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Volume 91 No. 5 May 2008

�Geriatric Neurology

157VOLUME 91 NO. 5 MAY 2008

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The Warren Alpert Medical School ofBrown UniversityEli Y. Adashi, MD, Dean of Medicine& Biological Science

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Quality Partners of Rhode IslandRichard W. Besdine, MD, ChiefMedical Officer

Rhode Island Medical SocietyNick Tsiongas, MD, MPH, President

EDITORIAL STAFFJoseph H. Friedman, MD

Editor-in-ChiefJoan M. Retsinas, PhD

Managing EditorStanley M. Aronson, MD, MPH

Editor Emeritus

EDITORIAL BOARDStanley M. Aronson, MD, MPHJay S. Buechner, PhDJohn J. Cronan, MDJames P. Crowley, MDEdward R. Feller, MDJohn P. Fulton, PhDPeter A. Hollmann, MDSharon L. Marable, MD, MPHAnthony E. Mega, MDMarguerite A. Neill, MDFrank J. Schaberg, Jr., MDLawrence W. Vernaglia, JD, MPHNewell E. Warde, PhD

OFFICERSNick Tsiongas, MD, MPH

PresidentDiane R. Siedlecki, MD

President-ElectVera A. DePalo, MD

Vice PresidentMargaret A. Sun, MD

SecretaryMark S. Ridlen, MD

TreasurerBarry Wall, MD

Immediate Past President

DISTRICT & COUNTY PRESIDENTSGeoffrey R. Hamilton, MD

Bristol County Medical SocietyHerbert J. Brennan, DO

Kent County Medical SocietyRafael E. Padilla, MD

Pawtucket Medical AssociationPatrick J. Sweeney, MD, MPH, PhD

Providence Medical AssociationNitin S. Damle, MD

Washington County Medical SocietyJacques L. Bonnet-Eymard, MD

Woonsocket District Medical Society

RHODE ISLANDPUBLICATION OF THE RHODE ISLAND MEDICAL SOCIETY

Medicine � Health VOLUME 91 NO. 5 May 2008

COMMENTARIES126 Introduction to Geriatric Neurology Issue

Joseph H. Friedman, MD

126 Some Thoughts On Ethical Guidelines for the Neurology-Impaired ElderlyStanley M. Aronson, MD

CONTRIBUTIONSSPECIAL ISSUE: Geriatric Neurology

129 Aging of the Human Nervous System: What Do We Know?Richard W. Besdine, MD, FACP, AGSF, and Difu Wu

132 Mild Cognitive Impairment, Healthy Aging and Alzheimer’s DiseaseChuang-Kuo Wu, MD, PhD

134 Gait In the ElderlyJoseph H. Friedman, MD

136 Parkinson’s Disease In the ElderlyMarie-Hélène Saint-Hilaire, MD, FRCPC

138 Epilepsy In the ElderlyAmanda M. Diamond, MD, and Andrew S. Blum, MD, PhD

142 Peripheral Neurology: Speech Concerns In the ElderlyGeorge M. Sachs, MD, PhD

144 Sleep Disorders In the ElderlyJean K. Matheson, MD

146 Driving Safety Among Older AdultsMelissa M. Amick, PhD, and Brian R. Ott, MS

148 Geriatric Neurorehabilitation In the New MilleniumStephen T. Mernoff, MD

COLUMNS151 HEALTH BY NUMBERS – The Value Equation: Costs and Quality of Rhode

Island’s Health PlansBruce Cryan, MBA, MS

153 PUBLIC HEALTH BRIEFING – Rhode Island Leads In Regulating Office-BasedCosmetic SurgeryShaun Najarian

154 POINT OF VIEW – Creative and Sensory Therapies Enhance the Lives ofPeople With AlzheimersJohn Stoukides, MD

155 PHYSICIAN’S LEXICON – The Prefixes of the PastStanley M. Aronson, MD

155 Vital Statistics

156 May Heritage

Cover: “Red Blooms in Spring,” watercolor, byTheresa Aiello. Ms. Aiello, age 91, painted RedBlooms in Spring as part of the art program atthe Hope Alzheimer’s Center. She has been par-ticipating at the Center since 2004 and lives inNorth Providence.The Hope Alzheimer’s Center specializes in caringfor people with memory loss and helping familieskeep their loved ones living at home. For moreinformation on the center, contact Cyndi Forcier,phone 946-9220. www.hopealzheimerscenter.org

158MEDICINE & HEALTH/RHODE ISLAND

In this issue we grapple with the neu-rology of aging. Excepting pediatricians,we all deal with the elderly, and neuro-logical problems become, like all otherproblems, increasingly common. Manynon-neurologists are neurology-phobicand, because neurology used not to be atreatment oriented discipline, often tendto overlook neurologic problems, or elseconsider them part of the process of nor-mal aging (“once you’re 80 everyone hastremors or falls down once in a while”).In this issue we hopefully are “userfriendly,” and help you in your day today care of the elderly.

These articles are summaries of a daylong course on geriatric neurology givenin Providence on Nov 3, 2007.

– JOSEPH H. FRIEDMAN, MD

Disclosure of Financial InterestsJoseph Friedman, MD, Consultant: Acarta

Pharmacy, Ovation, Transoral; Grant ResearchSupport: Cephalon, Teva, Novartis, Boehringer-Ingelheim, Sepracor, Glaxo; Speakers’ Bureau:Astra Zeneca, Teva,Novartis, Boehringer-Ingelheim,GlaxoAcadia, Sepracor, Glaxo Smith Kline

Some Thoughts On Ethical Guidelines for theNeurologically-impaired Elderly

�

Introduction To Geriatric Neurology Issue�

Commentaries

There is a widely accepted Inuit tale [denied as factual by manyanthropologists] that when their frail elders reach a point ofsenility requiring active nursing care, or when the food supplyof their community becomes perilously low, the demented el-ders are reverently placed upon an ice-flow to drift away intothe Eskimo equivalent of oblivion.

Two current social and geophysical realities have alteredthis aboriginal scenario: first, the intrusion of earnest ethicaldebate regarding the extent and merit of care for the elderlywho are neurologically impaired [such care ranging from thevery best technologically to utter abandonment]; and second,with the indisputable acceleration of global warming, there isthe diminution in the number and survivability of arctic ice-flows.

Age takes a toll. Mathematicians’ bestwork is behind them by their late twen-ties, if not earlier. Chess champions arenever elderly. No athletic records are heldby the elderly. Yet some people get wiser.The great novels are products of skillshoned with time, wisdom and experience,and, clearly a different sort of creativitythan required in mathematics and chess.Our brains start to lose neurons in ourtwenties. As an elderly Houston Merritt,MD, the author of one of the standardAmerican neurology texts, and a giant oftwentieth century neurology, once com-mented, “when it’s very quiet, I can some-times hear the splash a dying neuronmakes as it falls into the lacunar lakes inmy brain.”

In the 1930’s the great British neu-rologist, MacDonald Critchley, pub-lished a series of papers pointing out thataging produced, as a normal conse-quence, many of the features we identifyas pathological in Parkinson’s disease. Yetthese changes are not considered patho-logical. Perhaps they will be sometimesoon. These “normal” changes often pro-duce clinical challenges for physicianstrying to distinguish pathological from

normal. Essential tremor in an elderlyperson, for example, can be indistinguish-able from Parkinson’s disease, but theprognosis and treatments are quite dif-ferent. Gait disorders in an elderly per-son with widespread arthritis, multiplejoint replacements and diabetic neuropa-thy, are often impossible to accurately clas-sify, other than with the highly accuratedesignation, “multifactorial,” which may,or may not be helpful to all concerned.

In the course of my 25 years of prac-tice I have personally witnessed the as-tounding increase in the number of eld-erly and very elderly patients I treat. In arecent review I learned that I have caredfor 43 patients with Parkinson’s diseaseover the age of 90! Twenty years ago Iprobably hadn’t ever seen a PD patientof that advanced age. As we all know, thisis a mixed blessing. In Gulliver’s Travels,one of the lands Gulliver visits has a smallgroup of people who are immortal. Hethinks this a great miracle but is informedthat it is considered a curse because thepeople are not free of the diseases of ag-ing, thus becoming crippled and de-mented, and never granted the freedomof death.

There is little debate that a patient who is both elderly andneurologically impaired is effectively marginalized, certainly bycontemporary society – and sometimes even by members of thehealing community. Many patients with organic disabilities havea way of rehabilitating themselves; less so, though, for those withthe loss of neural or cognitive function, thus making the elderlywho are paralyzed or the elderly who are demented vulnerableto a more stringent standard of appraisal – outliers, perhaps – inthe calculus of care for the elderly American citizen.

In an appraisal of moral norms and moral hopes in thefield of geriatric neurology, there are substantially more ques-tions than there are confident answers or even flexible guide-lines. Geriatric neurology, particularly as it pertains to the de-mented elderly, presents an array of incorrigible problems


formally sensitized and educated in distinguishing between ademented elderly wandering the streets and an inebriated per-son wandering the same thoroughfares.

Years later the report was reviewed and our recommenda-tions [regarding the assignment of state hospital beds for thosewith advanced dementia] were accepted.

There is little debate now that organic dementia is morethan a medical problem; more than a public health problemdraining much of this nation’s health-care budget; and certaina compelling nightmare for those responsible for planning forthis nation’s future medical needs.

In 1950, 4% of this nation’s GNP was invested in healthcare. By 1994, this had risen to 14%; it is now verging upon20% - and rising. A decade ago this government was spending,on average, $14,000 per year on each elderly American underthe Medicare program; it is now approaching $20,000. And asthe nation – particularly its old-old segment – grows in number,and as the number of Americans burdened with dementia ofthe Alzheimer type increases exponentially, the cost of protect-ing and caring for these encumbered patients will grow at analarming rate. Finally these staggering costs will overweigh thehumanitarian beliefs in this country and—barring a medicalmiracle in discovering ways to prevent or cure the organicdementias—the rationing of care will become inevitable.

What may we expect in an elderly person with long-stand-ing dementia? At best a stabilization of the sense of personalidentity and cognitive awareness. Visitors, whose visits tend tobe brief and cursory, may comment that they experience nocommunication with their sick relatives, that they are no longerrecognized by the demented patients and view them as onestep removed from a persistent vegetative state. Nursing aideshowever, may attest to a measurable degree of communicationas well as preservation of some “selfness.” To exploit a com-mon cliché, is the cognitive cerebrum half-full or half-empty?

Despite the notable advances in biotechnology in recentyears, and despite some unsubstantiated claims that the progressof Alzheimer’s disease may be slowed by certain medications,the professional care of such patients remains largely in thedomain of care-takers such as nurses. Physicians continue toplay an identifiable role in initiating more aggressive therapiesfor such complications as decubitus ulcers, opportunistic in-fections and renal or cardiopulmonic failure. What guidelinesmay then be established for a disease that is both progressive—often relentlessly so—and without effective therapy?

Certainly, comfort measures, good nursing, pain-controlif needed and scrupulous attention to hygienic needs. Butbeyond these interventions, what then? Specifically, when inthe course of this ailment might discussions be begun about aregime confined to palliative care? Daniel Callahan has sug-gested three standards to observe in such trying situations:

1. No one should, in the modern world, have to live longerin the advanced stages of dementia than he or she wouldhave in a pre-technologic era.

2. The likely deterioration in individuals with advanced de-mentia should lead to a shift in the usual standard of treat-ment: that of stopping rather than continuing or extend-ing treatment.

readily distinguishable from the other sub-disciplines of medi-cine by the frequent use of such alien words as triage, eco-nomic utilitarianism, equity, social justice, palliation, hospicecare and the right to die; and the use of such needlessly inflam-matory words as euthanasia and “pulling-the-plug.”.

An ethical consideration - with any medical dilemma in-volving the elderly - certainly demands that a few basic ques-tions be confronted:

1. Does the patient’s age, per se, play any conscious role in deter-mining the employment [or abandonment] of any therapeu-tic intervention ? Should it ? Is there such a thing as age-relatedrationing of institutional care or medical interventions?

2. Rewording the question, does age-conscious triage be-come operative in elderly, neurologically impaired patientsmore so than in orthopedically-impaired elderly ?

3. Are stroke victims, beyond the age of 80, viewed differentlythan dementia victims of similar age ? Rewording this ques-tion: Does future prognosis play a role in determining presentmedical intervention ? Does the projected lifespan for thepatient influence the type and intensity of the therapy?

4. Concerning diagnostic or clinical interventions of doubt-ful merit, whose vision [or will] prevails ? The patient ? Thepatient’s assigned surrogate ? The family ? Clergy ? Physi-cian ? And when differences arise, whose decision prevails?

5. Are there occasions when palliation replaces active inter-vention ? And what are the thresholds when active inter-vention gets replaced?

6. When is the patient’s plea to die listened to and acted upon?

Before confronting these questions, let us consider a bit oflocal history as well as certain demographic verities. In 1984,Rhode Island’s General Assembly convened a task force as-signed with the problem of determining the extent to whichpatients with enduring dementia imperiled the health care sys-tem of the state. Our first task was to define the clinical state ofdementia [using standard criteria of duration of dementia, typeand extent of memory loss, degree of disorientation, loss of so-cial judgment, insight and the capacity to fulfill the minimaltasks of daily living]; then to survey each of the 107 registerednursing homes in the state to determine how many of theirresidents could be identified as organically demented; and fi-nally, to extrapolate from these data to estimate the total num-ber of the demented within the state [in hospitals, nursing homesand private homes]. We did not distinguish between dementiaof the Alzheimer’s type, multi-infarct dementia, Lewy bodydementia or other dementias such as the heritable ones as thoseassociated with Huntington’s disease.

We concluded, conservatively, that in 1985 there were about10,000 persons with dementia in a state population of aboutone million souls [about 1% of Rhode Island.] We presentedour data to the State legislature. The first response to our oralpresentation was: “Never heard of Alzheimer’s disease. What is it? Something new like AIDS?” Our demographic data—andour projections into the 21st Century—were treated with a com-bination of wry amusement and skepticism. And, accordingly,our recommendations were largely ignored—although the Statepolice did take to heart our recommendation that the police be


3. For the medical profession, there is as great an obligationto avoid a lingering, painful or degrading death as thereis to promote health and life.

Which avoids the crucial question: What clinical featuresforewarn the attending physician that the time has arrived towarrant cessation of interventions beyond those designed forcomfort, cleanliness, adequate hydration and freedom frompain ? The single criterion continues to be whether there isany residual sense of conscious selfness in the patient, any aware-ness—even if only episodic—of himself or herself. Just as fam-ily members, visiting briefly, may observe nothing beyond avegetative existence, so too with the physician visiting for a fewmoments. The insight into the patient’s sense of social identitymay come, more commonly, from the nurse or aide who feeds,bathes and interacts regularly with the patient.

The thoughts, wishes and religious observances of the fam-ily, the views of the concerned clergy must be listened to, butnot heeded blindly. The wishes of the patient remains para-mount, whether expressed in an advance directive, in a will orin any reliable document; or, expressed orally during his or hercurrent institutionalization.

• • •

We, as a society, must confront the realities of a near-fu-ture in which an avalanche of impaired elderly with dementiawill inundate the health care industry and its inpatient institu-tions, places ranging from nursing homes to tertiary care hos-pitals.

Our health-care professions are about to be overwhelmed by atragedy of human aging called dementia. We assemble earnest pa-pers such as this, make honorable declarations, admonish ourselvesfor alleged insensitivities, atone for our past negligences, pay obei-sance to the ethical standards of our vocations, recall oaths to do nowrong, identify the physical needs of the demented, decry the in-sensitive insurance industry for wanting to set explicit thresholds fortriage – but rarely do we listen to the secular voices of the demented.Let me end with a poem by Maya Angelou, a poem that says somuch more than any powerpoint presentation might convey:

The print is too small, distressing me.Wavering black things on the page.Wiggling polliwogs all about.I know its my age.I’ll have to give up reading.

The food is too rich, revolting me.I swallow it hot or force it down cold,And wait all day as it sits in my throat.Tired as I am, I know I’ve grown old.I’ll have to give up eating.

My children’s concerns are tiring me.They stand at my bed and move their lips,And I can’t hear one single word.I’d rather give up listening.

Life is too busy, wearying me.Questions and answers and heavy thought.I’ve subtracted and added and multiplied.And all of my figuring has come to naught.Today I’ll give up living.

– STANLEY M. ARONSON, MD

Disclosure of Financial InterestsStanley M. Aronson, MD, has no financial interests to disclose.

CORRESPONDENCEe-mail: [email protected]


Aging of the Human Nervous System: What Do We Know?Richard W. Besdine, MD, FACP, AGSF, and Difu Wu�

LEARNING OBJECTIVESDemonstrate the ability to identify and use in clinical care:

1. Nervous system changes with age2. Differences between pure aging in the NS and the ef-

fects of common diseases3. Age-related changes in key domains:

a. Cognition/Memoryb. Special sensesc. Strengthd. Balancee. Somatic sensation

OVERVIEW: AGING IN 21ST CENTURY AMERICAAmericans have gained >25 years of average life expectancy

during the 20th century, and there is no evidence of slowing in the21st. Although clinical and public health interventions have al-lowed gains in healthy life expectancy (average age of disabilityonset) to keep pace with the striking gains in longevity, the sheernumerical increases of older persons portend a burden of diseaseand disability that will overwhelm the social and financial capacityof our technologically advanced society to manage older persons’health and health care. And Congress dabbles by trying to trim 1-2% from the current Medicare growth rate. The tools to meetthese care needs are biomedical science coupled with strategicchanges in health care delivery for the very old and vulnerable;neurological problems of aging are a major contributor to themorbidity and healthcare costs for older adults.

NEUROLOGY OF AGINGThere is no greater fear among most Americans than loss of

brain function – whether the loss of the very persona from demen-tia (usually Alzheimer’s disease), the multiple other neurodegenerativeconditions that are increasingly common with age (e.g., Parkinson’sdisease, ALS) or the sudden devastation of stroke.

WHAT IS OBLIGATORY WITH AGING?As we age, many neurological disorders become common. What

are the changes occurring in the nervous system that are inevitablewith age in the healthiest adults, even those who exhibit all knownrisk-reducing behaviors? Using the term Pure Aging Syndromemakes clear that no disease, environmental, life style or behavioralrisk factor plays a role in the change. These are brain functionchanges that are inevitable, irreversible with current technology, andwhile mostly decremental, do not cause symptoms on their own.Although there is much in the literature about decrease in brain sizeand weight with age, secular trends of increasing size of humansmake such conclusions from cross-sectional data hazardous. In ad-dition, only in the past 50 years have large numbers of healthy adultssurvived into old age. Accordingly, great caution should be takenwhen concluding that brain shrinkage is due to age alone.

