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FACIAL PAIN-NON ODONTOGENIC FACIAL PAIN-NON ODONTOGENIC CAUSESCAUSES
Prof. A.V. SRINIVASAN,MD, DM, Ph.D, D.Sc(hon)F.A.A.N, F.I.A.N.
Emeritus Professor
The Tamilnadu Dr. M.G.R. Medical University
Former Head
Institute of Neurology, Madras Medical College
Prof. A.V. SRINIVASAN,MD, DM, Ph.D, D.Sc(hon)F.A.A.N, F.I.A.N.
Emeritus Professor
The Tamilnadu Dr. M.G.R. Medical University
Former Head
Institute of Neurology, Madras Medical College
Ragas dental college-7-09-11
Understanding, Impact and Understanding, Impact and AwarenessAwareness
Facial PainFacial Pain
We learn by thinking and the quality of the learning outcome is determined by the quality of our thoughts
R.B. Schmeck
“Pain May be Inevitable, but Misery is Optional”
Dee Malchow
Pain constitutes nearly 40% of the total of patient visits to doctors.1
1 Mäntyselkä et al. Pain as a reason to visit the doctor: a study in Finnish primary health care. Pain. 2001 Jan;89(2-3):175-80.
“By Nature All Men/ Women are alike butby Education widely different”
- Chinese
Pain is undertreatedPain is undertreated In 2001, Barry Furrow wrote “Pain is undertreated” in the American health-care
system at all levels.2
The term "opiophobia" has been coined to describe this remarkable clinical
aversion to the proper use of opioids to control pain.
The possible reasons for health-care providers' failures to properly manage pain are
many;
– Occasional lack of knowledge about appropriate treatment choices for pain
management
– A reflection of a Culture hostile to drug use
– Threats of legal action.
– Worry about tolerance and addiction and other adverse drug effects
– Something as trivial as the lack of insurance cover, can lead to patients
suffering unnecessary pain as a result.2. R.M. Marks and E.J. Sachar, "Undertreatment of Medical Inpatients with Narcotic Analgesics,"Annals of Internal Medicine, 78 (1973): 173.
Indian ScenarioIndian Scenario Despite an essentially stoic and less demanding Indian patient; the
obligation to manage pain comes to the fore not only to complete the
perfection of a clinicians management.
But also, it is an independent entity with physical and psychological
components that in adherence to best practices can neither be ignored nor
treated such that adverse effects eclipse the malady.
This importance of pain management is further increased when benefits for
the patient are realized,
– Early mobilization which tends to prevent the more dangerous
complication of a deep vein thrombosis;
– Shortening hospital stay
– Reducing costs
Decade of Pain Control and ResearchDecade of Pain Control and Research
In late 2000, US Congress passed into law a provision, which the president signed , that declared the 10 year period beginning Jan 1st 2001, as the Decade of Pain Control and Research.
The American Pain Society has actively supported the Decade of Pain Control Research, and it has been a focal point for the development of numerous programs to advance awareness and treatment of pain and funding for research.
What is Pain?What is Pain?• Pain is always a subjective experience
• Everyone learns the meaning of “pain” through
experiences usually related to injuries in early life
• As an unpleasant sensation it becomes an emotional
experience
• Pain is a significant stress physically, emotionally
(American Society of Anesthesiologists, 2002; Loeser et al, 2001; Merskey H et al, 1994; Portenoy et al, 1996)
The International Association for the Safety of Pain (IASP) defines pain an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage, or both.
Qualities of PainQualities of Pain Organic vs. psychogenic Acute vs. chronic Malignant or benign Continuous or episodic
Perceiving Pain• Algogenic substances – chemicals released at the site of the injury
• Nociceptors – afferent neurons that carry pain messages
• Referred pain – pain that is perceived as if it were coming from somewhere else in the body
Acute vs. Chronic PainAcute vs. Chronic Pain
ACUTE CHRONIC
Function To warn None (destructive)
Etiology Usually Clear Complex/obscure
Pt. Mood Anxiety/fear Depression/anger
MD impact Comforting Frustrating/draining
Role of Rx Control/cure Improve function/QOL
Categorization of Chronic painCategorization of Chronic pain
Types of PainTypes of Pain
Pain arising from pain receptors
[Nociceptive Pain]
Pain arising from pain receptors
[Nociceptive Pain]
(Psychogenic)
Pain with NO apparent cause(e.g. Low back pain or some
pelvic pain in women)
(Psychogenic)
Pain with NO apparent cause(e.g. Low back pain or some
pelvic pain in women)
Pain arising from Nervous system[Neuropathic Pain]
Pain arising from Nervous system[Neuropathic Pain]
Central(Brain and Spinal cord)
Central(Brain and Spinal cord)
Peripheral (Peripheral nervous
system)
Peripheral (Peripheral nervous
system)
Superficical / SomaticSuperficical / Somatic Deep / VisceralDeep / Visceral
Keay, KA; Clement, CI; Bandler, R (2000). "The neuroanatomy of cardiac nociceptive pathways". in Horst, GJT. The nervous system and the heart. Totowa, New Jersey: Humana Press. p. 304
Different types of painDifferent types of pain
Nociceptive descriptors Neuropathic descriptors
Cramping, tender Shooting
Gnawing, heavy Hot-burning
Aching Sharp
Splitting Stabbing
Multidimensional Classification of Pain Multidimensional Classification of Pain
IASP (International Association for the Study of Pain) expert multi-axial classification of chronic pain
Axis I: Anatomical location Axis II: Systems Axis III: Temporal Characteristics (intermittent, constant, etc.) Axis IV: Patient’s Statement of Duration/ Intensity / severity Axis V: Etiology Example:
Mild post-herpetic neuralgia of T5 or T 6; 6 months’ duration = 303.22e
Axis I: Thoracic regionAxis II: Nervous system (central, peripheral, or autonomic); physical
disturbance/dysfunctionAxis III: Continuous or nearly continuous, fluctuating severityAxis IV: Mild severity of 1 to 6 monthsAxis V: Trauma, operation, burns, infective, parasitic (one of these)
(Loeser et al, 2001; Merskey et al, 1994)
Dimensions of Chronic PainDimensions of Chronic Pain
Loneliness
HostilitySocial
Factors
Anxiety
DepressionPsychological
Factors
Pathological ProcessPhysical
Factors
TIM
E
A.G. Lipman, Cancer Nursing, 2:39, 1980
Chronic pain has a psycho-
social component that must
be dealt with before
depression becomes a part of
the clinical picture. Chronic
pain should be recognized as
a multi-factorial disease state
requiring intervention at
many levels.
