Presentation on theme: "Cerebral Vascular Disease. Risk factors for stroke Systolic or diastolic hypertension Diabetics Hypercholesterolemia Heart disease (afib) Cigarette smoking."— Presentation transcript:
Cerebral Vascular Disease
Risk factors for stroke Systolic or diastolic hypertension Diabetics Hypercholesterolemia Heart disease (afib) Cigarette smoking Heavy alcohol consumption High homocystine Oral contraceptive use
The major types of cerebrovascular disease Cerebral ischemia and infarction Transient Ischemic Attacks Atherosclerotic thrombosis Lacunes Embolism Hemorrhage Hypertensive hemorrhage Ruptured aneurysms and vascular malformations Other
Cerebral ischemia and infarction Anatomy and pathology The principal pathological process under consideration here is the occlusion of arteries supplying the brain. The two internal carotid arteries and the basilar artery form the Circle of Willis at the base of the brain, which acts as an efficient anatomotic device in the event of occlusion of arteries proximal to it.
Anatomy and pathology Occlusion leads to sudden severe ischemia in the area of brain tissue supplied by the occluded artery, and recovery depends upon rapid lysis or fragmentation of the occluding material: Reversal of neurological function within minutes or hours gives rise to the clinical picture of a transient ischemic attack.
Anatomy and pathology When the neurological deficit lasts longer than 24 hours, it may be called a reversible ischemic neurological deficit ( RIND ) if it recovers completely in a few days, or a completed stroke if there is a persistent deficit. Sometimes recovery is very slow and incomplete.
Neurological symptoms and signs – The loss of function that the patient notices, and which may be apparent on examination, entirely depends on the area of brain tissue involved in the ischemic process.
Neurological symptoms and signs The following suggest middle cerebral territory: – Dysphasia; Dyslexia, dysgraphia, dyscalculia; Loss of use of contralateral face and arm; Loss of feeling in contralateral face and arm.
Neurological symptoms and signs The following suggests anterior cerebral territory: Loss of use and/ or feeling in the contralateral leg. The following suggests posterior cerebral territory: Development of a contralateral homonymous hemianopia.
Neurological symptoms and signs The following suggests a deep-seated lesion affecting the internal capsule which is supplied by small perforating branches of the middle and posterior cerebral arteries close to their origins: Complete loss of motor and sensory function throughout the whole of the contralateral side of the body with a homonymous hemianopia.
Neurological symptoms and signs The following suggests ophthalmic artery territory (the ophthalmic artery arises from the internal carotid artery just below the Circle of Willis): Monocular loss of vision.
Neurological symptoms and signs The following suggest vertebro-basilar territory: double vision facial numbness facial weakness vertigo dysphagia dysarthria ataxia drop attacks;motor or sensory loss in both arms or legs.
Transient Ischemic Attacks(TIA) Definition of term Current opinion holds that TIAs are brief, reversible episodes of focal, nonconvulsive ischemic neurologic disturbance, Consensus has been that their duration should be less than 24 h.
Clinical picture Transient Ischemic Attacks can reflect the involvement of any cerebral artery. The loss of function entirely depends on the influenced artery. It may last a few seconds or up to 12 to 24 h, Most of them last 2 to 15 min. There are only a few attacks or several hundred. Between attacks, the neurologic examination may disclose no abnormalities. A stroke may occur after numerous attacks have occurred over a period of weeks or months.
Differential diagnosis of TIAs Transient episodes, indistinguishable from TIAs, are known to occur in patients with Seizure,Migraine,Transient global amnesia,and occasionally in patients with multiple sclerosis, meningioma, glioblastoma,metastatic brain tumors situated in or near the cortex,and even with subdural hematoma.
Cerebral thrombosis Most cerebrovascular disease can be attributed to atheroscleroses and chronic hypertension; until ways are found to prevent or control them, vascular disease of the brain will continue to be a major cause of morbidity.
