Cerebrovascular Disease

Cerebrovascular Disease

these are including the following important disease like as Ishaemic disease .Thrombotic disease ,Embolic disease ,Haemorrhagic disease
Cerebrovascular disease is the most frequent.causes of new rapid­ onset, non traumatic neurologic deficit It is a far more common etiology than seizures.or tumors. Vascular structures are subject to a variety of chronic pathologic processes which compromise vessel wall integrity. Diabetes, high cholesterol, high blood pressure, and smoking are risk factors for vascular disease. These conditions can lead to vascular damage by such mechanisms as atheroma deposition

causing luminal stenosis, endothelial damage promoting thrombo­genesis, and weakening of the vessel wall resulting in aneurysm formation or dissection. These processes may coexist. For instance, a vessel may contain an atheromatous plaque that significantly de­creases lumen diameter, and also have compromised endothelium over the plaque, providing the opportunity for thrombus formation, which can lead to acute total occlusion of the remaining lumen. Aneurysms and dissection often occur in atheromatous vessels. Spe­cific patterns of disease relevant to the cerebrovascular system are
atheromatous and thrombotic carotid occlusion, brain ischemia due
to embolus from a proximal source, vessel wall breakage leading to hemorrhage, and rupture of abnormal, thin-walled structures, specif­ically aneurysms and arteriovenous malformations.

Ischemic Diseases

Ischemic stroke accounts for approximately 85% of acute cerebrovascular events. Symptoms of acute ischemic stroke vary based on the functions of the neural tissues supplied by the occluded ves­sel, and the presence or absence of collateral circulation. The circle of Willis provides extensive collateral circulation, as it connects the right and left carotid arteries to each other and each to the verte­brobasilar system. Patients with complete occlusion of the carotid artery proximal to the circle of Willis may be asymptomatic if the
blood flow patterns can shift and provide sufficient circulation 
to the ipsilateral cerebral hemisphere from the contralateral carotid and the basilar artery. However, the anatomy of the circle of Willis is highly variable. Patients may have a hypoplastic or missing communicat­ing artery, both anterior cerebral arteries supplied by one carotid, or the posterior cerebral artery supplied by the carotid rather than the basilar. Similarly, one vertebral artery is often dominant, and the other hypoplastic. These variations may make disease in a partic­ular vessel more neurologically devastating than in a patient with full collateral circulation. Occlusion distal to the circle of Willis generally results in stroke in the territory supplied by the particular artery.

Neurologic deficit from occlusive disease may be temporary or
permanent. A patient with sudden-onset focal neurologic deficit that resolves within 24 hours has had a transient ischemic attack (TIA). If the deficit resolves between 24 hours and one week. then the patient has had a reversible ischemic neurologic deficit (RIND). A patient· with permanent deficits has had a cerebrovascular accident (CVA). CVA is a commonly used, but vague term. Some prefer the term completed stroke.

Thrombotic Disease

The most common area of neurologically Significant vessel throm­bosis is the carotid artery in the neck. Disease occurs at the carotid bifurcation. Thrombosis of a carotid artery chronically narrowed by atheroma can lead to acute carotid occlusion. As discussed above,. this may or may not cause symptoms. The more common concern is thromboembolus. Intracranial arterial occlusion by local thrombus formation may occur, but is considered rare compared to embolic occlusion.


Complete occlusion of the carotid artery without referable neu­rologic deficit requires no treatment. A patient with new neuro­logic deficit and an angiographically demonstrated complete carotid occlusion contralateral to the symptoms should be considered for emergency carotid endarterectomy.Surgery should not be per­formed on obtunded or comatose patients, and should be done within

 hours of symptom onset This time restriction significantly reduces the number of candidates

Embolic Disease

Emboli causing strokes may originate in the left atrium due to atrial fibrillation, on a hypokinetic left ventricular wall segment, or in valvular vegetations, an atheromatous aortic arch, or stenosed carotid bifurcations, or from the systemic venous system in the pres­ence of a right-to-left shunt, such as a patent foramen ovale. The majority of emboli enter the anterior (carotid) circulation rather than the posterior (venebrobasilar) circulation. Characteristic clini­cal syndromes result from embolic occlusion of the various vessels

