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)

Neuronal intranuclear hyaline inclusion disease (NIHID) has been recognized in 14 patients. It usually occurs in the first and second decades but has been seen in the sixth. Both sexes are affected by this sporadic multisystem degenerative disorder that has involved the central and peripheral nervous systems with fibrillar and granular intranuclear inclusions. NIHID appears to be several variants of a multisystem degenerative disease as illustrated by the combination of a spontaneous, degenerative central and peripheral nervous system disorder with neuronal intranuclear inclusions and severe atherosclerotic coronary artery disease in a 23-year-old white man. Beginning at 11 years of age, this patient had experienced diffuse muscle spasms, dysarthria, dysphagia, tremors, ataxia, oculogyric crises, progressive muscle weakness, and atrophy. At autopsy, neuronal intranuclear hyaline inclusions and neuronal loss were seen in his brain, brainstem, cerebellum, spinal cord, bowel, bladder, and esophagus. These fibrillary and granular Cowdry type A and B intraneuronal inclusions were consistent with the diagnosis of NIHID associated with severe coronary atherosclerosis.
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PMID:Neuronal intranuclear hyaline inclusion disease associated with premature coronary atherosclerosis. 244 45

This study included 125 cases of cerebellar infarction followed during an average period of 4.3 years. The diagnosis was made by CT or MRI. Infarctions localized to the territory of the superior cerebellar artery (SCA) and the territory of the posterior inferior cerebellar artery (PICA) occurred with the same frequency. Transient ischemic attacks preceded infarction in 26% of cases. Symptoms and signs were usual with sudden association of headache, dizziness, unsteadiness and vomiting. Vestibular signs were more important in infarctions of the PICA territory; cerebellar signs and dysarthria were more frequent in infarction of the SCA territory. A decreased level of consciousness developed in only 21% of cases. Surgical operation was required in 9 cases. Investigations have showed the large responsibility of cardiac embolisms and atherosclerosis. Short term outcome was more often favourable: 116 patients were alive at the end of the first month; 80% of survivors were independent one year later. At 5 years, 73% of patients were alive. After the acute period, mortality was mainly due to cerebro-vascular and cardiac events.
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PMID:[Clinical and evolutive aspects of cerebellar infarction]. 786 66

The territory of the lateral branch of the posterior inferior cerebellar artery (1PICA) supplies the anterolateral region of the caudal part of the cerebellar hemisphere. Because infarcts in the territory of the 1PICA have rarely been studied specifically, 10 patients with this type of infarct are reported. An 1PICA infarct was isolated in only three patients, whereas it was associated with brainstem infarct in four, with occipital infarct in one, and with multiple infarcts in two patients. The most common symptom at onset was acute unsteadiness and gait ataxia without rotatory vertigo (six patients). Unilateral cerebellar dysfunction was found in all patients, with limb ataxia (nine patients), dysdiadochokinesia (five patients), and ipsilateral body sway (four patients), but dysarthria and primary position nystagmus were notably absent. In the patients with a coexisting infarct in the brainstem, cranial nerve and sensorimotor dysfunction was prominent and often masked the signs of cerebellar dysfunction. Unlike other infarcts in the PICA territory, 1PICA territory infarcts were mainly associated with vertebral artery atherosclerosis (six patients), whereas cardiac embolism was less common (three patients). Unilateral limb ataxia without dysarthria or vestibular signs suggests isolated 1PICA territory infarction and should allow its differentiation from other cerebellar infarcts.
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PMID:Infarcts in the territory of the lateral branch of the posterior inferior cerebellar artery. 808 72

We studied 34 consecutive patients with non-mass-producing cerebellar infarcts using a standard protocol of investigations including magnetic resonance imaging (MRI). We analyzed the topography of infarcts to determine the involved arterial territories and we correlated the findings with neurological dysfunction and potential causes of stroke. Sixteen patients had an infarct in the territory of the posterior inferior cerebellar artery (PICA); 2, in the territory of the anterior inferior cerebellar artery (AICA); 13, in the territory of the superior cerebellar artery (SCA); and 8 had junctional infarcts between the territories of the medial and lateral branches of the PICA or PICA/SCA territories. PICA or medial PICA territory infarcts were manifested by acute vertigo and truncal ataxia, while the patients with lateral PICA territory infarcts presented with unsteadiness, limb ataxia and dysmetria without dysarthria. Patients with infarcts in the AICA territory were characterized by limb and trunk ataxia associated with signs of lateropontine involvement. Patients with SCA territory infarcts presented with dysarthria, unsteadiness and/or vertigo, limb ataxia, and dysmetria. Cardiac embolism was the main cause of large infarcts in the territories of the PICA (8/16) or SCA (4/7). Multiple small infarcts were associated with vertebrobasilar atherosclerosis (8/12). These clinical-MRI correlations allow better definition of the topographic and etiological spectrum of cerebellar infarction, which was previously based on pathological studies in subjects with severe infarction.
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PMID:The clinical and topographic spectrum of cerebellar infarcts: a clinical-magnetic resonance imaging correlation study. 849 23