Pathogenesis Pathogenesis of Ischemic neuronal death Ischemia ↓ Excitatory amino acid receptors ↓ Borderzone or penumbra ↓ Programmed cell death
Clinical picture In general, evolution of the clinical phenomena in relation to cerebral thrombosis is more variable than that of embolism and hemorrhage. The loss of function that the patient notices, and which may be apparent on examination, entirely depends on the area of brain tissue involved in the ischemic process.(above)
Clinical picture In more than half of patients, the main part of the stroke is preceded by minor signs or one or more transient attacks of focal neurologic dysfunction. The final stroke may be preceded by one or two attacks or a hundred or more brief TIAs, and stroke may follow the onset of the attacks by hours, weeks, or, rarely, months. The most occurrence of the thrombotic stroke is during sleep. The patient awakens paralyzed. Either during the night or in the morning. Unaware of any difficulty, he may arise and fall helplessly to the floor with the first step.
Clinical picture Associated symptoms – Seizures accompany the onset of stroke in a small number of cases (10-50%); in other instances, they follow the stroke by weeks to years. The presence of seizures does not definitively distinguish embolic from thrombotic strokes, but seizure at the onset of stroke may be more common with embolus.
Clinical picture Associated symptoms – Headache occurs in about 25% of patients with ischemic stroke, possibly because of the acute dilation of collateral vessels.
Laboratory Findings CT Scan or MRI: A CT scan or MRI should be obtained routinely to distinguish between infarction and hemorrhage as the cause of stroke, to exclude other lesions (eg, tumor, abscess) that can mimic stroke, and to localize the lesion. CT is usually preferred for initial diagnosis because it is widely available and rapid and can readily make the critical distinction between ischemia and hemorrhage. Lumbar Puncture: This should be performed in selected cases to exclude subarachnoid hemorrhage.
Laboratory Findings Cerebral Angiography: Intra-arterial angiography is used to identify operable extracranial carotid lesions in patients with anterior circulation TIAs who are good surgical candidates. It also can be used for intra-arterial thrombolysis ( r-tPA) Magnetic resonance angiography (MRA) may detect stenosis of large cerebral arteries, aneurysms, and other vascular lesion, but its sensitivity is generally inferior to that of conventional angiography.
Differential Diagnosis Vascular disorders are mistaken for ischaemic stroke include intracerebral hemorrhage, subdural or epidural hematoma, and subarachnoid hemorrhage from rupture of an aneurysm or vascular malformation. These condition can often be distinguished by a history of trauma or of excruciating headache at onset, a more marked depression of consciousness, or by the presence of neck stiffness on examination. They can be excluded by CT scan or MRI.
Differential Diagnosis Differential Diagnosis: Other structural brain lesion such as tumor or abscess can also produce focal cerebral symptoms of acute onset. Brain abscess is suggested by concurrent fever, and both abscess and tumor can usually be diagnosed by CT scan or MRI. Metabolic disturbances, particularly hypoglycemia and hyperosmolar nonketotic hyperglycemia, may present in stroke like fashion. The serum glucose level should therefore be determined in all patients with apparent stroke.
Treatment of Cerebral Thrombosis and Transient Ischemic Attacks The current treatment of it may be divided into four parts: Management in the acute phase Measures to restore the circulation and arrest the pathologic process 1. Thrombolytic agents ( t-PA only for completed stroke,w/in 3~6hrs ) 2.Anticoagulant drugs ( Heparin, LMWH & warfarin) 3. Antiplatelet drugs ( Aspirin or Clopidogrel, Dipyridamole or Ticlopidine ) 4. Neuroprotective agents: barbiturates, opioid antagonist naloxone, Manitol
Treatment – Treatment of cerebral edema and raised intracranial pressure – Acute surgical revascularization – Surgery for symptomatic carotid stenosis – Carotid endarterectomy, intralumenal stents, extracranial-intracranial bypass – Physical therapy and rehabilitation – Measures to prevent further strokes and progression of vascular disease.
