2. Ischemic stroke which result from occlusion
of an artery is the most common type of
stroke .
3. WHO defines stroke as a disease of sudden
onset focal neurological deficites ass. With
dysfunction in the brain , retina or spinal
cord due to occlusion or rupture of a
cerebral or spinal artery .
4. Previously defined as a neurological
impairment lasting less than 24 hours .
Now is defined as a transient neurological
deficit with-out the presence of infarction
on neuro-imaging .
5. Small proportion of all strokes but ass. With
higher short-term mortality .
6. Present with focal neurological deficit &
may include headache or impairment in
consciousness .
7. Present with sudden onset severe headache
& impairment in conciousness with-out
focal neurological deficit .
Clinical manifestations often overlap with
stroke .
10. Sensory changes .
Storke may present with more non-specific
sympyoms such as :
* Dizziness .
*Altered mental status .
*Sudden unexplained coma .
12. Common used scales is national institutes
of health stroke scale ( NIHSS ) .
13. Non contrast head CT most widely used
test.
High sensitivity for diagnosis hemorrhagic
stroke .
14. In ischemic stroke , initial head CT scan
often normal esp. in pts. Seen within 3
hours of symptom onset .
Even 24 hours after onset , may not show
evidence of infarction given poor resolution
of small infarct & those located in brain
stem .
15. CTA of the head & neck may performed
acutely if endovascular therapy is
considered or in unexplained acute coma to
rule out basilar artery thrombosis .
17. Visualize small strokes .
Multifocal or bilateral infarcts that may
suggest an embolic cause .
Presence of micro-bleeding .
18. However , MRI is never the initial test of
choice in acute suspected stroke because of
its longer acquisition time .
19. If pt. has symptoms suggestive of SAH &
non-contrast head CT findings are normal ,
LP required to evaluate for presence of
blood or xantho-chromia ( yellow color
stemming from erythrocyte breakdown .
20. Required if SAH is confirmed to diagnose &
treat a cerebral aneurysm .
21. Results most likely suggest the cause of
ischemic stroke such as presence of Atrial
Fibrillation or Carotid bruit .
22. Characterised by a temporary local
neurologic deficit with an absence of
infarction on neurologic imaging .
23. Hemiparesis .
Mono-ocular or visual field loss .
Dysartheria .
Aphasia & Sensory loss .
24. The presence of the following is more
consistent with migraine or seizure :
36. Aspirin 300 mg daily started immediately .
Specialist assessment & investigation within
24 hours of onset of symptoms .
Measures for secondary prevention
introduced as soon as the diagnosis is
confirmed including risk factors discussion .
37. Specialist assessment within 1 week of
symptom onset including decision on brain
imaging .
If vascular territory or pathology is
uncertain , refer for brain imaging .
38. 2 or more episodes in a week .
Should be treated as being at high risk of
stroke , even though they may have an
ABCD2 score of 3 or below .
39. Clopidogrel is recommended first line .
Aspirin + dipyridamole in pts. Who cannot
tolerate clopidogrel .
40. Pts. With internal carotid artery stenosis
who have TIA have the greatest short-term
risk of stroke .
41. AF .
Other cardio-embolic sources require
anticoagulation .
48. Infarcts occur in multiple arterial teriotories.
Located near cortical surface of brain with
normal arterial imaging .
49. AF most common cardio-embolic cause of
stroke .
New ventricular thrombus after MI .
Severe valvular diseases .
50. Isolated motor or sensory syndromes .
Rarely affect cognition or mental status .
Infaracts < 1.5 cm in diameter involve deep
white matter , basal ganglia & brain-stem .
51. Pathologically infarcts due to occlusion of
small penetrating arteries arising from ICAs
( most commonly the middle cerebral &
basilar arteries .
52. Hypertension is the main risk factor .
Artery to artery embolic thrombi .
Cryptogenic causes of stroke .
