Internal Medicine - Cerebrovascular Diseases

nianderthalNOTES

INTERNAL MEDICINE:

Cerebrovascular Diseases

INTRODUCTION

-include the following most common devastating disorders:

1. Ischemic Stroke 2. Hemorrhagic Stroke 3. Cerebrovascular anomalies -Intracranial aneurysms -Arteriovenous malformations (AVMs) -most cerebrovascular diseases manifest by the

abrupt onset of a focal neurologic deficit

STROKE

-DEFINITION: abrupt onset of a neurologic deficit that is attributable to a focal vascular cause

-laboratory studies and brain imaging are used to support the diagnosis

-clinical manifestations are highly variable because of the complex anatomy of the brain and its vasculature

STROKE

-OTHER TERMS:

-Cerebral ischemia – caused by reduction in blood flow that lasts longer than several seconds

-Cerebral infarction – if the cessation of flow lasts for more than a few minutes, death of brain tissue results

-Transient ischemic attack (TIA) – when blood flow is quickly restored, brain tissue can recover fully and the patient’s symptoms are only transient

-Ischemic Penumbra: tissue surrounding the core region of infarction that is ischemic but reversibly dysfunctional; imaged by using perfusion-diffusion imaging with MRI or CT

STROKE -a generalized reduction in cerebral blood flow due to systemic

hypotension usually produces SYNCOPE -Global hypoxia-ischemia: widespread brain injury due to

infarction in the border zones between the major cerebral artery distributions if low cerebral blood flow persists for a longer duration

-Hypoxic-ischemic encephalopathy: the constellation of cognitive sequelae that ensues

-Focal ischemia: usually caused by thrombosis of the cerebral vessels or by an emboli from a proximal arterial source or the heart

-Intracranial hemorrhage: bleeding directly into or around the brain; produces symptoms by:

a.) mass effect of neural structures b.) toxic effect of blood itself c.) increasing intracranial pressure

APPROACH TO THE PATIENT -patients with acute stroke often do not seek

medical assistance on their own because:

1. they are rarely in pain

2. they may lose appreciation that something is wrong (ANOSOGNOSIA)

*sudden onset of any of the following:

-unilateral loss of sensory/motor function

-changes in vision, gait, speech or comprehension

-sudden severe headache

APPROACH TO THE PATIENT -Neurologic symptoms may mimic stroke

SYMPTOM THAT MIMICS STROKE GUIDES TO DIAGNOSIS

-Seizure -history that indicates prior convulsive activity excludes seizure

-Intracranial tumor -present with acute neurologic symptoms due to hemorrhage, seizure or hydrocephalus

-Migraine -sensory disturbance is often prominent, sensory/motor deficits tend to migrate slowly across limbs over minutes rather than seconds as with stroke

-Metabolic encephalopathy -produce fluctuating mental status without focal neurologic finding

APPROACH TO THE PATIENT -Once a clinical diagnosis of stroke is made, a brain

imaging study is necessary to determine if the cause of stroke is ischemia or hemorrhage

-CT IMAGING of the brain is the STANDARD MODALITY to detect the presence or absence of intracranial hemorrhage

-Medical management to reduce the risk of complications becomes the next priority, then plans for secondary prevention

OVERVIEW OF DIFFERENCES

ISCHEMIC STROKE HEMORRHAGIC STROKE

-85% of stroke cases -administration of recombinant tissue plasminogen activator (rTPA) or endovascular mechanical thrombectomy may be beneficial in restoring cerebral perfusion

-15% of stroke cases -BP lowering primarily considered -usually caused by aneurysmal subarachnoid hemorrhage (SAH) and hypertensive intracranial hemorrhage

ISCHEMIC STROKE PATHOPHYSIOLOGY:

MAJOR MECHANISMS THAT UNDERLIE ISCHEMIC STROKE:

1. Occlusion of an intracranial vessel by an embolus that arises at a distant site – often affects large intracranial vessels

2. In situ thrombosis of an intracranial vessel – typically affecting the small penetrating arteries that arise from the major intracranial arteries

3. Hypoperfusion caused by flow-limiting stenosis of a major extracranial or intracranial vessel


1st: acute occlusion of an intracranial vessel causes reduction in blood flow to the brain region it supplies

-magnitude of flow reduction is a function of collateral blood flow and is dependent on:

1. individual vascular anatomy

2. site of occlusion

3. systemic blood pressure


2nd: decrease in cerebral blood flow to zero causes death of brain tissue within 4-10 minutes

-infarction within an hour: <16-18ml/100g tissue per minute

-ischemia without infarction (unless prolonged for hours or days): <20ml/100g tissue per minute


3rd: -if with restored blood flow: patient experiences TRANSIENT ISCHEMIC ATTACK

-if no change in flow: infarction of ischemic penumbra

*hence, saving the ischemic penumbra is the goal of REVASCULARIZATION THERAPIES

ISCHEMIC STROKE PATHWAYS OF FOCAL CEREBRAL INFARCTION:

1. Necrotic pathway

-with rapid cellular cytoskeletal breakdown due principally to energy failure of the cell

2. Apoptotic pathway

-cells are programmed to die

ISCHEMIC STROKE 1. NECROTIC PATHWAY: -Ischemia produces necrosis by starving neurons of

glucose and oxygen -Mitochondria then fails to produce ATP -NO ATP means cessation of membrane ion pump

function causing neuronal depolarization which leads to:

a. increase in intracellular Calcium b. glutamate release from pre-synaptic terminals -produces neurotoxicity *free radicals are produced by membrane lipid

degradation and mitochondrial dysfunction

ISCHEMIC STROKE 2. APOPTOTIC PATHWAY:

-Lesser degrees of ischemia within the ischemic penumbra favor apoptotic cellular death causing cells to die days to weeks later

*fever and hyperglycemia worsens brain injury during ischemia, both must be suppressed as much as possible

ISCHEMIC STROKE TREATMENT OF ACUTE ISCHEMIC STROKE: -After the clinical diagnosis of stroke is made, an orderly process

of evaluation and treatment should follow -FIRST GOAL: PREVENT OR REVERSE BRAIN INJURY -attend to the patient’s airway, breathing and circulation

(ABCs) -treat hypoglycemia or hyperglycemia -perform a non-contrast head CT scan *differentiates ischemic and hemorrhagic stroke since NO

reliable clinical finding conclusively separate the two HEMORRHAGIC ISCHEMIA

-more depressed level of consciousness -higher initial blood pressure -worsening of symptoms after onset

-deficit is maximal at onset, or remits

ISCHEMIC STROKE CATEGORIES OF TREATMENT:

-designed to reverse or lessen the amount of tissue infarction and improve clinical outcome

1. Medical Support

2. IV Thrombolysis

3. Endovascular Techniques

4. Antithrombotic Treatment

5. Neuroprotection

6. Stroke Centers and Rehabilitation

ISCHEMIC STROKE -IMMEDIATE GOAL: optimize cerebral perfusion in the

surrounding ischemic penumbra -attention is also directed toward preventing the common

complications of bedridden patients: -infections -deep venous thrombosis (DVT) -blood pressure is lowered in: -malignant hypertension -concomitant myocardial ischemia -BP >185/110 mmHg and thrombolytic therapy is

anticipated *B1-adrenergic blocker such as ESMOLOL can be a first

step to decrease cardiac work and maintain BP

1. MEDICAL SUPPORT

ISCHEMIC STROKE

-Fever should be treated with antipyretics and surface cooling

-Serum glucose should be monitored and kept at less than 110mg/dl using an insulin infusion if necessary

