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Stroke (CVA - Cerebrovascular Accidents)               See also Hypertension & Acute Stroke
Stroke Treatment     See TIA  |    stroke_ischemic2007.pdf  |  carotid_stenosis2008.pdf  

Stroke - CVA Cerebral Vascular Accident

Types of Stroke  Ischemic cerebrovascular disease (generally thromboembolic disease) 1.  Thrombotic disease (atherothrombotic disease) 2.  Embolic stroke - much less common than thrombosis, most brain infarcts under age 35 3. Intracranial Hemorrhagic Stroke hypertensive hemorrhage subarachnoid hemorrhage - berry aneurysm rupture other hemorrhage - vascular malformations , atherosclerotic aneurysms , mycotic aneurysms Lobar Intracerebral Hemorrhage 4.  Venous sinus thrombosis

Anterior circulatory occlusion Internal carotid artery occlusion Sx: contralateral weakness or numbness, dysphasia, apraxia, confusion if the dominant hemisphere is involve. Transient blurring of vision or ipsilateral blindness (amaurosis fugax), homonymous visual field loss, ipsilateral headache. Anterior cerebral artery occlusion Sx: paralysis of opposite foot & leg, paresis of opposite arm, urinary incontinentce, mental impairment, slowness, delay, lack of spontaneity, impairment of gait & stance (apraxia), cortical sensory loss over toes, foot, & leg.

Middle cerebral artery occlusion Sx: paralysis & sensory impairment of contralateral face, arm & leg; aphasia in left CVA, paralysis of conjugate gaze to the opposite site; homonymous hemianopia (often superior homonymous quadratanopia); Cheyne-Stokes respiration; pure motor hemiplegia in internal capsule posterior limb CVA; ataxia of contralateral limb in parietal lobe involvement; Sx of Upper division occlusion: hemiparesis & sensory loss, arm & face affected more than leg; Broca's aphasia, hemineglect. Sx of Lower division occlusion: Wenicke's aphasia or nondominant behavior disorder without hemiparesis; Sx of Penetrating Artery occlusion:  pure motor hemiparesis

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Types of Stroke 
Ischemic cerebrovascular disease (generally thromboembolic disease)
1.  Thrombotic disease (atherothrombotic disease)

Anterior circulatory occlusion
Internal carotid artery occlusion
Sx: contralateral weakness or numbness, dysphasia, apraxia, confusion if the dominant hemisphere is involve. Transient blurring of vision or ipsilateral blindness (amaurosis fugax), homonymous visual field loss, ipsilateral headache.

Anterior cerebral artery occlusion
Sx: paralysis of opposite foot & leg, paresis of opposite arm, urinary incontinentce, mental impairment, slowness, delay, lack of spontaneity, impairment of gait & stance (apraxia), cortical sensory loss over toes, foot, & leg.

Middle cerebral artery occlusion
Sx: paralysis & sensory impairment of contralateral face, arm & leg; aphasia in left CVA, paralysis of conjugate gaze to the opposite site; homonymous hemianopia (often superior homonymous quadratanopia); Cheyne-Stokes respiration; pure motor hemiplegia in internal capsule posterior limb CVA; ataxia of contralateral limb in parietal lobe involvement;
Sx of Upper division occlusion: hemiparesis & sensory loss, arm & face affected more than leg; Broca's aphasia, hemineglect.
Sx of Lower division occlusion: Wenicke's aphasia or nondominant behavior disorder without hemiparesis;
Sx of Penetrating Artery occlusion:  pure motor hemiparesis

Posterior circulatory occlusion
Anterior inferior cerebellar artery occlusion

Basilar artery occlusion

Posterior cerebral artery occlusion
Sx: homonymous hemianopia of bilateral homonymous hemianopia; cortical blindness; memory defect, dyslexia without agraphia, topographic disorientation, unformed visual hallucination.

Thalamic syndrome: sensory loss, spontaneous pain & dysesthesias, choreathetosis, intentional tremor, mild hemiparesis.

Thalamoperforate syndrome:  1. Superior, crossed cerebellar ataxia.  2. Inferior, crossed cerebellar ataxia with ipsilateral 3rd nerve palsy.

Weber syndrome: 3rd nerve palsy & contralateral hemiplegia.
Paralysis or paresis of vertical eye movement, skew deviation, sluggish pupillary light response, slight miosis & ptosis;  Contralateral ataxic or postural tremor; Decerebrate attacks;

Midbrain syndrome: oculomotor palsy & other movement abnormalities.

Bilateral inferior temporal lobe: amnesis.

Subthalamic nucleus: hemiballism
-superior cerebellar artery occlusion
-vertebral artery occlusion
-Posterior inferior cerebellar artery occlusion (lateral medullary syndrome)
Occlusion of vertebral artery or lower branch of basilar artery.
One side of lesion: paralysis with atrophy of half the tongue.
On opposite side of lesion: paralysis of arm & leg, spare the face, impaired tactile & proprioceptive sense over half of othe body.