Pain: Social and Psychological FactorsPain: Social and Psychological Factors
Chronic pain has high co-morbidity– Depression– Anxiety disorders– Sleep disorders
All diminish function and quality of life Addressing these issues is essential to optimal pain
management
Give us the GRACE to accept with serenity the things that cannot be changed the COURAGE to change the things that should be changed and the WISDOM to know the
difference
Current Understanding of PainCurrent Understanding of Pain
Chronic pain is NOT a normal part of aging. Emotions play a key role in painful experience Pain sounds a warning, signaling damage to tissues, and has survival value so pain receptors do not adapt
to prolonged stimulation and pain sensation may intensify as pain thresholds are lowered by continued stimulation.
The 19th Century viewed pain as a solely physiological entity with two theories dominating – the “specificity” & the “summation” theories. 8
Paradigm Shift: – Pain perception impulses are modified by ascending and by descending pain-suppressing systems
activated by various environmental and psychological factors. – 1965 Melzack & Wall: Gate Theory of Pain marked a turning point in understanding transmission
and modulation of nociceptive signals, and recognition of pain as a psychophysiological phenomenon.
The concept of Neuroplasticity was recognized and accepted adding dynamism to neuronal & brain structure with neuroimaging of the central nervous system in three domains; anatomical, functional, and chemical imaging helping measure changes in chronic pain.
Taken together these three domains have changed our thinking on pain; now considered an altered brain state in which there may be altered functional connections or systems and components of degenerative aspects of the CNS. 9
8) 11. J.A. Paice, C. Toy, and S. Short, "Barriers to Cancer Pain Relief: Fear of Tolerance and Addiction," Journal of Pain and Symptom Management, 16 July 1998): 1-9.9) Quick Reference Guide for Clinicians No. 1a. AHCPR Publication No. 92-0019: February 1993
Understanding Pain Understanding Pain PathophysiologyPathophysiology
What causes pain?What causes pain?
Trauma/ injury initiates immediate nerve impulses to brain
Injury to cells result in chemical release H+
K+
Substance P Bradykinin 5HT Phospholipids Prostaglandins
Blood vessels leak resulting in inflammation
Stimulate C-fibres (slow response)
Peripheral and Central Pathways for PainPeripheral and Central Pathways for PainAscending TractsAscending Tracts Descending TractsDescending Tracts
Cortex
Midbrain
Medulla
Spinal Cord
Thalamus
Pons
(Brookoff, 2000)
Pain PathwayPain Pathway
Nerve FibresNerve Fibres
( A delta) Myelinated Fast conductors Gentle pressure and pain
(A beta) Thinner – but still
myelinated Fast conductors Heavy pressure &temp
C - very thin Slow conductors PAIN, Pressure, temp &
chemicals
Pathophysiology of Chronic PainPathophysiology of Chronic Pain
In chronic pain, the nervous system remodels continuously in response to repeated pain signals
– nerves become hypersensitive to pain
– nerves become resistant to anti-nociceptive system
If untreated, pain signals will continue even after injury resolves
Chronic pain signals become embedded in the central nervous system
(Marcus, 2000)
Pain-Sensing System in the Malfunction in Chronic Pain
(Illustration: Seward Hung, 2000)
Acute pain:
Pain-sensing signals are initiated in response to a stimulus
• They elicit a pain-relieving response
Chronic pain:
Pain signals are generated for no reason and may be intensified
• Pain-relieving mechanisms may be defective or deactivated
Pain Sensing
In chronic pain, pain signals are generated without physiologic significance
Role of Serotonin and NorepinephrineRole of Serotonin and Norepinephrine
Reticulospinal fibers from raphe nuclei project to dorsal horn of spinal cord and release serotonin which stimulates interneurons to release enkephalin
Enkephalin inhibits transmission of pain and temperature signals in second order neurons
Reticulospinal fibers from locus coruleus also project to dorsal horn of spinal cord and release norepinephrine which inhibits pain and temperature signals by an unknown mechanism
Mental illnesses such as depression decrease serotonin and norepinephrine and lower pain thresholds while antidepressant drugs and therapies (e.g., exercise) which increase serotonin and norepinephrine levels raise pain thresholds
Pathophysiology of PainPathophysiology of Pain
Inferred from characteristics, etiology or pathophysiology
Types
– Nociceptive
– Neuropathic
– Idiopathic
Therapeutic implications
(Portenoy et al, 1996)
Nociceptive PainNociceptive Pain
Presumably results from ongoing activation of primary afferent neurons responding to noxious stimuli Pain consistent with degree of tissue injury
Described as aching, squeezing, stabbing, throbbing
Subtypes:
– Somatic: related to activation of somatic afferent neurons
