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)

Fifty-six closed head injured patients referred to a rehabilitation medicine center were examined to determine the presence and nature of verbal deficits. Eighteen (32 per cent) presented classical symptoms of aphasia, 21 (38 per cent) had motor dysarthria, and 17 (30 per cent) had no discernible aphasic deficit in spontaneous speech, but showed clear evidence of verbal deficit on testing. No patient admitted with sequelae of closed head injuries was spared some degree of verbal impairment, however mild or apparent. Dysarthric patients, without exception, showed subclinical linguistic deficits. Although the patients studied were thought to be more severe than most of those reported in the literature, our findings suggest the desirability of a careful linguistic evaluation of all closed head injured patients because of the potential impact of verbal deficits on rehabilitation out come.
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PMID:The nature of verbal impairment after closed head injury. 744 Dec 32

We report 3 cases of opercular myoclonic status epilepticus (OMASE), characterized by fluctuating cortical dysarthria without true aphasia associated with epileptic myoclonus involving bilaterally the glossopharyngeal musculature. In this syndrome, the inferior rolandic area of either one or the other hemisphere is involved by an epileptogenic lesion of various etiology. Ictally, clonic expression was consistent with epilepsia partialis continua (EPC) and bilaterally and symmetrically involved palatal muscles (cases 1-3), tongue (cases 2 and 3), lips and chin (case 3), and inferior jaw (case 1) due to bilateral projections of the inferior corticonuclear pathways. Postictally, the main clinical sign was pseudobulbar palsy, consistent with Todd's palsy. In our cases, OMASE was either of vascular (cases 1 and 2) or tumoral origin (case 3). In adulthood, early recognition of OMASE, although nonspecific, may be important for early management of carotid occlusive disease because it usually indicates an acute opercular infarction.
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PMID:Opercular myoclonic-anarthric status epilepticus. 761 13

Alteration of speech is a rare but distressing complication of orthotopic liver transplantation (OLT). We describe a characteristic speech disorder identified in a large series of consecutive patients undergoing OLT. Between 1988 and 1993, 525 adults underwent OLT. For all recipients with neurologic complications, we reviewed clinical findings, imaging and electrophysiologic test results, and perioperative laboratory data. Five patients (ages 23-52; UNOS status 3-4) exhibited a characteristic pattern of stuttering dysarthria, leading to complete loss of speech production, occasionally with elements of aphasia. In four of the five patients, right-sided focal seizures were subsequently noted. All cases presented within the first 10 postoperative days and improved with 1 month of cessation of cyclosporin (CyA), although halting, monotonous speech was evident to some degree in all five for up to 1 year. There was no correlation between onset of symptoms and CyA levels. None of the patients has clinical or radiologic findings suggestive of central pontine myelinolysis or akinetic mutism. EEGs and Spect scan results were consistent with dysfunction in the left frontotemporoparietal regions of the brain. A characteristic speech disorder, which may be described as cortical dysarthria or speech apraxia, occurs in approximately 1% of adults undergoing OLT. Prompt recognition of this syndrome and temporary cessation of CyA therapy may favorable affect the course.
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PMID:Loss of speech after orthotopic liver transplantation. 762 86