-Cerebral edema is treated in 5-10% of patients with water restriction and IV mannitol to reduce serum osmolarity watch out for HYPOVOLEMIA as this may contribute to hypotension and worsening infarction

*cerebral edema causes obtundation or brain herniation

*peaks on 2nd or 3rd day but can cause mass effect for 10 days

1. MEDICAL SUPPORT

ISCHEMIC STROKE MEDICAL SUPPORT:

-Hemicraniectomy: craniotomy with temporary removal of part of the skull; markedly reduces mortality

-Things that should alert physician:

-Cerebellar infarction may mimic labyrinthitis because of prominent vertigo and vomiting

-Head or neck pain mimics cerebellar stroke from vertebral artery dissection

-increasing ICP may lead to brainstem compression and cause respiratory arrest

*prophylactic suboccipital decompression of large cerebral infarcts before brainstem compression

1. MEDICAL SUPPORT

ISCHEMIC STROKE

rtPA:

-causes an increased incidence of symptomatic intracerebral hemorrhage

-treatment of IV rtPA within 3 hours of the onset of ischemic stroke improved clinical outcome

*efficacy likely extended to 4.5 hours if not 6 hours

-time of stroke onset: the time the patient’s symptoms began or the time the patient was last seen as normal. Patients who awaken with a stroke have the onset defined as the time they went to bed

2. IV THROMBOLYSIS

ISCHEMIC STROKE

rtPA:

2. IV THROMBOLYSIS

INDICATIONS CONTRAINDICATIONS

-Clinical diagnosis of STROKE -sustained BP > 185/110 mmHg despite Rx

-onset of symptoms to time of drug administration is LESS THAN 3 HOURS

-Platelets LESS THAN 100,000; Hematocrit LESS THAN 25%; Glucose LESS THAN 50 or GREATER THAN 400 mg/dl

-CT scan show no hemorrhage or edema of GREATER THAN 1/3 of the MCA territory

Use of Heparin within 48 HOURS and prolonged PTT or elevated INR ; GI bleeding preceding 21 DAYS

-Age > 18 years old -rapidly improving , minor stroke symptoms

-consent by patient or surrogate -prior stroke or head injury within 3 MONTHS; recent myocardial infarction

-Major surgery in preceding 14 days

-Coma or stupor

ISCHEMIC STROKE

rtPA: -administer through IV access with TWO PERIPHERAL

LINES (avoid arterial or central line placement -0.9 mg/kg IV (maximum 90 mg) IV as 10% of total

dose by bolus, followed by remainder of total dose over 1 hour

-frequent BP monitoring -no other antithrombotic treatment in 24 hours -for decline in neurologic status or uncontrolled BP

STOP INFUSION, give CRYOPRECIPITATE and reimage brain emergently

-avoid urethral catheterization for > 2 HOURS

2. IV THROMBOLYSIS

ISCHEMIC STROKE

-Vessels that involve a large clot volume and often fail to open with IV rtPA alone:

-middle cerebral artery (MCA)

-internal carotid artery

-basilar artery

-Endovascular mechanical thrombectomy:

-adjunctive treatment of acute stroke in patients who are ineligible for, or have contraindications to thrombolytics, or those who have failed to have vascular recanalization with IV thrombolytics

3. ENDOVASCULAR TECHNIQUES

ISCHEMIC STROKE

-MERCI: novel endovascular thrombectomy device restores patency of the occluded vessel within 8 hours of ischemic stroke symptoms; with successful recanalization at 90 days

3. ENDOVASCULAR TECHNIQUES

ISCHEMIC STROKE

PLATELET INHIBITION: -ASPIRIN: the ONLY antiplatelet agent that has been

proven effective for the acute treatment of ischemic stroke

-the use of aspirin within 48 hours of stroke onset reduced both stroke recurrence risk and mortality minimally

-ABCIXIMAB: a glycoprotein IIb/IIIa receptor inhibitor was found to cause excess intracranial hemorrhage and should be avoided in acute stroke

-CLOPIDOGREL: still being tested to prevent stroke following TIA and minor ischemic stroke

4. ANTITHROMBOTIC TREATMENT

ISCHEMIC STROKE

ANTICOAGULATION:

-low molecular weight Heparin: failed to show any benefit over aspirin, and increased bleeding rates

4. ANTITHROMBOTIC TREATMENT

ISCHEMIC STROKE

-the concept of providing a treatment that prolongs the brain’s tolerance to ischemia

-includes:

a. use of drugs that block excitatory amino acid pathways – protects neurons and glia in animals

b. hypothermia – neuroprotective in patients with cardiac arrest

5. NEUROPROTECTION

ISCHEMIC STROKE

-patient care in comprehensive stroke units followed by rehabilitation services improves neurologic outcomes and reduces mortality

-proper rehabilitation of the stroke patient includes early physical, occupational and speech therapy

-GOAL OF REHABILITATION: return the patient home and to maximize recovery by providing a safe, progressive regimen suited to the individual patient

6. STROKE CENTERS AND REHABILITATION

ISCHEMIC STROKE

-RESTRAINT THERAPY: immobilizing the unaffected side has shown to improve hemiparesis following stroke

6. STROKE CENTERS AND REHABILITATION

ISCHEMIC STROKE

ETIOLOGY:

-Although the initial management of acute ischemic stroke often does not depend on the etiology, establishing a cause is essential in reducing the risk of recurrence

-Focus on: a.) atrial fibrillation and b.) carotid atherosclerosis

ISCHEMIC STROKE

CLINICAL EXAMINATION:

FOCUS FINDINGS

-Peripheral and cervical vascular system

-carotid auscultation for bruits, BP, pressure comparison between arms

-Heart -dysrhythmias, murmurs

-Extremities -peripheral emboli

-Retina -effects of hypertension and cholesterol emboli (Hollenhorst plaques)

ISCHEMIC STROKE: Cardioembolic Stroke

EXAM/LABORATORIES/IMAGING: -a complete neurologic examination is performed to localized

the site of stroke -an imaging study of the brain is required for patients being

considered for thrombolysis -an ECG may demonstrate arrhythmias or reveal MI -Other tests include: -CXR -ESR -urinalysis -serum electrolytes -CBC -Creatinine/BUN -blood sugar -PT/PTT -serum lipid profile -serologic test for syphilis


-responsible for 20% of all ischemic strokes -stroke caused by heart disease is PRIMARILY DUE TO

EMBOLISM of thrombotic material forming on the atrial or ventricular wall of the left heart valves

-TIA: if the thrombus fragment or lyse quickly -Characteristics: -sudden onset -maximum neurologic deficit at once -petechial hemorrhage can occur within the ischemic

territory -Emboli from the HEART most often LODGE IN THE MCA,

posterior cerebral artery or one of their branches, infrequently, the anterior cerebral artery is involved


-Most significant causes: 1. non-rheumatic (non-valvular) atrial fibrillation -MOST COMMON cause of cerebral embolism -stroke risk can be calculated using CHADS2

score CHADS2 score:

CHADS2 SCORE

RECOMMENDATION

0 Aspirin or no antithrombotic

1 Aspirin or VKA

Greater than (>) 1

VKA

POINTS CONDITION

1 > 75 years old

1 Hypertension

1 Congestive heart failure

1 Diabetes

2 Stroke or TIA


-Most significant causes:

2. Myocardial Infarction

-especially when transmural and involves anteroapical ventricular wall

-risk is reduced by anticoagulation

3. prosthetic valves

4. rheumatic heart disease

-increased incidence with prominent mitral stenosis or atrial fibrillation

5. ischemic cardiomyopathy


-paradoxical embolization occurs when venous thrombi migrate to arterial circulation, usually via a PATENT FORAMEN OVALE or ATRIAL SEPTAL DEFECT; detected through bubble-contrast ECG

-Bacterial endocarditis can cause valvular vegatations that can give rise to septic emboli

*Mycotic aneurysms caused by septic emboli give rise to SAH or intracerebral hemorrhage

ISCHEMIC STROKE: Artery-Artery Embolic Stroke

-thrombus formation on atherosclerotic plaques may embolize to intracranial arteries producing an artery-to-artery embolic stroke

-Unlike the myocardial vessels, artery-to-artery embolism, RATHER THAN local thrombosis, is the DOMINANT VASCULAR MECHANISM causing brain ischemia.

