Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electro-oculographic recordings of dissociated vertical (oblique and upbeat) nystagmus were carried out in a patient in coma due to vascular lesions. Based on the clinical and neuropathological findings, it was suggested that dissociated vertical (oblique and upbeat) nystagmus in a patient in coma can be caused by bilateral lesions in the brachium pontis.
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PMID:Dissociated nystagmus in a comatose patient. A clinicopathological study. 615 92

A 17 year old high school boy experienced fever and diarrhea, which subsided within 4 days by appropriate medications. Six days later, however, he developed unsteadiness and limb spasm. On the morning of admission, he was found to have drowsiness, dysarthria, gait disturbance and involuntary jerks. When he was brought to the hospital, he was lethargic but could follow simple verbal commands. Frequent involuntary movements manifested by facial grimacings, limb spasms and twitchings with dystonic features were seen. Decorticate posturing was readily elicited by painful stimuli. There was no meningeal irritation sign or gross sensory impairment. The deep tendon reflexes were symmetrically exaggerated with bilateral Babinski signs. Bilateral lateral rectus muscle weakness was found together with mild ptosis and upward gaze limitation. Nystagmus was not present and the funduscopic examination was normal. Immediately he was placed on anticonvulsants, steroid hormone, gamma-globulin and antibiotics as well. A brain CT scan and a CSF examination revealed no abnormality. Meanwhile he continued to show a progressive deterioration associated with fever and status epilepticus, and within 24 hours he lapsed into coma in decorticate posture. An EEG obtained at the 3rd hospital day was compatible with spindle coma. In spite of aggressive treatment he remained febrile and comatous. Therefore, vidarabine (adenine arabinoside) was initiated from the 3rd hospital day for 5 days. Then he began to groan and show frequent choreic movements. For the subsequent 2 weeks he made a slow recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of brain stem encephalitis with complete recovery (Bickerstaff's encephalitis)]. 620 73

Fifty adult patients with partial motor status epilepticus were treated with a single intravenous (i.v.) injection of diphenylhydantoin (DPH), 20 mg/kg body weight at a rate of 1 mg/kg/min. Seizures were controlled in 32 patients (64%) during the injection or within the following hour; in 13 of them previous (i.v.) injections out of benzodiazepines had been ineffective. DPH was effective in 10 patients of 11 with a previous history of epileptic seizures and without problems of consciousness during their epileptic status. In contrast, 13 failures out of 18 concern occasional status in patients deeply comatose because of head trauma, neurosurgical operation or intracerebral hemorrhage. Total plasmatic levels of DPH, when measured 24 h after the injection, were found between 38 mumol/l in all patients, and were in the range of 40 mumol/l-100 mumol/l in 77% of cases. Adverse effects were: pain at the injection site (6 cases), horizontal nystagmus during injection (5 cases), transient cerebellar symptoms (3 cases). This study confirms that single loading doses of DPH can maintain DPH plasmatic levels within the therapeutic range during 24 h, with minor or transient side effects, provided that cardiovascular contra-indications are respected.
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PMID:[Treatment of partial motor status epilepticus in adults with intravenous diphenylhydantoin (DPH). Prospective study of 50 cases]. 644 81

A 14-year-old boy of Arabic origin presented with a pellagra-like rash and neurological manifestations including ataxia, dysarthria, nystagmus, and coma. There was a striking response to oral nicotinamide. The laboratory findings were not typical of Hartnup disease: aminoaciduris and indicanuria were absent and there was no evidence of tryptophan malabsorption. Tryptophan loading did not induce tryptophanuria nor did it increase excretion of xanthurenic or kynurenic acids. These findings support the possibility of a block in tryptophan degradation. The family history suggests a genetically-determined disorder.
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PMID:Familial pellagra-like skin rash with neurological manifestations. 645 Dec 1

Blood concentrations and clinical findings in 25 cases of overdose involving chlordiazepoxide (CDZ) alone ("pure") were compared with those in 23 cases of overdose involving ethanol in addition to CDZ ("mixed"). Both groups consisted predominantly of men who were chronic alcoholics. The mean blood CDZ concentrations did not show statistically significant difference between the two groups ("pure," 5 mg/L; "mixed," 6 mg/L). Following "pure" ingestion, patients were usually alert, and the level of consciousness showed no statistically significant correlation with the blood CDZ concentration. In contrast, after "mixed" ingestion patients were usually lethargic, and the level of consciousness correlated significantly with the blood CDZ concentration (P less than 0.05) but not with the blood ethanol concentration. In neither group was coma noted. For both groups the most common physical findings were tachycardia and dysarthria. Nystagmus was much more common following "mixed" ingestion while seizures, hyperreflexia, and hypertension were more frequent after CDZ overdose alone. Most patients were seen only in the emergency room and were discharged. The implications of these findings are discussed.
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PMID:Blood concentrations and clinical findings following overdose of chlordiazepoxide alone and chlordiazepoxide plus ethanol. 653 Jul 1