We report a 91-year-old man who had a stroke and died of renal failure. He had been treated for hypertension since 20 years before the onset of the present illness. In addition, he was operated on a gastric cancer 17 years previously. Otherwise he was doing well until May 29, 1991 (when he was 87-year-old) when he had sudden onset of dysarthria and right facial weakness. He was admitted to our hospital. On admission, general physical examination was unremarkable, and neurologic examination revealed a mentally sound man with slight dysarthria, right facial weakness, orolingual dyskinesia, and dysequilibrium in which he showed difficulty in tandem gait; however, no cerebellar ataxia was noted. A cranial CT scan revealed leukoaraiosis with multiple low density areas in the cerebral white matter. His BUN was 37 mg/dl and Cr 2.2 mg/dl. His neurologic symptoms cleared within the next few weeks and he was discharged with ticlopidine 100 mg q.d.. He had been doing well after the discharge except for gradual worsening of his renal function; his BUN was 65 mg/dl and Cr 3.27 mg/dl in April of 1994. On March 10, 1995, he fell down and hit his back; he became unable to walk because of pain, and he was admitted again on March 16, 1995. On admission, his blood pressure was 170/80 mmHg. There was an 1 + pitting pretibial edema; otherwise general physical examination was unremarkable. Neurologic examination revealed an alert and oriented man, however, Hasegawa's dementia scale was 23/30. Higher cerebral functions as well as cranial nerves were intact. He showed some unsteadiness of gait, however, no motor weakness or ataxia was noted. Deep tendon reflexes were diminished, but Chaddock sign was positive bilaterally. Vibration was diminished in the feet, however, pain and touch sensations were intact. Laboratory examination revealed a compression fracture of the twelfth thoracic vertebra. Blood count and chemistries were as follows; Hb 7.6 g/dl, Hct 23.3%, TP 6.0 g/dl, Alb 3.6 g/dl, BUN 87 mg/dl, Cr 4.53 mg/dl, T-Chol 174 mg/dl, HDL-Chol 49 mg/dl, Glu 156 mg/dl, Na 142 mEq/L, K 5.4 mEq/L, Cl 115 mEq/L. A urine specimen contained 1 + protein and 1 + glucose, and the sediments contained hyaline casts. A cranial CT scan was essentially same as that taken four years ago. His hospital course was complicated with pneumonia, congestive heart failure, and progressive renal failure. He was treated with intravenous fluid, chemotherapy, and other supportive measures, however, he expired from respiratory failure on April 30, 1995. He was discussed in a neurologic CPC, and the chief discussant arrived at the conclusion that the patient had Binswanger's disease in the brain, benign nephrosclerosis from arteriolosclerosis due to hypertension, congestive heart failure, and pneumonia. Opinions were divided regarding the question as to whether or not this patient had Binswanger's disease. Although his cranial CT scan revealed leukoaraiosis, his dementia and gait disturbance was only mild until his fall on March, 1995. Clinical features did not conform to those of Binswanger's disease. Postmortem examination of the right hemisphere revealed wide spread atherosclerosis and arteriolosclerosis. The kidney showed benign nephrosclerosis due to arteriolosclerosis. Sclerotic changes were also seen in the coronary arteries and the left middle cerebral artery with 70% stenosis. Myelin stain showed diffuse myelin pallor of the cerebral white matters with scattered small infarcts. Arterioles in the white matter showed arteriolosclerosis. Small infarcts were also seen in the putamen and in the thalamus. This patient appeared to have had circulatory disturbance of the white matter which is the basic abnormality causing Binswanger's disease. However, white matter changes in this patient were not quite severe enough to make a pathologic diagnosis of Binswanger's disease.
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PMID:[A 91-year-old man with a stroke, hypertension, and renal failure]. 899 Apr 84

A 47-year-old man developed progressive muscular weakness in the left arm. MR images revealed low intensity signal lesions with ring enhancement by Gd-DTPA in right fronto-parietal lobes. At that time cerebral angiography was not performed because he refused. A tuberculin skin test showed strongly positive reaction and then administration of anti-tuberculous drugs was started. His symptom had remained stable for one year, but left facial palsy and dysarthria added about two years later. MR images revealed expansion of the lesions in right parietal lobe, adding cortical high intensity signal lesions with Gd-DTPA enhancement on T1-weighted images. Angiography disclosed tubular stenosis of right internal carotid artery at the portion of cervical to petrous segment and the local stenosis at right renal artery. These lesions were considered to be caused by fibromuscular dysplasia, but not atherosclerosis, because we could not find any atherosclerotic lesions in other arteries including right carotid bifurcation. His manifesting symptoms were ascribed to slowly progressive cerebral ischemia. And peculiar MRI findings in his early stage resembled those of inflammatory granulomatous diseases.
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PMID:[A peculiar MRI findings in a case with slowly progressive cerebral ischemia caused by internal carotid artery stenosis possibly due to fibromuscular dysplasia]. 1065 64

