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

A retrospective review of colloid cysts diagnosed from 1974 to 1986 emphasizes the presenting symptoms of these lesions, their surgical management, and the contribution of modern imaging techniques to their diagnosis and therapy. In this 12-year period, 84 patients (45 men and 39 women) had a colloid cyst diagnosed. The patients' mean age was 46 years (range, 7-82 years). Surgery was performed in 55 patients, 7 of whom had undergone prior surgery elsewhere. The surgical approaches used were transfrontal-transventricular, transcallosal, computer-assisted stereotactic aspiration and resection by stereotactic craniotomy, and shunting of cerebrospinal fluid without removal of the lesion. There was no operative mortality, but complications occurred in 15 patients (27%). Preoperative imaging showed hydrocephalus in 93% of the patients: severe in 43%, moderate in 36%, and mild in 14%. In the surgically treated group, the most common presenting symptoms were headache, change in mental status, ataxia, nausea and vomiting, visual disturbance, emotional lability/inappropriate affect, depersonalization, and hypersomnolence. Twenty-four patients for whom surgery was not recommended are being followed up closely. Most of these patients had normal ventricles. The symptoms in this group included headache, anxiety/nervousness, ataxia, memory impairment, visual disturbance, and seizures. Five autopsy cases of patients with colloid cysts were available during this period and were reviewed. Direct removal of colloid cysts can be accomplished with low morbidity and mortality, avoiding the frequent revisions and complications related to shunt procedures. There is a subgroup of colloid cysts that can be operated upon electively or followed up closely with serial imaging studies.
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PMID:Colloid cysts: experience with the management of 84 cases since the introduction of computed tomography. 271 77

We report a case of primary position downbeating nystagmus due to an occult breast carcinoma in a 57-year-old woman with progressive oscillopsia and truncal ataxia. Acute nausea and vomiting precipitated hospitalization. Magnetic resonance imaging of the brain was normal, though a sterile mononuclear cerebrospinal fluid pleocytosis was present. Search for an occult malignancy disclosed an adenocarcinoma of the breast. Radical mastectomy and oral corticosteroid therapy did not alter the clinical course of the paraneoplastic syndrome in our patient. Primary position downbeating nystagmus is an uncommon manifestation of an occult malignancy. Our report and review of the literature suggests that investigations necessary for the diagnosis of occult malignancies of the lung, breast, uterus, and ovary be included in the search for cryptic causes of downbeating nystagmus.
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PMID:Paraneoplastic downbeating nystagmus. A sign of occult malignancy. 285 13

Acute, subchronic, and chronic studies were conducted in various species to evaluate and compare the toxicity of nabilone, a new synthetic 9-ketocannabinoid that is orally effective for the treatment of nausea and vomiting induced by cancer chemotherapy agents. The oral LD50 in mice and rats for nabilone formulated as a polyvinylpyrrolidone (PVP) codispersion was in excess of 1000 mg/kg. Among nonrodents, rhesus monkeys had a higher tolerance to the CNS depression induced by single oral doses of nabilone-PVP than did dogs. Rats fed dietary mixtures of nabilone-PVP which provided approximate daily nabilone doses of 1 to 93 mg/kg tolerated treatment for 3 months with no deaths. Treatment-related changes (at doses greater than or equal to 5 mg/kg) were limited to reduced body temperature, slight-to-moderate decreases in weight gain, and behavioral changes (e.g., hyperactivity, hyperirritability to touch, and hypoactivity). All dogs treated for 3 months with daily oral doses of up to 1.0 mg/kg survived; treatment-related effects were limited to transient episodes of ataxia and anorexia. Nabilone treatment of rats and dogs for 3 months produced no evidence of systemic toxicity in the clinical chemistry, hematology, or pathology parameters examined. Chronic treatment of dogs with daily oral doses of nabilone-PVP equal to 0.5, 1.0, or 2.0 mg of nabilone/kg produced cumulative toxicity; by the end of 7 months, 2, 6, and 7 dogs in the respective dose groups had died. In a number of instances, death was preceded by one or more convulsive episodes. In contrast to the dog, the toxic potential of nabilone was minimal in rhesus monkeys treated with nabilone-PVP for 1 year at daily oral nabilone doses of up to 2.0 mg/kg. The enzymatic reduction of the 9-keto group of nabilone to form carbinol metabolites was a major metabolic pathway for nabilone in dogs but not in rhesus monkeys. The carbinols were long-lived metabolites in the plasma of dogs and accumulated in the plasma compartment with time. Furthermore, the carbinol metabolites were found to concentrate in the brain tissues of treated dogs. Although the precise mechanism for this marked species difference in chronic toxicity is not known, the metabolic differences responsible for the presence of the carbinol metabolites at high concentrations in the plasma and brain over time may play a role in the toxicity observed in the dog.
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PMID:A species comparison of the toxicity of nabilone, a new synthetic cannabinoid. 288 99

