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)

Two patients with disulfiram-(Antabuse-)induced encephalopathy exhibited paranoid ideas, disorientation, impaired memory, ataxia, dysarthria, snout and grasp reflexes, and abnormal electroencephalograms. The first patient developed symptoms on two occasions, each time after disulfiram administration. The second patient experienced a generalized seizure followed by fulminant psychosis three weeks after starting disulfiram therapy. Spinal fluid examination in the latter patient revealed a low homovanillic acid (HVA) level. Since disulfiram inhibits dopamine oxidation, disulfiram-induced encephalopathy may be related to excess dopaminergic activity in the central nervous system.
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PMID:Disulfiram-induced encephalopathy. 125 49

Clinical and neuropathological studies of a case of pallido-nigro-luysian atrophy with thalamic degeneration and ossification of the posterior longitudinal ligament (OPLL) is reported. The patient was a 72-year-old man, suffering from gait disturbance caused by OPLL for about 3 years. The clinical features were characterized by gradual development of disorientation in place, time and person, memory disturbance, vertical gaze palsy and rigidity of extremities. Dysarthria, dysphagia, bradykinesia, masked face and neck dystonia appeared at the advanced stage of his illness. There was no tremor or other involuntary movements. A clinical diagnosis of parkinsonism was suspected. The main neuropathological findings were neuronal loss and gliosis in globus pallidus, substantia nigra, subthalamic nucleus and thalamus. In addition, neuronal loss of the anterior horn of the cervical spinal cord due to compression by OPLL (C4-C7) was recognized. The neuropathological findings of the present case were consistent with systemic degenerative disorder of the nervous system affecting the pallido-nigro-luysian tract. This rare disorder should be considered in the differential diagnosis of parkinsonism in old people.
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PMID:[An autopsy case of pallido-nigro-luysian atrophy associated with OPLL]. 251 8

Various types of associated movements of eyeballs with other cranial muscles have been described in the literature. Only a few observations, however, have been reported on the relation of ocular movements and facial muscles innervated by the facial nerve, especially the orbicularis oculi muscles. We report two cases presenting gaze-evoked involuntary contraction of the orbicularis oculi muscle and unilateral eyelid closure. Case 1 was a 38-year-old housewife who was admitted to our hospital because of gait disturbance and sensory deficits below the neck. She had a 5-year history of left facial palsy, disturbed horizontal eye movements, retrobulbar optic neuritis, spastic paraparesis and bladder and rectal disturbances, some of which had relapsed a few times. Neurological abnormalities were summarized as follows: bilateral pale discs, right Horner's sign, horizontal nystagmus, left facial nerve palsy of peripheral type, spastic paraparesis with left-sided predominance, sensory disturbances below the third cervical segment, truncal and limb ataxia, and bladder and rectal disturbances. Gaze-linked synchronized contraction of the left facial muscles was observed and on the left lateral gaze marked spasm of the left orbicularis oculi muscle with occasional lid closure was evoked. Case 2 was a 72-year-old female with cerebellar hemorrhage. Neurological abnormal findings included mild disorientation, meningeal irritation signs, horizontal nystagmus on lateral gaze, reduced response of reflex eye movement to the left, minimal weakness of the left facial muscles, ataxic dysarthria, mild left hemiparesis and hemisensory deficits with face, truncal and limb ataxia. She could move eyeballs to any direction but with effort to the left.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Gaze-evoked eyelid closure. Report of two cases]. 261 99

