Neuronal activity in the region of the thalamic principal sensory nucleus (ventralis caudalis) in patients with pain following amputations.

Thalamic neuronal activity has not been studied in a primate model of peripheral nerve injury. We now report neuronal activity in the region of the human principal sensory nucleus of thalamus (ventralis caudalis) in awake patients during the physiologic exploration that precedes surgical procedures for treatment of stump pain and movement disorders. All patients with amputations showed increased thalamic representations of the stump as reflected in both receptive and projected field maps. This suggested that thalamic re-organization involved both the afferent inputs from and the perceptual representation of the limb. The spontaneous activity of neurons in the region of ventralis caudalis representing the limb with the stump (stump area) was significantly different from that in other areas of the region of ventralis caudalis in patients with amputations (stump control areas) and in patients with movement disorders (control areas). The mean interspike intervals were significantly shorter for cells located in stump areas than for those located in stump control or control areas. Cells in all areas were found to fire in three different patterns: B group (burst) characterized by bursting activity, R group (relay) characterized as a Poisson process, and III group characterized by non-bursting, non-Poisson activity. Cells in the B group were significantly more common in stump control (41%) and stump areas (33%) than in control areas (15%). Bursting cells were found to have patterns consistent with the occurrence of a calcium spike (spike-burst pattern). The spike-burst pattern was most common among cells with receptive fields in the stump area. In these cells firing between bursts (primary event rate) was significantly higher than other cells in the region of ventralis caudalis, suggesting that spike-bursts are not due to hyperpolarization, i.e. low-threshold spikes. Spike-bursts often occur as a result of low-threshold spikes, when the cell is hyperpolarized. In contrast, spike-bursts in these patients were associated with increased interburst firing rates in cells with receptive fields. Thus bursting of these cells may have been due to high-threshold dendritic calcium spikes evoked by afferent input. In that case bursting could be involved in activity-dependent changes in thalamic function following deafferentation through a calcium-mediated mechanism.

Patterns of bursting occurring in thalamic cells during parkinsonian tremor.

It has been proposed that parkinsonian tremor is produced either by the activity of an intrinsic thalamic pacemaker or by the oscillation of an unstable long loop reflex arc. The former (central) hypothesis proposes that overactivity of neurons in the internal segment of the globus pallidus inhibits or hyperpolarizes thalamic neurons. When hyperpolarized, thalamic cells oscillate with bursting of the type associated with low threshold calcium spikes (low threshold spike-bursts). Low threshold spike-bursts can be identified by particular patterns of interspike intervals within the burst. The alternative (peripheral) hypothesis proposes that tremor results from oscillation of a reflex arc transmitting activity from muscle stretch receptors to thalamus, motor cortex, and back to the stretched muscle. When the gain of this reflex is increased, the arc may become unstable and oscillate. Oscillations produced by peripheral inputs may produce an acceleration-deceleration pattern within the burst which results in sinusoidal modulation of a spike train if bursting is periodic. We have assessed these two hypotheses by studying the pattern of interspike intervals occurring within bursts recorded in patients with parkinsonian tremor. The spike trains were analysed for 118 cells located in the ventral nuclear group including ventralis intermedius (thalamic cerebellar relay nucleus, n=48) and ventralis oralis posterior (thalamic pallidal relay nucleus, n=39) of patients with parkinsonian tremor. Two cells recorded in ventralis intermedius of a sleeping patient with chronic pain showed bursting activity similar to the low threshold spike-bursts recorded in sleeping animals, suggesting a common mechanism for low threshold spike-bursts across species. Forty-two cells recorded in patients with parkinsonian tremor (ventralis intermedius, n=19; ventralis oralis posterior, n=12) were classified as tremor-related cells because their activity was characterized by both a concentration of power at tremor frequency and significant correlation with tremor. Eleven tremor-related cells, 10 located in ventralis intermedius or ventralis oralis posterior and most responding to sensory inputs, had an acceleration-deceleration pattern of intraburst firing. Only one cell, a tremor-related cell in ventralis intermedius, showed the pattern expected of presumed low threshold spike-bursts. Therefore, intraburst interspike interval patterns consistent with either the central or the peripheral hypothesis were recorded in the thalamus of patients with parkinsonian tremor. Twenty-one tremor-related cells (15 cells in ventralis intermedius or ventralis oralis posterior) had bursts with intraburst interspike intervals which were independent of position of the interspike interval within the burst. Therefore, the activity of the majority of cells was not consistent with either hypothesis, suggesting that another oscillatory process may contribute to parkinsonian tremor.

Muscarinic receptors in rat cortex, hippocampus, hypothalamus and brainstem following transient forebrain ischemia and hemorrhagic shock.

