1/13. Transient ischemic attack in heavy cannabis smokers--how 'safe' is it?Drugs are lately considered high-risk factors for cerebrovascular disease. Three male patients (mean age 24.6 years) who were heavy cannabis smokers presented with transient ischemic attacks (TIA) shortly after cannabis abuse. The complete examination of all 3 consisted of: EEG, brain CT scan, brain MRI, cerebral vessel angiography (digital subtraction and magnetic resonance angiography); also a full cerebrospinal fluid, urine and blood analysis (immunological, biochemical and hormonal tests were included). urine was further examined for drug metabolites. An extensive cardiological investigation was carried out. Small vessel leukoencephalopathy was revealed by the brain CT and MRI. EEG recordings of the first patient showed paroxysmal sharp waves with left hemispheric dominance. The other 2 patients had diffuse delta and theta activity in their EEG tracings. The urine analysis was positive for cannabis metabolites. There were no other abnormal findings in the rest of the meticulous and thorough study of all 3 patients, which leads to the conclusion that cannabis was the only risk factor responsible for the observed TIA, contradictory to other studies, which support that cannabis is a 'safe' drug. More research is required in order for this issue to be completely elucidated.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
2/13. Mini-infarct encephalopathy associated with uncommon microvessel convolute formation presenting with presenile dementia.A female patient started to suffer from transient ischemic attacks when she was 47 years of age, followed by increasing predominantly left-side spastic tetraparesis, generalized seizures and progressive dementia over a period of 11 years. She died when she was 58 years of age. On gross examination the brain showed enlarged ventricles and arteriosclerotic changes of large extracerebral vessels of the circulus arteriosus. Microscopic examination of the atrophic brain showed innumerable incomplete microinfarcts in the white and gray matter throughout all parts of the brain. In the white matter these lesions were characterized by small foci of demyelination and loss of oligodendrocytes while occasionally some scavenger cells were seen. axons seemed to be unaffected or displayed irregular axonal regeneratory growth. Any inflammatory reaction failed. In the cerebral cortex and subcortical nuclei the lesions showed loss of neurons and decrease in synaptophysin expression. Intracerebral arteries showed fibrosis or fibrohyalinosis of the entire intracerebral small-vessel network. In addition, numerous uncommon clusters of angioma-like telangiectatic vessels were observed. Medium-sized ischemic infarcts were found in the right putamen and adjacent internal capsule region, left-side dorsolateral brain stem and cerebellar hemisphere as well as a left-side pyramidal tract degeneration. Contralateral pseudohypertrophy of the inferior olivary nucleus was seen. The clinical and the neuropathologic observations made in this patient are compatible with small vessel disease characterized by a multicentric special and not yet described type of incomplete mini-infarcts in cerebral cortex and white matter accompanied by some larger ischemic infarcts of the common type in brain stem and cerebellum.- - - - - - - - - - ranking = 4keywords = vessel (Clic here for more details about this article) |
3/13. Treatment-induced leukoencephalopathy in primary CNS lymphoma: a clinical and autopsy study.BACKGROUND: Treatment-related leukoencephalopathy is the leading toxicity after successful treatment of primary CNS lymphoma (PCNSL). Its mechanism is poorly understood and there are no autopsy data available on such patients. methods: From a database of immunocompetent patients with PCNSL diagnosed between 1985 and 2001, the authors identified five autopsied patients who died of leukoencephalopathy. The authors reviewed their clinical records, MRI, and autopsy findings. RESULTS: The median age was 74 years (range 41 to 79) at PCNSL diagnosis. Symptoms of neurotoxicity developed a median of 1 month after treatment completion, and median survival was 30 months (range 22 to 68 months) after neurotoxicity onset. All had white matter hyperintensity on T2-weighted MRI, and two developed enhancing lesions 5 and 14 months following completion of treatment. At autopsy no PCNSL was identified. Myelin and axonal loss, gliosis, pallor, spongiosis, and rarefaction of the white matter were found in all; two patients had tissue necrosis that correlated with the enhancement on MRI, and one had fibrinoid necrosis of vessels. Four of the five patients had atherosclerosis of large cerebral vessels in the circle of willis and all had small vessel disease; two had recent strokes at autopsy. CONCLUSIONS: Treatment-induced leukoencephalopathy is not a late delayed consequence of neurotoxic treatment but can be seen very early in some patients. Vascular disease may be a component of this white matter injury.- - - - - - - - - - ranking = 1.5keywords = vessel (Clic here for more details about this article) |
