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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The validity of a newly developed computer-aided "Visuospatial Cognitive-Performance Test" (VCP-Test) was examined in two populations, 68 normal elderly volunteers (mean age, 69.5% years) and 25 patients with dementia (mean age, 68.2 years). None of the cases in the two groups had either motor impairment or ataxia. The VCP-Test was a kind of vigilance task in which a subject is required to tap the key corresponding to the local change-over of the image on the computer display as quickly as possible. After 40 trials, consecutive data of performance efficiency were automatically displayed on the LCD display and printed out. A significant negative correlation between the VCP-Test and age in normal elderly population was recognized. Moreover, the relationship between the VCP-Test and the Hasegawa Dementia Scale (HDS), and the Mini-Mental State (MMS) was also significant in patients with dementia. In conclusion, the VCP-Test was considered to be useful for geriatric neurobehavioral functional assessment and for the detection of dementia.
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PMID:[Computer-aided visuospatial cognitive-performance test]. 187 Feb 83

A 7-year-old spayed bitch had a 3-year history of episodes of hind-limb weakness and ataxia. Neurologic abnormalities consisted of deficits in postural reactions, spinal reflexes, and conscious proprioception. A right-sided head tilt also was observed. Immediately after cervical radiography, CSF tap, and electroencephalography, the dog was alert, but it was found comatose the next morning and died within an hour. At necropsy, a 1.6- x 0.8- x 1.5-cm, thinly encapsulated mass was found on the left cerebellar peduncle. It had caused dorsal displacement of the left portion of the cerebellum and ventral compression of the fourth ventricle. Histologically, the mass was determined to be a dermoid cyst.
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PMID:Intracranial dermoid cyst in a dog. 335 Jul 47

Bismuth subsalicylate preparations are over-the-counter products for gastrointestinal complaints. Bismuth toxicity causes delirium, psychosis, ataxia, myoclonus, and seizures and is reversible over several weeks or months, when bismuth intake is stopped. We report a 54-year-old man with a 6-week history of progressive confusion and memory difficulty and a 2-3-week history of involuntary movements and gait impairment. His encephalopathy was further characterized by marked multifocal myoclonic jerks, coarse postural tremors, postural instability, and gait ataxia. He gradually improved. Extensive toxic, metabolic, and infectious workup demonstrated bismuth toxicity. Spinal tap and brain magnetic resonance scan were normal. Electroencephalography showed bihemispheric slowing. As his encephalopathy cleared, he reported using bismuth subsalicylate long term (daily intake of 8 oz). Bismuth levels 5 weeks after cessation of bismuth were elevated and normalized after 12 weeks. He followed a typical course for bismuth toxicity with subacute progressive encephalopathy and gradual recovery. Creutzfeldt-Jakob was strongly considered due to his rapidly progressive encephalopathy, multifocal myoclonus, and ataxia. Due to its rarity, bismuth toxicity is often overlooked. We hope this presentation will increase recognition of bismuth toxicity. We believe more detailed labeling of bismuth products is needed to avoid similar toxicity from this readily available product.
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PMID:Bismuth subsalicylate toxicity as a cause of prolonged encephalopathy with myoclonus. 775 66

