Copyright HandsOn Therapy Schools 2009 PATH… · function 25% is bulbar form Speech, swallowing, control of tongue Frequent, extreme mood swings (emotional incontinence) Tends to

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1 Functionand

Structureclick here

2 ChronicDegenerative

Disordersclick here

3 MovementDisorders

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4 InfectiousDisorders

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5 PsychiatricDisorders

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6 NervousSystemInjuriesclick here

7Other

NervousSystem

Conditionsclick here

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Function

Transmit electrical impulses to and from central nervous system (CNS)(sensation and motor control)

Interconnecting neurons in CNS provide for consciousness,learning, creativity, memory (outside this scope) pt 1

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Structure

Nerves are bundles of individual neurons. Each neuron has axon,cell body, dendrite;

Neurons communicate atsynapses, using

neurotransmitters

Peripheral nerves = bundles of axons and dendrites

___________________

Sensory neurons: long dendrites, cell body in dorsal rootganglion (DRG), short axons

Motor neurons: long axons, cell body and short dendrite inventral horn of spinal cord

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All motor neurons terminate in muscle or glandular tissue pt 1 Back Next

Copyright HandsOn Therapy Schools 2009 PATH4



Reflex Arc

Connects sensation to motor response Reaction to spinal cord response to synapses,whereby information travels up the spine into the

brain

Neurons covered with Schwann cellsform myelin and neurilemma

___________________

Myelin in CNS and peripheralnervous system (PNS):

Speeds transmission, electricalinsulation

___________________

Neurilemma in CNS only:

Promotes repair of PNS tissue

___________________

Most PNS nerves run close to bonefor protection

___________________

Vulnerable in a few places





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General Neurological Problems

Most disorders that massage can affect involve pinching or distortion ofperipheral nerves

Massage mayaggravate or relieve

pressure

_______________

Major cautions formassage therapists:

Numbness (moredangerous than pain)

Verbal communication(watch for nonverbal

signals)

Medications (may haveinteractions with

massage)

Brain and spinal cord injuries are inaccessible

Patients can benefit from massage to maintain function

Proprioceptive adaptation may be subject to interruption

___________________

Psychological disorders are a different class

May benefit from massage for stress balance

Risk of interpersonal complications

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Chronic Degenerative Disorders

Alzheimer Disease

Amyotrophic Lateral Sclerosis

Multiple Sclerosis

Peripheral Neuropathy

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Alzheimer DiseaseProgressive degenerative brain disorder; Memory loss,personality changes, death

DemographicsAbout 5% of U.S. population (4.5

million)Half of people in nursing homes

$100 billion/year in direct, indirectmedical costs

Incidence increases with age10% people > 65 years

About half of people > 85 yearsWomen > men; may be related to

longer life span

Copyright 2009 Walters Kluwers Health l Lippincott Williams & Wilkins

Etiology

First observations were plaques and tangles:still leading issues

Plaques

Beta amyloid deposits on neuronsin brain

Stimulates inflammatory response:kills affected and nearbyunaffected cells

Neurofibrillary tangles

Tau in cytoskeletons collapses;cells fall out of relationship,become twisted and tangled

Can’t transmit messages, shrinkand die

Brain shrinks (See Image)

Fewer brain cells function, neurotransmitterlevels drop

Remaining neurons don’t work aswell

Other issues may contribute



Chronic inflammation, history ofhead injury, exposure to toxins,high cholesterol, low estrogen,and other factors

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more Alzheimer Disease

Signs and Symptoms Diagnosis Treatments Massage

Staging protocols varyMild, moderate, severeProgressive memoryloss from mild cognitiveimpairment to completedisconnection, organfailure

Conclusive only withautopsy

Tests to ruleout othersources ofdementia,evaluatementalstatusImportant toidentifyearly:medicationcan preserveearly stage

Differential DiagnosisCauses of permanentmemory loss other thanAD include

Vasculardementia Stroke andtransientischemicattack (TIA) Parkinsondisease Lewy bodydementia Huntingtondisease

Medication to preventreuptake ofacetylcholine

Mood,behavioralmodifiers

Patients respond well totouch

Lessdisruptive,betterorientation,etc.

Cautions:

Elderlyclients haveother healthproblems Inability tocommunicateverbally



Creutzfeldt-Jakobdisease

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Amyotrophic Lateral SclerosisAlso called Lou Gehrig disease in the United States and motorneurone disease in the United Kingdom; Progressivedegeneration of motor neurons in CNS and PNS; Large motorneurons on lateral aspect of spinal cord are replaced with fibrousastrocytes

DemographicsThree types: sporadic (mostcommon); familial (genetic),

Mariana Island varietyMostly people 40–70 years oldAverage age at diagnosis = 55About 5,000 diagnoses/year;30,000 with ALS in the United

StatesMen > women

Etiology

Cause unknown

Degeneration of motor neurons inspinal cord → progressive,irreversible atrophy of skeletalmuscle One-third of motor neurons for amuscle must be destroyed forsymptoms to develop

Factors:

Tangled neural fibers, deposits ofplaque Glutamate accumulates insynapses Interrupts only motor function;intellect and memory stay intact

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more Amyotrophic Lateral Sclerosis


75% is spinal variation

Loss ofcoordination,fine motorskills inhands, feet Progressestoward core;breathingmuscles arelast to losefunction

25% is bulbar form

Speech,swallowing,control oftongue Frequent,extrememood swings(emotionalincontinence)

Tends to befasterprogression

Upper motor neuronproblems

Progressivespasticity Exaggeratedreflexes

Positive

History, physicalexamination, nerveconduction studies,electromyographs Rule out musculardystrophy,hyperthyroidism,multiple sclerosis,postpolio syndrome,peripheral neuropathy,spinal cord restriction

Palliative

Moderateexercise,physicaltherapy (PT),occupationaltherapy (OT) Heat,whirlpools Speechtherapy Assistivedevices:braces,wheelchairs,computers,voice aids

Medication for fatigue,spasms, infections

New drugsmay limitglutamateaccumulation

PrognosisMost patients die 2–10years after diagnosis

Pneumonia,cachexia

Some live for decades(Stephen Hawking); notclear why/how

Appropriate for pain,within client resilience Work with health careteam



Babinski sign

Lower motor neuronproblems

Weakness,atrophy,musclecramps,fasciculations

Pain develops as thebody collapses; noattack on sensoryneurons

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Multiple SclerosisInflammation, degeneration of myelin sheaths in CNS; Probablyautoimmune

DemographicsWhites more than other groups

Mostly among people who live far

from equator, especially beforeage 15

Usually diagnosed 20–40 yearsold

Young women> young menOlder women = older men

300,000–350,000 live with MS

now25,000 new diagnoses/year

Etiology

Myelin sheath in CNS is attacked, destroyed Oligodendrocytes multiply to repair damage;ultimately fail

Myelin is replaced with scartissue

Electrical impulses are slowed or obstructed

Motor, sensory paralysis

Runs in flare/remission

With persistent flares the neuronis damaged: this is permanent

CausesMost agree on immune system attack on myelin sheath Genetic predisposition for autoimmunity

Probably a combination of predispositionand exposure to a trigger

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more Multiple Sclerosis


The great imitator: looks likelots of other disorders

Weakness Spasm Changes insensation Optic neuritis Urologicaldysfunction Sexualdysfunction Difficulty walking Loss of cognitivefunction Depression Lhermitte sign Digestivedisturbances Fatigue

Progression

Five patterns:

Possible, probable,definite MS Symptoms, familyhealth history, spinaltap, magneticresonance imaging(MRI), nerveconduction tests Official diagnosticcriteria:

Evidence oftwo or moreepisodesEpisodes offlare areseparatedby at least 1monthNo otherexplanationforsymptomscan befound

Differential DiagnosisLyme disease HIV/AIDS Scleroderma Vascular problems inbrain

Steroids can reduceinflammation; goodfor short term only Interferon betas:limit immune systemactivity Plasmapheresis (foracute situations) Also exercise, PT,OT, diet, sleep,stress management

Safest in remission;take care not tooverstimulate (→spasms, pain)

