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Query: UMLS:C0013362 (dysarthria)
3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Broca's aphasia is characterized by disorders on the phonemic, syntactic and lexical level of linguistic description. It is not only the patient's speech which is impaired; abilities to comprehend, read and write are likewise impaired. Articulatory disorders (dysarthria) which are due to an impaired innervation of the phonatory and articulatory musculature may exist. However these disorders do not account for all the linguistic deficits found in cases of Broca's aphasia. The characteristic feature enabling a differential diagnosis of Broca's aphasia is agrammatism.
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PMID:[Broca's aphasia. The clinical picture and a consideration of the neurolinguistic structure (author's transl)]. 7 59

The mute or nearly mute patient who is alert and has good understanding of speech and a right hemiparesis could have Broca's aphasia, akinesia of speech (transcortical motor aphasia), or aphemia. The patient who has Broca's aphasia does not write well, and his speech does not improve greatly with repetition. The speech of a patient with akinesia of speech improves with repetition. The aphemic patient writes normally, but his speech does not improve with repetition. The mute patient whose eyes are open but who is poorly responsive and moves little or not at all could be an akinetic mute (with either a cingulate or a thalamomesencephalic lesion) or have a locked-in syndrome. The latter is diagnosed by asking the patient to look up and down or to open and close his eyes. If he obeys these commands, the physician questions him using a code of eye movement responses. If the patient fails to respond at all, he is an akinetic mute; intense stimulation may result in speech or movement. If the patient is drowsy and has third nerve involvement, the lesion is in the thalamomesencephalic reticular formation. If the patient appears alert and has episodes of agitation, he probably has bilateral lesions in the gyri cinguli. Patients with weakness of the bulbar musculature (facial, palatal, and tongue weakness and dysphonia) may have either upper motor neuron or lower motor neuron lesions. Only bilateral upper motor neuron lesions produce permanent dysarthria. As a typical example, a patient has a transient left hemiparesis with dysarthria and almost completely recovers. Later, however, a right hemiparesis develops and the patient experiences severe bilateral facial weakness, drooling, dysphagia, and severe dysarthria. The absence of atrophy of the bulbar musculature, a hyperactive jaw jerk and gag reflex and, sometimes, inappropriate laughing or crying episodes indicate that the lesion is located above the medulla in the corticobulbar tracts. Flaccid paralysis, absence of the jaw jerk or gag reflex, and absence of other upper motor neuron signs, such as upgoing toes, indicate a lower motor neuron or neuromuscular junction problem. Appropriate tests to rule out myasthenia gravis should be done. The other conditions discussed here are often obvious from their clinical presentation. Although the specific disorder of speech sometimes is helpful in localizing the cause, in most patients, the associated deficits on neurologic examination are of greatest value.
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PMID:Nonlanguage disorders of speech reflect complex neurologic apparatus. 16 83

A case of left atrial myxoma with repeated multiple cerebral emboli is reported. A-44-year-old man first developed a sudden right hemiparesis in October 1969. After intensive physical theraphy, strength improved and he was able to return to his work. In March 1970, he suddenly lost consciousness and remained comatose for a day. Upon waking, he had a profound right hemiparesis, motor aphasia and Gerstmann's syndrome. He was admitted to Hiroshima City Hospital on August 1, 1970. The cardiac examination, including an electrocardiogram, was entirely normal. Laboratory studies revealed a normal blood count and urinalysis; erythrocyte sedimentation rate was elevated (32mm/hour). On a left cerebral angiographic study, performed on September 6, 1971, multiple aneurysmal dilatations of the branches of the left middle cerebral artery were demonstrated. No specific diagnosis was made. In January 1973, he developed dysarthria, dysphagia and quadriplegia because of the recurrent cerebral attacks. He had a high temperature continuously for three days and died on May 30, 1974. At autopsy a myxoma with the peduncle was attached to the septal wall of left atrium, and there were old infarcts in the brain, the myocardium and the kidneys.
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PMID:[Left atrial myxoma with repeated multiple cerebral emboli]. 103 60