We report a 55-year-old man with papilledema and multiple cranial nerve palsies. He was well until 52 years of age when there was an onset of progressive difficulty in initiating urination; he visited the urology service of our hospital where a diagnosis of prostate cancer was made; the cancer was invading the bladder and was metastasizing to lymph nodes and bones. He was treated with oochiectomy and estrogen preparations with some improvement in his symptoms. Two years later, he developed difficulty in urination again, and transurethral resection of the tumor was performed in 1991. In December 1991, he noted tingling and numb sensation in his left face, which had become progressive worse within the next one month, and he developed blepharoptosis and deafness all on the left side. He was admitted to the urology service on February 4, 1992, and a neurological consultation was asked. On physical examination, general findings were unremarkable, except for lymph node enlargements of about 0.5 to 1.0 mm in size in cervical and inguinal regions. On neurologic examination, he was alert with normal mental activities; higher cerebral functions were intact. He had normal vision and visual fields, however, papilledema was present bilaterally; pupils and light reactions were normal. Extraocular muscles were intact on the right side, however, moderate restriction was noted in the left eye in that all the extraocular muscles except for the medial rectus were weak; blepharoptosis was noted on the left; no nystagmus was present. The sensation was diminished in the left face, and left facial paresis of the peripheral type was also noted; the taste sensation was also diminished in the left anterior two thirds of the tongue. He had sensorineural deafness on the left side. The other cranial nerves appeared intact. He walked normally; no weakness or muscle atrophy was noted; muscle tone was normal and no ataxia was observed. Deep reflexes were normally elicited and symmetric; the plantar response was flexor. No meningeal signs were present. Laboratory examination revealed following abnormalities: Hb 7.1 g/dl, platelet 47,000/cmm, WBC3,800/cmm, LDH 950IU/l, PAP232ng/ml (normal less than 1.6), PA2.631ng/ml (normal less than 7.4); a small amount of effusion was noted in the left pleural cavity; cytological examination of the fluid was class V. A cranial CT scan as well as MRI were entirely normal, as was the spinal tap. He was treated with glycerol, however, there was progressive increase in the pleural effusion, and he developed dyspnea; moist rale had become audible in the end of February.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 55-year-old man with prostate cancer, papilledema, and multiple cranial nerve palsies]. 794 37

We report a 32-year-old man who developed cerebellar ataxia and a posterior fossa mass 12 years after the radiation therapy for a cerebellar arteriovenous malformation (AVM). The patient was well until 19 years of the age when he had an acute onset of vertigo and vomiting. A spinal tap was performed and the CSF was bloody. He was admitted to another hospital where an arteriovenous malformation was found in the cerebellum by angiography. Four years after the onset, he developed tingling sensation in the distribution of the second division of the right trigeminal nerve. He was admitted to the neurosurgery service of our hospital where the cerebellar AVM was confirmed. He was transferred to University of California where Bragg peak stereotaxic radiotherapy was successfully performed; this utilizes high energy alpha-ray produced by a cyclotron. Three years after the radiotherapy, marked reduction in the size of the AVM was confirmed by angiography. Twelve years after the onset of his initial symptom, he noted unsteadiness of gait. He was readmitted to our neurosurgery service where obstructive hydrocephalus was found. He was treated by ventriculoperitoneal shunting and placement of a Ommaya reservoir. After these therapy, he noted marked improvement in his gait and ataxia. However, in 1993, his unsteadiness of gait recurred, and he was again admitted to our neurosurgery service on June 20, 1993. On admission, T1-weighted MRI revealed a slightly low signal intensity mass lesion in the right cerebellar hemisphere compressing the brain stem; a spotty high signal intensity lesion and another small low intensity lesion were seen within the mass. Vertebro-basilar angiograms revealed upward displacement of the superior cerebellar arteries. No arteriovenous nidus was visualized. On July, 3rd, the cyst was surgically drained and the Ommaya reservoir was removed. Post-operative course was uneventful, however, he developed head tremor after the surgery. Neurologic examination on July 20, 1993 revealed an alert and well oriented man in no acute distress. General physical examination was unremarkable. Neurologic examination revealed no dementia; higher cerebral functions appeared intact. The optic discs were flat, and visual fields were intact. Ocular movements were full but convergence was restricted. Horizontal gaze nystagmus was noted more in the right lateral gaze. Pupils were intact. Facial sensation and facial muscles were intact. Hearing was normal. His voice was of nasal quality. Pharyngeal reflex was diminished. The tongue showed deviation to the left without atrophy. Head tremor at 5 c/s was noted. He was able to stand with support but was unable to walk. No muscle atrophy or weakness was noted. The finger-to-nose and the heel-to-knee tests showed dysmetria and decomposition more on the right. Rapid alternating movements were ataxic on the right. Muscle tone was diminished on the right. Muscle stretch reflexes were normally elicited and were symmetric. The plantar response was flexor bilaterally. Sensation was intact. On July 21, a posterior fossa exploration was performed. After the surgery, he was treated with 30 mg/day of alotinolol which showed no effect on his head tremor. He was then treated with gradually increasing doses of clonazepam; when he received 8 mg/day of clonazepam, his tremor showed marked improvement. He was discussed in a neurologic CPC on the nature of the posterior fossa lesion and his tremor. Opinions were divided between delayed radiation necrosis and a radiation-induced brain tumor. The chief discussant arrived at the conclusion that the patient had delayed radiation necrosis compressing the brain stem and cerebellar hemispheres. Regarding the nature of his tremor, he thought that his head tremor was of cerebellar type of postural tremor. Histologic examination of the biopsied specimen revealed accumulation of relatively fresh blood constituents in the deep area of the cerebellum forming a mass. Most of the
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PMID:[A 32-year-old man who developed a posterior fossa mass 12 years after the radiation therapy for cerebellar arteriovenous malformation]. 867 25

