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

A 6-year-old boy developed a flaccid hemiplegia and dysarthria following several transient episodes of nausea, vomiting, and ataxia. An anomly of the dens was discovered, permitting subluxation of C-1 on C-2. A segmental occlusion of the right vertebral artery and an aneurysm of the left vertebral artery were found at the C-2 level, as well as a thromboembolic occlusion of the rostral end of the basilar artery. It appeared that the repeated cervical subluxation produced occlusive, aneurysmal, and embolic vascular disease, and that clinical symptoms were the result of ischemia in the territory perfused by the vertebrobasilar arteries.
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PMID:Occlusive vertebrobasilar artery disease associated with cervical spine anomaly. 113 Mar 56

A 73-year-old man was admitted with gait disturbance and dysarthria. He showed right-side cerebellar ataxia. Computed tomography of brain showed left thalamic bleeding. Nine months later, he was admitted again because of seizure and consciousness disturbance. He had a history of diabetes mellitus and gout for five years, but no hypertension. On physical examination the lungs and heart were normal. On neurological examination, he showed stupor,pupils and eye position were normal. He showed right hemiparesis and urinary incontinence. The deep tendon reflexes were (+) at the upper limbs and (2+) at the right knee and ankle. Blood pressure was 162/88 mmHg and glucose was 275 mg/dl. Other laboratory data were normal. Brain CT showed hemorrhage of the left frontal lobe. The cystatin C level in cerebrospinal fluid was 68 ng/ml. Therefore we suspected cystatin C deposit amyloid angiopathy. In this case, thalamic hemorrhage was initially thought to be amyloid angiopathy. In cases of cerebral hemorrhage in the elderly without hypertension, we must be considered amyloid angiopathy.
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PMID:[A case of recurrent cerebral hemorrhage considered to be cerebral amyloid angiopathy by cerebrospinal fluid examination]. 143 57

The common signs of hypoglycemia include: tachycardia, diaphoresis and vertigo which may be associated to disturbances of the consciousness. Occasionally, focal neurological signs occur with conservation of consciousness which are erroneously interpreted as cerebral vascular disease. An insulin dependent diabetic patient is presented with an initial diagnosis of transient ischemic attack (TIA) with right hemiparesis and dysarthria associated to hypoglycemia (35 mg %) whose remission occurred following the correction of glycemia. The different physiopathogenic mechanisms were also revised postulating (selective neuronal vulnerability, vasospasms and subjacent vascular disease) and the need for considering this diagnosis must be emphasized in those diabetic patients with focal neurological symptoms.
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PMID:[Hypoglycemic hemiparesis]. 161 Jun 4

The neurological spectrum of Borrelia burgdorferi infections is still enlarging. We review epidemiological, pathological and serological data of Lyme disease. The course of the disease is divided in three stages: stage 1 during the first month is characterised by erythema chronicum migrans and associated manifestations; stage 2 includes not only the classical European meningoradiculitis but also less specific neurological symptoms: isolated lymphocytic meningitis with an acute or even relapsing course, apparently idiopathic facial palsy, neuritis of other cranial nerves, polyneuritis cranialis, Argyll-Robertson sign, peripheral nerve involvement, acute transverse myelitis, severe encephalitis, myositis. During stage 3, three to five months or longer after the onset of the disease, chronic arthritis, acrodermatitis chronica atrophicans and various neurological symptoms can be observed: chronic neuropathy with mainly sensory or motor signs, recurrent strokes due to cerebral angiopathy and progressive encephalomyelitis; this third stage the central nervous system involvement is characterised by slowly progressive or fluctuating course during months or years, ataxic or spastic gait disorder, bladder disturbances, cranial nerve dysfunction including optic atrophy and hypoacusia, dysarthria, focal and diffuse encephalopathy. This chronic central nervous system disease can mimic multiple sclerosis, anorexia nervosa, psychic disorders or subacute presenile dementia. It is often associated with pleiocytosis, abnormal EEG and evoked potentials, sometimes multifocal and mainly periventricular white matter lesions visualised by CT or MRI, and as a rule high antibody titers against Borrelia burgdorferi. High doses of penicillin can halt the disease, sometimes induce spectacular regression of symptoms or sometimes be inefficient; ceftriaxone could be a more powerful therapy. Similarities between syphilis and Borreliosis are multiple: both of these spirochetes contain plasmids, can be transmitted through the placenta and progress for many years through successive stages, with multiorgan symptoms, including parenchymatous and vascular lesions of the central nervous system. Borrelia burgdorferi is the new great imitator.
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PMID:[Multiple neurologic manifestations of Borrelia burgdorferi infection]. 307 Jun 90

A case of multiple spontaneous intracerebral hematomas is presented. A 67-year-old man with 7 years history of hypertension had sudden clumsiness in his right hand and an hour later dysarthria appeared. A CT scan taken 3 hours after the onset revealed two well demarcated high density areas in the left putamen and in the parietal subcortex. A diagnosis of multiple intracerebral hematomas was made. On neurological examination he was midly stuporous (13 points of Glasgow Coma Scale). Dysarthria, right hemiparesis and right extensor plantar response were seen. CT scan of 6 hours later disclosed the same findings as the previous study. He recovered well and neurologically free in a few days. On the following CT scans both hematomas were isodense 2 weeks later, and ring-like enhancement effect was noted. CT scan showed normal appearance 7 weeks later. On MRI using 0.5 T unit t-1 and t-2 weighted spin echo images of these hematomas also showed the similar chronological changes. The history, these CT and MRI studies suggest that two hematomas of this case occurred almost simultaneously in one cerebral hemisphere. No causative factors such as blood dyscrasias, AVM, angioma, septicemia, malignancies or sinus thrombosis was identified. We consider that a hypertensive intracerebral hematoma of the putamen was followed by the parietal intracerebral hematoma within a few hours, although amyloid angiopathy was not completely excluded because no cerebral biopsy of the lesion was performed.
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PMID:[A case report of simultaneous multiple intracerebral hematomas]. 338 86

