2Risk factors for stroke Systolic or diastolic hypertensionDiabeticsHypercholesterolemiaHeart disease (afib)Cigarette smokingHeavy alcohol consumptionHigh homocystineOral contraceptive use
3The major types of cerebrovascular disease Cerebral ischemia and infarctionTransient Ischemic AttacksAtherosclerotic thrombosisLacunesEmbolismHemorrhageHypertensive hemorrhageRuptured aneurysms and vascular malformationsOther
4Cerebral ischemia and infarction Anatomy and pathologyThe 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.
9Anatomy and pathologyOcclusion 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.
10Anatomy and pathologyWhen 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.
11Neurological 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.
12Neurological 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.
13Neurological 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.
14Neurological 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.
15Neurological 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.
16Neurological symptoms and signs The following suggest vertebro-basilar territory:double visionfacial numbnessfacial weaknessvertigodysphagiadysarthriaataxiadrop attacks;motor or sensory loss in both arms or legs.
17Transient Ischemic Attacks(TIA) Definition of termCurrent 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.
18Clinical pictureTransient 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.
19Differential 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.
20Cerebral thrombosisMost 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.
21Pathogenesis Pathogenesis of Ischemic neuronal death Ischemia ↓ Excitatory amino acid receptorsBorderzone or penumbra ↓Programmed cell death
22Clinical pictureIn 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)
23Clinical pictureIn 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.
25Clinical 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.
26Clinical picture Associated symptoms Headache occurs in about 25% of patients with ischemic stroke, possibly because of the acute dilation of collateral vessels.
27Laboratory FindingsCT 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.
28Laboratory FindingsCerebral 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.
29Differential 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.
30Differential 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.
31Treatment of Cerebral Thrombosis and Transient Ischemic Attacks The current treatment of it may be divided into four parts:Management in the acute phaseMeasures to restore the circulation and arrest the pathologic process1. Thrombolytic agents ( t-PA only for completed stroke,w/in3~6hrs )2.Anticoagulant drugs ( Heparin, LMWH & warfarin)3. Antiplatelet drugs ( Aspirin or Clopidogrel, Dipyridamole orTiclopidine )4. Neuroprotective agents: barbiturates, opioid antagonistnaloxone, Manitol
32Treatment Treatment of cerebral edema and raised intracranial pressure Acute surgical revascularizationSurgery for symptomatic carotid stenosisCarotid endarterectomy, intralumenal stents,extracranial-intracranial bypassPhysical therapy and rehabilitationMeasures to prevent further strokes and progression of vascular disease.
33TreatmentSince the primary objective in the treatment of atherothrombotic disease is prevention , efforts to control the risk factors must continue.AspirinHypotensive agentsOversedation should be avoidedSystemic hypotension, severe anemia should be treated promptlyParticular care should be taken to maintain the systemic blood pressure, oxygenation and intracranial blood flow during surgical procedures, especially in elderly patient.
34Course and PrognosisWhen 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.
35Embolic infarctionThis 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.
36Clinical PictureOf 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.
37Clinical PictureIt 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.
38Causes of cerebral embolism: Cardiac origin Noncardiac origin Undetermined origin
39Laboratory FindingsNot 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.
40Laboratory FindingsIn 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.
41Course and prognosisMost 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.
42Treatment and prevention Three phases of therapy :General medical management in the acute phase,Measures directed to restoring the circulationPhysical therapy and rehabilitationThese are much the same as described above the prevention of atherothrombotic infarction.
43Lacunar infarctAs 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.
44Lacunar infarctIn 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.
45Lacunar infarctAs 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.
46Lacunar infarct Recognition of lacunar stroke is important Future lacunar stroke can be reduced bytreating HTNAnticoagulation is not indicated (No evidence)Aspirin is also of uncertainty
47Intracranial 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.
48Intracranial 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.
49Intracranial 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.
50Intracerebral Hemorrhage Of all the cerebrovascular diseases, brain hemorrhage is the most dramatic. It has been given its own name, “apoplexy”.
52Clinical PictureWith 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.
53Clinical 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.
54Clinical PictureLobar 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.
55Clinical PicturePontine 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.
56Laboratory FindingsAmong 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.
57Laboratory FindingsIn 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.
58Differential 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.
59TreatmentThe 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.
60TreatmentRapid 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.
61TreatmentIn 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.
62Course and PrognosisThe 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.
63Course and PrognosisA 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.
64Spontaneous 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
65Spontaneous 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.
66Clinical picturePrior 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).
67Clinical pictureRupture 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.
68Clinical pictureSince the hemorrhage is confined to the subarachnoid space, there are few or no focal neurologic signs.AVM is another most common cause for SAHConvulsive seizures, usually brief and generalized.
69Clinical pictureVasospasm 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.
70Laboratory FindingsA 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.
71Laboratory FindingsCarotid 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.
72Establish 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.
73Establish 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).
74TreatmentThis 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 restfluid administration to maintain above-normal circulating volume and central venous – pressureuse of elastic stockings and stool softenersadministration of beta-blockerscalcium channel blockers
75Treatment 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.
76TreatmentThe 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.
77TreatmentNotable 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.
78Treatmentlumbar 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.
79TreatmentAdvice 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
80RehabilitionSince 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.
81Course and prognosisPatients 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.