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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cyclosporine is a specially useful immunosuppressor agent in children subjected to renal transplantation, minimizing the deleterious effect of steroids on growth and the development of Cushing syndrome. However, side effects which require close supervision are well known, including liver, kidney and central nervous system toxicity. Seizures, cerebellar ataxia, aphasia, paresthesia and behavioral disorders are characteristic of the latter. Hypertension and hypomagnesemia have been identified as risk factors. In contrast to nephrotoxicity, CNS toxicity is not related to plasma levels of cyclosporine. In this paper 2 patients, 10 and 11 year old, manifesting cyclosporine neurotoxicity after renal transplant, are reported.
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PMID:[Neurotoxicity caused by cyclosporin A in renal transplantation in children]. 134 84

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

Central nervous system is rarely involved in progressive systemic sclerosis (PSS) unless there are concomitant abnormalities in renal or lung function or hypertension. A 72-year-old woman with typical PSS developed cerebellar bleeding. Medical history records revealed, she had noted the onset of Raynaud's sign on her upper extremities at the age of 37. This was followed by necrosis and repeated infection, and as a result, shortening of her fingers in her 40's. The disease progressed and involved lower extremities, and then face and body in her 50's. Aortic valve stenosis was diagnosed at 69 year old, cardiac myopathy at 70 and at the age of 71 infectious dermatitis in both inguinal regions. Mild anemia, hypoalbuminemia and the decrease of serum Fe were discovered in June 1988. At the same time, prolonged ESR, positive C-reactive protein, RA, and anti-nuclear-antibody were also noticed. A chest roentgenogram revealed pulmonary fibrosis. Systemic hypertension was not noticed on the clinical course. She developed an onset of vertigo and vomiting in the morning of August 8, 1988. Consequently, she was brought to our hospital. She was alert but a physical examination showed a swallowing disturbance, dysarthria, right cerebellar ataxia, nystagmus and hypertension (192/100 mmHg). A CT examination on admission revealed a slightly low density area in right cerebellar hemisphere without mass effect. She was treated with dextran and mannitol and her condition improved on the 6th day of her admission. She was alert and blood pressure calm down to 120/70 mmHg without the use of anti-hypertension drugs on August 21.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of progressive systemic sclerosis associated with a hemorrhagic infarction of the cerebellum]. 235 21

Severe acute thallium poisoning in a young man is described. He presented with transient loss of consciousness and paraesthesiae of finger tips and lips, with a blood thallium concentration of 5750 micrograms/l (levels above 200 micrograms/l are toxic). He rapidly lost limb sensation and power and later required temporary mechanical ventilation and nasogastric feeding. The neurological sequelae one year afterwards are a flaccid paraparesis, cerebellar ataxia and mental impairment. Immediate cardiovascular complications included hypertension, sinus tachycardia, ECG abnormalities and an episode of ventricular fibrillation. We were able to assess the relative merits of different methods advocated for enhancing thallium excretion. Oral Prussian blue, forced diuresis and haemodialysis were found to be the most effective: 2000 mg of thallium were eliminated over 20 days, 820 mg over 46 days and 225 mg over 25 days respectively by these methods. Haemofiltration was ineffective. Diethyldithiocarbamate, a chelating agent, brought about a rise in serum thallium concentration accompanied by clinical deterioration and its use should be abandoned.
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PMID:Clinical features and therapy of acute thallium poisoning. 327 37

In 19 children with acute infantile hemiplegia an ischemic cerebral infarct was found clinically and by serial computertomography. In 11 patients an angiography has been performed in addition. 9 of the children had chronic diseases which are known as predisposing factors for cerebrovascular disease (congenital heart disease in 7 and chronic renal failure with hypertension in 2). One child had a severe hypernatremic dehydration due to infantile diarrhea and in 1 child thrombosis of the internal carotid artery occurred 3 days after a perforating trauma of the soft palate. No obvious reason for the ischemic stroke could be evaluated in 8 children. The onset of symptoms was either acute or slowly progressive. An altered state of consciousness was present in 11 children. Hemiparesis was found in 18 patients (13 right, 5 left) accompanied by facial palsy in 12 and aphasia in 6. Seizures occurred in 6 patients. One patient with incomplete occlusion of a vertebral artery showed acute cerebellar ataxia. In children without predisposing factors the prevalence of girls was higher (2 : 6) and there was a history of a preceding acute febrile illness in 5 of 8 patients. Laboratory investigations showed polycythemia in 4 children with cyanotic heart disease and additional hypochromia in two. Blood sedimentation rate was increased in 6 out of 8 patients without a known predisposing factor. Cerebrospinal fluid (CSF) showed a slight increase of erythrocytes (36-88/cmm) in 4 children, in two others purulent CSF was obtained after the infarct had developed into a brain abscess. The etiology of ischemic stroke in childhood and the possibility of an inflammatory vascular disease are discussed.
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PMID:Acute infantile hemiplegia caused by cerebral ischemic infarction. Etiology, clinical features and investigations. 647 69

A 45-year-old woman with hypertension suffered four episodes of right hemiparesis and two attacks of left hemiparesis, within seven months. On examination she showed weakness and cerebellar ataxia of all four limbs. Computed tomography demonstrated a radiolucent area in the base of the pons, consistent with lacunar infarction.
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PMID:Ataxic tetraparesis from lacunar infarction in the pons. 688 7