A useful concept is “homeostenosis,” the progressive restric-tion of physiologic reserve capacity in organ systems as a conse-

quence of the pure aging syndrome. The resulting reduced ca-pacity to maintain homeostasis during stress often leads to earlyand unexpected decompensation under a variety of mild homeo-static perturbations. It is the superimposition of acute illness ordrug toxicity upon the pure aging syndrome that results in“homeostenotic” organ crises. There is no better example than theextraordinary vulnerability of elders to delirium when they arestricken with many illnesses or adverse drug effects.

Once the changes of pure aging are understood, the im-pact, evaluation and management of superimposed disease inolder adults can be appreciated. The complexity of these in-teractions of disease and aging defines the field of geriatrics.Nowhere are these interactions more complex and potentiallyconfusing for the clinician than in the nervous system.

I. COGNITIONA. Attention – There is a mild decline in overall accu-

racy, beginning in the 60s that progresses slowly, but sustainedattention very good in healthy older adults. Older adults aremore easily distracted, especially if irrelevant information ispresented concurrent with important material.

Clinical point: When giving crucial information to olderpatients, stick to core data, repeat it and write it down.

B. Learning and memory1. Sensory memory is the earliest stage (visual, auditory,

tactile); it is inherently unstable and decays rapidly.There is no age-related change.

2. Primary (short-term) memory is the stage after trans-fer of sensory memory. There is no loss with age.

3. Secondary (long-term) memory persists for hours, daysand years. There is a decline with age, mostly in freerecall; recognition is well preserved. The universal tem-porary decline in the ability to retrieve names generallybegins early in middle age, and worsens over time. Thelost name is almost always retrieved soon after the epi-sode. This phenomenon is not predictive of anyneurodegenerative disorder (e.g., Alzheimer’s disease).

4. Encoding strategies help retrieval - mnemonics, men-tal hierarchies, clusters—but they are used less by olderpersons. Training gives long-lasting improvements.

5. Distraction interferes with learning more in olderpersons than in young.

6. Clinical point: Give instructions directly and simply,encourage encoding strategies, refer to reputablememory training.

C. Language – Vocabulary increases well into the 50sand 60s, and shows no decline with age in those who continueto be engaged in complex language use. Similarly, syntacticskills – the ability to combine words in meaningful sequences –show no decline with pure aging.


D. Intelligence, as measured by the Wechsler Adult In-telligence Scale, declines with age, but the biggest, earliest losseswere reported in flawed studies. Cohort differences under-mined these cross sectional studies, causing selection bias re-garding education, gender, race, occupation and income. Sum-mary scores of “intelligence” per se are less useful in adults.Measuring specific intellectual functions has become usual.

1. Crystallized intelligence (learning and experience) re-mains stable or improves with age until the late 70sor beyond, especially in those who remain healthyand engaged in cognitively demanding activities.

2. Fluid intelligence (problem-solving with novel ma-terial requiring complex relations) declines rapidlyafter adolescence.

3. Perceptual motor skills (timed tasks) decline with age.

Special SensesE. Vision1. Pure aging includes decline in accommodation (pres-

byopia), low-contrast acuity, glare tolerance, adapta-tion, color discrimination and attentional visual field.Changes occur in components of the eye itself andin central processing. These numerous changes af-fect reading, balance and driving, but compensatoryglasses and behavior can maintain safety.

2. The common eye diseases in old age (glaucoma, macu-lar degeneration, cataracts, diabetic retinopathy) aresuperimposed upon these pure aging changes.

F. Hearing1. Conductive and sensory hearing losses (presbycusis)

occur with age; losses are primarily high tones, mak-ing consonants in speech difficult to discriminate.

2. Although impairment is defined as an auditory thresholdgreater than 25 decibels, the nearly half of Americans >80 who don’t reach the clinical threshold of 25 decibelsstill have diminution in acuity – pure aging effects.

3. Consequences include difficulty in localizing soundand understanding speech, usually accompanied byhypersensitivity to loudness.

4. Common diseases in old age are superimposed uponthese changes, often resulting in worsening hearingimpairment (e.g., cerumen impaction, otosclerosis,8th N drug toxicity).

G. Taste buds don’t diminish, but salt detection declines;perception of sweet is unchanged, and bitter is exaggerated. Thevolume and quality of saliva diminish. All changes combine tomake eating less interesting. These aging changes are com-pounded by common diseases (periodontal) and medications.

H. Smell acuity declines with aging. There is atrophyof olfactory bulb neurons, and central processing is altered.The result is decreased perception and less interest in food.Again, these age-related changes are compounded by disease(e.g., AD and PD have diminution and alteration of smell).

II. STRENGTHA. Muscle – Disuse and disease, as in many systems, are

major confounders of age effect.1. Age-related changes include loss of muscle mass,

though strength loss can be relatively preserved byexercise. Reduction in muscle fiber size occurs pri-marily in Type II (‘fast’) fibers, which are highlyanaerobic; Type I (‘slow’) fibers, which are aerobic,tend to retain their size during aging.

2. Muscle wasting in frail older persons, a disorderknown as sarcopenia, leads to higher incidence offalls and fractures and functional decline.

B. Spinal reflex changes include decline in amplitudeof the spinal stretch reflex with normal aging, due in part tostiffness of tendons.

D. Motor cortex changes with age include decrease inthe number of neurons and synapses; one hypothesis is thatdisuse atrophy occurs, arguing for a “use it or lose it” construct.

E. Basal Ganglia – Age-related changes in the striatuminclude decline in dopamine D1 receptor density in the cau-date and putamen. Age-related loss of dopamine neurotrans-mission may play a role in vulnerability of older adults to ex-trapyramidal disorders. In the substantia nigra, pigmentedneurons drop out; their loss is associated with motor dysfunc-tion, including bradykinesia, stooped posture and gait distur-bance. These aging changes mimic parkinsonian features, andmay account for the increase in prevalence of PD with age.

III. BALANCEBalance function declines with increasing age, but is rarely

the sole cause of falls in older persons. Strength, cerebellar integ-rity, vestibulo-cochlear function, hearing and vision all play a rolein maintaining balance. Degeneration of the otoconia (granulesof the otolith) is a mechanism for vestibule-cochlear decline withaging. Many diseases affect the vestibular portion of the 8th N,and it is also sensitive to drugs. Finally, proprioception also con-tributes to maintenance of balance. Muscle spindle and mechano-receptor functions decline with pure aging, further interferingwith balance. Clinical position sense does not decline with age.

IV. SENSATIONA. Pain – Typically painful disorders are often less or not

at all painful in elders.

1. Some cortical processing capacity for pain sensation ap-pears to decline with age. When functional magneticresonance imaging (fMRI) was used to compare corticalnociceptive responses to painful contact heat in healthyyoung and older subjects, older subjects had significantlysmaller pain-related fMRI responses in anterior insula(aINS), primary somatosensory cortex (S1), and supple-mentary motor area. Gray matter volumes in S1 and aINSwere significantly smaller in the elders, suggesting reducedprocessing capacity in these regions, perhaps accountingfor smaller pain-related fMRI responses.


2. Endogenous pain inhibition is reduced with aging. Opioid-mediated endogenous analgesic systems are particularlysusceptible to functional decline with aging. Additionally,older age is associated with reduced beta-endorphin levels.

3. Some pain thresholds show age-related changes. Al-though sensitivity to heat pain is decreased with age(above), sensitivity to pressure pain is enhanced.

4. Both Substance P and calcitonin gene-related pep-tide (CGRP), major neuro-transmitters of primary af-ferent nociceptive fibers, are decreased with aging,likely reflecting reduction in density or function ofnociceptive nerves. The rate of CGRP axonal trans-port also decreases with advancing age.

B. Sensory nerves lose myelin selectively, perhaps pre-disposing to neuropathy. Vibration sensation perception di-minishes with aging, especially in the legs. Since position senseis carried in the same tracts as vibration, diminished vibratorysense should be followed up by position sense testing.

REFERENCES1. Beers MH (Ed). The Merck Manual of Geriatrics. 3th Ed. NJ: Merck & Co., Inc, 2006.2. Boeve B, McCormick J, et al. Neurol 2003;60:477-80.3. Borson S, Scanlan J, et al. Int J Geriatr Psychiatry 2000;15:1021-74. Burke SN, Barnes CA.. Nat Rev Neurosci 2006;7:30–405. Craft S, Cholerton B, Reger M. Aging and Cognition: What is Normal? In:

Hazzard WR, Blass JP, , et al, eds., Principles of Geriatric Medicine & Gerontol-ogy, 5th Ed. NY: McGraw-Hill, 2003:1370-1.

6. Galban CJ, Maderwald S, et al. J Gerontol A Biol Sci Med Sci 2007;62:453-8.7. Gibson SJ, Farrell M. Clin J Pain 2004 ;20:227-39.8. Keuker JI, Luiten PG, Fuchs E. Neurobiol Aging 2003;24:157–65.9. Kirkwood TB. Cell 2005;120:437–47.10. Lindeboom J, Weinstein H. Eur J Pharmacol. 2004;490:83-6.11. Mattay VS, Fera F, et al. Neurol 2002;58:630-5.12. Mrak RE, Griffin ST, Graham DI. J Neuropathol Exp Neurol 1997;56:1269–75.13. Nanda A, Besdine RW. Dizziness. In. Halter JB et al, editors. Principles of

Geriatric Medicine and Gerontology. 6th Ed. New York. McGraw-Hill; 2003.14. Nusbaum AO, Tang CY, et al.. AJNR Am J Neuroradiol 2001;22:136-42.15. Peters R. Postgrad Med J 2006;82:84–8.16. Quiton RL, Roys SR, et al. Ann N Y Acad Sci 2007;1097:175-8.17. Raz N. The ageing brain: structural changes and their implications for cogni-

tive ageing. In New Frontiers in Cognitive Ageing, Dixon R, Backman L, NilssonL (eds). Oxford University Press: Oxford, 2004; 115–34.

18. Resnick SM, Pham DL, et al. J Neurosci 2003;23:3295–301.19. Rodríguez-Aranda C. Clin Neuropsychol 2003;17:203-15.20. Shaffer SW, Harrison AL. Phys Ther 2007;87:193-207. Epub 2007 Jan 23. Review.21. Smith CD, Chebrolu H, et al. Neurobiol Aging 2007;28:1075-87. Epub

2006 Jun 13.22. Smith DE, Rapp PR, et al. J Neurosci 2004;24:4373–41.23. Tumeh PC, Alavi A, et al.. Semin Nucl Med 2007;37:69-87. Review.24. Ward NS. Ageing Res Rev 2006;5:239-54. Epub 2006 Aug 14. Review.

Richard W. Besdine, MD, FACP, AGSF, is Professor of Medicine,GreerProfessor of Geriatric Medicine, Director, Division of Geriatrics (Medi-cine), and Director, Center for Gerontology and Healthcare Research, atThe Warren Alpert Medical School of Brown University.

Difu Wu is a student at The Warren Alpert Medical Schoolof Brown University.

Disclosure of Financial InterestRichard W. Besdine, MD, FACp, AGSF. Grant Research

Support: Donald W. Reynolds FoundationDifu Wu has no financial interests to disclose.

CORRESPONDENCERichard W. Besdine, MD, FACP, AGSFCenter for Gerontology and Healthcare ResearchThe Warren Alpert Medical School of Brown University2 Stimson AvenueBox G-STProvidence, Rhode Island 02912e-mail: [email protected]

8SOW-RI-GERIATRICS-053008

The Mini-Cog assessment instrument combines an uncued 3-item recall test with a clock-drawing test (CDT)that serves as a recall distractor. The Mini-Cog can be administered in about 3 min, requires no special equipment, and isrelatively uninfluenced by level of education or language differences.

ADMINISTRATION – The test is administered as follows:1. Make sure you have the patient’s attention. Instruct the patient to listen carefully to and remember 3 unrelated words

and then to repeat the words back to you (to be sure the patient heard them).2. Instruct the patient to draw the face of a clock, either on a blank sheet of paper, or on a sheet with the clock circle

already drawn on the page. After the patient puts the numbers on the clock face, ask him or her to draw the handsof the clock to read a specific time (11:10 and 8:20 are most commonly used and more sensitive than someothers). These instructions can be repeated, but no additional instructions should be given. If the patient cannotcomplete the CDT in =3 min, move on to the next step.

3. Ask the patient to repeat the 3 previously presented words.

SCORING – Give 1 point for each recalled word after the CDT distractor. Score 0–3 for recall.Give 2 points for a normal CDT, and 0 points for an abnormal CDT. The CDT is considered normal if all numbers are

depicted, once each, in the correct sequence and position, and the hands readably display the requested time.Add the recall and CDT scores together to get the Mini-Cog Score:

• 0–2 indicates positive screen for dementia.• 3–5 indicates negative screen for dementia.

THE ANALYSES UPON WHICH THIS PUBLICATION IS BASED wereperformed under Contract Number 500-02-RI02, funded bythe Centers for Medicare & Medicaid Services, an agency ofthe U.S. Department of Health and Human Services. The con-tent of this publication does not necessarily reflect the viewsor policies of the Department of Health and Human Services,nor does mention of trade names, commercial products, ororganizations imply endorsement by the U.S. Government.The author assumes full responsibility for the accuracy andcompleteness of the ideas presented.


Mild Cognitive Impairment, Healthy Aging andAlzheimer’s Disease

Chuang-Kuo Wu, MD, PhD

�As predicted in 1976, the growth ofthe elderly population has resulted in atremendous increase in Alzheimer’s dis-ease (AD).1 In 2007, there were prob-ably more than 5 million Americans suf-fering from AD.2 The major advances in-clude more clinical tools to diagnose ADand several medications approved by theFDA for treatment.

Our goals are:- Recognizing healthy, successful

aging of cognition and devel-oping strategies for primaryprevention

- Developing new disease modi-fying agents to alter the courseof AD.

- Defining mild cognitive im-pairment (MCI) as a diagnos-tic entity for early intervention.

HEALTHY AND SUCCESSFUL AGINGHealthy aging is defined by the lack

of a significant decline in physical andmental abilities.3 These people are sociallyactive and emotionally satisfied. One defi-nition of “successful aging” is that the eld-erly who perform in the upper end of adistribution of test scores are deemed suc-cessful.4 The effect of aging on cognitionis a hot topic. People older than 65 con-tinue to change through the rest of theirlives in different ways. A wide variety ofage-related phenomena have been de-scribed.5 Many studies have documentedvarious life styles leading to healthy or suc-cessful aging.3,4,5 Learning from these stud-ies, preventive strategies are postulated todelay the onset of dementia. Among them,education and participation in certain lei-sure activities are two areas which havedemonstrated benefit.6,7

From epidemiological data, Katzmanpointed out that elder people with pooror no education have an increased risk ofdeveloping dementia6 compared to thosebetter educated. It is postulated that edu-cation might generate brain “reserve”,which can compensate the initial presen-

tation of dementia.7 In a five-year, pro-spective, longitudinal study of healthy eld-erly adults (above 75 years of age),Verghese et al. reported that the elderly(n=345; age 78.9) who participated inthree kinds of cognitive activities and onephysical activity had a reduced risk of de-mentia.8 Reading, playing board gamesand playing musical instruments aredeemed beneficial cognitive activities;dancing is the only physical activity iden-tified that is associated with a lower risk ofdementia. They also observed that subjects(n=124; age 79.7) who eventually devel-oped dementia (the majority of them hadAD) were older individuals with lower lev-els of education (less than 12 grades) andrelatively lower test scores (on two memorytests) at baseline. This landmark study pro-vides evidence of risk-reducing activitiesto delay the onset of AD.

MILD COGNITIVE IMPAIRMENT(MCI)

The term, mild cognitive impair-ment (MCI), was initially used as stage 3of Reisberg’s Global Deterioration Scale(GDS) in the staging of AD.9 Petersen,et al then proposed MCI as a diagnosticentity for the transition between normalaging and AD.10 In 2001, the AmericanAcademy of Neurology published itsguideline for the diagnosis of MCI.11 Thecriteria include 1) memory complaint 2)objective memory impairment 3) normalgeneral cognitive function 4) intactADLs 5) not demented by DSM IV cri-teria. The clinical tools recommendedaccording to the guideline are the Mini-Mental State Examination (MMSE), theClinical Dementia Rating (CDR) scale

and other neuropsychological batteries,to be used as screening tests.

Clinicians encounter several pitfallswhen diagnosing MCI. It is caused by avariety of pathologies other than just AD.To predict that a MCI patient is in the pro-dromal stage of AD, we have to considerother differential diagnoses. In the elderly,the two most common conditions whichcan mimic MCI are depression and stroke.Patients with late-life depression commonlycomplain of memory and cognitive prob-lems. By sophisticated neuropsychologicaltesting, their cognitive functions are usu-ally within normal limits and subjectivememory problem can be restored by ad-equate treatment. Older adults who had asudden onset of cognitive impairment of-ten had a cerebrovascular event. Recentstudies have reported that patients with theamnesic-type of MCI often do have under-lying AD pathology. For example, Morrishas proposed that since so many amnesicMCI patients have AD pathology the di-agnostic criteria need to be revised.12 In con-trast, the Mayo clinic reported that 71%of amnesic MCI brains displayed the ADpathology but that 29% of them showednon-AD pathologies, which particularlyaffected the mesial temporal regions.13

Neurochemical studies of MCI brainshave demonstrated upregulation of the syn-thetic cholinergic enzyme, suggesting nodecline of acetylcholine in MCI brains. Thisfits with the observation that all publishedclinical trials to date of cholinesterase in-hibitors show no significant efficacy.14 Cur-rently the FDA approves no treatment forMCI because all the data indicate a clearlack of benefit.

ALZHEIMER’S DISEASEIn the near future, we will witness

major advances in the treatment of AD,such as the introduction of disease-modify-ing agents. None are yet available, however.The first crucial step in treating AD patientsis to classify the clinical stage. (Figure 1).Today only symptomatic treatments areavailable for AD, including cholinesteraseinhibitors (CEIs) and a NMDA receptor

Currently the FDAapproves no

treatment for MCIbecause all the dataindicate a clear lack

of benefit.


antagonist. Since 1992,the FDA has ap-proved five medications to treat Alzheimer’sdisease. We no longer prescribe tacrine be-cause of significant side effects. Donepezil,rivastigmine and galantamine are approvedfor treating mild to moderate stage of AD.In 2004, memantine was approved for themoderate to severe stage of AD. In 2007,donepezil won approval for the severe stageof AD; rivastigmine has a skin patch ap-proved to treat the mild to moderate AD.

