Biomedical subjects
Publications and source records attributed to M Collard.
A female adult without previous medical or surgical pathology nor specific treatment developed meningoencephalitis localised to the brainstem associated with bilateral subclinical optic neuritis. Serology showed that the disease was related to primary infection with cytomegalovirus. The patient spontaneously recovered.
A simplified method of renal scintigraphy carried out with 131I-Hippuran and 99mTc-DTPA diethylenetriaminopentacetate is described in man. Results were expressed as tubular clearance (with Hippuran) and glomerular clearance (with DTPA) per kidney, and compared to PAH and inulin clearances measured in the same patients. There was a close positive correlation between clearances calculated by means of renal scintigraphy and those measured by standard procedure for studying renal function. This study showed that a simple calculation allowed to express scintigraphical findings in terms of clearance.
From a series of 117 neurological patients presenting a pathological periventricular white matter signal on NMR, the authors discuss the differential diagnosis possibilities based on the configuration of the lesions, on their localization in the brain, and on the calculated apparent T2 (T2**) values achieved with the single multi-echos technique.
The distribution of HLA antigens A, B, C and DR was studied in 69 native Alsatian multiple sclerosis (MS) patients. Antigen DR2 was high in MS compared to healthy control subjects, as is known. Given antigens were more frequently, and, above all, more closely linked with certain clinical and organic parameters. Antigens A3, B7 and B40 were preferentially associated with progressive forms, and A32 with remitting forms. B7 may be predictive of the prognosis, as it was correlated with disease severity. B7 and DR2 were more frequent in MS patients presenting intrathecal immunoglobulin synthesis. Sex appeared to be a fundamental factor in the clinical expression of MS, interacting closely with the HLA system. These findings confirm the multi-factor etiology of MS. Several MS susceptibility genes may exist near the HLA complex, and their expression may modulate the clinical and organic signs of MS. Studies of this sort should be carried out on ethnically and geographically homogeneous populations.
Single or multiple parenchymatous anomalies were detected in 48 of 49 patients with multiple sclerosis by proton magnetic resonance imaging (MRI) combined with a spin-echo sequence in the 4 planes of the section passing through the ventricular bodies. Lesions were identified in the frontal, orbital and particularly juxta-ventricular white substance, and were of variable appearance, the most common being spots in the parenchyma and juxta-ventricular bands. A limited number of sections is sufficient for the MRI study of anomalies in clinically defined multiple sclerosis, the diagnostic value of this examination suggested by these findings requiring confirmation by prospective studies.
The behavior of 64 normal subjects was studied after they had been submitted to excentric lateral ocular fixation of gaze of more than 40 degrees for periods of one the three minutes. A significant proportion developed vertigo, slow segmental deviations and nystagmus. Nystagmus appearing during gaze fixation (physiological nystagmus of extreme lateral gaze) was distinguished from nystagmus in the opposite direction which appeared after cessation of fixation and was named "post-fixation nystagmus". The possible role of proprioceptive receptors in the extra-ocular muscles is discussed and a hypothesis proposed of an oculo-oculogyric reflex possibly through the vestibular nuclei and influencing the control mechanisms of posture and balance.
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A 36 year old psychotic man receiving treatment with slow-release pipotiazine and trihexyphenidyl developed nine days after addition of droperidol signs suggestive of a malignant neuroleptic syndrome: altered general condition, diffuse hypertonia, akinesia, fever and vomiting. Results of biologic tests and a muscle biopsy were suggestive of a severe rhabdomyolysis. Cessation of neuroleptic therapy and the administrative of nifedipine brought a gradual return return to normal conditions, and progressively increasing doses of neuroleptic could be given without complications 12 days later. Onset of hyperthermia during neuroleptic treatment raises two questions: 1) is the etiology related to a malignant neuroleptic syndrome or acute catatonia, or a heat stroke? 2) to what extent are neuroleptics responsible for these disorders?