Exacerbatedwith heat:avoid rapidchanges inenvironment



Benign MS: onlyone flare Relapse/remitting(RRMS): flareand remission:most commonpresentation Secondaryprogressive MS(SPMS): onlypartial recoveryduring remission Primaryprogressive(PPMS): steadydecline infunction Malignant MS:rapidlyprogressive

Complications ofencephalitis Herniated, ruptureddisc Lupus CNS tumors Fibromyalgia B , folic aciddeficiency

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Peripheral NeuropathySymptom or complication of underlying problem: nerve damage

EtiologyMononeuropathy Polyneuropathy Can affect sensation, motor control; voluntary orinvoluntary muscle function Can be genetic anomaly Usually a complication of some other problem

Injury: carpal tunnel syndrome, thoracicoutlet syndrome, Bell palsy, disc disease,trigeminal neuralgia Infection: herpes simplex, herpes zoster,HIV/AIDS, Lyme disease, hepatitis, syphilis,leprosy Systemic disease: diabetes (type 1 or type2), renal failure, vitamin B deficiency,cancer; also autoimmune diseases,including lupus, Sjögren syndrome,sarcoidosis, Guillain-Barré syndrome. Toxic exposure: chronic alcoholism, sniffingglue, some medications, exposure to heavymetals (especially lead and mercury),solvents, other environmental contaminants

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more Peripheral Neuropathy

Signs and Symptoms Treatments Massage

Usually has slow onset

Depends on whichneurons aredamaged

Sensory: pain, tingling,hypersensitivity, loss ofsensitivity, numbness

Usually atextremities

Motor: twitching, cramps,atrophy of muscles Autonomic: problems with heartrate, blood pressure, respiratoryrate, digestive and urinaryfunction

Depends on source of problem

Chronic pain: tricyclicantidepressants,antiseizure meds Topical ointments TENS (transcutaneouselectrical nervestimulation) units Biofeedback Acupuncture Relaxation techniques Massage

Numbness, tingling, changes insensation should be diagnosed Touch may soothe or irritate PN

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Chronic Degenerative Disorders

Dystonia

Parkinson Disease

Tremor

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DystoniaRepetitive, involuntary, sustained contractions in skeletalmuscles

DemographicsMost types: females > males (2–

3:1)Some = genetic anomaly

250,000–300,000 in the UnitedStates

EtiologyProblems at basal ganglia

Inability to process dopamine, gamma-aminobutyric acid) GABA, serotonin,acetylcholineBursts of electrical activity in affectedmuscles (not the same as tremor)

Types of dystonia:

Focal dystonia affects only one area Spasmodic torticollis Vocal dysphonia Oromandibular dystonia Blepharospasm Writer’s cramp

Others

Segmental dystonia affects two adjacent ornearby areas of the body Multifocal dystonia affects two disconnectedparts of the body Hemidystonia affects the left or right side ofthe body Generalized dystonia may progress to affectthe whole body



more Dystonia


Involuntary contractionof an area

Exacerbatedby stress orfatigue Maydisappearwithalternatingmovements

Progression varies

Sudden orslow onset May stabilizeor subside May spillover to othermuscles

Can cause otherproblems: headaches,functional blindness,muscle irritation, fibrosis

Rule out neck injuries,Parkinson disease,Tourette syndrome,other movementdisorders Genetic testing

Medications to changeneurotransmittersecretion/uptake Botox injections Deep brain stimulation Surgery at brain orspinal cord

Massage is safe, maybe helpful

Getinformationonmedications

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Parkinson DiseaseShaking palsy ; Progressive degenerative movementdisorder

Demographics1 to 1.5 million in the United States

60,000 new diagnoses/yearRare under age 40; about 1% of

people over 60Men > women, 3:2


EtiologyBasal ganglia help with voluntary movement Basal ganglia need dopamine from nearbysubstantia nigra

Substantia nigra cells die Dopamine shortage Basal ganglia don’t work Voluntary movement degrades

CausesNot clear

Environmental agents Lewy bodies Genetic predisposition

Parkinsonism = Parkinson-like symptoms

Drug use Pugilistic parkinsonism Neurovascular disease

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more Parkinson Disease


Primary symptoms (related todisease process):

Nonspecific achiness, weakness,and fatigue Resting tremor Bradykinesia Rigidity (not the same asspasticity) Poor postural reflexes Secondary symptoms (indirect

effects or related tomedications)

Shuffling, festinating gait Changes in speech Changes in handwriting Sleep disorders Depression Mental degeneration

Medication L-dopa, carbidopa (temporary,side effects) Other dopamine-affecting drugs Anticholinergic agents Antivirals Nondrug treatments

Deep brainstimulation Surgery to thalamus,midbrain PT, OT, speechtherapy

Massage can be safe andeffective

People don’t moveeasily Can reduce rigidity Can improve sleep

pt 2



TremorRhythmic oscillations of antagonistic muscle groups ; Movementoccurs in a fixed plane; Varies by velocity, body parts involved,and amplitude

EtiologyMost related to dysfunction in links between thebrainstem, cerebellum, thalamus Several classifications Resting tremor Action tremor

PosturalIsometricIntention

Psychogenic Physiological: exacerbated by fear, stress, underlyingproblem Pathological: idiopathic or caused by other disease Essential Tremor

Idiopathic, not secondary to other disease 10 million in the United States

Slowly progressive, not debilitating

Huntington disease

Hereditary degeneration of cerebrumSymptoms show in adulthood: tremors,progressive dementia5 in 1 million in the United States

Multiple system atrophy



Tremor and many other problemsShy-Drager syndrome, striatonigraldegeneration, olivopontocerebellar atrophy

Parkinson disease

Discussed elsewhere

Other factors

Alcohol withdrawal, peripheral

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more Tremor

Treatments Massage

Depends on causes

Medication, surgery

Appropriate for diagnosed conditions; may helpreconnect brain to muscles

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Infectious Disorders

Encephalitis

Herpes Zoster

Meningitis

Polio, Postpolio Syndrome

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EncephalitisInfection of brain ; Usually virus ; Occurs with myelitis, meningitis Demographics

Not always reported; difficult toestimate

Elderly and infants mostvulnerable to worst effects

EtiologyMostly viral

Can be bacterial, fungal

Viral infections can be primary or secondary (fromsomewhere else in the body) Primary infections:

Enteroviruses (directly communicable)Arboviruses (insect vector)

Secondary

Herpes simplex, mumps,measles, herpes zoster

Affect parenchyma of brain

Often mild with no lastingproblems

In young and old can cause permanent damage, death

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more Encephalitis


Mild to very severe

Fever,headache,drowsiness,irritation,disorderedthoughts Doublevision,confusedsensation,impairedspeech,hearing Partial,completeparalysis,changes inmemory,personality Convulsions,stupor, coma

Spinal tap, computedtomography (CT), MRI Blood test Electroencephalography(EEG)

Antivirals, steroids,sedatives, TLC

PrognosisDepends on virulence,health of patient Most survive with nolasting problems Can cause paralysis,cognitive changes

Contraindicated whileacute If in past, check forlasting problems andadjust accordingly

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Herpes ZosterAlso called shingles ; Viral infection of sensory dendrites:painful, fluid-filled blisters

Demographics500,000 diagnoses/year

Seldom occurs more than once,unless immunocompromised


Etiology

Causative agent is varicella zoster virus (VZV) (also forchickenpox)

Virus is never expelled from childhoodinfection Later in life virus reactivates: shingles

Causes

Stress, age, impaired immunity, trauma Communicable only to people with no exposure to VZV

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more Herpes Zoster


Pain is present for 1-3days before a blisterbreakout. Blisters may grow alongthe entire dermatome ofthe host dorsal rootganglion, but most oftenappear along isolatedstretch. Sensory nerves thatsupply trunk andbuttocks are mostfrequently affected.

Blood test

Antivirals may shortenoutbreak Soothing lotions,steroids for anti-inflammatory action andpainkillers.