In the clinic, patients can be evaluatedsimply by the MMSE as the first assessmenttool. Many clinical scales have been devel-oped to replace the MMSE. However, theMMSE yields a significant amount of datafor interpretation. The first step in establish-ing the diagnosis of AD is to rule out othermimicking conditions, both treatable anduntreatable. For example, a typical, highschool-educated, 70 year-old patient comesin with a caregiver complaining of a memoryproblem, and scores 24/30. Based on theeducation level and age, the score suggests ahigh probability of dementia. Using a set oflaboratory tests and a brain scan (CT orMRI), a clinician can confidently rule outother causes and establish AD as the causeof dementia (two-step approach). Scores of12 to 23 are usually considered the mild tomoderate stage of AD, as defined in the cho-linesterase inhibitor clinical trials. A score be-low 15 indicates the moderate to severerange. However, there is no consensus aboutthe defined score for the moderate stage ofAD. The Alzheimer’s Disease CooperativeStudy (ADCS) group reported that the abil-ity to perform a wide range of instrumentaland basic ADLs correlates well with theMMSE scores of AD patients. A significantdrop on the MMSE to below 20 correlates

with a significant decline in ADLs from themild to moderate stage; likewise, a score be-low 15 indicates a further decline towardthe moderate to severe stage.

Treating the cognitive problems of ADpatients is limited to those approved by theFDA. When AD patients receive treat-ment, we should monitor progress of dis-ease with the MMSE. A 4-point declinewithin a short period (6 months) deservesrepeated clinical evaluation for other medi-cal conditions which can worsen cognition.The combination of CEIs and memantineis recommended for treating the moderateto severe AD patient if side effects are toler-able. Memantine is not approved for mildAD or MCI diagnosis.

REFERENCES1. Katzman R. Arch Neurol 1976; 33:217-8.2. Hebert LE, Scherr PA, et al. Arch Neurol

2003;60:1119-22.3. Reichstadt J, Depp CA, et al. Am J Geriatr Psy-

chiatry 2007;15:194-201.4. Fritsch T, McKee MJ, et al. t Gerontologist

2007;47:307-22.

5. Baltes PB, Baltes MM. Psychological perspectiveson successful aging. In: Baltes PB, Baltes MM.Editors. Successful aging. Cambridge UniversityPress; 1990:1-34.

6. Katzman R. Neurol 1993;43:13-20.7. Zhang M, Katzman R, Dalmon D Ann Neurol

1990;27:428-37.8. Verghese J, Lipton RB, et al. NEJM

2003;348:2508-16.9. Flicker C, Ferris SH, Reisberg B. Neurol

1991;41:1006-9.10. Petersen RG, Smith GE, et al. Arch Neurol 1999;

56:303-8.11. Petersen RG, Stevens JC, et al. Neurol 2001;

56:1133-42.12. Morris JC. Arch Neurol 2006; 63:15-6.13. Jicha GA, Parisi JE, et al. Arch Neurol 2006;

63:674-81.14. DeKosky ST, Ikonomovic MD, et al. Ann Neurol

2002; 51:145-55.15. Jelio V, Kivipelto M, Winblad B. JNNP 2006;

77:429-38.

Chuang-Kuo Wu, MD, PhD, is AssociateDirector, Clinical core of NIA-Funded ADC Cog-nitive Neurology and Alzheimer’s Disease Center,and Assistant Professor, Department of Neurology,Northwestern University Feinberg School of Medi-cine. Until July 31, 2007, Dr.Wu was an assistantprofessor of clinical neurosciences, The WarrenAlpert Medical School of Brown University, andassociate director of the Alzheimer’s disease andmemory disorders center of Rhode Island Hospital.

Disclosure of Financial InterestsThe author has no financial inter-

ests to disclose.

CORRESPONDENCEChuang-Kuo Wu, MD, PhDNorthwestern Memorial Hospital675 North St. Clair StreetGalter 20-100Chicago, IL 60611phone: 312-695-9627e-mail: [email protected]

Figure 1.


Gait In the ElderlyJoseph H. Friedman, MD�

A number of impressive statistics onfalls in the elderly are routinely cited inreview articles.1,2 Interestingly, none ofthem are recent.1,2 My guess is that as thepopulation ages, these numbers willworsen. In addition, abandonment of the“chemical straitjacket” routinely used forthe demented twenty years ago whichrendered poor walkers into non-walkersmay have increased fall frequency.

For example, data from 1988, stillcited in recent articles, 1,2 state that one thirdof people over age 65 fall each year, andfor half of them this is an ongoing prob-lem.3,4 Ten percent of these falls results insignificant morbidity (data from early1990s).5 Presumably these numbers in-crease with age. Falls are the fifth most com-mon cause of death in the elderly. Only25% of patients who suffer hip fracturesregain their former level of function. Andfalls frequently induce a fear of falling,which itself contributes to the problem.

Impairment in mobility affects 14%of those between 65 and 74 but half of thoseover 85.6 This impairment occurs for anumber of reasons, including brainchanges, both normal and pathological, aswell as changes in muscles and the sensoryorgans (eyes, vestibular apparatus, periph-eral nerves). Normal aging produces physi-cal changes that overlap with the signs ofParkinson’s disease, except for tremor.7

The clinical importance of gait can-not be overestimated. In a nursing homeevaluation, every single patient seen bythis author had a significant gait abnor-mality. Of course, in many cases, that waswhy they were not living at home.

It is my hypothesis that gait abnormali-ties are often not identified by doctors becauseit has not been part of their training. In theoutpatient setting, doctors, for efficiency, tendto see patients in examining rooms, partiallyundressed, seated on the examining table. Inthe hospital, it is difficult to get patients out ofbed or off their stretchers, and a lot more dif-ficult to get them back on them, especially inthe emergency department where the stretch-ers are quite high.

The basic problem is the lack of alanguage for describing and classifyinggait problems.

Gait disorders may occur for a num-ber of reasons, and most are non-neuro-logical in origin. Joint pain, muscle weak-ness, deformities, blindness, vestibulardysfunction, psychological factors, poorlyfitting shoes (especially in those withedema and bunions) and deconditioningall may play a role. Pain, shoes, feet andblindness should be asked about.

Weakness and numbness may be pe-ripheral nervous system contributions to gaitdisorders or may result from central ner-vous disorders. Increased tone, ataxia, weak-ness and abnormal “motor programs” arecentral nervous system abnormalities.

COMPONENTS OF GAIT1. Ability to stand

The patient should be asked to standwithout using her arms. They may be keptfolded across the chest or put into a pray-ing position. If the patient cannot do this,she should try to stand pushing off fromthe armrests on her chair. A note shouldbe made of how easily the patient was ableto do this or whether the doctor neededto help.

2. PosturePatients with an abnormal posture will

generally have kyphosis, scoliosis or somedegree of both. Rare patients will have ahyperlordotic posture from lower spinalmuscle weakness or dystonia. Kyphosis isusually idiopathic, but may be due to com-pression fractures, Parkinson’s disease,spondylitis. The curvature may occur any-where from the lumbar spine up. In PD,for example, patients may have highly vari-able degrees of flexion in the thorax or theneck or both.

3. BaseThe normal width of foot placement

is considered the width of the shoulders.The base should be noted both whenstanding and when walking. Ataxic gaits,due to sensory problems, cerebellar or ves-tibular dysfunction will cause the base toincrease or to vary. Spastic problems, dueto corticospinal tract dysfunction, as seenin spastic forms of cerebral palsy, stroke orcervical myelopathies, cause a narrowing

of the base, with scissoring, the crossing offeet, being an extreme example, most of-ten seen in people who were born with aform of cerebral palsy.

4. Stride and foot strikeThe stride length depends on the speed

of gait as well as the height of the subject. Ex-cessively long strides are rare, and produce a“loping” quality, whereas short steps are com-mon, especially in the elderly, seen in parkin-sonian disorders as well as “fear of falling” inwhich people walk as if they are on ice. Inasymmetric disorders, such as Parkinson’s dis-ease, one stride length may be shorter thanthe other, producing a limping gait.

In normal gait the heel strikes theground first, but in Parkinsonian disor-ders there is a flat foot strike. In spasticdisorders the ball of the foot hits first.These different foot strike patterns maybe reflected in wear on the shoes.

5. ArmswingThis is not important in the biophysics

of walking but is extremely important in mak-ing diagnoses. The armswing is reduced inParkinsonism, for example, generally morereduced on the worse side, possibly absent onone side and normal on the other. Armswingis absent after a stroke. In patients with ataxicsyndromes the arms are often abducted, as ifsupplying extra balance. Tremor may be seenonly during walking in Parkinson’s disease,whereas tremor is not seen during walking inpatients with essential tremor. In choreiformdisorders, such as generalized tardive dyski-nesia or Huntington’s disease, the armswing isoften excessive. It may also be excessive in somedisorders in which there is a short stride, as ifto compensate.

6. Turning A normal turn requires a pivot. One

foot is kept on the ground and rotationoccurs on the ball of that foot. In Parkin-sonism the patient turns “en bloc,” in onepiece, using two or more steps. Some-times the patient turns in a large circle,as if making a U-turn. Turning fre-quently causes loss of balance, in all gaitdisorders.


7. Pull test This test, like the Romberg, tests bal-

ance. The pull test is performed by in-forming the patient that you are goingto pull him off balance and that heshould try to keep from falling, taking asfew steps as possible. It is important topull hard enough to make the patienttake a step or two. Taking more than threesteps is considered abnormal, indicativeof a balance problem.

INTERPRETATIONSAs in most aspects of the neurologi-

cal examination, the cardinal feature issymmetry. When the stride length is dif-ferent on the two sides, we usually see alimp or scuffing of one foot. Asymmetricarmswing is obvious, once you look forit. When the gait looks abnormal, try tobreak it down into the component partslisted above to see if the abnormality canbe localized. When the patient shiftsweight suddenly, it is often an indicationof joint pain, and this should be inquiredabout.

Examples:1. Foot drop: the affected foot is

lifted higher than normal and then theball of the foot is dropped onto theground or is thrown forward andslapped.

2. Hip weakness produces a wad-dling gait. To lift the swing leg and moveit forward, weight is shifted to the sup-porting leg by tilting the pelvis up on theswing side. This is usually a symmetricproblem so that the hip swivels up anddown.

3. Parkinsonism is one of the mostcommon gait in the elderly, and not al-ways pathological.7 The posture is stooped,the stride length is reduced and there is atendency for a flat foot strike. Armswingis reduced. Turning is without a pivot andbalance is impaired on the pull test. As thegait deteriorates, the patient will often beflexed at the knees, which causes a majorincrease in weightbearing problem for thethigh muscles.

4. Ataxic: this may be from cerebel-lar dysfunction, vestibular impairment orsensory denervation. The stance may benormal or wide, but the gait is irregularand often lurching, with a tendency toveer to one side, or to either side, withincreased problems on turning.

Armswing is normal, but sometimes re-duced when the arms are abducted, act-ing like a balancing rod used for tight-rope walkers. Alcohol intoxication pro-duces an ataxic gait.

5. Post stroke: armswing is lost on theaffected side, and the arm is often flexedat the elbow, and wrist, while adducted atthe shoulder. The affected leg is typicallykept in extension, as if acting like a crutch.The leg is moved in a circular fashion asthe knee is not bent. The ball of the footusually hits the ground first.

6. Spastic: this is seen in children oradults with cereral palsy, but also withother bilateral corticospinal dysfunction,typically after bilateral strokes, multiplesclerosis or cervical myelopathy, as occurswith cervical spondylosis. The posture isnormal. The legs are stif and do not bendnormally at the knees. The base narrows.Because the legs are kept extended, theball of the foot usually hits the groundfirst. Stride length is reduced. Armswingchanges are determined by the level ofthe lesions so that in brain diseases, thearmswing is reduced. When the spasticgait arises from a cervical process, it mayor may not be reduced.

7. Cautious gait. This is the gait ofsomeone fearful of falling, which, para-doxically, may increase the risk. The pa-tient walks as if on ice, with slow, deliber-ate steps, placing each foot flatly and sol-idly on the ground before advancing.

8. Astasia abasia. This is an old term,meaning “can’t sit, can’t stand,” used forconversion disorder, or psychogenic gaitdisorders. Although these are consideredrare in the elderly, they do occur. Gener-ally the gait is extremely bizarre, and,unlike other gait disorders where thebody tries to minimize risk and effort,these generally maximize effort and pro-duce convoluted postures, standing onone leg and other unusual stresses to thebalance systems. Contrary to popularbelief, these disorders are not generallyassociated with “belle indifference” orwith the absence of falls or injuries.

REFERENCES1. Moylan CK, Binder EF. Fall in older adults. Am J

Med 2007;120:493-7.2. Tinetti ME. Preventing falls in elderly persons.

NEJM 2003;348:42-9.3. Tinetti ME, Speechley M, Ginter SF. Risk factors

for falls among elderly persons living in the com-munity. NEJM 1988;319:1701-7.

4. Nevitt MC, Cummings SR, et al. Risk factors forrecurrent nonsyncopal falls. JAMA1989;261:2663-8

5. Nevitt MC, Cummings SR, Hudes ES. Risk factorsfor injurious fall. J Gerontol 1991;46:M164-M170.

6. Odenheimer G, Funkenstein H, et al. Compari-son of neurologic changes in “successful aging”persons vs the total aging population. Arch Neurol1994;41:573-80.

7. Critchley M. Neurolocial changes in the aged. ResPubl Assoc Res Nerv Mental Dis 1956;35:198-223.

ht tp : / /medl ib .med.utah.edu/n e u r o l o g i c e x a m / h t m l /gait_abnormal.html contains infor-mation on gait including video ex-amples of a doctor simulating andexplaining common gait disorders aswell as including examples. Otherwebsites cited include informationabout gait, both for health profes-sional and patient.

Joseph H. Friedman, MD, is execu-tive editor of Medicine & Health/RhodeIsland.

Disclosure of Financial InterestsJoseph Friedman, MD, Consultant:

Acarta Pharmacy, Ovation, Transoral;Grant Research Support: Cephalon, Teva,Novartis, Boehringer-Ingelheim, Sepracor,Glaxo; Speakers’ Bureau: Astra Zeneca,Teva,Novartis, Boehringer-Ingelheim,GlaxoAcadia, Sepracor, Glaxo Smith Kline

CORRESPONDENCEJoseph H. Friedman, MDNeurohealth227 Centreville Rd.Warwick, RI 02886e-mail: [email protected]

Two office suites on bottomFloor of medical building.

One @ 600 SF & one@ 900 SF. Can be combinedinto a single unit. Park Ave.,Cranston, minutes from RT95 & RT 10. Ample Parking.

Perfect for a specialist orallied health professional-internist on the 2nd floor.

Contact Sharli at401-275-0700

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Parkinson’s Disease In the ElderlyMarie-Hélène Saint-Hilaire, MD, FRCPC�

An 82 year old woman was ad-mitted to a rehabilitation hospi-tal after sustaining a pelvic frac-ture. She had a past history of os-teoporosis and chronic lower backpain treated with epidural ste-roids. For the past two years shehad had several falls associatedwith fractures. She also reporteddrooling, difficulties swallowing,gait shuffling and freezing, andtremor in the left hand, more atrest than with action. She had nocognitive impairment. She wasstarted on a small dose of levodopa/carbidopa 25/100, a half threetimes a day. She responded verywell, stopped drooling, and hadimprovement in swallowing, gait,and tremor. However, her balanceremained impaired and she con-tinued to need a walker.

This case exemplifies some of the chal-lenges in diagnosing and treating elderlypatients with Parkinson’s Disease (PD):1) concurrent medical conditions, such asarthritis, can affect mobility, and symptomscan overlap with the symptoms of PD, thusdelaying the diagnosis; 2) although treat-ment with levodopa is beneficial, it doesnot eliminate gait and balance problems,which are major causes of morbidity.

Age remains the single most impor-tant risk factor in PD. Although the av-erage age of onset of PD is around 60,the incidence rates consistently increasethrough age 85.1 Aging does appear todirectly influence the clinical expressionof PD, and late onset PD patients offerspecial challenges because of polyphar-macy, multiple pathology, and coexistingcognitive problems. This article will re-view the specific aspects of the clinicalpresentation, differential diagnosis andtreatment of PD and its complications inthe elderly population.

CLINICAL PRESENTATIONThe diagnosis of PD is based on the

history and the clinical examination. Itrequires the presence of two of the fol-lowing: rest tremor, bradykinesia or ri-

gidity. Asymmetry of physical findings isimportant to support the diagnosis, as isa good response to levodopa.

Several clinical features help to dis-tinguish idiopathic PD from other causesof parkinsonism. The presence of earlyfalls, a poor response to levodopa, sym-metry of signs at onset, or significant au-tonomic dysfunction should raise the sus-picion that the patient may not have id-iopathic PD.

In addition, significant cognitive de-cline and hallucinations, within one yearof onset of the parkinsonian signs is sug-gestive of a diagnosis of dementia withLewy Bodies. Concomitant PD andAlzheimer Disease (AD) are also possiblein this age group. The diagnosis can be dif-ficult, because some patients with AD haveparkinsonian features. The presence of anasymmetric rest tremor, and improvementof the motor signs with levodopa lend sup-port to a diagnosis of PD.

It is always necessary to review all themedications taken by the patient, becausemany have extrapyramidal side effects. Po-tential culprits include atypical neuroleptics,(i.e. risperidone), antiemetics (i.e.metoclopramide), some antidepressants (i.e.fluoxetine) and some antiepileptics (i.e.valproic acid). Other conditions to exclude,especially in the elderly, are cerebrovasculardisease and normal pressure hydrocephaluswhich usually present as a gait disorder or“lower body parkinsonism.”

Patients with late onset PD progress ata greater rate and are more cognitively im-paired than those with early onset disease.They also have more bradykinesia and pos-tural instability3. Lack of tremor, male sex,and associated comorbidities are also associ-ated with a more rapid rate of progression2.

NON-MOTOR SYMPTOMSNon-motor symptoms are increas-

ingly recognized as an intrinsic feature ofPD. Their prevalence is high: A surveyfound that 88% of PD patients had at leastone non-motor symptom, and 11% hadfive.4 With improvement in the treatmentof PD motor symptoms, non-motor symp-toms, such as dementia and depression,have become an important cause of dis-

ability.5 They are however under recog-nized because their symptoms can over-lap with the symptoms of PD.

Non-motor symptoms affect several do-mains: neuropsychiatric, autonomic, sensory,sleep, and dermatologic. Dementia, depres-sion and autonomic symptoms are often themost problematic in elderly PD patients.