-embolic sources are diseased vessels in the: -aortic arch -common carotid arteries -internal carotid arteries -basilar arteries -vertebral arteries -carotid bifurcation – MOST COMMON SOURCE


-Carotid Atherosclerosis:

-atheroscerois within the carotid artery occurs most frequently with the common carotid bifurcation and proximal internal carotid artery

-Risk factors:

-male -smoking

-older age -hypertension

-diabetes -hypercholesterolemia

-produces 10% of ischemic stroke


-Carotid Atherosclerosis:

-Classification is based on:

1. whether stenosis is symptomatic or asymptomatic

-symptomatic – patient has experienced a stroke within the vascular distribution of the artery

- associated with greater risk of subsequent stroke

2. degree of stenosis

ISCHEMIC STROKE: Artery-to-Artery Embolic Stroke

-Other causes of Artery-to-Artery embolic stroke:

1. Intracranial atherosclerosis

-produces stroke through an embolic mechanism or by in situ thrombosis

-common in Asian and African-Americans

ISCHEMIC STROKE: Artery-to-Artery Embolic Stroke

-Other causes of Artery-to-Artery embolic stroke: 2. Dissection -common source in the young: internal carotid, vertebral

arteries or vessels beyond the circle of Willis -characteristic: painful, precedes stroke by hours or days -causes: -connective tissue disorders (such as Ehlers-

Danlos type IV, Marfan’s disease, cystic medial necrosis and fibromuscular dysplasia), trauma (usually on carotid and vertebral arteries)

-most dissections heal spontaneously, and stroke or TIA beyond 2 weeks are uncommon

-treatment: anticoagulants antiplatelets

EXTRACRANIAL dissection INTRACRANIAL dissection

-do not cause hemorrhage because of tough adventitia of vessels

-may produce SAH because vessels are thin and may form pseudoaneurysms

ISCHEMIC STROKE: Small-Vessel Stroke

-lacunar infarction: infarction following atherothrombotic or lipohyalinotic occlusion a small artery (30-300 micrometer) in the brain

-account for 20% of all strokes PATHOPHYSIOLOGY: -arteries that give rise to 30-300 micrometer branches that

penetrate the cerebrum or brainstem: -MCA -circle of Willis -anterior and posterior communicating -basilar vertebral


PATHOPHYSIOLOGY:

-small branches can occlude either by:

1. atherothrombotic disease at its origin

-thrombosis cause small infarcts called lacunes

-infarct size: 3mm to 2cm

2. development of lipohyalinotic thickening

-Principal risk factors:

-age

-hypertension


CLINICAL MANIFESTATIONS: -Lacunar Syndromes: 1. Pure motor hemiparesis -infarct location: posterior limb of the internal

capsule or basis pontis -involves mostly the arms, face, legs 2. Pure sensory stroke -infarct location: ventral thalamus 3. Ataxic hemiparesis -infarct location: ventral pons or internal capsule 4. Dysarthria and clumsy hand -infarct location: ventral pons or genu of internal

capsule


CLINICAL MANIFESTATIONS:

-transient symptoms may occur several times a day and last only a few minutes

-a large-vessel source may manifest initially as a lacunar syndrome

SECONDARY PREVENTION:

-risk factor modification especially BP reduction

STROKE: LESS COMMON CAUSES

1. Hypercoagulable disorders 2. Venous sinus thrombosis 3. Sickle cell anemia 4. Fibromuscular dysplasia 5. Temporal giant cell arteritis 6. Necrotizing (granulomatous) arteritis 7. Primary Central Nervous System Vasculitis 8. Drugs: amphetamines, cocaine 9. Moyamoya Disease 10. Reversible posterior leukoencephalopathy 11. Leukoaraiosis / periventricular white matter disease 12. CADASIL (cerebral autosomal dominant arteriopathy with

subcortical infarcts and leukoencephalopathy)

LESS COMMON CAUSES OF STROKE: Hypercoagulable disorders

-primarily cause INCREASED RISK of VENOUS THROMBOSIS and therefore may cause VENOUS SINUS THROMBOSIS

-Protein S deficiency & Homocysteinemia: may cause arterial thromboses

-SLE with Libmann-Sacks endocarditis: can cause embolic stroke

-requires long term anticoagulation to prevent further stroke

LESS COMMON CAUSES OF STROKE: Venous sinus thrombosis

-affected location: lateral or sagittal sinus or small cortical vessels

-occurs as a complication of:

-oral contraceptive use

-pregnancy and the post-partum period

-inflammatory bowel disease

-intracranial infections (meningitis)

-dehydration

-thrombophilia

LESS COMMON CAUSES OF STROKE: Venous sinus thrombosis

-manifestations: -headache -focal neurologic symptoms -paraparesis and seizures -CT is normal unless presence of hemorrhage -signs of increased ICP/coma in greater degrees -Venous thrombosis is readily visualized by MR or CT

venography -treatment: IV heparin regardless of intracranial hemorrhage -Vitamin K antagonists – if without hypercoagulability *anticoagulation is continued indefinitely if

thrombophilia is diagnosed

LESS COMMON CAUSES OF STROKE: Sickle cell anemia (SS Disease)

-common cause of stroke in children

-predicted by high velocity of blood flow within MCAs using transcranial Doppler ultrasonography

-Treatment: aggressive exchange transfusion

LESS COMMON CAUSES OF STROKE: Fibromuscular dysplasia

-affects the cervical arteries

*carotid/vertebral arteries show multiple rings of segmental narrowing alternating with dilatation

-OCCLUSION is usually INCOMPLETE

-more common in women

-often asymptomatic but may be associated with audible bruit, TIA or stroke

-may involve renal arteries and cause hypertension

-Treatment: anticoagulation or antiplatelet

LESS COMMON CAUSES OF STROKE: Temporal giant cell arteritis

-common in elderly with the temporal arteries undergoing subacute granulomatous inflammation with giant cells

-blindness: due to occlusion of posterior ciliary arteries; prevented with GLUCOCORTiCOIDS

-rarely causes stroke because the internal carotid artery is not inflamed

-Takayasu’s arteritis: idiopathic giant cell arteritis involving great vessels arising from the aortic arch; may cause carotid or vertebral thrombosis

LESS COMMON CAUSES OF STROKE: Necrotizing (granulomatous) arteritis

-occurs alone or in association with generalized polyarteritis nodosa or granulomatosis with polyangiitis (Wgener’s)

-involves the distal small branches (<2mm diameter) of the main intracranial arteries

-produces small ischemic effects on the brain, optic nerve and spinal cord

-CSF: pleocytosis, increased protein level

LESS COMMON CAUSES OF STROKE: Primary Central Nervous System Vasculitis

-rare

-affects small or medium-sized vessels

-without apparent systemic vasculitis

-can follow the post-partum period and are self-limited

-differential diagnosis includes inflammatory and non-inflammatory causes

LESS COMMON CAUSES OF STROKE: Drugs – amphetamines, cocaine

-cause stroke by acute hypertension or drug induced vasculopathy

-Phenylpropanolamine, cocaine, methamphetamine: linked with intracranial hemorrhage

