Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 12-year-old boy was admitted to our hospital in May 1990. Since two years previously, he became restless and could not adapt himself to his new school mates and teacher. He came to refuse going to school, and his intellectual performance rapidly deteriorated, thereafter. During the following two years, he gradually became mutic and incontinent with dystonic involuntary movements, and was admitted to our hospital. Examination revealed melanoderma, mutism, dementia and grossly normal visual and auditory system except for bilateral optic atrophy. Volitional movements were severely limited because of marked truncal and extreme dystonia and spastic paresis. Urinary 17-KS and 17-OHCS were decreased. Serum cortisol did not increase normally on rapid ACTH test. Very-long-chain fatty acids in serum were increased. Serial CTs and MRI demonstrated marked ventricular dilatation and diffuse white-matter lesions involving the frontal lobes, corpus callosum, internal capsules, and less markedly parieto-occipital regions with slight calcification in the optic radiations. Those in the frontal lobes had been visualised in CTs taken 18 months after the onset. School refusal, the initial symptoms of the patient, is one of serious socioeducational problems in Japan. While the majority of children with school refusal might be of non-organic affections, those with apparent mental deterioration and behavioral abnormalities should undergo non-invasive CT or MRI evaluation during the early stage of the disorder. And if diffuse white matter lesions is suggested even in the frontal lobe, the possibility of adrenoleuko-dystrophy should be considered.
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PMID:[A case of adrenoleukodystrophy having progressed from the frontal lobes]. 142 38

During the period from January 1st 1983 up to the end of April 1989 in the Neurology Department and the Neurosurgery Department 1417 patients were treated due to subarachnoidal hemorrhage. Among these patients in 275 cases the inner hydrocephalus was diagnosed using computer tomography (19.4%). In 17 cases (6.2%) hydrocephalus was treated surgically. In all patients the ventricle-atrial Pudenz valve was implanted; in 15 patients the valve was implanted for low pressure and in 2 for moderate pressure. The diagnostics was based on the computed tomography and angiography of cerebral vessels. In all cases large hydrocephalus was diagnosed (the anterior horn index in the computed tomography was below 3.0). The most frequent clinical symptoms were: urine incontinence (15 cases), disturbances of orientation (8 cases), akinetic mutism (8 cases) and paresis of extremities (7 cases). Above symptoms together with radiologic image presented indication for the valve implantation. Very good and good results were obtained in 13 patients, bad results in 2 cases, 2 patients died. Longer observation showed that 6 patients remain in satisfactory state, 3 patients are in bad state and 3 others died.
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PMID:[Immediate and late results of surgical treatment of hydrocephalus after subarachnoid hemorrhage]. 208 43

Acute mutism with paralysis of the bulbar and facial muscles following discrete bilateral internal capsular infarction is a rare stroke syndrome. We describe a 62 year-old male who suddenly became unable to speak or swallow. The paucity of facial expression and inability to voluntarily move the facial, lingual and pharyngeal muscles were persistent and contrasted with a relatively mild limb paresis which recovered. High resolution CT scan revealed infarcts in the posterior limbs of both internal capsules. It is important to recognise this stroke syndrome because of the permanence of dysarthria and dysphagia associated with it.
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PMID:Persistent mutism and dysphagia of acute onset due to bilateral internal capsule infarction. 239 43

Locked-in Syndrome (LIS) is a rare clinical entity consisting of quadriplegia, paralysis of lower cranial nerves, mutism, and bilateral paresis of horizontal gaze. The prognosis is usually poor. Most patients who do survive have severe residual impairment or develop chronic LIS. Review of the literature shows that recovery has been reported but not systematically studied, particularly with respect to early prognostic signs. We report a case of LIS with bilateral pontine infarctions shown by MRI. Severe neurological deficits included quadriplegia, paresis of horizontal gaze, facial paralysis, and bulbar palsy. Horizontal eye movements were present and smooth by the second week after onset. The patient had almost full functional motor recovery within four months, after a comprehensive rehabilitation program. Fourteen other reported cases of LIS with full recovery had documented recovery of lateral gaze in the early stage. In addition, smooth horizontal gaze is the most frequent activity in incomplete LIS. Early recovery of horizontal eye movement may indicate that the brain lesion is limited and may be a good prognostic sign in LIS.
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PMID:Early smooth horizontal eye movement: a favorable prognostic sign in patients with locked-in syndrome. 292 43

The best-known example of motor deficits after cortical lesions is contralateral paresis and spasticity after damage to the precentral motor strip. After recovery the residual motor functions can be used in a purposive and skillful manner. In patients with lesions of the supplementary motor area (SMA) and cingulate gyrus transient akinesia and mutism have been described. Lesions restricted to more lateral parts of the premotor field interfere with proximal muscle function and interlimb coordination, whereas distal motor activity and bimanual coordination are unimpaired. In contrast, hand function in patients with parietal lesions is severely disturbed. This dysfunction includes deficits such as ataxia, dysmetria and postural instability that are typically observed in deafferented patients. Severe disturbances of the purposive behaviour of the hand during exploratory finger movements and manipulation of objects are seen in patients with posterior parietal lesions. Observations in human patients are compatible with the hypothesis that lesions of the frontal agranular motor fields interfere with the control of postural and force control whereas parietal lesions are associated with motor programme disorders affecting the use of the hand or the eye as a sense organ or affecting more complex motor behaviour.
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PMID:Differential effects of cortical lesions in humans. 332 19

A case of mutism due to left hemisphere infarction is described. Recovery revealed mild motor dysphasia. Review of the literature showed that the case resembles aphemia but is unique by virtue of its duration, and the absence of associated apraxia and paresis.
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PMID:Mutism following left hemisphere infarction. 621 Mar 46

