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 authors report a case of acute lithium poisoning, of double interest by virtue of its accidental origin and the fact that the patient suffered from chronic uraemia treated by intermittent haemodialysis, without residual diuresis. Neurological involvement consisted of a succession of dysarthria, behaviour disturbance, extra-pyramidal hypertonia and finally coma with respiratory difficulties. A favourable outcome was obtained by daily haemodialysis which made possible the elimination of almost all the lithium introduced into the body.
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PMID:[Accidental lithium poisoning in a patient with chronic hemodialysis]. 124 Nov 29

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

Cerebral dyspraxia associated with hemodialysis is a progressive, fatal syndrome. Patients suffer from a combination of psychiatric and neurological signs and symptoms. Psychiatric manifestations include anxiety, depression, paranoid ideation, and a progressive dementia with impaired concentration, decreased memory, personality changes, and hallucinations. Neurological findings include deliberate speech, stuttering, dysarthria, dyspraxia of speech and movement, tremulousness, myoclonic activity, asterixis, and seizures. These symptoms are aggravated during and immediately following dialysis. Patients usually die within 6 months of its onset. The etiology is unknown. Treatment efforts have failed to reverse its course. Recognition of this syndrome is highlighted so that informed, critical decisions can be made as to whether to continue dialysis therapy.
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PMID:Clinical and psychological test findings in cerebral dyspraxia associated with hemodialysis. 125 51

This report reviews 13 cases in which a dysarthria appeared, remitted, and reappeared within seconds. The speech pattern of each case was characteristic of ataxic dysarthria. A cinefluorographic film for one of the subjects provided a rare opportunity to study the articulatory dynamics of this disorder. Multiple sclerosis either was given as a diagnosis or was strongly suspected in each case, and carbamazepine has been an effective treatment. Speculations concerning the origin of the paroxysmal and ataxic character of the dysarthria are presented along with a preliminary checklist for identifying the disorder.
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PMID:Paroxysmal ataxic dysarthria. 125 44

The course of Motor Neurone Disease (MND) is described in 22 patients in respect of the extent and duration of the disabilities. The average stay in hospital in the terminal phase in 20 patients followed to the time of their death was 6.6 months for men and 4.7 months for women. The total duration of the disease ranged from 11 to 45 months, with an average of 28.7 months for men and 22.2 months for women. Between the bulbar cervical lumbar and mixed forms of the disease at the onset there emerged no difference in average survival. On woman of 32 is still alive 10 years after the onset, and one after 2-1/2 years. The hospital staff were exposed over many months to the progressive deterioration in breathing, swallowing, posture and mobility, and emotional crises and dysarthria aggravated the problems of management. Pain was a feature in one-third of the patients. In the treatment, physiotherapy with the accent on passive movements was found helpful. Although formal occupational therapy was not accepted by half of the patients, it was important to talk to them frequently, and encourage any means of expression such as painting, writing or dictating diaries, poems or essays. The indications for gastrostomy feeding are discussed, and the problem is raised of assisted respiration in this disease.
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PMID:The problems of motor neurone disease. 125 10

The Troyer syndrome was found by Cross & McKusick (1967) in 20 members of 12 Old Order Amish families in Holmes County, Ohio; it is a form of hereditary spastic paraplegia combined with distal muscle wasting, i.e. signs of involvement of lower motor neurons. The condition usually begins at 1 to 2 years and progresses at variable rates. Further manifestations include growth retardation, delayed speech development with dysarthria and drooling, and cerebellar signs; mental functions are usually not affected but severe emotional lability is a common finding. Brothers in a Wisconsin Old Order Amish family are reported with spastic diplegia, mental retardation, behavioral disorder and shortness of stature; the condition apparently is not progressive, and may be a "new" syndrome but could also represent a variant of the Troyer syndrome. Autosomal recessive inheritance is most likely, although consanguinity of the parents could not be proven. Another child in this family suffers from focal scleroderma (morphea) which is not related to the neurological syndrome.
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PMID:Familial spastic paraplegia with distal muscle wasting in the Old Order Amish; atypical Troyer syndrome or "new" syndrome. 126 Oct 70

