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)

The cases presented with psychic troubles and repeated somnolence episodes accompanied by dysarthria in 5 cases, myoclonic jerks in 4 cases and epileptic seizures in 1 case. In all cases the EEG was disturbed. It showed symetrical, paroxystic, bilateral, monomorph slow activity with more or less frequent paroxysms. The average serum aluminium level was at 407 microgram/l in the acute phase, at 161 microgram/l in the remission phase and at 123 microgram/l three months later. After interruption of oral and dialytic aluminium intake the remission is maintained. However in 2 cases the transitory readministration of aluminium gel was followed by reversible recurrency. The role of both aluminium gel and dialysate aluminium as the origin of encephalopathy is discussed.
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PMID:[Reversible dialytic encephalopathy after interruption of aluminium intake. 6 cases (author's transl)]. 49 78

A case of hypertensive intracerebellar hematoma surgically treated and cured was reported. The 41-year-old male had two cerebrovascular attacks with headache and vomiting followed by left hemiparesis. Drowsiness and dysarthria appeared the next day. The patient was admitted to a hospital, where right facial palsy, loss of right gag reflex and paralytic hemiplegia on the left side were noted. On the 7th day, the patient's consciousness became clear byt the other neurological evidences did not change. On the 14th day, bradycardia and central hyperventilation appeared and he became drowsy again. The patient was transferred to the authors' clinic. When the patient was admitted, he showed typical cerebellar signs such as nystagmus, ataxia, and slurring speech with pyramidal sign on left side and cranial nerves paralysis on right side, and also showed the changes of vital signs as a medullary syndrome in the late stage of the course. The vertebral angiogram revealed a space taking process in the right cerebellar hemisphere. The old blood (30g) was removed by suboccipital craniectomy. The hematoma cavity had a communication with the IVth ventricle through a small perforation in the medial wall of the hematoma. Spontaneour intracerebellar hematoma including of hypertensive origin is not rare in the reports of autopsy but surgically treated case has only rarely been reported. The main reason of few survivals should be in its fulminate course.
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PMID:[A cured case of hypertensive intracerebellar hematoma (author's transl)]. 94 80

A 48-year-old man, who took by mistake a sip of ointment containing dichloroethane, survived, and showed a course of two phases of toxic symptoms. After an initial narcosis and an interval with few pathological symptoms seizures, myoclonia and somnolence occurred. Irreversible final disturbances were lasting mental defects, cerebellar dysarthria, ataxia, and hydrocephalus. Concomitant diseases were acute liver dystrophy, nephropathy, and anemia. The clinical picture of dichoroethane posoning is outlines, the pathogenesis of this particular cerebral lesion described, and the therapy discussed.
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PMID:[Dichloroethane poisoning with myoclonic syndrome, seizures and irreversible cerebral defects (author's transl)]. 122 Jun 46

Four siblings aged 12-18 years with progressive myoclonus epilepsy demonstrated a subclinical stage at the age of 9-11 years, with visual blackouts and polyspike electroencephalographic (EEG) activity on photic stimulation, an early myoclonic stage at the age of 12-15 years, with increasing segmental, stimulus-sensitive myoclonus, occasional nocturnal buildup myoclonic "cascade" seizures, slowing of EEG alpha-activity, episodic 4-6 Hz bilateral sharp waves and polyspikes with myoclonias on photic stimulation, and a disabling myoclonic stage at the age of 16-18 years, with periodic generalized myoclonias, nocturnal myoclonic "cascade" seizures, ataxia, dysarthria, mental changes, intermittent wheelchair dependency, and continuous EEG slow waves with polyspikes and intense myoclonias on photic stimulation. One of the siblings died at the age of 18 years with no apparent cause of death. Treatment with antiepileptic drugs other than valproate may have contributed but none of the siblings were ever treated with phenytoin. Extensive clinical and laboratory investigations revealed no abnormalities and excluded other known possible causes of progressive myoclonus epilepsy. The diagnosis was consistent with Unverricht-Lundborg disease and rested on typical age of onset, clinical signs, EEG, and evoked response abnormalities. Buildup myoclonic seizures are typical in advanced stages of Unverricht-Lundborg disease. We have labeled these myoclonic "cascade" seizures. A typical seizure was studied with video-EEG and cardiorespiratory monitoring. Characteristics revealed were onset with continuous arrhythmic myoclonic jerks followed by intense rhythmic myoclonus with increasing muscle tone that successively reduced the amplitude of the jerks. The EEG during the whole seizure showed intense polyspike activity. Obstructive apnea was seen at the peak of the seizure. There were no cardiac dysrhythmias. Consciousness was normal or only slightly impaired. Postictal drowsiness was not observed. Myoclonic "cascade" seizures are easily confused with generalized tonic-clonic seizures.
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PMID:Clinical and neurophysiological development of Unverricht-Lundborg disease in four Swedish siblings. 174 64

An 85-year-old housewife was admitted owing to the sudden onset of amnestic syndrome on June 27, 1986. There was no history of abulia or somnolence. Though she showed severe amnesia, her understanding was not impaired. There was no aphasia, no dysarthria or other focal sings. The CT showed a low density area in the genu of the left internal capsule. The patient's amnestic syndrome did not improve during the following four years and thus she was readmitted for further examination in July, 1990. Although her WAIS scores were fairly good and intelligence was considered normal, she showed very poor performance on the Wechsler memory scale-R and Benton visual retention test. MRI of the brain showed infarction which extended from the genu to the anterior limb of the left internal capsule. The longstanding amnesia in the present case was induced probably by the infarction of the genu of the left internal capsule, where some fibers of memory pathways, such as the anterior thalamic peduncle, ansa peduncularis, and stria terminalis, may pass.
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PMID:[Persistent amnestic syndrome due to infarction of the genu of the left internal capsule]. 176 47

