P.L. De Riu

Hypoglossal nuclei participation in rat mystacial pad control

Recently, we showed that extra-trigeminal axons, originating from the hypoglossal nucleus, travel with the infraorbital division of the trigeminal nerve (ION), which is known to innervate the rat mystacial pad. Dil was monolaterally injected into the rat XII nucleus to analyse the peripheral distribution of hypoglossal axons to the mystacial pad, to evaluate their involvement in facial sensory–motor control. Electromyographic responses of mystacial pad motor units to electrical stimulation of the ION were recorded, along with the evoked responses to electrical stimulation of the ipsilateral XII nucleus. The results showed that hypoglossal axon terminals target the ipsilateral extrinsic musculature of the mystacial pad, but they do not have any contact with the intrinsic muscles. ION electrical stimulation increased electromyographic activity in the ipsilateral pad extrinsic muscles, even following VII nerve transection. Hypoglossal nucleus electrical stimulation induced field potentials and monosynaptic responses in the same motor units that persisted even following VII nerve transection, these disappearing after cooling the ION. We suggest that the small hypoglossal neurons projecting to the extrinsic musculature of the mystacial pad are part of a hypoglossal–trigeminal loop that participates in the sensory–motor control of the rat vibrissae system.

β-Endorphin and Cortisol Levels in Plasma and CSF Following Acute Experimental Spinal Traumas

beta-endorphin and cortisol were measured in cerebrospinal fluid (CSF) and plasma by radioimmunological method (RIA) in two groups of rabbits with spinal cord traumatic injuries at cervical and lumbar levels, respectively with and without concomitant spinal shock and arterial hypotension, and in a group of sham operated animals as controls. The two groups with spinal lesions displayed a significant beta-endorphin increase in CSF, whereas the cortisol level remained unchanged both in the spinal traumatized rabbits and in controls. Both the opioid and the cortisol concentration rose significantly in plasma in all three groups and in particular resulted significantly higher in the cervical traumatized group where spinal trauma was associated with spinal shock and hypotension. However, no significant difference was found when beta-endorphin concentrations in plasma were compared between the sham operated animals and the spinal lumbar traumatized animals without concomitant spinal shock. The results seem to suggest that the beta-endorphin increase in CSF is related to the nervous tissue lesion, while its increase in plasma, like that of cortisol, is due to surgery or other stress factors inherent in the experiment. This independent behaviour of beta-endorphin in plasma and in CSF suggests its different origin in these two compartments.

Hypoglossal nucleus projections to the rat masseter muscle

We investigated in the rat whether hypoglossal innervation extended to facial muscles other than the extrinsic musculature of the mystacial pad. Results showed that hypoglossal neurons also innervate the masseter muscle. Dil injected into the XII nucleus showed hypoglossal axons in the ipsilateral main trunk of the trigeminal nerve. After Gassers ganglion crossing, the axons entered into the infraorbital division of the trigeminal nerve and targeted the extrinsic muscles of the mystacial pad. They also spread into the masseter branch of the trigeminal nerve to target the polar portions of the masseter muscle spindles. Retrograde double labelling, performed by injecting Dil into the pad and True Blue into the ipsilateral masseter muscle, showed labelled hypoglossal neurons in the medio-dorsal portion of the XII nucleus. The majority of these neurons were small (15-20 microm diameter), showed fluorescence for Dil and projected to the mystacial pad. Other medium-size neurons (25 microm diameter) were instead labelled with True Blue and projected to the masseter muscle. Finally, in the same area, other small hypoglossal neurons showed double labelling and projected to both structures. Functional hypotheses on the role of these hypoglossal projections have been discussed.

An elderly female patient with tardive oromandibular dystonia after prolonged use of the histamine analog betahistine

Tardive oromandibular dystonia (OMD) is iatrogenic in origin and is characterised by orofacial and lingual stereotypes more frequently than the idiopathic form of OMD Tardive OMD is often associated with anti-dopaminergic treatment involving drugs such as anti-psychotics, anti-emetics, and anti-vertigo agents, although the syndrome can also be triggered by anti-epileptic or anti-depressant drugs that do not have anti-dopaminergic properties. We report an elderly female patient with OMD after prolonged, self-administered treatment with betahistine dihydrochloride, a histamine analogue.

Subcortical projections of the cerebral nystagmogenic area

Abstract In the present investigation we analyzed the connections of the cerebral nystagmogenic center with subcortical formations in the guinea pig by electrophysiological methods. Single-shock electrical stimulation of the parietotemporal nystagmogenic area elicited typical evoked potentials in various subcortical structures with latencies ranging from 0.7 msec up to 9 msec. Such evoked potentials could be recorded from ipsilateral internal capsule, most lateral part of the cerebral peduncle, lateral and medial geniculate bodies, lateral and posterior nuclei of the thalamus, superior and inferior brachia, superior and inferior colliculi, oculomotor nuclei, mesencephalic reticular formation, lateral lemniscus and lateral vestibular nuclei. Usually no contralateral responses were seen. Often the evoked potentials were localized in or around the mesodiencephalic nystagmogenic center, which in some experiments was also previously identified. In several cases the experimental arrangement was reversed and it was possible to elicit antidromic evoked potentials in the cerebral nystagmogenic center by stimulating the previously recorded subcortical sites. Thus the results of the present research on the anatomical connections of the cerebral nystagmogenic area with some subcortical formations confirm and extend preceding findings obtained with the Marchi method.

Effect of reperfusion on the uptake of [3H] uridine in the gerbil brain after prolonged ischaemia

SummaryThe uptake of labelled uridine is reduced in the whole ischaemic hemispheres of gerbils subjected to unilateral carotid artery occlusion. Following circulatory restoration, brain structures that had an ischaemic insult of moderate intensity exhibit a progressively increased uptake. However, during reperfusion there is a tendency towards a clear cut definition of dead zones. This progression of the lesions seems to be related to a maturation phenomenon occurring in areas with an irreversible damage at the end of the ischaemic period.

Spinal compensation of postural cerebral asymmetries

Abstract Unilateral ablation of the motor area in primates provokes contralateral hemiplegia and asymmetrical posture due to derangement of muscle tone. Such a phenomenon, however, fades away in approximately 35–55 days. Spinal cord transection at low thoracic levels or bilateral lumbo-sacral deafferentation induces reappearance of the acute symptoms in the forelimbs of well compensated animals following the previous cortical lesion. It seems reasonable that the spinal cord plays an important role in the peripheral compensation via afferent impulses.