– Visceral: related to activation of visceral afferent neurons
(Loeser et al, 2001; Portenoy et al, 1996)
Neuropathic PainNeuropathic Pain
Initiated by a primary lesion in the nervous system; believed to be sustained by aberrant somatosensory processing in the peripheral or central nervous system
Independent of obvious ongoing nociceptive activation
Burning, shooting, electrical quality; may be aching, throbbing, sharp
Subtypes:
– Presumed “central generator” deafferentation pain (central pain, phantom pain) Sympathetically-maintained pain
– Presumed “peripheral generator” Polyneuropathies and mononeuropathies
(Portenoy et al, 1996)
Idiopathic and Psychogenic PainIdiopathic and Psychogenic Pain
Idiopathic Pain
Usually exists in the absence of an identifiable physical or psychologic pathology that could account for pain
Uncommon in patients with progressive illness
Psychogenic Pain
Presents positive evidence of a predominant psychologic contribution and may be labeled with a specific psychiatric diagnosis
(Loeser et al, 2001; Merskey et al, 1994; Portenoy et al, 1996)
Recent Developments In Pain ManagementRecent Developments In Pain Management
Greater understanding of the pathophysiology underlying chronic pain syndromes
Scientific breakthroughs in molecular biology; insight into pain at the molecular level
Advances in drug therapy (drug delivery technologies)
Multimodal therapy
Multidisciplinary teams, shared decision-making that includes patients
Patients’ rights movement
(JCAHO, 1999; Loeser et al, 2001)
Therapeutic Modalities for
Chronic Pain Management
Assessment
Progress in Chronic Pain Management:Progress in Chronic Pain Management:
“Describing pain only in terms of its
intensity is like describing music only in
terms of its loudness”
von Baeyer CL; Pain Research and Management 11(3) 2006; p.157-162
Pain AssessmentPain Assessment
Characterize the pain
Characterize the disease, relationship between pain and disease and potentially treatable etiologies
Clarify syndromes and infer pathophysiology
Determine need for urgent therapy
Identify other needs
Develop a therapeutic strategy
(Portenoy et al, 1997)
Pain AssessmentPain AssessmentComponents History: temporal features, intensity, topography, quality,
exacerbating/alleviating factors Physical Exam: determine existence of underlying pathology Lab and Radiographic Tests: appropriate to pain syndrome
Assessment Tools Pain Intensity Scales: VAS, NAS, “faces” scale Multidimensional Pain Measures: Brief Pain Inventory, McGill
Pain Questionnaire
(Portenoy et al, 1997)
Pain Intensity Rating ScalesPain Intensity Rating Scales• Visual Analogue Scale (VAS)
No painNo pain ----------------------------------- ----------------------------------- Worst painWorst pain
•Categorical Scale None (0) Mild (1 – 4) Moderate (5 – 6) Severe (7 – 10) None (0) Mild (1 – 4) Moderate (5 – 6) Severe (7 – 10)
• Numerical Rating Scale0 0 -------------------------------------------------------------------------- 10 10
No painNo painWorst pain Worst pain imaginableimaginable
(Cleeland, 1991; Jacox et al, 1994)
00
No No hurthurt
22
Hurts just a Hurts just a little bitlittle bit
44
Hurts a little Hurts a little bit morebit more
66
Hurts even Hurts even moremore
88
Hurts a whole Hurts a whole lotlot
1010
Hurts as much Hurts as much as you can as you can
imagineimagine
• Pain Faces Scale
• Brief Pain Inventory Shade areas of worst pain. Put an X on area that hurts mostShade areas of worst pain. Put an X on area that hurts most
Progress in Chronic Pain Management
Therapeutic Modalities for Chronic Therapeutic Modalities for Chronic
Pain ManagementPain Management
TreatmentTreatment
Therapeutic Options for Chronic Pain ManagementTherapeutic Options for Chronic Pain Management
Pharmacotherapy (Analgesics) Non-opioids Adjuvant Analgesics
Antidepressants Anticonvulsants
Opioids Rehabilitative Approaches Psychologic Interventions Anesthesiological Approaches Neurostimulatory Techniques Surgery Complementary/Alternative Approaches Lifestyle Changes
(Cashman, 1996; Portenoy et al, 1997; Hanks et al, 1998; Galer, 1998; Stein, 1995)
Status of antidepressants in chronic pain managementStatus of antidepressants in chronic pain management
Best evidence: TCAs – Inhibit both NA and 5-HT reuptake
TCAs are superior to SSRIs in pain management
TCAs are superior to the anticonvulsant
There is no consensus regarding which of the many TCA
derivatives is most effective.
The choice of TCA is therefore dictated largely by adverse
effects
Neurologic Complications of Cancer Therapy Current Treatment Options in Neurology 1999, 1.428-437
Litsedge, A Double-Blind Comparison of Dothiepin and Amitriptyline for the Treatment of Depression with Anxiety, Psychopharmacologia (Berl.) 19, 153--162 (1971)
INTRODUCTIONINTRODUCTION
Major reason for seeking medical care.
90% is vasculr headache.
10% is mixture of inflammation,traction or dilatation of pain sensitive structure.