Contraindicated whileacute After blisters havehealed and the pain hassubsided, massage isappropriate

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MeningitisMeninges + itis: inflammation of the meninges, arachnoid layer,cerebral spinal fluid

Demographics5,000 diagnoses/year

Most in children <5 years orelderly

College students, military recruits

Etiology

Important to identify the causative factor for besttreatment Bacterial meningitis

More severe than viral; risk of permanentdamage is significantHearing loss, cognitive functionResponds to antibiotics if given early

Viral meningitis

Enteroviruses, herpes, othersLess severe than bacterial meningitis

Bacteria in CNS thrive in cerebrospinal fluid (CSF)

Increased permeability → cerebral edema,toxins in CSF Increased pressure in brain put cranialnerves at risk Hearing loss Obstructive hydrocephalus Blood clots, ischemic damage

Without treatment, autoregulating centers can bedamaged

11–19% all patients have permanentdamage

Bacteria can affect other areas in body



Pneumonia, rash, blood vessel damage withrisk of clotting, cell death in extremities

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more Meningitis


Rapid-onset high fever,chills Deep red, purple rash Headache, irritability,photophobia, stiff rigidneck

Can involvenausea,vomiting,delirium,convulsions,coma

Long incubation period;may take 10 days forbacterial infections topeak Viral infections areslower: 3 weeks topeak, 2–3 weeks toresolve

Spinal tap

For bacterial infection:antibiotics, steroids For viral infection:supportive therapy

CommunicabilityMucous secretions,contaminated surfaces Enteroviruses: oral-fecalcontamination

Prevention:HiB (Haemophilusinfluenzae type B)vaccine for childhoodbacterial meningitis Vaccine for 2 of 3meningococci isrecommended for high-risk groups

Contraindicated whileacute After recovery massageis appropriate

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Polio, Postpolio SyndromeUsed to be called infantile paralysis; Polio: viral attack ondigestive mucosa and anterior horn motor neurons; PPS:progressive muscular weakness that develops 10–40 years later

DemographicsWild polio almost extinct

PPS still affects people infectedmany years ago


EtiologyPoliovirus spreads through oral-fecal contamination

Contaminated water Into stomach, intestine (concentrates infecal matter) ; Infection looks like flu plusdiarrhea

1% of infected people: virustravels to CNS ; Destroys motorneurons in ventral horn ; Atrophyof supplied muscles, motorparalysis (sensation is intact)

Overlap of nerve supply allows function to remain inmuscle groups Anterior horns can grow new terminal axons

Puts more demand on each nerve cell Eventually they wear out: PPS

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more Polio, Postpolio Syndrome


PPS Sudden onset offatigue, pain, muscleweakness Dyspnea, dysphagia,sleep disturbances Cycles of lost function,some recovery, flareagain

Episode of polio plus

Onset ofmuscleweakness,loss ofstamina forat least 1year

Reduce muscular,neurological demand:

Change inactivitylevelsUsingbracesExercisingmuscles notaffected bypolio

Prevention

Polio vaccines:

Salk =inactivatedvirus tocreateantibodies(may spreadin feces ofpatient) Sabin = oraldose ofweakenedvirus, slightlyhigher risk ofinfection

For polio, becausesensation is intact,massage is indicated For PPS, massage isindicated to improvelocal nutrition, decreasetension

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Psychiatric Disorders

Anxiety DIsorders

Attention Deficit Hyperactivity Disorder

Autism Spectrum Disorders

Chemical Dependency

Depression

Eating Disorders

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Anxiety DisordersCollection of disorders; Irrational fears; Efforts to control them; Mildto debilitating

Demographics

Discussed with each type

40 million in the United Statesaged 18 years or older havesome type (lots of overlap)

Women> men 3:2

Low end of socioeconomic scale

More likely to become

substance abusers, depressive,suicidal

Etiology“Am I safe?”“Probably not.”Arousal: preparation for a stressful eventFear: the event is confirmedAnxiety: prolonged arousal or fear—without an event

Two major factors:

The limbic system and thehypothalamic-pituitary-adrenal(HPA) axis

Limbic system determines perceived safety

Amygdala, hippocampus Linked to hypothalamus: center forsympathetic/parasympatheticresponse

Hippocampus: center for verbal memory Amygdala: history of fear responses

Together they can stimulate the HPA axis to establish astress response

HPA axis : Chemical/electrical connections ;Excessive glucocorticoid secretion (cortisol)with prolonged stress

Weakens connective tissueSuppresses immunityShrinks hippocampus



Neurotransmitters

NorepinephrineGABASerotoninCRFTightly interdependent: disruptionin one → disruptions in all Types of anxiety disorders

General anxiety disorder (GAD)

6.8 million in the United StatesWomen > men 2:1Chronic, exaggerated, consuming worry;constant anticipation of disaster :Restlessness/edginess; Fatigue; Poorconcentration ; Irritability; Muscle tension; Sleeping problems

Panic disorder

6 million in the United States

Sudden onset of extremesympathetic reactions: Poundingheart, chest pain, sweatiness,dizziness, faintness; Feeling ofimpending doom, nearness ofdeath; 10 minutes to many hours Can have panic attack withoutpanic disorder

Complication: agoraphobia,shrinking safety zone

Acute and posttraumatic stress disorder

Acute (ATSD) = symptoms within 1 month oftriggering event Post (PTSD) = symptoms persist 3 or moremonths 7.7 million in the United States



Persistent visceral memories of ordeal: Combat, abuse, rape, assault, torture, naturaldisaster, terrorist attack; Patient may be awitness or participant

Memories relieved in nightmares, flashbacks Exaggerated startle reflex, dissociation,hypervigilance PTSD may have delayed onset

Obsessive-compulsive disorder (OCD)

2.2 million in the United States Men = women Can come and go, is not always progressive Unwelcome thoughts (obsessions)Efforts to control them (compulsions) Common obsessions : Fear of contamination(dirt, germs, sexual acts); Fear of violence,catastrophic events; Fear of committingviolent, sexual acts; Fear of disorder,asymmetry ; Common rituals; Repeatedhandwashing; Refusing to touch people,surfaces; Repeated checking locks, stove,irons, etc.; Counting telephone poles; Symmetrically arranging items; Repetition ofchants, prayers; Many hours/day devoted torituals

Phobias: social and specific

Social phobia

Also called social anxiety disorder15 million in the United StatesIntense, irrational fear of beingjudged negatively by others, publicembarrassmentCan limit ability to work, school,relationships



Specific phobias

19.2 million in the United StatesIntense irrational fear of somethingthat poses no, little threat :Animals (dogs, cats, birds, insects,spiders) ; Closed-in places,heights, flying, elevators, blood

Respond to desensitization and relaxationtechniques more than to medication

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more Anxiety Disorders

Treatments Massage

Medication and psychotherapyMost are treatable if patients can find itMedications

AntidepressantsAntianxietiesBeta-blockers

Psychotherapy

Supported resistance to compulsivebehaviors Controlled exposure to stimuli forphobics

Behavioral-cognitive therapies

Relaxation techniques, breathing exercises,biofeedback are often taught; massage Touch and massage can reduce self-reportedanxiety Indicated as long as the stimulus is perceived assafe and nurturing

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Attention Deficit Hyperactivity DisordersNeurobiochemical disorder → difficulties with attention,movement, impulse control

Demographics

Estimates only4.3% school-age children (= 4.4

million) in the United StatesSome surveys show higher, lower

numbersMay be both overdiagnosed and

underdiagnosedBoys > girls 2.5:1; may not be

accurate30–75% of children with ADHD

have it as adultsThey may raise kids with ADHD

EtiologyStill being explored Problems with dopamine production, transportation,reabsorption Noradrenaline disruption in frontal cortex and basalganglia (judgment, movement)

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more Attention Deficit Hyperactivity Disorders


Three behavior patterns:

InattentivenessHyperactivityImpulsivity

Behaviors are consistentin various settings

Observation and rulingout other disorders:

Depression,anxiety,learningdisabilities,sleepdisorders,fetal alcoholsyndrome,vision/hearingproblems,Tourettesyndrome,mooddisturbances,seizuredisorders,others

ComplicationsPoor self-esteem,difficulty withrelationships,performance at school,work High rate of motorvehicle accidents(MVAs), substanceabuse, other addictions

Counseling, training forcoping skills Medications

Psychostimulants

Medication side effects

Appetitesuppression Increased bloodpressure, heartrate Sleep problems Facial, vocal tics