[3H]Quinuclidinyl benzilate binding properties of cerebral cortex, hippocampus, hypothalamus and brainstem of rats subjected to transient forebrain ischemia or severe hemorrhagic shock were investigated. Maximal binding capacities (Bmax) were not significantly different from control animals in either model. On the other hand, significant increases in binding affinities at all four brain regions in the ischemia-reperfusion group and at hypothalamic and brainstem membranes in the hemorrhagic shock group were observed. Kd values obtained in cortex and hippocampus of animals in shock were similar to control values. It was concluded that in brain ischemia models, the number of brain muscarinic receptors do not change at early stages, but binding affinities increase most likely due to systemic hypotension rather than reperfusion. The well-developed circle of Willis seems to protect cortical and hippocampal muscarinic receptors from hypoxia-induced changes.

CT myelography in communicating syringomyelia.

Although the etiology of syringomyelia is not clearly understood, many surgical methods have been proposed for its treatment. One widely used technique in cases of communicating syringomyelia is that of posterior fossa decompression and plugging of the obex (Gardner's Operation). In this paper we present five cases of syringomyelia which were investigated using detailed myelo-computerized tomographic techniques, of which two appeared to be communicating syringomyelia and which were treated by posterior fossa decompression and obex plugging. We also discuss the place of computed tomography in the differential diagnosis of communicating syringomyelia.

Intradural rupture of cervical vertebral disc.

STUDY DESIGN: The authors discuss their experience with a patient who had cervical intradural disc herniation and relate the case to the relevant literature. OBJECTIVES: The patient was evaluated with direct radiographies, myelography, electromyography, and computerized tomography, as well as with neurologic examination. The follow-up period was 10 months post-operative. SUMMARY OF BACKGROUND DATA: Intradural disc herniation is a rare pathology nearly always confined to the lumbar region. In 1989, Katooka et al reviewed the existing literature and discovered 70 cases. Cervical intradural disc herniation, on the other hand, is much rarer, and there are only five cases in the literature. METHODS: The patient's neurologic, neuroradiologic, and operative findings were evaluated and compared with the cases reported in the literature. CONCLUSIONS: The five patients in the literature had signs of cord compression, but the present patient is the first with root compression.

Tizanidine is an effective agent in the prevention of focal cerebral ischemia in rats: an experimental study.

BACKGROUND: Focal cerebral ischemia secondary to cerebral vessel occlusion is still an important cause of mortality and morbidity. Excitatory neurotransmitters are gathered in the extracellular space during ischemia and initiate or stimulate a series of pathophysiological biochemical processes and consequently lead to neuronal death. Tizanidine (Sandoz compound DS 103-282, 5-chloro4,2 (2-imidazolin-2-yl-amino)-2,1,3-benzothiazol hydrochloride) is a selective alpha 2 adrenoreceptor agonist which shows its effect by stimulating presynaptic alpha 2 adrenoreceptors in central ASPergic and GLUergic system by inhibiting aspartic acid and glutamic acid release. In this study, the effect of Tizanidine on reversible focal cerebral ischemia was evaluated. METHODS: Cerebral blood flow to the left hemisphere of adult Sprague-Dawley rats (n=48) was temporarily interrupted by middle cerebral artery and bilateral common carotid artery occlusion for 3 hours in eight rats of each group. Tizanidine was given to each group of rats intraperitoneally before the ischemic insult, 2 hours after ischemia, right after the reperfusion, 2 h after reperfusion, and 4 hours after reperfusion; the animals survived for 24 hours after the reperfusion. After killing and triphenyltetrasoliumchloride staining of brain slices, infarction volumes and ratios of the brains were calculated and the results were compared with those of the control group. RESULTS: Infarction volumes and infarction ratios of the Tizanidine group 1/2 hours before ischemia (143.7+/-6.34 mm3 and 10.1+/-0.43%) and the Tizanidine group 2 hours after ischemia (145.6+/-6.32 mm3 and 10.3+/-0.43%) were found to be significantly lower in favor of the Tizanidine groups when compared with those of the control group (173.9+/-6.38 mm3 and 12,4+/-0.41%). Tizanidine is not effective if used just after reperfusion or later. CONCLUSION: This study shows that Tizanidine pretreatment before the ischemic insult and the administration of the drug within the 2 hours after ischemia reduces ischemic damage significantly. Therefore, this drug can be used as a protective and therapeutic agent in ischemic diseases.

A pontine tuberculoma mimicking an exophytic brain stem tumor.

A 21 year old man with a five month history of facial paresis, diplopia, and gait disturbance diagnosed with a brain stem tumor at another institution was evaluated. Computed tomography, magnetic resonance imaging, clinical and laboratory evaluations suggested a pontine astrocytoma, and the mass was excised. Pathological diagnosis was a tuberculoma confirmed by postoperative positive Mantoux testing. CT and MRI appearances of tuberculomas have been described, but can not differentiate them completely from other tumors such as astrocytomas. Because the incidence of tuberculomas has increased in recent years and they may mimic exophytic tumors of pons, it is important to include pontine tuberculoma in the differential diagnosis of pontine tumors.

