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)

We report a 52-year-old Japanese woman who developed dyskinesia, epilepsy, and gait disturbance. She was well until 35 years of age, when she noted the onset of gait disturbance. She also noted abnormal involuntary movements in her limbs. She also noted dysarthria at age 38. A neurologist examined her at age 41. The neurologist found cerebellar ataxia and dyskinesia. The atrophy of the brain stem and the cerebellum was on CT. She started to have generalized convulsion with loss of consciousness. Dementia became apparent at age 40. In October, 1993, she became psychotic in which she behaved violently taking off her clothes shouting as "Fire". She was treated with major tranquilizers and became quiet. However, choreic movements became prominent. Her subsequent course was complicated with dysphagia, dementia, convulsion, and frequent bouts of pneumonia. She expired on January 24, 2000 after developing pneumonia. Her father and one sibling had similar motor disturbances. She was discussed in a neurological CPC. The chief discussant arrived at conclusion that the patient had dentatorubral-pallidoluysian atrophy. Most of the participants agreed with this diagnosis. Postmortem examination revealed that entire brain looked smaller than normal including the brain stem and the cerebellum. The cerebellar dentate nucleus showed loss of neurons and gliosis; glumose degenerations were also seen. The external segment of the pallidum showed neuronal loss and gliosis. The subthalamic nucleus showed gliosis without neuronal loss. A demyelinated focus was found in the pons; the lesion looked similar to central pontine myelinolysis. The cerebral white matters were unremarkable. Other areas were unremarkable. The pathological diagnosis was dentatorubral-pallidoluysian atrophy. The pathologic lesion which might explain her dementia was not apparent.
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PMID:[A 52-year-old woman with dyskinesia, epilepsy and gait disturbance]. 1247 84

A previously neurodevelopmentally intact 5-year-old male was admitted to hospital with a right lower lobe pneumonia with pleural effusion, subsequently confirmed to be a Mycoplasma pneumoniae infection. On the seventh day of the illness he had a prolonged generalized tonic or tonic-clonic convulsion, requiring intubation and ventilation. He was slow to regain consciousness (Child's Glasgow Coma Score 7-10 over 6 days) and brain imaging with CT and then MRI demonstrated bilateral thalamic lesions with oedema and central haemorrhage suggestive of acute bilateral thalamic necrosis, without striatal or white-matter involvement. He was treated with a 2-week course of erythromycin, and as an autoimmune process was considered possible, 5 days of intravenous methylprednisolone (20 mg/kg/day) followed by a 4-week oral prednisolone taper. He made a slow recovery over the next few weeks with almost complete neurological recovery by 2 months but with significant dysarthria, drooling, and a mild left hemiparesis. At 9 months, significant dystonia continued to affect his speech and, together with tremor, his upper-limb fine motor function bilaterally. His gait, personality, and higher cognitive functions appeared to have recovered fully. Although acute striatal necrosis, acute disseminated encephalomyelitis, and encephalitis have been reported with Mycoplasma pneumoniae and a similar picture of acute bilateral thalamic necrosis with influenza-A ('acute necrotizing encephalopathy'), this is the first reported case of Mycoplasma pneumoniae-associated isolated acute bilateral thalamic necrosis.
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PMID:Acute bilateral thalamic necrosis in a child with Mycoplasma pneumoniae. 1499 91

We report a 66-year-old woman with Hashimoto's encephalopathy who showed rapidly developing cognitive deficits, inactivity, and gait disturbance without involuntary movements or convulsions. She had had right-sided hemiparesis and dysarthria caused by a lacunar infarction and had been admitted to our hospital for 2 weeks. Although the dysarthria and hemiparesis gradually improved, difficulty in walking, disorientation, and drowsiness developed 2 months after discharge. Upon readmission, the patient was alert but apathetic and sometimes sleepy. The right upper and lower limbs showed mild weakness, which was considered to be due to the previous infarction. Cerebrospinal fluid showed mild elevation of protein without pleocytosis. An electroencephalogram was normal, and a magnetic resonance imaging of the brain showed only the old lacunar infarction. Titers of antithyroglobulin antibodies and levels of thyroid stimulating hormone in serum were elevated. We made a diagnosis of Hashimoto's encephalopathy and treated the patient with high-dose corticosteroids. Within 1 week, her mental status improved and she was able to walk. Generalized seizure, myoclonus, and tremor, which are characteristic of Hashimoto's encephalopathy, never developed. The findings in this patient suggest that Hashimoto's encephalopathy, a treatable condition, should be included in the differential diagnosis of dementia.
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PMID:[A patient with Hashimoto's encephalopathy showing subacute global cognitive dysfunction]. 1450 57

We report a 46-year-old woman who extensively showed intracranial calcifications possibly due to neuropsychiatric systemic lupus erythematosus (NPSLE) and antiphospholipid syndrome (APS). She had been treated with oral prednisolone for SLE since age 15, and experienced two abortions due to APS at ages 28 and 35 respectively. After a convulsion attack due to NPSLE at age 30, she had been suffering from dysarthria and choreic movement in her extremities. On admission to our hospital brain CT demonstrated extensive and symmetrical calcifications bilaterally in basal ganglia, subcortical white matter of the frontal lobe and dentate nuclei. She was shown to have neither metabolic nor congenital disorders causing these intracranial abnormalities. In this patient both NPSLE and APS, therefore, might have contributed to the remarkable intracranial calcifications in a long clinical course.
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PMID:[Neuropsychiatric systemic lupus erythematosus associated with anti-phospholipid syndrome, showing massive intracranial calcifications]. 1463 17