Nondrug approaches

Nutritionalsupplements Avoid caffeine,sugar, stimulants

Indicated: mayimproveclassroombehavior,interpersonalrelationships May need toadjust length ofsession

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Autism Spectrum DisordersCommunication disorders ; Specific, predictable movementpatterns ; Sensory problems ; Usually begins early in childhood;diagnosable by age 3 ; Also called pervasive developmentaldisorders (PDD)

DemographicsThree to four in 1,000 school-aged

childrenNumber is rising; unclear why

EtiologyAbnormalities in neural systems that link brainstem,limbic system, basal ganglia, cerebellum, corpuscallosum, cerebral cortex Some causes identified:

Fragile X syndromeTuberous sclerosisGenetic predisposition

Theories

Mitochondrial dysfunction in neurons?Autoimmune response?Exposure to heavy metalsAllergies

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more Autism Spectrum Disorders


Three major issues

Deficit inverbal andnonverbalcommunication Problems withsocialinteractions Repetitivebehaviors,movements

Sometimes: extremereactions to sensorystimuli Locked insideperspective: nounderstanding of otherconsciousness

Nointerpretationof voice ortone People seemcompletelyunpredictable

Often appears with otherconditions

Seizures,cognitivedisability(However, if IQis over 35,

Identified in regularscreenings, then referredfor specialists

Rule out leadpoisoning,hearing loss

Types of autism spectrumdisordersAutistic disorder Asperger syndrome PDD-NOS: pervasivedevelopmental disorder,not otherwise specified Rett syndrome: Childhooddisintegrative disorder Related issues:

Semanticpragmaticcommunicationdisorder Nonverballearningdisabilities

High-functioningautism Hyperlexia

Depends on type ofdisorder, individualchild Highly structuredprograms that reinforcepositive behaviors Applied behavioralanalysis Sensory integrationtherapy Dietary adjustments:

Avoidgluten,casein SupplementB withmagnesium

Medication for anxiety,seizures, depression

Can be helpful

Improvessleep, morepositivesocialinteractions,more timeon task

Some may not toleratetouch: requiresadjustments fromtherapist

6



25% with ASDshow somesavantcharacteristics)

Signs (no babbling,delayed language,communication of anykind, no eye contact, etc.)usually appear by age 3,may not be diagnoseduntil 5 years or older

Earlyinterventioncan improvefunction

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Chemical DependencyUse ; Abuse ; Dependence Demographics

National Survey on Drug Use andHealth Issues:

22.5 million the United States olderthan 12 years = ongoing abusers

of drugs or alcohol3.8 million get help

Alcoholism = number 3 cause ofdeath from a preventable cause

85,000 alcohol-related deaths/year$185 billion in health care costs

EtiologyDepends on substance

Some drugs slow neurotransmitterabsorption, change number of receptor sites Disruptions in neural pathways

Alcoholism1 drink = 12 oz beer; 4–5 oz wine; 1.5 oz80-proof liquor Moderate consumption = 1–2 drinks/day Heavy consumption = 2–4 drinks/day Binge drinking = 4+ in a row for a man, 3+in a row for a woman Depresses CNS arousal, slows brain activity Loss of inhibitions can feel like a stimulant

Risk factors

Genetic predisposition Other mental illness Environmental factors Type of drug being used Age



Medical reasons

Body can become dependent on drug to dosome job (decongestant, painkiller) Body can develop tolerance, need moredrug to do same job The higher the tolerance, the stronger theaddiction

Types of addiction

Psychological addiction: using feels good! Physical addiction: withdrawal symptoms, not usingfeels like death!

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more Chemical Dependency


Persistent craving Person goes to great lengths forsupply Person can’t voluntarily control use Person develops increasingtolerance Cessation of use createsunpleasant, dangerous symptoms

Also devotes a lot oftime to use/recovery Neglects responsibilities Lives in denial

Complications of chemicaldependency

Paranoid delusions, coma, death Violent crime, car/industrialaccidents, spread of AIDS,domestic violence, child abuse

Complications of alcoholismThe digestive system

Irritates stomach lining(gastritis); ulcers; liverdamage and cirrhosis;cancer at esophagus,

Recognizing a problem Treatment program

Recurrence is highuntil 5 years ofsobriety

Goals: abstinence,rehabilitation, prevention ofrelapse Many programs begin withdetoxification

Sedatives,tranquilizers, otherversions of drug

Aftercare is most important partof treatment Some medications cansuppress cravings (temporarysolution only)

Can help with detox, helpperson reconnect with healthybody

Watch for otherhealth problems

Long-term recovery probablyfine for massage Clients who are high/drunk atappointment may get sick



pharynx, larynx, mouth;pancreatitis

The cardiovascular system

Arrhythmia,cardiomyopathy;agglutinates red bloodcells (RBCs); alsoreduced clotting factors,bleeding ; (Moderatealcohol use may protectfrom CV disease)

The nervous system:

Memory loss; slowedreflexes, slurredspeech, impairedjudgment; toxicity cancause brain damage

The immune system

Impedes resistance;vulnerable topneumonia

The reproductive system:

Reduced sex drive,erectile dysfunction,menstrual irregularity,infertility, fetal alcoholsyndrome (2,000births/year)

Alcoholic families

Children 3x risk ofsubstance abuse;depression, anxietydisorders, phobias

Other complications

Traffic injuries,drownings, falls, burns,unintentional shootings

pt 5



DepressionA genetic-neurochemical disorder requiring a strongenvironmental trigger whose characteristic manifestation is aninability to appreciate sunsets.

Demographics20% of women

12% of menWill experience some type of

depressionEvery year, 9.5% of the United

States population have depression(20.9 million people)

Etiology

Some distinguishing features Neurotransmitter imbalance: serotonin, norepinephrine,dopamine Hormonal imbalance: progesterone, estrogen,endorphins, cortisol HPA axis: high amounts of corticotropin-releasinghormone (CRH), adrenal stimulation Atrophy in the hippocampus: may be related to cortisollevels

CausesGenetics Environmental triggers Personality traits Chronic illness Other issues (hypothyroidism, smoking, drug use, sideeffects of medications, B and folate deficiency)

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more Depression


Depends on type

Sad, emptyfeeling Less pleasurefrom hobbies Sense of guilt,disappointmentwith self Hopelessness Irritability Change insleeping habits

Also

Poorconcentration Weightchanges Loss of energy Sense ofhelplessness Persistentphysical pain:headache,gastrointestinal

Rule out hypothyroidism,vitamin deficiencies, etc. Try to identify which typeof depression

In olderpeople adiagnosis iseasy to miss:physicalsymptomsoften lead

Complications

200,000 suicideattempts/year, 30,000suicides

Half relatedto depressiveepisodes 15% withmajordepressivedisordercommitsuicide Men >women 4:1 Number 2cause ofdeath amongadolescents

Most types are treatable

Can bechallenging tofind rightcombination,dosage Important totreat fully todecrease riskof repeatepisodes

Antidepressant drugsFour main categories

SSRIs :Selectiveserotoninreuptakeinhibitors:Prozac, Zoloft SNRIs :Serotoninnorepinephrinereuptakeinhibitors:Effexor,Cymbalta MAOIs :Monoamineoxidaseinhibitors:Nardil, Parate TCAs :Tricyclic

Benefits:

Improves HPA axisfunction Parasympatheticbalance Increase inserotonin,decrease in cortisol Shift in mood state Self-care

Risks:

Clients may wantto stop taking meds Complex emotionalissues, high risk forboundaryconfusion



(GI) discomfort

Types of depression

Major depressive disorder

6- to 18-month-longepisodes; canhappen 4–6times in alifetime

Adjustment disorder:

Triggered by aspecific event;symptomsoutlast anormalrecovery orgrieving period

Dysthymia:

Fewer, lessseveresymptoms; canlast for yearsat a time

Bipolar disease

Also calledmanicdepression,manicdepressivepsychosis

Mood swingsfrom majordepression tomania:heightenedenergy,elation,irritability,racingthoughts,increased sexdrive,

Also

Increasesrisk forstroke, heartattack Predictsrecoveryfrom stroke Accompaniesother long-termdiseases

