Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 14-year-old boy developed mutism 24 h after the removal of a vermian low-grade astrocytoma. The mutism was not accompanied by long tract signs or cranial nerve palsies. He started to regain his speech 3 weeks postoperatively, and 4 months after the operation he was minimally dysarthric. Seven similar cases of transient muteness following cerebellar operations and not accompanied by long tract signs or cranial nerve palsies have been reported in the literature. In most of them there was delayed postoperative onset of the mutism. In all patients the recovery of speech started to appear 2 weeks to 3 months postoperatively and passed through a dysarthric phase. The absence of long tract or other brain stem signs, together with the presence of dysarthria during the recovery of speech, suggests a cerebellar cause for the transient muteness.
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PMID:Transient mutism following removal of a cerebellar tumor. A case report and review of the literature. 264 39

A 43 year-old woman suffered a cardio-circulatory arrest with a post-anoxic coma during 24 hours. This was followed by and akinetic-hypertonic syndrome. There was also dystonia of both hands and of right big toe. After and initial mutism, the patient spoke with dysarthria, a monotonous weak voice of poor timbre and low vocal volume. She had in addition mood disturbances with indifference to her condition and compulsive activity. Extrapyramidal syndromes after ischemic anoxia are rare, when compared to their relative frequency after carbon monoxide poisoning. Early CT scan with contrast can identify symmetrical and bilateral lenticulocaudal high densities and MRI is also useful for the diagnosis.
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PMID:[Extrapyramidal syndrome after cardiocirculatory incompetence]. 274 Jun 88

A case is presented of a 13-year-old right-handed male who exhibited bilateral striato-capsular lesions following an episode of cerebral anoxia and a range of clinical features typical of aphemia. The findings of a neurological assessment, neuroradiological assessment and battery of speech/language tests are described and their implications for current theories regarding the role of the basal ganglia in speech/language function discussed. The patient initially demonstrated an isolated loss of the ability to articulate words without the loss of the ability to write or comprehend spoken language. His initial mutism later resolved into a dysarthria with features similar to those seen in hypokinetic dysarthria. It was concluded that striato-capsular lesions in childhood are capable of producing temporary language disturbances and in some cases a persistent dysarthria.
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PMID:Aphemia associated with bilateral striato-capsular lesions subsequent to cerebral anoxia. 292 38

A case of toxic leucoencephalopathy induced by 5 FU derivatives is reported. A 46-year-old woman was diagnosed as having breast cancer, and radical mastectomy was performed on May, 1982. After operation, she was given irradiation and 5FU derivative (tegafur or carmofur) 600 mg and Nolvadex 20 mg (tamoxifen citrate) were administered every day. After taking the medication for a month, she began to stagger and developed a tremor in both arms. She was admitted to our hospital on August 16, because she showed evidence of dysarthria and memory disturbance in addition to her initial complaints. Soon after admission, she developed akinetic mutism, and metastasis in the brain stem was suspected. In spite of her severe condition, she was given radiation over the posterior fossa and continued the medication. On September 22, CT disclosed low density area in the centrum semiovale bilaterally. She died of DIC on November 30. An autopsy was performed. The brain weight was 1110 g and the outer surface of the brain was normal. In frontal cut surfaces stained with K.B., bilateral degeneration of the centrum semiovale was apparent. Microscopically, the degree of myelin degeneration was stronger than that of axon, and numerous fatty granular cells were found in the degenerated area. There were no bizarre shaped astrocytes, inclusion body or cellular infiltration. Fibrillary gliosis was scanty. No metastasis was found in the central nervous system or other organs. Based on these pathological findings and clinical history, toxic leucoencephalopathy induced by 5 FU derivatives was suggested.
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PMID:[A case of toxic leucoencephalopathy induced by 5FU derivatives]. 393 66

We studied 30 necropsy cases of vascular dementia with a lacunar state. Manifestations included dementia, lack of volition, emotional lability, small-stepped gait, dysarthria, urinary incontinence, grasp reflex, pyramidal signs, paraplegia in flexion, and akinetic mutism. Pathologically, there was diffuse incomplete softening of white matter in all cases. Both lacunes and diffuse softening were found predominantly in the frontal lobes. The prominent clinical features were therefore frontal lobe symptoms, with good correlation between the symptoms and the distribution of pathologic lesions.
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PMID:Why do frontal lobe symptoms predominate in vascular dementia with lacunes? 395

Neurological examinations were made of 67 children and adults with congenital iodine-deficiency disorder (endemic cretinism) in four rural villages in highland Ecuador. There was a distinct and readily identifiable pattern of neurological deficits. These included, to varying degrees: deaf-mutism or lesser degrees of bilateral hearing-loss or dysarthria; spasticity, particularly involving the proximal lower extremities; mental deficiency of a characteristic type; and rigidity and bradykinesia. Not all of these elements were found in all cases. Less common features were strabismus, kyphoscoliosis and frontal-lobe signs. There were exceptional cases with hypotonia. In contrast, cerebellar function was largely spared, as were functions of emotion and attention, vegetative and autonomic functions, social interaction, and probably memory, except in the most severely involved.
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PMID:Neurological signs in congenital iodine-deficiency disorder (endemic cretinism). 401 26

Two young patients are described who made good recoveries from a "locked-in" syndrome presumed to be due to ventral pontine ischemia. The first patient recovered completely from quadriplegia and mutism. In the second patient the only permanent sequellae were slight dysarthria and mild spasticity. Since patients may recover nearly completely from a "locked-in" syndrome, aggressive supportive therapy seems justified during the initial weeks or months.
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PMID:Reversible "locked-in" syndromes. 404 98

We studied a case of language loss caused by an acquired vascular lesion in the putamen, anterior limb of the internal capsule, and lateral aspect of the head of the caudate nucleus in a 7-year-old right-handed girl. Acute right-sided hemiplegia, mutism, oral apraxia, and disturbance in language comprehension but no dysarthria were present. During recovery, a nonfluent aphasia with anomia was evident. After six months, only mild hemiparesis and minor spelling difficulties persisted. We compared this patient with an 11-year-old right-handed girl with right-sided hemiparesis and dysarthria but no language loss following a lesion in the globus pallidus, a portion of the posterior limb of the internal capsule, and the body of the caudate. The presence of a language disturbance in the first but not the second patient was attributed to the difference in lesion location. The symptoms and lesions were similar to those in recent reports of adult patients. To our knowledge, this is the first report of these findings in a child with a left-hemisphere lesion.
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PMID:Acquired capsular/striatal aphasia in childhood. 619 70

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


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