Thirty-eight patients who ingested ethchlorvynol were seen at our institution over an 8.7 year period. Eleven involved ethchlorvynol alone ("pure") while the remainder included at least one other drug ("mixed"). Twenty-three of the patients were women. Six patients required hospitalization. Five patients were chronic users of the drug. Admission ethchlorvynol blood concentrations ranged from 3 to 46 mg/L ("pure") and from 3 to 75 mg/L ("mixed"). For the "pure" cases the most common physical findings were depressed level of consciousness (10 cases), dysarthria (7), mydriasis (6), nystagmus (6), areflexia (4), tachycardia (4), and hypotension, ataxia, and respiratory depression (2 cases each). Following "pure" ingestion, ethchlorvynol concentrations greater than 19 mg/L were usually associated with dysarthria, mydriasis, nystagmus, and tachycardia. When concentrations exceeded 38 mg/L, coma, areflexia, hypotension, and respiratory depression were generally noted as well. All patients recovered with supportive care alone.
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PMID:Ethchlorvynol ingestion: interpretation of blood concentrations and clinical findings. 667 79

Eye movements induced by head rotation were studied in 6 patients in acute coma, 4 patients in a persistent vegetative state, and 6 healthy, alert control subjects. Results from control subjects suggest that the oculocephalic response in the supine position is principally a vestibulo-ocular reflex. A position-step rotation of the head produced an initial oppositely directed eye movement, followed by a drift of the eyes back toward midline with a negative exponential time course. The time constant of this drift was greater than or equal to 10 seconds in control subjects but less than or equal to 1.5 seconds in unconscious patients and less than or equal to 0.5 seconds in vegetative patients. The rapid drift back of the eyes in unresponsive patients implies dysfunction of reticular and, possibly, cerebellar connections; the rate of this drift may indicate the severity and extent of brain injury. Sinusoidal head rotation produced slow and quick phases of nystagmus in normal subjects. Quick phases were absent in patients in acute coma; although present in vegetative patients, the quick phases did not keep the eyes close to primary position, as was the case in control subjects.
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PMID:Eye movements induced by head rotation in unresponsive patients. 673 93

Magnesium deficiency may complicate many diseases. The causes include the following: inadequate intake during starvation or increased requirement during early childhood, pregnancy, or lactation; excessive losses of magnesium as a result of malabsorption from the gastrointestinal tract or from the kidneys during use of diuretics; and to a combination of the two, as in alcoholism. Most often the etiological factors have been operative for a month or more. Acute hypomagnesemia can occur without previous Mg deficiency after epinephrine, cold stress and stress of serious injury or extensive surgery. The clinical manifestations depend on the age of the patient and may begin insidiously or with dramatic suddenness, or there may be no overt symptoms or signs. The manifestations can be divided into the following categories: totally non-specific symptoms and signs ascribable to the primary disease; neuromuscular hyperactivity including tremor, myoclonic jerks, convulsions, Chvostek sign, Trousseau sign (rarely), spontaneous carpopedal spasm (rarely), ataxia, nystagmus and dysphagia; psychiatric disturbances from apathy and coma to some of all facets of delirium; cardiac arrhythmias including ventricular fibrillation and sudden death; hypocalcemia which is responsive only to Mg therapy; and hypokalemia which is not easily nor completely corrected without Mg therapy. The diversity of etiologies and the multiplicity of manifestations result in confusion and controversy. The documentation of normal renal function is absolutely necessary for maximum doses. The order of magnitude of dose is 1.0 meq Mg/kg on day 1, and 0.3 to 0.5 mEq/kg per day for 3 to 5 days. In emergencies such as convulsions or ventricular arrhythmias, a bolus injection of 1.0 gm (8.1 meq) of MgSO4 is indicated. Therapy of Mg deficiency in the presence of renal insufficiency requires smaller doses and frequent monitoring. Complete repletion occurs slowly.
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PMID:Magnesium deficiency. Etiology and clinical spectrum. 702 Mar 47

Four patients with an acute overdose of carbamazepine were examined with serial blood level determinations. The clinical spectrum consisted of coma, respiratory depression, seizures, myoclonus, nystagmus, hyperreflexia, hyporeflexia, delayed gastric emptying with cyclic coma, ataxia, sinus tachycardia, and atrioventricular conduction delay. Carbamazepine elimination half-lives varied from 10 to 29 hours, and in one case carbamazepine-10,11-epoxide was measured and had a half-life of 24 hours.
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PMID:Acute carbamazepine toxicity resulting from overdose. 719 79

In 1,000 cases of phencyclidine (PCP) intoxication evaluated at the time of first examination in an emergency department, the incidence of "typical" findings was found to be lower than has been reported previously. Nystagmus and hypertension occurred in only 57% of our cases; some patients had only one of these findings and many had neither. The incidence of violence was 35%; bizarre behavior, 29%; and agitation, 34%. Changes in sensorium consisted of coma, lethargy/stupor, and acute brain syndrome; however, 46% of patients were alert and oriented. Motor signs included grand mal seizures, generalized rigidity, localized dystonias, catalepsy, and athetosis. Profuse diaphoresis, hypersalivation, bronchospasm, and urinary retention occurred in less than 5%. A small percentage had severe disturbances in vital signs, including three cases (0.3%) of cardiac arrest and 28 cases (2.8%) of apnea. Hypoglycemia and elevated serum CPK, uric acid, and SGOT/SPGT were common. Urine PCP levels did not correlate with the severity of the clinical findings.
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PMID:Acute phencyclidine intoxication: incidence of clinical findings in 1,000 cases. 722 71


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