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)

Tetrahydroaminoacridine (T.H.A., Tacrine) 1 mg/kg, and 4-aminopyridine (Pymadin) 0.2 and 1.0 mg/kg i.v., significantly reduced the recovery time when the were administered after ketamine-diazepam anesthesia in Maccacus Rhesus monkeys. Anesthesia was induced with ketamine (50 mg), diazepam (1.2 mg) and sodium glycopyrrolate (0.02 mg) as a secretiondrying agent, as a single bolus injection. Anesthesia was continued with ketamine by constant infusion of a solution of 5 mg/ml, at a speed of 20 mg/ml, at a speed of 20 ml/hour, during 30 minutes. The 5 monkeys in the control group were allowed to recover spontaneously. The test series consisted of the same monkeys, with an adequate rest period of one or more weeks between anesthesias. Recovery was indicated by production of nystagmus, and by an awake pattern in the EEG. Clinical signs, restlessness and purposeful movements, were also used.
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PMID:Effect of tetrahydroaminoacridine and 4-aminopyridine on recovery from ketamine-diazepam anesthesia in the macacus rhesus monkey. 12 11

Fifteen patients with prolonged coma after craniocerebral injury were observed for a year or more, and their communicative functions were evaluated. Nine of them showed a considerable degree of recovery, while 6 remained in a vegative state. Of the 9 with recovery, 6 showed complete recovery of semantic functions, while 3 remained with aphasic deficits. Eight out of these 9 remained dysarthric. Communicative recovery began as late as 5.7 months after injury, and it roughly paralleled recovery in locomotion and A.D.L. Restlessness and sweating were favorable prognostic factors. Excessive salivation, snout reflex, corneomandibular reflex, retractory nystagmus and stereotypic movements were unfavorable. The 8 patients who remained dysarthric showed marked diminution of their expiratory and inspiratory reserves, and of their forced vital capacity.
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PMID:Recovery of communicative functions after prolonged traumatic coma. 64 59

In nine cases of phencyclidine hydrochloride poisoning, early signs of overdose included drowsiness, nystagmus, miotic pupils, blood pressure elevation, increased deep tendon reflexes, ataxia, anxiety, and agitation. In more severe cases, seizures, spasticity, and opisthotonos were seen in addition to deep coma and respiratory depression. Treatment included removal by emetics or lavage, hydration, and a quiet, reassuring environment. Spasticity, agitation, and ocular manifestions responded to diazepam. Psychiatric intervention was instituted after the patients were stable and no longer agitated.
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PMID:Phencyclidine. Nine cases of poisoning. 124 71

A series of seven children in Hawaii experienced transient cortical blindness following mild head trauma. All children, ages 3 through 8, recovered fully. The most prominent clinical feature was initial restlessness and agitation following relatively mild head trauma without significant loss of consciousness (LOC). One child may have experienced this several times. The clinical features associated with a benign outcome in this syndrome include: pediatric age group, mild head trauma, brief or no LOC, onset of blindness occurring within hours of the head injury, absent optokinetic nystagmus, duration of blindness less than 24 hours, agitation and restlessness, absence of skull fracture or visible cerebral injury on CT scan, absence of other neurological deficits, and EEG findings that initially show posterior slowing with subsequent normalization. Transiently fixed and dilated pupils have been described in these patients but should be viewed cautiously by clinicians in making this diagnosis, since cortical blindness is defined by sparing of the pupils. This syndrome may be underdiagnosed, since it may not be obvious that the child is blind unless the diagnosis is considered.
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PMID:Transient blindness following mild head trauma. Criteria for a benign outcome. 304 40