LESS COMMON CAUSES OF STROKE: Moyamoya Disease

-occlusive disease involving large intracranial arteries especially:

-distal internal carotid

-stem of MCA and ACA

-lenticulostriate arteries develop rich collateral circulation around the occlusive lesion, which gives the “puff of smoke” impression

-common in Asian chilren or young adults but appears the same in adults with atherosclerosis associated with diabetes

-Treatment: anticoagulation is risky

-surgical bypass of extracranial carotid arteries to the dura or MCAs may prevent stroke and hemorrhage

LESS COMMON CAUSES OF STROKE: Reversible posterior leukoencephalopathy -can occur in head injury, seizure, migraine,

sympathomimetic drug use, eclampsia and postpartum period

-may involve widespread cerebral segmental vasoconstriction and edema

-manifestation: headache, fluctuating neurologic symptoms especially visual

-ischemia reverses completely

LESS COMMON CAUSES OF STROKE: Leukoaraiosis / periventricular white matter disease

-result of multiple small-vessel infarcts within the subcortical white matter

-CT/MRI: areas of white matter injury surrounding the ventricles within the corona radiata; lacunar infarction are also seen

-caused by chronic hypertension leading to lipohyalanosis of small penetrating arteries within the white matter

-may lead to SUBCORTICAL DEMENTIA SYNDROME – which may be prevented/delayed with antihypertensive medications

LESS COMMON CAUSES OF STROKE:

CADASIL (cerebral autosomal dominant arteriopathy

with subcortical infarcts and leukoencephalopathy)

-an inherited disorder that presents as:

-small-vessel stroke

-progressive dementia

-extensive white matter changes seen in MRI

-manifestation: migraine with aura, transient motor or sensory deficits

-onset is usually on the 4th or 5th decade of life

-caused by mutation in Notch-3

LESS COMMON CAUSES OF STROKE: Other monogenic ischemic stroke syndrome

- CARASIL (cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy)

- Hereditary endotheliopathy, retinopathy, nephropathy, and stroke (HERNS)

- Fabry’s disease

TRANSIENT ISCHEMIC ATTACK

-episodes of stroke symptoms that last only briefly

-standard definition of duration is <24 hours, but most TIAs last <1 hour

-has similar causes as ischemic stroke; may herald stroke

-may arise from an emboli to the brain or an in situ thrombosis

-newer definitions of TIA categorize those with new infarct as having ischemic stroke rather than TIA regardless of symptom duration

TRANSIENT ISCHEMIC ATTACK -Amaurosis fugax: transient monocular blindness, occurs from

emboli to the central retinal artery of one eye -indicates carotid stenosis or local opthalmic artery disease -risk of stroke after TIA is 10-15% in the first 3 months with most

events occuring in the first 2 days -risk is estimated using ABCD2 method -improvement characteristic of TIA is contraindication to

thrombolysis

CLINICAL FACTOR SCORE

A: AGE: greater than/equal to 60 years 1

B: BLOOD PRESSURE: SBP >140 mmhg or DBP >90 mmHg 1

C: CLINICAL SYMPTOMS

-Unilateral weakness 2

-Speech disturbance without weakness 1

D1: DURATION

- greater than 60 minutes 2

-10 to 59 minutes 1

D2: DIABETES (oral medications or insulin) 1

TREATMENT: Primary and Secondary Prevention of Stroke and TIA

GENERAL PRINCIPLES:

-identification and control of modifiable risk factors is the best strategy to reduce the burden of stroke


ATHEROSCLEROSIS RISK FACTORS: 1. Older age 2. Family history of thrombotic stroke 3. Hypertension -most significant risk factor -Rx: use of thiazide diuretics, ACE-inhibitors 4. Tobacco smoking – discouraged 5. Abnormal blood cholesterol (high LDL, low HDL) -Rx: statin drugs 6. Prior stroke or TIA – greater risk 7. Cardiac conditions – atrial fibrillation, MI 8. Oral contraceptives and hormone replacement therapy 9. Hypercoagulable states 10. Diabetes -Rx: pioglitazone – agonist of peroxisome proliferator-activated

receptor gamma


ANTIPLATELET AGENTS: -inhibits the formation of intraarterial platelet aggregates -most commonly used: 1. Aspirin – acetylates platelate cyclooxygenase, which

irreversibly inhibits the formation in platelets of thromboxane A2, a platelet aggregating and vasoconstricting prostaglandin

-paradoxically inhibits formation of prostacyclin, an antiaggregating and vasodilating prostaglandin

-50-325 mg/day of aspirin for stroke prevention 2. Clopidogrel – block ADP receptor on platelets and thus prevent

the cascade resulting in activation of glycoprotein IIB/IIIa that leads to fibrinogen binding to the platelet and consequent platelet activation

-rarely causes TTP, but does not cause neutropenia


ANTIPLATELET AGENTS: 3. Dipyridamole (extended-release) – an antiplatelet agent that

inhibits the uptake of adenosine by a variety of cells, including those of the vascular endothelium accumulated adenosine is an inhibitor of aggregation

-potentiates effects of prostacyclin and nitrous oxide 4. Ticlopidine – rarely used, alternative to Clopidogrel -same action as Clopidogrel -more effective than aspirin but causes more side

effects such as diarrhea, neutropenia, thrombotic thrombocytopenic purpura (TTP)


ANTICOAGULATION THERAPY AND EMBOLIC STROKE: -anticoagulation is safe for patients with chronic nonrheumatic

atrial fibrillation and prevent cerebral embolism -the decision to use anticoagulation for primary prevention is

based primarily on risk factors *history of TIA or stroke favors anticoagulation -anticoagulation also reduces the risk of embolism in acute MI -3-month course of anticoagulation when there is: -Q wave infarction -substantial left ventricular dysfunction -congestive heart failure -mural thrombosis -atrial fibrillation (VKA if atrial fibrillation persists)


ANTICOAGULATION THERAPY AND NONCARDIOGENIC STROKE:

-warfarin has no benefit over aspirin

-no support for long-term use of VKAs for preventing atherothrombotic stroke for either intracranial or extracranial cerebrovascular disease

TREATMENT: Carotid Atherosclerosis

-can be removed surgically (endarterectomy) or mitigated with endovascular stenting with or without balloon angioplasty

-Surgical:

- Endarterectomy is most beneficial when performed within 2 weeks of symtpom onset, benefit is more pronounced in patients >75 years old, and benefit men more than women

-Endovascular Therapy:

-endovascular stenting with balloon angioplasty used to open stenotic carotid arteries

STROKE SYNDROMES

DIVISION OF STROKE SYNDROMES: 1. LARGE-vessel stroke within the ANTERIOR circulation

2. LARGE-vessel stroke within the POSTERIOR circulation

3. SMALL-vessel of either vascular bed

STROKE SYNDROMES CEREBRAL HEMISPHERE, LATERAL ASPECT:

STRUCTURES INVOLVED SIGNS AND SYMPTOMS

-Somatic motor area for face and arm -Fibers descending from the leg area to enter the corona radiata and corresponding somatic sensory sytem

-paralysis of the contralateral face, arm and leg -sensory impairment over the same are (pinprick, cotton touch, vibration, position, 2-point discrimination, stereognosis, tactile localization, barognosis, cutaneographia)

-Motor speech area of the DOMINANT hemisphere

-Motor aphasia

-Central, suprasylvian speech area -Parietooccipital cortex of the dominant hemisphere

-Central aphasia -word deafness -sensory agraphia -anomia -jargon speech GERSTMANN SYNDROME: -acalculia -alexia -finger agnosia -right-left confusion

