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In Capsule Series Neurology

Stroke
Definition :

 A sudden neurological deficit of vascular origin that persists for

longer than 24 hours or leading to death.
 Stroke is the third most common cause of death, after coronary
heart disease & cancer.

Types & causes :

I. Ischemic : ( Cerebral infarction ) 85% of all strokes.

a) Thrombosis :
 Atherosclerosis : The most common cause
 Extracranial : aorta , carotid or vertebral
 Intracranial : ACA , MCA , PICA
 Arteritis , Dissection.
 Hematological disorders : Polycythemia, leukemia, sickle cell
anemia & hypercoagulability state.

b) Embolism :

 From the heart :

 Atrial fibrillation ( AF )
 Infective endocarditis.
 Mitral Stenosis
 Myocardial infarction.
 Atrial myxoma
 Dilated cardiomyopathy
 Congenital heart disease.
 From carotid vessels

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Risk factors for ischemic stroke

 Risk factors of atherosclerosis : modifiable & non modifiable see cardiology

 Transient ischemic attacks.

II. Hemorrhagic : accounts for 15% of all strokes

a. Intracerebral : 2 HAT see hemiplegia

b. Subarachnoid hemorrhage. 2A , 2H , 2T

Clinical feature of ischemic stroke :

1- Focal neurological manifestations : according the occluded artery

Clinical features of occlusion of the MCA or its branches:

Cortical branch occlusion : Supplies the lower 3/4 of the anterior 3/5 of CC

- Contralateral UL monoplegia with cortical sensory loss.

- Other cortical manifestations : aphasia , agraphia , apraxia ( If the left

hemisphere is involved )

Capsular branch occlusion : capsular hemiplegia 6 criteria P4

Clinical features of occlusion of the ACA or its branches:

Cortical branch : supplies upper 1/4 of the anterior 3/5 of the cerebrum

- Contralateral monoplegia in LL with cortical sensory loss

- Mentality & personality changes.

Capsular branch : supplies ventral surface of the anterior limb of the internal capsule.

- Contralateral facio-brachial monoplegia.

Vertebro-basilar system : supplies the posterior 2/5 of the cerebrum

, the cerebellum , the brain stem & the spinal cord.
1- anterior spinal artery occlusion:
 Quadriplegia if above C5
 Paraplegia if below C5. ( complete flaccid paraplegia )
2- Brainstem branches occlusion : Brainstem hemiplegia

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3- Posterior inferior cerebellar artery (PICA):

 Ataxia. ( …….. )
 It is NOT associated with hemiplegia.
 Lateral medullary syndrome ( Wallenberge syndrome ) : 

1- Sympathetic: Horner`s syndrome :

- Ptosis - Myosis - Anhidrosis - Enophthalmos - Nasal congestion

2- Spinothalamic tract : loss of pain & temperature from the opposite side.
3- Cranial nerves: 10th cranial nerve lesion  palatopharyngeolaryngeal
manifestations as (nasal tone, nasal regurge, dysphagia, horseness of voice).
4- Vestibular of the 8th cranial nerve : Vertigo & Vomiting.
5- Spinal nucleus of the trigeminal nerve: loss of pain & temperature from the same
side of the lesion ( crossed hemianaethesia ).

Stages : Flaccid then spastic stage P3

2- Negative in quality :
Loss of function rather than positive ( e.g. Paralysis rather than jerking ,
blindness rather than visual hallucination )
3- Rapidly developing : The onset is sudden and acute.
4- Maximum at onset : Over minutes to hours.
5- 80% of stroke patients have at least one vascular risk factor and most
are elderly. Stroke is uncommon ( but not rare ) in young people.
Investigations of ischemic stroke

1- First line investigations :

o CBC & ESR.

o INR , PTT
o Plasma glucose , cholesterol, urea , electrolytes.
o Urinalysis.
o ECG.

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2- Cerebral imaging :

i. CT brain :
o To exclude non vascular causes e.g. tumor.
o To differentiate an ischemic stroke ( hypodense blackish lesion )
from hemorrhagic stroke ( hyperdense whitish lesion )
ii. MRI : Usually detects area of evolving infarction within hours, CT
is sometimes negative for up to several days after acute infarction.