A 27-year-old Algerian patient presented a slowly progressive disease clinically characterized by a cerebellar syndrome, absence of deep reflexes, bilateral sign of Babinski, deep sensory disturbances, ophthalmologic disorders and pes cavus. The diagnosis of ceroid lipofuscinosis resulted from the presence of lipofuscin deposits evidenced as autofluorescent bodies, and a particular type of curvilinear, crystalloid ultrastructural inclusion bodies in muscle, lymphocytes and liver. Biochemical tests showed reduction in levels of linoleic and arachidonic acids, and of superoxide dismutase activity in lymphocytes. These findings suggest that the biochemical anomalies result from disturbances in polyunsaturated fatty acids metabolism. These results can be related to pathogenetic hypotheses for ceroid lipofuscinosis suggesting a predominant role for peroxidation of fatty acids.
Stuporous states induced by sodium valproate (VPA) are accompanied by an isolated marked hyperammonemia. In reality, hyperammonemia occurs after administration of VPA even in the absence of neurological complications. The hyperammonemia is of purely renal origin and results from modifications in glutamine metabolism, this compound being the main precursor of amino acid neurotransmitters. Combined administration of VPA and phenobarbitone increases the level of hyperammonemia due to lack of detoxification by the liver of the excess of ammonia produced by the kidneys. The anatomical site of origin of the ammoniogenesis, and its intensity, were studied in two patients with a history of stuporous states during combined VPA-phenobarbitone treatment. A single injection of VPA at a later date when they were being treated by combined phenobarbitone-carbamazepine therapy, induced disturbances in ammonia metabolism which did not differ qualitatively from those observed when intolerance to VPA is lacking. It is therefore not possible to rely on simple biological tests to detect patients at risk. Correlation is also lacking between the degree of hyperammonemia and disorders of vigilance. Ammonia does not therefore appear to be the only factor responsible for neurological complications and the role of other factors must be investigated. These include: disturbances of metabolism of inhibitory and excitatory aminoacid neurotransmitters, the condition of the cerebral parenchyma, and the excitatory effect of sodium valproate which could act to varying degrees in synergy with the hyperammonemia to provoke a stuporous state.
The effects of prolonged tobramycin administration (given in repeated injections over a 15-day period) on auditory and vestibular functions were studied in normal subjects, in patients with renal impairment, and in chronic nephritic patients undergoing hemodialysis. With the doses used in this study, the repeated administration of tobramycin resulted in blood accumulation only in the group of patients with renal impairment. In one single case, administration of tobramycin was followed by a transient aggravation of a pre-existing renal impairment. Cochlear and vestibular functions were evaluated before treatment and repeated during and after drug administration. In normal subjects, a dosage of 50 mg/8 h failed to produce cochlear and vestibular dysfunction; but with dosages of 75 mg/8 h and 100 mg/8 h, changes in vestibular reflectivity occurred frequently, mostly of the irritative type. Generally moderate, but quite often slight changes persisted (5 of 10 cases). They were not accompanied by auditory or vestibular clinical signs. In patients with impaired renal function and in those undergoing chronic hemodialysis, vestibular impairment is customary and most often of the deficiency type. Half of the cases still showed detectable changes on follow-up evaluation that was performed 10 days after discontinuation of the drug.
A similar affection has developed in eight members from four generations of a family living in the Alsace. The disease is characterized by the onset of a pyramidal, pseudobulbar syndrome and dementia during the third or fourth decade of life. The outcome is fatal after a mean period of three years. Cerebral biopsies in three cases have demonstrated multicentric amyloid plaques differing from senile plaques. Clinical and pathological findings are similar to those currently reported in the literature as being typical of Gerstmann-Sträussler-Scheinker's syndrome. The affection appears as a separate entity: the multicentric plaques, clinical symptomatology, pyramidal or pseudobulbar, cerebellar syndromes, usually preceding dementia, age of onset, course, and familial character or the disorder distinguish it among presenile dementias. Its clinical profile and course are very similar to that of familial cases of Alzheimer's disease, some of which are probably cases of Gerstmann-Strässler-Scheinker's syndrome. Transmission to animals, though inconstant, places it within the group of transmissible dementias among kuru, Creutzfeldt-Jakob's, and familial forms of Alzheimer's disease. The familial nature of the affection and the variability of clinical and pathological features in the same family illustrate the complex relationships between hosts and pathogenic agents in the clinicopathological expression of a disease.
