Cases reported "Cerebral Infarction"

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11/825. Localized scleroderma associated with progressing ischemic stroke.

    We present a 73 year-old Japanese woman with localized scleroderma involving the right side of the scalp accompanied by continuous tingling pain, who developed insidiously progressive left hemiparesis. In magnetic resonance imaging of the brain, an infarct first appeared in the watershed region of the right middle cerebral artery territory and subsequently extended to deep white matter accompanied by scattered hemorrhages. Focal stenosis in the M2 portion of the right middle cerebral artery was revealed on magnetic resonance angiography, and the distal vessels were only shown faintly. A biopsy specimen from the sclerotic scalp lesion showed obvious thickening of vessel walls and mild mononuclear cell infiltration. We believe that the progressing ischemic stroke was caused by hemodynamic disturbances from localized sclerotic obstruction of the middle cerebral artery, with an autoimmune pathogenesis.
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12/825. Midbrain infarction: a rare presentation of cryptococcal meningitis.

    A 20-year-old farmer who had headache and fever for 1 month, suddenly developed left hemiplegia, tremor in left arm and titubation followed by deep coma. Cranial CT scan revealed an infarction in right crus of midbrain. His CSF revealed 66 mg/dl protein, 10 lymphocytes/mm3, and 70 mg/dl glucose. CSF was positive for cryptococcal antigen. He improved following i.v. amphotericin 0.5 mg/kg and fluconazole 200 mg daily, continued for 6 and 12 weeks respectively. Infarctions though rare in cryptococcal meningitis should be considered in patients with chronic meningitis with vasculitis.
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13/825. Vertebrobasilar artery territory infarction as an initial manifestation of systemic lupus erythematosus.

    cerebral infarction is a well-documented complication of systemic lupus erythematosus (SLE), that usually occurs several years after the diagnosis of SLE. To our knowledge, however, strokes associated with vertebrobasilar artery involvement were not reported to present as an initial manifestation of SLE. We report two patients, who presented with vertebrobasilar territory infarction as an initial manifestation of SLE. Patient 1 was a 16-year-old girl, who developed dysarthria and ataxia. MRI showed multiple infarcts in the pons, cerebellum and thalamus. Four-vessel cerebral angiography showed multifocal stenoses in the vertebral and basilar arteries with beaded appearance. Patient 2 was a 26-year-old woman, who developed headache associated with dysarthria, dizziness and ataxia. MRI showed multiple infarcts in the cerebellum, medulla, pons, midbrain and thalamus. cerebral angiography revealed occlusion of both vertebral arteries at the first cervical vertebral level with non-visualization of the basilar artery. Both patients were diagnosed as having SLE supported by laboratory results. Although rare, posterior circulation stroke can present as an initial manifestation of SLE, which may be attributed to vasculitis or dissection in the vertebral/basilar artery.
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14/825. Posterior fossa ischemia and bilateral vertebral artery hypoplasia.

    OBJECTIVE: To discuss cerebellar infarct in a patient with bilateral hypoplasia of the vertebral arteries. CLINICAL FEATURES: A 67-year-old woman suffered neck pain and headaches immediately after a minor motor vehicle accident. Fracture and dislocation were radiographically ruled out. Within a few days, the patient began to experience symptoms of vertigo and dizziness. Computed tomography scanning of the brain revealed a cerebellar infarct, and an angiogram of the vertebral arteries demonstrated bilateral hypoplasia. INTERVENTION AND OUTCOME: The cerebellar infarct created mild, stable symptoms, and the patient was monitored closely in a hospital setting until the risk of possible complications was negligible. After an uncomplicated and full recovery, the patient was given recommendations regarding critical neck positions to decrease the potential for further ischemic events. CONCLUSION: Cerebellar infarcts are rare and may be associated with rare vascular anomalies.
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15/825. White matter dementia in cadasil.

    Cerebral white matter disorders may be associated with profound neurobehavioral dysfunction. We report a 62-year-old man who had a slowly progressive 25-year history of personality change, psychosis, mood disorder, and dementia. neurologic examination disclosed abulia, impaired memory retrieval, and preserved language, with only minimal motor impairment. Neuropsychological testing found a sustained attention deficit, cognitive slowing, impaired learning with intact recognition, and perseveration. magnetic resonance imaging of the brain revealed extensive leukoencephalopathy. Right frontal brain biopsy showed ill-defined white matter pallor with hyaline narrowing of white matter arterioles. Granular osmiophilic material adjacent to vascular smooth muscle cells on electron microscopy of a skin biopsy, and an arginine for cysteine replacement at position 169 in the 4 EGF motif of the notch 3 region on chromosome 19q12 established the diagnosis of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (cadasil). This case illustrates that cadasil can manifest as an isolated neurobehavioral disorder over an extended time period. The dementia associated with cadasil closely resembles that which may occur with other white matter disorders, and represents an example of white matter dementia.
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16/825. Non-typhoid salmonella meningitis complicated by a infarction of basal ganglia.

    A previously healthy 16-month-old Korean girl with symptoms of fever, vomiting, and generalized tonic seizure was diagnosed to have Group D non-typhoid salmonella meningitis. The patient was treated with ceftriaxone (100 mg/kg/day) and amikin (22.5 mg/kg/day) initially and ciprofloxacin (30 mg/kg/day) was added later because of clinical deterioration and disseminated intravascular coagulation. Brain CT performed on the second day showed a well-demarcated low density lesion in the right lentiform nucleus and both caudate nuclei, without evidence of increased intracranial pressure. MRI performed on the 11th day confirmed CT scan findings as well as right subdural fluid collection, brain atrophy, and ventriculomegaly. She underwent subdural drainage and later ventriculo-peritoneal shunt operation. Despite receiving intensive treatment, she still has severe neurologic sequelae. Our case shows that infarctions of basal ganglia and thalami are not specific for tuberculous meningitis and that meningitis complicated by infarction is indicative of grave prognosis.
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17/825. When the left brain is not right the right brain may be left: report of personal experience of occipital hemianopia.

