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)

We reported a case of a 32-year-old female who had a transient mutism after resection of a malignant astrocytoma in the left frontal lobe. Preoperatively magnetic resonance (MR) imaging revealed a cystic tumor in the left frontal lobe. The patient underwent surgery. She was alert but did not speak immediately after surgery. She could follow verbal commands, comprehend written language, and write letters. She had no cranial nerve or extremity paresis. Seven days postoperatively, she began to say simple words, and one month postoperatively she could talk normally. Postoperative MR imaging revealed a hypointensity area on T1 weighted image in the frontal lobe including a part of the anterior cingulate cortex and the anterior part of the corpus callosum. It appears that a dominant hemisphere lesion of both the anterior cingulate cortex and the corpus callosum may be responsible for the development of postoperative mutism.
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PMID:[Transient mutism after resection of left frontal lobe astrocytoma in adult: case report]. 899 Apr 70

A 30-year-old female became comatose due to embolic occlusion of the basilar artery, caused by surgical injury to the origin of the vertebral artery during removal of a neurinoma in the upper thoracic paravertebral region. The basilar artery occlusion was treated by local fibrinolysis through a microcatheter. Two weeks later she recovered her consciousness but suffered mutism. Her speech disturbance was characterized by severe ataxic dysarthria known as "cerebellar mutism" but without cranial nerve paresis. The mutism gradually improved during the following 3 months. This is case of cerebellar mutism was apparently due to ischemic stroke. Disturbance by hypoperfusion of the cerebellum and brain stem may have been involved in the pathogenesis of cerebellar mutism.
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PMID:Cerebellar mutism after basilar artery occlusion--case report. 980 3

Among the numerous clinical syndromes observed after severe traumatic head injury, post-traumatic mutism is a disorder rarely reported in adults and not studied in any detail in children. We report seven children between the ages of 3 1/2 and 14 years who sustained severe head injury and developed post-traumatic mutism. We aim to give a precise clinical characterization of this disorder, discuss differential diagnosis and correlations with brain imaging and suggest its probable neurological substrate. After a coma lasting from 5 to 25 days, the seven patients who suffered from post-traumatic mutism went through a period of total absence of verbal production lasting from 5 to 94 days, associated with the recovery of non-verbal communication skills and emotional vocalization. During the first days after the recovery of speech, all patients were able to produce correct small sentences with a hypophonic and monotonous voice, moderate dysarthria, word finding difficulties but no signs of aphasia, and preserved oral comprehension. The neurological signs in the acute phase (III nerve paresis in three of seven patients, signs of autonomic dysfunctions in five of seven patients), the results of the brain imaging and the experimental animal data all suggest the involvement of mesencephalic structures as playing a key role in the aetiology of post-traumatic mutism.
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PMID:Post-traumatic mutism in children: clinical characteristics, pattern of recovery and clinicopathological correlations. 1072 32

A 26-year-old man, who had received a ventriculo-peritoneal shunt for obstructive hydrocephalus after possible encephalitis, complained of disturbance of upward gaze and difficulty in movement seven months after the shunt implantation. One month later, neurological examination revealed upward gaze paresis and rigidity of all four limbs, but the neuroimaging studies revealed no ventricular dilatation. His symptoms deteriorated, and tremor of the extremities appeared. He was admitted to our hospital 10 months after the shunt implantation. He developed akinetic mutism soon after admission. Cerebrospinal fluid protein was elevated (62 mg/dl). At that time, the shunt reservoir was found to be insufficiently filled, and neuroimaging showed dilatation of the lateral and third ventricles with no dilatation of the fourth ventricle. A neuroendoscopic third ventriculostomy with removal of the previous shunt system gradually resolved the parkinsonism within two months, and the patient became capable of walking. The dilatation of the ventricles improved on neuroimaging. The present report suggests that shunt malfunction should be suspected when parkinsonism occurs in patients who have undergone a shunt placement, even though hydrocephalus on neuroimaging is not observed.
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PMID:[A case of severe parkinsonism induced by failure of ventriculo-peritoneal shunt for aqueductal stenosis]. 1458 70


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