Treatment – Since the primary objective in the treatment of atherothrombotic disease is prevention, efforts to control the risk factors must continue. – Aspirin – Hypotensive agents – Oversedation should be avoided – Systemic hypotension, severe anemia should be treated promptly – Particular care should be taken to maintain the systemic blood pressure, oxygenation and intracranial blood flow during surgical procedures, especially in elderly patient.
Course and Prognosis When the patient is seen early in the cerebral thrombosis, it is difficult to give an accurate prognosis. As for the eventual or long-term prognosis of the neurologic deficit, there are many possibilities. It must be mentioned that having had one thrombotic stroke, the patient is at risk in the ensuing months and years of having a stroke at the same or another site, especially if there is hypertension or diabetes mellitus.
Embolic infarction This is one of the most common cause of stroke. In most cases of cerebral embolism, the embolic material consists of a fragment that has broken away from a thrombus within the heart. Embolism due to fat, tumor cells, fibrocartilage, amniotic fluid, or air is a rare occurrence and seldom enters into the differential diagnosis of stroke.
Clinical Picture Of all strokes, those due to cerebral embolism develop most rapidly. The embolus strikes at any time of the day or night. Getting up to go to the bathroom is a time of danger. The neurologic picture will depend on the artery involved and the site of obstruction.
Clinical Picture It is important to repeat that an embolus may produce a severe neurologic deficit that is only temporary; symptoms disappear as the embolus fragments. In other words, embolism is a common cause of a single evanescent stroke that may reasonably be called a prolonged TIA. Also as already pointed out, several emboli can give rise to two or three transient attacks of differing pattern or, rarely, of almost identical pattern.
Laboratory Findings Not infrequently the first sign of myocardial infarction is the occurrence of embolism; therefore it is advisable that an ECG and echocardiogram be obtained in all patients with stroke of uncertain origin. Prolonged study of heart rhythm with Holter monitoring should be undertaken.
Laboratory Findings In some 30 percent of cases, cerebral embolism produces a hemorrhagic infarction. CT scanning or MRI may be helpful in showing the more intense hemorrhagic infarcts, particularly if the scan is repeated on the second or third day.
Course and prognosis Most patients survive the initial insult, and in many the neurologic deficit may recede relatively rapidly, as indicated above. The eventual prognosis is determined by the occurrence of further emboli and the gravity of the underlying illness- cardiac failure myocardial infarction, bacterial endocarditis and so on.
Treatment and prevention Three phases of therapy : General medical management in the acute phase, Measures directed to restoring the circulation Physical therapy and rehabilitation These are much the same as described above the prevention of atherothrombotic infarction.
Lacunar infarct As one might surmise, small penetrating branches of the cerebral arteries may become occluded, and the resulting infarcts may be so small or so situated as to cause no symptoms whatever. As the softened tissue is removed, it leaves a small cavity, or lacune.
Lacunar infarct In our clinical and pathologic material, there has always been a strong correlation of the lacunar state with a combination of hypertension and atherosclerosis and, to a lesser degree, with diabetes. In all the cases of lacunar infarction, the diagnosis depends essentially on the occurrence of the certain unique stroke syndromes of limited proportions.
Lacunar infarct As mentioned above, CT scanning is less reliable than MRI in demonstrating the lacunes. The EEG may be helpful in a negative sense; in the case of lacunes in the pons or the internal capsule, there is a notable discrepancy between the unilateral paralysis or sensory loss and the negligible electrical changes over the affected hemisphere.
Lacunar infarct Recognition of lacunar stroke is important Future lacunar stroke can be reduced by treating HTN Anticoagulation is not indicated (No evidence) Aspirin is also of uncertainty
Intracranial Hemorrhage This is the common, well-known “spontaneous” brain hemorrhage. It is due predominantly to chronic hypertension and degenerative changes in cerebral arteries. Hemorrhage may interfere with cerebral function through a variety of mechanisms, including destruction or compression of brain tissue and compression of vascular structures, leading to secondary ischaemia and edema.