Blood pressure, which ist the product of cardiac output and peripheral vascular resistance is regulated by a complex feedback mechanism involving the sympathetic and parasympathetic systems and hormones. An acute disturbance of regulation may lead to a life-threatening increase in blood pressure. Diagnosis is based upon a careful measurement of blood pressure, which must be performed under internationally standardized conditions. Hypertensive crisis refers to a rapid blood pressure increase greater than 30 mmHg above the age-related 95th percentile. The main causes of hypertension in childhood are renal diseases, which may be aggravated by additional conditions either by the clinician himself (e.g. cyclosporin, steroids) or by the patient (lack of compliance). Crisis affects the brain (hypertensive encephalopathy), the heart (left ventricular insufficiency), the retina (visual disturbances) and the mucous membranes (epistaxis). Hypertensive encephalopathy is induced by a break-through of the autoregulation of brain flow, leading to hyperperfusion and, thus to cerebral oedema. The clinical manifestations are characterized by restlessness, severe and diffuse headache, vomiting, nystagmus, impaired vision, dizziness, paraesthesia, seizures and palsies, which may lead - if untreated - to coma and death. The course is usually prolonged and reversible by adequate treatment. The morphological consequences are purpura cerebri, fresh retinal haemorrhages and papillary oedema, apart from left ventricular dilatation and hypertrophy. The diagnostic procedure rests on the quick realization of essential anamnestic (blood pressure, renal disease, drugs), clinical (oedema, cardiac action, central nervous system, fundus) and laboratory parameters (serum creatinine, electrolytes, glucose, blood count, urine). Treatment should start before the manifestation of clinical signs (hypertensive emergency) with rapidly acting antihypertensive drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The hypertensive crisis in childhood]. 305 87

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

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

Dextrorphan HCl (Ro 01-6794/706) is an NMDA receptor antagonist with clinical potential for administration in an elderly population of acute ischemic stroke patients. In vivo experience with such patients demonstrated a consistent pharmacologic effect/adverse experience profile that is typical of an NMDA receptor antagonist (e.g., nystagmus, nausea, vomiting, agitation, somnolence, hallucinations and hypertension). For the most part, these pharmacologic effects were mild to moderate in severity; short-lived; reversible; not life-threatening and subjectively tolerated. The most serious pharmacologic effect produced by dextrorphan administration was hypotension, which occurred within a well-defined window of 90 minutes from the start of the loading dose infusion in patients who received 200 mg/hr or greater loading dose infusions. In all cases it was reversible without neurologic sequelae. Careful review of demographic and pharmacokinetic parameters did not demonstrate any overriding factor(s) to the production of hypotension other than the rate of the loading dose infusion. Severe hypotension, severe decreased levels of consciousness and respiratory depression should not be generally expected at loading doses less than 200 mg/hr. In summary, dextrorphan can be safely given to an elderly population of ischemic stroke patients as a loading dose rate below 200 mg/hr and as a maintenance dose rate between 50-90 mg/hr for 24 hours when patients are monitored carefully for pharmacologic effects.
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PMID:Safety, tolerability and pharmacokinetics of the N-methyl-D-aspartate antagonist Ro-01-6794/706 in patients with acute ischemic stroke. The Dextrorphan Study Group and Hoffmann-La Roche. 748 11

Dextromethorphan (DM), the dextrorotatory isomer of 3-hydroxy-N-methylmorphinan, is the main ingredient in a number of widely available, over-the-counter antitussives. Initial studies (Bornstein 1968) showed that it possessed no respiratory suppressant effects and no addiction liability. Subsequently, however, several articles reporting abuse of this drug have appeared in the literature. The drug is known to cause a variety of acute toxic effects, ranging from nausea, restlessness, insomnia, ataxia, slurred speech and nystagmus to mood changes, perceptual alterations, inattention, disorientation and aggressive behavior (Rammer et al 1988; Katona and Watson 1986; Isbell and Fraser 1953; Devlin et al 1985; McCarthy 1971; Dodds and Revai 1967; Degkwitz 1964; Hildebrand et al 1989). There have also been two reported fatalities from DM overdoses (Fleming 1986). However, there are no reports describing the effects of chronic abuse. This report describes a case of cognitive deterioration resulting from prolonged use of DM.
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PMID:Cognitive deterioration from long-term abuse of dextromethorphan: a case report. 780 71

Review was made of the symptoms, treatment and outcome of 151 cases of severe envenomation by the scorpion Centruroides sculpturatus treated with antivenom, 1988-1989. The most frequent symptoms were restlessness, nystagmus, paresthesiae, hypersalivation, fasciculation, blurred vision and dysphagia with an average of four symptoms. Medications before antivenom, given to about half of the subjects, included antihistamines, sedatives, analgesics and epinephrine. In 71% of patients, symptoms were relieved within 30 minutes of receiving one vial. Immediate hypersensitivity reactions occurred in 8%, but were generally mild. Skin tests had a sensitivity of 96% and specificity of 68%. Delayed reactions were not addressed. In conclusion, the antivenom appears safe and effective.
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PMID:Response to specific Centruroides sculpturatus antivenom in 151 cases of scorpion stings. 814 56


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