Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 74-year-old man was admitted to our hospital with abrupt onset of hemichorea-hemiballism in the left arm and leg. On admission, the blood glucose level was 296 mg/dl, glycosylated hemoglobin Alc was 17.0%, and the serum osmolality was 296 mOsm/l. Urinalysis was negative for ketone bodies, but was strongly positive for glucose. After normalization of the blood glucose level, ballistic movement disappeared, but choreiform movement of the left arm and leg continued for 10 months. Brain CT showed a slight high density of the right putamen, which disappeared on 37th day after the onset. MRI showed high intensity on T1-weighted images and low intensity on T2-weighted images in the right putamen, which disappeared 10 months after the onset. SPECT on the 21th day after the onset showed hyperperfusion in the right putamen. 4 months later, the blood flow slightly reduced in the right putamen. The abnormality in the right putamen was considered to be the cause of his involuntary movements. High intensity in the putamen on T1-weighted MR images in the present case are presumed to have developed following mild ischemia and the reversible deposition of calcium or other material which occurred in association with nonketotic hyperglycemia.
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PMID:[Hemichorea-hemiballism associated with nonketotic hyperglycemia and presenting with unilateral hyperintensity of the putamen on MRI T1-weighted images--a case report]. 760 83

We report two diabetic patients with hemichorea-hemiballism associated with striatal lesions detected by MRI. Case 1 was a 57-year-old woman. On May 5, 1990, hemichorea-hemiballism of the right upper extremity developed suddenly. The blood glucose level at the time of onset was 695 mg/dl. Plain cranial CT scanning revealed a small high-density lesion in the left putamen. On MRI, this lesion showed a high signal intensity on T1-weighted images, while it showed as an irregular low-intensity area on T2-weighted images. Three and a half months later, the high intensity lesion on MRI decreased gradually and almost disappeared. Case 2 was a 68-year-old woman. In late August 1992, hemichorea-hemiballism of the right upper and lower extremities developed suddenly. The blood glucose level at the time of onset was 365 mg/dl. Plain cranial CT scanning was normal. MRI revealed a high signal intensity lesion involving the left putamen, globus pallidus and head of the caudate nucleus on T1-weighted images, while the lesion was almost isointense on T2-weighted images. The high-intensity lesion on MRI thereafter decreased gradually and disappeared almost completely one year after the onset. It is characteristic that the lesions responsible for hemichorea-hemiballism showed high-intensity areas on T1-weighted MRI in these two diabetics. In the hyperglycemic state, the Krebs cycle is inhibited and GABA is utilized as an energy source. The possibility has been suggested that striatal ischemia is likely to occur in diabetics because the GABA content of the corpus striatum is decreased by hyperglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two diabetics with hemichorea-hemiballism and striatal lesions]. 766 16

Stroke-related nonepileptic transient dyskinesias are rare, and the site of ischemia remains often undetermined. Five cases out of 47 consecutive thalamic infarcts (10.6 per cent) are reported. Patients presented with monochorea (1 case), hemiballism-hemichorea (2 cases), choreoathetosis (1 case with subsequent arm painful dystonia and hand tremor), and asterixis (1 case). Magnetic resonance imaging demonstrated that the subthalamic nucleus was spared in all cases. Transient dyskinesias occurred at any time in the course of infarction (as a warning sign in 1 case, as an associated symptom in 3 cases, or during recovery in 1 case). Moreover, this study suggests that: 1) transient dyskinesias are mainly related to thalamic ischemic injury, and 2) small vessels disease is the main etiology.
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PMID:[Transient involuntary movement disorders and thalamic infarction]. 830 59

Four patients presented with hemiballism-hemichorea as a clinical manifestation of white matter ischemia. These patients illustrate "positive" motor phenomena rather than limb weakness as a consequence of cerebral ischemia. In each patient, the involuntary movements disappeared following worsening of paresis. Subcortical white matter infarction in three patients and hemodynamic hypo-perfusion in the cerebral hemisphere contralateral to dyskinetic movements were possible causes. Neuroradiologically, none had pathological changes in the vicinity of the subthalamic nucleus. We presume from these observations that ischemia of the subcortical white matter, without involvement of the basal ganglia or the subthalamic nucleus, may cause hemiballism-hemichorea.
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PMID:Hemiballism-hemichorea induced by subcortical ischemia. 831 49

Hemiballism and hemichorea following anesthesia-induced hypotension has rarely been described, but a recent case suggests an association. After experiencing marked hypotension during spinal anesthesia, a 70-year-old woman developed hemiballism and hemichorea. Involuntary ballistic movements with writhing, consisting of repetitive rotation and flexion-extension without apparent muscle weakness, affected her left limbs proximally. Low-amplitude, involuntary, choreiform movements involved the distal portions of these limbs. Magnetic resonance imaging demonstrated an area of high signal intensity in the contralateral subthalamic nucleus, suggestive of a focal ischemic lesion. Although such occurrences are rare, anesthesiologists should be aware of the risk of subthalamic nucleus ischemia following marked hypotension.
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PMID:Hemiballism-hemichorea from marked hypotension during spinal anesthesia. 952 38