53. Autoimmune & hyper-coagulable disorders.
Cerebral vasculitis present with numerous
infarcts affecting multiple arterial
distribution .
54. Common consequence of SAH >> increase
ICP from obstructive hydrocephalus or
global cerebral edema .
55. Common consequence of SAH >> increase
ICP from obstructive hydrocephalus or
global cerebral edema .
56. Most common cause of SAH is saccular
( berry ) aneurysm rupture .
59. Altered mental status .
Nuchal rigidity
Sub-hyaloid hemorrhage on fundoscopy .
60. Pupillary dilation from compression of
occulomotor nerve ( 3rd Cranial Nerve ) by a
posterior communicating artery aneurysm .
61. CTA .
MRA .
Catheter-based angiography necessary for
the definitive diagnosis of aneurysm & other
causes of SAH .
62. Impairment in consciousness .
Loss of brainstem reflexes .
Stereotyped posturing movements to
painful stimuli .
63. Presence of hydrocephalus on neuro-
imaging is ass. With high mortality >>
should prompt neurosurgical placement of
external ventricular drain to relieve &
measure elevated ICP .
64. Impaired consciousness due to non-
convulsive status epilepticus may occur >>
require electroencephalographic monitoring
for diagnosis .
65. Presentation similar to ischemic stroke with
headache & impaired consciousness as
distinguishing characteristics .
66. Most common cause of ICH is hypertension
affects deep structures of the brain
( thalamus , basal ganglia , pons &
cerebellum ) .
67. Cerebral amyloid angiopathy in pts. Older
than 55 Years esp. in those with-out
hypertension in cerebral amyloid
angiopathy syndrome >> amyloid protein
deposits in cerebral arterioles >>
weakening the arterial wall >> making it
prone to rupture .
69. Blood pressure control is the main-stay of
acute treatment & prevention .
Hematoma expansion is the main-cause of
early neurologic deterioration .
70. Early withdrawal of care esp. within the first
48 hours is the leading cause of death .
71. Ischemic Stroke Treatment > Thrombolysis
& Endovascular Therapy .
Thromboysis should only be given if :
72. It is administered within 4.5 hours of onset
of stroke symptoms ( the thrombolytic
window ) .
Haemorrhage has been definitively
excluded ( imaging has been performed ) .
73. IV recombinant tissue plasminogen
activator ( TPA ) .
Only thrombolytic agent approved for use in
acute ischemic stroke .
74. Most effective when administered early .
Treatment within 3 hours of ischemic stroke
onset with disabling symptoms is ass. With
a significant reduction in disability at 3
months .
75. Treatment within 4.5 hours may have
clinical benefit .
Treatment beyond 3 hours is not approved
by FDA .
76. Age over 18 Years .
Clinical diagnosis of acute ischemic stroke .
Known time of onset .
77. CT scan consistent with diagnosis .
And treatment can be given within 180
minutes .
79. Gastrointestinal bleed in the last 21 days .
Major surgery in last 14 days .
History of intracranial bleed .
80. Serious head injury in last 3 months .
Pregnancy .
Active Pancreatitis .
81. Main complications of Alteplase treatment
is symptomatic ICH present with headache
or worsening level of consciousness .
82. Before treatment with alteplase Bp should
be < 185 / 110 mmHg .
Higher reading , should administration of IV
Labetalol or Nicardipine before alteplase
treatment .
83. Nitrates should be avoided because of
potential to increase ICP so Sodium
Nitropruside not used for hypertension
management .
84. Endovascular therapy primarily with intra-
arterial mechanical thrombectomy within 24
hours of stroke onset can considered for
pts. With clinically suspected large vessel
occlusion .
85. Start Aspirin .
Allow Bp up to 220 / 120 mmHg unless
evidence of end-organ damage exists .
Start deep venous thrombosis prophylaxis .
86. Aspirin administer within 48 hours of stroke
Clopidogrel monotherapy not established
benefit in acute stroke setting .