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In 11 patients with complex partial epileptic seizures stuporous states were observed during treatment with valproate (VPA) (2 cases), with VPA and phenobarbitone (PB) (4 cases), or with VPA, PB and a third anti-epileptic drug (5 cases). Based on 3 characteristic cases, an attempt is made to define the role of VPA, the nature of the stuporous states, and the origin of digestive disorders which often herald the onset of behavioural disorders. Several clinical studies have suggested the direct responsibility of VPA even if the adverse effects are potentiated by many other anti-epileptic drugs. Stuporous states are not due to VPA overdose and do not depend on the mode of administration. No correlation has been found between electroclinical signs and plasma or CSF levels of the different anti-epileptic drugs. Reported data and the present cases suggest a paradoxical epileptogenic role for VPA on complex partial seizures: there exists a close similarity of electroclinical findings between spontaneous epileptic seizures and stuporous states during DPA treatment. Digestive disorders appear to result from a central mechanism and not from digestive tract intolerance. In some cases, it is likely that partial seizures with digestive symptoms and signs do occur.
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This study was undertaken following a first paper describing cerebral clinicopathological correlations in aphasiology using computerized axial tomography. Its originality lies in the fact that we studied the correlations starting from the lesional sites and deducing the aphasiologic diagnosis. Our conclusions are similar but show that a small proportion of the patients do not follow the usual pattern of correlations. In view of future prospective studies, the authors emphasize the importance of information to analyze and compare well-individualized clinical syndromes. We suggest that such clinicopathological correlations could be used in other fields of neuropsychology.
A review of the literature shows the extreme frequency of nystagmus and changes in vestibular reflexes in disseminated sclerosis. During the course of this disease, it is possible to detect nystagmus in at least two-thirds of cases and in a similar proportion there are changes in vestibular reflexes, usually a hyperreflexia, especially in the early phases of disseminated sclerosis. Subjectively the patients rarely complain of vertigo and such symptoms are in any case part of the early form of the disease. On the other hand, disorders of balance are much more frequent but the factors involved are numerous, and the role of the vestibular system is often debatable. Electronystagmography and oculography demonstrate the extreme frequency of spontaneous or fixed gaze nystagmus in this disease, as well as the extreme frequency of changes in conjugated eye movements; changes in reflex, voluntary and automatic conjugated eye movements. As a matter of fact, there are many kinds of nystagmus which are not related to any changes in the vestibular system, but which are rather more part of the overal changes of conjugated eye movements. Seen in this light, electronystagmography and oculography, by exploring the different kinds of conjugated eye movement, can help decisively in the diagnosis of disseminated sclerosis by revealing changes which reflect damage to the brain stem, lesions which are clinically very often silent. In this way the diagnosis of disseminated sclerosis may be confirmed. Furthermore, electronystagmography can easily suggest another diagnosis, other than the early form of disseminated sclerosis of the vestibular type.
Oculographic examinations were conducted in 24 cases of Arnold-Chiari malformation. Disorders in vertical eye movements with a spontaneous vertical nystagmus were frequently observed, together with disturbances in visual tracking. There was no case of paralysis of lateral eye movements, but an adduction internuclear ophthalmoplegia might be present. Though these anomalies are not specific, they differ for example from those usually observed in multiple sclerosis, which is often a differential diagnosis in such cases. Oculography therefore may be of particular value.