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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nine cases have been presented in detail to illustrate some of the varied causes of sudden neurological deficit in childhood: arteriovenous malformation, cryptic hamartoma, berry aneurysm, mycotic aneurysm, intraspinal arteriovenous malformation, brain tumor, migraine, arteritis, and multiple sclerosis. The Boston Children's Hospital experience with aneurysms and intracranial arteriovenous malformation has been summarized. It is noteworthy that a cutaneous hemangioma overlay one cranial and one intraspinal arteriovenous malformation. One small but deep cerebral arteriovenous malformation apparently destroyed itself after its second hemorrhage. Not only have multiple sclerosis and a brain tumor mimicked a vascular lesion, but a series of vascular accidents was misdiagnosed first as multiple sclerosis then as a thalamic tumor. The many possible causes of childhood strokes has been thoroughly cataloged in the Report of the Joint Committee for Stroke Facilities in 1973 (11). Children may be more susceptible to strokes because of congenital abnormalities such as congenital heart disease, hemophilia, and sickle cell anemia, or by diseases which more commonly occur in this age group, such as leukemia. The likelihood of brain abscess in cyanotic congenital heart disease is stressed. Arteriographic studies in our series have been safe; however, there have been reports of probable worsening of symptoms in children with multiple cerebral occlusive lesions in the presence of homocystinuria.
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PMID:Strokes in children. 98 45

Although families with several members suffering a cerebral haemorrhage have been reported previously, a family history of this stroke sub-type has not yet been firmly established as a risk factor for the disease. A family in whom cerebral haemorrhage has been clearly documented in five members, spanning three generations, is reported. In three a berry aneurysm was detected. There was no evidence of hypertension among any of the five cases. A sixth member of the family probably died of a cerebral haemorrhage but no necropsy was performed. By using established incidence rates for cerebral haemorrhage in the population, the probability of five such unrelated events arising in any family of similar size and longevity was calculated to be 4.9 x 10(-10). This family strengthens the case that an underlying genetic susceptibility does exist for a proportion of patients who have a cerebral haemorrhage. This susceptibility appears to be consequent upon berry aneurysm formation. The distribution of cases within this family is consistent with an autosomal dominant pattern of inheritance.
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PMID:Cerebral haemorrhage and berry aneurysm: evidence from a family for a pattern of autosomal dominant inheritance. 195 6

By selectively infiltrating and destroying the internal elastica of a major cerebral artery, Aspergillus fungus (Af) induces disruption and incipient dilatation of the vascular wall with or without inflammation. This unique pathogenetic mechanism of forming "true" fungal mycotic aneurysms (FMAs) was clearly demonstrated in a middle-aged adult male who died of a pontine stroke. The latter was secondary to thrombosis in the basilar artery of which the internal elastica was infiltrated and replaced by Af hyphae. The patient had diabetes, liver cirrhosis with oesophageal varices, and received multiple blood transfusions. However, leukopenia was not present and immunosuppressive drugs were not used. This case prompted comparison of the natural history and pathogenesis of bacterial and fungal mycotic aneurysms in cerebral arterial branches. Selective destruction of the internal elastica with progressive dilation at a segment of vascular wall insinuates a potential pathogenetic process involved in the formation of saccular or berry aneurysm. Management and therapeutic approaches for FMA are discussed.
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PMID:A proposed pathogenetic process in the formation of Aspergillus mycotic aneurysm in the central nervous system. 821 10

Cerebral vasospasm and related ischemic stroke continue to be significant complicating factors in the course of many patients with subarachnoid hemorrhage from berry aneurysm rupture. The risk of this well-recognized but poorly understood complication can be estimated on the basis of patient medical history, neurologic examination, and head CT findings. Every patient with possible risk needs specialized neurologic intensive care unit care after aneurysm obliteration. Surgical and pharmacologic wash-out of subarachnoid blood around the basal arteries, proper management of intracranial pressure and fluid status, hyponatremia, hypomagnesemia, and fever, as well as use of calcium channel blockers, have been considered helpful in patient management prior to and with the symptomatic vasospasm development. Transcranial Doppler (TCD) ultrasound is important in detecting vasospasm before the patient suffers ischemic neurologic deficit or infarct. Elevated TCD velocities often initiate the use of triple-H (HHH: hypertension, hemodilution, and hypervolemia) therapy and subsequently guide it. Up to the end of the first 3 weeks after subarachnoid hemorrhage and aneurysm obliteration, development of any focal neurologic deficit or mental deterioration, unless convincingly proven otherwise, is assumed to be from cerebral vasospasm. When a hemodynamically significant vasospasm in the arterial segments of clinical concern is suggested, emergency cerebral angiography with balloon dilatation angioplasty or intra-arterial infusion of vasodilating agents may be helpful in relieving ischemic symptoms.
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PMID:Cerebral Vasospasm Following Subarachnoid Hemorrhage. 1219 10