Analysis of 893 patients of ischaemic stroke in the stroke registry of Nizam's institute of Medical Sciences, Hyderabad is presented. 16% of them had lacunar infarction. The mean age at presentation was 56.9 years and male to female ratio was 3.5:1. The common risk factors included hypertension(62%),diabetes(38%) and smoking(28%). Six percent had an underlying cardiac source of embolism and none had significant (>50%) extracranial carotid atherosclerosis. In 22% of patients, no obvious risk factors could be identified. The frequency of risk factors was similar in patients with lacunar and non- lacunar infarctions. However, patients with lacunar infarction had higher frequency of diabetes and absence of significant (>50%) extracranial carotid artery disease. Pure motor hemiparesis was the presenting syndrome in 45% patients. Ataxic hemiparesis and sensorimotor stroke accounted for 18% each and dysarthria-clumsy hand syndrome for 14%. This study suggests that the frequency, risk factors and clinical profile of lacunar infarction in our stroke registry is similar to most of the western stroke registries.
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PMID:Frequency, clinical features and risk factors of lacunar infarction (data from a stroke registry in South India). 1087 73

A 68-year-old man was admitted to St Marianna University Hospital on account of loss of consciousness with left hemiplegia. During the hospital recovery course with a rehabilitation procedure, the patient's blood pressure was very unstable, fluctuating between high (210/110 mmHg) and low (110/70 mmHg) values accompanied by a fainting sensation. A second stroke of left hemiplegia took place 1 month later. Afterwards, his condition worsened to tetraplegia with dysarthria. Three months later, lung cancer with multiple metastasis including his left neck was found and he died from adynamic ileus 6 months after the onset of the present illness. Autopsy revealed nearly complete atheromatous obstruction and more than 50% stenosis, respectively, of his right common and internal/external carotid arteries. His intracranial arterial trunks and main branches were all patent with localized atherosclerosis of only moderate degree. The pathology of the brain existed predominantly in the right hemisphere in the border zone area between the anterior and middle cerebral arteries systematically with numerous disseminated foci of complete or incomplete necrosis, white matter and gray matter being involved independently. Involvement of centrum semiovale white matter is more extensive and intensive than that of gray matter. Of the gray matter, cerebral cortex as well as striatum, periventricular (the third ventricle) gray and cerebellar cortex was involved. The specific characteristic topography and distribution of the lesions together with their histopathology are described in detail with illustration. It is concluded that this case represents an outstanding example of hemodynamic cerebral circulatory insufficiency doubly caused by hemilateral carotid artery stenosis and repeated episodes of systemic hypotension.
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PMID:An autopsy case of hemilaterally dominant and systematic/extensive border zone infarction: sequela of preceding atherosclerotic obstruction of one common carotid artery followed by repeated episodes of systemic hypotension. 1183 34

Head and neck irradiation may lead to accelerated atherosclerosis over several years. Delayed stroke has been described after head and neck irradiation administered for a number of conditions. However, brain stem stroke has only rarely been associated with irradiation. We report a patient with medullary hemorrhagic infarction 6 years after radiotherapy for nasopharyngeal carcinoma. A 42-year-old normotensive Chinese male had rapid onset of vertigo, diplopia, ataxia, dysphagia, hypophonic dysarthria, hemiparesis, and respiratory distress. Cranial MR imaging 2 days after symptom onset showed medullary infarction, and cranial MR imaging 5 days after symptom onset showed medullary hemorrhage. He needed ventilatory support and died of bacterial pneumonia 1 month later. Other risk factors for stroke were absent. Hemorrhagic infarction in this patient was likely associated with the radiotherapy. Radiotherapy is the first choice of treatment for nasopharyngeal carcinoma, however, it may induce fatal medullary hemorrhagic infarction.
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PMID:Medullary hemorrhagic infarction after radiation for nasopharyngeal carcinoma. 1747

We report a case of a 55-year-old female presenting with headache. Neuroradiological investigations revealed a fusiform aneurysm at the M3 part of the right middle cerebral artery. The aneurysm rapidly developed in the course of one year. She underwent a craniotomy for superficial temporal artery middle cerebral artery bypass (STA-MCA bypass) and resection of the aneurysm. Pathological examination suggested that atherosclerosis was a predisposing factor for aneurysm formation. Although she had developed transient dysarthria and left-hand clumsiness after the operation, she was able to be discharged after 26 days with no neurological deficits. On reviewing the literature, fusiform aneurysms seem to be an important cause of subarachnoid hemorrhage and cerebral infarction of unverified origin. Etiology and treatment of spontaneous fusiform aneurysms in a branch of the middle cerebral artery are also discussed.
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PMID:[A case of unruptured fusiform aneurysm in a middle cerebral artery branch]. 1993 66


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