Cases reported "Acute Disease"

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1/13. Non-ketotic hyperglycemia in a young woman, presenting as hemiballism-hemichorea.

    We report a 22-year-old girl presenting with acute onset left sided hemiballism-hemichorea (HH) and non-ketotic hyperglycemia (NKH). Initial brain CT revealed faint hyperdensities, sharply confined to the contralateral nucleus caudatus and putamen. Sequential MRI investigations yielded increasing hypersignal intensities on T1-weighted images and resolving hypodensities on T2-weighted images of the right striatum, leaving small sequelae in the head of the right caudate nucleus. NKH is an unusual cause of HH. The abnormalities seen in neuroimaging are rare, but seem to be quite specific to this syndrome. We give an update on current literature regarding the possible pathophysiological processes underlying this specific clinical entity.
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2/13. A case of Japanese encephalitis: CT and MRI findings in acute and convalescent stages.

    We studied the CT and MR images of a patient with Japanese encephalitis. The first symptom was general malaise with high fever. The diagnosis of meningoencephalitis was made by spinal tap and clinical presentation. CT on the third day of illness showed no significant findings. MRI on the fifth day of illness demonstrated that the left thalamus and bilateral putamen were hyperintense on T2-weighted images. On CT one month later, the density in the thalamus and bilateral putamen was normal. MRI two month later showed high signal intensity only in the left thalamus. The patient recovered, but was judged to have dementia according to the simple dementia scale of Hasegawa. Flaccid paralysis was observed during the acute period.
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3/13. Infantile acute encephalopathy with combined symmetrical hypodensities in the thalami and the putamen on computed tomography.

    An eight-month-old boy with clinical features of acute encephalopathy with symmetrical low-density areas in the thalami and the putamen on computed tomography is presented. These particular computed tomography features suggest potential aetiology common to acute encephalopathy with low-density areas in the thalami and infantile bilateral striatal necrosis with an acute onset. The therapeutic consideration of these conditions is also discussed.
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keywords = putamen
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4/13. Acute bilateral basal ganglia lesions in patients with diabetic uremia: an FDG-PET study.

    PURPOSE: head CT and MRI show characteristic changes in the syndrome of acute bilateral basal ganglia lesions in patients with diabetic uremia. However, they do not provide further insight into the underlying pathophysiology. To further clarify the biologic mechanism of the syndrome, F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) was used in 2 patients. methods: PET studies were performed in 2 diabetic uremic patients with acute movement disorders. The cerebral glucose metabolic rates in these 2 patients were compared with 11 normal age-matched controls. The images were further analyzed with statistical parametric mapping to identify regions of significant metabolic abnormality. RESULTS: The cases showed markedly reduced glucose metabolism in the bilateral basal ganglia, especially in the bilateral putamens, where the glucose uptake was nearly absent. CONCLUSIONS: FDG-PET correlates better with the clinical conditions and provides more pathophysiological information than head CT or MRI scans in bilateral basal ganglia lesions in patients with diabetic uremia. We propose that acute exacerbation of a long-term glucose utilization failure in the basal ganglia cells produced these lesions.
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5/13. Acute limbic encephalitis: a new entity?

    Clinical cases similar to herpes simplex virus (HSV) encephalitis have accumulated in japan. Detailed examinations have failed to demonstrate HSV infection. Recently, these cases have been named "non-herpetic acute limbic encephalitis". Only a single autopsy case was so far reported in an abstract form, because many cases showed a good prognosis. The case presented here was that following fever, a 59-year-old woman developed disturbance of consciousness and uncontrollable generalized seizures. brain MRI revealed abnormal signals in the bilateral medial temporal lobe and along the lateral part of the putamen. Autoantibody against the NMDA glutamate receptor (GluR) IgM-epsilon2 was detected in the serum, and the GluR IgG-delta2 antibody was positive in cerebrospinal fluid. She died 12 days after onset. An autopsy examination revealed scattered foci consisting of neuronal loss, neuronophagia and some perivascular lymphocytic infiltration in the hippocampus and amygdala, but no haemorrhagic necrosis in the brain. HSV-1, -2 and human herpes virus-6 were negative immunohistochemically. We believe that our autopsy case may contribute to understanding the neuropathological background of non-herpetic acute limbic encephalitis.
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6/13. Delayed choreoathetosis following acute carbon monoxide poisoning.