A true commitment is a heart felt promise to yourself from which you will not back down
- D. Mcnally
PATHOPHYSIOLOGYPATHOPHYSIOLOGY
Pain Referred pain
– Pattern of referred pain
Success in life is a matter not so much of talent and opportunity
as of concentration and perseverance
- C.W. Wendte
CLINICAL ASSESSMENTCLINICAL ASSESSMENT
History– Hx of present illness
– Past medical hx
– Family hx
– Social hx
Physical examination
We possess by nature the factors out of which personality can be made, and to organize them into effective personal life is every man’s primary responsibility
- Harry Emerson Fosdick
CLINICAL ASSESSMENTCLINICAL ASSESSMENT
Clinical features suggesting serious cause– Crescendo– Early morning– Vomiting– Fever– Seizures & other neurological symptomes– Worst headache in my life– Known malignancy– Tenderness
Facial painFacial pain
Typical Neuralgias1) Trigeminal neuralgia
• Characterized by recurring paroxysmal severe pain, brief duration (seconds) in the territory of the trigeminal nerve, spontaneously or initiated by chewing, talking, touching the affected side of the face.
• Unknown aetiology, an arterial loop pushing on the sensory root in the posterior fossa.
• Females affected more than males• Analgesics, surgery, destruction of the sensory
neuron, division of nerve root.
Facial painFacial pain
Typical Neuralgias2) Glossopharyngeal neuralgia
• Unknown cause• Equal both sexes• Severe, sudden episodes of pain in the
tonsil region one side only, ipsilateral ear.• Pain - severe for 1-2 hours, recur daily• Treated like trigeminal
Facial painFacial pain
Typical Neuralgias3) Sluder’s neuralgia and Vidian neuralgia
• Intractable pain in the nose, eye, cheek and lower jaw.
• Could be due to lesion of the sphenopalatine ganglion, or vidian nerve.
• Analgesics, vidian neurectomy
Facial painFacial pain
Posttraumatic neuralgia– Neuroma
– Parietal & occipital
– 90% recovery
Experience can be defined as
yesterday’s answer to today’s problems
Facial PainFacial Pain
Atypical facial pain Pain felt over the cheek, nose, upper lip or
lower jaw Usually bilaterally symmetrical Aching, shooting, burning, accompanied by
reddening of the skin and lacrimation or watering of the nose
Lasts for hours, days or weeks Psychological consultation, analgesics
Symptomatic NeuralgiasSymptomatic Neuralgias
Intracranial lesions1) Central lesions
• Tumours of the brain stem, M.S., thrombotic lesions, metastasis, occult naso-pharyngeal ca.
• No precipitant, sensory loss.2) Post herpetic neuralgia
• Herpes zoster may affect trigeminal nerve ganglion
• Vesicular rash covers one division commonly the 1st with severe pain.
Symptomatic NeuralgiasSymptomatic Neuralgias
Extracranial lesions1) Sinus disease
• Infective and neoplastic lesions of the paranasal sinus.
• Facial pain & dental pain, loss teeth.• Clinical suspicion.• Treatment
2) Dental neuralgia• Dental carries• Dental extraction
3) Temporomandibular joint pain
HeadacheHeadache
Headache is one of the commonest symptoms in medical practice.
Aetiology:
1) Raised intracranial pressure Due to tumours, abscesses, subdural
haematoma, brain haemorrhage.
2) Inflammation of the brain and meninges e.g. meningitis, cerebritis, others
HeadacheHeadache3) Migraine
Congenital predisposition Triggered by hunger, certain foods, sleep - too much or too
little, hormonal variations, stress. Pathology-vascular dilatation Females affected more than males ? Proceeded by aura usually visual, paraesthesiae of hands,
weakness Headache is unilateral or bilateral, affects any area of the
head, aching or throbbing often accompanied by nausea and vomiting
Diagnosis - by history alone Treatment - prevention by avoiding precipitating factors,
appropriate medication.
HeadacheHeadache
4) Tension headache More common in adult females Positive family history (40%) Maybe associated with migraine Produced by persistent contraction of the
muscles of the neck, head and face Caused by emotional tension, secondary to
other headaches, posture habit Treated by analgesics, muscle relaxants,
physiotherapy
HeadacheHeadache
5) Cluster headache 90% are men Age 20 - 30 Attacks occur in groups, no aura Caused by vascular dilatation of branches of
external carotid Triggered by histamines, alcohol Treated by analgesics, anti-histamine, steroids
Pains from head and neck Pains from head and neck musclesmuscles
Pain from temporalis muscles Can arise from grinding teeth at night
(bruxism), impacted wisdom teeth, temporomandibular joint dysfunction, anxiety when the patient clenches the jaws too tightly
Treatment: Refer to interested dental surgeon.
Pains from head and neck Pains from head and neck musclesmuscles
Pain from upper neck muscles Can radiate over the head
Treatment by physio-therapist or rheumatologist
Pain from frontalis muscles Usually due to bad posture at work or
while drivingTreatment: physio-therapy
Pains from head and neck Pains from head and neck musclesmuscles
Cervical spondylosis Pain mediates upwards from the neck to the
occiput or vertex to the front of the head, down to the shoulders
Due to cervical discs prolapse Diagnosis - x-ray
Treatment: Physio-therapy, referral to rheumatologist
Pains from head and neck Pains from head and neck musclesmuscles
Temporal arteritis Due to acute inflammation of the artery, the cause
unknown, affects men and women over the age of 60
Pain over the temples and frontal region, intense, throbbing, tenderness over the scalp, swelling and redness of the overlying skin with general malaise, partial or complete loss of vision.