Lacunar disease

2.  Embolic stroke - much less common than thrombosis, most brain infarcts under age 35

3.  Venous sinus thrombosis

Intracranial Hemorrhagic Stroke

• hypertensive hemorrhage
• subarachnoid hemorrhage - berry aneurysm rupture
• other hemorrhage - vascular malformations , atherosclerotic aneurysms , mycotic aneurysms
• Lobar Intracerebral Hemorrhage (NEJM January 27, 2000 -- Vol. 342, No. 4)
  The apolipoprotein E genotype can identify patients with lobar intracerebral hemorrhage who are at highest risk for early recurrence. (N Engl J Med 2000;342:240-5.)
  Although intracerebral hemorrhage is a less frequent cause of stroke than cerebral infarction, it is more often fatal. It is usually attributed to hypertensive small-vessel disease, and the most common sites of hemorrhage are the basal ganglia, cerebellum, and pons. Treatment is largely restricted to the control of hypertension and rehabilitation.
  In some patients with intracerebral hemorrhage, however, the hemorrhage is lobar in location, such as in the frontal, parietal, temporal, or occipital cortex, and such patients often do not have hypertension. This category of hemorrhage, referred to as lobar intracerebral hemorrhage, may represent a distinct pathogenetic subgroup.   Cerebral amyloid angiopathy, also known as cerebral congophilic angiopathy or cerebral amyloidosis, has been recognized as a frequent cause of lobar intracerebral hemorrhage. The main pathological feature is the infiltration of cortical vessels by amyloid beta-protein , a homogeneous eosinophilic substance found in the brain in elderly persons and an important component of the senile plaques found in patients with Alzheimer's disease. The clinical syndrome is characterized by lobar intracerebral hemorrhage with no other definite cause of the hemorrhage.   Affected patients are usually over the age of 60 years and may have antecedent memory loss.

Cryptogenic stroke - often medium vessel disease

(Ref: DynaMed Web - Stroke)             ----------

Clinician Information on Stroke:

• Acute Stroke Toolbox (Rx Guidelines, etc.) 

Hypertension & Acute Neurologic Patients
Rodrigo Rodriguez,Jr. MD  Dec. 7, 2001 KP Conference

Cerebral Perfusion Pressure (CPP) = MAP - ICP   (Normal range 70 - 100 mmHg)

Mean Arterial Pressure (MAP) = (SBP + 2 DBP)/3

Intracranial Pressure (ICP) = 5- 15 mm Hg normally

Summary Statement:

• In acute neurologic illness CPP takes on a linear relationship with MAP
• Beta-adrenergic blocking agents as Labetalol are agents of choice in neurologic illness.
• ACE Inhibitors are second line agents
• Vasodilators should be avoided if possible
• Nitroprusside may be used with caution in severe HTN

For Intracerebral Hemorrhage patients:

• Rebleeding may occur if the Bp remains elevated
• Optimal target BP should take into account the premorbid degree of Hypertension
• Target Mean Arterial Pressure MAP of 120-130 mmHg

For Ischemic Stroke patients:

• Usually are hypertensive on admission
• Cerebral autoregulation is impaired
• Regional CBF (Cerebral Blood Flow) becomes pressure-dependent
• Elevated BP may be needed to aid blood flow to the ischemic prenumbra
• Target MAP of 120-140 mmHg

For Traumatic Brain Injury patients:

• Increased Bp may be secondary to a hyperadrenergic state vs elevated ICP
• Elevated ICP will decrease CBF
• Target MAP of 110-120 mmHg or a CPP of 70 mmHg

For Hypertensive Encephalopathy patients:

• It is an hypertensive emergency
• Co-existent cerebral vasospasm
• Autoregulation breaksdown
• Both ischemia and cerebral edema develop
• Decrease MAP slowly by 25% over hours to avoid cerebral hypoperfusion.

Final Clinical Conclusions:

• CPP should be maintained between 70 - 100 mmHg
• CPP can be adjusted by controlling the MAP
• CPP can be achieved by maintaining a MAP of 100-120 mmHg
• Elevated ICP wil decrease CPP
• Labetolol does not affect cerebral vascular tone and is the first choice agent .

REF:

The Diagnosis and Management of Hypertensive Crises  (Review)
(Chest. July 2000;118:214-227  American College of Chest Physicians)

How to manage blood pressure in critically ill neurologic patients.  
(Journal of Critical Illness  April, 2001)

12182001

Antihypertensive agents frequently used in neurologically ill patients Mechanism Initial (bolus)
Ref: How to manage blood pressure in critically ill neurologic patients.  (Journal of Critical Illness  April, 2001)

Medication	Mechanical of action	Initial bolus dose	Infusion rate	Advantages	Disadvantage
Labetalol	Alpha & Beta antagonist	5-20 mg IV q15min (Max: 340 mg)	0.5 - 2 mg/min	Rapid onset of action No effect on ICP	CHF, bronchospasm, Bradycardia
Esmolol	B1 selective blocker	500 ug/kg over 1 min	50 - 200 mg/kg/min	Rapid onset of action No effect on ICP	Bradycardia
Nicardipine	Ca-blocker	none	5 - 15 mg/h	Rapid onset of action	Hypotension, increase ICP & heart rate
Na-Nitroprusside	Vasodilator	none	0.25 - 10 ug/kg/min	Rapid onset of action Short duration of action	cyanide toxicity, increase CBF, ICP
Nitroglycerin	Vasodilator	50 ug IV	5 - 200 ug/min	Rapid onset of action Short duration of action	Methemoglovin production, increase CBF, ICP
Clonidine	Alpha 2 agonist	0.1 - 0.2 mg PO	not available	May be helpful in alcohol withdrawal syndrome	decrease CBF
Hydralazine	Vasodilator	2.5 - 10 mg IV q20-30 min (Max 40 mg)	usually used as boluses	Good antihypertensive effect	Longer duration of action, increase CBF, ICP; lupus like syndrome, hemolytic anemia, glomerulonephritis
Enalaprilat	ACE inhibitor	0.625 - 5 mg IV q6h	usually used as boluses	no efect on ICP or CBF	may cause abrupt decrease in BP; potential for increased ICP in pts with poor intracranial compliance; renal dysfunction

        2008