We reported here three infants aged 11 to 12 months who, according to their parents, suddenly became unwilling to stand up. All the patients had barely achieved the ability to stand or to walk at the time of the illness. The symptom developed relatively acutely in the winter months from 1997 to 1998 with a probable preceding infection. On examination, no paralysis of the lower extremities was observed, and muscle weakness was minimal. There were neither violent tremors, nystagmus, nor sensory disturbance. Orthopaedic disorders were considered unlikely. Biochemical examinations of the serum were not diagnostic, and imagings of the central nervous system were normal. Spinal tap revealed mild cerebrospinal fluid pleocytosis in two of the patients. All the children showed almost complete recovery without any medication during the following period of 2 days to 2 months. Although no definite signs of ataxia were recognized in the three patients, a diagnosis of acute cerebellar ataxia was considered to be appropriate. Mild, infantile acute cerebellar ataxia may be overlooked because of the obscure complaints of the parents and the difficulty in performing a thorough neurological examination of infants.
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PMID:[Three infants who suddenly became unwilling to stand up presumably due to acute cerebellar ataxia]. 1100 38

Aim of our study was to find a specific measure for the intensity of upper limb tremor and other ataxic symptoms in Multiple Sclerosis (MS) patients, and to establish standard values and test quality parameters. Three hundred and forty-two consecutive patients with different symptoms in the upper limbs (upper motor neuron symptoms, cerebellar upper limb ataxia, and/or sensory deficits in the upper limbs) and 140 healthy controls took part in the study. All patients and controls had to trace over a 25 cm high figure '8' on a graphic tablet, to tap with the stylus on the tablet and to perform the nine-hole-peg test (9HPT). Patients were additionally examined using clinical standard scales to classify motor dysfunctions of the upper limbs. One hundred and eighty-nine patients and 27 controls were tested twice to investigate the test reliability. Kinematic analysis of the tablet data was performed by kernel estimators, oscillatory activity by spectral analysis. Total power in the 2--10 Hz band was very specific for ataxia versus other motor symptoms. Tapping and 9HPT could well distinguish patients from controls, and patients with predominant motor neuron or cerebellar symptoms from patients with predominant sensory dysfunctions. Mean drawing error did not differ between motor and sensory dysfunctions. The test--retest reliability was similarly high for both spectral analysis and 9HPT.
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PMID:Measurement of ataxic symptoms with a graphic tablet: standard values in controls and validity in Multiple Sclerosis patients. 1145 15