A series of six patients with movement disorders associated with cerebral arteriovenous malformations (AVM) is reported. The AVMs were classified according to the Spetzler-Martin classification as grade V (one patient), grade IV (four patients), and as grade III (one patient). One patient had action-induced hemidystonia caused by a contralateral frontoparietal AVM which compressed the putamen and was supplied partially by enlarged lenticulostriate arteries. Two patients presented with unilateral cortical tremor associated with contralateral high-frontal cortical/subcortical AVMs sparing the basal ganglia. Another patient developed hemidystonia and hemichorea-hemiballism after bleeding of a contralateral temporooccipital AVM and subsequent ischemia. Two patients had focal dystonia after thalamic and basal ganglia hemorrhage from AVMs. Five patients were operated on. The movement disorder was abolished in one patient postoperatively. Different mechanisms were identified that are relevant for the development of AVM-related movement disorders: mass effect, diaschisis, local parenchymal altered cerebral blood flow, and hemorrhagic or ischemic structural lesions.
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PMID:Cerebral arteriovenous malformations and movement disorders. 1046 3

A 72-year-old man presented with paroxysmal and transient involuntary movements, or "limb shaking". The attacks occurred alternately from one side of the body to the other and ceased spontaneously. Surface EMG study showed synchronous grouping discharges in multiple limb muscles, being compatible with hemiballism-hemichorea. Cerebral angiography demonstrated marked stenosis of the bilateral internal carotid arteries. Bilateral carotid endarterectomy led to complete disappearance of the involuntary movements. Alternating paroxysmal hemiballismhemichorea might be a transient ischemic attack, and alternating striatal dysfunction induced by cerebral hemodynamic or microembolic ischemia probably plays a central role in the occurrence of such involuntary movements.
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PMID:Alternating paroxysmal hemiballism-hemichorea in bilateral internal carotid artery stenosis. 1151 31

A 54-year-old woman presented choreic movements in left face and extremities for three months. Cerebral angiography revealed occlusions of bilateral internal carotid arteries (right: after the furcation of posterior communicating artery; left: after the furcation of opthalmic artery) and net-like collaterals around the basal ganglia region (Moyamoya vessels). Haloperidol rapidly resolved the choreic movements and no recurrence was observed. PET demonstrated misery perfusion at bilateral temporo-parietal cortices. Especially, right peri-sylvian region showed the most severe ischemia. MRI demonstrated no infarcts. Therefore, ischemia of the right striatum was suspected to be the cause of the left-sided hemichorea. Previously, Moyamoya disease presenting chorea was infrequently reported in young people of less than 20 years of age. This is the first report of the aged patient of Moyamoya disease presenting with hemichorea and severe misery perfusion.
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PMID:[An adult case of Moyamoya disease presenting with transient hemichorea]. 1235 53

In 1998 some patients with hyperglycemia-related hemichorea-hemiballism have been reported with a hyperintense putamen on T1-weighted MR images, presumably resulting from petechial hemorrhage. I questioned this explanation from my experience because (1) the areas of hyperintense lesions and their time evolutions did not match with those of the high density lesions on CT, (2) these hyperintense lesions persisted for years, and (3) the hyperintense lesions extended inferiorly to the midbrain. Therefore, a biopsy was performed in one patient and disclosed a fragment of gliotic brain tissue with abundant gemistocytes, which I proposed was sufficient to explain the shortening of T1 relaxation time. In addition, because two of our patients were associated with cortical infarcts and without hyperglycemia, I have suggested that cerebral ischemia might be a more important cause. In 1999 Fujioka et al reproduced the MR finding in animals 7 days after 15-minute occlusion of the middle cerebral artery. Therefore, both studies have suggested that the MRI finding resulted from a progressive pathological reaction in an incomplete infarction. In 2003 Fujioka et al further reported that the hyperintensity on T1-weighted MR images after mild ischemia may involve a paramagnetic effect resulting from tissue manganese accumulation in reactive astrocytes.
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PMID:Hemichorea-hemiballism associated with hyperintense putamen on T1-weighted MR images: an update and a hypothesis. 1566 92

Dyskinesias are infrequent presentations in acute stroke (1%). They can be found more frequently as delayed presentations after a stroke, but the prevalence is not available from the literature. The full spectrum of hyper- and hypo-akinetic syndromes has been described, but three main pictures are rather specific of an acute stroke: limb shaking, hemichorea-hemiballism and unilateral asterixis. Besides limb shaking, that seems to reflect a transient diffuse ischemia of the frontosubcortical motor pathway, lesions are described at all levels of the frontosubcortical motor circuit including the sensorimotor frontoparietal cortex, the striatum, the pallidum, the thalamic nuclei, the subthalamic nucleus, the substantia nigra, the cerebellum, the brainstem and their interconnecting pathways, as ischemic or hemorrhagic strokes. The preferentially late development of dyskinesia could reflect the return to a more ancestral motor control level, the most functional possible with the remaining configuration of structures, elaborated by brain plasticity after stroke.
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PMID:[Movement disorders in stroke]. 1876 Apr 32


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