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)

Cerebellar infarcts have been neglected for a long time and are now shown well by CT and especially MRI. Some infarcts involve the full territory supplied by a cerebellar artery. They are frequently complicated by edema with brain stem compression and supratentorial hydrocephalus, requiring at times emergency surgery, and are often accompanied by other medullary, medial pontine, mesencephalic, thalamic and occipital infarcts. On the other hand, partial territory infarcts are usually confined to the cerebellum and have a benign outcome with total recovery or minimal disability. They are more common than full territory infarcts. However, clinical presentations are similar to those full territory infarcts, differing mainly by the lack of drowsiness or unconsciousness. The main symptoms are vertigo, headache, vomiting, unsteadiness of gait and dysarthria. Signs include ipsilateral limb dysmetria, ipsilateral axial lateropulsion, ataxia and dysarthria. Vertigo is more severe and rotary in posterior inferior cerebellar artery territory infarcts, whereas dysarthria and ataxia are prominent in superior cerebellar artery territory infarcts. A few brain stem signs are sometimes added. In these territorial cerebellar infarcts, cardioembolism is the most common cause. Atherosclerotic occlusion comes next, involving the intracranial part of the vertebral artery and, less frequently, the lower basilar artery, both locations inaccessible to surgery. Other causes are artery to artery embolism from a vertebral artery origin stenosis, or the aortic arch, in situ intracranial branch atherosclerotic occlusion, and vertebral artery dissection. Border zone cerebellar infarcts occur in one third of the cases. They are small cortical or deep infarcts. They have the same symptoms and signs as territorial infarcts except for more frequent postural symptoms occurring over days, weeks or months after the ischemic event. The infarcts mainly have a thromboembolic mechanism, and sometimes have a hemodynamic mechanism: 1) focal cerebellar hypoperfusion due to large artery occlusive disease in more than half the cases, 2) small or end (pial) artery disease due to hypercoagulable state (thrombocythemia, polycythemia, hypereosinophilia, disseminated intravascular coagulation), arteritis or intracranial atheroma, and 3) rarely systemic hypotension due to cardiac arrest.
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PMID:[Cerebellar infarctions and their mechanisms]. 809 Oct 85

A 56-year-old man with vertebrobasilar insufficiency and associated findings including quadriparesis, dysarthria, cerebellar ataxia, nystagmus, and somnolence underwent left occipital artery (OA) to anterior inferior cerebellar artery (AICA) anastomosis with interposition of a superficial temporal artery (STA) graft. This procedure was chosen because cerebral angiograms demonstrated occlusion of the right vertebral artery (V3) and severe stenosis of the V4 segment of the left vertebral artery, with perfusion of the territory of the left posterior inferior cerebellar artery via the ipsilateral AICA, and because dissection of the OA is a relatively difficult and time-consuming procedure. Dissection of the STA, on the other hand, is much easier. Preoperative measurements of local cerebral blood flow in the vertebrobasilar circulation before and after intravenous administration of acetazolamide (500 mg) were obtained, and demonstrated low flow and hemodynamic compromise in the posterior circulation. The patient's hemodynamic and neurological status improved following surgery. In this report, we present a new and simplified method of OA-AICA anastomosis with interposition of STA graft.
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PMID:Anastomosis of occipital artery to anterior inferior cerebellar artery with interposition of superficial temporal artery. Case report. 836 56

INTRODUCTION. Acute intermittent familial ataxia is a rare disorder with autosomal dominant inheritance and unknown etiology which usually in childhood or adolescence. CASE 1. A 33-years-old woman who suffered from giddiness, gait ataxia, dysarthria and somnolence episodes. These episodes lasted between 4 and 72 hours. They generally occurred within a framework of emotional or physical stress. The following tests were performed: hemogram and biochemistry, blood and urine toxicology, immunological tests, cerebrospinal-fluid study, electrocardiogram, electroencephalogram, trunk and visual evocated potentials, cerebral computed tomography and cerebral magnetic resonance imaging. None of them gave significative results. CASE 2. A 12-years-old boy, son of the previous woman, who suffered from somnolence, gait ataxia and dysarthria with acute beginning. The same tests than in the above case were performed together with metabolic studies. There were no pathological findings in this case, either. The symptoms disappeared gradually in 6 days. His familial history led to a diagnosis of acute intermittent familial ataxia. A year later he suffered from a similar disorder and he was immediately treated with acetazolamide. The symptoms disappeared in 2 hours. CONCLUSIONS. Acute intermittent familial ataxia is a disorder of difficult identification. It can be easily confused with other periodical ones, because its diagnosis has to be based on the clinical findings and on the familial history. For this purpose, a therapeutic test with acetazolamide can be useful, since in most cases a spectacular clinical improvement has been observed.
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PMID:[Acute intermittent familial ataxia: report of a new family]. 868 Nov 77

Although chlorobutanol is available in a large number of preparations, the incidence of toxicity appears to be low. However, with continued exposure to high-dose chlorobutanol, significant toxicity may occur. It seems prudent to use caution in the continued administration of products containing chlorobutanol. The lack of pharmacokinetic data warrant that extra care be used when administering chlorobutanol-containing products to patients with hepatic or renal dysfunction. Patients should be monitored for possible increased somnolence, alterations in speech pattern, dysarthria, and hemodynamic changes. Chlorobutanol toxicity should be ruled out by serum analysis if the patient exhibits any of the above reactions.
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PMID:Chlorobutanol toxicity. 889 27