Ethanol, a highly lipid-soluble compound, appears to exert its effects through interactions with the cell membrane. Cell membrane alterations indirectly affect the functioning of membrane-associated proteins, which function as channels, carriers, enzymes and receptors. For example, studies suggest that ethanol exerts an effect upon the gamma-aminobutyric acid (GABA)-benzodiazepine-chloride ionophore receptor complex, thereby accounting for the biochemical and clinical similarities between ethanol, benzodiazepines and barbiturates. The patient with acute ethanol poisoning may present with symptoms ranging from slurred speech, ataxia and incoordination to coma, potentially resulting in respiratory depression and death. At blood alcohol concentrations of greater than 250 mg% (250 mg% = 250 mg/dl = 2.5 g/L = 0.250%), the patient is usually at risk of coma. Children and alcohol-naive adults may experience severe toxicity at blood alcohol concentrations less than 100 mg%, whereas alcoholics may demonstrate significant impairment only at concentrations greater than 300 mg%. Upon presentation of a patient suspected of acute ethanol poisoning, cardiovascular and respiratory stabilisation should be assured. Thiamine (vitamin B1) and then dextrose should be administered, and the blood alcohol concentration measured. Subsequent to stabilisation, alternative aetiologies for the signs and symptoms observed should be considered. There are presently no agents available for clinical use that will reverse the acute effects of ethanol. Treatment consists of supportive care and close observation until the blood alcohol concentration decreases to a non-toxic level. In the non-dependent adult, ethanol is metabolised at the rate of approximately 15 mg%/hour. Haemodialysis may be considered in cases of a severely ill child or comatose adult. Follow-up may include referral for counselling for alcohol abuse, suicide attempts, or parental neglect (in children). The ethanol withdrawal syndrome may be observed in the ethanol-dependent patient within 8 hours of the last drink, with blood alcohol concentrations in excess of 200 mg%. Symptoms consist of tremor, nausea and vomiting, increased blood pressure and heart rate, paroxysmal sweats, depression, and anxiety. Alterations in the GABA-benzodiazepine-chloride receptor complex, noradrenergic overactivity, and hypothalamic-pituitary-adrenal axis stimulation are suggested explanations for withdrawal symptomatology.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute ethanol poisoning and the ethanol withdrawal syndrome. 304 Dec 44

A Phase I trial of AT-125 was completed for the bolus dose every three week schedule. Dose limiting toxicity was primarily central nervous system (CNS) in the form of ataxia, confusion, hallucinations and dysarthria. Although this was most severe at doses of 150 mg/m2, lesser symptoms were reported at all dose levels. Nausea and vomiting were moderate to severe at higher doses. Myelosuppression did not occur. This schedule is not recommended for Phase II studies until methods are developed to reduce drug-related CNS toxicity.
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PMID:Phase I evaluation of AT-125 single dose every three weeks. 651 Dec 37

Spinal cavernous hemangioma is rare, and it is extremely rare for cavernous hemangioma to develop in the cauda equina. There has been only one report of hydrocephalus associated with cavernous hemangioma in the cauda equina. We report a case of cavernous hemangioma in the cauda equina diagnosed on the basis of the headaches due to hydrocephalus. A 67-year-old man was being treated for Parkinson's disease because of tremor of both upper extremities for several years. In December 1991 he complained of occasional headaches. On February 15, 1992 the headaches became severe and frequent, with nausea and vomiting, and his gait became unsteady. Four days later he came to our hospital. Neurological examination revealed fine finger tremor and truncal ataxia. Computerized tomography scanning and magnetic resonance imaging of the head revealed ventricular enlargement, but there were no mass lesions obstructing the cerebrospinal fluid pathway. Lumbar puncture at the L3-L4 level yielded bloody cerebrospinal fluid, and the pressure had increased to 410 mmH2O. Cerebral angiography showed no abnormal findings. Magnetic resonance imaging of the lumbar spine demonstrated an intradural tumor at the level of vertebral body L2. Spinal angiography showed no evidence of abnormal vascularity in the mass at the L2 level. On March 10, 1992, laminectomy at three levels, L1 to L3 was performed, and a well-defined blueberry-like intra-cauda equina tumor 1 cm. in diameter, was removed. One spinal nerve root passed through the tumor. The pathological diagnosis was cavernous hemangioma. After removal of the tumor, the patient's headaches improved, and a follow-up computerized tomography scan six months later showed normal ventricle size.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cauda equina cavernous hemangioma associated with hydrocephalus--case report]. 754 25

A 59-y-old with a history of chronic renal failure on hemodialysis was diagnosed with herpes zoster and begun on 800 mg acyclovir 5 times daily. Two days later the patient developed visual hallucinations, ataxia, confusion and memory loss along with focal myoclonus, nausea and vomiting. No fever, elevated WBC count or significant electrolyte imbalance was found. CT scan of the brain was unremarkable. The patient was then dialyzed for presumed acyclovir toxicity. Her acyclovir level was later found to have been 3.4 micrograms/ml (normal peak range 0.4-2 micrograms/ml) prior to dialysis. After 3 h of hemodialysis, her post-dialysis acyclovir level was 1.9 micrograms/ml. After a second course of hemodialysis the next day the patient's mental status improved, and she was discharged 5 d later. Due to its low volume of distribution (0.6 L/kg), low protein binding (about 15%) and water solubility, acyclovir is an example of the ideal drug that can be removed by hemodialysis. About 45% of the total body amount can be extracted through a 3-h course of hemodialysis with resultant improvement in symptoms.
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PMID:Hemodialysis removal of acyclovir. 757 52