ESR Elevated
Treatment: Cortisone, analgesics
Pains from head and neck Pains from head and neck musclesmuscles
Psychologic headache Usually accompanied by depression,
anxiety
No organic lesion
It is a great misfortune not to possess sufficient wit to speak well
nor sufficient judgment to keep silent
La Broyers character
Dedicated to my family for making everything worthwhile
Thank youThank you
THANKYOUTHANKYOU
My sincere thanks to P.Sampath
READ not to contradict or confute
Nor to Believe and Take for Granted
but TO WEIGH AND CONSIDER
Cerebrovascular Cerebrovascular EmergenciesEmergencies
Is survival a mere stroke of Luck?
“My Opinions are founded on knowledge but modified by experience”
Every minute matters: ‘time is brain’Every minute matters: ‘time is brain’
Expert is one who think to his chosen mode of ignorance
INTRODUCTIONINTRODUCTION
Perceptual Sense (Observation) Word Sense (Recording) Common Sense (Thinking)
– Will lead you to get - Clinical Sense
“ He who cannot forgive others destroys the bridge over which he himself must pass” - Annoy
Cerebrovascular disease – Cerebrovascular disease – Mind boggling factsMind boggling facts
CVD is the most disabling of all neurologic diseases. 50% of survivors have a residual neurologic deficit.
Greater than 25% require chronic care.
World wide incidence: 2/1000 population/annum1
Incidence in people aged 45 – 84 years: about 4/10001
Incidence in India: was 36/100,000 for the year 1998-19993 in a study in Calcutta
Incidence of mortality due to stroke (India: WHO study): 73/100,000 per year2
1.A practical approach to management of stroke patients; 1996; 360-3842. Epidemology of cerebrovascular disorders in India; 1999; 4-19
3. Neuroepidemiology 2001;20:201-207
If you think you can or you can’t You are always right
• CVD 6.7 %
• MI 2.5 %
• Death 7.2 %
• CVD, MI, Vascular death 8.6 %
• CVD, MI, Death 10.3 %
Annual risk CVD, MI, vascular Annual risk CVD, MI, vascular death following TIA, minor CVDdeath following TIA, minor CVDAnnual risk CVD, MI, vascular Annual risk CVD, MI, vascular
death following TIA, minor CVDdeath following TIA, minor CVD
Experience can be defined as yesterday’s answer to today’s problems
Indian scenario
1880 death / daydue to stroke in India
Equal to 6 Boeings 737 crashes every dayEqual to 6 Boeings 737 crashes every day
22 times that due to malaria 4 times that due to RHD 1.4 times that due to TB Almost equal to deaths due to IHD
Indian scenarioIndian scenarioNumber of deaths due to strokeNumber of deaths due to stroke
Indian immigrants to England have higher risk or dying due to stroke than local population
ComparisonComparisonIndia vs. established market economiesIndia vs. established market economies
(Age adjusted stroke mortality)(Age adjusted stroke mortality)
2 to 3 times stroke 2 to 3 times stroke mortality higher in Indiamortality higher in India
– Increase life expectancy (aging population)– Urbanization
ComparisonComparison USA – stroke mortality decline since 1940’sUSA – stroke mortality decline since 1940’s
India likely to increaseIndia likely to increase
Stroke units Aspirin Thrombolysis Heparin
Acute stroke interventions – Acute stroke interventions – reasonable evidencereasonable evidence
Neurologists
StrokeStroke
Vascular event due to atherosclerosisVascular event due to atherosclerosis
CardiologistsCardiologists PhysiciansPhysicians
Relevant to all of usRelevant to all of us
Limb weakness – 77% Urinary disturbance – 48% Dysphagia – 45% Cognitive deficit – 44%
Stroke disability worldwideStroke disability worldwide
35% functionally dependent at 1 year35% functionally dependent at 1 year
Stroke care units vs general wards– 9% relative risk reduction– 56 deaths or dependency avoided / 1000 acute
strokes treated / year Aspirin
– 3% relative risk reduction– 12 deaths or dependency avoided / 1000 active
strokes treated / year
Acute stroke interventions – Acute stroke interventions – evidence based medicineevidence based medicine
Thrombolysis – (even in USA only 1% of strokes are thrombolysed)– 10% relative risk reduction– 63 deaths or dependency avoided
(91 early deaths due to haemorrhage) Heparin
– No benefit
Acute stroke interventions – Acute stroke interventions – evidence based medicineevidence based medicine
People who survive stroke – 90% are left with deficit – minimal / mild / moderate / severe
None of the presently available therapy has any major impact hence prevention is critical
ConclusionConclusion
New role of doctorsNew role of doctors
““Managers of Change”Managers of Change”
““Preventors of Change”Preventors of Change”(Health ill health)(Health ill health)
GlobalGlobal
15 million deaths globally 15 million deaths globally every year due to vascular disease every year due to vascular disease
(30% of all deaths) (30% of all deaths)
GlobalGlobal
By 2020 – stroke and myocardial By 2020 – stroke and myocardial infarction will constitute leading cause infarction will constitute leading cause
of death / disabilityof death / disability
Lowering blood pressure Primary prevention – 17 randomised trials –
reduction of 5 to 6 mmHg diastolic and 10.12 mmHg systolic BP – 38% reduction of stroke
Secondary prevention – have we made PROGRESS
Common Stroke MimicsCommon Stroke Mimics Hypoglycemia Post ictal state Drug overdose Concussion with neck injury Migrainous accompaniment Encephalopathies with focal signs Hyponatremia Subdural hematoma, Empyema Focal Encephalitis: Herpes
Being ignorant is not so much a shame as being unwilling to learn
Level of Evidence
Level A: Based on RCT or Meta analysis of
RCT
Level B: Based on Robust Experiment or Observation Studies
Level C: Based on Expert opinion.