Common Types of Strokes

Anterior Cerebral Artery Stroke. The ACA supplies the medial frontal and parietal lobes, including the motor strip, as it courses into the interhemispheric fissure. ACA stroke results in con­tralateral eg weakness

Middle Cerebral Artery Stroke. The MCA supplies the lateral frontal and parietal lobes and the temporal lobe. MCA stroke results in contralateral face and arm weakness. Dominant­ hemisphere MCA stroke causes language deficits. Proximal MCA occlusion causing ischemia and swelling in the entire MCA territory can lead to significant intracranial mass effect and midline shift

Posterior Cerebral Artery Stroke. The PCA supplies the occipital lobe. PCA stroke results in a contralateral homonymous hemianopsia 
Posterior Inferior Cerebellar Artery Stroke. The PICA supplies the lateral medulla and the inferior half of the cerebel­lar hemispheres. PICA stroke results in nausea, vomiting, nystag­mus, dysphagia, ipsilateral Horner's syndrome, and ipsilateral limb ataxia. The constellation of symptoms resulting from PICA occlu­sion is referred to as lateral medullary syndrome or Wallenberg's syndrome.


Ischemic stroke management has two goals: reopen the occluded vessel and maintain blood flow to borderline ischemic tissues on the border of the vascular territory. This bordering tissue is referred to as the ischemic penumbra. The first goal. reopening the ves­sel, may be attempted with recombinant TPA. TPA administration within 3 hours of the onset of neurologic deficit improves outcome

at 3 months. Obtain a head CT immediately in the setting of 
suspected ischemic stroke to differentiate ischemic from hemorrhagic stroke. Intracranial hemorrhage. major surgery in the previous 2 weeks, gastrointestinal or genitourinary hemorrhage in the previous 3 week
  platelet count < lOO,OOO uL and systolic blood pressure (SBP) > 185 mm Hg are among the contraindications to tPA therapy. The neurology stroke team should be called while taking the patient to head CT

Patients not eligible for tPA require hemodynamic optimization and neurologic monitoring. Admit such patients to the ICU stroke service for blood pressure management and frequent neurologic checks. Allow the blood pressure to run high to maximize cerebral perfusion. SBP more than 180 mm Hg may require treatment. Give normal saline solution without glucose (which could injure neu­rons in the penumbra), and aim for normovolemia. A stroke patient

who worsens clinically should undergo repeat head CT to evaluate for hemorrhage or significant mass effect from

typically peaks 3 to 5 days after the stroke. Significant swelling from an MCA stroke or cerebellar stroke may be life threatening and re­quire hemicraniectomy or suboccipital craniectomy, respectively

Hemorrhagic Diseases

Intracranial hemorrhage (ICH) from abnormal or diseased vascular structures accounts for approximately 15% of acute cerebrovascu­lar events. Hypertension and amyloid angiopathy account for most intraparenchymal hemorrhages, although arteriovenous malforma­tions (AVMs), aneurysms, venous thrombosis, tumnors, hemorrhagic conversion of ischemic infarct, and fungal infections may also be the cause. The term intracranial hemorrhage is frequently used to mean intraparenchymal hemorrhage, and will be used here. lCH causes local neuronal injury and dysfunction, and can also cause global dysfunction due to mass effect if of sufficient volume. AVM or aneurysm rupture results in subarachnoid hemorrhage (SAH), be­ cause the major cerebral and cortical blood vessels travel between the pia and the arachnoid membrane, in the subarachnoid space. SAH can cause immediate concussive-like neuronal dysfunction by exposure of the brain to intra-arterial pressure pulsations during the hemorrhage, and can cause delayed ischemia from cerebral arterial vasospasm

Patients presenting with ICHs that do not follow typical patterns should undergo
   angiography or MRI to evaluate for possible underlying lesions, such as AVM or tumor

Patients who suffer a hemorrhagic stroke are more likely to
present lethargic or obtunded than those who suffer an ischemic stroke. Depressed mental status results from brain shift and hernia­tion secondary to mass effect from the hematoma. Ischemic stroke does not cause mass effect acutely, therefore patients are more likely to present with normal consciousness and a focal neurologic deficit, Hemorrhagic strokes tend to present with a relatively smooth onset of symptoms as the hematoma expands, rather than the immediately maximal symptoms caused by ischemic stroke. Table 1 provides
a listing of relative incidences of ICH by anatomic distribution


