Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reported a rare case of cerebral infarction with somatoparaphrenia (SP) caused by involvement of the dominant cerebral hemisphere. The patient was 77-year-old right-handed woman who was noted to have atrial fibrillation, right hemiplegia, hemisensory disturbance and ipsilateral homonymous hemianopsia. Neuropsychologically, there were anosognosia (AG) for hemiplegia and SP arguing her hand as doctor's hand. In addition, there also were noted disorientation, right unilateral spatial neglect and mild amnestic aphasia. Brain CT and MRI demonstrated infarctions in the left lateral thalamus, internal capsule, lateral geniculate body, hippocampus, caudate nucleus and medial occipitotemporal gyrus. IMP-SPECT showed extensive hypoperfusion areas in the left cerebral hemisphere. These lesions were thought to have resulted from occlusion of the left anterior choroidal artery and partial occlusion of the left middle and posterior cerebral arteries caused by cardiogenic embolism. AG persisted and SP disappeared 80 days after the onset. While AG and SP are generally believed to be associated with non-dominant hemispherical lesion, the present case suggests the possibility that those symptoms were seen in the case of dominant hemispherical lesion without severe aphasia.
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PMID:[Somatoparaphrenia caused by the lesion in the dominant cerebral hemisphere--a case report]. 886 40

Fourteen children with congenital hemiplegia were studied with a detailed assessment of various aspects of vision (linear acuity, stereopsis, visual fields) and MRI. The aim of this study was to evaluate the effect of a congenital lesion on visual function. The results showed a very high incidence (78%) of children who had abnormal results on at least one of the visual tests. Visual abnormalities were not correlated with the clinical severity of hemiplegia or with a specific pattern of lesion on MRI. Similarly no constant association could be found between visual structures (optic radiations and primary visual cortex) and visual function. Finally, our results would suggest that all the children with congenital hemiplegia need to be investigated irrespective of the clinical severity or of the type or the extent of the lesion. This would help to identify children with minor visual abnormalities which can affect everyday life performance.
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PMID:Visual outcome in children with congenital hemiplegia: correlation with MRI findings. 889 66

Two cases of traumatic internal carotid artery occlusion probably related to the seat belt shoulder strap are reported. Case 1. A 20-year-old woman was driving and was struck on the right front side of her car by another car. There were neither bruises, abrasions on her neck, nor weakness in her extremities. About 4 hours later, she developed left hemiplegia, and CT scan taken on the following day revealed low density areas in the capsulostriatal area on the right. The right carotid angiography revealed occlusion of the internal carotid artery about 3 cm distal to the bifurcation. Case 2. A 43-year-old man was driving and was struck on the front of his car by a hard iron railing. He sustained a sternum fracture, but there was no disturbance of consciousness or paresis of the extremities. His neck was unremarkable externally. About 50 days later, he developed left hemiplegia. CT scan and MRI revealed a massive infarction in the distribution of the right middle cerebral artery territories. The carotid angiography revealed occlusion of the right internal carotid artery about 3 cm distal to the bifurcation. In each cases, the driver was wearing a three-point shoulder seatbelt when the car was struck on the front or on the right front. Previous experimental studies have revealed in these situations the neck is flexed right anteriorly, and then quickly overextended left posteriorly. The overextension of the neck probably injured the intima of the internal carotid artery ipsilateral to the shoulder fixed in the seatbelt, resulting in the subsequent occlusion by a thrombus.
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PMID:[Internal carotid artery occlusion related to seat belt shoulder strap: report of two cases]. 890 87

We report a case of Prader-Willi syndrome (PWS) complicated with juvenile stroke. The patient is a 19-year-old man with right hemiplegia, who has had a history of non-insulin-dependent diabetes mellitus (NIDDM) for ten years. The diagnosis of PWS was confirmed genetically by the method of fluorescence in situ hybridization which showed the deletion of chromosome 15. His brain MRI revealed abnormal signal intensities in the left basal ganglia and around the right trigone of the lateral ventricle. Angiographic examination showed occlusions of bilateral proximal middle cerebral arteries with basal moyamoya vessels. The left vertebral artery was also occluded at its origin. Only a few cases of PWS complicated with stroke have been reported before and, to date, there has been no case with arterial occlusion similar to our case. Though the cause of these arterial occlusions is unknown, it may be related to arteriosclerosis following NIDDM.
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PMID:[A case of Prader-Willi syndrome with bilateral middle cerebral artery occlusion and moyamoya phenomenon]. 893 99

The combination of pure motor hemiplegia and horizontal gaze palsy is a rare but identifiable lacunar syndrome. Among horizontal gaze palsies, one-and-a-half syndrome and abducens nerve palsy are reported to be associated with pure motor hemiplegia in pontine lacunar infarction. Although conjugate lateral gaze palsy is also hypothesized, pure motor hemiplegia with conjugate lateral gaze palsy has never been reported. We present a 75-year-old man who showed right hemiparesis and impaired left horizontal conjugate eyeball movement. Both the findings of the brain CT scan and those of the MRI study were consistent with a small infarction in the left midpontine tegmentum. Magnetic resonance angiography revealed no stenotic narrowing of the vertebrobasilar artery. Radiological findings suggested that pure motor hemiplegia with conjugate lateral gaze palsy, in our patient, might have been produced by the occlusion of a single penetrating branch of the basilar artery.
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PMID:Pure motor hemiplegia with conjugate lateral gaze palsy in pontine lacunar infarction. 896 15