-Central speech area -Conduction aphasia

STROKE SYNDROMES CEREBRAL HEMISPHERE, LATERAL ASPECT:


-non-dominant parietal lobe (corresponds to speech area in dominant hemisphere)

-Apractagnosia of the dominant hemisphere -inaccurate localization on the half field -distortion of visual coordinates -agnosia for the left half of external space -visual illusions -upside-down reading -anosognosia -unilateral neglect -hemiasomatognosia -dressing apraxia -constructional apraxia -inability to judge distance

-Optic radiation deep to second temporal convolution

-homonymous hemianopia -homonymous inferior quadrantonopia

-Frontal contraversive eye field -Projecting fibers

-paralysis of the conjugate gaze to the opposite side

STROKE SYNDROMES CEREBRAL HEMISPHERE, MEDIAL ASPECT:


-Motor leg area -Paralysis of the opposite foot and leg

-Arm area of cortex -fibers descending to corona radiata

-A lesser degree of paresis of opposite arm

-Sensory area for foot and leg

-Cortical sensory loss over toes, foot, and leg

-Sensorimotor area in paracentral lobule

-Urinary incontinence

-Medial surface of the posterior frontal lobe; likely supplemental motor area

-Contralateral grasp reflex -sucking reflex - gegenhalten (paratonic rigidity)

STROKE SYNDROMES CEREBRAL HEMISPHERE, MEDIAL ASPECT:


-Uncertain localization—probably cingulate gyrus and medial inferior portion of frontal, parietal, and temporal lobes

-Abulia (akinetic mutism) -reflex distraction to sights and sounds -intermittent interruption -slowness -lack of spontaneity -delay -whispering

-Frontal cortex near leg motor area

-Impairment of gait and stance (gait apraxia)

-Corpus callosum -Dyspraxia of left limbs -tactile aphasia in left limbs

STROKE SYNDROMES LEVEL OF MEDULLA:

SYNDROME VESSEL(S) OCCLUDED

SIDE OF LESION

INNER STRUCTURES INVOLVED

SIGNS AND SYMPTOMS

-Medial medullary syndrome

-vertebral artery -branch of vertebral or lower basilar artery

-same -Ipsilateral twelfth nerve

-Paralysis with atrophy of one-half half the tongue

-opposite -Contralateral pyramidal tract and medial lemniscus

-Paralysis of arm and leg, sparing face -impaired tactile and proprioceptive sense over one-half the body

-Lateral medullary syndrome

-vertebral artery -posterior inferior cerebellar artery -superior, middle, or inferior lateral medullary arteries

-same -Descending tract -nucleus fifth nerve

-Pain, numbness, impaired sensation over one-half the face



SIDE OF LESION


SIGNS AND SYMPTOMS



-same -Uncertain—restiform body, cerebellar hemisphere, cerebellar fibers, spinocerebellar tract

-Ataxia of limbs, falling to side of lesion

-same -Vestibular nucleus -Nystagmus -diplopia -oscillopsia -vertigo -nausea -vomiting

-same -Nucleus and tractus solitarius

-Loss of taste



SIDE OF LESION


SIGNS AND SYMPTOMS



-same -Descending sympathetic tract

Horner's syndrome: -Miosis -Ptosis -Decreased sweating

-same -Issuing fibers ninth and tenth nerves

-Dysphagia -hoarseness -paralysis of palate -paralysis of vocal cord -diminished gag reflex

-same -Cuneate -gracile nuclei

-Numbness of ipsilateral arm, trunk, or leg



SIDE OF LESION


SIGNS AND SYMPTOMS



-same -Genuflected upper motor neuron fibers to ipsilateral facial nucleus

-Weakness of lower face

-opposite -Spinothalamic tract

-Impaired pain and thermal sense over half the body, sometimes face

-Total unilateral medullary syndrome

-vertebral artery -Combination of medial and lateral syndromes



SIDE OF LESION


SIGNS AND SYMPTOMS

-Lateral pontomedullary syndrome

-vertebral artery -Combination of lateral medullary and lateral inferior pontine syndrome

-Basilar artery syndrome

-basilar artery -arteries arising in the posterior cerebral artery distribution

-Bilateral long tract -cerebellar and peripheral cranial nerves

-Bilateral long tract signs (sensory and motor; cerebellar and peripheral cranial nerve abnormalities)

-Corticobulbar and corticospinal tracts bilaterally

-Paralysis or weakness of all extremities, plus all bulbar musculature

STROKE SYNDROMES LEVEL OF THE INFERIOR PONS:


SIDE OF LESION


SIGNS AND SYMPTOMS

-Medial inferior pontine syndrome

-paramedian branch of basilar artery

-same -Center for conjugate lateral gaze

-Paralysis of conjugate gaze to side of lesion (preservation of convergence)

-Vestibular nucleus -Nystagmus

-Likely middle cerebellar peduncle

-Ataxia of limbs and gait

-Abducens nerve -Diplopia on lateral gaze

-opposite -Corticobulbar and corticospinal tract in lower pons

-Paralysis of face, arm, and leg



SIDE OF LESION


SIGNS AND SYMPTOMS

-Medial inferior pontine syndrome

-paramedian branch of basilar artery

-opposite -Medial lemniscus -Impaired tactile and proprioceptive sense over one-half of the body

-Lateral inferior pontine syndrome

-anterior inferior cerebellar artery

-same -Vestibular nerve or nucleus

-Horizontal and vertical nystagmus -vertigo -nausea -vomiting -oscillopsia

-Seventh nerve -Facial paralysis

-Center for conjugate lateral gaze

-Paralysis of conjugate gaze to side of lesion



SIDE OF LESION


SIGNS AND SYMPTOMS

-Lateral inferior pontine syndrome

-anterior inferior cerebellar artery

-same -Auditory nerve or cochlear nucleus

-Deafness -tinnitus

-Middle cerebellar peduncle and cerebellar hemisphere

-Ataxia

-Descending tract and nucleus fifth nerve

-Impaired sensation over face


-Impaired pain and thermal sense over one-half the body (may include face)

STROKE SYNDROMES LEVEL OF THE MIDPONS:


SIDE OF LESION


SIGNS AND SYMPTOMS

-Medial midpontine syndrome

-paramedian branch of midbasilar artery

-same -Pontine nuclei -Ataxia of limbs and gait (more prominent in bilateral involvement)

-opposite -Corticobulbar and corticospinal tract


-Medial lemniscus -Variable impaired touch and proprioception when lesion extends posteriorly

-Lateral midpontine syndrome

-short circumferential artery

-same -Middle cerebellar peduncle

-Ataxia of limbs

Motor fibers or nucleus of fifth nerve

-Paralysis of muscles of mastication

STROKE SYNDROMES LEVEL OF THE MIDPONS:


SIDE OF LESION


SIGNS AND SYMPTOMS

-Lateral midpontine syndrome

-short circumferential artery

-same -Sensory fibers or nucleus of fifth nerve

-Impaired sensation over side of face


-Impaired pain and thermal sense on limbs and trunk

STROKE SYNDROMES LEVEL OF THE SUPERIOR PONS:


SIDE OF LESION


SIGNS AND SYMPTOMS

-Medial superior pontine syndrome

-paramedian branches of upper basilar artery

-same -Superior and/or middle cerebellar peduncle

-Cerebellar ataxia (probably)

-Medial longitudinal fasciculus

-Internuclear ophthalmoplegia

-Localization uncertain—central tegmental bundle, dentate projection, inferior olivary nucleus

-Myoclonic syndrome, palate, pharynx, vocal cords, respiratory apparatus, face, oculomotor apparatus, etc



