Nervus intermedius neuralgia (Hunt).
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Biomedical subjects
Publications and source records attributed to G W Bruyn.
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To define more closely the clinical relationship between migraine and intracranial arteriovenous malformation (iAVM), the clinical features of 57 reported instances and of 7 personal cases were analysed. Migraine attacks symptomatic of AVM include: late onset, frequent absence of (familial) migraine history, diminution or even inversion of the usual sex-ratio in migraine, brevity of attacks, disruption of the usual sequence of attack symptoms and, finally, unusual or permanent neurologic deficit. An attempt has also been made to clarify the epidemiological relationship. The reported frequency of migraine in cases of AVM, and AVM in cases of migraine is reflected against an inquiry into the number of annually diagnosed cases of AVM in 20 Dutch neurological/neurosurgical centres, covering 12.10(6) inhabitants in 8 of the 11 provinces. The annual incidence of migraine is estimated at 1:3,500 population, that of diagnosed iAVM is 120, i.e. 1:100,000. Coincidental occurrence of the two conditions works out at 1:4 X 10(8) per year. The presented case series of 7 seen in 2 of the 20 centres strongly militates against such a chance hypothesis.
An analysis is presented of 35 cases of chorea as a symptom of polycythaemia. This analysis reveals: (a) whereas polycythaemia occurs predominantly in males (3:2), polycythaemic chorea (PC) occurs predominantly in females (5:2), at a real ratio of female:male = 4:1, the prevalence being 1-2.5% of polycythaemic patients; (b) PC manifests predominantly after the age of 50 (8 cases before, 27 after 50 years), making polycythaemia the first disorder to be considered in cases of so-called 'senile' chorea; (c) PC is generalised, with predominant involvement of faciolingual and brachial muscles, and associated with muscular hypotonia; (d) PC may last from periods of weeks to years, usually responds to haloperidol, venesection or 32P-treatment, but may persist, or recur with treatment, or remit spontaneously, and (e) no relationship exists between the choreatic syndrome and (the rare finding of) a small infarct in the caudate nucleus. The cause of the choreatic syndrome in polycythaemia is presumably to be explained as a neostriatal hyperviscosity syndrome producing venous stasis, reduced brain blood flow and impaired tissular O2/glucose metabolism. The state of dopaminergic hyperactivity is presumably enhanced by relatively increased neostriatal catecholestrogens. The hypothesis of polycythaemic excess of dopamine-laden platelets releasing excess of dopamine in the neostriatum needs to be confirmed by laboratory evidence of platelet counts.
A critical analysis of 52 cases of systemic lupus erythematosus (SLE) and chorea is presented. Choreatic movements occurred early in the course of the disease in most cases; the duration varied from several days to 3 years. No sex predominance was found and no relationship could be demonstrated between chorea and other neurological signs, or between chorea and other SLE manifestations. Also, the neuropathological findings offered no simple explanation for the emergence of chorea. Immunological pathomechanisms might be present.
A critical analysis of cases of systemic lupus erythematosus (SLE) and chorea is presented. Choreatic movements occurred early in the course of the disease in most cases; the duration varied from several days to 3 years. No sex predominance was found and no relationship could be demonstrated between chorea and other neurological signs, or between chorea and other SLE manifestations. Also, the neuropathological findings offered no simple explanation for the emergence of chorea. Immunological pathomechanisms might be present.
A review is presented of the clinical features of glossopharyngeal neuralgia, as analysed from 304 reported instances. The sex-ratio of the condition is equal, the peak-age at onset is between 40 and 60 yrs, and left-side involvement predominates in females. The clinical features are detailed in 18 specific items. In a review of the aetiology it is argued that the so-called "idiopathic" type of IXth nerve neuralgia (which, upon careful analysis, may still rest upon either an obscure tumor or infection or elongated styloid process) should be primarily attributed to vascular elongation and looping ("Jannetta mechanism"). The cardiovascular type of the neuralgia, with bradycardia, or asystole and convulsions or coma, receives special emphasis. The differential diagnosis, particularly in view of the not-infrequently occurring combination with trigeminal neuralgia, is set out briefly.
This disorder has failed to achieve the status of general recognition among the cephalic neuralgias. Whether its orphanage derives from narrow-minded expulsion from the neurological domain of cephalic neuralgias to the ENT-field, or can be attributed to its rarity (though this did not keep glossopharyngeal neuralgia from rightfully assuming its place among equals), or to the hazy outlines of the disorder, remains a question more readily posed than answered. Yet, if it shares with Sluder's sphenopalatine neuralgia an uncertain clinical identity, there are a sufficient number of observable clinical data from which to conclude the reality of this neuralgia. A review of pertinent reports should enable the reader to make up his own mind.
For 1100 patients with Huntington's Chorea in 102 families from The Netherlands the average age at death per family is presented. This average ranges from 72 to 38 years. An analysis of variance of the data is strongly indicative of genetic heterogeneity. For the patients with the relatively high age at death little or no difference is observed from the age at death of their non-affected parents and non-affected sibs. Eleven children who presented with the juvenile form of the disease had all inherited the abnormal gene from their father. These 11 children were found only in families with an average age at death below 57 years. Other factors that might possibly influence the variation of average age at death between families are discussed, but cannot explain the observed differences.
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The effect of Tiapride on dyskinesia was evaluated in 12 patients with tardive dyskinesia in a double-blind controlled cross-over trial. The effect was measured by a Doppler-radar device and by counting the number of involuntary movements from video-recordings. Besides these methods, subjective assessments were made on analogue scales by family, nurses and attendant doctors. The subjective evaluation appeared to be useless because of many inconsistent answers. The quantitative methods revealed a significant diminution of the involuntary movements in the Tiapride therapy period (P less than 0.01). It appears that tiapride is an effective drug in the treatment of tardive dyskinesia. No clinically important side-effects have been observed. The drug appeared not to induce parkinsonism.
Twenty-two patients with Huntington's chorea were investigated in a double-blind controlled cross-over trial. The effect was measured by counting the number of involuntary movements from video-recordings and by a Doppler-radar device. Besides these methods, subjective assessments were made on analogue scales by patients, family, nurses and attendant doctors. The quantitative methods revealed no significant diminution of the involuntary movements in the Tiapride therapy period. The subjective evaluation turned out to be useless because of many inconsistent answers.
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The Tolosa-Hunt syndrome is a superior orbital fissure and/or anterior cavernous sinus syndrome. Because the etiology is unknown, the differential diagnosis is essentially one of localization. The pathological substrate consists of a non-specific inflammation. An exhaustive literature search up to 1 January 1981 yielded altogether 214 cases. Seven personal cases are reported. A consistent pathogenesis still lacking. Observations made in four cases led to the hypothesis that the syndrome results from dysregulation of the adaptation to stressful events, involving enhanced serotonergic activity which suppresses ACTH secretion and promotes non-specific inflammation of perivascular (venous/arterial) tissue.
Several red cell membrane properties and activities of membrane-bound enzymes were investigated in blood samples of patients with Huntington's disease. (Na(+)+K(+)) ATPase activity and cell deformability appeared to be normal, in contradiction to preceding reports from other laboratories. With other techniques sensitive to relatively small changes in membrane structure, no abnormalities were found in Huntington's disease red cell membranes. These investigations do not support the concept that a generalised membrane abnormality is present in Huntington's disease.