1. FACIAL PAIN-NON ODONTOGENIC
CAUSES
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

2. Facial Pain
Understanding, Impact and
Awareness
We learn by thinking and the quality of the learning outcome
is determined by the quality of our thoughts
R.B. Schmeck

3. “Pain May be Inevitable, but Misery is Optional”
Dee Malchow
Pain constitutes nearly 40% of the total of patient visits to doctors. 1
“ByNature All Men/W en are alike but
om
byEducation widelydifferent”
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.
- Chinese

4. Pain 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.

5. Indian 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

6. Decade 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.

7. 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
The International Association for the
• Pain is a significant stress physically, emotionally pain an
Safety of Pain (IASP) defines
unpleasant sensory and emotional
experience associated with actual or
potential tissue damage, or described in
terms of such damage, or both.
(American Society of Anesthesiologists, 2002; Loeser et al, 2001; Merskey H et al, 1994; Portenoy et al, 1996)

8.  Qualities 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

9. Acute 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

10. Categorization of Chronic pain
Types of Pain
Types of Pain
(Psychogenic)
(Psychogenic)
Pain arising from
Pain arising from Pain arising from
Pain arising from
pain receptors
pain receptors Pain with NO apparent cause
Pain with NO apparent cause
Nervous system
Nervous system
[Nociceptive Pain]
[Nociceptive Pain] (e.g. Low back pain or some
(e.g. Low back pain or some [Neuropathic Pain]
[Neuropathic Pain]
pelvic pain in women)
pelvic pain in women)
Peripheral
Peripheral
Central
Central
Superficical / /Somatic
Superficical Somatic Deep / /Visceral
Deep Visceral
(Brain and Spinal cord)
(Peripheral nervous
(Peripheral nervous
(Brain and Spinal cord) system)
system)
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

11. Different types of pain
Nociceptive descriptors Neuropathic descriptors
Cramping, tender Shooting
Gnawing, heavy Hot-burning
Aching Sharp
Splitting Stabbing

12. 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 region
Axis II: Nervous system (central, peripheral, or autonomic); physical
disturbance/dysfunction
Axis III: Continuous or nearly continuous, fluctuating severity
Axis IV: Mild severity of 1 to 6 months
Axis V: Trauma, operation, burns, infective, parasitic (one of these)
(Loeser et al, 2001; Merskey et al, 1994)

13. Dimensions of Chronic Pain
Chronic pain has a psycho-
Depressio
Hostil
social component that must
ity
be dealt with before
n depression becomes a part of
Psychological
Loneline
the clinical picture. Chronic
Pathological
Anxie
pain should be recognized as
Factors
Physical
Process
Social
Factors
Factors
a multi-factorial disease state
ss
ty
requiring intervention at
many levels.
A.G. Lipman, Cancer Nursing, 2:39, 1980
TIME

14. Pain: 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 GR ACE to acce pt with se re nity the thing s that canno t be
chang e d the COURAGE to chang e the thing s that sho uld be chang e d
and the WISDOM to kno w the diffe re nce

15. Current 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

16. Understanding Pain
Pathophysiology

17. 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)

18. Peripheral and Central Pathways for Pain
Ascending Tracts Descending Tracts
Cortex
Thalamus
Midbrain
Pons
Medulla
(Brookoff, 2000)
Spinal Cord

19. Pain Pathway

20. Nerve Fibres
 Αδ ( A delta)
 Myelinated
 Fast conductors
 Gentle pressure and pain
 Αβ (A beta)
 Thinner – but still
myelinated
 Fast conductors
 Heavy pressure &temp
 C - very thin
 Slow conductors
 PAIN, Pressure, temp &
chemicals

21. Pathophysiology 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)

22. Pain-Sensing System in the
Malfunction in Chronic Pain
Acute pain:
Pain Pain-sensing signals
Sensing are initiated in
response to a stimulus
In chronic • They elicit a pain-
pain, pain relieving response
signals are
generated
Chronic pain:
without
physiologic Pain signals are
significance generated for no
reason and may be
intensified
• Pain-relieving
(Illustration: Seward Hung, 2000) mechanisms may be
defective or
deactivated

23. Role 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

24. Pathophysiology of Pain
 Inferred from characteristics, etiology or pathophysiology
 Types
– Nociceptive
– Neuropathic
– Idiopathic
 Therapeutic implications
(Portenoy et al, 1996)

25. Nociceptive 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)

26. Neuropathic 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)

27. Idiopathic 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)

28. Recent 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)

29. Progress in Chronic Pain Management:
Therapeutic Modalities for
Chronic Pain Management
Assessment

30. “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

31. Pain 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)

32. Pain Assessment
Components
 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)

33. Pain Intensity Rating Scales
• Visual Analogue Scale (VAS)
No pain ----------------------------------- Worst pain
• Numerical Rating Scale
0 ------------------------------------- 10
Worst pain
No pain
imaginable
•Categorical Scale
None (0) Mild (1 – 4) Moderate (5 – 6) Severe (7 – 10)
• Pain Faces Scale
0 2 4 6 8 10
No Hurts just a Hurts a little Hurts even Hurts a whole Hurts as much
hurt little bit bit more more lot as you can
imagine
• Brief Pain Inventory Shade areas of worst pain. Put an X on area that hurts most
(Cleeland, 1991; Jacox et al, 1994)