Diagnosis ofdepression can makeother diseases more

manageable

antidepressants:Elavil

Two major disadvantages:

Take severalweeks toestablishchanges

Produce sideeffects beforebenefitsappear

Lithium: for bipolar

Psychotherapy

Cognitive-behavioraltherapy: life skills Interpersonal therapy:relationships Psychodynamic:unresolved inner conflict

Other therapies

Light therapy for SAD Electroconvulsive therapy(ECT) (unclear why itworks, but it does forsome) St. John’s Wort may beeffective for dysthymia Others: transcranialmagnet stimulation; vagusnerve stimulation; SAM-e,omega-3 fish oil; 5-HTP,others



decreasedinhibitions,unrealistic orgrandiosenotions thatlead todecisionsmade withextremely poorjudgment

Seasonal affectivedisorder (SAD)

Absence ofsunlight, lowlevels ofmelatonin

Postpartum depression

Sleepdeprivation,hormonalshifts, unmetexpectations Majordepressionwith fear ofharm, doingharm to baby Can lead topsychosis

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Eating DisordersAnorexia nervosa: self-starvation ; Bulimia nervosa: normal orhigh calorie consumption, with compensatory activities toprevent absorption ; Binge eating: overeating withoutcompensatory activity

DemographicsAnorexia, bulimia: girls 12–35

years old1% may have anorexia2–5% may have bulimiaFemales > males 10:1

Binge eating: hard to guess2–5% of the United States

population binges within any 6-month period

64% of United States adults areoverweight

59 million in the United States areobese (body mass index 30+)

Etiology

Anorexia and bulimia

High expectations, overachievers Athletes (dance, gymnastics, track) Power issue: patients can control what goesin their mouth ; May have some brainchemistry issues

Prolonged eating habits can becomepermanent, difficult to reverse, terminal

Binge eating

Mixture of physical/psychological issues

Touch: “hugging” inner skin

Protection: from hostile world

May relate to history of touch abuse

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more Eating Disorders


AnorexiaAvoid eating in public Baggy, shapelessclothes

Restrictive:not enoughcalories

Purge type:barelyenoughcalories andpurgebehaviors

Lanugo

Bulimia

Eat normally in public;binge in private Triggered by emotionalstress

Purge type:uselaxatives,diuretics,vomiting

Non–purgetype:excessiveexercise,fasting

No extensive weightloss; more internal

AnorexiaRefusal to maintainweight at or above anormal level; weight isbelow 85% of normalbody mass index Intense fear of gainingweight Distorted self-perception; the patientsees herself as heavierthan she is Menstrual periods stop(amenorrhea) for atleast 3 months in a row

BulimiaRecurrent episodes ofbinge eating A sense of lack ofcontrol; the patientcouldn’t stop eatingeven if she wanted to Inappropriatecompensatorybehaviors, includingself-induced vomiting,laxative or enema use,or excessive exercise(persisting in exercisewhen exhaustion orinjury are present)

Address control issues,not weight management Education, therapy Neurotransmitterbalance?

Within resilience, can bebeneficial:

Positivetouch

Self-awareness

Goodexperience ofliving in thebody

Risks

CV problems,othercomplications



damage

Binge eating

Public, private, both Triggered by stress,feeling out of control Weight gain, possiblyover short time

Long-termdangers aremorereversiblethan withanorexia,bulimia

Complications

Mental/emotional

Depression,irritability,sleepdisorders,anxiety(especiallyOCD)

PhysicalAnorexia

Bradycardia,hypotension, arrhythmia Amenorrhea,osteopenia,osteoporosis Colon dysfunction Tooth damage,esophageal damage,imbalanced electrolytes

A binge/compensationpattern occurs at leasttwice a week for at leastthree months in a row

Behaviors areinfluenced by body

image



Special risk for girls withtype 1 diabetes

Bulimia

Related to vomiting,laxative use Tooth erosion, callus onknuckles Esophageal ulcers,stricture, rupture Colon dysfunction Permanent difficultywith keeping food down

Binge eating

Cardiovascular (CV)disease Type 2 diabetes Osteoarthritis Can be reversed ifhabits change

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Nervous System Injuries

Bell Palsy

Cerebral Palsy

Complex Regional Pain Syndrome

Spina Bifida

Spinal Cord Injury

Stroke

Traumatic Brain Injury

Trigeminal Neuralgia

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Bell PalsyDamage to cranial nerve (CN) VII, the facial nerve; Mostlymotor

Demographics40,000/year in the United States

Mostly young, middle-aged adultsEspecially pregnant women, peoplewith diabetes, immunosuppressed


Etiology

Type of peripheral neuritis CN VII is inflamed, irritated at some point in pathway Usually preceded by herpes outbreak or cold:inflammation presses on nerve Leads to flaccid paralysis of one side of face,platysma Nerve heals; most people have full or nearly fullrecovery




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more Bell Palsy


Sudden onset of flaccidparalysis to one side offace

Hard to eat,drink, blink

Distortedtaste

Hyperacusis

May bepainful—because ofmusculardrag, notattack onsensoryneurons

Complications

85% have full, nearly fullrecovery within a fewmonths Can damage eye(inadequate lubrication,blinking) As nerve heals, it makesnew connections

Unpredictablemuscleactivity offace(synkinesis)

Excessive

Through client history Herpes, Lyme disease,other pathogens maybe trigger Bilateral symptomsprobably not Bell palsy:

Guillain-Barrésyndrome,sarcoidosis,tumors,Ramsay-Huntsyndrome

Steroidal anti-inflammatories,acyclovir to shortenviral activity Take care of affectedeye Massage to stretch,mobilize muscles whilenerve heals

Indicated for musclehealth; sensation isintact



tears withsalivation

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Cerebral PalsyGroup of brain injuries that happen during gestation, birth, earlyinfancy

Demographics2–4 in 1,000 live births in the

United States500,000–1 million patients in

United States8,000 babies, 1,500 toddlers

diagnosed/year

Etiology

Damage to motor areas at basal ganglia, cerebrum

Prenatal causes

Most cases develop during pregnancy: maternalinfection, diabetes, hyperthyroidism, Rh sensitization,abdominal trauma, PIH

Birth trauma

Anoxia, asphyxia, head trauma during birth (relativelyrare)

Acquired CP

Develops in infancy: jaundice, head trauma, infection,brain hemorrhage, neoplasms in brain

Types

Spastic cerebral palsy

Most common form (50–80%) Spasticity in some areas

Athetoid cerebral palsy

Weak muscles, involuntary writhing movements

Ataxic cerebral palsy

Rare: shaking, intention tremor, poor balance



Dystonic cerebral palsy

Slow, involuntary twisting movements of trunk,extremities

Mixed cerebral palsy

Combinations of forms

Complications

Many patients have changes in sensation (hearing,vision loss); digestive difficulties; possibility of cognitiveproblems, seizures, contractures, pain from disorderand treatment interventions

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more Cerebral Palsy


Vary, depending on type, area ofbrain damage

Hypotonicity,hypertonicity, poorcoordination, poorcontrol, weakmuscles, randommovements, etc.

