The anatomical basis of the pyramidal tract is reviewed with respect to its proposed role in the conduction of the motor evoked potential. The fiber diameter profiles are discussed in relation to the measured conduction velocities of the corticospinal tract in humans. Stimulus parameters utilized to obtain the motor evoked potential are reviewed in relation to the laterality of response, response threshold, and properties of spatial and temporal summation. A discussion of the major descending tracts involved with walking as opposed to fine distal use of the digits is undertaken in the context of the possible prognostic capabilities of the motor evoked potential.
S-UMMARY1. Dopamine applied iontophoretically to neurones of the caudate nucleus of cats caused excitation of some (9 % of those encountered) and depression of others (60 %). Some cells have been found affected both by dopamine and by acetylcholine.2. The effects of dopamine could be prevented by the previous iontophoretic administration of phenoxybenzamine, but not by dichloroisopropylnoradrenaline.3. Responses evoked in caudate neurones by electrical stimulation of substantia nigra were depressed by dopamine. No evidence for enhancement of the effects of nigral stimulation through the application of dopamine were detected.
The relationship between intracranial pressure (ICP) and latency of visual evoked potentials (VEP) was investigated in hydrocephalic patients with severe head trauma. A positive correlation of increase in latency of wave N2 (normal latency 71 +/- 9.2 msec) of the VEP with elevations in ICP was observed. A potential role for VEP in both the assessment of shunt function and the monitoring of patients with severe head injury is suggested by these findings.
SUMMARY1. The dorsal lateral geniculate nucleus (LGN) of the cat stains densely for acetylcholinesterase, which is present in intra-axonal and extracellular locations.2. Acetylcholine (ACh), cholinomimetic drugs, anticholinesterases and ACh antagonists were administered iontophoretically to neurones in the LGN.3. ACh excited eighty-six of 184 (46.7 %) geniculate neurones and depressed seven (3.8 %).4. The excitatory response to ACh was frequently larger than that to L-glutamate and had a comparable time course.5. There was a considerable variation in the proportion of ACh sensitive cells in different animals. ACh firing was facilitated by optic nerve or visual stimulation.6. Carbamylcholine was the most active of the choline esters tested, frequently exceeding ACh in potency. The other choline esters and nicotine were consistently less active than ACh.7. Anticholinesterases, eserine, neostigmine and edrophonium potentiated the action of ACh, and often caused excitation. Eserine caused an initial small enhancement in the amplitude of the focal potential evoked by optic nerve stimulation followed by a reduction in amplitude and prolongation of duration of the potential.8. Atropine and benzoquinonium effectively prevented the ACh excitation of many cells. Dihydro-,8-erythroidine failed to cause a significant reduction in the magnitude of the ACh response. All three ACh antagonists failed to reduce the excitant effects of optic nerve or visual stimulation.9. Stimulation of the mesencephalic reticular formation caused either an enhancement or a reduction in the excitability ofACh sensitive neurones in the LGN. Benzoquinonium abolished the excitatory effects of reticular formation stimulation.
SUMMARY1. A cooling plate was implanted over the forelimb representation in area 2 of the post-central region of cerebral cortex in two monkeys.2. Recordings were made of the discharges of thirty-seven movement-related neurones (thirty-four precentral and three post-central) in the forelimb motor representation of the cerebral cortex during active and passively, imposed limb movements before, during and after cooling area 2 and local surrounding regions.3. Perfusion of the cooling plate with ice-cooled water for 3-5 min caused marked clumsiness of the conscious animal's forelimb movement and anaesthesia of the contralateral hand.
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