Stroke is a major cause of morbidity and mortality but the brain and other relevant tissues are often examined only cursorily when stroke patients come to autopsy. The pathological findings and clinical implications vary according to the type of stroke and its location and cause. Large ischaemic strokes are usually associated with atherosclerosis of extracranial or major intracranial arteries but can be caused by dissection. Most small cerebral infarcts are caused by arteriosclerosis or, in the elderly, cerebral amyloid angiopathy (CAA). However, vasculitides and coagulopathies can cause a range of different patterns of ischaemic (and, occasionally, haemorrhagic) stroke. Global brain ischaemia, caused by severe hypotension or raised intracranial pressure, produces damage that is accentuated in certain regions and neuronal populations and may be confused with hypoglycaemic injury. The main cause of subarachnoid haemorrhage is a ruptured berry aneurysm but CAA, arteriovenous malformations and infective aneurysms are occasionally responsible. These can also cause parenchymal brain haemorrhage, although this most often complicates hypertensive small vessel disease. Sometimes the haemorrhage arises from a neoplasm. Performing an adequate autopsy in stroke requires proper preparation, awareness of the likely pathological processes, familiarity with intracranial vascular anatomy, careful gross examination and dissection, and appropriate use of histology.
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PMID:Autopsy approach to stroke. 2066 47

The study aimed to determine the clinical characteristics of fatal methamphetamine-related stroke in Australia, 2009-2015. There were 38 cases, 60.5% male, with a mean age of 40.3 years. In no case was there evidence that this was the first time methamphetamine had been used by the decedent, and 52.6% had known histories of injecting drug use. The stroke was hemorrhagic in 37 of 38 cases. In 21.1% of cases, the stroke was purely parenchymal and, in 18.4%, involved purely the subarachnoid space. A ruptured berry aneurysm was present in 31.6% and in 68.8% of initial subarachnoid hemorrhages. There was evidence of systemic hypertension in 8 of 25 cases in which full autopsy findings were available. With increased use of methamphetamine, there is a high probability of increased hemorrhagic stroke incidence among young people. In cases of fatal hemorrhagic stroke among young cases presenting to autopsy, the possibility of methamphetamine use should be borne in mind.
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PMID:Clinical Characteristics of Fatal Methamphetamine-related Stroke: A National Study. 2883 7

Subarachnoid hemorrhage is a medical emergency. Berry aneurysm rupture is the second most common cause following trauma. Diagnosis is often challenging. Neurogenic heart syndrome often complicates subarachnoid hemorrhage. A concomitant pheochromocytoma can be deadly causing sudden cardiac arrhythmia. Here, we describe a case of subarachnoid hemorrhage with concomitant incidental pheochromocytoma in a relatively young female who died suddenly, diagnosed during autopsy. A 57-year-old Hispanic woman with past medical history of asthma, prediabetes, and uncontrolled hypertension collapsed unexpectedly. She initially had ventricular tachycardia, followed by pulseless electrical activity and finally asystole without response to resuscitation. In the emergency department she was on epinephrine, calcium, naloxone, and tPA with suspected thrombotic stroke. Despite measures, she was pronounced dead. Autopsy revealed subarachnoid hemorrhage due to a ruptured berry aneurysm. Additionally, pheochromocytoma was detected in the right adrenal gland. Subarachnoid hemorrhage has a grave prognosis by itself. This case describes the uncommon detection of pheochromocytoma in the setting of subarachnoid hemorrhage.
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PMID:A Case of Sudden Death: Subarachnoid Hemorrhage, Pheochromocytoma, Berry Aneurysm. 3128 1