Skills, equipment to live asfunctionally as possible:

Braces, other aids

OT, PT, speechtherapy

Adapted computers

Extensive massage/physicaltherapy may yield surprisingresults: interferes withproprioceptive limitations Medication:

Antiseizure, reducemuscle spasm, Botoxfor excessivesalivation, involuntarymuscle contractions

Surgery for dislocations, bonecorrections

Adults with Cerebral Palsy

Essentially a new populationgroup: longer lifespan than everbeforeAge faster, more vision problems

Fatigue, exhaustion,overuse syndromes

Many benefits: can work withproprioceptors to increase ROM,maintain function Be careful about communication,nonverbal signals for people whocan’t speak clearly

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Complex Regional Pain SyndromeCollection of signs and symptoms: long-lasting pain andchanges to the skin, muscles, joints, nerves, and bloodvessels of the affected areas : CRPS 1 = mostly inextremities (used to be called RSDS) ; CRPS 2 = painoutlives nerve injury, spills over boundaries of affectednerve (used to be called causalgia)

DemographicsMost are 40–60 years old

Women > men 3:1


Etiology

Initial trauma (usually to hand or foot) starts a painstimulus

Bullet, shrapnel

Also minor strains/sprains, postsurgery, fracture, injection site, discdisease, post stroke, no trigger

Sympathetic response reinforces pain; painsensors become more sensitive

Pain becomes self-fulfilling prophecy

Physiological changes may become irreversible;may spread proximally or to contralateral limb

Sympathetically maintained pain (SMP)

Source of pain is sympathetic nervous system(SNS) activity; blocking SNS nerves stops pain

Sympathetically independent pain (SIP)

Pain is more resistant; SNS blocks don’t work Comes as late-stage CRPS Nerves may develop fibrosis where nerve blocksare injected



more Complex Regional Pain Syndrome


Vary widely; three mainissues:

Burning painat site ofinjury

Autonomicdysfunction:changes inskintemperature,texture,edema, hairand nailgrowth, bonedensity loss,

Motordysfunction:weakness inlocalmuscles,goes tostiffness,contractures,atrophy

CRPS 1: 3 stages

(progression varies)

Stage I:1–3 months, severeburning at site, musclespasm, reduced rangeof motion (ROM), hairgrowth, hot red skin Stage II:3–6 months; painful

History and physicalexamination Triple-phase bone scan,thermography New diagnostic criteriafor more standardizedresearch: An initiating trigger orevent (type 1) or aspecific nerve injury(type 2) Persistent pain thatoutlasts a typicallyhealing process; in type2 the pain may exceedthe boundaries of theaffected nerve Marked edema,sweating, hair or nailgrowth, shiny skin,discoloration, andtemperature differencesin the affected area (thisalso includes changesin bone density asregulated by local bloodvessels) No other contributingfactors can be identified(these would includesimple nerveentrapment, arthritis,thrombophlebitis, or

PT, OT to preservefunction, delay atrophy Psychotherapy fordepression, anxiety,sleep disorders Chemical nerve blocks Intrathecal pumps Sympathectomy

Local contraindicationwherever stimulus is toointense Anything well toleratedcan be helpful



swelling spreadsproximally; hair stopsgrowing, skin turns blue,muscles atrophy Stage III:Bones become brittle,joints are immobile,muscle contractures; Symptoms spreadelsewhere Pain is self-sustaining

local infection

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Spina BifidaCleft spine: neural tube defect in which the vertebral arch fails toclose completely over the spinal cord ; Ranges from subtle tosevere

Demographics1:1,000 live births

1,500–2,000/year in the UnitedStates

Hispanics and European whiteshave highest rates


EtiologyNeural tube defects occur day 14–28 of gestation:fetus is the size of grain of rice Main risk factor is folate deficiency

Spina bifida occulta (SBO)

Vertebral arch may not completely fuse; no signs arevisible May not know until radiography for something else May be common: 5–10% of population? May show dimple, tuft of hair at low back Can be serious: tethered cord

Spina bifida meningocele

Rarest form Only dura, arachnoid press through cleft to form a cystvisible at birth Repaired with surgery, few long-term consequences

Spina bifida myelomeningocele

Most common, most serious diagnosed form: 94% allcases



Cauda equina protrudes with meninges through cleft Skin may or may not cover cyst (risk of CNS infection)



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more Spina Bifida


SBO may be silent Cystic SB is obvious,usually at lumbar spine

Complications85% of patients havehydrocephalus

Treated witha shunt

Some may havecognitive impairment Latex hypersensitivitycan become dangerous Decubitus ulcers, GIproblems, urinaryproblems, obesity,muscle imbalances,scoliosis

Can be detectedprenatally Some cases can becorrected in utero; highrisks, of course

Surgery to reduce cystwithin a few days ofbirth PT to retain function,build leg muscles Assistive equipment asnecessary Additional surgeries torelease tethered cord,deal withhydrocephalus, etc.

Depends on sensation,level of function, othercomplications Can be helpful in thecontext of PT topromote good function

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Spinal Cord InjurySelf-evident ; Concussion, contusion, compression,laceration, transaction ; Paraplegia, tetraplegia,quadriplegia

Demographics10,000–11,000/year

250,000 living with SCIMale > female 4:1

MVA → 50%Gunshot wound (GSW), violence →

11%Falls → 24%Sports → 9%

Other: nontraumaticArthritis, bone spurs, tumors

EtiologyUsually starts with crushing blow Could also be slow compression New injury → spinal cord shock

Blood pressure is low, bradycardia,peripheral vasodilation

Muscles may be flaccid

When inflammation subsides

Muscles supplied by damaged axonstighten

Reflexes become hyperreactive

Spasticity

(Flaccid paralysis indicates PNS damage; spasticparalysis indicates CNS damage—both mayoccur with cauda equina/spinal cord pressure)

Secondary problemsA lot of damage occurs post trauma withinflammation, other processes Limiting this improves prognosis Excessive bleeding can cause pressure in CNS,low blood pressure Local edema can damage neurons throughpressure or hypoxia Free radical activity: destroys cell membranes



Excitotoxicity: excessive glutamate damagesmotor neurons Immune system activity: inflammatory cytokinesdamage cells, lead to scar tissue Apoptosis: especially of oligodendrocytes (myelinin CNS)

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more Spinal Cord Injury


Higher the lesion → moredamage Anterior cord → motor damage Posterior, lateral cord → sensorydamage

Complications

Respiratory infectionEspecially if injury is above T12;leading cause of death for SCIpatients is pneumonia Deep vein thrombosis,pulmonary embolismPulmonary embolism is number2 cause of death for SCI patients Urinary tract infectionNeurogenic bladder, catheteruse carries high risk of urinarytract infection (UTI), kidneyinfection Decubitus ulcersHigh risk for infection, bloodpoisoning Heterotopic ossificationUsually around hips, knees; canbe painful Corrected surgically

Acute: remove pressure onspinal cord Limit inflammation, secondarydamage Later Implant electrodes in muscles;surgical transfer of healthytendons, work with spinalreflexes Work to provide living skills New branches of research:influence growth medium in CNSfor regeneration of damagedcells

Respect complications Otherwise indicated for improvedfunction, pain relief,proprioceptive training



Autonomic hyperreflexiaEspecially with damage aboveT6 Minor stimulus createssympathetic reaction: poundingheadache, increase heart rate,high blood pressure; can bemedical emergency Cardiovascular diseaseRelated to immobility NumbnessAllows minor injuries to beignored; risk of infection PainFrom damaged nerve tissue,secondary injury, heterotopicossification, musculoskeletalinjury Spasticity, contracturesSome is related to CNS damage Can be reinforced byproprioceptive messages(Some of this may beinterruptible with PT, massage) Damaged sensation may →painful temporary spasms)

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StrokeAlso called brain attack, cerebrovascular accident (CVA) ;Damage to brain cells due to oxygen deprivation

DemographicsMost common CNS disorder

Number 3 cause of death in the United

States

Number 1 cause of adult disability

700,000/year (1:45 seconds)160,000 deaths/year

Of survivors: 15–30% disabled

20% need institutional care

4.7 million stroke survivors alive today

EtiologyOxygen deprivation from bleeding or ischemia

Ischemic strokes (about 80%):

Cerebral thrombosis: blood clot forms in cerebralarteries, obstructs blood flow Embolism: Clot or other debris travels fromelsewhere (heart, carotid artery)

TIA is warning sign

PFO: patent foramen ovale allows blood to crossthe atrial septum: a factor in strokes in people <55 years old.