SIDE OF LESION


SIGNS AND SYMPTOMS

-Medial superior pontine syndrome

-paramedian branches of upper basilar artery

-opposite -Corticobulbar and corticospinal tract


-Medial lemniscus -Rarely touch, vibration, and position are affected

-Lateral superior pontine syndrome

-superior cerebellar artery

-same -Middle and superior cerebellar peduncles, superior surface of cerebellum, dentate nucleus

-Ataxia of limbs and gait, falling to side of lesion

-Vestibular nucleus -Dizziness -nausea, vomiting -horizontal nystagmus



SIDE OF LESION


SIGNS AND SYMPTOMS



-same -Pontine contralateral gaze

-Paresis of conjugate gaze (ipsilateral)

-Uncertain -Skew deviation

-Descending sympathetic fibers

Horner's syndrome: -Miosis -Ptosis -Decreased sweating over face

-Dentate nucleus -superior cerebellar peduncle

-Tremor



SIDE OF LESION


SIGNS AND SYMPTOMS




-Impaired pain and thermal sense on face, limbs, and trunk

-Medial lemniscus (lateral portion)

-Impaired touch, vibration, and position sense, more in leg than arm (there is a tendency to incongruity of pain and touch deficits)

STROKE SYNDROMES LEVEL OF THE MIDBRAIN:


SIDE OF LESION


SIGNS AND SYMPTOMS

-Medial midbrain syndrome

-paramedian branches of upper basilar arteries -proximal posterior cerebral arteries

-same -Third nerve fibers -Eye "down and out" secondary to unopposed action of fourth and sixth cranial nerves -with dilated and unresponsive pupil

-opposite -Corticobulbar and corticospinal tract descending in crus cerebri


STROKE SYNDROMES LEVEL OF THE MIDBRAIN:


SIDE OF LESION


SIGNS AND SYMPTOMS

-Lateral midbrain syndrome

-small penetrating arteries arising from posterior cerebral artery

-same -Third nerve fibers -third nerve nucleus

-Eye "down and out" secondary to unopposed action of fourth and sixth cranial nerves -with dilated and unresponsive pupil

-opposite -Red nucleus -dentatorubro-thalamic pathway

-Hemiataxia, hyperkinesias, tremor

STROKE WITHIN THE ANTERIOR CIRCULATION

-The internal carotid artery and its branches comprise the ANTERIOR CIRCULATION of the BRAIN

-causes of occlusion:

-intrinsic disease of the vessel

-emboli from proximal source

-occlusion of each major intracranial vessel has distinct clinical manifestations


OCCLUSION of the MIDDLE CEREBRAL ARTERY: -occlusion of the proximal MCA or one of its major branches

is MOST OFTEN due to an embolus RATHER THAN intracranial atherothrombosis

-collateral formation via leptomeningeal vessels prevents MCA stenosis from becoming symptomatic

-cortical branches of the MCA supply the lateral surface of the hemisphere except for:

1. the frontal pole and a strip along the superomedial border of the frontal and parietal lobes supplied by the ACA

2. the lower temporal and occipital pole convolutions supplied by the PCA


OCCLUSION of the MIDDLE CEREBRAL ARTERY: -proximal MCA (M1 segment) gives rise to lenticulostriate

arteries (penetrating branches) that supply the following: -putamen -outer globus pallidus -posterior limb of the internal capsule -adjacent corona radiata -most of the caudate nucleus -MCA divides into superior and inferior divisions (M2

branches) in the sylvian fissure: -inferior – supply inferior parietal & temporal complex -superior – supply frontal & superior parietal complex


OCCLUSION of the MIDDLE CEREBRAL ARTERY: -occlusion of the entire MCA at its origin, with limited distal

collaterals lead to the following clinical findings: -contralateral hemiplegia -hemianesthesia -homonymous hemianopia -1-2 day gaze preference to the ipsilateral side -dysarthria (due to facial weakness)

DOMINANT HEMISPHERE INVOLVEMENT

NONDOMINANT HEMISPHERE INVOLVEMENT

-Global aphasia -anosognosia -constructional apraxia -neglect


OCCLUSION of the MIDDLE CEREBRAL ARTERY:

COMPLETE SYNDROME PARTIAL SYNDROME

-most often occlusion of MCA stem -presence of cortical collateral blood flow -emboli that causes incomplete occlusion -occlusion of distal MCA branches or fragment and move distally



LOCATION OF OCCLUSION SYMPTOMS

-single branch -hand or hand and arm weakness (brachial syndrome) -facial weakness with Broca’s aphasia with or without arm weakness (opercular syndrome)

-proximal superior division and infarcted frontal and parietal cortices

-sensory disturbance -motor weakness -Broca’s aphasia

-inferior division supplying posterior part (temporal cortex) of the dominant hemisphere

-Wernicke’s aphasia without weakness -Jargon speech and inability to comprehend written and spoken language -contralateral homonymous superior quadrantanopia

inferior division of the nondominant hemisphere

-hemineglect -spatial agnosia without weakness




-lenticulostriate vessel (stroke within the internal capsule)

-pure motor stroke or sensory-motor stroke contralateral to the lesion

-ischemia in the genu of the internal capsule (moving posteriorly)

-1st: facial weakness arm weakness leg weakness -contralateral hand: ataxia, dysarthria

-lacunar infarction in globus pallidus and putamen

-few clinical symptoms -parkinsonism -hemiballismus


OCCLUSION of the ANTERIOR CEREBRAL ARTERY: -ACA is divided into 2 segments: 1. precommunal (A1) circle of Willis or stem – -connects the internal carotid to the anterior

communicating artery -gives rise to deep penetrating branches that supply the: -anterior limb of the internal capsule -amygdala -anterior perforate substance -anterior hypothalamus -inferior part of the head of the caudate nucleus 2. postcommunal (A2) – -distal to the anterior communicating artery


OCCLUSION of the ANTERIOR CEREBRAL ARTERY: -occlusion of the ACA is usually well tolerated due to

collateral flow through the anterior communicating and through the MCA and PCA


-single A2 segment -contralateral symptoms

-A2 segments from a single anterior cerebral stem (contralateral A1 segment atresia)

-may affect both hemispheres and thus result to: -profound abulia –delay verbal and motor response -bilateral pyramidal signs with paraparesis and quadriparesis -urinary incontinence


OCCLUSION of the ANTERIOR CHOROIDAL ARTERY: -anterior choroidal artery arises from the internal carotid

artery and supplies the posterior limb of the internal capsule and the white matter posterolateral to it, through which GENICOLOCALCARINE fibers pass

-collateral: penetrating vessels of the proximal MCA, posterior communicating artery, posterior choroidal arteries

*presence of collateral cause minimal deficits -anterior choroidal strokes are often caused by IN SITU

thrombosis, and iatrogenic occlusion during surgical clipping of aneurysms arising from the internal carotid artery


OCCLUSION of the ANTERIOR CHOROIDAL ARTERY:


-anterior choroidal artery -COMPLETE syndrome consists: -contralateral hemiplegia -hemianesthesia (hypesthesia) -homonymous hemianopia


OCCLUSION of the INTERNAL CAROTID ARTERY: -clinical picture depends on cause of ischemia: -thrombus -embolism -low flow -the cortex supplied by the MCA territory is affected

MOST OFTEN -may go unnoticed with a COMPETENT circle of Willis -in stenotic lesions, a high-pitched carotid bruit fading

into DIASTOLE is heard becomes fainter and disappears when occlusion is imminent


OCCLUSION of the INTERNAL CAROTID ARTERY:


-propagation into the MCA -symptoms of proximal MCA -may have massive infarction of deep white matter and cortical surface