4/13. Postpartum angiopathy with reversible posterior leukoencephalopathy.BACKGROUND: Postpartum angiopathy (PPA) is a cerebral vasoconstriction syndrome of uncertain cause that affects large and medium-sized cerebral arteries. Postpartum angiopathy is frequently complicated by ischemic stroke. The reversible posterior leukoencephalopathy syndrome (RPLS) is a distinct clinical-radiological entity characterized by transient vasogenic edema on brain imaging. The pathophysiological features of RPLS are related to small-vessel dysfunction and breakdown of the blood-brain barrier. OBJECTIVES: To report the coexistence of PPA and RPLS in 4 patients and to discuss possible interrelationships between these 2 entities. DESIGN: Four case reports and a review of the literature. RESULTS: Four women developed a clinical-radiological syndrome overlapping PPA and eclampsia shortly after an uncomplicated pregnancy. All had acute severe ("thunderclap") headaches and hypertension. Three developed seizures. All patients had reversible angiographic narrowing of large and medium-sized cerebral arteries. Serial magnetic resonance imaging showed transient nonischemic brain lesions, resembling the lesions described in patients with RPLS. The results of extensive tests for cerebral vasculitis were negative. CONCLUSION: These cases, and the literature, suggest an interrelationship between RPLS and cerebral vasoconstriction syndromes such as PPA.- - - - - - - - - - ranking = 0.5keywords = vessel (Clic here for more details about this article) |
5/13. Neuropathological correlates of reversible posterior leukoencephalopathy.The pathogenesis and neuropathology of reversible posterior leukoencephalopathy (RPLE; a clinical and radiographical syndrome linked to malignant hypertension, eclampsia, immunosuppressive drugs, and chemotherapy) remain poorly understood. Autopsies on patients with hypertensive encephalopathy have demonstrated arteriolar fibrinoid necrosis with micro-infarcts and failed to show brain edema; nonetheless, magnetic resonance imagings (MRIs) of patients with RPLE generally show findings most consistent with vasogenic edema. This article reports a patient with RPLE in whom brain biopsy revealed edematous white matter with no evidence of vessel wall damage or infarction. This supports the concept that the imaging changes on MRI represent vasogenic edema and suggests that the changes observed on autopsy in malignant hypertension may be an epiphenomenon.- - - - - - - - - - ranking = 0.5keywords = vessel (Clic here for more details about this article) |
6/13. An adult case of leukoencephalopathy with intracranial calcifications and cysts.We describe a 44-year-old woman with progressive headache, ataxia, and seizures in association with multifocal cerebral and cerebellar leukoencephalopathy, intracranial calcifications, and cysts. The cause of death was intracerebellar hemorrhage while taking warfarin. Pathologic features on biopsy included angiomatous-like blood vessels, intense gliosis, and Rosenthal fiber formation in the white matter. Genetic analyses did not identify any significant mutations in two candidate genes.- - - - - - - - - - ranking = 8.1697283423212keywords = blood vessel, vessel (Clic here for more details about this article) |
7/13. hypertension and vascular dementia.Postmortem surveys on patients treated for chronic hypertension often fail to demonstrate significant vessel changes. Nevertheless, hypertensive alterations in the brain can include infarcts and hemorrhages. Autopsies in a primary care hospital have shown that hypertension can affect arteries, arterioles, and capillaries in various patterns and degrees in the brain. These vascular lesions may be associated with large and small infarcts and hemorrhages in isolated or diffuse patterns. Widespread cerebral edema can occur with rapidly progressive hypertension. atherosclerosis, arterial and arteriolar fibrinoid necrosis, and micro-aneurysms may be observed. Chronic hypertensive encephalopathy causes vascular dementia and can be associated with subcortical arterial and arteriolar leukoencephalopathy, leukoaraiosis and/or Binswanger's disease. Epidemiologic evaluations based on complete autopsy studies need to be correlated with compliance of therapy, appropriate diagnosis of hypertension, and its long-term effects on the nervous system. Although persistent poorly controlled hypertension is known to damage the brain both acutely and chronically, the effects of intermittent hypertension remain to be defined.- - - - - - - - - - ranking = 0.5keywords = vessel (Clic here for more details about this article) |