“The True Art of Memory is The Art of Attention” - S.Johnson
Guidelines for 24 hrs – MandatoryGuidelines for 24 hrs – Mandatory
1. History And Examination
a. Stroke clerking Performa (1994) R.C.P.1. Improved patient Assessment2. Improved Management - not clear3. Improved outcome - not clear
b. Examination1. Secure Diag of Stroke2. Specify Impairment3. Identify sub type of Ischemic stroke4. Rule out stroke mimics
“ We Sometimes think we have forgotten something when in fact we never really learned it in the first place”
Imp.Your Memory Skills
Guideline: 3 (B) - CPR– CPR is rarely successful in the setting of stroke – Sneeder
1993.
Guideline: 4(B) Investigations:(Sagar 1995)-435 PTS)– Chest x-ray 16% ABN – Only 4% change clinical management– Order x-ray chest if weight loss or chest symptoms
present
Through Action You Create your Own Education - D.B. ELLIS
Guideline 5: (B) ECG:– Cardiac cause of Death (30 days) Ebrahim 1990.– All conscious patients to have ECG
Guideline 6: (C) CT:– Routine CT Head is a must– King’s fund forum(1988) gives useful framework– Weir 1994 Clinical scoring cannot distinguish – CT done if: a) Uncertainty of Stroke
b) If Anticoagulation or Anti Platelet treatment contemplated
c) IV rtPA
Thought is the labour of the intellectReverie is its pleasure
Guideline 7:(B) M.R.I.
– Mohr 1995, - Unclear for Implications for clinical practice
– 2004 – PWI > DWI – IV rtPA very useful
Whatever the Mind can conceive and Believe, the mind can Achieve -Napoleon Hill
Imagination is more Important than KnowledgeImagination is more Important than Knowledge
Guideline 8: (B) ECHO no Routine
– Echo in Acute Stroke – Cardiac cause/Thrombus LV– TEE is superior to TTE– Amer Heart Asson (1997) - same conclusion– Yield is very low. (Leung 1993; Chambors 1997)– Only when abnormal ECGS - change clinical management
Guideline 9: (A) – Doppler scan for selected patients – > 80% stenosis benefits from Endarterectomy– Subst Storke -Good recovery - do doppler– Useful in posterior circulation
A open foe may prove a curse ; but a pretended friend is worse
Guideline 10: (B) Management:
– Fever (Worst Prog.) Reith 1996 – Hypoxia (Moroney 1996) - Exac. by seizures
Pneumonia and Arrythmias - Worst outcome
– Hyperbaric O2 ineffective (Nighoghossaln 1995)
– Haemodilut. Plasm Expanders; venesection – No evidence for efficacy (As plund - 1997)
Check ABG only if Hypoxia suspected.
It is a great misfortune not to possess sufficient wit to speak well nor sufficient judgment to keep silent - La Broyers character
Guideline 11: (A) Steroids and Hyperosmolar agents Unproven treatment –
– Tumor oedma responds but not cytotoxic stroke oedma qialbash 1997 - No effect on survival or improv. In funct. Outcome
– Mannitol - (Boysen 1997) - short term effective statistically in conclusive
You are what you think and not what you think you areYou are what you think and not what you think you are
We learn by thinking and the quality of the learning outcome is We learn by thinking and the quality of the learning outcome is determined by the quality of our thoughtsdetermined by the quality of our thoughts
R.B. SchmeckR.B. Schmeck
Guideline 12: (B) - Blood Pressure
– Defer - acute reduction of BP - 10 days unless HT Encephalopathy or aortic dissection present
– Moris 1997 - Increase BP - falls in 10 days– UK - 5mm in D.B.P. 1/3 storke - Low BP prompt correct of
hypovoll. and withdrawal of hypotonic drugs– Collins 1994 - HT - Prim. stroke prevent– Neal 1996 (Current RCT) - HTs in stroke survivors -study
needed– Acute reduction of BP only if thrombolysis considered
Guideline 13: (A/B) – AF
– AF / ISCH Stroke/ Mild disability - Warfarin after 48 Hrs (Longer for larger)
– Aspirin for others EAFT 1995 Less than 2 PT - No effect SPAF 1996 > 5 - Bleeding
Discipline Weighs ounces; Regret weighs Tons
A great many people think they are thinking when they are A great many people think they are thinking when they are merely re arranging their prejudicesmerely re arranging their prejudices
W. JamesW. James
Guideline 14:(B/C) - Blood sugar
– Weir (1997) > 8 mm d/Lit - Poor outcome– Acute MI + 11 mm d/Lit - Intensive Insulin - improved
(Malmberg 1997)
Many Ideas grow better when transplanted into another mind than Many Ideas grow better when transplanted into another mind than in the one where they sprang UPin the one where they sprang UP
O.W. HolmosO.W. Holmos
Guideline 15: (A) Cholesterol
– Prosp. Study collob.: 1993 - Epidem study do not support
– Blaun 1997: Metranauetic - Chollest & statin 30% decrease - stroke in CAHD patients.
– Sacks 1996 - Tot chol: decrease to 4.8 mmol/Lit benefits
Guideline 16: (A/C) Deep vein thrombosis
– Kalra 1995 - 10 days - stroke Pts - 50% – Sandercock 1993 - Pul embol 6-16% only– Ist 1997 - 5000 IV or 12500 twice daily - Hemorrage greater– Gradual stocking value - useful in Surg - pts but its value not
evaluated - (Wells 1994)– Use with caution - if periph artery insuf. is present hence do
not use heparin on stockings.