87. Anticoagulation therapy whether related to
AF or not > not reduce short term risk of
reccurent stroke & increase risk of
hemorrhage into territory of cerebral
infarction ( Hemorrhagic conversion ) .
88. Statins have not been shown to reduce the
risk of recurrent stroke but can be
considered after a dysphagia evaluation has
been completed esp. in pts. With
atherosclerotic stroke subtype .
89. Osmotherapy with mannitol or hypertonic
saline , temporary reduce ICP in ICH .
90. IV Nitrates such as Nitroglycerin &
Nitroprusside may raise increase ICP &
reduce blood flow to the ischemic region &
should be avoided in pts. With ICH .
91. Blood glucose , hydration , oxygen
saturation and temperature should be
maintained within normal limits .
Blood Pressure should not be lowered in the
acute phase unless there are complications
e.g Hypertensive encephalopathy .
92. Aspirin 300 mg orally or rectally should be
given as soon as possible if a haemorrhagic
stroke has been excluded .
93. With regards to atrial fibrillation , the Royal
college of Physicians state : anticoagulants
should not be started until brain imaging
has excluded haemorrhage and usually not
until 14 days have passed from the onset of
an ischemic stroke .
94. If the cholesterol is > 3.5 mmol/l pts.
Should be commenced on a statin , many
physicians will delay treatment until after at
least 48 hours due to the risk of
haemorrhagic transformation .
95. Stroke thrombolysis with TPA >> only
consider if less than 4.5 hours &
haemorrhage excluded .
The National Institute of Neurological
Disorders & Stroke ( NINDS ) issued a
protocol with inclusion & exclusion criteria .
96. NICE published a technology appraisal in
2010 on the use of Clopidogrel &
Dipyridamole for prevention of further
occlusive vascular events ( OVE ) .
97. Clopidogrel .
Aspirin plus dipyridamole .
Dipyridamole alone ( not to be used in
acute phase ) .
98. Pt. with ischemic stroke at discharge from
hospital after 14 days >> he should receive
( Clopidogrel + Statin if the cholesterol is >
3.5 ) .
99. The endarterectomy should be performed
as soon as the pt. is fit for surgery ,
preferably within 2 weeks of a TIA .
100. Symptomatic pts. With greater than 50 %
stenosis .
Healthy asymptomatic pts . With greater
than 60 % stenosis .
101. Used as an alternative to endarterectomy .
Less invasive revascularisation strategy &
uses an embolic protection device .
Indicated in selected cases such as re-
stenosis .
106. Contrast arteriography of the neck vessels .
A CT brain showed middle cerebral artery
territory .
107. Aim at preventing cerebral infarction .
Treatment similar to acute stroke .
Stenting can be used if there is ongoing
ischemia .
108. Usually affects the posterior circulation (
posterior cerebral artery territory is the
commonest ) .
109. A thrombotic event resulting from cardio
embolism or Antiphospholipid syndrome
would usually only affect intracranial
vessels & therefore a Horner’s syndrome
would be unusual .
110. Pts. Who are under 60 Years with large
cerebral infarctions arising in MCA territory
should be considered for decompressive
hemicranioectomy which is removing part
of skull to reduce ICP & should be carried
out within 48 hours of index event .
118. Locked-in’ syndrome : pt. is awake but is
unable to respond in anyway except by
vertical gaze & blinking ( lesion is in ventral
pons ) .
119. Present with either isolated hemiparesis ,
hemisensory loss or hemiparesis with limb
ataxia .
Strong association with HTN .
Common sites include basal ganglia ,
thalamus & internal capsule .
120. Visual field defects is a manifestation of the
following pathology :
122. Right homonymous hemianopia means
visual field defect to the right = lesion of
left optic tract .
Incongruous defects = optic tract lesion .
Conguous defects = optic radiation lesion
or occipital cortex .