3- Echocardiography : if cardiogenic embolism is suspected.

4- Duplex carotid ultrasound : When carotid artery occlusion is suspected.

5- Angiography : it plays an important role in the preoperative

evaluation of carotid artery disease.

Treatment of ischemic stroke

 As in hemiplegia : 6 items P7 plus

 Carotid endarterectomy for patient with severe carotid stenosis.

1- General care of the comatosed patient :  b

2- Symptomatic ttt : 
3- Rehabilitation :
o Physiotherapy
o Speech therapy.
4- Control of blood pressure : Antihypertensive therapy is indicated in severe
hypertension ( ≥ 220/120 ) or in those with hypertensive encephalopathy,
aortic dissection, acute pulmonary edema or myocardial infarction.
5- Specific treatment :
 Thrombolytic therapy
 Anticoagulants
 Anti-platelets
6- Neuroprotective.

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Indications of thrombolytic therapy in stroke :

- Acute ischemic stroke with clearly definable time of onset.
- 3 hours time window. ( time is brain )
- A baseline CT excluding ICH & SAH.
- Age is 18 years or older.
- Dose of i.v. alteplase ( tissue plasminogen activator ) : 0.9 mg/kg
(max. 90 mg) infused over 1 hour.
Absolute contraindications : 11
o CT scan today shows intracranial bleeding.
o Symptoms suggestive of subarachenoid hge, even if the CT is
normal.
o CT scan today shows multilobar infarction ( hypodense area > ⅓ of
cerebral hemisphere.
o Prior history of intracranial bleeding.
o Any of the following within the past 3 months : intracranial or
intraspinal surgery, serious head trauma.
o Blood pressure > 185 mmHg ( systolic ) or > 110 mmHg ( diastolic )
o Evidence of active internal bleeding.
o Patient has an arteriovenous malformation or aneurysm.
o Lab evidence of coagulopathy : e.g. platelets count < 100000
o Patient received heparin in the past 48 h and PTT above normal range
o Patient received warfarin & INR > 1.7
Relative contraindications : 4
o Major surgery or serious trauma in past 2 weeks.
o GIT or urinary tract bleeding within past 3 weeks.
o Acute MI in past 3 months or post MI pericarditis.
o Blood glucose < 50 or > 400 mg/dl

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Prognosis

Complete recovery is uncommon, but the sooner improvement begins,

the better the prognosis.

Depends on :

o Site & size of infarction.

o Patient age
o Other comorbidities.
o Impaired consciousness , aphasia , or severe brain stem signs
suggest poor prognosis.

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Hemorrhagic stroke
Types & Etiology :

1) Intracerebral hemorrhage : See above 2H, 2A, 2T

o Primary intra-cerebral hemorrhage : intracerebral hemorrhage
due to chronic hypertension. “hypertensive ICH”
o Chronic hypertension produces fibrinoid necrosis, lipohyalinosis,
and medial degeneration, which make the vessels susceptible to
rupture.
2) Subarachnoid hemorrhage : 2A , 2H , 2T

Clinical picture of intracerebral hemorrhage :

1) ICH occurs characteristically during activity (rarely during sleep).

2) Symptoms typically begin abruptly.
3) The clinical presentation has 2 elements :
a) Increased Intracranial pressure : headache , vomiting , loss of
conscious in some cases. Seizures are uncommon at the onset in
7% of cases but are found in 32% of lobar hemorrhages.
b) Specific clinical manifestations : which are related to the site of
hematoma.

4) In order of frequency, the most common site of primary cerebral

hemorrhage are :
1- Putamen. ( a basal ganglia nucleus )
2- Lobar hemorrhage : central white matter of frontal, parietal, temporal & occipital.
3- Thalamus.
4- Cerebellum.
5- Pontine hemorrhage.

