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Biomedical subjects

J Dostrovsky

Publications and source records attributed to J Dostrovsky.

8 recordsLinked to original sources

Neuronal recordings in Parkinson's disease patients with dyskinesias induced by apomorphine.

Dopaminergic agents reverse parkinsonism but commonly induce dyskinesia in patients with Parkinson's disease (PD) on long-term levodopa therapy. The aim of this study was to determine the neurophysiologic correlates of the amelioration of parkinsonism and the involuntary movements produced by the dopamine agonist apomorphine. Seventeen PD patients were given apomorphine (2-6 mg) before surgery. Neural activity was recorded for individual neurons and for populations of neurons before and after apomorphine. Both internal (GPi) and external (GPe) segments of the globus pallidus were sampled in patients undergoing pallidal surgery. The subthalamic nucleus (STN) was sampled in STN surgery patients. Results suggest that dopaminergic agents act by decreasing GPi and STN activity, and increasing GPe activity, and that drug-induced dyskinesias results from a large reduction in GPi firing.

Action Potentials↗

Regulation of expression of galanin and galanin receptors in dorsal root ganglia and spinal cord after axotomy and inflammation.

Galanin can normally be detected only in a few dorsal root ganglion (DRG) neurons, but it is dramatically upregulated after peripheral nerve injury in both rat and monkey. Galanin is stored in large dense core vesicles, which after axotomy are often found close to the membrane of afferent nerve endings in the dorsal horn. In the monkey there is an increase in galanin in many nerve terminals in the superficial dorsal horn after axotomy, but such an increase is more difficult to detect in the rat. Galanin is also present in local dorsal horn neurons, where it is upregulated by peripheral inflammation. Both galanin-R1 and galanin-R2 receptor mRNAs are expressed in rat DRGs, mainly in, respectively, large and small DRG neurons. Galanin-R1 receptor mRNA is downregulated in DRG neurons after axotomy, and a small decrease in galanin-R2 receptor mRNA levels can also be seen. After peripheral tissue inflammation galanin-R1 receptor mRNA levels decrease and galanin-R2 receptor mRNA levels increase. The present results show that galanin and galanin receptors are present in sensory and local dorsal horn neurons and are regulated by nerve injury and inflammation. Galanin may therefore be involved in processing of pain information, primarily exerting analgesic effects. Whereas local dorsal horn neurons represent a defense system against inflammatory pain, we have proposed that a second defense system, against neuropathic pain, is intrinsic to DRG neurons.

Animals↗

Methods for microelectrode-guided posteroventral pallidotomy.

Methods for localizing the posteroventral globus pallidus intermus are described. The authors' techniques include the use of microelectrodes to record single-unit activity and to microstimulate in human pallidum and its surrounding structures. This technique allows a precise determination of the locations of characteristic cell types in sequential trajectories through the external and internal segments of the pallidum. The location of the optic tract can be determined from microstimulation-evoked visual sensations and recordings of flash-evoked potentials. In addition, microstimulation-evoked motor and sensory responses allow the internal capsule to be identified. The data collected using this technique are an important adjunct to selecting optimum sites to place electrocoagulation lesions for stereotactic posteroventral pallidotomy for refractory Parkinson's disease.

Catheter Ablation↗

Comparison in man of short latency averaged evoked potentials recorded in thalamic and scalp hand zones of representation.

Recordings were performed in the thalamus of 13 patients suffering from either abnormal movements or intractable pain, with the aim of delimiting the region to be destroyed or stimulated in order to diminish the syndrome. In 11 of these patients averaged evoked potentials were recorded simultaneously from the scalp and specific thalamus (VP) hand area levels following median nerve stimulation. These recordings were done during the operation or afterwards when an electrode was left in place for a program of stimulation. The latencies of onsets and peaks on the scalp 'P15' were compared with those of the VP wave; a clear correspondence was found. Moreover, when increased stimulation was used, both waves began to develop in parallel. Thus in the contralateral 'P15' a component exists due to the field produced by the thalamic response. To explain the presence of an ipsilateral scalp 'P15' wave, we propose that a second wave having the same latency and a slightly shorter peak exists on the scalp due to a field produced by a brain-stem response. This double origin of 'P15' is also shown by the different changes which the ipsilateral and contralateral waves present during changes in alertness. The scalp 'N18-N20' is also composed of at least 2 components. The first peak appears on the scalp with a latency shorter than that of the negativity which develops in the thalamus. The N wave, moreover, increases in latency with rapid stimulus repetition. We propose with others that 'N18' is a cortical event reflecting the arrival of the thalamo-cortical volley. The second component, 'N20,' has a peak latency closely correlated to that of the thalamic negativity. This component was present alone in 'N' when rapid stimulation (greater than 4/sec) was used, which did not change the thalamic response. It must be a field produced by the thalamic negativity.

Electrodes↗