A 39 year old caucasian man was admitted in 1994 to the neurological department with a left pure motor hemiplegia that appeared suddenly. This patient showed typical features of Werner's syndrome. He had a hoarse voice, a diffuse muscle weakness and atrophy in the upper and lower limbs with chronic ulcers on the legs. His scalp and public hair were sparse. Cranial MRI revealed several lesions in the white matter, low signal intensity on T1 weighted images and high signal on T2 weighted images. Cerebrospinal fluid (CSF was inflammatory with hypercytosis and proteinorachia was 0.50 g/l with synthesis of IgG. Sural nerve biopsy revealed muscle atrophy and the loss of myelinated fibers. Thus, central and peripheral nervous systems were affected in this case.
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PMID:[Neurologic complications in a case of Werner syndrome]. 903 57

The acute pathophysiologic changes during hemiplegic spells and the long-term outcome of alternating hemiplegia remain obscure. In a 41-year-old male with familial alternating hemiplegia we found an increase in right frontal cerebral blood flow 3 h into a 5-h left hemiplegic episode. A repeat high-resolution brain SPECT study performed 26 h after the resolution of the left hemiplegia revealed normalization of the frontal blood flow accompanied by hyperperfusion in the right parietal lobe. An interictal SPECT scan several weeks later showed no asymmetries. Head CT and MRI scans were negative. Neuropsychologic assessment and neurologic examination revealed evidence of a diffuse disorder which predominantly involved the right hemisphere. To our knowledge, there are no previous correlative studies of serial high-resolution brain SPECT with MRI, or of detailed neuropsychologic assessment, in adult patients with such an advanced course of alternating hemiplegia of childhood.
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PMID:Focal brain dysfunction in a 41-year old man with familial alternating hemiplegia. 908 4

We examined a patient with alternating hemiplegia of childhood (AHC) who had over a 23-year history of AHC to investigate the origin of the neurological deterioration with increasing age. Hemiplegic attacks had occurred consistently at a frequency of a few per week since infancy, and he first experienced attacks of cerebellar ataxia at the age of 23 years. Intellectual impairment, dysarthria, dystonic posturing, and a wide-based gait had been slowly progressive, but they had been stable since he turned twenty. The electromyographic response to transcranial magnetic stimulation was normal between attacks and showed reversible alteration during an attack. MRI revealed slight dilatation of the lateral ventricles, and MR angiography showed normal cerebral blood flow. Proton MR spectroscopy between attacks showed normal peak area ratios for N-acetyl groups, choline-containing compounds, and creatine and phosphocreatine, and it also demonstrated no lactic peak. 123I-IMP SPECT between attacks demonstrated diffuse cerebral hypoperfusion despite no evidence of ischemic change in the above MR study. These results suggest that the slowly progressive neurological deficits are due to the primary underlying pathology rather than the secondary neuronal loss as a result of frequent ischemic attacks.
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PMID:Alternating hemiplegia of childhood: report of a case having a long history. 913 95

We reported five patients having presented only with clumsy hand and dysarthria which resulted from motor paresis confined to one side of the fingers and the ipsilateral face and tongue. All of them were right-handed, and their manifestation was transient. They had no abnormalities of muscle tonus and sensation, and no ataxia. The features of these cases differed from those of the dysarthria-clumsy hand syndrome because of absence of ataxia, and could be distinguished from pure motor hemiplegia by a motor paresis with cheiro-oral topography. MRI examinations showed a localized lesion at the border between internal capsule and corona radiata (two cases), or in the corona radiata just over this region (three cases). In the former cases in which the internal capsule was involved, we confirmed the lesion in the genu and anterior half of the posterior limb of the internal capsule. The lesion was on the left side in all five patients. It has been known that the pyramidal tract consists of the large and small fibers. The large ones are localized in the posterior part of the posterior limb of the internal capsule, and the damage of them produces sustained and serious motor paralysis. The small ones are widely distributed in the genu and the posterior limb of the internal capsule. The findings of our study suggest that the small fibers have adjacent somatotopy for the hand and mouth in the region of the genu and the anterior part of the posterior limb of the internal capsule, and that the damage of them may lead to mild, transient motor paresis without spasticity.
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PMID:[Motor paresis with cheiro-oral topography due to small infarct in the internal capsule or the corona radiata]. 914 66

Twenty-three infants with an infarct in the territory of the middle cerebral artery are reported. The diagnosis was made using cranial ultrasound in all, confirmed on postmortem in two cases and on MRI, performed during the neonatal period or in infancy, in 18 of the 20 survivors. Involvement of the main branch was present in 7 cases and three of these had a gestational age of less than 35 weeks. In the other 16 infants, involvement of a cortical branch or one or more of the lenticulostriate branches was present and all but three of these had a gestational age of 34 weeks or less. While involvement of the main branch was usually diagnosed on postnatal day 1 or 2 using ultrasound, involvement of the lenticulostriate branches was noted as a wedgeshaped echogenic lesion in the caudate nucleus, thalamus or putamen, between day 4 up till day 24, and at term age in one of the cases. Neurodevelopmental outcome of those with involvement of the main branch was disappointing as all survivors developed a hemiplegia, associated with epilepsy in two; while so far only three of the other 16 infants developed cerebral palsy, one a hemiplegia and one athetoid cerebral palsy. Global delay was present in a further three cases. Infarcts in the region of the middle cerebral artery can occur in both preterm as well as fullterm infants. Involvement of the main branch also occurred in infants with a gestational age below 35 weeks and resulted in the development of a hemiplegia in all survivors. Involvement of one of the other branches was especially common in preterm infants, who had a more favourable outcome. As the lesion in the latter group was usually not present before the end of the first week, serial ultrasound up till term age is needed in order to identify these lesions.
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PMID:Infarcts in the vascular distribution of the middle cerebral artery in preterm and fullterm infants. 920 8


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