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1- Putamen :

o This is the commonest type.

o Clinical manifestations vary with the size of hemorrhage, but
include hemiparesis, headache, and alterations of consciousness.
2- Lobar hemorrhage : Headache is a first and most prominent symptom.
o Frontal hematoma : hemiparesis more in upper limb
o Parietal hematoma : sensorimotor deficit
o Dominant temporal hematoma : fluent aphasia
o Occipital hematoma : homonymous hemianopia.
3- Thalamic hemorrhage : 15%
o hemiparesis or hemiplegia in nearly all cases with severe sensory deficit
o Aphasia may be present with lesion of the dominant side.
o Extension into the subthalamus & high midbrain may cause ocular
disturbances ( downward deviation of the eyes & irreactive pupil )
o Rupture into the 3rd ventricle may lead to early hydrocephalus.
4- Cerebellar hemorrhage : 10%
o Acute onset of headache , vertigo , vomiting & inability to stand
and walk.
o characteristic syndrome of ipsilateral ataxia, LMN facial palsy, and
ipsilateral gaze paresis
o Coma & death may occur due to brainstem compression.
5- Pontine hemorrhage : 6%
o Characterized by coma, quadriplegia, absence of light reaction,
pinpoint pupil , decerebrate rigidity, respiratory disturbance,
tachycardia, hyperthermia. Death usually occurs within few hours.
o Less severe cases arising from hemorrhage confined to one side of
the pons are also recognized.

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Diagnosis of intracerebral hemorrhage

1) Clinical feature : suggested by :

o Acute hypertension exceeding the patient’s chronic hypertensive
level.
o Vomiting at onset.
o Severe headache.
NB : Although the absence of headache or vomiting does not rule out the diagnosis of ICH,
presence of these symptoms is in favor of ICH or SAH as it is reported in less than 10% of
occlusive strokes.

o Focal seizure.
o Hypertensive changes of the retina.
2) Brain CT : is the procedure of choice to detect the intracerebral
hemorrhage ( white mass ) with surrounding brain edema.
3) MRI.
4) Lumbar puncture : must performed cautiously as it may
precipitate or aggravate an impending cerebellar herniation.
5) Others : PT , PTT , Platelets count , Liver function tests.
Prognosis

o 1/3 of the patient die in the first 1 to 30 days

o Death occurs due to either :
1) Marked rise of intracranial pressure   brain perfusion.
2) Compression of vital centre such as hypothalamus , brainstem.

NB : Patients who survive usually show a surprising degree of restoration of

function , since in contrast to infarction the hemorrhage pushes the brain
tissue rather than destroys it.

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Treatment : see hemiplegia

1- Intracerebral hemorrhage :

 As ischemic infarction but surgical evacuation of blood instead of

thrombolytic & anticoagulant therapy.
 Antihypertesive therapy is initiated when the systolic blood
pressure is > 180 mmHg or the diastolic blood pressure > 105
mmHg.

2- Subarachnoid hemorrhage : see later p51

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Transient ischemic attacks ( TIAs )

Definition :
o TIAs are short transient attacks of cerebral ischemia lasting less than 24h
o Most TIAs last only 10 seconds to 15 minutes.
o RIND ( Reversible Ischemic Neurological Deficit ) : If the attack lasts over 24 h .
o Patients with TIAs have a higher risk of developing a stroke.
Etiology : The same as ischemic infarction
o Cerebral thrombosis.
o Cerebral embolism.
Clinical picture :
o Carotid TIAs : see before
o Vertebro-basilar TIAs : see before
Investigations : The same as ischemic stroke

Treatment :
I. Medical :
o Antiplatelets : Aspirin , plavix.
o Anticoagulants : Heparin , Warfarin.
o Neuroprotective : Trental , Trivastal.
o Treatment of risk factors : e.g. hypertension , DM, hyperlipidemia,
smoking.
NB : LDL goal < 70, TG goal < 150 & glucose concentration of 140-180 mg/dL
II. Surgical :
Endarterectomy : An incision is made to open the carotid
artery , the plaque is removed.
III. Carotid angioplasty : Introduction of balloon to dilate the stenotic artery.

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