Recently, cerebral amyloid angiopathy is stressed as an unusual and infrequent cause of cerebral infarct or intracerebral hemorrhage. This report described a case of cerebral amyloid angiopathy complicated by multiple cerebral infarcts and multiple intracerebral hemorrhages. This 70-year-old man was admitted to our hospital on November 10, 1984 for evaluation of the gradual onset of dysarthria. Examination showed only slight dysarthria. There was no history of hypertension or dementia. A computed tomography (CT) showed enlarged ventricles with cortical atrophy and multiple low-density lesions, deep in the left frontal, left parietal, right parietal lobes, and in the both basal ganglias. The patient discharged from the hospital with only slight dysarthria. On November 20, 1984, he was admitted to our hospital again, because he was found unresponsive on the floor. He was somnolent but arousable. Examination showed disorientation, impairment of recent memory and impairment of calculation, A CT scan demonstrated three small intracerebral hemorrhages in the left frontal, right parietal lobes and left basal ganglia. On the fifth hospital day he deteriorated acutely, becoming semicomatose and hemiparetic on the right side. A repeated CT scan showed two new intracerebral hemorrhages in the left frontal lobe. Cerebral angiograms showed only minimal changes due to the occupying lesions in the above mentioned area. The hematomas was evacuated via left fronto-parietal craniotomy. The specimens removed with hematoma (stained with hematoxylin-eosin, Congo red and thioflavin T) showed extensive amyloid angiopathy. Postoperatively he made a good recovery, although he had residual mental dysfunctions. He expired by pneumonia on March 30, 1985.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebral amyloid angiopathy complicated by multiple cerebral infarcts and intracerebral hemorrhages: case report]. 361 33

This work is to study the ultrastructure of the neuronal lipofuscin that occurred in the brain and the spinal cord of an autopsy case of familial Alzheimer's disease and to compare with those in several other diseases. The patient was a 46-year-old male, whose father and elder brother were diagnosed as Alzheimer's disease and died at the age of 42, respectively. He became afflicted with forgetfulness and disorientation at the age of 36. He developed a grand mal seizure at the age of 39 and thereafter, his clinical course was characterized by pyramidal signs, dysarthria and the symptoms of Gerstmann's syndrome, visuo-spatial agnosia, apraxia for dressing and constructive apraxia. He became bedridden at 45 years old and died of general prostration. The brain weighed 1,250 g, and the cerebral cortex showed mild atrophy. The neuronal loss, senile plaques and Alzheimer's neurofibrillary tangles were found throughout the cerebral cortex. The senile plaques were also found in the basal ganglia, the cerebellar medulla and cortex. There was severe amyloid angiopathy in the occipital and cerebellar cortices. The specimens for electron microscopy were taken from the cerebral cortex, the basal ganglia, the thalamus, the midbrain, the medulla oblongata, the cerebellum and the spinal cord. The ultrastructural study revealed three different types of the neuronal lipofuscin, though different stainability between these lipofuscin granules could not be manifested by several histochemical methods. Their morphological differences seemed to be based on the sites of the central nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ultrastructural study of the neuronal lipofuscin--an autopsy case of familial Alzheimer's disease]. 648 35

Complications from mydriatic and cycloplegic drugs are rare compared with their extensive use. Adverse effects are often related to dosage or other factors. The ocular complications include increased intraocular pressure, pigmentation of the conjunctiva and cornea, pigment in the anterior chamber, lacrimal duct blockage, macular edema, corneal endothelium damage, hyperemia, allergy, discomfort, and blurred vision. The systemic complications are those common to sympathomimetic and parasympatholytic drugs and include tachycardia, hypertension, headache, faintness. pallor, trembling, excessive sweating, palpitations, arrhythmias, confusion, hallucinations, drowsiness, ataxia, flushed skin, high fever, dysarthria, thirst, dry mouth, convulsions, disorientation, nervousness, coma, and death. An understanding of all possible side effects is of paramount importance to those using these drugs in the treatment of anticholinesterase poisoning. This review is intended as a ready reference to the adverse effects of mydriatic and cycloplegic drugs.
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PMID:Mydriatic and cycloplegic drugs: a review of ocular and systemic complications. 703 29

A double-blind study was performed on 20 patients comparing the safety and efficacy of Iopamidol and Metrizamide in cervical myelography. The radiographic qualities of the Iopamidol and Metrizamide examinations were equivalent when using the same volume (12 to 13 ml), concentration (200 mg I/ml), and a C1-2 route of administration. The performance of a CT scan on selected patients in specified areas of interest provided additional diagnostic information in some patients (e.g syringomyelia, degenerative spondylosis). The adverse reactions were mild in the Iopamidol group with 4 of the 10 patients experiencing no adverse reactions. The more severe reactions, including disorientation, agitation, dysarthria, asterixis, hyperreflexia and EEG abnormalities were limited to the Metrizamide group with one or more occurring in 2 of the 10 patients studied. Only one Metrizamide patient experienced no adverse reactions. In this study containing a limited number of patients, Iopamidol was shown to be a diagnostically effective and safer contrast medium for performing cervical myelography.
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PMID:Iopamidol vs metrizamide: a double blind study for cervical myelography. 717 74