Three patients, who subsequently developed the locked-in state characterised by quadriplegia and mutism with an alert sensorium, initially had mild dysarthria and uncrossed hemisensory or hemimotor deficits involving the face and ipsilateral extremities. Case one initially mimicked a left cerebral lesion with right hemisensory deficits, a mild right facial paresis and a right homonymous field deficit. Case two initially developed both left hemimotor and hemisensory deficits and later developed a paresis of right conjugate gaze. Case three presented with left hemimotor deficit, and mild paresis of conjugate gaze to the right. All three patients died. Rostral brainstem infarctions were found at necropsy in cases one and two. Case three had a radiolucent area of the brainstem demonstrated by CT Scan. Hemisensory and hemimotor deficits also have been noted to precede reported cases of pontine infarction with the locked-in state. Acute onset of uncrossed hemisensory and hemimotor deficits with dysarthria may be caused by infarction of the pons which may predispose to the locked-in state.
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PMID:Premonitory symptoms of stroke in evolution to the locked-in state. 684 29

Five patients were examined suffering from bilateral paramedian thalamic infarction, caused by occlusion of the posterior paramedian thalamo-subthalamic arteries, when they begin from one single pedicle. All cases began with obnubilation or transitory coma, followed by hypersomnia. Four patients showed vertical gaze paralysis, and the fifth vertical nystagmus. In three cases, nuclear lesion of the III cranial nerve was observed along with alteration of the photomotor reflexes, and there was miosis in one case. All were suffering from weakness in one or another limb or facial paresis and generalised acute hypotonia: only one patient had hemihypostesia. All five had dysarthria, ataxy and dysmetria, one had asterixis and two spasmodic crying. Between 5 and 12 months later, one had akinetic mutism and vertical gaze paralysis as the most noteworthy signs. The neuroradiological images show a bilateral ischemic lesion in the paramedian thalamic region, which extends in some cases to the anterior nucleus and in one case to the pulvinars; the lesion continues through the subthalamic regions and the medial part of the mesencephalic tegmentum, with a clear extension to the medial region of the cerebral peduncles in three cases and to the tectum in one case.
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PMID:[Paramedian bithalamic infarct syndrome: report of five new cases]. 749 75

We report a 57-year-old woman with progressive gait disturbance, headache, character change, convulsion and coma. She was well until 55 years of age, when she noted an onset of unsteady gait. At times she experienced transient weakness in her right hand, which was followed some difficulty in articulation. She was admitted to our service for the work up on April 6, 1992. Neurologic examination at that time revealed an alert Japanese lady in no acute distress. She was oriented to all spheres, however, she was somewhat bradyphrenic and had some disturbance in recent memory. Higher cerebral functions appeared intact. The visual acuity and visual fields were normal as were the optic fundi. Pupils were round and isocoric reacting promptly to light. Ocular movement was full, however, horizontal nystagmus was noted upon right lateral gaze. The sensation of the face was intact. She showed right facial paresis of the central type. Hearing was intact. She showed slurred speech and some difficulty in swallowing. The tongue was deviated to the right. Her gait was wide based and unsteady; tandem gait was difficult, however, walking on toes and on heels were performed well. No cerebellar ataxia was noted, but she showed some clumsiness in her right hand. Deep reflexes were symmetric and normally reactive; plantar response was extensor bilaterally. Sensation was intact; no meningeal sign was elicited. Routine laboratory work up was unremarkable; the CSF was under a borderline pressure (180 mmH2O) and contained 39 mg/dl of protein and 59 mg/dl of sugar. Cranial CT scan revealed diffuse low density areas involving bilateral cerebral white matter as well as the brain stem; MRI revealed high signal intensity lesions in those areas; gadolinium enhancement was negative; cortical sulci were effaced and the anterior part of the left lateral ventricle was compressed without deviation of the midline structure. The patient was treated with steroid pulse therapy without effect. She was discharged for out patient follow up, however, she developed a convulsion which was followed by loss of consciousness, and was admitted again to our service. She had never gained consciousness after this episode, and remained in the state of akinetic mutism. Follow-up CT and MRI did not show much change, although the area of high signal density lesions slightly enlarged on June 1, 1993. Her clinical course was complicated by drug induced bone marrow suppression and nephrotic syndrome. She expired on September 8, 1993 after developing sudden drop of blood pressure and bradycardia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 57-year-old woman with gait disturbance, headache, character change, convulsion, and coma]. 761 89

We report a 70-year-old man who had a sudden onset of right hemiparesis and mutism. The lower extremity was more involved than the upper one. He had a long history of diabetes and chronic renal failure for which hemodialysis was necessary. On August 30, 1990, he had an sudden onset of right hemiparesis and mutism. Neurological examination revealed awake but mute in no acute distress. He could only respond to very simple commands such as opening his mouth or protruding his tongue. He did not appear to understand more difficult questions. In addition, he could not answer verbally. He was totally mute. Cranial nerves appeared intact except for slight right central facial paresis and severe diabetic retinopathy. He had complete paralysis of his right leg and a moderate weakness in his right upper extremity. Deep reflexes were diminished in both upper extremities and absent in the lower limbs. Frotal signs such as grasp and snout reflexes were present. Cranial CT scans revealed an ill-defined low density area in the left parasagittal subcortical area and a part of the anterior cerebral artery territory. The supplementary motor area appeared at least in part to be involved. He was treated with glycerol and other supportive cares, however, his clinical course was complicated by pneumonia, heart failure, septicemia, and he expired two months after his stroke. The patient was discussed in a neurological CPC, and the chief discussant arrived at a conclusion that he had an artery-to-artery embolism at the internal carotid bifurcation resulting in the cerebral infarction mainly in the territory of the anterior cerebral artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 70-year-old man with right hemiparesis and mutism]. 836 54


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