DEMENTIAThe prevalence of dementia in PD var-

ies between 10 and 44% depending on thediagnostic criteria used and the nature of thepopulation studied. The risk increases withage, with one study finding that 65% of PDpatients over the age of 85 were demented.6

Risk factors include older age at onset, andinitial manifestations of hypokinesia and ri-gidity.7 The dementia in PD usually does notappear at the onset of the disease. It is char-acterized by impaired executive function,visuospatial abnormalities, impairedmemory, and language deficits.8 In elderlypatients, superimposed cerebrovascular dis-ease can contribute to cognitive problems.Dementia is a major factor in the manage-ment of PD, limiting the drug therapy thatcan be used, and leading to earlier nursinghome placement and decreased survival.2

DEPRESSIONAround 40% of subjects will have

depression.9 Although there may be a psy-chological response to living with a pro-gressive neurological disease, there is evi-dence that depression in PD is related tothe underlying pathology of the disease.

There is overlap between the symptomsof depression and those of PD which canmake the diagnosis challenging. The natureof the depression in PD is more character-ized by pessimism, hopelessness and poormotivation, with less feeling of guilt and selfblame than in depressed elderly subjects with-out PD. Psychotic features are rare.10

AUTONOMIC DYSFUNCTIONSymptoms of autonomic dysfunction

become more prominent as PD progresses.They also increase with age and medica-tion use.11 They include bladder dysfunc-tion, constipation, orthostatic hypotension,abnormal sweating and sexual dysfunction.


In addition, age itself affects autonomicfunction, as do concurrent diseases such asdiabetes and hypertension, and medica-tions, including some used to treat PD.

Orthostatic hypotensionFalls in blood pressure (BP) occur

particularly when getting up in the morn-ing, or after meals. They manifest as dizzi-ness when the patient stands, but can alsopresent as fatigue or episodes of confusion.Critical review of all prescribed medica-tions is necessary but sometimes specifictreatment such as fludrocortisone orproamatine must be instituted.

Bladder symptomsSymptoms of urgency, frequency, noc-

turia, and incontinence are common in ad-vanced PD. They result from detrusor hyper-reflexia with or without detrusor/sphincterdyssynergia. In addition, they can be compli-cated by prostatic hypertrophy in males. Un-fortunately medications for detrusor hyper-reflexia are anticholinergic and can exacer-bate confusion in elderly PD patients. Theirrisks and benefits must be carefully weighed.

ConstipationConstipation is very common in PD,

because of a combination of autonomicdysfunction with delayed transit time,and immobility, drug therapy, poor dietand lack of appropriate hydration. An ag-gressive bowel regimen may be necessaryto avoid impaction.

TREATMENTTreatment must be individualized to

each patient’s needs, and the functional andcognitive status. Symptomatic therapy is in-troduced when the patient is functionallydisabled. Levodopa/carbidopa is still the mosteffective medication for the motor symptomsof PD, and is better tolerated than Dopam-ine Agonists, amantadine or anticholinergicsin elderly patients. It is initiated at a low dose,and increased slowly to minimize side effects.The optimal dose is the lowest one that willmaintain adequate function. As the symp-toms of PD progress, the dosage of the medi-cation will need to be adjusted. Howevercertain symptoms such as gait freezing, falls,hypophonia, and dysphagia do not respondwell to drug treatment, and in these casesphysical therapy and speech therapy may behelpful.12, 13

The treatment of the non-motor symp-toms of PD must be addressed specificallyand separately from the treatment of themotor symptoms. The only medication ap-proved for the treatment of PD dementiais Rivastigmine.14 There is no medicationspecifically approved for the treatment ofdepression, bladder or sexual dysfunction,constipation, or orthostatic hypotension inPD. For any treatment being considered,the clinician must weigh the potential ben-efit versus the risk of side effects.

CONCLUSIONElderly PD patients have more gait

and balance difficulties, more depression,cognitive problems, and autonomic dys-function, in addition to concurrent diseasessuch as cardiac and cerebrovascular disease.Drug therapy can be limited by neuropsy-chiatric side effects, and has marginal ben-efit for gait, balance, and swallowing diffi-culties. In this situation a non-medical ap-proach involving physical and speech thera-pies becomes an important part of the man-agement. A dietitian can also be involvedto recommend strategies to maintainweight, and an occupational therapist canevaluate the home environment to improvesafety. As the disease progresses, it may be-come increasingly difficult for patients togo to a specialty clinic. The primary careprovider then becomes more involved inthe management of the patient but musthave access to consultation with the patient’sspecialist if necessary. The care of patientswith advanced PD is complicated by thefact that the caregiver, usually a spouse, isalso likely to be elderly and to suffer from achronic illness.

REFERENCES1. Mayeux R, Marder K, et al. The frequency of

idiopathic Parkinson’s disease by age, ethnic group,and sex in northern Manhattan, 1988-1993. AmJ Epidemiol 1995; 142:820-7.

2. Suchowersky O, Reich S, et al. Practice Parameter.Report of the Quality Standards Subcommitteeof the American Academy of Neurology. Neurol2006; 66: 968-75.

3. Diederich NJ, Moore CG, et al. Parkinson diseasewith old-age onset. Arch Neurol 2003; 60:529-33.

4. Shulman LM, Taback RL, et al. Comorbidity ofthe nonmotor symptoms of Parkinson’s disease.Mov Disord 2001; 16: 507-10.

5. Weintraub D, Moberg PJ, et al. Effect of psychiatricand other nonmotor symptoms on disability inParkinson’s disease. J Am Geriatr Soc 2004; 52:784-8.

6. Mayeux R, Chen J, et al. An estimate of the inci-dence of dementia in idiopathic Parkinson’s dis-ease. Neurol 1990; 40:1513-6.

7. Miyasaki JM, Shannon K, et al. PracticeParameter.Report of the Quality Standards Sub-committee of the American Academy of Neurol-ogy. Neurol 2006; 66: 996-1002.

8. Aarsland D, Andersen K, et al. Prevalence andcharacteristics of dementia in Parkinson disease.Arch Neurol 2003; 60:387-92.

9. Cummings JL. Depression and Parkinson’s dis-ease. Am J Psychiatry 1992; 149, 4: 443-54.

10. Brown RG, MacCarthy B. Psychiatric morbidityin patients with Parkinson’s disease. Psycholog Med1990; 20: 77-87.

11. Verbaan D, Marinus J, et al. Patient-reported au-tonomic symptoms in Parkinson disease. Neurol2007; 69: 333-41.

12. de Goede CJ, Keus SH, et al. The effects of physi-cal therapy in Parkinson’s disease. Arch Phys MedRehabil 2001; 82: 509-15.

13. Ramig LO, Sapir S, et al. Changes in vocal loud-ness following intensive voice treatment (LSVT)in individuals with Parkinson’s disease. Mov Disord2001; 16: 79-83.

14. Emre M, Aarsland D, , et al. Rivastigmine fordementia associated with Parkinson’s Disease.NEJM 2004, 351: 2509-18.

Marie-Hélène Saint-Hilaire, MD,FRCPC, is Medical Director of theParkinson’s Disease and Movement Disor-ders Center, Boston University School ofMedicine.

Disclosure of Financial InterestsGrant Research Support: Eisai,

Bayer, Novartis; Speaker’s Bureau: Teva,Boeringher Ingelheim, Valeant

CORRESPONDENCEMarie-Hélène Saint-Hilaire, MD, FRCPCBoston University School of MedicineDepartment of Neurology715 Albany Street, C-329Boston, MA 02118Phone: (617) 638-8640e-mail: [email protected]

Patients with lateonset PD progressat a greater rate

and are morecognitively impaired

than those withearly onset disease.


Epilepsy In the ElderlyAmanda M. Diamond, MD, and Andrew S. Blum, MD, PhD�

People over age 65 are the most rap-idly increasing segment of the population.The incidence of epilepsy rises signifi-cantly with age, starting with 25.8/100,000 person-years for the ages of 60-74 and increasing to 101.1/100,000 forthe ages of 75-89.1 The prevalence ofepilepsy is 1.5% in the elderly, twice thatof young adults.2 Also, the prevalence ofepilepsy in nursing home residents is evenhigher than that in the general popula-tion. Review of elderly nursing homeresidents reveals that up to 10.5% arereceiving anticonvulsants, along with anaverage of 5.6 other medications.3,4

ETIOLOGY AND SEMIOLOGYIn the elderly, cerebrovascular dis-

ease accounts for 30-40% of cases.2 Therisk of seizures within the first year afterstroke has been estimated to be 23 timesthat of the general population.5 Othercauses include Alzheimer’s disease,trauma, brain tumors and infection.About half of cases are cryptogenic, andit is presumed that vascular etiologies ac-count for much of this group too.2

Further complicating the diagnosisis the sometimes vague history. Theevents are often unwitnessed and mayinvolve confusional symptoms. Elderlypatients do not always have classical sei-zure semiologies or auras as in youngerpatients. Symptoms that may suggest al-ternate diagnoses can further confound;these may include tremor, headache anddizziness, among others.6 In a recentVA study, 27% of patients ultimately di-agnosed with epilepsy were initially mis-diagnosed as having syncope, alteredmental status and confusion.6 Postictalperiods tend to be more prolonged in thisage group, at times lasting for severaldays.7

DIFFERENTIAL DIAGNOSIS ANDWORK-UP

The differential diagnosis in thispopulation is extensive and includes tran-sient cerebrovascular symptoms (TIA),syncope (including convulsive syncope),confusional migraine, drug intoxication,infection, psychiatric disorders, transient

global amnesia and dementia. Multiplemetabolic etiologies can also be consid-ered, including hypo- or hyperglycemia,thyroid dysfunction, hypercapnia, ure-mia and hyponatremia.7

Electroencephalography can bepivotal, but one must be aware of po-tential false positive findings. Rhythmicruns of temporal theta activity may beseen in drowsiness as a normal or benignfinding. Focal slowing may be presentwith underlying cerebrovascular insults.Wicket spikes and subclinical rhythmicelectrographic discharges in adults(SREDA) are two other benign variantpatterns that can be misinterpreted.Long-term video-EEG monitoring(LTM) may prove invaluable in evalu-ating recurrent spells. Brain imagingshould be performed, preferably MRI.Other testing considerations include ba-sic metabolic screens, sleep studies,Holter monitoring, echocardiogram,tilt-table and/or vestibular testing,where appropriate, to rule out compet-ing diagnoses.

MANAGEMENTThe assistance of family members and

caregivers may be needed to ensure pa-tient safety. In some, help with medica-tions may be critical and the importanceof compliance should be emphasized.Patients may need a home safety evalua-tion. Medication lists should be reviewedfor potentially pro-convulsive medications.

Medical management of epilepsy inthe elderly poses several distinct challenges.Pharmacokinetic and pharmacodynamicparameters change significantly with age,making the potential for side effects of anti-epileptic drugs (AEDs) greater and de-creasing the predictability of dose – blood

level relationships.8 Decreased proteinbinding is more common in the aged; thismay lead to higher AED free fractions,which can lead to earlier toxicity with morehighly protein bound AEDs such as pheny-toin and valproate. Also, the elderly mayhave a lower volume of distribution. De-creased clearance due to hepatic or renalinsufficiency may also promote higher thanexpected serum AED levels.9 The CNSthreshold for AED toxicity may also belower in the elderly. Delayed esophagealand gastric emptying, altered postprandialgastric pH, and delayed intestinal transitall affect absorption in the elderly.10

Several medications more common inthe elderly can pose significant interactionswith some AEDs. For example, highlyprotein bound AEDs (e.g. phenytoin andvalproate) may interact with warfarin andother highly protein bound concomitantmedications, leading to complex untowardinteractions. Cytochrome P450-inducingAEDs (phenytoin, carbamazepine, phe-nobarbital) accelerate the clearance ofsome hepatically cleared drugs, includingsome chemotherapeutics.9

Several AEDs are known to contrib-ute to accelerated bone demineralization.The older generation of AEDs seems tobe worse in this regard. The elderly are ata higher risk of osteoporosis and relatedfractures, so this may be relevant. Balanceand cognitive concerns are also enrichedin the elderly. Some AEDs appear to posegreater balance risks (e.g. phenytoin,carbamazepine)11 or cognitive risks (e.g.phenobarbital, topiramate). Hyponatre-mia, a problem occasionally provoked bycarbamazepine and oxcarbazepine, ismore frequent in the aged, particularlywith concomitant diuretic use.

The elderly are likely to have moremedical diagnoses and take more medica-tions than a younger population and thusare far more susceptible to drug-drug in-teractions.3 AEDs that act as hepatic en-zyme inducers or inhibitors will greatlyaugment this problem of drug-drug in-teraction burden in this age group. Thisis more often the case for the older AEDs.The newer (2nd generation) AEDs exhibitless hepatic affects and are more often

Several medicationsmore common in

the elderly can posesignificant

interactions withsome AEDs.


renally cleared, have lower protein bind-ing, and hence have fewer drug interac-tions as a group. Additionally, the elderlymay have more difficulty paying for AEDs,contributing to potentially poor compli-ance or restricted choice of agent.

ANTIEPILEPTIC CHOICES IN THEELDERLY

Little comparative efficacy data existto help guide the use of AEDs in the eld-erly. Most clinical trials of AEDs have beenconducted in younger and healthier adultpopulations. In the UK, Brodie et al12 com-pared the efficacy and tolerability oflamotrigine vs. carbamazepine in elderlypatients with new onset epilepsy. Theyfound similar efficacy but better tolerabil-ity in the lamotrigine arm.12 A similar USstudy compared gabapentin vs. lamotriginevs. carbamazepine in the elderly and foundbetter tolerability in the gabapentin andlamotrigine arms vs. carbamazepine withno significant efficacy distinctions.13 How-ever, a later international study that com-pared lamotrigine and carbamazepine us-ing a more flexible dosing schedule and slowrelease carbamazepine did not observe asmarked a tolerability difference.14

It is helpful when treating the eld-erly with epilepsy to keep the regimen assimple as possible. Medication choicesshould be tailored to seizure type, withmost being partial onset rather than gen-eralized in this population. Tolerabilityconcerns should be considered carefullyin AED selection and individualized ac-cordingly. Doses should generally beginquite low and titration should be as slowas possible .15 Levels may be helpful. Costmay be a deciding factor for some.

Fortunately, the majority of elderlycases are very responsive to treatment.Refractory epilepsy may be infrequentlyencountered in this group. Non-phar-macologic treatment options may be lim-ited. Surgical resection is not as com-monly used in this age group. Vagal nervestimulation may prove an option for somewhen AEDs prove inadequate and sur-gery is not a viable option.

SUMMARYThe incidence of epilepsy is higher in

the elderly than in younger adults. This com-munity presents a challenging set of consid-erations in diagnosis and management.Numerous other processes may mimic sei-

zures in the elderly. After careful diagnosis,AED choices should take into account me-tabolism, drug-drug in interactions, co-mor-bidities, and side effect profiles while striv-ing to achieve seizure freedom.

REFERENCES1. Hussain SA, Haut SR, et.al. Incidence of epilepsy

in a racially diverse, community-dwelling, elderlycohort. Epilepsy Res 2006;71:195-205.

2. Hauser WA. Epidemiology of Seizures in the eld-erly. In: Seizures and Epilepsy in the Elderly. RowanAK, Ramsay RE, Eds. Boston, Butterworth-Heinemann, 1997:7-18.

3. Lackner TE, Cloyd JC, et al. Antiepileptic druguse in nursing home residents, Epilepsia1998;39:1083-7.

4. Garrard J, Cloyd JC, et.al. Factors associated withantiepileptic drug use among nursing home eld-erly. J Gerontol Med Sci 2000 ;55:384-92.

5. So EL, Annegers JF, et.al. Population-based studyof seizures disorders after cerebral infarction.Neurol 1996;46:350-355.

6. Ramsay RE, Rowan AJ, Pryor FM. Special con-siderations in treating the elderly patient with epi-lepsy. Neurol 2004;62(Suppl 2):S24-S29.

7. Ramsay RE, Macias FM, Rowan AJ. Diagnosingepilepsy in the elderly. In “The Neurobiology ofEpilepsy and Aging” (RE Ramsay, ed.) Int RevNeurobiol 2007;81:1-14.

8. Perucca E, Berlowitz D, et.al. Pharmacological andclinical aspects of antiepileptic drug use in theelderly. Epilepsy Res 2006;68S:S49-S63.

9. Boggs JG. Elderly patients with systemic disease.Epilepsia 2001;42:18-23.

10. Gidal BE. Drug absorption in the elderly. Epi-lepsy Res 2006;68S:S65-S69.

11. Fife TD, Blum D, Fisher RS. Measuring the ef-fects of antiepileptic medications on balance inolder people. Epilepsy Res 2006;70:103-9.

12. Brodie MJ, StephenLJ. Outcomes inelderly pa-tients with newly diagnosed and treated epilepsy.Int Rev Neurobiolo 2007;81:253-63.

13. Rowan AJ, Ramsey MD, et al. New onset geriat-ric epilepsy, Neurol 2005;64:1868-73.

14. Saetre E, Perucca E, et al. An internationalmulticenter randomized double-blind controlledtrial of lamotrigine and sustained-releasecarbamazepine in the treatment of newly diag-nosed epilepsy in the elderly. Epilepsia2007;48:1292-302.

15. Leppik IE. Epilepsy in the elderly. Epilepsia2006;47(Suppl 1):65-70.

Amanda M. Diamond, MD, is a Fel-low in Clinical Neurophysiology, RhodeIsland Hospital and The Warren AlpertMedical School of Brown University.

Andrew S. Blum, MD, PhD, is Direc-tor, Comprehensive Epilepsy Program, RhodeIsland Hospital, and Assistant Professor ofClinical Neurosciences, The Warren AlpertMedical School of Brown University.

Disclosure of Financial InterestsAmanda M. Diamond, MD. Con-

sultant: Guidant, TEVA, Berlex (Bayer),Genentech.

Andrew S. Blum, MD. Grant Re-search Support: Abbott Laboratories.Speaker’s Bureau: Glaxo SmithKline,ICB Pharmos, Ortho-McNeil.

Discussion of off-label usage of anyproduct: gabapentin and lamotrigine.Reference is made to studies performedon the use of these medications in eld-erly patients with epilepsy.

CORRESPONDENCEAndrew S. Blum, MD, PhD110 Lockwood St., Ste. 342Providence, RI 02903Phone: (401) 444-4364E-mail: [email protected]


Peripheral Neurology: Special Concerns In the ElderlyGeorge M. Sachs, MD, PhD�

Changes in the peripheral nervous systemproduce a major impact on safety andquality of life in the elderly. The chal-lenges of aging reflect alteration of bothneuromuscular and sensory function. Ofparticular concern are motor and prop-rioceptive deficits increasing the risk offalls. In addition, changes in sensory path-ways may predispose the elderly to neu-ropathic pain. This review will focus onaspects of aging in muscle and nerve rel-evant to these issues.