Hemorrhagic strokes (about 20%)

Intracerebral hemorrhage: rupture of blood vesselinside the brain Subarachnoid hemorrhage: rupture of bloodvessel on surface of the brain Secondary damage from inflammation, freeradicals causes a lot of damage; limiting thesecan improve prognosis

Risk factors that can be controlled

High blood pressure: chronic high blood pressureraises risk by 400–600% Smoking: nicotine constricts blood vessels andraises blood pressure



Atherosclerosis, high cholesterol: contributes tohigh blood pressure, raises risk of emboli C-reactive protein (CRP): associated with long-term inflammation Atrial fibrillation: forms emboli that may travel tobrain High alcohol consumption: >2 drinks/day Drug use: cocaine, crack, and marijuana Obesity and sedentary lifestyle Diabetes: untreated or poorly treated raises risk300% High-estrogen birth control pills, especially whentaken by a smoker Hormone replacement therapy Depression Overall stress

Risk factors that can’t be controlled

Age: Three-fourths > 65 years; risk doubles eachdecade after 55 Gender: men > women; women more likely to die Race: African Americans two times more likely tohave stroke than whites, almost two times morelikely to die Family history: genetic influence oncardiovascular disease, strength of blood vessels





Previous stroke

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more Stroke


Sudden onset ofunilateral weakness,numbness or paralysison the face, arm, leg orany combination of thethree Suddenly blurred ordecreased vision in oneor both eyes;asymmetrical dilation ofpupils Difficulty in speaking orunderstanding simplesentences; confusion Sudden onset ofdizziness, clumsiness,vertigo Sudden very extremeheadache Possible loss ofconsciousness TIA looks like stroke:temporary Pursue it as medicalemergency to limitdamage

Complications

Partial, full paralysis of

Determine whetherischemic orhemorrhagic (impactstreatment options) Physical examination,CT, MRI, arteriography,blood tests

Prevention Identify who is at risk,change what factors arepossible For ischemic strokeThrombolytics For aneurysmRepair before rupture After strokePT, OT, speechtherapy, massage

Get information oncardiovascular health Be cautious withparalysis, numbness,problems with language Otherwise, massagecan help with recovery,proprioceptive training,etc.



one side (hemiparesis,hemiplegia) Aphasia Dysarthria Memory loss Personality changes Sensory problems:numbness, vision loss Depression (can predictrecovery)

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Traumatic Brain InjurySome damage to brain not from congenital or degenerativecondition ; Altered consciousness, cognitive impairment,disruption of function ; Mostly from MVAs, GSWs, sports, fall,violence

Demographics1.5 million diagnosed/year

1 million emergency departmentvisits

270,000 rated as moderate tosevere

80,000 are disabled, 60,000develop seizures, 70,000 people

die/year2.5 million to 6.5 million TBI

patients alive today

Etiology

Skull fracture

Bones of cranium are broken Open injury less dangerous than closed

Penetrating injury

GSW, knife wound High mortality

Concussion

Most common form of TBI, 300,000/year Jarring of cranium Can lead to second impact syndrome: more serious

Contusion

Bruising inside cranium Coup-contrecoup

Diffuse axonal injury

Internal tearing of nerve tissue in brain Whiplash accidents, shaken baby syndrome



Anoxic brain injury

Complete oxygen deprivation: airway obstruction,sudden apnea

Hypoxic brain injury

Inadequate oxygen: stroke, edema, toxins (carbonmonoxide)

Hemorrhage

Bleeding inside brain, ruptured aneurysm

Hematoma

Blood coagulates in brain or cranium

Edema

Secondary inflammatory response; can cause moredamage than initial trauma

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more Traumatic Brain Injury


Vary, according to area affectedand severity Frontal lobe is most common, →language, motor dysfunction Brainstem → massive loss ofautonomic function At trauma: CSF may leak fromears, nose; asymmetrical pupils;visual disturbances; dizzinessand confusion; apnea or slowedbreathing; nausea and vomiting;slow pulse and low bloodpressure; loss of bowel andbladder control; possibleseizures, paralysis, numbness,lethargy, or loss ofconsciousness Long-term: mild to severecognitive dysfunction, memory,learning; movement disorders;seizures; behavior/personalitychanges; at brainstem: coma,persistent vegetative state

Surgery to remove pressurePT, OT, speech, recreationaltherapy

Prevention

Most related to transport injury:altercation between wheeledvehicles Drive alert, sober; wear helmetsetc. Store firearms carefully Make homes safe for children,elderly

Depends on client’s ability toadapt Watch for numbness, languagedifficulties Massage can work with PT,other therapies to restore motorfunction, improve mood, workwith proprioception For comatose clients: can helpprevent bedsores (with caution!) Work with health care team

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Trigeminal NeuralgiaNeuro-algia (nerve pain) along one or moreof the three branches of CN V ; Also calledtic douloureux

Demographics40,000 in the United States

Women > men 3:2Usually 60–70 years old

EtiologyPrimary or secondary CN V is irritated → sharp,electrical, burning orstabbing pain on one sideof the face Cause is questionable Artery or vein wrapsaround CN V as it emergesfrom pons(not completely consistent) Blood vessel may wearaway myelin, causingmisfires Can be secondary to bonespur, infection, multiplesclerosis Type 1: sharp blasts ofpain on one side of facerelated to mild trigger Type 2: long-lastingburning pain, ache, withoccasional bolts of extremepain



more Trigeminal Neuralgia


Sharp, electrical stabbing orburning sensations 10 seconds to 2 minutes orseveral jabs in succession Muscular tic may accompanypain Triggers: chewing, swallowing,speaking, a draft, light touch Episodes may come and go overyears No pain during sleep, nonumbness, weakness or hearingloss

Rule out sinus, tooth infection Acupuncture Anticonvulsant drugs (oftentemporary) Controlled destruction of parts ofthe trigeminal nerve Microvascular surgery

Local contraindication; facecradles may also be problematic Otherwise massage is safe andappropriate

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Other Nervous System Conditions

Guillain-Barre Syndrome

Headaches

Meniere Disease

Seizure Disorders

Sleep Disorders

Vestibular Balance Disorder

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Guillain-Barre SyndromeAcute inflammation and destruction of the myelin layer of peripheralnerves

DemographicsMostly 15–35 years old or

50–75 years oldMen > women

3,000/year in the UnitedStates

EtiologyUsually preceded by infection of respiratory or GI tract May stimulate an immune system attack directed at Schwanncells Linked to infection with

Campylobacter jejuni, Haemophilus influenzae,Mycoplasma pneumoniae, Borrelia burgdorferi,cytomegalovirus, Epstein-Barr virus, HIV

Also seen with pregnancy, surgery, some vaccines (swine flu,1976) Myelin on peripheral nerves is attacked and destroyed bymacrophages and lymphocytes Damage progresses proximally May affect cranial nerves Many patients need ventilator before resolution GBS includes several demyelinating diseases

Acute inflammatory demyelinating polyneuropathy(AIDP) (90% of diagnoses)

Acute motor axonal neuropathy (AMAN)

Acute motor-sensory axonal neuropathy (AMSAN)

Miller-Fisher syndrome

pt 7



more Guillain-Barre Syndrome


Unpredictable Fast, severe onset(hours to days) Symmetrical Progresses proximallyfrom extremities to trunk Weakness, tingling inlimbs Reflexes diminish If GBS is at cranialnerves: facialweakness, pain,speech, swallowingdifficulty Respiratory control islost Symptoms peak 2–3weeks after onset,linger, then subside

Signs/symptoms aredistinctive Spinal tap Nerve conduction tests

PlasmapheresisPatients diagnosedearly in the course ofthe disease and thosewho are acutely ill oftenrespond well to bloodplasma exchangePlasmapheresis isthought to remove thesubstances thatdamage myelin. It canshorten the course ofGBS, alleviatesymptoms, and preventparalysis.ImmunoglobinLarge doses ofimmunoglobin givenintravenously can helpshorten the duration ofsymptoms.Overall, about 70% ofpatients respond toplasmapheresis orimmunoglobin.res.

MedicationOver-the-counteranalgesics such asaspirin.If necessary, strongerpain medication (e.g.,acetaminophen withhydrocodone) may beprescribed. Musclespasms can becontrolled with relaxantssuch as diazepam(Valium®).

