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 Case of Marchiafava-Bignami disease demonstrated by MR diffusion-weighted image (DWI) was reported. A 55-year-old male with chronic alcoholism demonstrated dysarthria, disorientation and apraxia of left-hand. Sagittal view on MRI showed a swelling of the corpus callosum. The body and splenium of the corpus callosum showed symmetrically iso-intensity in T1 WI and hyperintensity in T2 WI, and remarkable hyperintensity in fluid attenuated inversion recovery images. DWI showed a definite hyperintensity area on the corpus callosum and the apparent diffusion coefficient (ADC) map presented the decreased water self-diffusion. These findings differed from the other demyelinating diseases, such as multiple sclerosis. We considered these DWI findings were the initial changes on MBD which preceded the demyelination. To our knowledge, this is the first report of DWI that was used in a case of Marchiafava-Bignami disease.
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PMID:[A case of Marchiafava-Bignami disease demonstrated by MR diffusion-weighted image]. 1093 26

Using systematic investigations, including neurological and neuropsychological examinations and computed tomography and magnetic resonance imaging analyzed on anatomical maps, we prospectively studied 12 patients (age range, 63+/-19 years) with an isolated anterior thalamic infarct. They had acute, severe, perseverative behavior, which was apparent in thinking, speech, and all memory and executive tasks, combined with increased sensitivity to interference. They also showed superimposition of mental activities normally processed sequentially (e.g., giving biographical information while working on a calculation test), which we called palipsychism (from the Greek palin [again] and the Greek psyche [soul]). In addition, all 12 patients (8 with a left-sided infarct, 4 with a right-sided infarct) had word-finding difficulties, 7 of 12 with impaired naming, 8 of 12 with dysarthria, and 5 of 12 with hypophonia. Comprehension, repetition, written abilities, and reasoning were consistently preserved, but apathy was usual. All patients had anterograde memory impairment, with a delayed recall deficit, primarily verbal in left-sided infarcts and visuospatial in right-sided infarcts. Dysexecutive features such as difficulty in programming motor sequences were always present. Visual neglect or topographic disorientation was found in 3 patients. Magnetic resonance imaging emphasized involvement of the anterior group of thalamic nuclei, the mamillothalamic tract, and the anterior part of the internal medullary lamina, with structural sparing of the dorsomedial and ventrolateral nuclei. Sequential follow-up examinations showed spectacular improvement within a few months, with the only significant persisting abnormalities being memory dysfunction and apathy. The acute behavioral syndrome of anterior thalamic infarction is dominated by palipsychism, which corresponds to an overlap of sequential cognitive processes in two or more domains. Its association with severe perseverative behavior with increased sensitivity to interference, anterograde memory retrieval deficit, intrusions, naming difficulties with dysarthria and hypophonia, and apathy is suggestive of this type of infarct.
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PMID:The acute behavioral syndrome of anterior thalamic infarction: a prospective study of 12 cases. 1093 73

We report the case of a 60-year-old man with autopsy-proven dementia with motor neuron disease (D-MND) and Alzheimer's disease lesion. The patient presented with clumsiness of his right hand at the age of 55 years old and subsequently developed dysarthria, weakness and atrophy of his upper limbs. He was unaffectionate towards his family, repeated the same phrase, and showed severe disorientation of time and place. Neurological examination on admission showed not only diffuse lower motor neuron signs, such as weakness, atrophy, fasciculation and areflexia in both upper limbs, but also dementia (HDS-R 9/30). He died of respiratory insufficiency. Neuropathological examination showed mild atrophy of the frontal and temporal lobes and anterior spinal roots. Microscopic examination of cortical sections revealed degenerative changes with simple atrophy and gliosis, and these changes were predominant in layers 1 and 2 of the frontal and temporal cortices. Using immunohistochemical staining, ubiquitin-positive but tau-negative inclusions were frequently found in neurons of the hippocampal granular cell layers and temporal lobes. Many senile plaques and neurofibrillary tangles were present in all sections of the brain. Our final diagnosis was dementia with motor neuron disease accompanying Alzheimer's disease lesion, because of hypoperfusion in the parietal lobe as well as the frontal lobe demonstrated by SPECT, and the presence of many senile plaques and neurofibrillary tangles in the cerebral cortex. Overlapping of pathologically-proven D-MND and Alzheimer's disease lesion is extremely rare, and this case may improve our understanding of the process of neurodegeneration.
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PMID:[An autopsy case of dementia with motor neuron disease accompanying Alzheimer's disease lesion]. 1188 31

