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Cause of stroke

This category includes patients with rare causes of strokes such as nonatherosclero-tic vasculopathies, cerebral venous thrombosis, hypercoagulable states, or hematologic disorders. Two such disorders are discussed below. [Pg.152]

Dissection of the internal carotid and vertebral arteries is a common cause of stroke, particularly in young patients. Although many occur due to trauma, it is estimated that over half occur spontaneously. The mechanism of stroke following arterial dissection is either by artery-to-artery embolism, by thrombosis in situ, or by dissection-induced lumenal stenosis with secondary cerebral hypoperfusion and low-flow watershed infarction. Occasionally, dissection may lead to the formation of a pseudoaneurysm as a source of thrombus formation. Vertebrobasilar dissections that extend intracranially have a higher risk of rupture leading to subarachnoid hemorrhage (SAH). ° ... [Pg.152]

Tests for hypercoagulable states, such as protein C deficiency and antiphospholipid antibody, should be done only when the cause of stroke cannot be determined based on the presence of well-known risk factors for stroke. [Pg.165]

Atrial fibrillation (most important and treatable cardiac cause of stroke)... [Pg.165]

Increasing Oxygen. It was once believed that the cause of Alzheimer s dementia was poor oxygen snpply to the brain. This theory suggested that atherosclerosis, hard plaques of fat and calcium, accumulate in blood vessels and block the arteries that snpply the brain, depriving it of oxygen-rich blood. In fact, atherosclerosis does occnr in the carotid arteries that snpply the brain and is the most common cause of stroke and vascnlar dementia. There is no evidence that this mechanism is involved in the pathology of Alzheimer s disease. [Pg.296]

TIA-related infarctions on DWI can be predicted on the basis of certain clinical TIA features. Transient motor symptoms, preceding non-stereotypic attacks, the presence of an established cause of stroke, and presentation with aphasia are independent predictors of infarction on DWI (Ay et al. 2002 Crisostomo et al. 2003). In contrast, limb paresthesias, slurred speech, and brief attacks of dizziness or imbalance are not associated with occurrence of infarction. Of note, most symptoms that are not associated with infarction on DWI are based on patients subjective feelings and sensations in contrast to motor deficit or aphasia, it is not possible to objectively assess such symptoms and mark the brain as their origin. Of particular relevance to this point is that, according to a recent study, the independent predictors of infarction on DWI such as motor deficit and speech impairment are also independently associated with increased risk of stroke after TIA (Johnston et al. 2003), suggesting a potential role for DWI in the risk stratification for stroke following TIA. [Pg.190]

This was systematically studied with DWI in 62 consecutive patients who presented with a classic lacunar syndrome (Ay et al. 1999). DWI showed subsidiary acute lesion(s) in addition to the index lacunar lesion in ten patients (16%). The additional lesions were punctuate and lay within the leptomen-ingeal arterial territories in the majority. Patients with subsidiary infarction(s) more frequently harbored an embolic cause of stroke. This finding is critical because underlying embolic cause may give rise to recurrent strokes with more extensive brain injury. Identification of subsidiary infarctions on DWI should have an impact in prompting the physician to introduce the best effective treatment for secondary stroke prevention in a patient with lacunar infarction. [Pg.199]

Use of MRI to Identify Other Causes of Stroke in Patients with Occlusive Carotid Disease 234... [Pg.225]

Q1 A stroke involves significant reduction in blood flow to a part of the brain. It can be caused either (i) by an embolus or by intravascular clotting, which blocks blood flow to an area (approximately 85% of strokes), or (ii) by haemorrhage from a ruptured blood vessel, which compresses the brain tissue (approximately 15% of strokes). Patients with extensive atherosclerosis are at risk of intravascular coagulation and blockage of cerebral blood flow, but a vessel can be blocked by a thrombus originating in another part of the circulation. This cause of stroke is common in elderly patients >60 years of age. Aneurysms which rupture suddenly are a more common cause of stroke in younger patients. [Pg.187]

A few strokes are clearly familial with a simple Mendelian pattern of inheritance of the underlying cause (Table 3.2). Some of these genetic causes of stroke are described below ... [Pg.32]

Giant cell arteritis is the most common vascuUtic cause of stroke and is associated particularly with posterior circulation ischemia (Nesher 2000 Ronthal et al. 2003 Eberhardt and Dhadly 2007). Medium and large arteries are affected, especially branches of the external carotid artery, the ophthalmic artery and the vertebral artery. The patients are elderly, with the diagnosis being rare under age 60 years. Malaise, polymyalgia and other systemic symptoms are frequently present. The erythrocyte sedimentation rate is usually raised, often to over 100 mm/h in the first hour. [Pg.72]

Thrombophilias and other causes of hypercoagulability are rare causes of stroke (Matijevic and Wu 2006). Antithrombin III deficiency, protein C deficiency, activated protein C resistance owing to factor V Leiden mutation, protein S deficiency and plasminogen abnormality or deficiency can all cause peripheral and intracranial venous thrombosis. Thrombosis is usually recurrent and there is often a family history. Thrombophilia may cause arterial thrombosis, although the alternative diagnosis of paradoxical embolism should always be considered in patients with these disorders. It should be noted that deficiencies in any one of the factors associated with thrombophilia may be an incidental finding and cannot necessarily be assumed to be the cause of stroke. [Pg.75]

Sometimes arterial occlusion is demonstrated by angiography in migrainous stroke and the cause is hypothesized to be in-situ thrombosis complicating vasospasm. No provoking factors are known. Other possible causes of stroke in the context of headache must be considered carotid dissection, mitochondrial cytopathy, ruptured vascular malformation, antiphospholipid antibody syndrome and CADASIL (cerebral autosomal dominant arterio-pathy with subcortical infarcts and leukoencephalopathy). Migraine auras without headache may be confused with TIA (Ch. 8). [Pg.78]

Vascular risk factors (Ch. 2) and diseases should be sought. It is unusual for an ischemic stroke or TIA to occur in someone with no vascular risk factors, unless they are very old, or are young with some unusual cause of stroke (Ch. 6). A history of heart disease may be relevant and cardiac symptoms should be specifically inquired about. [Pg.126]

Determining the cause of stroke clues from the examination... [Pg.127]

Second-line investigations (Table 13.2) must be targeted appropriately since the likelihood of a relevant result depends on the selection of patients and further investigation will incur more cost. There are numerous rare causes of stroke (Ch. 6) for which highly specialized tests may be required. [Pg.173]

Solomon RA, Loftus CM, Quest DO etaL (1986). Incidence and etiology of intracerebral haemorrhage following carotid endarterectomy. Journal of Neurosurgery 64 29-34 Spencer MP (1997). Transcranial Doppler monitoring and causes of stroke from carotid endarterectomy. Stroke 28 685-691 Steed DL, Peitzman AB, Grundy BL et al. (1982). Causes of stroke in carotid endarterectomy. Surgery 92 634-639... [Pg.302]


See other pages where Cause of stroke is mentioned: [Pg.203]    [Pg.322]    [Pg.21]    [Pg.226]    [Pg.289]    [Pg.47]    [Pg.48]    [Pg.477]    [Pg.502]    [Pg.33]    [Pg.75]    [Pg.77]    [Pg.79]    [Pg.101]    [Pg.295]   


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Stroke, cause

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