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)

We studied the effects of ketamine, an antagonist of the N-methyl-D-aspartate receptors, on (1) the spontaneous saccades, (2) the vestibulo-ocular reflex (VOR), and (3) the optokinetic nystagmus (OKN) in 8 cats. Ketamine was given intramuscularly at four dosages (1, 2, 8, and 16 mg/kg). Eye movements were measured using the magnetic field-search coil technique. Ketamine did not prevent the occurrence of saccades, but each of them was followed by a centripetal postsaccadic drift. The time-constant of the drift induced by ketamine was 1.0 s when the given dosage was 1 mg/kg and 0.35 s when the given dosage was 16 mg/kg. Post-saccadic drift caused by a low dosage of ketamine may reflect only a mismatch between the pulse and the step commands that create saccades. The highest used dosages of ketamine aggravated the post-saccadic drift probably by disturbing the oculomotor neural integrator. To elicit the horizontal VOR, the head was submitted either to sinusoidal rotations (+/- 20 degrees; 0.05 to 1 Hz) or to a rotation at a constant velocity (100 degrees/s during 40 s). In darkness, the VOR step gain was reduced by ketamine in a dosage-dependent manner. VOR phase lead at 0.10 Hz oscillation in darkness increased from 4.0 degrees +/- 2.4 degrees to 51.6 degrees +/- 7.5 degrees after administration of ketamine at 16 mg/kg. This suggests that ketamine, at least at higher dosages, induces a failure of the neural integrator. Chemical blockade of the vestibular commissure by ketamine may also be responsible for the reduction of the VOR gain. Horizontal OKN was tested using a step stimulus (30 degrees/s during 40 s). When ketamine was given at 1 mg/kg, the average steady-state gain of the OKN diminished from 0.6 +/- 0.2 to 0.3 +/- 0.1. After administration of ketamine at 2 mg/kg, the OKN was abolished. The sensitivity of OKN to ketamine is explained at least partly by the fact that ketamine acts against the visual pathways in the retina, in the geniculate nucleus, and in the visual cortex. The time course of the optokinetic afternstagmus (OKAN) and that of the decrease of the prerotatory and postrotatory VOR were not reduced by ketamine administered at 1 or 2 mg/kg. This shows that ketamine does not affect the velocity-storage mechanism at these dosages.
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PMID:Effects of ketamine on ocular movements of the cat. 167 Jan 65

Attention plays an important role in oculomotor function. We studied the effect of attentional stimuli on eye movements induced by ketamine. The experiments were carried out on three monkeys. Ketamine injected intramuscularly induced nystagmus. When we switched on a new stimulus these eye movements stopped and the animal made a saccade toward it. This may be due to a new motor program, triggered by a visual stimulus, that among its characteristics is able to engage the animal's attention. The program of evoked saccade is overwritten on induced oculomotor activity. Our results suggest that attentional processes modify the dynamic characteristics and induce in particular behavioral condition a new motor program.
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PMID:Does attention affect the motor programs of pharmacologically induced eye movements? 226 29

Intrathecal ketamine, which has not previously been described in man, has been administered to 16 patients with war injuries of the lower limbs. The first five received varying doses from 5 to 50 mg in a volume of 3 ml of 5% dextrose, to determine a dose-response curve (Group 1). The optimal dose was then administered to a further 11 patients who received ketamine 50 mg in a volume of 3 ml in 5% dextrose with the addition of adrenaline 0.1 mg (Group 2). A distinct sensory level was obtained in all patients. In Group 2, nine of the eleven patients obtained satisfactory surgical analgesia and two required supplementation with local anaesthetic. Central effects (drowsiness, dizziness, and nystagmus) also occurred in nine patients, but they remained conscious throughout; one patient experienced no central effects, and one patient developed dissociative anaesthesia. Central effects were more intense the higher level of block. There were no significant changes in mean systolic arterial blood pressure, pulse, or respiratory rates. Surgical analgesia for the blocked dermatomes lasted for a mean of 58 minutes (range 45-90), and recovery was complete and uncomplicated; mild generalised analgesia persisted for a further one to three hours following return of sensation. Ketamine alone did not produce motor block, but addition of adrenaline resulted in complete motor block, and may have intensified sensory blockade. Motor loss persisted for the same duration as surgical analgesia. Adrenaline neither delayed the onset of central effects, nor reduced their intensity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intrathecal ketamine for war surgery. A preliminary study under field conditions. 649 99

