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)

Foix-Chavany-Marie syndrome (FCMS) is a syndrome that presents facio-pharyngo-glosso-masticatory diplegia with automatic voluntary dissociation. Its most common etiology is stroke in the regions of bilateral opercula. We described a 75-year-old woman with FCMS and crossed aphasia. She had cerebral infarction of left middle cerebral artery territory 23 years before. At that time she had transient right hemiparesis, but no aphasia. This time, she suddenly became mute and was brought to our hospital. Neurological examination revealed severe weakness in her bilateral lower face, pharynx, tongue, and sternocleidomastoideus. She had no weakness of limbs. Her listening comprehension was moderately disturbed and handwriting was paragraphic. Her emotional facial movement was maintained despite of disturbed volitional facial movement. CT scan disclosed fresh infarction at the right corona radiata and old infarction at the left middle cerebral artery territory. In this patient, lesions at the left operculum and right corona radiata with the preserved right operculum gave rise to FCMS. This implies following possibilities: 1) the corticobulbar tract and corticospinal tract run separately at the corona radiata, 2) volitional and emotional tracts of facial movement run separately at the corona radiata. It was demonstrated that FCMS is not always caused by bilateral operculum lesions. Our patient did not show aphasia after the first stroke including left language area, but became severely aphasic after the right corona radiata infarction. Simultaneous occurrence of FCMS and aphasia after corona radiata lesion suggested that the corticobulbar tract and a tract that conducts linguistic information are running adjacently in the corona radiata. Our case suggested that restricted corona radiata lesion may cause severe subcortical aphasia and in case of additional contralateral corticobulbar tract lesion, severe dysarthria may occur.
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PMID:[A case of Foix-Chavany-Marie syndrome and crossed aphasia after right corona radiata infarction with history of left hemispheric infarction]. 1020 73

Cerebral infarction is a well-documented complication of systemic lupus erythematosus (SLE), that usually occurs several years after the diagnosis of SLE. To our knowledge, however, strokes associated with vertebrobasilar artery involvement were not reported to present as an initial manifestation of SLE. We report two patients, who presented with vertebrobasilar territory infarction as an initial manifestation of SLE. Patient 1 was a 16-year-old girl, who developed dysarthria and ataxia. MRI showed multiple infarcts in the pons, cerebellum and thalamus. Four-vessel cerebral angiography showed multifocal stenoses in the vertebral and basilar arteries with beaded appearance. Patient 2 was a 26-year-old woman, who developed headache associated with dysarthria, dizziness and ataxia. MRI showed multiple infarcts in the cerebellum, medulla, pons, midbrain and thalamus. Cerebral angiography revealed occlusion of both vertebral arteries at the first cervical vertebral level with non-visualization of the basilar artery. Both patients were diagnosed as having SLE supported by laboratory results. Although rare, posterior circulation stroke can present as an initial manifestation of SLE, which may be attributed to vasculitis or dissection in the vertebral/basilar artery.
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PMID:Vertebrobasilar artery territory infarction as an initial manifestation of systemic lupus erythematosus. 1035 Feb 8

Little information is available concerning the latent effects of silent cerebral infarction (SCI) on dysarthria (DA), dysphagia (DP), or both. A detailed analysis of MR images of multiple cerebral infarction was carried out to determine whether SCI is associated with the development of DA or DP. In this study MR images of the supra- and sub-tentorial regions were obtained from 14 patients presenting with persistent DA and DP (DA + DP group) and 9 patients presenting with DA alone (DA group) after the first episode of cerebral infarction. The DA + DP inducing lesion was identified from the change in signal intensity and the side with symptoms in 6 patients. Involvement of 3 lesions of the bilateral cortical branches, striatum, and pons on the line connecting the contra-lateral SCI with the lesion were noted in 4 patients (67%, vs. 40% for the DA group). Latent association of SCI with the development of supra-nuclear DA and DP was noted in 1 patient each from the DA + DP and DA groups. The results of this study support the concept that SCI patients include those in which SCI is involved in the development of supra-nuclear DA or DP, and suggest that SCI should be treated.
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PMID:[Association of silent cerebral infarction with cerebral hemispheric--sub-tentorial infarction in patients with supra-nuclear dysarthria or dysphagia]. 1046 53

