The document provides an extensive overview of cerebrovascular disorders and Parkinson's disease, covering assessment, classification, risk factors, and management strategies. It details clinical features of strokes, including ischemic and hemorrhagic types, and outlines diagnostic investigations like CT and MRI scans. Furthermore, it discusses Parkinson's disease, its symptoms, staging, and treatment options, including pharmacological and surgical approaches.

1. CENTRAL
NERVOUS
SYSTEM

2. CEREBROVASCULAR
DISORDERS

3. BEDSIDE ASSESSMENT
 History
 Neurological examination

4. HISTORY
 The time of onset of symptoms
 The nature of symptoms
Abruptly : vascular etiology
Risk factors for vascular disease,history of
seizures,migraine,insulin use or drug abude
Accompanying symptoms(severe
thunderclap headache-Sub arachnoid
hemorrhage)

5.  History of present illness:
Time of symptoms onset
Evolution of symptoms,recovery
Convulsion or loss of consciousness at
onset
Headache
Chestpain at onset
 Medical History:
Prior intracerebral hemorrhage,H/O
stroke,recent head trauma.myocardial
infarction

6.  Surgical History
Recent surgical procedures
 Medications-
Anticoagulant therapy

7. Record:
 Vital signs
 Blood glucose
 Level of consciousness
 Severity of deficits

8. NEUROLOGICAL EXAMINATION
 Identify signs of lateralised hemispheric
or brainstem dysfunction consistent with
focal cerebral ischemia.
 Level of consciusness, the presence of a
gaze deviation,Aphasia,neglect or
Hemiparesis

9. WHO DEFINITION OF STROKE
 A neurological deficit of sudden onset
accompanied by focal dysfunction and
symptoms lasting more than 24 hours
that are presumed to be of a non-
traumatic vascular origin.

10.  Major Causes
• Age • Obesity
• Hypertension • Smoking
• Diabetes mellitus • Atrial fibrillation
• Heart disease • Dyslipidaemia
• Hyperfibrinogenaemia • Alcohol
• Coagulopathies
• Contraceptive pill
• Markers of arterial atheroma

11. Risk Factors for Stroke
MAJOR
 1. Hypertension 2. Smoking
 3. Diabetes mellitus 4. Obesity
 5. Hyperlipidaemia 6. Polycythaemia
 7. High plasma fibrinogen
 8. Cardiac lesion — Atrial fibrillation —
Mitral valve prolapse — Mitral stenosis —
Rheumatic heart disease — Ischaemic
heart disease — Infective endocarditis.
 9. Thrombocythaemia

12.  Minor
1. High alcohol intake
2. Positive family history of stroke
3. Oral contraceptive pills
4. Trauma.

13. Clinical Classification of Stroke
 1. Completed stroke: This is rapid in
onset with persistent neurological deficit
which does not progress beyond 96
hours.
 2. Evolving stroke: There is a gradual
step-wise development of neurological
deficit.

14.  3. Transient ischaemic attack: The focal
neurological deficit resolves completely
within 24 hours
 4. Reversible ischaemic neurological
deficit (RIND): The neurological deficit
completely resolves within a period of 1
to 3 weeks.

15. Classification of Stroke
(Based on pathophysiology)
 Ischemic(85%)
 Hemorrhagic(15%)

16. ISCHEMIC STROKE:
 Thrombotic(55%)
 Embolic (30%)
HEMORRHAGIC STOKE:
 Subarachnoid hemorrhage
 Intracerebral and cerebellar .H
 Subdural & Extra dural.H

17. ISCHEMIC STROKE
THROMBOTIC
 Usually develops at night during sleep
 Symptoms perceived in morning
 Suspect in h/o of hypercoagulable
states,atherosclerosis and collagen
vascular disorders.

18. EMBOLIC
 Occurs at any time
 Frequently during periods of vigorous
activity
 H/O Atrial fibrillation,Valvular
vegetations,Thromboembolism from
MI,Ulcerated plaques incarotid system
 Seizures in 20% of cases

20. HEMORRHAGIC STROKE
 Occur during stress or exertion
 Focal deficits rapidly evolve
 Signs of raised ICT
 Confusion, coma or immediate death

27. Investigations
 I. Baseline investigations Full blood count,
ESR
2. Serological tests
3. Blood glucose and urea
4. Serum electrolytes and proteins
5. X-ray chest
6. ECG and ECHO
7. Carotid Doppler.