Ketamine 3-6 mg kg-1 given by mouth to paediatric patients for anaesthetic premedication was evaluated. Forty-three children, ages 2-9 years were randomly allocated to receive either ketamine (3 or 6 mg kg-1) or placebo (cola 0.2 mL kg-1). Oral use of ketamine made separation from the families easier, gave an increased level of sedation, made acceptance of mask application easier and improved the emotional state in the recovery phase. These improvements were present with ketamine 3 mg kg-1 and 6 mg kg-1 in comparison with the placebo. We conclude that 3 mg kg-1 ketamine given by mouth to premedicate paediatric patients is as effective as 6 mg kg-1 but has a decreased incidence of side effects such as nystagmus and vomiting.
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PMID:Oral ketamine premedication in children (placebo controlled double-blind study). 895 93

Several lines of evidence suggest that the glutamatergic N-methyl-D-aspartate (NMDA) receptor is involved in schizophrenia pathophysiology. Post-mortem studies have revealed a lower density of glutamatergic receptors in patients with schizophrenia. Other studies of cerebrospinal fluid reported lower levels of glutamate in patients with schizophrenia in healthy comparison subjects. The most compelling evidence is provided by the psychomimetic effects of the NMDA antagonists phencyclidine and ketamine. Recently, much interest has been given to the study related to the role of NMDA receptor in pathophysiology of schizophrenia by administration of sub-anesthetic doses of ketamine. A phencyclidine hydrochloride derivate, ketamine, is a dissociative anesthetic and a non competitive antagonist of the NMDA receptor. In healthy subjects, ketamine produces: 1) positive symptoms of psychosis, such as illusions, thought disorder and delusions; 2) negative symptoms similar to those associated with schizophrenia including blunted emotional responses, emotional detachment, and psychomotor retardation; 3) cognitive impairments, in particular impairments on tests of frontal cortical function including increased distractibility, reduced verbal fluency and poorer performance on the Wisconsin Card Sorting Test. During smooth pursuit eye tracking, ketamine induces nystagmus as well as abnormalities which are among the characteristics of schizophrenia. In patients with schizophrenia, the administration of ketamine produces an activation of their psychotic symptoms, which have striking similarities to symptoms of their usual psychotic episodes. Ketamine effects on memory and other cognitive functions in schizophrenic patients are controversial. The psychomimetic effects of ketamine are transitional, reversible and influenced by time, dose and administration conditions. Susceptibility to the psychotomimetic effects of ketamine is minimal or absent in children and becomes maximal in early adulthood. The similarity between ketamine effects and endogenous psychoses created interest in the capacity of antipsychotic medications to block ketamine effects. Haloperidol failed to block this ketamine-induced psychomimetic effects in healthy subjects and in schizophrenic patients. However, clozapine, the prototype of atypical antipsychotic agents significantly reduced the ketamine-induced increase in positive symptoms in schizophrenic patients. Recently, lamotrigine significantly decreased ketamine-induced positive and negative symptoms in healthy subjects. Brain regions responsible for NMDA-mediated psychosis have not been established. Using positron emission tomography and [18F] fluorodeoxyglucose, the sub-anesthetic ketamine administration produces bilateral increases in metabolic activity in the prefrontal cortex. In a [15O] H2O positron emission tomography study, ketamine selectively increases cerebral blood flow in the anterior cingulate cortex and reduces cerebral blood flow in the hippocampus and primary visual cortex. The mechanism of neuropsychiatric effects of sub-anesthetic ketamine is not clear. A dysfunction in glutamate-dopaminergic interactions has been suggested as a mechanism for these effects of ketamine. Ketamine has been reported to primarily block NMDA receptor complex giving support to a glutamate deficiency hypothesis in schizophrenia. In addition, ketamine caused increases in cortical and striatal synaptic dopamine concentrations. The effects of NMDA receptor antagonist administration are argued to support a neurobiological hypothesis of schizophrenia, which includes pathophysiology within several neurotransmitter systems, manifested in behavioral pathology. Pharmacological modulation of the effects of NMDA receptor antagonists, such as ketamine, may lead to development of novel therapeutic agents for psychiatric illnesses such as schizophrenia.
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PMID:[Glutaminergic hypothesis of schizophrenia: clinical research studies with ketamine]. 1129 39

Ketamine, an N-methyl-d-aspartate antagonist, blunts central pain sensitization at sub-anesthetic doses (0.3 mg/kg or less) and has been studied extensively as an adjunct for perioperative analgesia. At sub-anesthetic doses, ketamine has a minimal physiologic impact though it is associated with a low incidence of mild psychomimetic symptoms as well as nystagmus and double vision. Contraindications to its use do exist and due to ketamine's metabolism, caution should be exercised in patients with renal or hepatic dysfunction. Sub-anesthetic ketamine improves pain scores and reduces perioperative opioid consumption in a broad range of surgical procedures. In addition, there is evidence that ketamine may be useful in patients with opioid tolerance and for preventing chronic postsurgical pain.
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PMID:Intravenous sub-anesthetic ketamine for perioperative analgesia. 2727 42