Intracranial Hemorrhage Intracranial hemorrhage is classified by its location as intracerebral, subarachnoid, subdural, or epidural, all of which- except subdural hemorrhage- are usually caused by arterial bleeding.
Intracranial Hemorrhage The bleeding occurs within brain tissue, and rupture of arteries lying in the subarachnoid space is practically unknown apart from aneurysms. The extravasation forms a roughly circular or oval mass that disrupts the tissue and grows in volume as the bleeding continues. Adjacent brain tissue is distorted and compressed. If the hemorrhage is large, midline structures are displaced to the opposite side and reticular activating and respiratory centers are compromised, leading to coma and death.
Intracerebral Hemorrhage Of all the cerebrovascular diseases, brain hemorrhage is the most dramatic. It has been given its own name, “apoplexy”.
Clinical Picture With smaller hemorrhages, the clinical picture conforms more closely to the usual temporal profile of a stroke, i.e, an abrupt onset of symptoms that evolve gradually and steadily over minutes, hours, or a day or two, depending on the size of the ruptured artery and the speed of bleeding. Headache and vomiting are cardinal features.Very small hemorrhages in “silent” regions of the brain may escape clinical detection.
Clinical Picture Clinical features vary with the site of hemorrhage. Deep cerebral hemorrhage The two most common sites of hypertensive hemorrhage are the putamen and the thalamus, which are separated by the posterior limb of the internal capsule. This segment of the internal capsule is traversed by descending motor fibers and ascending sensory fibers, including the optic radiations.
Clinical Picture Lobar hemorrhage Hypertensive hemorrhages also occur in subcortical white matter underlying the frontal, parietal, temporal, and occipital lobes. Symptoms and signs vary according to the location.
Clinical Picture Pontine hemorrhage With bleeding into the pons, coma occurs within seconds to minutes and usually leads to death within 48 hours. Ocular findings typically include pinpoint pupils. Horizontal eye movements are absent or impaired, but vertical eye movements may be preserved. Cerebellar hemorrhage The distinctive symptoms of cerebellar hemorrhage (headache, dizziness, vomiting, and the inability to stand or walk) begin suddenly, within minutes after onset of bleeding.
Laboratory Findings Among laboratory methods for the diagnosis of intracerebral hemorrhage, the CT scan occupies the foremost position. In CT scans, fresh blood is visualized as a white mass as soon as it is shed. The mass effect and the surrounding extruded serum and edema are hypodense. By MRI, either in T1-or-T2 weighted images, the hemorrhage is not easily visible in the 2 or 3 days after bleeding.
Laboratory Findings In general, lumbar puncture is ill advised, for it may precipitate or aggravate an impending shift of central structures and herniation. The white cell count in the peripheral blood may rise transiently to 15,000 per cubic millimeter, a higher figure than in thrombosis.
Differential Diagnosis Putaminal, thalamic, and lobar hypertensive hemorrhages may be difficult to distinguish from cerebral infarctions. To some extent, the presence of severe headache, nausea and vomiting, and impairment of consciousness are useful clues that a hemorrhage may have occurred; the CT scan identifies the underlying disorder definitively. CT scan or MRI is the most useful diagnostic procedure, since hematomas can be quickly and accurately localized.
Treatment The management of patients with large intracerebral hemorrhages and coma includes the maintenance of adequate ventilation, use of controlled hyperventilation to a Pco2 of 25 to 30 mmHg, monitoring of intracranial pressure (ICP) in some cases and its control by the use of tissue-dehydrating agents such as mannitol (osmolality kept at 295 to 305 mosmol/L and Na at 145 to 150 meq), and limiting intravenous infusions to normal saline.