28. II. Special investigations (especially
young patients)
 1. Antinuclear antibodies (ANA) for SLE,
rheumatoid arthritis
 2. Antibodies to double stranded DNA
(SLE)
 3. Anticardiolipin antibodies (SLE)
 4. Lupus anticoagulant
(antiphospholipid antibodies)—SLE
 5. Serum cholesterol (familial
hyperlipidaemia).

29.  III.CT Scan—Indications
CT scan is mandatory for proper
initial evaluation in all cases of stroke to
categorise them into either ischaemic or
haemorrhagic origin.
1. To confirm diagnosis (haemorrhage can
be detected immediately whereas it
may take 48 hours for infarcts to be
detected).

30. 2. To decide the line of management (to
decide on therapy with anticoagulants
or antiplatelet drugs).
3. To identify the presence of underlying
tumour, haematoma or vascular
malformation which can simulate stroke.
4. Head CT scan is diagnostic of SAH in 90%
of cases in the first 24 hours.

31.  IV.MRI: It is the preferred modality of
investigation in cases of posterior fossa
infarcts and for patients having TIA.
MR angiography is a useful non-
invasive test to evaluate large arteries
and veins.
 V.Cardiac Evaluation (for sources of
thromboembolism).

32.  VI. Angiography: It is not usually
indicated but indicated only to rule out
specific causes such as arterial
dissection.
• Definitive study for vascular
malformations
• Essential test prior to endarterectomy
• Pre-surgical evaluation of saccular
aneurysms

33. Infarct in anterior cerebral artery territory

34. CT Brain- Intracerebral bleed
with intraventricular extension

35. MANAGEMENT OF ISCHEMIC
STROKE
Specific Management
Medical Management
a. Blood pressure:A patients blood
pressure at presentation should not be
lowered unless it is more than 185/110
mmHg, as the ischaemic penumbral
tissue will infarct with even minor drop
in systemic blood pressure, because
cerebral autoregulation in this zone is
impaired.

36.  b. Anticoagulants
 c. Treatment of cerebral oedema
 d. Thrombolysis
 e. Antiplatelet drugs
2. Surgical Management
Carotid endarterectomy is useful in
patients with TIA with haemodynamically
significant (> 70%) carotid stenosis.

37. MANAGEMENT OF HEMORRHAGIC STROKE
 1. Maintenance of fluid and electrolyte
balance (Ryle’s tube feeding in
unconscious patients and bladder
catheterisation).
 2. Regular change of posture and care
of skin to avoid bed sores. 3. Monitoring
of blood pressure (diastolic pressure not
to be lowered below 110 mmHg in the
first 48 hours).

38.  4. Antioedema measures with mannitol
0.5–1.0 gm/ kg as rapid IV infusion or with
10% glycerol 500 ml IV infused over 4
hours daily for 6 days.
 5. Surgery: It is indicated in cerebellar
haemorrhage, whereby the haematoma
can be surgically removed. This is not
recommended in haemorrhage at other
sites, as this may result in permanent
neurological deficit.

39. II. General Management
 a. Attend to bladder, bowel, back, base
of lungs and eyes
 b. Patients should be ideally placed in
the semiprone position if unconscious to
prevent aspiration
 c. Proper nursing, feeding (if needed,
through Ryle’s tube)
 d. Intake and output chart should be
maintained

40.  e. Physiotherapy
i. It is started immediately to prevent
joint contractures and to promote
recovery of strength and coordination
ii. Physiotherapy of the chest is done
to prevent lung infection.

41. PARKINSON’S
DISEASE

42. PARKINSON’S DISEASE
 It is a movement disorder of unknown
aetiology due to degeneration of the
neurons in the nigrostriatal dopaminergic
system.
 There is an imbalance between
dopamine and acetylcholine
neurotransmitters (either an increase in
acetylcholine or a decrease in
dopamine level).