The authors report a case of glioblastoma in which MR images with Gd-DTPA enhancement changed rapidly during the early stage. A 61 year-old male presented with sudden right facial spasm and dysarthria. However, both a plain and an enhanced CT failed to demonstrate any abnormal lesions. On the other hand, T2 weighted MR image revealed a well circumscribed high intensity lesion in the left frontal lobe without mass effect. This lesion could not be differentiated from cerebral infarction, since no contrast enhanced lesion was able to be observed in T1 weighted MR image with Gd-DTPA. His symptoms gradually became aggravated and at 3 months from the onset, MR image with Gd-DTPA disclosed a small enhanced lesion in the left frontal lobe near the cortical surface. After 6 months from the onset, he suffered from right hemiparesis and motor aphasia. The MR image with Gd-DTPA at this time showed a large enhanced lesion in the left frontal lobe with mass effect. He was admitted to our hospital, and subtotal removal of the tumor and intraoperative radiation was carried out. The patient did well postoperatively without additional neurological deficit, and then he received additional radiation therapy. It should be noted that Gd-DTPA enhanced MR image might fail to reveal the lesion of glioblastoma in its early stage, while T1 weighted image discloses only the gyral swelling.
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PMID:[A case of glioblastoma in which early diagnosis was difficult by MRI]. 194 85

A 47-year-old right-handed man underwent craniotomy for clipping of an aneurism at the trifurcation of the left middle cerebral artery. Subsequently, he suffered a left hemisphere CVA after which his speech and language resembled that of Broca's aphasia with accompanying apraxia of speech. Medical, behavioral, and acoustical data amassed over a period of several months indicated numerous contraindications to traditional diagnoses of Broca's aphasia, apraxia of speech, and dysarthria. Ultimately, it was determined that the patient had a selective impairement of phonation or laryngeal apraxia. This was illustrated dramatically when he was taught to use an electrolarynx which allowed him to bypass his disrupted phonatory system. Speaking with the electrolarynx, the patient communicated normally. Any semblance of Broca's aphasia disappeared. Supralaryngeal articulation was normal; apraxia of speech behaviors were absent. This case report indicates that dissociation of oral and laryngeal gestures due to brain injury is possible. Mechanisms underlying such a dissociation for this case are reviewed. The possibility of discrete center lesions in the frontal motor association area causing different types of apraxia of speech is discussed.
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PMID:Selective impairment of phonation: a case study. 320 76

The aim of this study is to determine to what extent a phonologically contrastive function of the prosodic feature of length is resistant to impairment in aphasia. The language chosen for investigation is Thai, a language which contrasts short and long vowels. Subjects included two Broca aphasics, one transcortical motor aphasic, one Wernicke aphasic, one conduction aphasic, one nonaphasic right-brain-damaged patient, one nonaphasic cerebellar dysarthric patient, and five normal controls. The subjects read a list of words containing short and long vowels. Vowel durations were measured from spectrograms. The results showed that the timing of vowel duration for signaling the contrast between short and long vowels remains relatively intact in nonfluent as well as fluent aphasic patients. These data are brought to bear on issues concerning the specialization of the left hemisphere for temporal processing, the contribution of the right hemisphere to the processing of nonaffective components of prosody, the nature of prosodic disturbance in Broca's aphasia and cerebellar dysarthria, and the separate disruption of prosodic features.
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PMID:Prosodic disturbance in aphasia: vowel length in Thai. 608 17