SARCOPENIASaracopenia refers to the degenera-

tive loss of muscle mass and strength withincreasing age. It begins in mid-life andaccelerates significantly in the seventhand eighth decades. Both active and sed-entary individuals suffer sarcopenia,though it is worsened by inactivity.Muscle mass decreases earlier in womenbut men experience greater overall loss,averaging 30-40% of their muscle massby age 80.1

The causes of sarcopenia are mul-tiple. They include loss of muscle cells aswell as hormonal changes that influencethe growth and regeneration of differ-ent cells within muscles. In addition, de-generation of spinal motor neurons has aprofound effect on the muscles they in-nervate.1,2

Satellite cells are essentially stem cellsresiding in muscle. In response to physi-cal trauma or even vigorous exercise, sat-ellite cells proliferate to form new musclefibers or fuse with damaged fibers to re-pair them. Most studies have shown re-duction in the number of satellite cellswith aging. This, along with changes ingrowth factor and hormone levels, de-creases the regenerative capacity ofmuscle over time.3

Testosterone (T), growth hormone(GH) and insulin-like growth factor (IGF)all regulate protein synthesis within muscle..IGF appears to increase synthesis of actinand myosin (the principal contractile pro-teins in muscle), while GH and T promoteprotein stability. Decreasing levels for allthree of these hormones in mid to late lifepresumably contribute to sarcopenia. The

role of estrogen is less well established,though its sharp perimenopausal fall mayhelp explain the relatively early onset ofmuscle loss in women.1,2

The interaction of nerve and musclecan be described in terms of “ motor units”.One motor unit consists of a single spinalmotor neuron and the muscle fibers it sup-plies through the branches of its axon. Amotor unit in hand muscles typically in-cludes about 100 muscle fibers, where calfand thigh muscle motor units include1000-2000.4 In addition to transmittingelectrical excitation, each motor neuronprovides trophic support to the muscle fi-bers in its motor unit. Once a muscle fi-ber loses its nerve input, it undergoes at-rophy unless connection with anothernerve terminal can be restored.

Anatomical and physiolgical studieshave shown that the number of motorunits (i.e. the number of spinal motor neu-rons) supplying limb muscles remains fairlyconstant up to age 60. Beyond that,healthy individuals typically lose about halfof their motor units between ages 60 and80.5 Sprouting of terminal axons fromremaining motor neurons initially com-pensates for those that are lost, however asthis process continues, muscle fibers areinevitably left to atrophy without nervesupply. This neurogenic atrophy is likelythe major cause of sarcopenia.1,2

CHANGES IN MUSCLE DYNAMICSTwo major types of motor units can

be distinguished by their morphologicand physiologic characteristics. In Type1 motor units, small motor neurons in-

nervate muscle fibers with slow contrac-tion times. Type 2 motor units containlarger motor neurons and muscle fibersthat contract more quickly. Aging musclesmay show a shift toward the slower con-tractions of Type 1 units for a few rea-sons. First, aging leads to selective Type 2fiber atrophy. Whether this simply re-flects decreased physical activity or someother more specific feature of agingmuscles is not clear. Secondly, muscle fi-bers may actually transform from Type 2to Type 1 as a result of the denervationand reinnervation that follows loss ofmotor neurons.6

The predominance of Type 1 fibercontraction in aging muscles inhibits theability to make quick, forceful move-ments. This poses particular problems forrapid postural reflexes important in main-taining balance. In addition to overallmuscle weakening and proprioceptivedeficits (described below), slowing ofpostural adjustments presents a major riskfor falls in the elderly.

THERAPEUTIC CONSIDERATIONS FORTHE AGING NEUROMUSCULAR SYSTEM

The literature regarding testosteronereplacement for sarcopenia presents amixed picture. Meta-analyses have sug-gested that injected testosterone can pro-duce a moderate increase in muscle massand strength in older men.7 Concernsover adverse effects temper any currententhusiasm. In particular, no large, pro-spective studies have looked at rates ofprostate cancer in older men receivingtestosterone supplementation.8

Growth hormone supplementationhas not demonstrated improvement inmuscle mass or strength in elderly menor women. Furthermore, the addition ofgrowth hormone to a resistance exerciseprogram does not appear to confer addi-tional benefit. Adverse effects includingcarpal tunnel syndrome, hyperglycemia,edema and orthostatic hypotension ledto high drop-out rates in treatmentgroups of some studies.2

Relatively few clinical trials haveevaluated the muscular effects IGF-1administration. A study assessing a two

Growth hormonesupplementation

has notdemonstrated

improvement inmuscle mass or

strength in elderlymen or women.


month course of IGF-1 complexed to abindng protein, found that grip strengthimproved by 11%.9 The effect of estro-gen replacement on sarcopenia has alsoreceived little study to date. Reportedeffects of estrogen on lean body masshave been mixed and changes in strengthor contraction speed have yet to be in-vestigated.10

Exercise, in the form of resistancetraining, appears to be the most effectivetreatment to counteract muscular declinein the elderly. Resistance training pro-grams can achieve the same percentagegain in muscle mass and strength at age80 as they do in young adults.2 Althoughthe mechanism is not understood, resis-tance training also increases whole musclecontraction speed with an associated im-provement in balance.

This likely reflects adaptive coordi-nation among different motor units sincethe contraction speed of individualmuscle fibers may actually decrease withresistance training.

AGING IN PERIPHERAL SENSORYNERVES

Signs of peripheral sensory loss be-come increasingly prevalent with advanc-ing age. Loss of ankle reflexes and decreas-ing distal vibration sense are particularlycommon. One study revealed that at leastone of these deficits occurred in 26% ofindividuals aged 74-84 and in 54% ofthose older than 85.11 Correspondingly,anatomic studies have documented lowernumbers of sural nerve fibers and physi-ologic studies have shown lower ampli-tudes of sural nerve response in “normal”older individuals.

Since these findings are so common,they are often considered part of “nor-mal aging.” This notion overlooks theimpact of peripheral sensory deficits onbalance and gait in the elderly. A num-ber of studies have documented that pe-ripheral sensory loss is an important riskfactor for falls. In some studies, the exist-ence of lower extremity neuropathy in-creased the frequency of falls about 20-fold.12 Even modest loss of propriocep-tion can pose significant risk when com-bined with slowed muscular response andvisual or vestibular disturbances so often

seen in the elderly. Though neuropathyin older individuals is not frequently re-versible, simple preventive measures in-cluding use of a cane, nightlights andshower chairs should not be neglected.

NEUROPATHIC PAINThe age-related changes discussed

above concern the largest sensory fibers.Evaluation of small caliber sensory fibersis more challenging but crucial to under-standing neuropathic pain. This is animportant issue for aging populationsgiven the striking predominance of cer-tain neuropathic pain conditions in theelderly.13

In contrast to the clear age-related lossof large sensory fibers, anatomic studieshave demonstrated relative preservation ofsmall-caliber, pain sensing fibers in the eld-erly.14 This raises an interesting possibilityregarding the development of post-her-petic neuralgia, a condition which is rarebelow the age of 50 but complicates 20-40 % of zoster cases past the age of 60.Studies testing sensory function in patientswith post herpetic neuralgia have indicatedthat vibratory sensory loss (presumablydue to large-fiber failure) is more promi-nent than small-fiber (pain and tempera-ture) deficit.15 This suggests that prefer-ential large fiber loss with aging may bean important risk factor for the develop-ment of neuralgias and neuropathic pain.If small sensory fibers are relatively pre-served, they may present an important tar-get for treatments. The use of local or topi-cal agents aimed at small fibers couldsupplement or replace systemic medica-tions that are limited by adverse reactionsin elderly patients.

REFERENCES1. Thomas DR. Loss of muscle mass in aging. Clin

Nutrition 2007;26:389-99.2. Borst SE. Interventions for sarcopenia and muscle

weakness in older people. Age Ageing 2004;33:548–55.

3. Shefer G,Van de Mark DP, et al. Satellite-cell pool sizedoes matter. Development Biol 2006;294:50-66.

4. Feinstein B,Lindegard E, Nyman E. Morpho-logical studies of human motor units in normalhuman muscles. Acta Anat 1955; 2:127-39.

5. Doherty TJ, Vandervoort AA, Brown WF. Ef-fects of aging on the motor unit. Can J Appl Physiol1993;18:331-58.

6, Doherty TJ. Aging and sarcopenia. J Appl Physiol2003;95:1717-27.

7. Ottenbacher KJ, Ottenbacher ME, et al. Andro-gen treatment and muscle strength in elderly men.J Am Geriatr Soc 2006;54:1666-73.

8. Brand TC, Canby-Hagino E, Thompson IM. Tes-tosterone replacement therapy and prostate can-cer. Curr Urol Rep 2007;8:185-9.

9. Boonen S, Rosen C, et al. Musculoskeletal effectsof the recombinant human IGF-1/IGF bindingprotein 3 complex in osteoporotic patients withproximal femoral fracture. J Clin Endocrinol Metab2002;67:1593-9.

10. Thorneycroft JH , Lindsay R, Pickar JH. Bodycomposition during treatment with conjugatedestrogens with and without medroxyprogesteroneacetate. Am J Obstet Gynecol 2007;197:e1-7.

11. Resnick HF, Vinik AI, et al. Age 85+ years acceler-ates large-fiber peripheral nerve dysfunction JGerontol Med Sci 2001;56:M25-M31.

12. Richardson JK, Hurvitz EA. Peripheral neuropa-thy. J Gerontol Med Sci 1995; 50:M211- M215.

13. Hall GC, Carroll D, et al. Epidemiology and treat-ment of neuropathic pain. Pain 2006;122:156-62.

14. Lauria G, Holland N, et al. Epidermal innerva-tion. J Neurol Sci 1999;164:172-8.

15. Baron R, Haendler G, Schulte H. Afferent largefiber neuropathy predicts the development ofpostherpetic neuralgia. Pain 1997; 73:231-8.

George M. Sachs, MD, PhD, is Asso-ciate Professor (Clinical) of Neurology, TheWarren Alpert Medical School of BrownUniversity.


ests to disclose.Discussion of off-label usage of any

products or services*use of supplemental testosterone,

growth hormones and IGF-1 to reducesacropenia is investigational

CORRESPONDENCEGeorge M. Sachs, MD, PhD593 Eddy St., APC 689Providence, RI 02903e-mail: [email protected]


Sleep Disorders In the ElderlyJean K. Matheson, MD�

Older patients frequently complain ofdifficulty initiating sleep, sleep mainte-nance or excessive daytime sleepiness,while bed partners or caretakers are dis-traught by episodes of nocturnal confu-sion or belligerence.

Sleep disorders may represent a pri-mary disorder of mechanisms regulatingsleep or failure of a specific organ systemmanifesting in a unique way during sleep.Sleep complaints should not be ignoredor treated empirically with pharmaco-logic agents without analysis of the etiol-ogy.

POLYSOMNOGRAPHYPolysomnography is the term ap-

plied to the simultaneous and continu-ous measurement of multiple physiologicparameters during sleep. In practice, thepolysomnogram (PSG) has come tomean a specific type of polysomnographicstudy in which measurements allow for1) the identification of sleep stage, 2)monitoring of cardio-pulmonary func-tion and 3) monitoring of body move-ments during sleep.

SLEEP STAGING AND ARCHITECTURERapid eye movement (REM) sleep,

sometimes called dreaming sleep, andnon-REM (NREM) sleep are the twosleep states. NREM and REM sleep alter-nate in recurring cycles of approximately90 minutes. NREM sleep had been di-vided into four stages (1-4), representingprogressive deepening of sleep. A recentrevision of staging nomenclature nowidentifies these stages as N1, N2 and N3.1

In what has been thought to benormal aging nocturnal awakeningsand wake time increase. N3 sleep de-creases and REM time usually remainsrelatively constant. Stage one sleep in-creases as a reflection of sleep disrup-tion. Sleep efficiency, the ratio of timeasleep to time in bed, decreases second-ary to both increased time in bed andincreased wake. However, many ofthese changes attributed to “normal”aging may also be exacerbated or in-duced by what we now know to be com-mon and treatable sleep disruptors such

as sleep apnea and periodic leg move-ments as described below.

SLEEP- RELATED BREATHINGDISORDERS (SRBDS)

The most important cause of sleep dis-ruption is sleep-disordered breathing. Theterm “sleep-disordered breathing” prima-rily refers to the sleep apnea syndromes, butalso includes disorders that result in noc-turnal hypoventilation and hypoxemia suchas restrictive and parenchymal pulmonarydiseases. While well known to cause exces-sive daytime sleepiness, the sleep apnea syn-dromes, both central and obstructive, arealso important contributors to difficultyinitiating and maintaining sleep because offrequent nocturnal arousals. Current defi-nitions that have the most widespread clini-cal use are based on guidelines providedby the Center for Medicare and Medic-aid Services (CMS);2

Apnea: An apnea is defined as the ab-sence airflow for at least 10 seconds.There are three types:

Obstructive apnea: Absence of airflowfor at least 10 seconds with evidenceof persistent respiratory effort.

Central apnea: Absence of airflow for10 seconds without evidence of anyof respiratory effort.

Mixed Apnea: Absence of airflow for10 seconds with initial absence ofeffort followed by a return of respi-ratory effort before resumption ofairflow.

Hypopnea: The term hypopnea refers to adecrease in airflow. By CMS criteria:“Hypopnea in adult patients is definedas an abnormal respiratory event last-ing at least 10 seconds with at least a30% reduction in thorocoabdominalmovement or airflow as compared tobaseline, and with at least a 4% oxy-gen desaturation.”2

Apnea Hypopnea Index (AHI): Thetotal number of apneas andhypopneas are summed and dividedby the number of hours of sleep.When used with the definitionsabove, the index is useful as a stan-dardized measure that reflects sever-

ity of sleep disordered breathingRespiratory Effort Related Arousal: When

airway resistance increases, oxygensaturation and airflow may stay thesame as respiratory effort increases toovercome obstruction. This increasedrespiratory effort may induce anarousal that disturbs sleep termed,RERA, respiratory effort- relatedarousal. This event is NOT recognizedby CMS and is sometimes called a“hypopnea without desaturation”.1

The presence of 5 apneas/hour ofsleep was previously deemed necessary toestablish the presence of either “obstruc-tive sleep apnea” or “central sleep apnea”.It is now clear, however, that either in-complete obstructions or centralhyoventilatory episodes without apneainduce physiologic changes of the samemagnitude as apneas. CMS currentlyaccepts a minimum AHI of 5 as evidenceof sleep apnea that justifies treatment.However, RERAs, often occult contribu-tors to sleep disruption, are not includedin the CMS definition of sleep apnea, butare accepted by the American Academyof Sleep Medicine as determinants ofobstructive sleep apnea syndrome.4

Well-documented risk factors for ob-structive sleep apnea include obesity, largeneck, upper airway structural abnormali-ties, nasal congestion, endocrine abnormali-ties, muscular weakness and sedating drugs.

In aging and degenerative neurologi-cal disease there are additional risk factorsincluding laryngeal dysfunction and cen-trally- induced dysynergy of upper airwaymuscle activation in relationship to chestwall and diaphragmatic activation.

Central sleep apnea episodes usuallyrepresent Cheyne-Stokes breathing, a cre-scendo-decrescendo breathing pattern,common in the elderly, especially thosewith congestive heart failure. Periods ofcentral apnea or hypopnea predispose toobstruction as well, because low airflowcontributes to airway collapse. This typeof breathing abnormality, once consid-ered benign, may markedly disruptsleep.4


TREATMENT OF SLEEP-DISORDEREDBREATHING:

Continuous positive airway pressure(CPAP) is the mainstay of treatment forobstructive sleep apnea and for some pa-tients with predominantly central apnea.Airway pressure acts as a pneumatic splintto maintain upper airway patency duringsleep. Bi-level positive pressure (BIPAP) isoften better tolerated in the elderly becauseit provides an expiratory pressure alwayslower than inspiratory pressure, makingexpiration more natural and less effortful.The inspiratory–expiratory pressure differ-ence also acts to augment ventilation in dis-orders associated with hypoventilation.New devices termed servo-ventilators arebased on bi-level positive pressure technol-ogy, and can be used at home to treat pa-tients with central components of theirsleep-disordered breathing, especiallyCheyne-Stokes respirations. These devicesare an important addition to the treatmentof sleep-disordered breathing in heart fail-ure. Many new mask styles and variationson these devices including “smart” auto ti-trating machines can improve patient tol-erance dramatically. Full face masks arenow comfortable and useful in patients whomay have rejected positive pressure previ-ously because of nasal obstruction.3

Cheyne-Stokes respirations often re-spond to low-flow oxygen deliveredthrough nasal prongs that generally arebetter tolerated than positive pressure. O

2

tends to decrease over-responsiveness toCO2 that perpetuates the hyperventilation-apnea cycle. Obstructive episodes exacer-bated by central apneas may also improve.Sedating medications, especially hypnoticsand narcotics, can exacerbate sleep disor-dered breathing and are best avoided whensleep-disordered breathing is suspected.3

SLEEP RELATED MOVEMENTDISORDERS

Sleep-related movement disordersinclude conditions in which simple ste-reotyped movements are present duringsleep and induce sleep disruption. Diffi-culty initiating and/or maintaining sleepare the typical complaints.

Periodic Limb Movement DisorderThe most prevalent of these disor-

ders is periodic limb movement disor-der (PLMD), characterized by periodsof repetitive stereotyped leg movements

that disturb sleep (PLMS). Many medi-cations are implicated in the inductionof periodic and aperiodic leg move-ments, most commonly SSRIs, SNRIsand tricyclic antidepressants.

Restless Legs SyndromeRestless legs syndrome (RLS) is char-

acterized by 1) an urge to move accompa-nied by uncomfortable sensations, predomi-nantly in the legs, that are 2) relieved bymovement, 3) occur when sedentary and 4)are worse in the evening.5 This syndrome isclosely associated with PLMD. Restless legssyndrome, however, is a syndrome based onclinical, not polysomnographic criteria. Thedisorder is familial in approximately 50% ofcases. Prevalence estimates vary between 5and 20% of the general adult population inNorth America and the disorder appears toincrease with age.5 Abnormalities of bothdopamine and iron metabolism are impli-cated in the underlying pathophysiology.Iron deficiency is known to exacerbate orprecipitate restless legs and periodic leg move-ments in familial and non-familial cases. Sec-ondary causes of RLS are subject to somedebate due to limited data and include ure-mia, neuropathy, and medications, especiallyanti-dopaminergic drugs and SSRIs.