43. Causes of Parkinsonism

44. CLINICAL FEATURES
 A. Motor
 1. General • Expressionless face with
staring look with infrequent blinking
• Greasy skin
• Soft, rapid, indistinct
monotonous speech
• Flexed posture (universal
flexion).

45.  2. Gait
• Patients walk with short steps, with a
tendency to run
• Slow to start walking
• Shortened stride • Rapid small steps,
tendency to run (festination)
• Reduced arm swinging • Impaired
balance on turning
• Propulsion and retropulsion and
lateropulsion
• Kinesia paradox (patients can run fast
during emergency).

46. 3. Tremor
 Resting tremor (4–6 Hertz)
• Usually first in fingers/thumb
• Coarse, complex movements,
flexion/extension of fingers (pill rolling
and drumbeating movements)
• Abduction/adduction of thumb
• Supination/pronation of forearm
• May affect arms, legs, feet, jaw, tongue
• Intermittent, present at rest and when
distracted
• Diminishes on action and disappears
during sleep.

47.  4. Rigidity
• It is seen predominantly in the limbs •
Cogwheel type, mostly appreciated in
upper limbs especially in wrist joints
(there is a phasic element to stiffness in
all directions of movement)
• Plastic (lead pipe) type, mostly
appreciated in the legs and trunk • In
the trunk, rigidity manifests itself by the
presence of a flexed, and stooped
posture.

48.  5. Hypokinesis
• Slowness in initiating movements
• Impaired fine movements, especially of
fingers
• Poor precision of repetitive movements
• Handwriting–micrographia.

49. B. NON-MOTOR
• Neuropsychiatric symptoms – anxiety,
depression, psychosis, dementia, impulse
control disorder
• Autonomic failure
• Sensory symptoms.

50. STAGING
Grading Clinical features
Grade I Unilateral involvement
Grade II Bilateral involvement
Grade III Bilateral with mild
postural imbalance
Grade IV Bilateral with moderate
postural imbalance and requires
assistance
Grade V Bedridden

51. Eye Signs in Parkinsonism
 Decreased blink rate
 Hypometric saccades
 Impaired smooth pursuit
 Reflex blepharospasm (glabellar,
Myerson’s sign)
 Blepharoclonus

52.  Spontaneous blepharospasm
 Oculogyric crises (postencephalitic
parkinsonism)
 Reversed Argyll Robertson pupil
(postencephalitic parkinsonism).

53. INVESTIGATIONS
 1. Serological tests for syphilis (all
patients)
 2. CT brain
Indications a. Patients under age 50
b. Signs entirely unilateral
c. Atypical signs (e.g.
pyramidal).

54.  3. Tests to exclude Wilson’s disease (in
young patients (2nd to 4th decade)
a.Serum ceruloplasmin
b. Serum copper
c. Urine copper
d. Liver function tests.
4. MRI brain

55. TREATMENT
 1. Treat the underlying disease
 2. Withdraw the drugs in drug-induced
parkinsonism
 3. Drug therapy.

56. 3. Drug therapy
I. Drugs • Dopamine agonists
• Carbidopa/levodopa
• MAO-A inhibitors
• MAO-B inhibitors
• COMT inhibitors
• Amantadine
• Anticholinergics

57.  II. Neuroprotective agents
• L-carnitine
• Creatine monohydrate
• Dopamine agonists
• Seligiline
 III.Surgery
• Deep brain stimulation
• Substantia nigra ablation

58.  IV.Neurotransplantation
• Stem cell
• GDNF infusion (Glial cell derived
neurotrophic factor)
NON-MOTOR SYMPTOMS:
• Anti-depressants – Tricyclic anti-
depressants, SSRI
• Dementia – Donepezil, Rivantigmine
• Psychosis – Atypical antipsychotics

59. CT brain—basal ganglia calcification in
hypoparathyroidism—causing Parkinsonism

60. Parkinsonism—smudging of pars compacta
of substantia nigra between low signals of
red nucleus and pars reticularis

61. MRI normal—Pars compacta and
reticularis with red nucleus

62. MULTIPLE SCLEROSIS

73. THANK YOU