-origins of ACA and MCA at the top of carotid artery

-abulia -stupor with hemiplegia -hemianesthesia -aphasia -anosognosia

-fetal posterior cerebral artery (PCA arises from the internal carotid artery)

-symptoms referable to its peripheral territory

-opthalmic artery -recurrent transient monocular blindness (amaurosis fugax)


OCCLUSION of the COMMON CAROTID ARTERY:

-Signs and symptoms the same with internal carotid occlusion

-Jaw claudication: low flow in external carotid branches

-Bilateral common carotid artery occlusion: Takayasu’s arteritis

STROKE WITHIN THE POSTERIOR CIRCULATION

-the POSTERIOR CIRCULATION is composed of: -paired vertebral arteries join to form -basilar artery divides -paired posterior cerebral arteries *these arteries give rise to circumferential and deep

penetrating branches that supply the: -cerebellum -brainstem -diencephalon -hippocampus -medial temporal and occipital lobes *occlusion of each vessel produces its own distinctive

symptom


OCCLUSION of the POSTERIOR CEREBRAL ARTERY:

-origin of the PCA:

75% - from bifurcation of the basilar artery

20% - one from the ipsilateral internal carotid artery via the posterior communicating artery

5% - both from the respective ipsilateral internal carotid arteries


OCCLUSION of the POSTERIOR CEREBRAL ARTERY: -PCA syndromes: -usually result from atheroma formation or emboli that lodge at

the top of the basilar artery -may also be due to vertebral artery dissection or fibromuscular

dysplasia -2 clinical syndromes are COMMONLY observed with PCA occlusion: 1. P1 syndrome -midbrain, subthalamic, thalamic signs -due to disease of the proximal P1 segment or its penetrating

branches 2. P2 syndrome -cortical temporal and occipital lobe signs -due to occlusion of the P2 segment distal to the junction of

the PCA with the posterior communicating artery



P1 SYNDROMES


-Ipsilateral subthalamus and medial thalamus -Ipsilateral cerebral peduncle and midbrain

-CLAUDE’S SYNDROME: third nerve palsy with contralateral ataxia -WEBER’S SYNDROME: third nerve palsy with contralateral hemiplegia

-red nucleus -dentatorubrothalamic tract

-ataxia

-cerebral peduncle -hemiplegia

-subthalamic nucleus -hemiballismus

-artery of Percheron -paresis of upward gaze -drowsiness -abulia

-extensive infarction in the midbrain and subthalamus with bilateral PCA occlusion

-coma -bilateral pyramidal signs -unreactive pupils -decerebrate rigidity


OCCLUSION of the POSTERIOR CEREBRAL ARTERY: P1 SYNDROMES Thalamic Dejerine-Roussy syndrome: -consists of: -contralateral hemisensory loss -agonizing, searing, burning pain in the affected area -persistent and responds poorly to analgesics -anticonvulsants (carbamazepine or gabapentin) or tricyclic

antidepressants show benefits


-penetrating branches o f thalamic and thalamogeniculate arteries

-less extensive thalamic and thalamocapsular lacunar syndromes



P2 SYNDROMES

LOCATION OF OCCLUSION/INFARCTION SYMPTOMS

-distal PCA (infarction of medial temporal and occipital lobes)

-contralateral homonymous hemianopia WITH macula sparing *occasionally, only the upper quadrant of visual field is involved

-calcarine cortex -patient is aware of visual defects

dominant hemisphere: -medial temporal lobe -hippocampus

-acute disturbance in memory but clears

dominant hemisphere: -splenium of the corpus callosum

-alexia WITHOUT agraphia *amnestic aphasia may occur even without callosal involvement

-PCA -peduncular hallucinosis: visual hallucinations of brightly colored scenes and objects



P2 SYNDROMES


-bilateral infarction in the distal PCA -cortical blindness (blindness with preserved PLR) -ANTON’S SYNDROME: unaware/deny blindness

-infarction secondary to low flow in the “watershed” between distal PCA and MCA territories *as occurs after cardiac arrest

-BALINT’S SYNDROME: disorder of orderly visual scanning of the environment -palinopsia: persistence of visual image for several minutes -asimultanagnosia: inability to synthesize whole image

-top of the basilar artery -central or peripheral territory symptoms -HALLMARK: sudden onset of bilateral signs – -ptosis -pupillary asymmetry -somnolence -lack of reaction to light


OCCLUSION of the VERTEBRAL and POSTERIOR CEREBELLAR ARTERIES:

-The vertebral artery arises from the INNOMINATE artery on the RIGHT and the SUBCLAVIAN artery on the LEFT

SEGMENT COURSE

V1 -from origin to entrance of 5th/6th transverse vertebral foramen

V2 -traverses the vertebral foramina from C6 to C2

V3 -passes through the vertebral foramen and circles around the arch of the atlas to pierce the dura at the foramen magnum

V4 -courses upward to join the other vertebral artery to form the basilar artery -ONLY V4 gives rise to branches that SUPPLY THE BRAINSTEM and CEREBELLUM



-Atherothrombotic lesions have a predilection for V1 and V4 segments of the vertebral artery

-V1 may produce posterior circulation emboli but collateral flow from contralateral vertebral artery, ascending cervical, thyrocervical or occipital arteries prevent low flow TIAs or stroke

-but when one vertebral artery is atretic, collateral flow may be insufficient

-low flow TIAs consist of:

-syncope

-vertigo

-alternating hemiplegia



-Atherothrombotic lesions have a predilection for V1 and V4 segments of the vertebral artery

-V4 can promote thrombus formation as:

-embolism

-basilar artery thrombosis – with propagation

-if the SUBCLAVIAN ARTERY is occluded proximal to the origin of the vertebral artery there is reversal in the direction of blood flow in the ipsilateral vertebral artery

*exercise of the ipsilateral arm may increase demand on vertebral flow, producing posterior circulation TIAs / “SUBCLAVIAN STEAL”



-V2 and V3 are subject to:

-dissection

-fibromuscular dysplasia

-encroachment by osteophytic spurs within the vertebral foramina



-The posterior inferior cerebellar artery (PICA):

-PROXIMAL segment supplies the LATERAL MEDULLA

-DISTAL branches supply the INFERIOR surface of the cerebellum

-stenosis proximal to the origin of the PICA can threaten both the lateral medulla and the inferior surface of the cerebellum




-V4 segment (ischemia of lateral medulla) -vertigo -numbness of ipsilateral face; contralateral limbs -diplopia -hoarseness -dysarthria -dysphagia -ipsilateral Horner’s syndrome (lateral medullary / Wallenberg’s syndrome)

-medullary penetrating branches -PICA

-partial syndromes

-infarction of the pyramid -rarely, medial medullary syndrome -contralateral hemiparesis of the arm and leg, sparing the face



-Gait unsteadiness, headache, dizziness, nausea and vomiting may

be the only early symptoms and signs and should arouse suspicion of impending complication, which may require neurosurgical decompression, often with an excellent outcome


-medial lemniscus -emerging hypoglossal nerves

-contralateral loss of joint position sense -ipsilateral tongue weakness

-cerebellar infarction with edema -sudden respiratory arrest (due to raised ICP in the posterior fossa) -before arrest ensues, the following are absent or present briefly: -drowsiness -Babinski signs -dysarthria -bifacial weakness


OCCLUSION of the BASILAR ARTERY: -the basilar artery supply the base of the pons and the superior

cerebellum; they fall into 3 GROUPS: 1. Paramedian -7-10 in number -supply a wedge of pons on either side of the midline 2. Short circumferential -5-7 in number -supply the lateral 2/3 of the pons and middle and

superior cerebellar peduncles 3. Bilateral long circumferential -2 in number -course around the pons to supply superior and

anterior inferior cerebellum


OCCLUSION of the BASILAR ARTERY:

-atheromatous lesions occur anywhere the basilar trunk but are MOST FREQUENT in the PROXIMAL BASILAR and DISTAL VERTEBRAL segments

-clinical picture depends on the availability of retrograde collateral flow from the posterior communicating arteries

-emboli from the heart or proximal vertebral or basilar segments are MORE COMMONLY responsible for “top of the basilar” syndromes

-COMPLETE BASILAR OCCLUSION: constellation of bilateral long tract signs (sensory and motor) with signs of cranial nerve and cerebellar dysfunction



- “LOCKED-IN” state of preserved consciousness with quadriplegia and cranial nerve signs suggest COMPLETE PONTINE and LOWER MIDBRAIN infarction

-TIAs in the proximal basilar distribution may produce vertigo, other symptoms include diplopia, dysarthria, facial or circumoral numbness and hemisensory symptoms

-symptoms of BASILAR BRANCH affect ONE side of the brainste; symptoms of BASILAR ARTERY affect BOTH sides

-TIAs are short lived (5-30 minutes) but repititive

-Rx: heparin to prevent clot propagation




-basilar artery with infarction -bilateral brainstem signs: -gaze paresis/internuclear opthalmoplegia -ipsilateral hemiparesis -unequivocal signs of bilateral pontine disease

-branch of basilar artery -unilateral symptoms: -signs involving motor, sensory and cranial nerves

-superior cerebellar artery -severe ipsilateral cerebellar ataxia -nausea and vomiting -dysarthria -contralateral loss of pain and temperature sensation over the extremities, body and face Rarely: -partial deafness -Horner’s syndrome -ataxic tremor of ipsilateral upper limb -palatal myoclonus




-anterior inferior cerebellar artery ipsilateral : -deafness, facial weakness, vertigo, nausea and vomiting, nystagmus, tinnitus, cerebellar ataxia, Horner’s syndrome, paresis of conjugate lateral gaze contralateral: -loss of pain and temperature sensation *an occlusion close to the origin may cause CORTICOSPINAL TRACT SIGNS

-one of the short circumferential branches of the basilar artery

-affects the lateral 2/3 of the pons and middle or superior cerebellar peduncle

-one of the paramedian branches -affects a wedge-shaped area on either side of the medial pons

IMAGING STUDIES: CT SCANS

-identify or exclude hemorrhage as the cause of stroke and they identify extraparenchymal hemorrhages, neoplasms, abscesses, and other conditions masking as stroke

-CT OBTAINED in the FIRST SEVERAL HOURS after an infarction generally SHOW NO ABNORMALITY

-Infarct may not be seen reliably for 24-48 hours

-CT may fail to show small ischemic stroke in the posterior fossa because of bone artifact, also on the cortical surface

IMAGING STUDIES: CT SCANS

-contrast enhanced CT allow visualization of venous structures

-CT angiography readily: - identifies carotid disease and intracranial vascular

occlusions -area of brain infarct, ischemic penumbra after IV

bolus of contrast -sensitive in detecting SAH -NON-CONTRAST HEAD CT IS THE IMAGING

MODALITY OF CHOICE IN PATIENTS WITH ACUTE STROKE

IMAGING STUDIES: MRI

-reliably documents the extent and location of infarction in ALL AREAS of the brain, including the posterior fossa and cortical surface

-LESS SENSITIVE than CT in DETECTING ACUTE BLOOD -diffusion-weighted imaging and fluid-attenuated inversion

recovery (FLAIR) is MORE SENSITIVE for EARLY BRAIN INFARCTION than MR sequences or CT

-MR perfusion studies use IV GADOLINIUM contrast -MR angiography is highly sensitive for stenosis of

extracranial internal carotid arteries and large intracranial vessels

-MRI with fat saturation visualize extra or intracranial arterial dissection

IMAGING STUDIES: MRI

-compared to CT, MRI is:

-less sensitive for acute blood products

-more expensive

-time consuming

-less readily available

-limited with Claustrophobia

-MRI is more useful outside the acute period by:

-more clearly defining the extent of tissue injury -discriminating new from old regions of brain infarction

IMAGING STUDIES: CEREBRAL ANGIOGRAPHY

-conventional X-RAY cerebral angiography is the GOLD STANDARD for:

-identifying and quantifying atherosclerotic stenoses of the cerebral arteries

-characterizing other pathologies -coupled with endovascular techniques for cerebral

revascularization -risks of cerebral angiography: -arterial damage -groin hemorrhage -embolic stroke -renal failure from contrast nephropathy *reserved when less invasive means are inadequate

IMAGING STUDIES: ULTRASOUND TECHNIQUES

-Transcranial Doppler (TCD)

-can detect stenontic lesions in large intracranial arteries because such lesions increase systolic flow velocity

-can assist thrombolysis and improve large artery recanalization following rTPA administration

IMAGING STUDIES: PERFUSION TECHNIQUES

-both xenon techniques (xenon-CT) and PET can quantify cerebral blood flow

-generally used for research BUT can be useful for determining the significance of arterial stenosis and planning for revascularization surgery

-CT perfusion increases the sensitivity of detecting ischemia and can measure ischemic penumbra

INTRACRANIAL HEMORRHAGE

INTRODUCTION:

-Hemorrhages are classified by their location and underlying vascular pathology.

-Types:

-Subdural and epidural hemorrhage – usually caused by trauma

-Subarachnoid hemorrhages – produced by trauma and rupture of intracranial aneurysms

-Intraparenchymal and Intraventricular hemorrhages


DIAGNOSIS:

-Intracranial hemorrhage is often discovered on non-contrast CT imaging of the brain during the acute evaluation of stroke

*CT imaging is preferred method for acute stroke evaluation over MRI since it is more sensitive on acute blood


EMERGENCY MANAGEMENT: -Airway – reduction in the level of consciousness is common

and progressive -Initial BP is maintained until CT scan results are reviewed *BP can be safely lowered using nicardipine , labetalol or

esmolol (non-vasodilating IV drugs) -Mean arterial pressure is maintained <130mmHg, unless an

increase in ICP is suspected -Stuporous or comatose patients generally are treated

presumptively for elevated ICP with: -tracheal intubation -mannitol administration -hyperventilation -elevation of the head of bed

INTRAPARENCHYMAL HEMORRHAGE

-MOST COMMON TYPE OF INTRACRANIAL HEMORRHAGE

-particularly high in Asians and Blacks

-Major causes:

1. hypertension

2. trauma

3. cerebral amyloid angiopathy

-Risk factors:

-advanced age

-heavy alcohol consumption

-cocaine and methamphetamine use (most important cause in the young)

HYPERTENSIVE INTRAPARENCHYMAL HEMORRHAGE

PATHOPHYSIOLOGY:

-usually results from spontaneous rupture of a small penetrating artery deep in the brain

-can also be due to hemorrhagic disorders, neoplasms, vascular malformations

*suspected in non-hypertensives and in uncommon sites

-Most Common Sites:

-basal ganglia especially the putamen

-thalamus

-cerebellum

-pons

HYPERTENSIVE INTRAPARENCHYMAL HEMORRHAGE

PATHOPHYSIOLOGY:

-hemorrhage may lead herniation and death

-most develop over 30-90 minutes compared hemorrhage caused by anticoagulant therapy that evolve for 24-48 hours

Internal Medicine - Cerebrovascular Diseases

Health & Medicine

Transcript of Internal Medicine - Cerebrovascular Diseases