Contraindicated forcirculatory work whileacute Later with PT etc. canbe helpful

Work withhealth careteam



PrognosisMost have full or nearlyfull recovery Some have permanentloss of function 5–10% have permanentdisability 10% have relapse later 5–7% die

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HeadachesMost are self-contained temporary problems ; Some are related toserious underlying conditions

Types of headaches:Primary versus secondary

Primary = freestandingSecondary = symptom of

another problem

Classifications (with overlap):

Tension-type headaches

Most common type of headache (90–92%)

Triggered by muscle tension, bonymisalignment, postural patterns,eyestrain, temporomandibular joint(TMJ) disorders, myofascial painsyndrome, ligament irritation, othermusculoskeletal imbalances

May be episodic or chronic

Vascular headaches

Any collection of too much fluid in thehead

Classic/common migraines, clusterheadaches, sinus headaches

Migraine/cluster: triggered by stress,food sensitivities, alcohol use, hormonalshifts

Vasoconstriction (prodrome) followed byvasodilation and pain

Hemi-craine: half of head

28 million in the United States getmigraines; women > men

EtiologyFor tension and vascular

Serotonin activity leading to vasodilation inarteries in the periphery of brain

Prostaglandin release → inflammatoryresponse

Main difference between tension and vascular: trigger,throbbing



(Men > women for cluster headache)

Sinus headaches: allergies, infection ofsinuses (Chapter 7)

Chemical headaches

Low blood sugar (hunger headache),hormone shifts, and dehydration,including dehydration brought about byalcohol use (hangovers)

Rebound headaches (also calledmedicine overuse headaches)

Exposure to toxins

Traction-inflammatory headaches

Indicate serious underlying problem:tumor, aneurysm, stroke, hemorrhage,infection

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more Headaches

Treatments Massage

Avoid/manage triggersHeadache journal for chronic situationsMedication to manage pain

Can be problematic for migraine(nausea)

NSAIDs for tension when necessary

Depends on type of headache

Tension types respond extremely well

Vascular usually prefer not to receivetouch, stimulus (hydrotherapy works)

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Meniere DiseaseInner ear dysfunction leading to vertigo, tinnitus,hearing loss

DemographicsMostly 20s–50s

625,000 in the United States45,000 diagnoses/year

Men = women


EtiologyStill being explored Accumulation of excess fluid in theendolymph inside the membranous labyrinth Idiopathic endolymphatic hydrops Possible causes

Rupture of the membranouslabyrinth

Autoimmune activity

Viral infection

Pressure from a tiny blood vesselwrapping around thevestibulocochlear nerve

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more Meniere Disease


Four major symptoms Starts in one ear, canprogress to the other Usually fast onset Ménière attack can last20 minutes to 24 hours

Hearing loss

Tinnitus

A sense offullness inthe middleear

Rotationalvertigo

Rule out any otherpossibilities: multiplesclerosis, neuroma Two episodes of vertigoand feeling of fullness >20 minutes Documented hearingloss

Symptomatic control Identify triggers ifpossible Avoid food/habits thatraise blood pressure Medication to managevertigo Disablevestibulocochlear nerve

No contraindications aslong as client iscomfortable on table

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Seizure DisordersAny kind of problem that can cause seizures ; Epilepsy is onetype ;Two or more seizures with no other medical problem

Demographics10% of the U.S. population will have

a seizure at some time2.7 million diagnosed with epilepsy

200,000 new diagnoses/year

Etiology

Interconnecting neurons in brain give off bursts ofenergy

Triggers vary:

Changes in light, strobe effect, flashing,sounds, anxiety, sleep deprivation,hormonal changes, infection

Causes

Some can be linked to specific problems in brain

Birth trauma, traumatic brain injury,stroke, tumor, penetrating wounds, toxicexposure

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more Seizure Disorders


Partial seizures Motor cortex, temporallobes most oftenaffected

Simplepartial

Complexpartial

Generalized seizures

Absenceseizures

Tonic-clonicseizures

Myoclonicseizures

Statusepilepticus

EEG, CT, MRI Rule out migraines,stroke, fainting,arrhythmia, narcolepsy,hypoglycemia, etc.

Anticonvulsantmedication High-fat low-fiberketogenic diet Surgery if specific massis determined to because Vagus nerve stimulation

Contraindicated duringseizure; consult withclient for best strategies Other times massage isfine

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Sleep DIsordersAnything that interferes with falling asleep, stayingasleep, or waking refreshed ; 70 types defined; fivediscussed here

Demographics40 million in the United States

Increases with age

Types of sleep disordersParasomnia: disruption of sleep (night terrors, etc.)Dyssomnia: can’t initiate, maintain sleep (thisdiscussion)

Insomnia ; Lack of sleep can be transientor chronic

Obstructive sleep apneaApnea = absence of breath.Estimated 18 million in the United StatesAir passage collapses during sleep; when oxygenlevels fall, muscle tighten (gasp, snore)May happen hundreds of time in a night Central sleep apneaNeurological problem: decreased respiratory driveCan cause brain damage Restless leg syndrome (RLS)Can be geneticAssociated with pregnancy, diabetes, anemia,fibromyalgia, attention deficit hyperactivity disorder(ADHD)Sensation in legs relieved by pressure, rubbingSimilar to periodic limb movement disorder (PLMD)An estimated 12 million in the United StatesResponds to drugs for Parkinson disease:movement disorder NarcolepsyNarco = stupor, lepsis = seizureSleep attacks in response to stress, laughing, angerAn estimated 350,000 in the United States

Etiology

Humans cannot adapt to insufficient sleep Sleep deprivation → slowed reflexes, loweredcognitive skills, poor immune system efficiency,fibromyalgia, chronic pain, depression,hallucinations, psychosis Now being linked to weight gain, increased riskof type 2 diabetes Circular relationship:

A person doesn’t feel well; doesn’tsleep well; doesn’t feel well

Stages of Sleep

Stage I: light sleep Stage II: eyes stop moving Stage III: delta waves appear Stage IV: only delta waves; growth hormone(GH) is secreted REM sleep: breathing is rapid, shallow,irregular; heart rate, blood pressure nearwaking levels; dreaming Cycle is completed in 90–100 minutes Healthy balance:



20–25% in REM

50% stage II

30% other stages

Cataplexy, sleep paralysis, hypnagogichallucinations Circadian rhythm disruptionActivity outside of daylight cycleShift work, travel25 million in the United States don’t work a day shiftHigher than normal risk for MVA, job injuries, cold,flu, hypertension, weight gain, irregular menstrualcycle, GI problems

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more Sleep Disorders


Excessive daytimesleepiness Irritability, decreasedability to focus orconcentrate, moodchanges, poor short-term memory

Complications

100,000 MVAs/year Job injuries, otherproblems (psychosis,fibromyalgia, poorhealing, etc.)

Check for sleep apnea Rule out other disorders Polysomnograph

Sleep hygiene: quietbedroom, no caffeine,exercise close tobedtime, etc. Sleeping aids generallydiscouraged if possible

Habitforming, maysuppressrespiratorydrive

For sleep apnea:surgery, CPAP(continuous positiveairway pressure)machine

Indicated! Increasestime in stages III and IV May recognize sleepapnea breathingpatterns

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Vestibular Balance DisordersDysfunction of vestibular branch of CN VIII → vertigo ; May lastseconds to hours

DemographicsMost common in elderly

2 million doctor visits/yearLeading cause of falls, accidental

deaths among elderly

Etiology

Changes in vestibule, other problems can → vertigo

Benign paroxysmal positional vertigo (BPPV)

Small bits of calcium debris are displacedinto the semicircular canals; maneuver maymove the otoliths back into place

Labyrinthitis

Inflammation inside bony or membranouslabyrinth; lasts a few days or weeks, andthen gradually subsides

Acute vestibular neuronitis

Inflammation of the vestibular portion of CNVIII

May involve hearing loss

Usually self-limiting

Ménière disease: discussed elsewhere

Head injury

Inner ear fluid can leak into middle ear

Others

Stroke, tumor, multiple sclerosis, migraines,allergies, anxiety, depression, medications,some drugs



more Vestibular Balance Disorders


Perception that theworld is spinning ortilting

Nystagmus

Nausea, vomiting

Can be difficult: manycauses, may overlap

MRI, CT to rule outCNS problems

Hearing, blood tests,electronystagmogram,posturography

Depends on type ofdisorder

BPPV: head maneuvers

Drugs for nausea,vomiting

Exercises for CNSadaptation

Appropriate if client iscomfortable

BPPV maneuvers maybe helpful

Some neck triggerpoints may mimicsymptoms

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Copyright HandsOn Therapy Schools 2009 PATH… · function 25% is bulbar form Speech, swallowing, control of tongue Frequent, extreme mood swings (emotional incontinence) Tends to