A woman’s desire for revenge outlasts all her other emotions
Every discovery contains an irrational element or Every discovery contains an irrational element or 4 creative intuition4 creative intuition
Guideline 17: (A/B) Pressure sure
– Event health care (1995) specialised low pressure mattress systems to be used than stand Hospital - mattress
I have never let my Medical schooling interfere with my education I have never let my Medical schooling interfere with my education Mark TwainMark Twain
Management of infarction– Guideline 18: (A)
Aspirin 75 - 150 /Day 3 yrs 40% reduces of vascular events in 1000 pts (APTC -
1994) Stroke sub type value ? (TACI, PACI, LACI, POCI) Dienners - 1996, synergy possible with Clopidogrel
Ticlopidine etc.
Anti CoagulationAnti Coagulation Warfarin - AF
– In sinus rhythm - uncertain – Spirit 1997 low dose ABP + Warfarin in TIA &
Minor stroke - Stopped of HE– Heparin (IST 1997) – Significant reduction in
early death (12 fewer in 1000) not better than aspirin
– So avoid Heparin (A)
“ He who cannot forgive others destroys the bridge over which he
himself must pass” - Annoy
When they tell you to grow up, they mean stop growing When they tell you to grow up, they mean stop growing PiccasoPiccaso
Thrombolysis (A)
Warlow 1997 - Uncertain clinical benefit 2004 – NINDS – Thrombolysis
conclusively proved its efficacy – first 3 hrs
A (Neurologist’s) life is like a piece of paper on which everyone who A (Neurologist’s) life is like a piece of paper on which everyone who passes by leaves an impressionpasses by leaves an impression
- Chines proverb- Chines proverb
Guideline 20: (I) Hemorrhage
– Hankey and hon 1997: Supra tentorial evacuation for ICH is controversial - Avoid
– Infra tentorial - Yes– Main Indication - Deteriorating or depressed
consciousness
A medical school should not be a preparation for life. A medical school should not be a preparation for life. A school should be lifeA school should be life
3 D ied
3 4 R ed tag
7 D ied
2 1 d isch ton ver h om e
3 D ied
8 D isc fo rp a llim a
1 D iscH om e
6 4 D isch ar 6 7 D ied
1 3 1In tu b a tion
9 3N ot In tu b
2 2 4 P ts
Guideline 21 : Ventilation -Decreased level of consciousness - increased mortality and poor final outcome - Absent pupillary light responses - poor prognosis
PITFALLSPITFALLS Basing treatment of stoke on brain imaging
along without a vascular work-up Missing early infarct signs on CT Underestimating the time of symptom onset
for patients who wake up with a stoke Overtreatment of hypertension in acute
stoke
Three can be seen in the divisions of a human in mind, body and spirit
PITFALLSPITFALLS Overuse of carotid endarterectomy in
asymptomatic patients Not investigating both extracranial and
intracranial circulations Failure to distinguish severe cartid stenosis
from total occlusion Not obtaining spinal fluid for patients with
suspected subarachnoid hemorrhage
“Social Isolation is in itself a pathogenicFactor for disease production”
PITFALLSPITFALLS Not treating patients with large artery
ischmic stroke indefinitely with antiplatelet terapy
Failure to recognize lacunar stoke Inadequate use and dosing ofHMG Co-A
reductase inhibitors (statins) inpatients with cerebrovascular disease
Through Action You Create your Own Education - D.B. ELLIS
PROGNOSTIC PEARLSPROGNOSTIC PEARLS Flaccid Paralysis for more than 96 hrs When tendon reflexes recover without return of voluntary
movement – prognosis poor Recovery of sensory less in usual to a degree. Postion sense
recovers but not pain and temperature Recovery from Dysphasia is never complete Dysarthria usual improves and Dysphagia never improves Diplopia due to brain stem is usually permanent Conjugate gaze – recovers Vertigo improves but hearing loss is permanent Pseudobulbar palsy permanent
“By Nature All Men/ Women are alike butby Education widely different”
STOKE MYTHOLOGYSTOKE MYTHOLOGY
GENERAL MYTHS DIAGNOSTIC MYTHS THERAPEUTIC MYTHS
Serious, sincere, systematic study surely secures supreme success
GENERAL MYTHSGENERAL MYTHS
PHYSICIAN + MRI = NEUROLOGIST MINISTROKE CVA
CHAOTIC
COMMUNICATION
Discipline Weighs ounces Regret weighs Tons
DIAGNOSTIC MYTHSDIAGNOSTIC MYTHS
Self evident cause Ischaemic stroke + AF Lacunes, Lacunar infarcts and small vessel
disease Cryptogenic stroke PFO and Cardiogenic stroke
Experience can be defined as
yesterday’s answer to today’s problems
Ultrasound DiagnosisUltrasound Diagnosis
In skilled hands, ultrasound may show:• Carotid occlusion or stenosis• MCA occlusion or stenosis• Vertebrobasilar occlusion• Extracranial dissection
The secret of walking on water is Knowing where the stones are
UCLA Stroke CT ProtocolsUCLA Stroke CT ProtocolsSequence Time CT
WWOCT
Stroke
CT Stroke WWO Diamo
x
CT Stroke reduced Dye
CT Stroke
reduced Dye
WWO Diamox
SCOUT 0’15” ++ ++ ++ ++ ++
CT 0’30” ++ ++ ++ ++ ++
CTA-COW
16’
-- ++ ++ ++ ++
CTA-Neck
-- ++ ++ ++ ++
CTP 20’ -- ++ ++ ++ ++
CTP W diamox
30’ -- -- ++ -- ++
Post-contrast
0’30” ++ -- -- -- --
Magnetic Resonance Imaging (MRI)Magnetic Resonance Imaging (MRI)11
High level of anatomic detail for precisely locating the stroke and determining the extent of damage.