Despite the accumulation of knowledge over the years, the postoperative results of shunt implantation in patients with normal pressure hydrocephalus (NPH) have shown little improvement. This means that reliable predictors of the course of the disease need to be identified. In a prospective study carried out between 1982 and 2000 we re-examined 155 (78%) of 200 NPH patients treated by shunt implantation, 7 months after their operation. On the basis of the results of the intrathecal infusion test NPH was graded early stage (no brain atrophy) or late stage (brain atrophy). We looked at the following factors as possible predictors: patient's age, disease duration, idiopathic or secondary aetiology, clinical signs such as gait ataxia, dementia and urinary incontinence, results of spinal tap, valve type and valve infection, and resistance to cerebral spinal fluid outflow and postoperative changes in ventricular size. As a measure for outcome we used the NPH recovery rate, and the Pearson chi-square test for statistical evaluation. 80 patients with early stage NPH, a history < 1 year, absence of dementia and an implanted Miethke dual-switch valve proved to be significant predictors of a positive outcome. Outflow resistance proved to have only minimal impact on outcome. The 75 patients with late-stage NPH had better outcome when dementia was absent, outflow resistance was > 20 mmHgmin/ml, the CSF tap test was positive, and a Miethke dual-switch valve was implanted.
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PMID:[Outcome predictors in patients with normal pressure hydrocephalus]. 1274 84

Despite knowledge emerging over the last 40 years, the postoperative results after shunt implantation in patients diagnosed with normal-pressure hydrocephalus (NPH) have not improved significantly over the last decade. For that reason predictors have to be identified in order to preoperatively predict outcome. From 1982 to 2000 we prospectively studied 200 patients diagnosed with NPH. From the patients, who were surgically treated by a shunt implantation we reexamined 155 (78%) postoperatively a mean time interval of 7 months. The NPH was graded according to the results of the intrathecal infusion test in an early stage NPH (without brain atrophy) and late stage NPH (with brain atrophy). In our study, we focussed attention on the possible predictors: patients age, length of disease, clinical signs (gait ataxia, dementia and bladder incontinence), aetiology idiopathic/secondary as well as implanted valve type and the value of resistance to cerebrospinal fluid outflow. To measure the outcome we used the NPH recovery rate and as the statistical test the chi(2) according to Pearson. In 80 patients with an early stage NPH (without cerebral atrophy), a short course of disease (<1 year), a slight degree of dementia and an implanted Miethke-Dual-Switch valve were significant predictors for a positive postoperative outcome. The outflow resistance measured in the intrathecal infusion test showed only a minimal relevance to outcome. Those 75 patients with a late state NPH (with cerebral atrophy) had a better outcome when dementia was not present, the outflow resistance was above 20mm Hg/min/ml, the CSF tap-test was positive and a Miethke-Dual-Switch valve was implanted.
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PMID:Predictors of outcome in patients with normal-pressure hydrocephalus. 1285 85

Despite emerging knowledge of over 40 years, the postoperative results after shunt implantations in patients diagnosed for normal-pressure hydrocephalus (NPH) have not improved significantly in the last decade. For this reason, predictors have to be identified in order to preoperatively predict the course of disease. From 1982 to 2000, we examined in a prospective study 200 patients diagnosed for NPH. Of the patients who were surgically treated by a shunt implantation we could re-examine 155 (78%) in a mean time interval of 7 months after operation. The NPH was graduated according to the results of the intrathecal infusion test in an early state NPH (without brain atrophy) and late state NPH (with brain atrophy). In the study we focused our attention on the possible predictors: patient's age, length of disease, clinical signs--like gait ataxia, dementia and bladder incontinence, etiology idiopathic/secondary as well as implanted valve type and the value of resistance to cerebrospinal fluid outflow. To measure the outcome we used the NPH recovery rate, as statistical test the chi(2) according to Pearson. In 80 patients with an early stage NPH (without cerebral atrophy) and a short course of disease (<1 year), slightly distinct dementia and an implanted Miethke Dual-Switch valve were significant predictors for a positive postoperative outcome. The outflow resistance measured in the intrathecal infusion test showed only a minimal relevance for the outcome. Those 75 patients with a late state NPH (with cerebral atrophy) had a better outcome when dementia was not present, the outflow resistance was >20 mm Hg.min/ml, the CSF tap test was positive and a Miethke Dual-Switch valve was implanted.
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PMID:Predictors of outcome in patients with normal-pressure hydrocephalus. 1466 Aug 79


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