34. Progress in Chronic Pain Management
Therapeutic Modalities for Chronic
Pain Management
Treatment

35. Therapeutic 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)

36. Status 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)

38. INTRODUCTION
 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

39. PATHOPHYSIOLOGY
 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

40. CLINICAL 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

41. CLINICAL ASSESSMENT
 Clinical features suggesting serious cause
– Crescendo
– Early morning
– Vomiting
– Fever
– Seizures & other neurological symptomes
– Worst headache in my life
– Known malignancy
– Tenderness

42. Facial pain
Typical Neuralgias
1) 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.

43. Facial pain
Typical Neuralgias
2) 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

44. Facial pain
Typical Neuralgias
3) 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

45. Facial pain
 Posttraumatic neuralgia
– Neuroma
– Parietal & occipital
– 90% recovery
Experience can be defined as
yesterday’s answer to today’s problems

46. Facial 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

47. Symptomatic Neuralgias
Intracranial lesions
1) 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.

48. Symptomatic Neuralgias
Extracranial lesions
1) 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

49. Headache
Headache is one of the commonest symptoms in
medical practice.
Aetiology:
1) Raised intracranial pressure


50. Headache
3) 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.

51. Headache
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

52. Headache
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

53. Pains from head and neck
muscles
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.

54. Pains from head and neck
muscles
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 driving
Treatment: physio-therapy

55. Pains from head and neck
muscles
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

56. Pains from head and neck
muscles
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

57. Pains from head and neck
muscles
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

58. Dedicated to my family for
making everything worthwhile

59. Thank you

60. READ not to contradict or confute
Nor to Believe and Take for Granted
but TO WEIGH AND CONSIDER
THANKYOU
My sincere thanks to
P.Sampath

62. Cerebrovascular
Emergencies
Is survival a mere stroke of Luck?
“My Opinions are founded on knowledge but modified by experience”

63. Every minute matters: ‘time is brain’
Expert is one who think to his
chosen mode of ignorance

64. INTRODUCTION
 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

65. Cerebrovascular disease –
Mind boggling facts
 World wide incidence: 2/1000 population/annum 1
 Incidence in people aged 45 – 84 years: about 4/1000 1
 Incidence in India: was 36/100,000 for the year 1998-1999 3 in a
study in Calcutta
 Incidence of mortality due to stroke (India: WHO study):
73/100,000 per year2
CVD is the most disabling of all neurologic diseases.
50% of survivors have a residual neurologic deficit.
Greater than 25% require chronic care.
1.A practical approach to management of stroke patients; 1996; 360-384
2. 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

66. Annual risk CVD, MI, vascular
death following TIA, minor CVD
• CVD 6.7 %
• MI 2.5 %
• Death 7.2 %
• CVD, MI, Vascular death 8.6 %
• CVD, MI, Death 10.3 %
Experience can be defined as yesterday’s answer to
today’s problems

67. Indian scenario
1880 death / day
due to stroke in India
Equal to 6 Boeings 737 crashes every day

68. Indian scenario
Number of deaths due to stroke
 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

69. Comparison
India vs. established market economies
(Age adjusted stroke mortality)
2 to 3 times stroke
mortality higher in India
 Indian immigrants to England have higher
risk or dying due to stroke than local
population

70. Comparison
USA – stroke mortality decline since 1940’s
India likely to increase
– Increase life expectancy (aging population)
– Urbanization

71. Acute stroke interventions –
reasonable evidence
 Stroke units
 Aspirin
 Thrombolysis
 Heparin

72. Stroke
Vascular event due to atherosclerosis
Relevant to all of us
 Neurologists Cardiologists Physicians

73. Stroke disability worldwide
 Limb weakness – 77%
 Urinary disturbance – 48%
 Dysphagia – 45%
 Cognitive deficit – 44%
35% functionally dependent at 1 year

74. Acute stroke interventions –
evidence based medicine
 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

75. Acute stroke interventions –
evidence 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

76. Conclusion
 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

77. New role of doctors
“Managers of Change”
“Preventors of Change”
(Health ill health)

78. Global
15 million deaths globally
every year due to vascular disease
(30% of all deaths)

79. Global
By 2020 – stroke and myocardial
infarction will constitute leading cause
of death / disability

80. 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

81. Common 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

82. Guidelines for 24 hrs – Mandatory
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

83. 1. History And Examination
a. Stroke clerking Performa (1994) R.C.P.
1. Improved patient Assessment
2. Improved Management - not clear
3. Improved outcome - not clear
b. Examination
1. Secure Diag of Stroke
2. Specify Impairment
3. Identify sub type of Ischemic stroke
4. 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

84.  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

85.  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 intellect
Reverie is its pleasure

86.  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

87.  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
Imagination is more Important than Knowledge

