Cases reported "Cerebrovascular Disorders"

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1/13. Near infrared spectroscopy and transcranial Doppler in monohemispheric stroke.

    We simultaneously performed near infrared spectroscopy (NIRS) and transcranial Doppler (TCD) to evaluate the effects of hypercapnia as well as of scalp ischemia on the blood flow at two different depth levels within the brain and of the scalp vessels. A decrease in the backscattered light intensity, meaning an increment of blood volume, was detected at the end of hypercapnia in all healthy subjects. This decrement was partly masked by ischemia in the cutaneous vessels. In 2 patients with a monohemispheric lesion in the middle cerebral artery (MCA) territory, an increase in NIRS response was found in the healthy hemisphere, while in the stroke side the CO2-induced changes were negligible. TCD data showed a similar increment of blood flow velocity to the hypercapnia in both hemispheres, with no differences between the affected and normal side in 1 patient, whereas in the second one, no increment was observed on the affected side, probably due to internal carotid artery stenosis. The two methods nicely integrate: TCD mainly tests subcortical changes in the MCA flow, while NIRS is exquisitely sensitive to cortical arterioles and capillary blood flow modifications.
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2/13. acetazolamide effect on vascular response in areas with diaschisis as measured by Tc-99m HMPAO brain SPECT.

    The effects of acetazolamide (Diamox) on vascular response were investigated in areas with intrahemispheric thalamic diaschisis and crossed cerebellar diaschisis using consecutive Tc-99m HMPAO brain SPECT studies before and after Diamox administration. All six patients with thalamic diaschisis and five of eight patients with crossed cerebellar diaschisis at baseline showed significantly augmented perfusion after Diamox administration in the affected thalamus and cerebellum compared with that in the contralateral unaffected areas. These results suggest more dilatation of the arterioles in areas with diaschisis after Diamox administration than in areas without diaschisis. Diamox may produce relative luxury perfusion in areas with diaschisis.
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3/13. MELAS of infantile onset: mitochondrial angiopathy or cytopathy?

    An 83-day-old male infant had convulsions, hypertrophic cardiomyopathy, and lactic acidosis. Cranial computed tomography revealed low-density areas in both parieto-occipital lobes and in the left temporal lobe. Muscle biopsy did not reveal ragged-red fibers, but abnormal mitochondria were found in the capillary endothelial cells as well as in the muscle fibers. At 5 months of age, the patient developed purpura on the soles and palms. skin biopsy showed degeneration of the endothelial cells with abnormal mitochondria in the arterioles and capillaries. Myelinated nerves in the skin had vacuolated axons with swollen mitochondria, and their myelin sheaths showed vacuolation. At 9 months of age, he died of heart failure, and autopsy revealed abnormal mitochondria in the myocardium but not in the coronary vessels. Our findings indicate that the symptoms of the mitochondrial encephalopathy, myopathy, lactic acidosis, and strokelike episodes (MELAS) syndrome cannot be fully explained by the mitochondrial angiopathy alone.
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4/13. Severe cerebral and systemic necrotizing vasculitis developing during pregnancy in a case of systemic lupus erythematosus.

    We describe a fatal case of systemic lupus erythematosus (SLE) developing cerebral and systemic necrotizing vasculitis during pregnancy. The patient was discovered to have SLE at 14 weeks' gestation. Although the symptoms disappeared without treatment with corticosteroid in the 2nd trimester, she presented with meningoencephalitis due to vasculitis in the 3rd trimester. polyarteritis nodosa (PAN)-like necrotizing vasculitis of the small muscular arteries and arterioles, with acute and healing lesions in the leptomeninges, brain parenchyma and visceral organs was observed at postpartum autopsy. PAN-like vasculitis in the central nervous system is quite rare in SLE. This case is also suggestive in terms of the influence of pregnancy on the activity of SLE.
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5/13. Bilateral posterior cerebral artery strokes in a young migraine sufferer.

    We report a young migraine sufferer who developed bilateral posterior cerebral artery territory infarcts during the course of his classic migraines, the second of which was associated with intraluminal clot in the posterior cerebral artery. To our knowledge, bilateral posterior cerebral artery stroke from spontaneous migraine has not been reported. Head computed tomographic, magnetic resonance imaging, and angiographic correlation is presented. The mechanism of migrainous infarction may be in part explained by caliber changes in arterioles and capillaries leading to flow reduction in the more proximal conduit arteries combined with the associated coagulopathy that has been previously documented during migraine attacks.
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6/13. Generalized racemose livedo with cerebrovascular lesions (sneddon syndrome): an occlusive arteriolopathy due to proliferation and migration of medial smooth muscle cells.