The differential diagnosis of developmental speech disorders may be very difficult. We tried to differentiate between the developmental dysphasia and dysarthria by means of CERA, using the different kinds of stimuli--tone bursts, words and white noise. The BERA was performed using the filtered clicks as stimuli. We have found the responses to tone, verbal and noise stimuli in children with developmental dysarthria. The latency times were prolonged to verbal and noise stimuli. We did not find any responses to verbal and noise stimuli in children with developmental dysphasia. At the BERA investigation we did not find the auditory evoked brainstem responses in children with developmental dysarthria on the side of motoric innervation lesion. The latency times of waves N3 and N5 were prolonged in children with developmental dysphasia. The CERA and BERA seems to be a good differential diagnostic tool for differentiation between these two kinds of developmental speech disorders. The results confirmed also that there are the mixed forms of those developmental speech disorders.
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PMID:Diagnostic possibilities of ERA in developmental speech disorders. 128 Mar 54

A 68-year-old right-handed woman was admitted to Tokyo Metropolitan Geriatric Hospital because of slowly progressive dysarthria and writing disability over 2-year period. On admission, severe dysarthria was observed, but no dysphagia. The dysarthria mostly resembled a type of pseudobulbar palsy, although it was associated with effortful speech production. An oro-facial apraxia was also found. She could name objects, and could understand spoken words correctly. Examination using the Western Aphasia Battery showed diminution of word fluency, impaired repetition and perseveration and writing errors. On the Wechsler Adult Intelligence Scale-R verbal IQ was 100 and performance IQ was 87. These scores did not suggest any significant degree of general intellectual deterioration. Wisconsin card sorting test disclosed mild frontal dysfunction. Magnetic resonance imaging showed cortical atrophy in the bilateral frontal and temporal lobes. Measurements of regional cerebral metabolic rate by 18F-FDG-PET demonstrated decreased uptake in the latero-dorso-inferior area of the bilateral frontal lobes, especially on the left side. The present case showed slowly progressive dysarthria and progressive aphasia without generalized dementia, and without typical aphasia. These symptoms are speculated to be related to the atrophy in the bilateral frontal and temporal lobes shown by MRI and the decreased metabolic rate in the left dominant bilateral frontal lobes on PET study. The pathologic process responsible for these lesions remains obscure.
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PMID:[Slowly progressive dysarthria and impaired language function--a case report]. 128 97

A case of hemihyperhidrosis and non-paralytic pontine exotropia due to brainstem infarction is reported. A 55-year-old hypertensive man developed right hemiparesis with slight dysarthria and nausea upon awaking. The right side of his face and right upper limb and trunk to the level of the Th8-9 territory showed hyperhidrosis, which disappeared in a week. Ocular motor examination revealed that during forward gaze with the left eye fixing, the right eye deviated outward. The patient was able to adduct the right eye to midposition with the right eye fixing. Rightward gaze elicited full abduction and right-beating nystagmus of the right eye, but the left eye did not adduct. When he attempted to gaze leftward, both eyes made the full excursion, but saccades were slow in that direction. Convergence was intact. Vertical gaze was full, and he did not show Horner's sign. This ocular sign, non-paralytic pontine exotropia, disappeared three days later. T2-weighted spin echo magnetic resonance imaging disclosed a small lesion with high intensity in the inner side of the left middle pons. This hyperhidrosis was thought to be caused by destruction of inhibitory fibers thermoregulating sweating. These findings suggest that at the level of the middle pons inhibitory fibers descend along the inner side of facilitatory fibers thermoregulating sweating, which are speculated to descend the dorso-lateral part of the pontine tegmentum. These findings also suggest that lesions of non-paralytic pontine exotropia may be located in the paramedian pontine reticular formation rostral to the abducens nucleus with ipsilateral medial longitudinal fasciculus lesion, but further investigation is necessary.
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PMID:[A case of hemi-hyperhidrosis and non-paralytic pontine exotropia due to brainstem infarction]. 129 Nov 62

A 51-year-old woman, with progressive gait disturbance and dysarthria, had been diagnosed as Menzel-type spinocerebellar degeneration. Later, she developed dystonic posture of upper limbs and bulging eyes. She was diagnosed as Machado-Joseph disease from neurological findings, which consisted of cerebellar signs, pyramidal tract signs and extrapyramidal tract signs and peripheral neuropathy. She died suddenly of unknown origin. Her illness lasted about 13 years. Neuropathological findings showed moderate neuronal loss with gliosis in the subthalamic nucleus, globus pallidus, substantia nigra, dentate nucleus, oculomotor and hypoglossal nucleus and anterior horn. Positron emission tomography (PET) using 15O steady state inhalation technique revealed reduction of cerebral blood flow and cerebral metabolic rate of oxygen in not only cerebellum but also cerebral cortex. These findings are different from typical PET findings of spinocerebellar degeneration.
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PMID:[A case of Machado-Joseph disease--cerebral blood flow and cerebral metabolic rate of oxygen]. 129 Nov 71


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