Hypertension increases the relative risk of ICH by approximately fourfold, likely due to chronic degenerative vasculopathy. Hyper­tensive hemorrhages often present in the basal ganglia, thalamus, or pons, and result from breakage of small perforating arteries that branch off of much larger parent vessels
Most hypertensive hemorrhages should be medically managed. The hematoma often contains intact, salvageable axons because the blood dissects through and along neural tracts, and surgical clot

evacuation destroys these axons. Factors that indicate that surgery may be appropriate include superficial clot location, young age, non­ dominant hemisphere, rapid deterioration, and significant mass ef­fect. Most studies fail to show overall improved outcomes. Medical management includes moderate blood pressure control, normalizing platelet and clotting function, phenytoin, and electrolyte manage­ment. Intubate patients who cannot clearly follow commands, to prevent aspiration and hypercarbia. Follow and document the neu­rologic exam and communicate with the family regarding appropri­ateness for rehabilitation versus withdrawal of care.

Amyloid Angiopathy

The presence of pathologic amyloid deposition in the media of small cortical vessels compromises vessel integrity, predisposes to more superficial (lobar) hemorrhages, and may cause multiple hemorrhages over time.

The superficial location of amyloid hemorrhages may make sur­gical evacuation less morbid than for typical deep hypertensive hem­orrhages. Approach medical management and family counseling similarly to patients with hypertensive hermorrhages.

Cerebral Aneurysm

An aneurysm is focal dilatation of the vessel wall, and is most often a balloon-like outpouching, but may also be fusiform. Aneurysms usually occur at branch points of major vessels [e.g., internal carotid artery (lCA) bifurcation], or at the origin of smaller vessels (e.g., posterior communicating artery or ophthalmic artery). Approximately 85% of aneurysms arise from the anterior circulation (carotid) and 15% from the posterior circulation (vertebrobasilar). Table 2 shows the percentage distribution of cerebral aneurysms by location. Aneurysms are thin-walled and at risk for rupture. The major cerebral vessels, and therefore aneurysms, lie in the subarach­ noid space. Rupture results in SAR. The aneurysmal tear may be small and seal quickly or not. SAH may consist of a thin layer of blood in the CSF spaces, or thick layers of blood around the brain and extending into brain parencbyma. resulting in a clot with mass effect. The meningeal linings of the brain are sensitive, so SAH usu­ally results in a sudden, severe "thunderclap" headache. A patient will classically describe the worst headache of my life." Present­ing neurologic symptoms may range from mild headache to coma to sudden death. The Hunt-Hess grading system categorizes patients clinically

Patients with symptoms suspicious for SAH should have a head
CT immediately. Acute SAH appears as a bright signal in the fis­sures and CSF cisterns around the base of the brain,  CT is rapid, noninvasive, and approximately 95% sensi­tive. Patients with suspicious symptoms but negative head CT should undergo lumber puncture , a lumbar puncture (LP)  with Xanthochromia and high red blood cells counts is consistent with SAH , negative CT and LP essentially rules out SAH patients diagnosed with SAH  require four vessels cerebral angiography within 24 hours to assess for aneurysm or other vascular malformation , catheter angiography remains the gold standard for assessing the patients cerebral vasculature SAH patients should be admitted to the neurologic ICU  hunt Hess grade 4 to 5 patients require intubation and hemodynamic monitoring and stabilization , the current standard of care for ruptured aneurysms requires early aneurysmal occlusion there are two options for occlusion the patient may under go craniotomy with  microsurgical dissection and placement of a titanium clip acros
the aneurysm neck to exclude the aneurysm from the circulation and reconstitute the lumen of the parent vessel. The second option is to take the patient to the interventional neuroradiology suite for en­dovascular placement of looped titanium coils inside the aneurysm dome. The coils support thrombosis and prevent blood flow into the aneurysm. Factors favoring craniotomy and clipping include young age, good medical condition, and broad aneurysm necks. Factors favoring coiling include old or medically-frail patients and narrow aneurysm necks. Clipping results in a more definitive cure, because coils can move and compact over time, requiring repeat angiograms and placement of additional coils. The decision to clip or coil is com­plex and should be fully explored. The International Subarachnoid Aneurysm Trial (lSAT) researchers suggested that endovascular oc­clusion resulted in better outcomes for certain types of cerebral aneurysms, although this trial was marred by poor selection and randomization techniques, and the validity of its conclusions have been questioned.  Debate also continues regarding optimal care for unruptured intracranial aneurysms.