A 15-year-old woman with a history of transient dysarthria two years before, suddenly developed weakness of right upper extremity, right facial palsy, and dysarthria. She was admitted to our hospital on the third day. She had no hypertension, heart murmur and oedema. On neurological examination, she had mild right hemiparesis including face muscles and mild dysarthria. The right knee jerk was brisk with no Babinski's sign. Ataxia and sensory disturbance were not present. T2-weighted MRI showed a hyperintensity at the posterior limb of the left internal capsule. Cerebral angiography was unremarkable. Ultracardiography and 24-hour electrocardiography were normal. Laboratory data revealed no inflammatory findings, liver dysfunction, hyperglycemia and hyperlipidemia. Antinuclear and anticardiolipin antibodies were negative. Prothrombin time was normal, but activated partial thromboplastin time was slightly prolonged (35.4 sec, normal 25.2-34.4). Protein C, protein S and antithrombin III were normal. Heparin cofactor II (HC II) activity was decreased (44%) with normal HC II antigen (79%) and so she was diagnosed as heparin cofactor II deficiency type II (heparin cofactor II abnormality). Her father manifesting thromboangitis obliterans also had low HC II activity with normal HC II antigen. However, on her genetic analysis, we didn't detect any mutations in the coding region of HC II gene. Until now she has no recurrence of cerebrovascular attacks. On the basis of these results, we suspect that HC II deficiency was a possible risk factor of cerebral infarction in this case because she was so young and had no general risk factors except for HC II. No stroke associated with HC II deficiency type II has been reported up to date. This case is worth considering etiologies of juvenile cerebral infarction.
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PMID:[Juvenile cerebral infarction associated with heparin cofactor II abnormality. A case report]. 1096 62

We report a very rare case of pure anarthria with lesion analysis. A 44-year-old right-handed man suffered from a cerebral infarction with a mild right hemiparesis and speech disturbance. An MRI of the brain 1.5 months post onset revealed a lesion confined to the left central gyrus. One month after the onset, his spontaneous speech was dysprosodic and laborious. It was contaminated with dysarthria and phonological paraphasias. However, language comprehension, repetition and naming abilities were normal. Most remarkably he showed no impairment in writing with his left hand. Over the following months, his difficulties in verbal output showed general amelioration, but the isolated impairment in the domain of articulation characterized by dysprosody, dysarthria, and phonological paraphasia persisted. As for the symptomatology of pure anarthria resulting from precentral gyral lesions, there have been controversies about its pureness. Some argue that the so called pure anarthria always shows some degree of writing disturbances, albeit mild in degree. Others maintain there certainly exists the pure type without any signs of agraphia. In the present case lesions were limited to the central gyrus but spared the lowest opercular portion. The previous reports of pure anarthria that had mild agraphia all had lesions involving the opercular portion. We conclude the sparing of this area is most likely related with sparing of writing capacity in pure anarthria.
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PMID:[The left central gyral lesion and pure anarthria]. 1100 29

A 61-year-old man with recurrent ischemic attacks was examined by diffusion-weighted MRI (DWI). He had reversible right hemiparesis and dysarthria five times during admission. DWI was obtained on the first two attacks, the last attack and four days after the last attack. The first two attacks were clinically diagnosed as transient ischemic attack (TIA), and the last attack was cerebral infarction with symptoms persistent for one week with Babinski's sign. In the first and last images the apparent diffusion coefficient (ADC) declined to approximately 80% of the corresponding area. We conclude that different images showed TIA with ADC declining, TIA without ADC declining, the hyperacute phase of cerebral infarction before ADC declining, and cerebral infarction after ADC declining. Consecutive DWIs were helpful to understand the character of recurrent ischemic attacks.
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PMID:[A case of recurrent ischemic attacks: consecutive diffusion-weighted magnetic resonance imaging]. 1130 40