Medial medullary infarctions (MMI) were reported in less than 40 patients with satisfactory clinicotopographic documentation. We studied seven patients with MRI-proven acute MMI seen in two neurologic departments over a 5-year period (1990-1994). MMI represented less than 1% of ischemic strokes in the posterior circulation. Five patients had an infarction above the pyramidal decussation. All patients had contralateral hemiparesis and lemniscal sensory loss, accompanied by ipsilateral lingual palsy (Dejerine's syndrome) in three. Two patients had infarction below the pyramidal decussation, with ipsilateral hemiparesis and lemniscal sensory loss. Accompanying symptoms and signs of MMI were vertigo and nausea (n = 5), mild ipsi- or contralateral decrease in pain sensation (n = 6), headache (n = 4), ipsilateral limb ataxia (n = 6), contralateral truncal lateropulsion (n = 5), mild ipsilateral ptosis (n = 4), nystagmus (n = 4), dysarthria (n = 3), and somnolence (n = 2). Presumed causes of MMI were stenosis, occlusion or dissection of the ipsilateral vertebral artery (n = 5), and cardioembolism (n = 1). Outcome at 3 months was favorable in five patients. In conclusion, the clinical features of MMI are more heterogeneous than commonly thought, whereas its etiology seems fairly constant (vertebral artery disease).
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PMID:Medial medullary stroke: report of seven patients and review of the literature. 971 65

We report a 29-year-old HIV-positive patient admitted with dysarthria, ataxia and somnolence. Imaging findings were typical of Wernicke's encephalopathy, but autopsy revealed cytomegalovirus encephalitis and primary cerebral lymphoma.
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PMID:Cytomegalovirus encephalitis and primary cerebral lymphoma mimicking Wernicke's encephalopathy. 912 41

A 40-year-old conductor was admitted because of increasing drowsiness and confusion. Two years before admission he had had a first seizure. One year before admission he had a generalized convulsive status epilepticus; the following months he was less able to concentrate. A second status epilepticus was followed by transient weakness of his left arm and a depressed level of consciousness for several weeks. After awakening, he had delusions, and his wife found him demented. In the following months his confusion and drowsiness gradually deteriorated. He had previously had gonorrhoea, an episode of fever and exanthema, and was found to have oligospermia as cause of his infertility. On examination he was disoriented, and he had dysarthria. His left pupil was smaller, but both pupils reacted normally. There was left hemianopia and cerebellar ataxia. CT and MR showed large ventricles and periventricular diffuse lesions in the white matter. CSF examination revealed leucocytosis and increased protein content. Further examination were focussed on serological evidence of syphilis, and finally neurosyphilis was diagnosed. After treatment with penicillin, the patient started to recover.
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PMID:[Clinical judgment and decision making in clinical practice. A music conductor with epilepsy followed by memory disorders]. 921 89

The side-effects and complications of posteroventral pallidotomy are analysed in 138 consecutive patients who underwent 152 pallidotomies. Transient side-effects, lasting less than three months, appeared in 18% of the patients, that is, 16.5% of the surgical procedures. Long term complications, lasting more than 6 months, were noted in 10% of the patients, that is, 9.2% of the surgical procedures. Sixteen complications occurred alone or in various combinations in 14 patients and included fatigue and sleepiness (2), worsening of memory (4), depression (1), aphonia (1), dysarthria (3), scotoma (1), slight facial and leg paresis (2) and delayed stroke (2). Complications such as dysarthria and paresis could be attributed to MR- or CT-verified pallidal lesions lying too medially and encroaching on the internal capsule. Two of the patients with deterioration in memory had some memory impairment before surgery, and the aphonic patient had dysphonia preoperatively. The study suggests that stereotactic MRI and careful impedance monitoring and macro-stimulation of the posteroventral pallidum area should be sufficient for minimizing the risk of complications; the stereotactic lesion should be centered within the posterior ventral pallidum without involvement of internal capsule. It is concluded that pallidotomy is a safe procedure if performed on cognitively alert patients, and it seems that both the incidence and especially the severity of complications are lower for posteroventral pallidotomy than for thalamotomy.
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PMID:The side-effects and complications of posteroventral pallidotomy. 923 12

Topiramate is a new antiepileptic drug, which is not yet marketed in Germany. The anticonvulsive activity is probably mediated by sodium-channel blockade combined with gabaergic and weak antiglutamatergic properties. We investigated 23 patients with partial seizures in this open prospective study. The efficacy was analysed under stable concurrent antiepileptic drugs. Two of the patients became seizure free. Ten patients had a reduction of seizure frequency of at least 50%. The responder rate was 57%. The maximum daily dosages were 400 to 850 mg. Side-effects without relationship to dose were nervousness and aggression. In two patients an psychotic episode occurred. Dose-related side-effects were ataxia, dizziness, somnolence and dysarthria. This study is underlining that topiramate is efficacious in the treatment of partial onset seizures but also associated with a narrow therapeutic width.
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PMID:[Topiramate--an effective new anticonvulsant. An open prospective study]. 944 Dec 57

Benign epilepsy of childhood with centrotemporal spikes (BECT) is the most common partial epilepsy syndrome in the pediatric age group, with an onset between age 3 and 13 years. The typical presentation is a partial seizure with parasthesias and tonic or clonic activity of the lower face associated with drooling and dysarthria. Seizures commonly occur at night and may become secondarily generalized. They are usually infrequent and may not require antiepileptic drugs but, if treated, they tend to be easily controlled. Children with BECT are neurologically and cognitively normal. The EEG shows characteristic high-voltage sharp waves in the centrotemporal regions, which are activated with drowsiness and sleep. In this typical form, BECT is easily recognized. However, atypical cases are common and the definition of BECT can become blurred. Although further investigations are not required in cases with typical clinical and EEG findings and normal neurologic examinations, neuroimaging studies may be required in atypical cases to rule out other pathology. The long-term medical and psychosocial prognosis of BECT is excellent, with essentially all children entering long-term remission by mid-adolescence.
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PMID:Benign epilepsy of childhood with centrotemporal spikes. 963 91


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