    Ten days after accidental exposure to carbon monoxide, a 17-year-old youth developed transitory choreoathetosis of both arms, face, and neck, with moderate dysarthria. CT revealed symmetric bilateral infarction in the head of the caudate nucleus, the putamen, and the small parts of the anterolateral globus pallidus.
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7/13. Hypertensive putaminal hemorrhage presenting with hemichorea.

    A progressive motor deficit primarily manifested by hemichorea developed in a 42-year-old hypertensive man. CT scan demonstrated contralateral putaminal hemorrhage. The patient's course was benign. Previous cases of acute hemichorea familiar to use and documented by CT scans have involved nonhemorrhagic lesions of either the putamen or caudate.
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keywords = putamen
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8/13. Cerebral metabolism in a case of multiple sclerosis with acute mental disorder.

    Acute mental disorder in early multiple sclerosis (MS) is rare and little is known about the structural and metabolic changes in this relation. We present an MS patient with discrete motor and sensory deficits, who developed severe behavioral changes over a period of nine months during the initial course of the disease. The cerebral metabolic rate of glucose (CMRglc) was measured using positron emission tomography (PET), and the patient underwent MRI as well as a comprehensive battery of neuropsychological tests. Significantly reduced values of CMRglc were found bilaterally in the frontal and temporal cortex, the putamen, the thalamus and the hippocampus. The MRI revealed progression of MS lesions in the frontal lobes during the development of mental symptoms. Neuropsychological examination showed wide spread cognitive dysfunction, and a pronounced frontal lobe syndrome. The study demonstrates the remote metabolic effects of lesions affecting subcortical neural connections in an MS patient with severe cognitive dysfunction.
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9/13. Suspected acute encephalopathy with symmetrical abnormal signal areas in the basal ganglia, thalamus, midbrain and pons diagnosed by magnetic resonance imaging.

    A 4-year-old boy was admitted with disturbed consciousness following a convulsion. He developed bilateral pyramidal tract signs and showed a decerebrate posture. Laboratory findings revealed severe liver dysfunction and disseminated intravascular coagulation. On the eighth day eight in hospital he developed parkinsonism. However, 5 months from onset he had recovered almost completely. brain CT on admission showed low density areas in the basal ganglia, thalamus, midbrain and pons. A T2-weighted scan in magnetic resonance imaging (MRI) showed almost symmetrical high signal intensities in both basal ganglia (including putamen, caudate nucleus, globus pallidus), external capsule, internal capsule thalamus, midbrain, pons and white matter of the peribasal ganglia; but a T1-weighted scan showed low signal intensities in the same regions during all phases. Therefore hemorrhagic lesions or the presence of thalamic methemoglobin were excluded. It was considered that the pathogenesis may be cytotoxic cellular edema due to cytotoxic agents or acute metabolic factors. Clinical presentation, laboratory findings and radiological findings were most suggestive of acute necrotizing encephalopathy. As differential diagnoses, acute disseminated encephalomyelitis and brainstem encephalitis were considered.
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keywords = putamen
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10/13. Acute hydrocephalus following carbon monoxide poisoning.

    Carbon monoxide remains a significant cause of poisoning in children. Cerebral edema is often the cause of significant morbidity and mortality in exposed children. While lesions of the basal ganglia have been well documented, the advent of neuroimaging has allowed antemortem demonstration of infarctions of the globus pallidus and putamen with carbon monoxide intoxication. Acute hydrocephalus following carbon monoxide poisoning has been a rare occurrence. We report a 2 year 6 month-old boy who, to our knowledge, represents the first reported case in which repeat computed tomography documented the evolution of hydrocephalus due to carbon monoxide exposure in a child.
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