Spontaneous dissection of the intracranial vertebral artery has been increasingly recognized as a cause of vertebrobasilar ischemic stroke. However, little is known about its natural history and clinical course. The authors report a young patient with repeated cerebral infarction in the posterior cerebral circulation caused by dissection of the vertebral artery, which was not detected on the first angiogram. The otherwise healthy 22-year-old male suddenly developed visual disturbance. Neuroradiological examination revealed right occipital infarction, but cerebral aniography revealed no caliber change or other pathological findings. He was treated with antiplatelet therapy. Two years later, he suffered vertigo, nausea, and dysarthria due to newly developed left cerebellar and medullary infarction. Cerebral angiography revealed left vertebral artery occlusion. T1-weighted MR image demonstrated Gadlinium-enhanced intramural hematoma in the occluded left vertebral artery, which was compatible to the arterial dissection. The present case argues serial neuroimaging studies especially in young patients with vertebrobasilar stroke in order to rule out the arterial dissection, even if initial angiography failed to demonstrate any radiographical evidence.
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PMID:[Repeated vertebrobasilar ischemic stroke caused by an intracranial vertebral artery dissection not detected on the initial angiogram: a case report]. 1151 95

We report two cases of cerebral infarction in which swallowing function improved following swallowing rehabilitation. Patient 1 was an 82-year-old man, who was admitted due to rheumatoid arthritis and multiple cerebral infarction, suffering from aspiration pneumonia. The abnormality of swallowing was assessed by the water swallowing test and videofluorography. It has been reported that videofluorography is useful in the diagnosis of aspiration. Three weeks after the start of swallowing rehabilitation, the serum level of inflammatory markers and the chest X-ray had returned to normal. His score on the water swallowing test had improved. Patient 2 was a 68-year-old [correction of 62] man, who was admitted with severe hemiplegia, dysphagia and dysarthria. One month after the swallowing rehabilitation, videofluorography showed that the magnitude of aspiration into the trachea had decreased and the pooling of barium in the piriform sinus had disappeared. The patient could begin taking a little food by mouth. These results suggest that swallowing rehabilitation will be affect the clinical improvement of swallowing function and help preventing aspiration pneumonia in our hospital.
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PMID:[Swallowing rehabilitation in two elderly patients with cerebral infarction]. 1152 72

A case of cerebral infarction in a 4-year-old male is described. The child presented with an acute onset of right hemiplegia, central facial palsy, and dysarthria. He had no predisposing factors for cerebral infarction. A computed tomography scan showed a diffuse low-density area in the territory of the left miiddle cerebral artery. Magnetic resonance angiography disclosed multiple irregular narrowings in the left anterior and middle cerebral arteries. He recovered spontaneously from the stroke with minimal long-term complications, and repeated angiography disclosed a complete regression of the vascular changes 2 months after the stroke. There was no recurrence of stroke after 2-year follow-up. This case demonstrates the importance of longitudinal angiographic follow-up in childhood cerebral infarction of idiopathic origin.
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PMID:Reversible vascular changes in children with cerebral infarction. 1191 76

A 38-year-old man was admitted to our hospital with headache, dysarthria and paraparesis. Brain CT and diffusion MRI disclosed cerebral infarction at bilateral anterior cerebral artery (ACA) territories. His symptoms and signs deteriorated in several days despite intensive antithrombotic therapy, resulting in right hemiparesis, akinetic mutism, memory disturbance, change of personality, urinary incontinence, forced grasping, and starting delay of speech and motion. Cerebral angiography demonstrated occlusion with contrast pooling at the right ACA A2 portion. Stenosis and dilatation were found at left ACA A2 portion. An intimal flap was also demonstrated on serial angiography. This case was diagnosed as cerebral infarction caused by dissection of bilateral ACA. Although no definite primary arteriopathy was demonstrated, bilateral dissection could be occurred simultaneously.
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PMID:[A case of juvenile cerebral infarction caused by bilateral anterior cerebral artery dissection]. 1266 Nov 8


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