The neurologic changes following lightning injury include coma with cerebral edema, inappropriate secretion of antidiuretic hormone (ADH), seizures, cerebellar ataxia, and painful sensory disturbances. Deteriorating neurologic status may warrant the use of intracranial pressure monitoring devices. Myocardial injury and transient hypertension are generally evident at the onset. Monitoring of the cardiac rhythm may be needed for as long as a week for late onset arrythmia. Abnormalities of memory, mood, and affect noted on recovery of consciousness may persist for months, necessitating close psychiatric and neurlologic follow-up.
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PMID:Neurologic, psychiatric, and cardiovascular complications in children struck by lightning. 692 48

The etiology to the empty sella syndrome (ESS) is not known. Increased intracranial pressure (ICP) has been suggested to be one of the possible causes. In the present study the CSF circulation was analyzed in 48 subjects with ESS with gamma cisternography, pneumoencephalography (PEG) and computed tomography (CT). In 80% of the subjects the CSF circulation was retarded with convexity block which was combined with widened CSF transport pathways and basal cisterns. These findings were correlated with the clinical signs and symptoms, most of which seemed to be related to the imparied CSF circulation (i.e. impared memory, balance disturbances, cerebellar ataxia, papilledema, hypertension and pituitary disorders). Headache, psychiatric symptoms, visual field defects and obesity, however, were not related to the impaired CSF circulation. It is concluded that impaired CSF dynamics leading to intermittent increase of ICP has a major impact on the development of the ESS and that most of the patients' complaints are related to this disturbance. Thus it is important to obtain information of the CSF dynamics concurrent with the diagnosis of ESS. For this purpose PEG or CT may be used as the first examination. Moreover, the patient should be examined at least every second year for symptoms and signs of progressive impairments of the CSF circulation.
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PMID:CSF circulation in subjects with the empty sella syndrome. 725 14

Clinical features of cerebellar infarction in the territory of the superior cerebellar artery (SCA) were investigated in six male patients, ranging in age from 50 to 69 years. In all patients, there were MR images of infarction located in the area supplied by the SCA. The lesion was on the left-side in 2, right-side in 3 and bilateral (recurrent) in 1 patient. The onset of disease occurred with nausea, vomiting and floating sensation, with no overt brain stem signs other than symptoms of unilateral cerebellar ataxia and dysarthria. Five of the 6 patients had heart disease and cerebral angiography without definite evidence of SCA occlusion, strongly suggesting occlusion of the artery at its periphery due to cardiogenic embolism. A comparison of these 6 patients with those reported previously in Japan suggests that patients with SCA occlusion may be divided into two distinct subgroups: one manifesting diffuse brain stem signs in addition to cerebellar signs, and the other showing cerebellar signs as the only neurologic manifestation. In the former group, comprising the vast majority of patients, SCA occlusion occurred at the origin of the vessel due to a thrombus under a state of hypertension, diabetes mellitus or malignancy, producing signs of brain stem involvement, such as dissociating sensory disturbance and Horner's sign. While in the latter group, which included these 6 patients, paucity of brain stem signs, absence of definite cerebral angiographic evidence of SCA occlusion, and the presence of heart disease were distinguishing clinical features. Cardiogenic cerebral embolism was probably the underlying pathology in many of the cases and the functional prognosis was favorable.
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PMID:[Cerebellar infarction in the territory of the superior cerebellar artery, presenting a predominant cerebellar symptom--with special reference to its pathophysiology]. 761 47

We present two siblings with hereditary cortical cerebellar atrophy (CCA), who showed peculiar clinical features. Their unaffected parents are cousins. The mode of inheritance in this family was autosomal recessive. Both patients developed involuntary movement and ataxia during the fourth decade. The proband (patient 1) was the elder sister. She developed choreoathetoid involuntary movement and cerebellar ataxia at the age of 32. At the age of 39, she showed mental deterioration and marked gait disturbance due to severe ataxia and amyotrophy. At the age of 40, she took medication for hypertension. At the age of 42, she was bedridden and had generalized convulsions and dysautonomia. Involuntary movement continued until her death at age 44. She had amenorrhea since the age of 25 years. Neuropathological findings. The brain weighed 1,010 g. We found marked degeneration in the cerebellar cortex including the molecular, Purkinje cells, and granular cell layers, and in the inferior olivary nuclei. In the basal ganglia, the putamen and caudate nuclei were moderately affected, but the substantia nigra and globus pallidus were spared. The cerebral cortex was spared, but the cerebral white matter showed diffuse myelin pallor without fibrillary gliosis. In the pons, the volume of the tegmentum was moderately decreased, but the base was spared. The spinal cord was normal. The findings of the patient differed from those of the case originally reported by Gordon Holmes in 1907. Holmes autopsied a case showing severe degeneration in both the cerebellar cortex including all three layers and the inferior olivary nucleus as in our patient. However, the striatum of his case spared and the patient did not develop involuntary movement as did other patients. The patients presented here should be distinguished from Holmes' original case clinicopathologically.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Autosomal recessive hereditary cortical cerebellar atrophy with striatal degeneration--two siblings showing choreoathetoid movement, ataxia, dementia, and amenorrhea]. 806 39


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