The clinical, laboratory and EEG findings of 4 uremic patients on hemodialysis who accidently developed acute hypercalcemia were reviewed. An acute central nervous system syndrome developed, associated with the clinical changes of disorientation, dysarthria, seizures, myoclonic jerks, hallucinations, irritability, confusion, memory and judgment defects plus bizarre behavior. The EEG findings demonstrated diffusely severe slow background activity in all tracings. In addition, the EEG abnormalities as well as the clinical findings disappeared when serum calcium returned to normal. Hypercalcemia, a reversible condition, seems to have been the cause of this clinical syndrome which should be differentiated from dialysis dementia, a condition known to be irreversible and fatal.
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PMID:Acute hypercalcemia in hemodialysis patients: distinction from 'dialysis dementia'. 738 36

A 25-year-old woman suffered from hyperemesis gravidarum when she was seven weeks pregnant. Since her vomiting continued, she received intravenous dextrose and electrolytes without thiamine in a hospital. One month later, she developed gait disturbance, followed by confusion and dysarthria. On admission to our department, she was confusional and had ataxic dysarthria. Spontaneous and gaze evoked nystagmus was present. Limb coordination was bilaterally ataxic. Based on her clinical course and symptoms, she was diagnosed as having Wernicke's encephalopathy. From the admission day, intravenous infusion of vitamin B1 (600 mg/day) was started. A few days later, her consciousness and limb ataxia began to improve. However, truncal ataxia and polyneuropathy became evident. Eight weeks after onset, she developed Korsakoff's psychosis such as anterograde and retrograde amnesia, disorientation and confabulation. We administered large amounts of corticosteroid (methylprednisolone 500 mg/day) in order to reduce brain edema or stabilize the impaired blood-brain barrier. Soon after, her psychosis began to improve gradually. She recovered remarkably from the psychosis, but she was left with persistent nystagmus, mild ataxic gait and polyneuropathy. The present case suggests that corticosteroid may have the beneficial effect on Wernicke-Korsakoff syndrome.
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PMID:[Beneficial effect of steroid pulse therapy on Wernicke-Korsakoff syndrome due to hyperemesis gravidarum]. 795 22

A 28-year-old man was admitted to our hospital, because of double vision, memory disturbance and dysarthria. These symptoms developed in November, 1994. His mental activity was gradually decreased and he became apathetic. A physical examination on admission was unremarkable. There were no lymphadenopathy, hepatosplenomegaly or skin rash. Neurological examination revealed disorientation, decreased mental activity and left gaze-evoked nystagmus. Neuropsychological tests demonstrated impairment of recent memory and performance but frontal lobe functions were maintained. Laboratory data showed hyponatremia, elevation of antinuclear antibodies and IgG-antibodies to Epstein-Barr virus capsid antigen and Epstein-Barr virus nuclear antigen. A brain MRI revealed multiple lesions in the cerebral subcortex, cerebellum and brainstem. These lesions showed high signal intensity on T2-weighted images and enhanced high signal intensity on T1-weighted images using Gd-DTPA injection. A cystic mass was seen between bilateral lateral ventricles and contacted with the fornix and thalamus. Lymphomatoid granulomatosis was diagnosed by an open brain biopsy, which showed diffuse infiltration of small lymphocytes, histiocytes and plasma cells, especially around the small vessels. Epithelioid granuloma or necrosis was not seen. An immunohistochemical study showed that nearly all lymphocytes were MT-1 positive T lymphocytes. The patient was treated by whole brain irradiation (30Gy) and pulse therapy of methylprednisolone. Multiple lesions in the brain responded to these modalities with complete resolution of the lesions and clinical improvement. In this case, impressive multiple and cystic lesions seen on brain MRI disappeared by whole brain irradiation and steroid. Since etiologies of multiple lesions on MRI includes many possibilities, histological diagnostic methods should be performed to obtain a definitive diagnosis. This is the first case of lymphomatoid granulomatosis that showed multiple and cystic lesions on brain MRI in Japan.
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PMID:[Lymphomatoid granulomatosis of the brain with multiple lesions on MRI]. 893 97


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