Twenty-two cases of cerebellar infarction were diagnosed by clinical findings, computerized tomography (CT), magnetic resonance image (MRI) and autopsy. Most of the infarctions occurred in the territory of the posterior inferior cerebellar artery (18/22). The most common and earliest symptoms were dizziness or vertigo (19/22), which occurred repeatedly and were accompanied by nausea and vomiting. The symptoms and signs of cerebellar lesion such as unsteady gait, limb and/or trunk ataxia, dysarthria were also the main clinical manifestations. However, in a number of patients there were no cerebellar symptoms or signs (9/22). Rapid deterioration of consciousness suggested acute compression of the brainstem, where the prognosis would be poor. CT scan made it possible to diagnose cerebellar infarction in the patients. But CT is not a satisfactory instrument in identifying this disease. MRI without bony artifacts from the posterior fossa has much higher resolution and renders the infarction to be visualized earlier. It may be regarded as the most ideal instrument in diagnosing this disease.
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PMID:Cerebellar infarction. Analysis of 22 cases. 808 78

Small asymptomatic cysts of the pineal gland represent a common incidental finding in adults undergoing computerized tomography or magnetic resonance (MR) imaging or at postmortem examination. In contrast, large symptomatic pineal cysts are rare, being limited to individual case reports or small series. The authors have reviewed 24 cases of large pineal cysts. The mean patient age at presentation was 28.7 years (range 15 to 46 years); 18 were female and six male. Presenting features in 20 symptomatic cases included: headache in 19; nausea and/or vomiting in seven; papilledema in five; visual disturbances in five (diplopia in three, "blurred vision" in two, and unilateral partial oculomotor nerve palsy in one); Parinaud's syndrome in two; hemiparesis in one; hemisensory aberration in one; and seizures in one. Four lesions were discovered incidentally. Magnetic resonance imaging typically demonstrated a 0.8- to 3.0-cm diameter mass (mean 1.7 cm) with homogeneous decreased signal intensity on T1-weighted images, increased signal intensity on T2-weighted images, and a distinct margin. Hydrocephalus was present in eight cases. The cysts were surgically excised via an infratentorial/supracerebellar approach (23 cases) or stereotactically biopsied (one case). Histological examination revealed a cyst wall 0.5 to 2.0 mm thick comprised of three layers: an outer fibrous layer, a middle layer of pineal parenchymal cells with variable calcification, and an inner layer of hypocellular glial tissue often exhibiting Rosenthal fibers and/or granular bodies. Evidence of prior hemorrhage, mild astrocytic degenerative atypia, and disorganization of pineal parenchyma were often present. Postoperative follow-up review in all 24 cases (range 3 months to 10 years) revealed no complications in 21, mild ocular movement deficit in one, gradually resolving Parinaud's syndrome in one, and radiographic evidence of a postoperative venous infarct of the superior cerebellum with ataxia of 1 week's duration in one. Of the patients referred for study, the cysts were most often initially misdiagnosed as a pineocytoma in eight and a pilocytic astrocytoma in three. Only two patients were correctly diagnosed as having pineal cysts. This stresses the importance of recognizing the histopathological spectrum of pineal cysts, as well as correlation with radiographic findings, if a correct diagnosis is to be attained.
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PMID:Symptomatic glial cysts of the pineal gland. 811 58

A 21-year-old man with acute cerebellar ataxia and sympathotonic orthostatic hypotension, following Epstein-Barr (EB) virus infection, was reported. He noticed unsteady gait 2 weeks after the development of cough, nausea and vomiting. On admission, he was unable to sit and walk due to truncal ataxia and orthostatic hypotension with marked tachycardia. Limb ataxia of moderate degree was also noted. The blood pressure was 112/42 mmHg, and the pulse rate was 64/min in supine position, and 5 minutes after standing, they were 82/42 mmHg and 128/min. In laboratory studies, no atypical lymphocytes were detected in the peripheral blood. However, the titers of antibodies, VCA-IgM, against EB virus, were x80 and x160 in serum, respectively. And the titer of VCA-IgM subsequently decreased to the normal level in two months. They were negative in the cerebrospinal fluid. The results of the autonomic function studies revealed dysfunctions of the sympathetic post-ganglionic nerves, especially of alpha-adrenergic system, with preservation of beta-adrenergic system. He recovered from cerebellar ataxia and from sympathotonic orthostatic hypotension 3 and 8 months after the onset, respectively, without residuals.
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PMID:[Acute cerebellar ataxia with sympathotonic orthostatic hypotension following Epstein-Barr virus infection--a case report]. 839 87


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