    We describe two cases of livedo racemosa generalisata with cerebrovascular defects (sneddon syndrome). The histology is characterized by a proliferation and migration of medial smooth muscle cells in ascending arterioles of the upper subcutis and deep dermis. Migrating smooth muscle cells with a high content of intermediate filaments colonize the sub-endothelial intimal space, with subsequent narrowing of the vessel lumen. Since the discoloration of the skin is provoked by a reactive dilatation of venules, the biopsy should be performed in the adjacent normal-looking skin, taking in the upper subcutis.
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7/13. Binswanger's disease: progressive subcortical encephalopathy or multi-infarct dementia?

    Since Binswanger's description of subcortical arteriosclerotic encephalopathy in 1894, numerous cases have been reported. Several authors doubt the validity of this malady, although the majority consider it to be a disease entity. We report seven cases with this type of pallor of myelin, only two of which are accompanied by a history of dementia. Among the seven cases, two had arteriosclerosis of penetrating arteries and arterioles in cerebral white matter. Electron microscopy showed splitting of myelin sheaths, probably the result of edema. In reviewing the blood supply of the cerebral white matter, we conclude that no pathological alterations of medullary branches of the cerebral arteries, the same vessels supplying the white matter, can give rise to such diffuse pallor of white matter and spare the arcuate fibres. This pallor can only be due to cerebral edema, most likely of hypoxic-ischemic, hypotensive, or acidotic origin. We also contend that arteriosclerosis can only cause dementia through multiple infarcts or lacunae, if it indeed leads to dementia.
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8/13. Amyloid angiopathy combined with granulomatous angiitis of the central nervous system: report on two patients.

    We report here two cases of isolated angiitis of the central nervous system associated with congophilic angiopathy. The clinical history lasted 9 months in the first patient (65 years old) and 9 years in the second patient (59 years old). It was characterized by progressive intellectual deterioration, increased protein content of the CSF and evidence of focal brain lesions in the CT scan. One patient showed chronic intracranial hypertension. Vascular lesions were limited to the brain and were characterized by granulomatous and necrotizing angiitis of the small leptomeningeal and intracortical vessels. Amyloid deposits were present in large amounts along vascular segments showing vasculitis, in foreign body giant cells, in plaque-like structures surrounding diseased perforating arterioles, along cortical microvessels and in many neuritic plaques. Close proximity and topographic overlap of vasculitis and amyloid changes suggest a possible pathogenetic relationship.
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9/13. Isolated benign cerebral vasculitis.

    A young woman south medical care for headache, nausea, and evolving focal neurologic signs. The CSF was normal; cerebral angiography showed segmental narrowing and irregularity of intraparenchymal arterioles. Isolated cerebral vasculitis was the clinical diagnosis made by careful exclusion; the illness reponded well to steroids and there was later angiographic evidence of healing.
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10/13. Familial cerebral amyloid angiopathy presenting as recurrent cerebral haemorrhage.

    Eleven patients belonging to two generations of a Dutch family with cerebral and cerebellar haemorrhage, haemorrhagic infarction and infarction are described. Their ages varied from 44 to 58 years. The principal clinical characteristics was recurring cerebral haemorrhages, sometimes preceded by a history of migrainous headaches or mental changes. In 4 of the 6 autopsied cases, old and new multiple cerebral haemorrhagic infarcts and infarcts were found, in one case a single cerebral haemorrhage and in another a cerebellar haemorrhage. In 5 cases this resulted in secondary subarachnoid haemorrhage. In one case the infarcts were only slightly haemorrhagic and did not result in subarachnoid haemorrhage. This patient presented as dementia. Microscopically, in these 6 cases and in one biopsy specimen hyaline thickening of the walls of cortical arterioles was found. The arteries of the arachnoid showed marked tortuosity, concentric proliferation, and focal hyalinization of the walls. Amyloid was found in the hyalinized vessels in 5 cases, but not outside the central nervous system. We believe that we are dealing with an inherited disorder with an autosomal dominated mode of inheritance, in which microangiopathy leads to cerebral haemorrhage and (haemorrhagic) infarction. It seems likely that amyloidosis underlies the angiopathy, and that this family suffers from a condition similar to the one described by Gudmundsson in 1972.
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