SAH patients often require I to 3 weeks of lCU care after
aneurysm occlusion for medical complications that accompany neu­rologic injury. In addition to routine ICU concerns, SAH patients are also at risk for cerebral vasospasm. In vasospasm, cerebral arteries constrict pathologically and can cause ischemia or stroke from 4 
 to 21 days after SAH. Current vasospasm prophylaxis includes maintaining hypertension and mild hypervolemia
 to optimize perfusion, and administering nimodipine, a calcium channel blocker that may decrease the incidence and degree of spasm. Neurointerventional

options for treating symptomatic vasospasm are intra-arterial papaverine and balloon angioplasty
, Aneurysmal SAH has an approximate mortality rate of 50% in the first month. Approximately one-third of survivors returns to pre­ SAH function, and the remaining two-thirds have mild to severe disability. Most require rehabilitation after hospitalization

Arteriovenous Malformations

AVMs are abnormal, dilated arteries and veins without an in­tervening capillary bed. The nidus of the AVM contains a tangled mass of vessels. but DO neural tissue. AVMs may be asymptomatic or present with SAH or seizures. Small AVMs present with hem­orrhage more often than large AVMs, which tend to present with seizures. Headache, bruit, or focal neurologic deficits are less com­mon symptoms. AVMs hemorrhage at an average rate of 2 to 4% a year. demonstrates the angiographic appearance of an AVM in arterial and venous phases.

There are several management differences for SAH due to AVM versus aneurysm. Definitive therapy for the AVM is usually de­layed 3 to 4 weeks to allow the brain to recover from acute injury. There is less risk of devastating early rebleeding from AVMs. and vasospasm is less relevant Adjacent brain may be hyperemic after removal of the high-flow arteriovenous (A-V) shunt, so hypertension and hypervolemia are not beneficial. Three therapeutic modalities for AVMs are currently in common use: microsurgical excision, en­dovascular glue embolization, and stereotactic radiosurgery. AVMs that are large, near eloquent cortex, or that drain to deep venous structures are considered high grade and more difficult to surgically resect without Causing significant neurologic deficit Radiosurgery can treat these lesions, although it is limited to lesions less than 3cm in diameter
  and has a 2-year lag time (i.e., the AVM may bleed in the interval). Embolization reduces flow through the AVM. it is usually considered adjunctive therapy, but may rarely be the sole treatment for deep, inaccessible lesions

table1 showing anatomic distribution of intracranial haemorrhages(ICHs) and correlated symptoms 

classic symptoms
 of ICHs%
Contralateral hemiparesis
Basal ganglia (putamen ,globus . pallidus) internal capsule
Contralateral hemiparesis loss
Depends on location weakness numbness partial loss if visual field
Cerebral white matter
Hemiparesis may be devasting
Lethargy or coma due to brain stem compression and or hydrocephalus3
Often devasting
Brain stem excluding pons

  Prevalence of cerebral Aneurysm by location
table 2

Aneurysm location


30%anterior communicating artery(A-Comm
25%posterior communicating artery(P-Comm
20%Middle cerebral artery bifurcation (MCA
10% Other 
Anterior circulation 85%
10%Basilar artery most frequently at the basilar tip
5%Vertebral artery usually at the posterior inferior cerebellar artery (PICA
Posterior circulation 15%
Table 3 The Hunt - Hess Clinical Grading System for Subarachnoid Haemorrhage

Clinical Presentation Hunt-Hess Grade
Asymptomatic unruptured aneurysem

Awake asymptomatic or mild headache , mild nuchal rifidity
Awake , moderate to severe headache cranral nerve palsy ,nuchal rigidity
Lethargic , mild focal neurologic deficit

Suporous , significant neurologic deficit eg hemiplegia

Comatose, posturing

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