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Biomedical subjects

O Keren

Publications and source records attributed to O Keren.

44 records · Page 3Linked to original sources

Enkephalin mydriasis in mice.

Morphine is known to produce mydriasis in mice. We have found that enkephalins caused a similar effect. Morphine was twice as active as D-Ala-D-Leu-enkephalin (BW-180C), 5 times as active as Met-enkephalin and 7 times as active as Leu-enkephalin. The time course of the effect was shortest for the enkephalins ( t 1/2 = 8-12 min), intermediate for BW-180C (60 min) and longest for morphine (80 min). Naloxone antagonised the effect of all agents to a similar extent. The question whether enkephalins are involved in the physiological regulation of pupillary diameter was investigated by administering either naloxone or D-phenylalanine to mice. None of these agents changed pupillary size, thus making such an involvement unlikely.

Animals↗

Tolerance to the Mydriatic effects of morphine in mice.

When injected to mice, opiates produce mydriasis. Animals treated chronically with morphine, developed tolerance to the mydriatic effects of morphine. The degree and consistency of the response make the pupil a valuable tool in opiate research.

Animals↗

Asymmetry of turning behaviour of rats induced by amphetamine and apomorphine.

Turning behaviour of rats following injection of amphetamine is in the same direction as following apomorphine. Unilateral common carotid artery ligation does not affect this asymmetry. Thus the reason for the asymmetry in turning behaviour following injection of amphetamine is probably due to postsynaptic dopaminergic asymmetry within the corpus striatum.

Amphetamine↗

Somatosensory evoked potentials in prolonged postcomatose unawareness state following traumatic brain injury.

Somatosensory evoked potentials (SEPs) were found by several authors to have a prognostic value in traumatically brain-injured (TBI) patients and can serve for monitoring changes in the state of TBI patients. Most of the studies were performed in the acute phase of trauma and most of reports have dealt with the short-latency components. The present study reports on seven patients (mean age 26.2 years) who suffered severe blunt TBI and were in prolonged post-comatose unawareness (PCU) state, in whom early and late SEP components were recorded at least 5 weeks after sustaining trauma. The SEPs studied could not reveal a uniform pattern apart from prolonged central conduction time (CCT), which was common to all patients. This may be due to individual non-homogeneous patterns of brain damage in our severe TBI patients. Meaningful late recovery of consciousness occurred in one patient and correlated with shortening of CCT. We suggest that the prolonged CCT found in our patients is related to diffuse subcortical axonal injury and that the shortened CCT found during the second examination in this patient actually reflects late partial recovery--either structural or functional--of affected brain regions. This patient is also an example of the possible relationship between reduction of CCT and recovery of consciousness a long time after injury.

Activities of Daily Living↗

Electrophysiological findings in poliomyelitis patients at the subacute phase.

Electrodiagnostic tests-needle EMG, nerve conduction and somatosentory evoked potential (SEP) studies of the upper and the lower limbs were performed in three patients during the subacute phase of poliomyelitis. Although poliomyelitis is traditionally considered a "pure motor" disease, involvement of the sensory system was demonstrated by prolonged sensory nerve conduction and by delayed latencies and amplitude asymmetries of SEPs obtained from the lower limbs. Sensory deficit in poliomyelitis is well known to exist during the acute phase of illness. The present report describes the electrophysiological findings in patients during the subacute phase, several months after onset of illness. Sensory nerve action potentials and sensory evoked potentials were abnormal, especially those elicited by lower limb stimulation although the patients had no overt signs of sensory loss at that time. The associated EMG findings are described, and the probable pathologic changes of the motor unit are discussed.

Adolescent↗