Especially useful for small blood vessels due to high sensitivity
Advances in the early detection of stroke involve using diffusion and perfusion weighted imaging.
1. Curr Opin Neurol. 2004 Aug;17(4):447-51
Memory, the daughter of attention, is the teeming mother of knowledge - Martin Tupper
UCLA Stroke MRI ProtocolsUCLA Stroke MRI ProtocolsSequence Time Brain
WWOTIA Stroke Thromb
olysis 1Thrombolysis 2
SCOUT 0’25” ++ ++ ++ ++ ++
MRA-Neck 6’44” -- ++ ++ - ++
DWI 0’40” -- ++ ++ ++ ++
T2 3’42” ++ ++ ++ ++ ++
MRA-COW 6’12” -- ++ ++ ++ --
FLAIR 2’41” ++ - ++ ++ --
GRE 2’35” - - ++ ++ ++
PWI 2’ - - - ++ ++
T1 3’ ++ - - - -
T1 post Gad
3’ ++ - - - -
Other Diagnostic Tools-1Other Diagnostic Tools-1
Magnetic Resonance Angiography1
(MRA) Carotid Duplex Scanning2: Transcranial Doppler (TCD)3
Xenon CT Scanning4
1.Neurol Res. 2004 Jun;26(4):429-342. J Vasc Surg. 2003 Sep;38(3):422-30. 3. .Neurology. 2004 May 11;62(9):1468-81,4. Keio J Med. 2000 Feb;49 Suppl
1:A25-8
Science is below the mind; Spirituality is beyond the mind
Other Diagnostic Tools -2Other Diagnostic Tools -2
Radionuclide SPECT Scanning1
PET Scanning2
Transesophageal Echocardiography3
1. AJNR Am J Neuroradiol. 2001 May;22(5):928-36
2.Neuroimaging Clin N Am. 2003 Nov;13(4):741-583. Heart Dis. 2003 Sep-Oct;5(5):320-2
Success is a prize to be won. Action is the road to it. Chance is what may lurk in the shadows at the road side.
THERAPEUTIC MYTHSTHERAPEUTIC MYTHS
Evidence based medicine = Randomized Clinical Trials– Best Research Evidence– Clinical Expertise– Patient Values
Systematic Escalation of anti thrombotic therapy Brain Hemorrhage Demands Neuro surgical
Consultation
Dead/dependent follow-upDead/dependent follow-up
Deaths by day 14Deaths by day 14
Deaths during follow-upDeaths during follow-up
Deaths ordered by antithromboticDeaths ordered by antithrombotic
Deaths ordered by thrombolyticDeaths ordered by thrombolytic
Deaths ordered by stroke severityDeaths ordered by stroke severity
Symptomatic ICH by 14 dysSymptomatic ICH by 14 dys
Fatal ICH by 14 dysFatal ICH by 14 dys
Dead/dependent follow-up < 3 hr.Dead/dependent follow-up < 3 hr.
Dead follow-up < 3 hr.Dead follow-up < 3 hr.
62% vs 69% s.62% vs 69% s.
22% vs 12% s.22% vs 12% s.
22% vs 19% s. 22% vs 19% s.
40% 30% 17% 10% 40% 30% 17% 10%
3% 20% ns.3% 20% ns.
11% 29% ns.11% 29% ns.
9.3% vs 2.5% s.9.3% vs 2.5% s.
6% vs 1% s.6% vs 1% s.
55% vs 71% s.! 55% vs 71% s.!
20% vs 25% ns.20% vs 25% ns.
Thrombolysis in acute strokeThrombolysis in acute strokeThrombolysis in acute strokeThrombolysis in acute stroke
NATURE, TIME AND PATIENCE are the 3 great physicians
NINDS ConsensusNINDS Consensus
Door to MD evaluation 10 min
Door to CT completion 25 min
Door to CT read 45 min
Door to treatment 60 min
Access to neurological expertise 15 min
Access to neurosurgical expertise 2 hrs
Admit to monitored bed 3 hrs
Memory, Pity and Beauty are short lived in life; But tinged with emotion persist in life
CONCLUSION CONCLUSION
• MYTHS
• PITFALLS
• PROGNOSTIC PEARLS
It is the disease of not listening, the malady of not marking,
that I am troubled withal - Shakespeare
CVD – Prevention or Cure?CVD – Prevention or Cure?
While number of curative methods are available, preventive therapy is undoubtedly the main strategy
in the management of CVD
Lijec Vjesn. 2003 Nov-Dec;125(11-12):322-8
The sign wasn’t placed there
By the Big Printer in the sky
Where are we ……?Where are we ……?
6-8 HO
UR
S
Call Call emergencemergency servicesy services
ER stroke teamER stroke team
ActivatedActivated(15 minutes)(15 minutes)
NeuroprotectivNeuroprotective drug infused e drug infused during during transporttransport
Brain scanBrain scan
Drugs Drugs administered administered
‘stroke-‘stroke-treatment’ treatment’
cocktailcocktail
Full Full recoveryrecovery
Stroke onsetStroke onsetSecondarySecondarypreventionprevention
The art of medicine is caring for the heart of the patient
Dedicated to my family for Dedicated to my family for making everything worthwhile making everything worthwhile
READ not to contradict or confute
Nor to Believe and Take for Granted
but TO WEIGH AND CONSIDER
THANK YOUMy sincere thanks to Thudhimugan .K for
his meticulous computer work My sincere thanks to Thudhimugan .K for
his meticulous computer work