    OBJECTIVES: To make a personal report of a hemianopia due to an occipital infarct, sustained by a professor of neurology. methods: Verbatim observation of neurological phenomena recorded during the acute illness. RESULTS: Hemianopia, visual hallucinations, and non-occipital deficits without extraoccipital lesions on MRI, are described and discussed. CONCLUSIONS: Hemianopia, due to an occipital infarct, without alexia, is not a disability which precludes a normal professional career. Neurorehabilitation has not been necessary.
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18/825. Second harmonic imaging In acute middle cerebral artery infarction. Preliminary results.

    BACKGROUND: Second harmonic imaging (SHI) is a new ultrasound technique that is able to detect microbubbles in the tissue vascular space. The aim of this pilot study was to prove that this technique may detect focal abnormalities of cerebral echo-contrast enhancement in acute hemispheric stroke. CASE DESCRIPTIONS: Two male patients (aged 72 and 64 years) were included who presented with acute onset of severe hemiparesis and no established demarcation of the ischemic area in CT scans. After bolus application of galactose-based microbubbles, axial SHI examinations in a diencephalic plane of sections were performed using the transtemporal approach. Ultrasound investigations were recorded and evaluated offline. In both individuals demarcated focal abnormalities of cerebral contrast enhancement were detectable: in patient 1 the region of the lentiform nucleus and the adjacent parts of the temporoparietal lobe was affected, and in patient 2 a large region including the lentiform nucleus and cortical white matter was involved for at least 24 hours. Follow-up CT scans demonstrated a striatocapsular infarct in patient 1 and complete MCA infarction in patient 2, correlating with the presumed ischemic area in acute ultrasound examinations. The patient with complete MCA infarction showed missing contrast enhancement in the entire hemisphere of the affected side in follow-up SHI examinations. He died of malignant space-occupying brain edema. In the patient with the striatocapsular infarction, reappearance of echo-contrast enhancement in the ischemic area was assessable after 1 week. CONCLUSIONS: SHI may identify focal abnormalities of cerebral echo-contrast enhancement in acute hemispheric stroke. Furthermore, this technique helps to determine size, localization, and prognosis of the ischemic region and could be useful for bedside assessment of echo-contrast agent distribution related to brain tissue perfusion.
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19/825. Outcome of acute ischemic lesions evaluated by diffusion and perfusion MR imaging.

    BACKGROUND AND PURPOSE: diffusion and perfusion MR imaging have been reported to be valuable in the diagnosis of acute ischemia. Our purpose was to ascertain the value of these techniques in the prediction of ischemic injury and estimation of infarction size, as determined on follow-up examinations. methods: We studied 18 patients with acute ischemic stroke who underwent echo-planar perfusion and diffusion imaging within 72 hours of symptom onset. Quantitative volume measurements of ischemic lesions were derived from relative mean transit time (rMTT) maps, relative cerebral blood volume (rCBV) maps, and/or apparent diffusion coefficient (ADC) maps. Follow-up examinations were performed to verify clinical suspicion of infarction and to calculate the true infarction size. RESULTS: Twenty-five ischemic lesions were detected during the acute phase, and 14 of these were confirmed as infarcts on follow-up images. Both ADC and rMTT maps had a higher sensitivity (86%) than the rCBV map (79%), and the rCBV map had the highest specificity (91%) for detection of infarction as judged on follow-up images. The rMTT and ADC maps tended to overestimate infarction size (by 282% and 182%, respectively), whereas the rCBV map appeared to be more precise (117%). Significant differences were found between ADC and rMTT maps, and between rCBV and rMTT maps. CONCLUSION: Our data indicate that all three techniques are sensitive in detecting early ischemic injury within 72 hours of symptom onset but tend to overestimate the true infarction size. The best methods for detecting ischemic injury and for estimating infarction size appear to be the ADC map and the rCBV map, respectively, and the diffusion abnormality may indicate early changes of both reversible and irreversible ischemia.
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20/825. Failure of a saphenous vein extracranial-intracranial bypass graft to protect against bilateral middle cerebral artery ischemia after carotid artery occlusion: case report.

    OBJECTIVE AND IMPORTANCE: We present the case of a patient who experienced bilateral middle cerebral artery infarctions after Hunterian ligation and trapping of a ruptured right cavernous aneurysm, despite a high-flow extracranial-intracranial bypass. This is a rare complication, and it highlights the need for further refinements in our understanding of the hemodynamic insufficiency created by major vessel sacrifice. CLINICAL PRESENTATION: The patient was a 59-year-old woman who experienced multiple episodes of massive epistaxis before undergoing angiography, which revealed left internal carotid artery occlusion and an irregular right cavernous aneurysm. The patient was then transferred to our center for treatment. The patient was neurologically intact at presentation, and her epistaxis was controlled by nasal packing. INTERVENTION: The patient underwent an extracranial-intracranial bypass from the external carotid artery to the M2 segment of the right middle cerebral artery, followed by trapping of the aneurysm. Despite evidence of graft patency, the patient experienced bilateral middle cerebral artery distribution infarctions after surgery. CONCLUSION: Although extracranial-intracranial bypasses protect the majority of patients who undergo carotid artery ligation from ischemic complications, this case demonstrates that hemodynamic insufficiency can occur even with a high-flow saphenous vein graft. Better ways to quantitate the hemodynamic needs of the brain after major vessel sacrifice may facilitate matching of the revascularization strategy to the specific needs of each patient, thus further reducing the likelihood of ischemic complications.
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