We report a 74-year-old man with a lung cancer, who developed right leg weakness, neurogenic bladder, and multiple cranial nerve palsies. The patient was well until December of 1992, when he was 74-year-old, when he noted transient double vision; in February of 1993, he noted numb sensation and weakness in his right leg. Later in the same month, he developed overflow incontinence of urine and weakness in his right face. He also noted deafness in his left ear (he had a marked loss of hearing in his right ear since childhood because of otitis media). His weakness in his right leg had progressed, and he was admitted to our service on March 19, 1993. On admission, he was afebrile and BP was 130/50 mmHg. General physical examination was unremarkable. On neurologic examination, he was alert and oriented to all spheres; no dementia was noted nor were detected aphasia, apraxia, and agnosia. His optic fundi were unremarkable; ocular movement appeared normal, however, he complained of diplopia in far vision. Sensation of the face was intact. He had right facial palsy of peripheral type; he was unable to close his right eye, and Bell's phenomenon was observed on attempted eye closure. On the left side, he had facial spasm. He had marked bilateral deafness. He had no dysarthria or dysphagia. The remaining of the cranial nerves were intact. Motor wise, he was unable to stand or walk alone; weakness did not appear to account for his difficulty in gait; manual muscle testing revealed 4/5 weakness in his tibialis anterior muscle, 1/5 in the peroneus longus, 0/5 in his extensor hallucis longus and extensor digitorum longus, all on the right side. Brachioradial and quadriceps femoris reflexes were increased to 3/4; plantar response was equivocal on the right side, and flexor on the left. Sensory examination revealed loss of touch and pain sensation in the L5 and S1 distributions in his right leg: vibration and position sensations were also diminished in his right foot. He had overflow urinary incontinence with loss of bladder sensation. Marked nuchal stiffness was noted, however, no Kernig's sign or eye ball tenderness was present. Pertinent laboratory findings were as allows; WBC 8,100/microliters, Ht 42.5%, platelet 326,000/microliters, TP 6.8 g/dl, BUN 16 mg/dl, creatinine 0.54 mg/dl, glucose 95 mg/dl, Na 136 mEq/l, K 4.4 mEq/l, Cl 100 mEq/l; liver profile was normal; CEA 436.6 ng/ml, CA19-93 U/ml; urinalysis was normal.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 74-year-old man with urinary incontinence, right leg weakness and multiple cranial nerve palsies]. 766 22

We describe a clinico-pathological variant of a degenerative disorder involving Broca's, Wernicke's, and supplementary motor areas, which presented as primary progressive aphasia, dysarthria, bucco-facial apraxia, and hearing loss as initial symptoms, followed by organic personality changes. Postmortem examination revealed severe focal atrophy of the cerebral convolutions in the frontal operculum, superior frontal gyrus, and superior and transverse temporal gyri in addition to diffuse atrophy of the frontal and temporal lobes in both hemispheres. Microscopical examination revealed argyrophilic neuronal inclusions (ANIs) in the neuronal perikarya and presynaptic terminal throughout the central nervous system, as well as neuronal loss and swollen chromatolytic neurons in the affected cortices. Neocortical ANIs showed a positive immunoreaction with an anti-tau antibody but only a weak reaction with an anti-ubiquitin antibody immunohistochemically. Ultrastructurally, neocortical ANIs consisted of 15-nm thick smooth-surfaced tubules and tubules with constrictions at 120-150-nm intervals; thus they were different from the typical paired helical filaments of the 80-nm interval constrictions observed in the subiculum. ANIs were also found in the basal ganglia, brain stem nuclei, and cervical cord. Accordingly, ANIs appear distinct from neurofibrillary tangles (NFTs) of progressive supranuclear palsy, NFTs of Alzheimer-type dementia, and Pick bodies. The authors consider that this case fits the histopathological criteria of corticonigral degeneration with neuronal achromasia except for the unusual extension to the temporal lobes.
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PMID:Corticonigral degeneration with neuronal achromasia presenting with primary progressive aphasia: ultrastructural and immunocytochemical studies. 770 78

Disturbances of vocal function in patients with apraxia of speech are well known in the literature and have often been described. Although apraxia of phonation is presumed, only 1 case is mentioned in the literature. We present a 51-year-old man (with missing signs of dysarthria and aphasia after spontaneous right temproparietal hemorrhagia) who had aphonia and missing respiration during speaking, whereas articulation was nearly undisturbed. After differential diagnostic exclusion of other central disorders of phonation we classify this patient as having apraxia of phonation or laryngeal apraxia.
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PMID:[Apraxia of the larynx]. 772 79