88.  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

89.  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

90.  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 are

91.  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
We learn by thinking and the quality of the learning outcome is
determined by the quality of our thoughts
R.B. Schmeck

92.  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

93.  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)
A great many people think they are thinking when they are
merely re arranging their prejudices
W. James

94.  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
Many Ideas grow better when transplanted into another mind than
in the one where they sprang UP
O.W. Holmos

95.  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

96.  Guideline 17: (A/B) Pressure sure
– Event health care (1995) specialised low
pressure mattress systems to be used than stand
Hospital - mattress
Every discovery contains an irrational element or
4 creative intuition

97.  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.
I have never let my Medical schooling interfere with my education
Mark Twain

98. Anti 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)
“ H who cannot forgive others destroys the
e
bridge over which he himself must pass” -

99.  Thrombolysis (A)
 Warlow 1997 - Uncertain clinical benefit
 2004 – NINDS – Thrombolysis
conclusively proved its efficacy – first 3 hrs
When they tell you to grow up, they mean stop growing
Piccaso

100.  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 (Neurologist’s) life is like a piece of paper on which everyone who
passes by leaves an impression
- Chines proverb

101. 2 2 4 P ts
Guideline 21 : Ventilation
131
I n t u b a tio n
93
N o t In tu b -Decreased level of
consciousness - increased
6 4 D is c h a r 6 7 D ie d
mortality and poor final
3 4 R e d ta g 2 1 d is c h t o
n ver h om e
8 D is c fo r
p a llim a
1 D is c
H om e outcome
- Absent pupillary light
3 D ie d 7 D ie d 3 D ie d
responses - poor prognosis
A medical school should not be a preparation for life.
A school should be life

102. PITFALLS
 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

103. PITFALLS
 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 pathogenic
Factor for disease production”

104. PITFALLS
 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

105. PROGNOSTIC 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
“ByNature All Men/W en are alike but
om
byEducation widelydifferent”

106. STOKE MYTHOLOGY
 GENERAL MYTHS
 DIAGNOSTIC MYTHS
 THERAPEUTIC MYTHS
Serious, sincere, systematic study surely secures supreme success

107. GENERAL MYTHS
 PHYSICIAN+ MRI = NEUROLOGIST
 MINISTROKE
CHAOTIC
 CVA
COMMUNICATION
Discipline Weighs ounces Regret weighs Tons

108. DIAGNOSTIC 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

109. Ultrasound 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

110. UCLA Stroke CT Protocols
Sequence Time CT CT CT CT CT Stroke
Stroke Stroke reduced
WWO Stroke
WWO reduced Dye
Diamox Dye WWO
Diamox
SCOUT 0’15” + + + + +
CT 0’30” + + + + +
CTA-COW - + + + +
16’
CTA-Neck - + + + +
CTP 20’ - + + + +
CTP W 30’ - - + - +
diamox
Post- 0’30” + - - - -
contrast

111. Magnetic Resonance Imaging (MRI)1
 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

112. UCLA Stroke MRI Protocols
Sequence Time Brain TIA Stroke Thrombol Thrombol
WWO ysis 1 ysis 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 3’ + - - - -
Gad

113. Other Diagnostic Tools-1
Magnetic Resonance Angiography1 (MRA)
Carotid Duplex Scanning2:
Transcranial Doppler (TCD)3
Xenon CT Scanning4
Science is below the mind; Spirituality is beyond the mind

114. Other 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):741-58
3. 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.

115. THERAPEUTIC 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

116. Thrombolysis in acute stroke
Dead/dependent follow-up 62% vs 69% s.
Deaths by day 14 22% vs 12% s.
Deaths during follow-up 22% vs 19% s.
Deaths ordered by antithrombotic 40% 30% 17% 10%
Deaths ordered by thrombolytic 3% 20% ns.
Deaths ordered by stroke severity 11% 29% ns.
Symptomatic ICH by 14 dys 9.3% vs 2.5% s.
Fatal ICH by 14 dys 6% vs 1% s.
Dead/dependent follow-up < 3 hr. 55% vs 71% s.!
Dead follow-up < 3 hr. 20% vs 25% ns.
NATURE, TIME AND PATIENCE
are the 3 great physicians

117. NINDS 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

118. CONCLUSION
• MYTHS
• PITFALLS
• PROGNOSTIC PEARLS
It is the disease of not listening, the malady of not marking,
that I am troubled withal - Shakespeare

119. 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

120. Where are we ……?
Call
Stroke onset emergency
Secondary
prevention services
Full recovery
U RS
Activated
(15 minutes)
Neuroprotective
drug infused
Drugs administered
‘stroke-treatment’ 6-8 O during transport
cocktail H ER stroke team
Brain scan
The art of medicine is caring for the heart of the patient

123. Dedicated to my family for
making everything worthwhile

124. READ not to contradict or confute
Nor to Believe and Take for Granted
but TO WEIGH AND CONSIDER
THANK YOU
My sincere thanks to Thudhimugan .K for
his meticulous computer work