The authors describe percutaneous radiofrequency (rf) thermocoagulation of the sphenopalatine ganglion used to treat seven patients with sphenopalatine ganglion neuralgia. The procedure was effective in relieving pain, without significant side-effects. All the patients have actually been free of pain during a follow-up of 6-28 months. The surgical technique and the rationale for its use are pointed out.
To test the hypothesis of opiate-like peptide release after transcutaneous electrotherapy we measured beta-endorphin cerebrospinal fluid (CSF) content in 13 patients without pain problems. The results indicate a time dependent increase of CSF beta-endorphin in the group of patients studied. This fact suggests that the analgesic properties of the treatment may be ascribed to an involvement of the endogenous opiates system, independently from the basal clinical conditions of the patients.
The effect of trigeminal electrical stimulation on cerebral blood flow has been studied in conditions of normal or reduced cerebral blood flow (CBF). Autologous blood was injected into the subarachnoid space of ten Pittmann-Moore pigs to induce subarachnoid haemorrhage (SAH) accompanied by cerebral blood flow (CBF) reduction. One week later, in six of ten animals, a considerable decrease of CBF was noted as evaluated by means of a recording-system monitoring over the right parieto-temporal calvarium the washout of 133Xenon injected into the internal carotid artery after the external carotid had been clamped. Continuous electrical stimulation of the Gasserian ganglion performed in the six animals with severely induced CBF reduction produced a remarkable cerebrovascular dilation and increase of CBF lasting over 3 h. Electrical stimulation of the Gasserian ganglion produced a similar pattern of vasodilation in six pigs in which no blood was injected and no reduction of CBF was evident. The mechanisms and the anatomical pathways which underlie these results are discussed.
One hundred and forty consecutive subarachnoid haemorrhages (SAH) which presented either an intracranial vascular malformation (102 cases: aneurysm 80 cases, AVH 22 cases) or remained of "unknown aetiology" (38 cases) were studied. SAH caused by other factors (neoplasms, thrombo-embolisms, systemic diseases etc.) were excluded. The 38 cases with bleeding of "unknown aetiology" have been studied by complete cerebral angiography, pneumoencephalogram or CT scan, and have been followed for two years. The most important clinical factors in the three groups have been compared by a statistical method to verify the hypothesis that SAH of "unknown aetiology" is caused by vascular micromalformations which are angiographically not evident either because of their small size or because of their "spontaneous" recovery after bleeding due to thrombosis and disappearance of the malformation. From the data collected it may be concluded that SAH of "unknown aetiology" is a benign lesion, typically occurring in middle age, but with no clear characteristics that enable identification of the anatomical substratum from it originates.
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