A 70-year-old man developed a slowly progressive cerebellar syndrome after having been exposed to carbon disulfide (CS2) in a viscose rayon plant for 27 years. Ataxia, dysmetria, dysarthria and adiadochokinesia appeared 7 years after retirement from work (at age 54), and were later accompanied by cognitive deterioration, dysmnesia, spatio-temporal disorientation, emotional lability, and paranoid-obsessive disturbances. Brain computed tomography (CT) and magnetic resonance imaging (MRI) showed advanced global cerebellar atrophy, and a picture of less severe cerebrocortical atrophy. The case illustrates the possibility of chronic toxic encephalopathy among patients with previous long-term exposure to CS2. In such instances, cerebellar damage may develop as an exceptional, delayed manifestation of neurotoxicity: brain imaging techniques can significantly contribute to the diagnosis and follow-up, in addition to occupational anamnesis and neuropsychiatric evaluation. The patient presented also serves as a remainder that neurodegenerative disorders of apparently unknown origin sometimes derive from occupational toxic exposures suffered in the past. The clinical manifestations may appear several years after retirement from work, when the effects of toxic damage combine with age-related neuronal loss to overcome the brain functional reserve.
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PMID:Cerebellar atrophy as a delayed manifestation of chronic carbon disulfide poisoning. 1267 53

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

This is the case report of a 44-year-old woman presented with an acute stroke immediately after electroconvulsive therapy (ECT). The patient had no significant medical history other than chronic depression. She was taking sertraline, and she had had multiple previous ECT treatments without any complications. While being monitored in the recovery room within 10 minutes after the last ECT session, she was found to have sudden onset of left-sided flaccid hemiplegia and numbness along with slurred speech. On arrival to our hospital, she was found to have flaccid hemiplegia on the left side involving the face, arm, and leg (face and arm more than the leg involvement), severe dysarthria, and mild neglect syndrome (National Health Institute Stroke Scale of 14). Noncontrast computed tomography (CT) of the head showed no signs of early ischemia, and iodine contrast CT angiography revealed right middle cerebral artery (MCA) (distal M1 segment) clot. Patient received intravenous recombinant tissue plasminogen (rt-PA) at 2.5 hours after the onset of symptoms, and then a total of 3.0 mg of intra-arterial (IA) rt-PA. Angiography at the end of the procedure showed successful recanalization of the M1 segment and normal vessel caliber with adequate distal flow. After the procedure, the patient made rapid improvements in all of her initial symptoms during the first 24 hours. An extensive stroke workup failed to reveal any cause of the stroke, including usual stroke and hypercoagulable risk factors. This was an acute embolic stroke immediately following an ECT, and without the aggressive thrombolytic therapy, the patient's outcome would have been poor because there was an M1 segment clot with a major MCA syndrome with relatively high National Institute of Health Stroke Scale. The neurological side effect profile of ECT is reported to be minimal with most common symptoms being headache, disorientation, and memory complaints. There is no clear cause-and-effect relationship in this case, and the stroke after ECT is extremely rare. In such rare event of stroke while receiving ECT, there is an effective treatment available using both intravenous and IA thrombolysis as reported in this case.
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PMID:Acute embolic stroke after electroconvulsive therapy. 1663 11