Neurologic manifestations, afflicting up to 70% of SLE patients, include psychosis, seizures, chorea, neuropathies, and stroke. MRI is useful in evaluation of lupus patients and several reports have documented cerebral atrophy or focal hyperintensities. We report an unusual MRI appearance in a 56-year-old woman with SLE, diagnosed on the basis of pleuritis, lymphopenia, anti-DNA antibodies, and neurologic involvement. She reported recent onset of Raynaud's phenomenon and generalized macular rash. She presented after two months of gradual deterioration with memory loss, flattened affect, dysphagia, dysarthria, anomia, and somnolence, without focal neurologic signs. Investigations included elevated ESR, reduced complement, normal CSF without oligoclonal bands, negative viral serology, normal hormone and vitamin levels, normal renal and hepatic function. Neuropsychologic testing showed widespread impairment (WAIS-R: FSIQ-63; WMS-69; DRS-98; RCPM-14; WAB AQ-78.8). CT was normal but MRI showed strikingly symmetric, confluent hyperintensities extensively involving cerebral and cerebellar white matter on T1 and T2 weighted scans. Basal ganglia and subependymal and subcortical white matter were spared. Treated with prednisone, the patient made a gradual, but incomplete, recovery. These MRI findings may reflect widespread vasculopathy or direct immunologic brain insult with or without immunologic blood-brain barrier disruption.
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PMID:Dementia with leukoencephalopathy in systemic lupus erythematosus. 191 71

A 28-year-old woman developed central pontine myelinolysis (CPM) following severe hyponatremia. Radiological examinations demonstrated a characteristic pontine lesion of CPM. Her neurological symptoms (drowsiness, emotional lability, dysarthria, dysphagia, and quadriparesis) were improved dramatically by treatment with thyrotropin-releasing hormone (TRH) and rehabilitation. However, results of repeat computed tomographic (CT) scans of the brain remained unchanged. This case therefore suggests that TRH may be beneficial for the treatment of CPM, and that CT findings appear to be a limited prognostic indicator for CPM.
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PMID:Dramatic recovery from neurological deficits in a patient with central pontine myelinolysis following severe hyponatremia. 192 Sep 71

The central anticholinergic syndrome (CAS) includes central signs (somnolence, confusion, amnesia, agitation, hallucinations, dysarthria, ataxia, delirium, stupor, coma) and peripheral signs (dry mouth, dry skin, tachycardia, visual disturbances and difficulty in micturition). It occurs when central cholinergic sites are occupied by specific drugs and also as a result of an insufficient release of acetylcholine. The CAS can be caused by atropine sulphate, hyoscine (scopolamine), promethazine, benzodiazepines, opioids, halothane, influrane, ketamine. The incidence of CAS during the postoperative period depends on choice and dose of anaesthetic agents, type of surgery, patient's condition and diagnostic criteria. It is close to 10% following general anaesthesia and 4% following regional anaesthesia with sedation. The differential diagnosis of CAS includes an overdose of anaesthetic drugs or an alteration in pharmacokinetics, altered hydratation, electrolyte or acid-base state, hypoglycaemia, hypoxia, hypercapnia, hypocapnia, hyperthermia, hypothermia, hormonal disorders, neurological damage resulting from surgery, embolism, haemorrhage or trauma. The diagnosis of CAS is often determined by a process of exclusion and not actually made until a positive therapeutic response to physostigmine, a centrally active anticholinesterase agent has taken place.
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PMID:[Central anticholinergic syndrome during postoperative period]. 219 41

The patient, a 37-year-old female, was hospitalized with a severe headache. Neurological examination on admission revealed no deficits except for neck stiffness and somnolence. Computed tomography showed a subarachnoid hemorrhage, which was especially prominent in the supracerebellar and quadrigeminal cisterns, but demonstrated no ventriculomegaly. Cerebral angiography on admission revealed no apparent abnormalities, but repeat angiography 8 days later disclosed a saccular aneurysm (2 X 3 mm) arising from the hemispheric branch of the left superior cerebellar artery (SCA). Three days after admission, the patient developed cerebellar dysarthria, which was assumed to be due to vasospasm. On the 24th day after admission, the aneurysm was successfully clipped through the infratentorial-supracerebellar approach. The postoperative course was uneventful and the patient was discharged with no neurological deficit. Nineteen other cases of peripheral SCA aneurysm have been reported in the literature. The presence of this type of aneurysm should be considered in patients who are fairly young and have focal neurological signs, such as third or fourth nerve palsy and/or cerebellar dysfunction. The prognosis for such patients is good, except in cases in which the neurological status is poor at the onset.
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PMID:[Peripheral superior cerebellar artery aneurysm. Case report]. 247 59

The antimanic effect of zotepine was investigated in 16 patients with manic-depressive psychosis or manic schizoaffective psychosis. Zotepine markedly improved manic symptoms in 75% and afforded at least slight improvement in all patients studied. However, in 50%, zotepine caused conversion from mania to depression. The most frequent side effects were dysarthria in 50%, parkinsonian symptoms in 33%, dry mouth in 28%, and sleepiness in 28%. EEG abnormalities were noted in 22% of patients. The antimanic effect of zotepine was enhanced by lithium carbonate; however, concomitant use of zotepine and lithium possibly increased the incidence of EEG abnormalities. The conversion-to-depression effect of zotepine was not inhibited by lithium. Overall, the concomitant use of zotepine and lithium may be important in the treatment of manic psychoses.
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PMID:Antimanic effect of zotepine. 308 26


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