Management of Restless Legsand Periodic Limb Movements

Periodic leg movements are oftenfound incidentally on sleep studies and arenot generally treated unless they are eitheraccompanied by symptomatic restless legs,or clearly contribute to arousals. Recom-mendations for the management of restlesslegs have recently been published.6 Serumferritin should be checked in all patients;iron replacement is recommended in pa-tients with ferritins below 45-50 ug/ml.Response to iron replacement may not oc-cur in all patients and usually takes monthsto years; some clinicians advocate intrave-nous replacement in severe cases. Becauseantidepressant and antihistamine medica-tions may exacerbate restless legs theyshould be avoided if possible. Some clini-cians routinely screen for neuropathy withexam and metabolic studies. Ropinirole(Requip) and pramipexole, (Mirapex), bothdopaminergic agonists FDA approved forRLS, are markedly effective. Because of thepossibility of inducing a syndrome termed“augmentation”, it is best to use as low asingle evening dose as possible. Augmen-

tation refers to the development of symp-toms earlier in the day with increasing se-verity, further exacerbated by dosage in-creases. This phenomenon occurs most dra-matically with the use of levodopa and lessfrequently with the dopaminergic agonistsropinirole and pramipexole. Gabapentinand low dose opioids are useful second linedrugs that can be used alone or in combi-nation with dopaminergic agonists for dos-age sparing. Benzodiazepines are third linedrugs because of limited efficacy and thedevelopment of tolerance.

REM Behavior DisorderLow muscle tone observed on PSGs

during REM correlates with the normalparalysis that occurs during dreaming. Thistemporary paralysis, termed REM sleepatonia, prevents the dreaming subjectfrom enacting dreams. REM BehaviorDisorder is characterized by incompleteREM atonia associated with motoric acti-vation during dreams.7) Typically the pa-tient, bed partner, or caretaker complainsof violent, often injurious, activity duringsleep. The patient may complain of achange in dream content with violenceand running as typical themes. Sometimesthe patient is able to incorporate ongoingconversation and activity into the dream,giving rise to the misperception that he isconfused or hallucinating until he sud-denly awakens and appear to “clear” hismental status. Underlying dementia oracute illness may impair the patient’s abil-ity to report the perception of dreaming,resulting in misdiagnosis. Hospital care-takers usually dismiss even detailed dream-ing reports as confusion. The disorder isfrequently mistaken for “sundowning” or,because of the violent quality of thedreams, post-traumatic stress disorder.

REM behavior disorder occurs mostfrequently in older men with a mean ageof 60. Over time it has become clear thatRBD precedes other clinical signs or symp-toms of some degenerative diseases, espe-cially Parkinson’s disease, dementia withLewy bodies and multisystem atrophy, (the“synucleinopathies.”) by years. Conversely,the prevalence of RBD in Parkinson’s dis-ease is in the range of 33-60%. The com-bination of degenerative dementia andRBD is highly correlated with the diag-nosis of dementia with Lewy bodies, basedon clinical and pathologic criteria. Thereare rare published reports of RBD with a


“tauopathy” (e.g. pure Alzheimer’s disease,frontotemporal dementia, progressive su-pranuclear palsy). Some medications, es-pecially NSRIs and SSRIs are known toprecipitate and exacerbate the disorder.Idiopathic RBD also exists.7

Circadian Rhythm Disorders:Advanced Phase Sleep Disorder

The tendency for elderly patients tospend more time asleep during the dayand less time asleep at night raises the pos-sibility that neurological dysfunction of thebiologic clock within the suprachiasmaticnucleus of the hypothalamus mediatesthese changes. Advanced phase sleep dis-order is a well-recognized circadian disor-der in which patients complain of diffi-culty staying awake in the evening andearly morning awakening.5 This disorderis common in the elderly and may be mis-taken for early morning insomnia.

Phase advance is exacerbated by vi-sual impairment and low light exposureduring the day; evening light exposurecan therapeutically delay rhythms andimprove sleep maintenance.8

REFERENCES1. The AASM manual for the scoring of sleep and

associated events. Westchester, IL: American Acad-emy of Sleep Medicine, 2007.

2. Medicare National Coverage DeterminationsManual Chapter 1, Part 4 Section 240.4. http://www.cms.hhs.gov/manuals/downloads/ncd103c1_Part4.pdf

3. Kryger MH, Roth T, Dement WC. Principles andPractice of Sleep Medicine. 4th ed. Philadelphia,PA: Elsevier/Saunders, 2005.

4. The international classification of sleep disorders: Diagnostic & coding manual, ICSD-2. 2nd ed.Westchester, IL: American Academy of SleepMedicine, 2005.

5. Allen RP, Picchietti D, et al. Restless legs syndrome:Diagnostic criteria, special considerations, and epi-demiology. A report from the restless legs syn-drome diagnosis and epidemiology workshop atthe National Institutes of Health. Sleep Med2003;4(2):101-119.

6. Silber MH, Ehrenberg BL, et al. An algorithm forthe management of restless legs syndrome. MayoClin Proc 2004;79:916-22.

7. Boeve BF, Silber MH, et al. Pathophysiology ofREM sleep behaviour disorder and relevance toneurodegenerative disease. Brain 2007.

8. Campbell SS, Dawson D, Anderson MW. Alle-viation of sleep maintenance insomnia with timedexposure to bright light. J Am Geriatr Soc1993;41:829-36.

Jean K. Matheson, MD, is Neurologi-cal Medical Director, Sleep Disorders Cen-ter, Beth Israel Deaconess Medical Center,and Associate Professor of Neurology,Harvard Medical School.


ests to disclose.Discussion(s) of off-label usage of any

products or services: gabapentin for rest-less legs syndrome, clonazepam for REMBehavior Disorder

CORRESPONDENCEJean K. Matheson, MDSleep Disorders Center, CCE866Beth Israel Deaconess Medical Center330 Brookline AveBoston MA 02215Phone: (617) 667-4307e-mail: [email protected]

Driving Safety Among Older AdultsMelissa M. Amick, PhD, and Brian R. Ott, MD

�The number of individuals in the UnitedStates who are age 65 and older is expectedto double by 2030.1 As this population in-creases, so will the number of licensed olderdrivers. Increasing age is a significant riskfactor for unsafe driving. The risk for crashinvolvement increases dramatically after theage of seventy; and drivers 85 and olderhave the highest driver fatality rate.2 Driv-ers over the age of 70 have the highest an-nual fatality rate per miles driven comparedto all age groups, except those aged 25 andyounger.2 In a study of mild dementia andnon-demented drivers, baseline age signifi-cantly predicted performance on a road testindependent of cognitive status.3 Thesefindings suggest that, as older people age,the risk of unsafe driving increases, and careproviders will need to monitor their agingpatients’ driving safety.

Research on driving safety in the eld-erly has mainly focused on drivers with de-mentia, who consistently perform morepoorly on open road tests and simulated

driving tests compared to their non-de-mented counterparts.4 For example,Duchek and colleagues found that 43%of participants with mild Alzheimer’s dis-ease (AD) failed the road test, comparedto 13% of patients with very mild AD and3% of non-demented control participants.3

Longitudinal data indicated that patientswith mild AD experienced a more rapiddecline in driving skills compared to thecontrol group; however, patients with verymild AD did not differ significantly fromeither group.3 Comparing crash raterecords collected by the state registries, onlyone study has observed that patients withdementia are more frequently involved inaccidents compared to a control group.4

There is also concern about the driv-ing skills of patients with Parkinson’s dis-ease (PD), because of the motor and non-motor symptoms (visual changes and cog-nitive dysfunction). Interestingly, motorsymptom severity and visual functioning donot consistently predict driving skills.5

While performance on neuropsychologi-cal measures does predict driving abilities,our research has found that PD drivers areinfrequently observed to be unsafe drivers:only one of 25 participants assessed actu-ally failed our road test. Rather, most par-ticipants received marginal or safe ratings.5

Research in dementia and Parkinson’s dis-ease emphasizes that mild degrees of motorslowing, cognitive dysfunction, and changesin vision may not adversely affect drivingskills, and that these diagnoses alone are notabsolute indicators of unsafe driving.

The American Medical Association’sPhysician’s Guide to Assessing and Coun-seling Older drivers lists acute medicalevents such as myocardial infarction, stroke,syncope, seizure, surgery, and delirium aswell as chronic conditions such as diseaseaffecting vision, cardiovascular disease, neu-rological disorders, psychiatric illnesses,metabolic conditions, musckuloskeletalimpairments, and respiratory disease as riskfactors for unsafe driving.6 Detailing the


accidents and traffic violations, whereas lessaccurate raters emphasized dementia his-tory, global neuropsychological perfor-mance, eye examination results, generalmedical history, and language skills9. Takentogether, these findings suggest that driv-ing safety is best not determined by perfor-mance on a single measure, but ratherbased on consideration of many patientcharacteristics. Importantly, compared tophysical examinations or neuropsychologi-cal tests, a road test conducted by a profes-sional driving instructor or certified occu-pational therapist appears to be the goldstandard for determining driving safety.

OLDER DRIVER RE-EDUCATIONChanges in sensory, motor, or cogni-

tive functioning do not always mean thatthe older patient should retire from driv-ing. In some cases evaluation and trainingby an occupational therapist or private driv-ers’ education program may help olderadults become safe drivers again. Modifi-cations can be made to vehicles to makethem easier to use. For example, older adultswith limited range of motion in their necksmay benefit from parabolic mirrors. Driv-ers with limited motion in their arms mayneed a knob on their steering wheel.

The most common driving re-educa-tion program is the AARP Driver SafetyProgram, which is run as a classroom courseand available on-line. AAA and state agen-cies also offer informational materials as wellas classroom education. Research on thebenefits of older driver re-education is verylimited. Kua and colleagues performed asystematic review of the older drivers re-education literature and found that onlyeight studies demonstrated sufficient inter-nal validity to be included.10 Limited ben-efits of physical (range of motion exercises

or at home physical therapy exercises) andvision interventions (speed of informationprocessing training or at home exercises toimprove visual perception) were reported.10

Educational programs were associated withsome improvements in driving safety be-haviors.10 Unfortunately the two studies (selfmonitoring program and California’s ma-ture drivers program) that examined thebenefit of driver education programs uponcrash rates found no significant effect.10.

The limited research should not com-pletely dissuade clinicians from recom-mending these “refresher courses” to theirolder drivers. Driver education programscan help individual drivers, and some in-surers provide discounts to older adults whoparticipate in AARP’s driver reeducationprogram. Until these programs are empiri-cally validated, however, it is difficult tojudge their relative benefit as well as whichelements of the course are associated withthe best remediation of driving skills.

CESSATION OF DRIVINGThe AMA Guide has compiled each

states’ reporting procedures for easy refer-ence.6 In Rhode Island “Any physician whodiagnoses a physical or mental conditionwhich, in the physician’s judgment, will sig-nificantly impair the person’s ability to safelyoperate a motor vehicle may voluntarily re-port the person’s name and other informa-tion relevant to the condition to the medicaladvisory board within the Registry of Mo-tor Vehicles. Any physician reporting in goodfaith and exercising due care shall have im-munity from any liability, civil or criminal.No cause of action may be brought againstany physician for not making a report.”6

Massachusetts is a self-reporting state. It isthe responsibility of the driver to report tothe Registry of Motor Vehicles any medicalcondition that may impair driving ability.However, physicians are encouraged to re-port unfit drivers to the Registry of MotorVehicles. The law does not provide any pro-tection from liability, nor does it promise con-fidentiality due to the “Public Records” lawwhich states simply that a driver is entitledto any information upon receipt of writtenapproval” 6 pg30-31.

Clinicians who recommend driving ces-sation to their patients should suggest alter-native transportation. In Rhode Island patientscan be referred to the Department of ElderlyAffairs Pocket Manual of Elder Services,11

which lists the different RIDE programs as

specific conditions that may be associatedwith unsafe driving is beyond the scope ofthis brief review. Interested readers arereferred to chapter 2 of the AMA’s guide.

OFFICE BASED ASSESSMENTS FORDRIVING SAFETY

In a sample of 460 primary care phy-sicians in Canada approximately 72% in-dicated that physicians should be legallyresponsible for reporting unsafe drivers tostate licensing authorities.7 Strikingly, only55% of the surveyed physicians believedthey were most qualified to make this de-cision, and 88% felt that they would ben-efit from additional training in this area.7

The AMA’s guide recommends that phy-sicians assess visual function (acuity andvisual fields), cognition (Clock drawingtest and Trails B, a visual motor task re-quiring participants to alternate betweenconnecting numbers and letters) and mo-tor function (20 foot walk and manual testof range of motion and motor strength),with cutoff scores for each measure.6

While office-based tests can assist cli-nicians in making recommendations aboutdriving safety, some have argued that thereis not enough research linking these mea-sures to unsafe driving. For example,Molnar and colleagues performed a system-atic review of research studies (1984-2005)examining the predictive utility of office-based screening measures for determiningdriving safety.8 They found only sixteen ar-ticles were of high enough quality to includein the review and only one study providedcutoff scores for determining driving safety.The review indicated that Trails B was vari-ably related to driving performance; andnone of the studies examined clock-draw-ing performance. At the present time clini-cians are expected to make recommenda-tions, without empirical evidence to sup-port office-based assessments.

Ott and colleagues examined the ac-curacy of physician assessments (based onchart review) for determining a professionaldriving instructor’s rating of AD patients’standardized road test performance.9 Phy-sicians’ accuracy ranged from 62% to 78%.9

Clinicians also indicated which portions ofthe evaluation they relied upon for makingtheir decision.9 Raters with higher accuracyemphasized dementia duration, dementiaseverity (CDR and MMSE), neuropsycho-logical measures of praxis, visuospatial abil-ity, executive function, attention, history of

…a road testconducted by a

professional drivinginstructor or certified

occupationaltherapist appears tobe the gold standard

for determiningdriving safety.


Geriatric Neurorehabilitation In the New MilleniumStephen T. Mernoff, MD�

Rehabilitation interventions have changedlittle in the last few decades, aside from im-provements in materials and medical care.Most neurorehabilitation research involvesgeriatric patients since most disabling neu-rologic disease occurs in older populations.Proving rehabilitation intervention efficacyis difficult for methodological reasons.

New technologies and neuroscience ad-vances allow us to foresee development of evi-dence-based neurorehabilitation interventionsimproving functional outcomes. The needfor such interventions will increase as the popu-lation ages. Developing patient-specific reha-bilitation programs using selected tools at selectedtimes during recovery now seems within reach.

REHABILITATION SETTINGSApproximately 6-8% of Medicare pa-

tients admitted to acute care hospitals will

well as a phone number to schedule paratansitfor individuals unable to use public transpor-tation. Care providers will want to closelymonitor these patients for signs of depression,self-neglect, and isolation as all can occur as aresult of loss of driving privileges (see the AMAguide for specific monitoring methods). 6

FUTURE DIRECTIONSThere is much research to be done in

the area of assessing older driver safety. AsMolnar and colleagues point out, the estab-lishment of empirically validated cut scoresfor visual functioning, motor skills, and cog-nition is necessary to help physicians confi-dently identify truly at risk drivers.8

A second priority is to establish clini-cally meaningful outcome measures. Cer-tainly poor performance on a simulated driv-ing test or pre-determined driving route isan indication for concern and monitoring,but there is not a perfect correlation betweenthese measures and crash risk. In this regard,a new study examining risk factors for poordrivers in a naturalistic setting has begun atRhode Island Hospital. In this study, fundedby the National Institute of Health, olderdrivers both with and without dementia willbe examined by video camera recordings intheir own cars and driving in their neigh-borhoods. These recordings will be com-pared to performance on a standardized road

test and computerized office tests. For moreinformation about participation or referrals,contact Lindsay Miller at 444-0789.

A third and final priority is to exam-ine the benefits of driver education pro-grams. If physicians are going to recom-mend these interventions, as with any othertreatment, efficacy trials are necessary.

REFERENCES1. US Interim Projections by Age, Sex, Race, and His-

panic Origin. Table 2a. Projected Population of theUnited States, by Age and Sex: 2000 to 2050. http://www.census.gov/ipc/www/usinterimproj/

2. US Department of Transportation National High-way Traffic Safety Administration. Traffic SafetyFacts 2000. http://www-nrd.nhtsa.dot.gov/Pubs/2000OLDPOP.PDF

3. Duchek JM, Carr DB, et al. Longitudinal drivingperformance in early-stage dementia of the Alzheimertype. J Am Geriatr Soc 2003;51:1342-7.

4. Man-Son-Hing M, Marshall SC, et al. Systematicreview of driving risk and the efficacy of compen-satory strategies in persons with dementia. J AmGeriatr Soc 2007;55:878-84.

5. Amick MM, Grace J, Ott BR. Visual and cognitivepredictors of driving safety in Parkinson’s diseasepatients. Arch Clin Neuropsychol 2007;22:957-67.

6. The American Medical Association. Physician’s Guideto Assessing and Counseling Older Drivers. http://www.ama-assn.org/ama/pub/category/10791.html

7. Jang RW, Man-Son-Hing M, et al.Family physicians’ attitudes and practices regard-ing assessments of medical fitness to drive in olderpersons. J Gen Intern Med 2007;22:531-43.

8. Molnar FJ, Patel A, et al. Clinical utility of office-basedcognitive predictors of fitness to drive in persons withdementia. J Am Geriatr Soc 2006;54:1809-24.

9. Ott BR, Anthony D, et al. Clinician assessmentof the driving competence of patients with de-mentia. J Am Geriatr Soc 2005;53:829-33.

10. Kua A, Korner-Bitensky N, et al. Older driver retrain-ing. J Safety Res 2007;38:81-90. Epub 2007 Feb 14.

11. The Rhode Island Department of Elderly Affairs.Pocket Manual of Elder Services. http://w w w . d e a . s t a t e . r i . u s / d o c u m e n t s /2007%20Pocket%20Manual.pdf

Melissa Amick, PhD, is Staff Neuropsy-chologist, Memorial Hosiptal of RI, and Clini-cal Assistant Professor, The Warren AlpertSchool of Medicine at Brown University.

Brian R. Ott, MD, is Director, TheAlzheimer’s Disease & Memory DisordersCenter, Rhode Island Hospital, and Profes-sor, Department of Clinical Neurosciences,The Warren Alpert Medical School ofBrown University.

Disclosure of Financial InterestsThe authors have no financial inter-

ests to disclose.

CORRESPONDENCEMelissa M. Amick, PhDMemorial Hospital of RIDepartment of Medical Rehabilitation111 Brewster StreetPawtucket RI, 02860Phone: (401) 729-2326e-mail: [email protected]

need inpatient rehabilitation. Medicare re-cipients comprise 75-80% of admissions toacute rehabilitation facilities (ARFs). In2007, the average age of patients admittedto ARFs in the US was 67 years. After anaverage stay of 16 days,1 73% of these pa-tients returned home. With limited staffingand ill patients, acute care hospitals usuallyprovide one or two brief therapy treatmentsa day. Immobilization for even only a fewdays causes deconditioning which takeslonger to reverse than to develop; therapyshould be initiated as soon as possible. Long-term acute care (LTAC) facilities managepatients with persistent intensive nursing andmedical care needs. Acute rehabilitation hos-pitals admit 50-60% of their patients withneurologic diagnoses, generally providingthe most intensive rehabilitation programsavailable for patients who can tolerate and

benefit from at least three hours of therapyper day. Subacute rehabilitation units pro-vide programs for patients who cannot tol-erate, or will not benefit from, more inten-sive therapy. Home therapy may often besuboptimal due to lack of equipment andinefficient scheduling. Outpatient therapyvaries between one and five sessions a weekfor medically stable patients. Patients maymove between these settings, depending onmedical status and rehabilitation needs.