A 43-year-old woman was undergoing radiofrequency catheter ablation of a symptomatic supraventricular tachycardia when a patent foramen ovale (PFO) was detected with passage of the diagnostic electrocatheter into the left atrium. Prior echocardiographic studies had been unrevealing. Upon questioning during the procedure, the patient now admitted to frequent and disabling daily migraine attacks, while her family described two recent brief episodes of disorientation and dysarthria, consistent with transient ischemic attacks. The patient was informed of the option of future closure of the PFO, but she insisted on having this done concurrently with her ablation procedure. After successful ablation of the slow pathway considered responsible for the supraventricular tachycardia, an Amplatzer closure device was utilized and the PFO was successfully closed during the same procedure. A postprocedural transesophageal echocardiogram showed complete sealing of the PFO, while over the ensuing 10 months the patient reported virtual elimination of her daily attacks of migrainous headaches, limited to a single episode the day after the procedure and none thereafter.
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PMID:Transcatheter closure of patent foramen ovale during a radiofrequency ablation procedure. 1693 79

A case of brainstem encephalitis in a man positive for both anti-Hu and anti-Ri antibodies is reported. This case had an unusual double step evolution and progressive involvement of different CNS subdivisions at MRI. Brainstem encephalitis developed abruptly, mimicking a posterior vascular deficit with vertigo and dizziness. These symptoms transiently remitted completely after a few days to relapse acutely 1 month later with sudden loss of consciousness, followed by confusion, disorientation, dysarthria, dysphagia and reduced thermic sensation on the right side. Within another few days, the patient developed acute respiratory failure and died some weeks later. MRI was negative at the beginning but later showed a progressive ascending involvement of the brainstem and thalamus. At autopsy, this picture corresponded to lymphocytic infiltration, preferentially B cells into the perivascular spaces and T cells in the brainstem parenchyma, confirming that T cells could be the effector of cytotoxicity, probably in the presence of cooperation with B cells that were well represented in this setting.
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PMID:Double step paraneoplastic brainstem encephalitis: a clinicopathological study. 1944 98

We describe the cases of two men, one of whom was a non-alcoholic 50-year-old man who had been on hunger strike for 50 days and who was admitted to hospital with dysarthria, unstable gait, disorientation, ophthalmoplegia and ataxia. The suspected diagnosis was Wernicke's encephalopathy and treatment consisted of intramuscular thiamine shots followed by oral administration of the same drug, which produced rapid symptom resolution. In both patients, magnetic resonance imaging showed bilateral and symmetrical injuries around Silvio's aqueduct and in the periventricular region of both thalami.
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PMID:[Two cases of Wernicke's disease]. 1969 16

Sarcoidosis is a chronic disease of unknown aetiology. Neurosarcoidosis is registered in 5% of patients with sarcoidosis. Clinical manifestations of sarcoidosis are numerous and diverse. Manifestation of Neurosarcoidosis includes partial- and grand-mal seizures, low-grade fever, headache, increased intracranial pressure, visual disturbances, diabetes insipidus, amenorrhea- galacterorrhea syndrome and pituitary failure, hypogonadotropic hypogonadism, hyperprolactinemia, unilateral and bilateral facial palsy, infiltration of meninges (aseptic meningitis) and nerve roots, leptominingitis, pachymeningitis with cranial neuropathies, pseudotumor, mild cognitive disorder, psychosis, delirium, dementia, disorientation, amnesia, progressive visual deterioration and proptosis, axonal polyneuropathies, mononeuropathies, chronic polyradiculoneuritis, peripheral neuropathy, cranial nerve abnormalities, radiculopathies, peripheral neuropathy, mononeuritis multiplex, progressive numbness and deep sensation disturbance in bilateral lower extremities, hemiplegia, hyperreflexia with pathological reflexes and hypesthesia, upward gaze palsy, spinal cord compression, dysarthria, dysphagia, weakness, episodes of blurred vision, diplopia, intracerebral hemorrhage, neuro-ophthalmic manifestations, intranuclear ophthalmoplegia, dysorientation, vasculitis presenting with strokes, intracranial hypothalamic lesion, paresthesis, hemiparesis, myelopathy in the cervico-thoracic region, lumbar pain, sensory level and inability of lateral gaze (Tab. 2, Ref. 60).
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PMID:Clinical manifestations of neurosarcoidosis. 1982 43


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