A syndrome of dysarthria following the appearance of small left frontal-lobe lesions has been recognized for many years but identified by numerous labels. Varied terminology has led to confusion in the literature and inadequate recognition of this syndrome as a distinctive clinical entity. We gathered clinical and anatomic (computed tomographic) data on four patients with this dysarthric syndrome and reviewed cases from the literature that contained sufficient clinical and anatomic data for comparison. These patients had a distinctive syndrome of dysarthria without aphasia, caused by small lesions of the motor system for articulation: pars opercularis, inferior prerolandic gyrus, or white matter deep to those regions. This syndrome should be distinguished from Broca's aphasia, Broca's area aphasia, transcortical aphasia, and subcortical aphasia. Aphemia is not mild Broca's aphasia; it is severe dysarthria, at times in the setting of transient Broca's aphasia.
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PMID:Aphemia. Clinical-anatomic correlations. 662 83

We present a rare case of thalamic germinoma with crossed aphasia in a dextral. A patient, 17-year-old righat-handed male, was admitted to Nippon Medical School Hospital with chief complaints of headache, abnormality of visual field and speech disturbance. There were pigmentations on the back of hand, foot and the perineum. Neurological examination revealed left homonymous hemianopsia, right slight degree of ptosis, left facial palsy, a mild paresis of the left upper extremity and motor aphasia. Right carotid angiography showed marked unrolling and midline shift of right anterior cerebral artery. CT scan revealed ring-like high density area in the right thalamic region, which was enhanced after constant infusion. Brain scintigraphy also showed an abnormal accumulation at the same site. The hen-egg sized tumor of 40 g. weight was almost totally removed by the right fronto-parietal craniotomy. The tumor was characterized histologically by the so-called two cell pattern with teratomatous components. As postoperative treatment local injection of adriamycine, irradiation and immunotherapy with picibanil were performed, and then left hemiparesis was markedly improved without sign of recurrence. Language evaluation was performed after operation. There were dysarthria, remarkable word amnesia, paraphasia and perseveration. Repetition was also impaired. His speech function was concluded to be a mixed type aphasia mainly composed of Broca's aphasia. The speech function of thalamus and crossed aphasia with dextrales were discussed.
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PMID:[A case of thalamic germinoma with crossed aphasia in a dextral (author's transl)]. 743 99

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

Posteroventral pallidotomy (PVP) was carried out in 86 patients with Parkinson's disease, who presented marked bradykinesia, freezing of gait and postural defect associated with rigidity and tremor in 82 patients (bradykinesia type), and similar gait and postural problems with minimum signs of rigidity and tremor in 4 (pure akinesia type). The stereotactic coordinates of Leksell's device were calculated from MRI and conventional ventriculography. The final target was defined by microelectrode techniques in the basal ganglia. The microrecording study revealed a very high background activity in the internal pallidum in patients of the bradykinetic type, however, a much lower pallidal activity in patients of the pure akinesia type. Fifty-eight patients underwent unilateral PVP, and 28 underwent bilateral surgery. Following PVP, rigidity tremor and poor reciprocal movements were significantly improved especially in the contralateral extremities. The most dramatic findings were the reversal of akinetic symptoms and wearing-off phenomena. The patients were followed up for 3-30 months (mean = 8) after surgery. Of the 82 bradykinesia type patients, good result were obtained in 48 (58%), fair results in 26 (32%), and minor improvement or no change in 8 (10%). In all the 4 patients of the pure akinesia type, recurrence of the akinetic symptoms occurred after a temporal improvement lasting a few days to 3 month after surgery. There was worst dysarthria in 3 patients, hemiparesis in 1 and partial motor aphasia in 1. The visual field problem was not complicated in any patients. These findings suggest that akinetic symptoms in PD are implicated in overactive pallidal outputs with putative GABAergic modulator by excessively inhibiting pedunculopontine nucleus activity (midbrain locomotor and posture regions) as well as thalamic activity. Partial interruption of the pallidal efferents eliminates the akinetic symptoms by disinhibitory effects on the target structures. The pathology of PD of the pure akinesia type is supposedly in the brainstem and should be excluded from indication of pallidotomy.
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PMID:Surgical control of akinesia in Parkinson's disease. 879 Oct 23


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