We report a 78-year old woman with 30 years history of rheumatoid arthritis and nephrotic syndrome, who developed right hemiparesis and renal failure recently. The patient was diagnosed as having rheumatoid arthritis in 1965, and had been treated with gold -sol, steroid hormone, and non-steroidal anti-inflammatory drugs intermittently. Later on her clinical course was complicated by nephrotic syndrome, however, her renal function was well compensated. Otherwise, she was apparently doing well until October of 1988 when she had an onset of anomic aphasia; she was 73-year-old at that time. She was admitted to our hospital; a cranial CT scan at that time revealed a low density area in the left temporal region, and she was diagnosed as suffered from an atherothrombotic infarction involving the left middle cerebral artery territory. She recovered soon and was discharged for out patient follow up with ticlopidine 100 mg/day. She was doing well until December 15, 1990, when she had an acute onset of nausea, vomiting, and speech disturbance; she was admitted to our hospital for the second time. On admission, she was alert, but she had motor aphasia, right hemiparesis, and dysarthria. A cranial CT scan revealed a low density area in the left temporal region extending into adjacent frontal and parietal areas including the angular gyrus; in addition, leukoaraiosis, cortical atrophy, and ventricular dilatation were noted (Fig. 1A, B). She was treated supportively, and she showed improvement in her aphasia, however, moderate weakness remained in her right upper and lower extremities. She was discharged for out patient follow up. She was doing well until May 21, 1993, when she developed difficulty in swallowing and speech. She became unable to take foods orally and she was admitted again on May 31. On admission, she was afebrile and BP was 120/80 mmHg. General physical examination was unremarkable except for pitting edema and multiple contracture of her joints. On neurologic examination, she was alert but appeared to have aphasia and dementia; she could utter only a few simple words, and was able to understand only simple questions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 78-year-old woman with rheumatoid arthritis, right hemiparesis, and renal failure]. 789 38

Communication impairments, with or without a swallowing disorder, are common among older adults. Aphasia, which is usually caused by a focal lesion, can affect spoken and written language, auditory comprehension, and reading ability but by itself does not affect intellectual and cognitive abilities. A cognitive-communicative impairment is related to underlying cognitive deficits in memory, attention, or visual perception and is seen with traumatic brain injury and nontreatable dementia. Voice and speech impairments such as dysarthria and apraxia of speech may lead to self-imposed social isolation and depression. Dysphagia may accompany a communication disorder or exist independently. As a primary care physician, your in-office workup can help diagnose a communication disorder and identify candidates for referral to an otolaryngologist and/or speech-language pathologist.
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PMID:Communication disorders: what to look for, and when to refer. 800 59

We report a case of foreign accent syndrome (FAS) without aphasia. The patient was a right-handed, 44-year-old woman, a native Japanese. Disposition and inversion of pitch accents and appearance of unnecessary stress accents made her speech sound foreign, like that of a Korean. MRI demonstrated an infarction in the middle fifth of the posterior lateral aspect of the left precentral gyrus. Limited motor cortex damage causes FAS without dysarthria, apraxia of speech, or aphasia.
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PMID:A case of foreign accent syndrome without aphasia caused by a lesion of the left precentral gyrus. 819 Mar 23

The purpose of the present study was to survey and compare the knowledge and attitudes of final year occupational therapy, physiotherapy and speech-language therapy students, concerning the role of the speech-language therapist as a member of the stroke rehabilitation team in the hospital setting. In order to achieve this aim, a questionnaire was administered to final year students in these three disciplines, and included questions on most areas of stroke rehabilitation with which the speech-language therapist might be involved, as well as the concepts of rehabilitation and teamwork in relation to stroke rehabilitation. Results suggested a fairly good understanding of the concepts of rehabilitation and teamwork. Students appeared to have a greater understanding of those disorders following a stroke, with which the speech-language therapist is commonly involved, such as Aphasia, Dysarthria, Verbal Apraxia and Dysphagia. However, students appeared to show less understanding of those disorders post-stroke, for which the speech-language therapist's role is less well defined, such as Agraphia, Alexia and Amnesia. In addition, a high percentage of role duplication/overlapping in several aspects of stroke rehabilitation, such as family and social support, was found. Several implications for facilitating communication, collaboration and understanding between paramedical professions, as well as for further research are also provided.
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PMID:The knowledge and attitudes of occupational therapy, physiotherapy and speech-language therapy students, regarding the speech-language therapist's role in the hospital stroke rehabilitation team. 860 43


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