ROLE OF PHYSICIANS INREHABILITATION

Primary care physicians and/orphysiatrists provide general medical manage-ment and help to prevent complications. Im-mobility increases risks of infection, deepvenous thrombosis, and skin breakdown,which can usually be effectively prevented.


to months, cells in the ischemic penumbrarecover somewhat. These cells may havegreater potential for synaptic plasticity via in-creased expression of genes for neurotrophinsand angiogenesis.3 The third stage is thoughtto consist of distant undamaged tissue takingon the functions of lost tissue. Several mecha-nisms may subserve neural plasticity includ-ing synaptogenesis, axonal regrowth,neurotrophins, and neurogenesis(stem cells).4

These mechanisms seem to be inhibitedin more mature tissue. Enhancing naturalmechanisms of plasticity may improve recov-ery. For example, antibodies to MAG promoteaxonal regrowth.5 Although motor control isvirtually fixed after adolescence, the reorgani-zation occurring in damaged neurologic tissuemay present an opportunity to intervene. Po-tential interventions, including neurotrophins,stem cells, and pharmacologic potentiation, aretechnically challenging and expensive. Elegant,noninvasive, and less expensive methods thatmay enhance neural plasticity are being inves-tigated. Different approaches will likely be ap-plicable in different situations.

NEW NEUROREHABILITATIONTECHNOLOGIES UNDERINVESTIGATION

Neurorehabilitation research is comingof age. Improvements in outcome measuresand study design allow new techniques tobe investigated in the context of random-ized, controlled, often multi-centered trials(RCTs). The EXCITE trial, a study of Con-straint-Induced Movement Therapy, dem-onstrates that multicenter RCTs for rehabili-tation interventions are feasible, and is serv-ing as a model for design of future studies.6

The Center for Restorative and Regen-erative Medicine (a collaboration of BrownUniversity and the Providence VA MedicalCenter led by Roy Aaron, MD, and JohnDonoghue, PhD), in collaboration with MITand Harvard, is becoming a major center forsuch research. Other local entities, includingCyberkinetics, Inc. (Foxboro, MA), AfferentCorporation (Providence, RI), and Rehabili-tation Hospital of Rhode Island (RHRI,North Smithfield), are at the forefront of theseefforts. Some of these investigational interven-tions are briefly described below.

“LOW TECH” INTERVENTIONSConstraint-Induced Movement

Therapy (CIMT) is based on the concept of“learned nonuse” in monkeys, a behavioralsuppression in which lack of success with use

of an impaired arm leads to preferential useof the unaffected arm.7 CIMT is a “forceduse” paradigm. The use of the unaffected armis limited (by a sling or mitt) and the affectedarm/hand undergoes intense therapy. Mul-tiple animal and human studies, including thelandmark EXCITE trial, have demonstratedthe technique to be quite effective in certainpopulations. There is some evidence that mea-surable cortical reorganization results. CIMThas been investigated mainly in patients withstroke and cerebral palsy, but is also beingapplied to lower limb impairment, traumaticbrain injury, and even aphasia.

STROKE INPATIENT REHABILITATIONREINFORCEMENT OF WALKINGSPEED (SIRROWS)8

Gait speed may be a surrogate markerfor gait quality, often the major limiting factorfor home discharge. Faster gait improvementin the inpatient rehabilitation setting mightresult in more efficient recovery with shorterlengths of stay. The World Federation ofNeurorehabilitation (WFNR), in collabora-tion with the American Society ofNeurorehabilitation (ASNR), is running theSIRROWS trial to determine if this is true.This elegant and simple RCT involves givingpatients daily feedback about their walkingspeed, with encouragement to walk faster,safely. SIRROWS is the first attempt to de-velop an internationally controlled multicentertrial in neurorehabilitation. Twenty centers,mostly outside of the US, are involved. RHRIwill soon become a SIRROWS study site.

“MEDIUM TECH” INTERVENTIONSSensory Enhancement

Afferent Corporation (Providence, RI) hasseveral devices under development. Afferent’stechnology involves applying subthresholdmechanosensory stimuli to affected limbs toenhance afferent information flow to the brain.The premise is that sensory impairment con-tributes to functional impairment after nervoussystem injury. Improving sensory functioncould improve recovery by enhancing plastic-ity. Studies show the system to be effective insensory-mediated gait disorders.9 A pilot study,using the technology in patients with arm weak-ness after stroke, is being conducted atSpaulding Rehabilitation Hospital in Boston.

“HIGH TECH” INTERVENTIONSRobotics

Various robotic devices are being stud-ied for use in rehabilitation settings. The MIT-

Inadequate sleep interferes with therapy, pos-sibly contributing to cognitive impairments.Obesity and depression must be treated earlyand aggressively. Reassessment of medicationsis critical; patients often come to rehabilita-tion on medications they no longer need.

The role of the neurologist has expandedas patients survive acute neurologic disease atprogressively higher rates and more is knownabout neurologic recovery. First and foremostis accurate diagnosis; some patients arrive torehabilitation with incorrect diagnoses. Pa-tients with traumatic brain injury must bemonitored for hydrocephalus and subduralhematomas. The neurologist’s role in educat-ing therapists, patient, and family, by describ-ing impairments, expected course of recov-ery, and prognosis, is critical to program de-sign and realistic goal-setting.

EVOLUTION OFNEUROREHABILITATION AS ACLINICAL SPECIALTY2

Rehabilitation Medicine as a medicalsubspecialty, the disciplines of Physical, Oc-cupational, and Speech Therapies, and dedi-cated Rehabilitation Units developed in theearly to mid 20th century as a result of warinjuries (amputations) and polio. The “tradi-tional” rehabilitation model was based onstatic impairments and compensation for,rather than restoration of, function. In thelate 20th century, improved survival fromacute neurologic injury and an emphasis onevidence-based practice resulted in improvedoutcome measures and a “neurologic” modelof rehabilitation incorporating pathology andprognosis. Powerful technologies and greaterunderstanding of plasticity present the possi-bility of enhancing natural recovery processesand evaluating these techniques. Clinicianswill be able to develop the rehabilitation “holygrail”: evidence-based patient-specific reha-bilitation programs using selected techniquesat selected times during recovery.

MECHANISMS OF RECOVERY ANDTHE CONCEPT OF NEUROPLASTICITY

A brief summary of recovery mecha-nisms in stroke with a three-stage model is in-structive. In the first stage, reduction of edema(causing mass effect and metabolic depression)over days to weeks improves the function ofnoninfarcted tissue as intercellular commu-nication improves. The second and third stagesof recovery are marked by spontaneous neu-rophysiologic adaptations referred to as neu-ral plasticity. In the second stage, over weeks


MANUS robots, under development over thelast 15 years at the MIT biomedical engineer-ing department, are devices designed to pro-vide consistent doses of intense limb exercise.They provide decreasing levels of assistance asthe patient’s own abilities improve. The devicesalso provide kinematic data that measure ef-fectiveness of the technique and give insightinto natural recovery. Initial studies are encour-aging, and demonstrate improved motor func-tion in involved limbs which appears to be sus-tained for years after a therapeutic trial of 4-8weeks.10 A VA multicenter trial (supervised byAlbert Lo, MD, PhD, of the Providence VA)utilizing various versions of MIT-MANUS ro-bots for stroke patients is currently underway.

Treadmill DevicesSeveral devices combining a treadmill

with partial-weight-bearing-support havebeen developed over the last 10 years. TheLokomat (Hocoma, Inc., Switzerland) de-vice has the added feature of a lower bodyexoskeleton providing partial assistance forstepping, and has shown benefit in patientswith spinal cord injury. Studies of benefitto patients with stroke have been mixed.Results of the first study of its use in pa-tients with multiple sclerosis (Albert Lo,MD, PhD) should be available shortly. TheAutoambulator, a similar device developedfor HealthSouth, is also being studied.

Cortical StimulationBrain stimulation might enhance neu-

ral plasticity. Noninvasive devices (includingTranscranial Magnetic Stimulation and DCCurrent Stimulation) designed to stimulatethe cerebral cortex during therapy are un-der investigation. A multicenter controlledtrial is currently underway to determine ifan epidurally implanted electrode (NorthstarNeuroscience), providing subthresholdstimulation during physical therapy, en-hances recovery (Spaulding RehabilitationHospital in Boston is a participant).

Brain-Computer InterfacesPatients with severe neurologic disabili-

ties usually have some residual muscle func-tion (finger, eyelid, or eye movements) allow-ing at least rudimentary communication.Some patients (e.g., ALS, brainstem stroke)are completely paralyzed despite having nor-mal or only mildly impaired cognition(“locked-in”), resulting in inability to com-municate or influence the environment.Brain-computer interfaces (BCI) are devices

that detect and decode brain signals, allow-ing control of external devices. The Braingate(Cyberkinetics, Inc, Foxboro, MA) device,developed in John Donoghue’s laboratoryat Brown University, is an electrode arrayimplanted on the cerebral cortex. A com-puter decodes detected signals to determinethe individual’s intended movements. A pi-lot trial with human subjects has demon-strated that patients can operate cursors oncomputer screens with their thoughts,11,12 al-lowing control of external devices such astelevisions and robotic arms.

A less invasive device, the WadsworthBCI Home System (Laboratory of NervousSystem Disorders, The Wadsworth Center,NY State Dept of Health), uses surface elec-trodes and software to detect and compileEEG signals which patients learn to modu-late to select characters on a computer screen.This system has enabled some patients withALS and other severely disabling disordersto communicate and send email. Amulticenter trial is being planned to betterassess the effectiveness and efficacy of thissystem with ALS patients on a larger scale.

CONCLUSIONSPlasticity exists particularly in the post-

injury period, even in the older population.Many possible new treatments are being de-veloped. Particular epochs during thepostinjury period may be windows of oppor-tunity for intervention. Optimization of thera-pies for different types of patients is a majorchallenge. Ongoing research will determinewhich treatments should be done for whichpatients, and when. New models of recoveryare under development to enable us to capi-talize on advances in neuroscience and tech-nology to improve rehabilitation outcomes.

Several landmark studies (recent, on-going, and upcoming) are demonstratingthat neurorehabilitation research is no longerin the back reaches of anecdotal evidenceand unprovable theories. Both low-tech butelegant interventions and sophisticated tech-nologies clearly have roles in improving thefunctioning of patients with both mild andsevere neurologic disabilities, by enhancingthe nervous system’s natural plasticity. Thisgoal is a huge challenge, particularly in thegeriatric population. We now have tech-niques to perform valid and reliable studiesof these interventions. Neurorehabilitationis worthy of being considered a medical sub-specialty subject to the standards of evidence-based medicine.

REFERENCES1. eRehabdata.com and Bazemore, Lisa (eRehab)

personal communication 10/17/07.2. Dobkin BH. The Clinical Science of Neurologic Reha-

bilitation, 2nd edn. Oxford University Press, 20033. Wei L, et al. Collateral growth and angiogenesis

around cortical stroke. Stroke 2001; 32:2179-84.4. Kempermann, et al. J Neurosci 2002;22:635-8.5. Lehmann M, et al. Inactivation of Rho signaling

pathway promotes CNS axon regeneration. JNeurosci 1999; 19:7537-47.

6. Wolf SL, et al. Effect of CIMT on upper extrem-ity function 3-9 months after stroke. JAMA 2006;296:2095-104.

7. Taub E, et al. Technique to improve chronic motordeficit after stroke. Arch PM&R 1993; 74:347-54.

8. Latham N, et al. Physical therapy during strokerehabilitation for people with different walkingabilities. Arch PM&R 2005; 86:41-50.

9. Priplata AA, et al. Noise-enhanced balance con-trol in patients with diabetes and patients withstroke. Ann Neurol 2006;59:4-12.

10. Volpe B, et al. Is robot-aided sensorimotor train-ing in stroke rehabilitation a realistic option? CurOp Neurol 2001;14:745-52.

11. Serruya MD, Hatsopoulos NG, et al. Instant neu-ral control of a movement signal. Nature2002;14;416:141-2.

12. Hochberg LR, Serruya MD, et al. Neuronal en-semble control of prosthetic devices by a humanwith tetraplegia. Nature 2006; 442: 164-71.

Stephen T. Mernoff, MD is Chief,Neurology Section, Providence VA Medi-cal Center, Clinical Assistant Professor ofClinical Neurosciences, The Warren AlpertMedical School of Brown University, Di-rector, Neurorehabilitation Program, Re-habilitation Hospital of Rhode Island, andDiplomate, American Board of Psychiatryand Neurology (Neurology).


ests to disclose.Discussion(s) of off-label usage of any

products or services: Several devices de-scribed in the article are investigationalbut are approved by the FDA for inves-tigational use: devices by AfferentCoporation, MIT-MANUS robot,Locomat, Autoambulator, Northstartdevice, Braingate (Cyberkinetics, Inc.),and Wadsworth BCI Home System.

CORRESPONDENCEStephen T. Mernoff, MDProvidence VA Medical Center, 111N830 Chalkstone AvenueProvidence, RI 02908 Phone: (401) 273-7100x3427e-mail: [email protected]


The Value Equation: Costs and Quality ofRhode Island’s Health Plans

Bruce Cryan, MBA, MS

RHODE ISLAND DEPARTMENT OF HEALTH • DAVID GIFFORD, MD, MPH, DIRECTOR OF HEALTH EDITED BY JAY S. BUECHNER, PHD

Two health plans, Blue Cross and Blue Shield of Rhode Is-land (Blue Cross), and United Healthcare of New England(United), provide health coverage to a large majority of RhodeIsland (RI) residents who are commercially insured. To assesswhether the purchasers of these plans’ products are receiving value,one must necessarily examine its two components, cost and qual-ity. For Rhode Islanders to receive good returns from their expen-ditures for health insurance, that coverage should be equally orless expensive and deliver the same or better quality services thansimilar plans elsewhere. Information about how these two plansperform is therefore essential toevaluating their relative value.

In response to this need forinformation, the RI GeneralAssembly passed the HealthCare Accessibility and QualityAssurance Act in 1996 (RhodeIsland General Laws 23-17.13).1 The Act institutedhealth plan performance re-porting in the state, which issummarized annually, and mostrecently in the Rhode IslandHealth Plans’ Performance Re-port (2006).2 The informationpresented here is derived fromthat report.

METHODSThe Rhode Island Depart-

ment of Health’s Center forHealth Data and Analysis con-ducts an annual health plan datacollection from three primaryaudited sources: Statutory Filingsto the state’s Department of Busi-ness Regulation and Health PlanEmployer Data and InformationSet (HEDIS) reports and Con-sumer Assessment of HealthcareProviders and Systems(CAHPS) survey data submittedto the Department of Health.3

From these data, 32 mea-sures are evaluated, comprisingeight separate dimensions ofperformance (enrollment, costs,utilization, prevention, screen-

ing, treatment, access, and satisfaction). For definitions of thesemeasures, see the source report.2 To ascertain relative perfor-mance, the measures for each plan are compared to the aver-age of all commercial health plans in New England.3

RESULTSOf Rhode Island’s 342,000 commercially insured popu-

lation, most are covered by two carriers, Blue Cross, with a2006 market share of 64.8%, and United, with a share of14.6%. The remainder of the market (20.6%) consists of a

Figure 1. Average health plan premium per member per month, by component, Blue Cross ofRhode Island, United Healthcare of New England, and New England aggregate, 2006.

Figure 2. Health plan member satisfaction with health plan and health care, Blue Cross ofRhode Island, United Healthcare of New England, and New England average, 2006.


number of smaller plans, none of which are domiciled in RhodeIsland. [Note that these data include only the insurers’ “fully-insured” members and exclude members of plans where thepurchaser (employer) is self-insured.]

On average in 2006, commercial health insurance costslightly less in RI than in New England. (Figure 1) Blue Cross’monthly premiums were 2% lower than regional premiums($317 vs. $325), and United’s premiums were 6% lower($305 vs. $325). In addition, both RI plans spent relativelyless on medical services for their members (2% less for BlueCross and 15% less for United).

With few exceptions, both Blue Cross and United gener-ally performed at or below average when their clinical qualitymeasures were compared to the New England values. (Table1) For Blue Cross, 12 of its 20 quality measures were equiva-lent to the regional averages, one measure was better, and theremaining seven were worse than these comparables. ForUnited, nine of its 20 quality measures were equivalent to theregional averages, two measures were better, and the remain-ing nine were worse than these comparables. Given that NewEngland health plans consistently post some of the highest qual-ity (and satisfaction) scores in the country, this regional com-parison provides a rigorous benchmark for RI plans.

In addition to an individual plan’s relative performance onthe clinical measures, the absolute values on some of the clinical

measures are worth examination. For example,the low rates of chlamydia screening (BlueCross: 40%; United: 39%) and antidepressantmedication management (Blue Cross: 26%;United: 24%) highlight the need for furtherimprovement in these areas.

Proxy measures of whether members per-ceive value in their plans may be obtained frommember satisfaction surveys. Member satisfac-tion with Blue Cross’ performance as a healthplan was 4 percentage points higher than theregional rate in 2006 (69% versus 65%), whilemember satisfaction with United was 15 percent-age points below that comparable (50% versus65%). (Figure 2) There was little difference inmembers’ satisfaction with their healthcare ser-vices between the two plans and in comparisonwith the New England rate. Interestingly, re-gardless of geographic area or health insurer,more members were satisfied with theirhealthcare services than with their health plans.

DISCUSSIONIncreasingly, the public, purchasers, pro-

viders, and policymakers are requiring mean-ingful information about health plans. Since1998, the Department of Health has trackedthe performance of this industry and producedannual reports on the subject.2

With the small number of health plansin the state and the market dominance ofBlue Cross, most Rhode Islanders have lim-

ited choice of carrier. The lack of widespread selective con-tracting also means that most plans deliver services through asimilar network of physicians, hospitals, and other providers,and the lack of differentiation between the two plans in theirhealthcare satisfaction rates bears this out.

Therefore, the real value in publishing this information isless in aiding consumer choice and more in fostering account-ability of the industry. Purchasers deserve to know how wellthe plans are performing and policymakers need empirical evi-dence to inform their efforts. An added benefit is that theperformance of health plans will likely improve if for no otherreason than the results are made public.