8/13. Amyloid beta-protein in cerebral amyloid angiopathy, senile plaques, and preamyloidotic lesions in subcortical arteriosclerotic encephalopathy (Binswanger disease).Cerebral vascular amyloid deposits, senile plaques and neurofibrillary tangles have been found in subcortical arteriosclerotic encephalopathy (Binswanger disease). A mouse antiserum, prepared against a 43-amino acid synthetic peptide homologous to the amyloid beta-protein of alzheimer disease (anti-SP43), revealed immunoreactive amyloid deposits in meningeal and intracortical blood vessels, senile plaques, intraneuronal amyloid and preamyloid in a neuropathologically confirmed case of Binswanger disease previously reported to have cerebral vascular amyloid deposits. These lesions contained sulfated glycosaminoglycans as determined by the alcian blue/critical electrolyte concentration method. Similar findings were not observed in a case of Binswanger encephalopathy without cerebral amyloid deposits. Our study indicates that amyloidotic lesions in Binswanger encephalopathy with cerebral amyloid deposits contain amyloid beta-protein and sulfated glycosaminoglycans.- - - - - - - - - - ranking = 8.1697283423212keywords = blood vessel, vessel (Clic here for more details about this article) |
9/13. Hepatic aging as an etiological factor in the development of Alzheimer's disease.Alzheimer's disease is a frequent cause of dementia in the elderly. The prevalence and incidence increase with aging. It is hypothesised that the age related decline in liver size and lysosomal function results in decreased clearance as well as decreased or altered proteolysis of the Alzheimer precursor protein, and results in the deposition of A4 protein in cerebral blood vessels and brain with congophilic angiopathy and senile/amyloid plaque formation.- - - - - - - - - - ranking = 8.1697283423212keywords = blood vessel, vessel (Clic here for more details about this article) |
10/13. Vascular pathology in three cases of progressive cognitive deterioration.The clinical condition known as vascular dementia remains poorly defined. Few studies have attempted a correlative link between the clinical syndrome and the structural abnormalities of the brain. Classically the clinical progression of the vascular dementing process is thought to be a multi-step process punctated by repeated episodes of ischemia, that are clinically expressed as strokes. In most instances it has been assumed that the substrate of vascular dementias consists of atherothrombotic infarcts. The objective of this report is to illustrate 3 cases of progressive (rather than stepwise) cognitive deterioration without clinical evidence of stroke, evolving over a period of several years, in which there were prominent vascular lesions. A complete autopsy and detailed neuropathologic examination demonstrated cerebral vascular lesions involving small arterial vessels (< 200 microns in diameter). The lesions consisted of moderate-to-severe arteriolosclerosis in two cases, and mild-to-moderate arteriolosclerosis in a case of Alzheimer's disease with severe cerebral amyloid angiopathy. Parenchymal lesions consisted of small cortical and subcortical infarcts, most of them smaller than 0.1 cm in average diameter, and subcortical leukoencephalopathy severe in two cases and mild-to-moderate in the third case. Severe atherosclerosis not accompanied by large infarcts was also present in one case. Arterial changes affecting small, distal branches causing sometimes small parenchymal lesions in association with diffuse cerebral white matter disease, appear to be the anatomical substrate that accompanies progressive cognitive impairment in some patients who are frequently diagnosed with Alzheimer's disease because in their clinical records there is neither history of strokes nor stepwise progression of symptoms.- - - - - - - - - - ranking = 0.5keywords = vessel (Clic here for more details about this article) |
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