Recently, cerebral amyloid angiopathy is stressed as an unusual and infrequent cause of cerebral infarct or intracerebral hemorrhage. This report described a case of cerebral amyloid angiopathy complicated by multiple cerebral infarcts and multiple intracerebral hemorrhages. This 70-year-old man was admitted to our hospital on November 10, 1984 for evaluation of the gradual onset of dysarthria. Examination showed only slight dysarthria. There was no history of hypertension or dementia. A computed tomography (CT) showed enlarged ventricles with cortical atrophy and multiple low-density lesions, deep in the left frontal, left parietal, right parietal lobes, and in the both basal ganglias. The patient discharged from the hospital with only slight dysarthria. On November 20, 1984, he was admitted to our hospital again, because he was found unresponsive on the floor. He was somnolent but arousable. Examination showed disorientation, impairment of recent memory and impairment of calculation, A CT scan demonstrated three small intracerebral hemorrhages in the left frontal, right parietal lobes and left basal ganglia. On the fifth hospital day he deteriorated acutely, becoming semicomatose and hemiparetic on the right side. A repeated CT scan showed two new intracerebral hemorrhages in the left frontal lobe. Cerebral angiograms showed only minimal changes due to the occupying lesions in the above mentioned area. The hematomas was evacuated via left fronto-parietal craniotomy. The specimens removed with hematoma (stained with hematoxylin-eosin, Congo red and thioflavin T) showed extensive amyloid angiopathy. Postoperatively he made a good recovery, although he had residual mental dysfunctions. He expired by pneumonia on March 30, 1985.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebral amyloid angiopathy complicated by multiple cerebral infarcts and intracerebral hemorrhages: case report]. 361 33

This work is to study the ultrastructure of the neuronal lipofuscin that occurred in the brain and the spinal cord of an autopsy case of familial Alzheimer's disease and to compare with those in several other diseases. The patient was a 46-year-old male, whose father and elder brother were diagnosed as Alzheimer's disease and died at the age of 42, respectively. He became afflicted with forgetfulness and disorientation at the age of 36. He developed a grand mal seizure at the age of 39 and thereafter, his clinical course was characterized by pyramidal signs, dysarthria and the symptoms of Gerstmann's syndrome, visuo-spatial agnosia, apraxia for dressing and constructive apraxia. He became bedridden at 45 years old and died of general prostration. The brain weighed 1,250 g, and the cerebral cortex showed mild atrophy. The neuronal loss, senile plaques and Alzheimer's neurofibrillary tangles were found throughout the cerebral cortex. The senile plaques were also found in the basal ganglia, the cerebellar medulla and cortex. There was severe amyloid angiopathy in the occipital and cerebellar cortices. The specimens for electron microscopy were taken from the cerebral cortex, the basal ganglia, the thalamus, the midbrain, the medulla oblongata, the cerebellum and the spinal cord. The ultrastructural study revealed three different types of the neuronal lipofuscin, though different stainability between these lipofuscin granules could not be manifested by several histochemical methods. Their morphological differences seemed to be based on the sites of the central nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ultrastructural study of the neuronal lipofuscin--an autopsy case of familial Alzheimer's disease]. 648 35

A case of juvenile Alzheimer's disease is reported with onset at 34 years of age, a clinical course of 6 years, had myoclonic jerks, generalized convulsions, dysarthria and ataxic symptoms. The neuropathological examination indicated kuru-plaques, amyloid angiopathy and grumose alteration (degeneration) in the dentate nucleus. In this case, the plaques in Alzheimer disease is quite rare. This case also demonstrates the complex interrelationship between Alzheimer's disease and various multisystemic degeneration mainly involving the dentate nucleus.
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PMID:Juvenile Alzheimer's disease with myoclonus: amyloid plaques and grumose alteration in the cerebellum. 649 95

We describe a 68-year-old woman who presented with falls, mild limb bradykinesia, axial rigidity, and a severe supranuclear gaze palsy, which failed to benefit from levodopa. She subsequently developed severe apraxia, progressive dysarthria, dysphagia, and a frontal cognitive impairment. Pyramidal weakness with fasciculations and widespread chronic partial denervation appeared shortly before her death from bronchopneumonia, 6 months after disease onset. A severe cerebral amyloid angiopathy diffusely involving the cerebral hemispheres and cerebellum was present at autopsy as well as a second pathological condition indicative of motor neurone disease. Cerebral amyloid angiopathy may rarely present with a progressive supranuclear palsy-like phenotype.
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PMID:Cerebral amyloid angiopathy and motor neurone disease presenting with a progressive supranuclear palsy-like syndrome. 1262 39

We report the case of a 72-year-old left-handed woman presenting with episodes of paresthesias of the left arm and dysarthria consistent with transient ischemic attacks. The diffusion MRI showed hypersignals of the right corona radiata suggesting recent ischemic process whereas gradient-echo MRI revealed multiple small hypointense regions consistent with petechial hemorrhages restricted to the corticosubcortical regions. Gadolinium-enhanced, T1-weighted MRI showed focal meningeal enhancement. The diagnosis of cerebral amyloid angiopathy was supported by leptomeningeal biopsy. The association of ischemic suffering, petechial haemorrhage and meningeal enhancement as demonstrated by multisequence MRI highly suggest a cerebral amyloid angiopathy.
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PMID:[Cerebral amyloid angiopathy revealed by transient ischemic events: contribution of MRI to diagnosis and pathophysiology study]. 1266 May 74


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