Bruce Cryan, MBA, MS, is a Health Policy Analyst in the Cen-ter for Health Data and Analysis, Rhode Island Department of Health.

Disclosure of Financial InterestsThe author has no financial interests to disclose.

REFERENCES1. See http://www.rilin.state.ri.us/Statutes/TITLE23/23-17.13/INDEX.HTM.2. Cryan B. Rhode Island Health Plans’ Performance Report 2006. Providence RI:

Rhode Island Department of Health and Office of the Health Insurance Com-missioner. In press.

3. For information on the HEDIS and CAHPS programs, see the website of theNational Committee for Quality assurance (NCQA) - http://www.ncqa.org.


A recent decision by the Rhode Island Director of Healthto close an unlicensed ambulatory surgery center and to sus-pend the medical license of the owner underscores the needfor the appropriate regulation of cosmetic surgery.

In September 2007, the Rhode Island Department of Health(HEALTH) closed an ambulatory surgery center owned and oper-ated by a physician licensed in the State of Rhode Island after theRhode Island Board of Medical Licensure and Discipline (“theBoard”) concluded that the owner/operator had performed a vari-ety of cosmetic surgeries in an unlicensed outpatient facility. As well,the Board concluded that the physician had allowed unqualifiedemployees to deliver anesthesia to patients at the facility.

Public Health is invested in the accreditation, licensure, andregulation of physicians, surgeons and their facilities. Many stateshave considered legislation regarding the licensure and regulationof office-based surgery, but few have followed though. At present,only six states have statutes of this type in place: Rhode Island, Cali-fornia, Florida, New Jersey, Pennsylvania, and Texas.1 In Rhode Is-land, legislation was passed in 1999 requiring physicians to be spe-cially licensed by HEALTH in order to perform office-based sur-gery, and in 2001, the law was amended, requiring that the facilitiesbe accredited for Level II and Level III anesthesia (intravenous andgeneral) within 24 months of licensure.2 To ensure the highest levelof patient safety, all states should consider similar legislation.

Under Rhode Island law, as specified by “Rules and Regu-lations for the Licensure of Physician Ambulatory Surgery Cen-ters and Podiatry Ambulatory Surgery Centers (R23-17-PASC),”surgery is defined as follows:

1.21 “Surgery” means the excision or resection partial/com-plete, destruction, incision or other structural alteration ofhuman tissue by any means. Surgery shall have the samemeaning as “operate.”

Certain procedures are exempt from R23-17-PASC:

1.8 “Exempt procedures” means: a) Minor surgical proce-dures such as excision of skin lesions, moles, warts, lipomasand repair of lacerations, incision and drainage of superficialabscesses, or surgery limited to the skin and subcutaneoustissue performed under topical or local anesthesia not in-volving drug induced alteration of consciousness other thanminimal pre-operative tranquilization of the patient; b) Pro-cedures not requiring or using conscious sedation techniquesor pre-operative medications other than minimal pre-opera-tive tranquilization of the patient; c) Procedures requiring orusing only local, topical, or no anesthesia.”

All medical laser procedures fall under the aegis of the RhodeIsland statute, including ablative and non-ablative skin rejuvena-tion procedures, tattoo removals, treatment of pigmented and vas-cular lesions, and laser hair removal. The reason for regulating allmedical laser procedures, including laser hair removal, is the sheervariety (and changing variety) of laser devices – including a wide

range of output – and the potential for lasers to do irreparableharm to a patient if used incorrectly. Thus, in Rhode Island, indi-viduals who wish to perform any of these cosmetic laser surgeries inan office setting must apply for a special license.

In December 2003, the Rhode Island Board of MedicalLicensure and Discipline strengthened its regulatory positionon the use of medical lasers with the following decision:

12/15/2003 - Policy statement on office based estheticprocedures:

It is the position of the Board that office based cosmetic oresthetic procedures that require the use of medical lasers, high-frequency radio waves, or injection of sclerosing chemicals orbiologically active compounds [e.g. Botulinum toxin A, Botox]are medical procedures.

Therefore, prior to undergoing such procedures patients mustreceive a medical evaluation for appropriateness by a licensedand qualified physician or other practitioner acting withinhis/her scope of practice. Although these procedures may beperformed by an appropriately trained nonphysician workingunder the supervision and direction of a physician or otherpractitioner acting within his/her scope of practice, it is thesupervising physician’s [or other practitioner acting within his/her scope of practice] responsibility to assure that proceduresare conducted appropriately; with appropriate assessment, con-sent and follow-up; and upon appropriate patients; and thatall patient records are maintained according to standards ap-plicable for medical records; and that patient privacy is pro-tected. The supervising physician or other practitioner actingwithin his/her scope of practice is responsible for any proce-dures carried out by nonphysicians under his/her direction.

Physicians [or other practitioner acting within his/her scope ofpractice] who perform and supervise such procedures must beable to demonstrate appropriate training and experience. Suchtraining and experience may include, but is not limited to, resi-dency or fellowship. The physician or other practitioner actingwithin his/her scope of practice is responsible to assure and docu-ment adequate training for individuals under his/her supervision.

Additionally, other cosmetic procedures such as dermabrasion orthe application of potentially scarring chemical treatments [e.g.so-called chemical peels] should also meet this same standard.

[Rhode Island Board of Medical Licensure and Discipline. “Policystatement on office based esthetic procedures.” December 15,2003. http://www.health.ri.gov/hsr/bmld/positions.php]

Despite increased vigilance such as this, office-based laserhair removal remains especially troublesome to regulatethroughout the United States. Many unlicensed facilities per-form the work, unaware of potential dangers and of existingsafety regulations, e.g., those that limit maximum laser expo-sure or require eye protection. At least one death in the UnitedStates has been attributed to an overdose of anesthetic creambefore laser hair removal.3

Rhode Island Leads In Regulating Office-Based Cosmetic SurgeryShaun Najarian

DAVID GIFFORD, MD, MPH, DIRECTOR OF HEALTH

RHODE ISLAND DEPARTMENT OF HEALTH EDITED BY JOHN P. FULTON, PHD


Several national organizations seek to improve the qualityof office-based surgical practices:

• The American Association for Accreditation of Ambu-latory Surgery Facilities (AAAASF)

• The Accreditation Association for Ambulatory HealthCare (AAAHC)

• The Joint Commission for Accreditation of HealthcareOrganizations (JCAHO)

The JCAHO recently released safety goals for office-basedsurgeries.

Despite the best efforts of HEALTH, some health profes-sionals may continue to perform cosmetic surgical procedures inunlicensed facilities. It is important for healthcare providersthroughout the state to be vigilant for this possibility. At present,in addition to licensed hospitals and licensed freestanding surgi-cal centers, only five “office operatories” are licensed in RhodeIsland. Those who wish to verify the license status of a facility or

of a service provider may consult HEALTH’s website: http://www.health.ri.gov/hsr/professions/license.php.

REFERENCES1. Lapetina EM, Armstrong EM. Preventing errors in the outpatient setting.

Health Affairs 2002; 21: 28.2. Springer R. An update on office surgical regulations. Plastic Surgical Nurs

2004;24: 172.3. On February 18, 2005, National Public Radio’s (NPR’s), Adam Hochberg dis-

cussed the dangers of an unregulated laser industry on his show “All Things Consid-ered.” Hochberg reported on the case of a North Carolina woman who died from anoverdose of anesthetic cream that she applied before her laser treatment in January.

Shaun Najarian is an undergraduate at Providence Collegewho served as an intern for the Rhode Island Department ofHealth, Office of Medical Licensure and Discipline.


Today physicians have access to an enormous body of researchand knowledge regarding the pathophysiology of Alzheimer’s dis-ease. Pharmacologic treatment options have also increased signifi-cantly over the past few years. However, pharmacologic treatmentis only one part of the overall care plan for improving the quality oflife of patients suffering from Alzheimer’s and related dementias.

Long-term care facilities and adult day centers throughout RhodeIsland use a variety of creative and sensory therapies to enhance the livesof people with Alzheimer’s including aromatherapy and massage; paint-ing, pottery, sculpting; music and dance; exercise and cooking.

The “Memories Fade…Love Inspires” art exhibit, recently held atthe Bellini Ruggeri Gallery in Providence, showcased a collection ofwatercolor paintings and pottery pieces created by participants at theHope Alzheimer’s Center. The cover of this journal features the beau-tiful work of Theresa Aiello, a long time participant in the therapeuticart program at the Hope Center. Although Theresa, age 91, has had noformal art training, she is able to express herself through vivid color

Since opening its doors in 1995, art therapy has been a center-piece of the adult day program at the Hope Center. Through theyears, the Center has reported seeing many withdrawn and quietparticipants begin to engage in lively conversations about a specialplace or time in their life reflected in the painting.

Research conducted in the field of Alzheimer’s shows clear evi-dence that art therapy is a powerful, nonmedical way to engageminds in the grip of this disease. For people with memory loss,creative and sensory activities can help:

Promote well being Help maintain skillsAid communication by Enhance relationships

using sensory rather Utilize past skillsthan cognitive pathways Express emotion

Facilitate decision making Encourage cooperationCombat depression with others

Point of ViewCreative and Sensory Therapies Enhance the Lives of People With Alzheimers

John Stoukides, MD

Although treatment is not available today that can delay orstop the deterioration of brain cells in Alzheimer’s disease, studieshave consistently shown that active medical management ofAlzheimer’s and other dementias can significantly improve qualityof life through all stages of the disease for diagnosed individualsand their caregivers. Active medical management includes the inte-gration of support services like adult day services that offer creativeand sensory therapies into the overall treatment plan.

Most of the participants in the Hope Center’s art therapy pro-gram live at home, where they are cared for by family and friends.Even when care is provided at home, most families also seek othersources of help, particular as the disease progresses. As a trustedinformation source for family caregivers, physicians can discuss thebenefits of choosing an adult day program or long-term care pro-vider that offers creative and sensory therapies for people withAlzheimer’s and other forms of memory loss.

John Stoukides, MD, is Medical Director of the Rhode Island Mood& Memory Research Institute and Director of Geriatric Medicine atRoger Williams Medical Center.


CORRESPONDENCEJohn Stoukides, MDe-mail: [email protected]


The Prefixes of the Past�

Physician’s Lexicon

Number (a)223201

364350

Number (a) Rates (b) YPLL (c)2,730 255.2 3,601.52,261 211.4 6,077.5

388 36.3 562.0565 52.8 9,003.0434 40.6 392.5

Reporting Period

12 Months Ending with May 2007May

2007

UnderlyingCause of Death

Live BirthsDeaths

Infant DeathsNeonatal Deaths

MarriagesDivorces

Induced TerminationsSpontaneous Fetal Deaths

Under 20 weeks gestation20+ weeks gestation

Number Number Rates942 13,521 12.7*826 9,943 9.3*

(9) (108) 8.0#(6) (74) 5.5#

394 6,879 6.4*187 3,026 2.8*386 4,919 363.8#

49 994 73.5#(45) (920) 68.0#

(4) (74) 5.5#

Reporting Period12 Months Ending with

November 2007November

2007Vital Events

Rhode Island MonthlyVital Statistics Report

Provisional OccurrenceData from the

Division of Vital Records

(a) Cause of death statistics were derived fromthe underlying cause of death reported byphysicians on death certificates.

(b) Rates per 100,000 estimated population of1,067,610

(c) Years of Potential Life Lost (YPLL)

Note: Totals represent vital events which occurred in RhodeIsland for the reporting periods listed above. Monthly pro-visional totals should be analyzed with caution because thenumbers may be small and subject to seasonal variation.

* Rates per 1,000 estimated population# Rates per 1,000 live births

RHODE ISLAND DEPARTMENT OF HEALTH

DAVID GIFFORD, MD, MPHDIRECTOR OF HEALTH EDITED BY COLLEEN FONTANA, STATE REGISTRAR

VITAL STATISTICS

Diseases of the HeartMalignant Neoplasms

Cerebrovascular DiseasesInjuries (Accidents/Suicide/Homicde)

COPD

The prefix, particularly when employedfor the technical terms such as those whichserve medicine, informs us about the rootof the noun: its size [eg, macro-, micro-,], itsspatial relationship [eg, juxta-, infra-, supra-], as well as an array of attributes to definefor us more precisely the modified mean-ing of the root word. A special group ofprefixes, either Latin or Greek, also tells uswhether or not the noun is old, ancient,backwards or primitive. These prefixes in-clude the following: ante-, paleo-, palin-,pre-, presby-, pretero- and proto-.

Ante-, Latin signifying before or priorto, is seen in words such as antecubital andantenatal [but not antigen or antacid.]Paleo-, from the Greek meaning primitiveor ancient, appears in such technical termsas paleopathology, paleontology, paleo-striatum [a synonym for the globus

pallidus] and Paleocene [the geologic ep-och preceding the Eocene.] Palin-, inGreek meaning backwards, appears inwords such as palindrome [a word orphrase reading the same backward or for-ward], palingenesis [meaning regenerationor rebirth] and palinopsia [a recurrent vi-sual disorder.]

The pal- prefix such as in palinopsia,however, can be confusing. Palisade, forexample, is derived from the Latin word,palus, meaning a stake. Palliation, mean-ing to extenuate, to cloak [and, specifically,to lessen pain] comes from the Latin, pal-lium, meaning a cloak. Pallid, meaningashen or pale, is from the Latin, pallidus,meaning pale or colorless [as in globuspallidus.] Paludism, an archaic name formalaria, is from the Latin, palus, meaningmarsh or swamp. And pallesthesia, mean-

ing the appreciation of vibration, is fromthe Greek, pallo, meaning to quiver.

The Greek prefix, presby-, meaning ven-erable or ancient, is seen in words such as pres-byopia, presbycusis, an older euphemism fordeafness, and Presbyterian. The Latin prefix,pretero-, meaning coming before or beyond,appears in words such as preternatural [a syn-onym for supernatural] and preterition.

Medical terms beginning with theLatin prefixes pro- and pre- are too numer-ous to list. Precocity, for example, is fromthe Latin praecox, meaning to ripen early,thus explaining the phrase, dementia prae-cox, an older term for schizophrenia. Pre-cipitation is from the Latin, praecipitare,meaning to cast down headlong, and ulti-mately derives from capitus, meaning head.

– STANLEY M. ARONSON, MD


�

�

�

�VOLUME 1 PER YEAR $2.00NUMBER 1 SINGLE COPY, 25 CENTSPROVIDENCE, R.I., JANUARY, 1917

The Official Organ of the Rhode Island Medical SocietyIssued Monthly under the direction of the Publications Committee

NINETY YEARS AGO, MAY, 1918Frank J. McCabe, MD, in “Eye Strain as Related to Gen-

eral Practice,” discussed types of asthenopia: accommodative,“due to errors of refraction and to strain of the…muscle;”muscular, “due to an abnormal condition of the…muscles ofthe eye;: nervous, “due to some faulty condition of the nervoussystem;” and reflex, “due to abnormalities in the organism out-side of the eye and the nervous system.” Accommodative strainswere the most common.

Frederick V. Hussey, MD, in “A Review of 100 Consecu-tive Cases of Acute Diseases of the Appendix, Gall Bladder,Duodenal and Gastric Ulcers Which Have Come to Opera-tion,” faulted general physicians’ “lack of courage – reluctanceto advise radical measures in the beginning, without first try-ing out some of the older methods of treatment, which bringshis patient into an extreme condition.” The author concededthat often patients wanted to avoid surgery. Of 46 cases of acutegangrenous appendicitis, all drained, three died; the averagehospital length of stay for those patients was 3 weeks.

In a War Department memo, the Office of the SurgeonGeneral, Washington, reminded physicians of the rule forbid-ding publication of professional papers related to officialrecords or military service, without permission.

An editorial, “Illegal Operations,” described the case of awoman recently convicted of an “illegal operation.” “Thewoman had enjoyed a lucrative clientele for some time, pursu-ing her work in a respectable residential section of Providence.”The editor assumed that this was the first case of a woman con-victed in Rhode Island for the “crime of performing abortions,and, furthermore, … the conviction did not depend upon thedeath of the unfortunate patient.” The editorial congratulatedboth the police and the Attorney General. “…decent publicopinion cannot fail to approve of the outcome.”

FIFTY YEARS AGO, MAY 1958Eugene T. Lothgren, MBA, general agent, Northwestern

Mutual Life Insurance Company, contributed “Tax Savings inEstate Planning for Physicians.” He urged: “action is essentialto security and peace of mind.”

The Division of Vital Statistics of the Rhode Island De-partment of Health contributed “Acute Poliomyelitis in RhodeIsland, 1948-57.” Many Americans, including Rhode Island-ers, were not yet vaccinated. “Unless there is a speedup in thepolio vaccination program it is the opinion of the Surgeon Gen-eral, Leroy E. Burney, that serious outbreaks of poliomyelitiscould occur this summer.” The State traced wide fluctuationsin incidence: in 1948, 8 cases; in 1949, 157 cases; in 1950, 55cases; in 1951, 15 cases. The toll rose to 295 in 1953, droppedto 123 in 1954, peaked at 421 in 1955.

Robert W. Hyde, MD, in “Butler Health Center Today,”described the 1957 reorganization of Butler Hospital into aHealth Center, with outpatient and day services.

David S. Liang, MD, and Asdrubal De Carvalho, MD, in“Leiomyoma of the Prostate,” described an 87 year-old man,admitted to Joseph’s with “painful gross hematuria for 2 days.”Surgeons found and removed an intravesical tumor.

Bencel L. Schiff, MD, in “Dermatitis from Acetozolamide(Diamox),” discussed the case of a 45 year-old woman whohad been given 250 mg daily for treatment of glaucoma, andthe case of a 57 year-old man, treated for hypertension and leftventricular failure.

TWENTY-FIVE YEARS AGO, MAY 1983Carl H. Critz, MD, W. Martin DeLuca, PA, and Arun K.

Singh, MD, in “Iatrogenic Extra-Corporeal Hemolysis duringCardiac Surgery in a Child: A Case Report,” postulated “shear-stress in transfusion filter as the cause of the hemolysis.” A fouryear-old girl had been admitted to Rhode Island Hospital forsurgical correction of both an atrial septal defect and pulmo-nary valvular stenosis.

Frank Newman, PhD, President, The University of RhodeIsland, delivered the 1982 Fiorindo A. Simeone oration at TheMiriam Hospital: “Notes from Underground.” His subject wasthe anatomy of recovery. He detailed his experience of hospi-talization, including “coping with fear,” and “role of the self inhealing.”

A.J. Migliaccio, MD, FACS, and A.V. Migliaccio, MD,FACS, contributed “The Use of a Feeding Gastrostomy as aMeans of Preventing Staple Line Disruption in Gastric Opera-tions for Morbid Obesity.”

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