Treatment Rapid reduction in blood pressure, in the hope of reducing further bleeding, is not recommended, since it risks compromising cerebral perfusion in cases of raised intracranial pressure. On the other hand, sustained mean blood pressure of greater than 110mmHg may exaggerate cerebral edema and risk extension of the clot. It is at approximately this level of acute hypertension that the use of beta-blocking drugs(esmolol, labetalol) or angiotensin-converting enzyme inhibitory drugs is recommended.
Treatment In contrast to cerebral hemorrhage, the surgical evacuation of cerebellar hematomas is a generally accepted treatment and is a more urgent matter because of the proximity of the mass to brainstem and the risk of abrupt progression to coma and respiratory failure.
Course and Prognosis The immediate prognosis for large and medium-size cerebral clots is grave; some 30 to 35 percent of patients die in 1 to 30 days. Either the hemorrhage extends into the ventricular system or intracranial pressure is elevated to levels that preclude normal perfusion of the brain. Sometimes the hemorrhage itself seeps into vital centers such as the hypothalamus or midbrain.
Course and Prognosis A volume of 30 ml or less, calculated from the CT scan, predicted a generally favorable outcome. In patients with clots of 60 ml or larger and an initial Glasgow Coma Scale score of 8 or less, the mortality was 90 percent. As remarked earlier, it is the location of the clinical effects.
Spontaneous Subarachnoid Hemorrhage This is the fourth most frequent cerebrovascular disorder following atherothrombosis, embolism, and primary intracerebral hemorrhage. Saccular aneurysms are also called berry” aneurysms; actually they take the form of small, thin-walled blisters protruding from arteries of the circle of Willis or its major branches. Their rupture causes a flooding of the subarachnoid space with blood under high pressure. Aneurysms are multiple in 20 percent of patients
Spontaneous Subarachnoid Hemorrhage In childhood, rupture of saccular aneurysms is rare, and they are seldom found at routine postmortem examination; beyond childhood, they gradually increase in frequency to reach their peak incidence between 35 and 65 years of age. Approximately 90 to 95 percent of saccular aneurysms lie on the anterior part of the circle of Willis.
Clinical picture Prior to rupture, saccular aneurysms are usually asymptomatic. Exceptionally, if sufficiently large to compress pain-sensitive structures, they may cause localized cranial pain. The presence of a partial oculomotor palsy with dilated pupil may be indicative of an aneurysm of the posterior communicating-- internal carotid junction. With rupture of the aneurysm, blood under high pressure is forced into the subarachnoid space(where the circle of Willis lies).
Clinical picture Rupture of the aneurysm usually occurs while the patient is active rather than during sleep, and in some instances sexual intercourse, straining at stool, lifting heavy objects, or other sustaining exertion precipitates the ictus. In patients who survive the initial rupture, the most feared complication is rerupture, an event that may occur at any time from minutes up to 2 or 3 weeks later. In less severe cases, consciousness, if lost, may be regained within a few minutes or hours, but a residual of drowsiness, confusion, and amnesia accompanied by severe headache and stiff neck persists for several days.
Clinical picture Since the hemorrhage is confined to the subarachnoid space, there are few or no focal neurologic signs. AVM is another most common cause for SAH Convulsive seizures, usually brief and generalized.
Clinical picture Vasospasm Delayed hemiplegia or other focal deficit usually appears 3 to 12 days after rupture and rarely before or after this period. These delayed accidents and the focal narrowing of a large artery or arteries, seen on angiography, are refered to as vasospasm. Hydrocephalus If a large amount of blood ruptures into the ventricular system or floods the basal subarachnoid space, The patient then may become confused or unconscious as a result of acute hydrocephalus. A subacute hydrocephalus due to blockage of the CSF pathways by blood may appear after 2 to 4 weeks.
Laboratory Findings A CT scan will detect blood locally or diffusely in the subarachnoid spaces or within the brain or ventricular system in more than 90 percent of cases and in practically all cases in which the hemorrhage has been severe enough to cause momentary or persistent loss of consciousness. In all other cases a lumbar puncture should be undertaken when the clinical features suggest a subarachnoid hemorrhage. Usually the CSF is grossly bloody within 30 min of the hemorrhage, with RBC counts up to 1 million per cubic millimeter or even higher.