A previously healthy 30-year-old woman was admitted to our hospital because of impaired consciousness after convulsion. A temporary diagnosis of herpes simplex encephalitis was made, and intravenous acyclovir (ACV) therapy (250 mg four times daily in normal saline over 2 hours) was started. Three days later, she became confused, and was having hallucinations, dysarthria and generalized painful seizures occurred without focal neurologic deficit. Whether the neuropsychiatric symptoms were related to herpes simplex encephalitis or acyclovir neurotoxity was initially unclear. The brain MRI and lumbar puncture findings were initially normal, but abnormal FLAIR lesions appeared later. ACV-associated encephalopathy was considered. ACV was discontinued, and she recovered from the neurological disorder within 24 hours. Although blood levels of acyclovir were not determined, it is unlikely that they were in a toxic range, in view of her normal renal function.
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PMID:[A young patient of acute encephalitis complicated with acyclovir encephalopathy without renal dysfunction]. 1465 98

A 3-year-old girl developed right hemiplegia with acute onset, followed by generalized convulsion, choreic movement, and severe motor deterioration. She became bed-ridden a few months after the onset. Intravenous cyclophosphamide pulse therapy resulted in a remarkable improvement of her clinical symptoms. At age of six, she has recovered markedly with the residual symptom of minimum dysarthria. Autoimmune mechanism similar to the antiphospholipid syndrome was considered to be the pathogenesis of this case.
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PMID:[A child with choreic movement, generalized convulsion and severe neurological deterioration responded to cyclophosphamide]. 1602 99

Ethylene glycol is recognised as a potentially lethal poison if ingested. Approximately 100 mls may be fatal in a 70 kg adult. Current Toxbase guidelines are the accepted standard of treatment of such poisonings in the United Kingdom. These guidelines suggest that symptoms of significant poisoning are usually present within 30 minutes of ingestion i.e. ataxia, dysarthria, nystagmus, nausea and vomiting, haematemesis, coma and convulsions. In the absence of these symptoms, metabolic acidosis or ethylene glycol concentration more than 8 mmol/l a single loading dose of ethanol and observation were the recommended course of management until recently. We report a case of a patient who remained relatively asymptomatic for almost 24 hours but then developed clinical symptoms with marked metabolic acidosis and renal impairment requiring intensive treatment including haemodialysis.
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PMID:Toxic alcohol but not intoxicated--a case report. 1616 3

As onset time and duration of sensory block are intermediate, mepivacaine is widely used for regional anaesthesia. Few reports of systemic adverse effects are available following nerve blockade with mepivacaine. We report the case of a 54-year-old patient suffering from terminal renal failure who needs the confection of an arteriovenous shunt under axillary brachial plexus block. At completion of the injection of 25 ml (375 mg) of 1.5% mepivacaine the patient presented dysarthria, mental confusion followed by a loss of verbal contact and agitation, but no convulsion or cardiac dysrythmia. The patient received midazolam and surgery was planned the following day under general anaesthesia. Plasma mepivacaine concentration at time of neurological signs was measured at 5.1 microg/ml. Prevention and treatment of systemic toxic effects after regional anaesthesia are discussed.
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PMID:[Systemic toxicity with mepivacaine following axillary block in a patient with terminal kidney failure]. 1625 73

It is known that rotavirus gastroenteritis can accompany some neurological manifestations, including encephalitis/encephalopathy or seizures. However, the detailed pathogenesis involved has not been fully understood. To date, acute cerebellitis associated rotavirus gastroenteritis has not been previously reported, except for one case. Herein, we describe two cases of acute encephalitis/encephalopathy and concurrent cerebellitis, associated rotavirus gastroenteritis. Following vomiting and diarrhea, case 1 experienced convulsions and consciousness disturbance and case 2, transient loss of consciousness with eye deviation. After these symptoms subsided, cerebellar signs became evident and a brain MRI showed cerebellar involvement in both cases. Both cases showed speech disturbances, such as mutism, slow speech and dysarthria. In this report, we will discuss the possible pathogenesis of rotavirus associated acute encephalitis/encephalopathy and concurrent cerebellitis.
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PMID:Rotavirus associated acute encephalitis/encephalopathy and concurrent cerebellitis: report of two cases. 1753 86

Central nervous system (CNS) involvement is uncommon in brucellosis. Neurological complications of brucellosis may be divided into 2 major groups: 1) those related to the acute-febrile state that occurs in acute disease (toxic-febrile neurobrucellosis), and 2) those related to actual invasion and localization of the pathogen in the CNS (classical neurobrucellosis). In this paper, we present 4 cases of toxic-febrile neurobrucellosis and discuss clinical findings and outcome of treatment in these cases. All patients had fever, headache, stupor or coma with neuropsychiatric symptoms such as hallucination, delirium, convulsion, dysarthria, psychosis, and night raving. Peripheral and cranial vasculitis was present in case 3 and bilateral sensorioneural hearing loss in case 4. Neither pleocytosis nor hyperproteinorrachia was present in any patient in lumbar puncture. Brucella melitensis was isolated in case 3 from bone marrow, and in case 4 both from blood and bone marrow. All patients received combined treatment consisting of ceftriaxone, rifampicin, and doxycycline. They were discharged from the hospital with full recovery. No recurrence or any complaint was observed during the follow-up. In conclusion, despite the rapid course and serious complications, outcome from febrile-toxic neurobrucellosis is excellent especially when effective antimicrobial therapy is started early in the course of illness.
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PMID:Toxic-febrile neurobrucellosis, clinical findings and outcome of treatment of four cases based on our experience. 1785 20


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