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)

4 cases of accidental fenfluramine poisoning in children are reported. Excitation, coma, convulsions, tachycardia, mydriasis, nystagmus, and rubeosis of the face were the most important signs. They appeared 30--60 min after ingestion, and some of them lasted for several days. 2 children had severe trismus and therefore had to be given muscle relaxants before intubation and gastric lavage became possible. These observations agree well with informations collected in our poisoning control center and with previously published data. Less than 5 mg/kg of body weight are toxic, 5--10 mg/kg may produce coma and convulsions, and the smallest lethal doses were 28,7 and 33,3 mg/kg. Early gastric lavage, good monitoring of the vital functions and, if necessary, administration of anticonvulsive drugs, beta-blocking agents, lidocaine, chlorpromazine, and artificial ventilation and cardiac defibrillation are the most important therapeutical measures.
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PMID:[Fenfluramin (ponderax) intoxications in children (author's transl)]. 3 42

In a series of 53 fenfluramine intoxications (15 taken from the literature), 10 were lethal after doses of 28.7--70 mg/kg of body weight. Cardiac arrest occurred 1--4 hr after ingestion in 9 cases; all these 9 patients died. Two out of 3 patients with more than 15 mg/kg had coma and convulsions. Other frequent signs were mydriasis, tachycardia, and rubor of the face. The additional signs of nystagmus, hypertonia, trismus, hyperreflexia, clonus, excitation, hyperthermia, and sweating define the clinical syndrome of fenfluramine intoxication. Symptoms begin 30--60 min after ingestion and can persist during several days. Early gastric lavage, instillation of activated charcoal, diazepam in case of seizures, chlorpromazine for malignant hyperthermia, propranolol for extreme tachycardia, and lidocaine in the event of ventricular extrasystoles are recommended. If trismus is a prominent sign, muscle relaxants must be given before gastric lavage can be done. The relatively benign course after survival of the first 4 hr suggests supportive therapy only in the later phase of intoxication.
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PMID:Fenfluramine poisoning. 43 87

For 24 hours after an automobile accident, a 19-year-old comatose man exhibited spontaneous, intermittent, see-saw, rotatory, and downward eye movements with synchronous lid elevation. These unusual movements, which appear most closely related to nonpendular see-saw nystagmus and atypical ocular bobbing, probably resulted from the severe pontomedullary tegmental damage found at autopsy.
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PMID:Intermittent see-saw eye movements. Report of a patient in coma after hyperextension head injury. 62 64

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

The authors report a case of posterior fossa acute subdural hematoma diagnosed preoperatively through extravasted contrast media from the hemispheric branch of the posterior inferior cerebellar artery along a linear fracture across the transverse sinus unto the pyramis. In a review of the literature it is to be noted that in acute cases, nystagmus and cerebellar signs are very rare and patients fall in coma within 24 hours after injury with promptly advancing severe brain stem compression signs in contrast to subacute or chronic cases. Therefore, whenever the diagnosis is suspected, time should not be lost for a burr hole opening and decompressive craniectomy. Vertebral angiography is sometimes very confirmative but it should be done only when time affording.
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PMID:[A case of posterior fossa acute subdural hematoma diagnosed through extravasated contrast media (author's transl)]. 90 22

In 32 patients with coma of varying intensity and aetiology the effect of light on caloric nystagmus was studied. During consciousness disturbances a light stimulus provoked or increased the intensity of induced caloric nystagmus. This reaction was thus a reverse (paradoxical reaction) of that observed in waking state. Photic stimulation may provoke the rapid phase of nystagmus through facilitating impulses coursing from the subcortical or cortical visual centres to Cajal's nuclei and then through the reticular formation to the vestibulo-oculomotor system. In waking state these impulses are inhibited while in precomatic state they may become prevalent. The paradoxical reaction disappears in deep coma together with all vestibular reactions.
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PMID:[Paradoxical vestibular reaction in patients with consciousness disorders (nystagmographic recording)]. 108 Feb 59

Although old or recent infarcts of a cerebellar hemisphere in the territories of the posterior inferior (PICA), superior, or anterior inferior cerebellar arteries are commonplace autopsy findings, in no case have corresponding clinical symptoms been clearly identified. We have studied three cases, two clinocaopthologically and one clinicosurgically, in which an acute infarct involving only the cerebellum lay in the PICA territory distal to the branches to the medulla oblongata. The clinical manifestations consisted of rotatory dizziness intensified by motion, nausea, vomiting, imbalance, and nystagmus. In two cases, the clinical diagnosis had been a benign labyrinthine disorder. Recognition of a syndrome corresponding to cerebellar infarction in the PICA territory is important insofar as it assists in the differential diagnosis of dizziness. It becomes of crucial importance when cerebellar infarction is the prelude to cerebellar swelling and brain stem conpression leading to coma and death unless surgically relieved.
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PMID:Acute cerebellar infarction in the PICA territory. 113 Oct 70

Two cases of acute meningoencephalitis, presumably viral in origin, with brainstem involvement are reported. Common to both patients during the course of their illness was coma, downbeat nystagmus, and ataxia. Although both reached what appeared to be a terminal state, recovery began following treatment with corticosteroids. The significance of the neurologic signs, particularly the unusual occurrence of downbeat nystagmus, is discussed, as is the appropriate management of the disorder.
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PMID:Downbeat nystagmus as a sign of brainstem involvement in acute meningoencephalitis. 116 35

Phencyclidine is now one of the most frequently used main ingredients of "street drug" preparations. Its effects are highly dose dependent and three varieties of acute intoxication have been seen clinically associated with different dosages and routes of administration. Most persons using phencyclidine smoke it sprinkled on parsley in low doses. The presence of horizontal and vertical nystagmus associated with hypertension in a patient who is agitated or comatose are diagnostic of a phencyclidine intoxicated state. Sensory isolation and intravenous administration of diazepam in the event of seizure activity have proved effective in the treatment of acute intoxicated states. Phencyclidine has pronounced behavioral toxicity and several deaths due to this agent have now been documented. It is unknown whether seizure activity or respiratory depression is the primary cause of death in pharmacological overdoses.
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PMID:Phencyclidine--states of acute intoxication and fatalities. 121 Mar 29

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


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