Laboratory Findings Carotid and vertebral angiography is the only certain means of demonstrating an aneurysm and does so in some 85 percent of patients in whom the correct diagnosis of spontaneous subarachnoid hemorrhage is made on clinical grounds. MRI and MRA detect most aneurysms of the basal vessels but are as yet of insufficient sensitivity to replace conventional angiography. Even when MRA or “ CT angiography “ demonstrates the aneurysm, the surgeon usually requires the kind of anatomic definition that can only be obtained by conventional angiography.
Establish the diagnosis If there is a typical history, marked neck stiffness and no focal neurological deficit, lumbar puncture is still the best way to make the diagnosis, revealing uniformly blood-stained CSF.
Establish the diagnosis If the history is typical with marked neck stiffness, but the patient remains in coma or shows a marked focal neurological deficit, a CT scan is a safer way to establish the diagnosis (revealing blood in the subarachnoid space),since lumbar puncture may lead to worse condition in this group of patients (whose coma or focal neurological deficit may indicate the presence of an associated intracerebral blood clot).
Treatment This is influenced by the neurologic and general medical state of the patient as well as by the location and morphology of the aneurysm. The general medical management in the acute stage includes the following, in all or part: bed rest fluid administration to maintain above-normal circulating volume and central venous – pressure use of elastic stockings and stool softeners administration of beta-blockers calcium channel blockers
Treatment intravenous nitroprusside or other medication to reduce greatly elevated blood pressure and then maintain systolic blood pressure at 150 mmHg or less; and pain-relieving medication for headache ( this alone will often reduce the hypertension ). The prevention of systemic venous thrombosis is critical, usually accomplished by the use of cyclically inflated whole-leg compression boots.
Treatment The use of anticonvulsants is controversial; many neurosurgeons administer them early, with a view of preventing a seizure-induced risk of rebleeding. Calcium channel blockers are being used extensively to reduce the incidence of stroke from vasospasm. Nimodipine 50 mg, administered intravenus, is currently favored.
Treatment Notable advances in the techniques for the obliteration of aneurysms, particularly the operating microscope, and the management of circulatory volume have significantly improved the outcome of patients with ruptured aneurysms. Both the risk of rerupture of the aneurysm and some of the secondary problems that arise because of the massive amount of blood in the subarachnoid space can be obviated by early obliteration of the aneurysm.
Treatment lumbar puncture is carried out for diagnostic purposes if the CT scan is inconclusive; thereafter this procedure is performed only for the relief of intractable headache, to detect recurrence of bleeding, or to measure the intracranial pressure prior to surgery.
Treatment Advice from specialist neurosurgical units should be sought. Patients who have withstood their first bleed well are submitted to carotid and vertebral angiography within a few days to establish whether or not an operable aneurysm is present. Patients who do not recover from their first bleed well, patients with inoperable aneurysms should be nursed in bed for a few weeks and then mobilized over a further few weeks, being encouraged to return to full normal activities at about 3-4 months. Prevent re-bleeding
Rehabilition Since the incidence of significant damage to the brain is high in patients surviving subarachnoid haemorrhage, many will not be able to return to normal activities. They will need support from relatives, nurses, physiotherapists, speech therapists, occupational therapists, social workers and specialist units in rehabilitation.
Course and prognosis Patients with the typical clinical picture of spontaneous subarachnoid hemorrhage in whom an aneurysm or arteriorvenous malformation cannot be demonstrated angiographically have a distinctly better prognosis than those in whom the lesion is visualized. Vasospasm and rebleeding were the leasing causes of morbidity and mortality in addition to the initial bleed. In respect to rebleeding, this occurred within 2 weeks in 20 percent of patients, with a peak incidence in the 24 h after the initial bleed.