Microvascular decompression in the surgical management of trigeminal neuralgia.

The pathophysiological mechanisms underlying trigeminal neuralgia are not clearly understood and several therapeutic modalities have been advocated. Microvascular decompression (MVD) is a widely used surgical approach for the decompression of the affected root entry zone (REZ) of the fifth cranial nerve. In this paper, we present our experience based on 32 patients with trigeminal neuralgia who were treated with MVD, and discuss the role of this procedure in the surgical management of trigeminal neuralgia. All patients had typical TN pain and had had previous medical management which was unsuccessful. Fourteen patients (44%) had been previously treated with other surgical procedures and had persisting pain at the time of admission. Preoperatively, computerized tomography was obtained in all patients; twelve patients (37.5%) were evaluated with magnetic resonance imaging. These neuroradiological studies revealed an asymmetrical vascular structure at the involved REZ in nine patients (28%). All patients underwent MVD, and a vascular loop causing compression on the REZ of the fifth cranial nerve was demonstrated in each case. No mortality was observed, and the only permanent morbidity was cerebellar infarction in one patient (3%). Symptoms disappeared in all patients in the early postoperative period, and only three recurrences (12%) were observed within the follow-up period (mean: 26 months).

Human thalamic nucleus mediating taste and multiple other sensations related to ingestive behavior.

Until now, taste was the only primary sensory modality for which the human central nervous system pathways were unknown. We report sensations evoked by stimulation at microampere current levels in the region of the human thalamic nucleus (ventralis caudalis parvocellularis internis) corresponding to the monkey taste relay nucleus. Stimulation in this region during awake neurosurgical procedures evoked special visceral/somatic (taste/pungent smell), general visceral (fullness of a hollow viscus), as well as painful and nonpainful general somatic sensations. General somatic or visceral sensation was evoked by stimulation at 80% of sites where special visceral/somatic sensation was evoked. These results suggest that primate taste relay mediates multiple sensations in addition to taste.

Painful stimuli evoke potentials recorded from the parasylvian cortex in humans.

Cutaneous stimulation of the face and hand with a CO2 laser in three awake patients evoked potentials (LEPs) recorded from the dominant left parasylvian cortex. These were recorded by means of a subdural grid of electrodes implanted for evaluation of epilepsy. Stimulation of the contralateral face resulted in waveforms consisting of a negative potential (N2, 162 +/- 5 ms; mean +/- SE) followed by a positive potential (P2, 340 +/- 18 ms). Both waves occurred at longer latency after hand than after facial stimulation. N2 and P2 potentials recorded from the grid correspond well in morphology to those recorded from the scalp in four additional patients tested with the same stimulation paradigm. The N2 waves recorded from the subdural grid occurred at significantly shorter latencies than did those recorded from the scalp (184 +/- 6 ms), but the P2 waves at the grid occurred at significantly longer latencies than did those recorded at the scalp (281 +/- 13 ms). The amplitudes of the potentials recorded from the grid were maximal over the parietal operculum both for contralateral stimulation of the face or hand and for ipsilateral stimulation of the face. Potentials also were recorded in this area after stimulation of the ipsilateral hand. The cortical distributions of these potentials suggest that their generators are located in the parietal operculum or in the insula, or in both, consistent with previous PET, magnetoencephalographic, and scalp LEP source analyses. These previous analyses provide indirect evidence of nociceptive input to parasylvian cortex because the interpretation of each analysis incorporates multiple assumptions. The present results are the first direct evidence of nociceptive input to the human parasylvian cortex.

Magnetic resonance imaging in the diagnosis of idiopathic giant-cell granulomatous hypophysitis: a rare cause of hyperprolactinaemia.

Idiopathic giant cell granulomatous hypophysitis is a rare disorder of pituitary gland characterised by a chronic inflammatory process. It can also be an extremely rare cause of hyperprolactinaemia. In this paper, we present our experience with two cases of idiopathic giant cell granulomatous hypophysitis manifested by hyperprolactinaemia, and their neuroradiological evaluation including preoperative MRI studies in one of them, and discuss our findings in the light of the literature.

Thalamic neuronal activity correlated with essential tremor.

Animal studies suggest that an olivocerebello-bulbospinal pathway mediates harmaline induced tremor, which resembles essential tremor in humans. However, recent evidence suggests that thalamocortical pathways participate in essential tremor. Thalamic single neuron activity has been analysed during thalamotomy for essential tremor. It has been shown by spectral cross correlation analysis that thalamic activity has a significant, linear relation to forearm EMG activity during tremor. The presence of this tremor related activity at the site where a lesion abolishes essential tremor suggests that the thalamus has an important role in the mechanism of essential tremor.