Biomedical subjects
Publications and source records attributed to P Boulu.
A 55 year-old, right-handed, man developed a progressive writer's cramp spreading to a right hemidystonia. He had a left paramedian frontal meningioma. The association of an hemidystonia with contralateral lesions in the basal ganglia has been often reported. Its occurrence with a frontal lesion appear to be much less frequent. This association suggests a possible disorder of frontostriatal connections.
The term "idiopathic diffuse polyalgia syndrome" is suggested to designate an entity well known to neurologists, rheumatologists and all physicians interested in pain. In this syndrome pain is diffuse but often predominates in a given region. Physical examination shows excessive tenderness in well-defined areas. Radiological and laboratory examinations are negative. Psychological factors are not always obvious. Several arguments are in favour of dysfunction of the pain control mechanisms. The effectiveness of the various treatments prescribed is related to the quality of the doctor-patient relation.
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The characteristics of the late components of the somatosensory evoked potential (SEP) as a function of stimulation intensity have been studied in 10 normal volunteers following electrical stimulation of the distal cutaneous branches of the median nerve. The stimulus intensity (either single shock or train) was adapted in order to produce the following 4 types of sensation: liminal tactile (ST); frankly tactile but never painful (4 times ST); pain threshold (SD); and 1.5 time SD. A significant relationship was observed between the amplitude of the late component (N150-P220-N400), of the SEP and the stimulus intensity for a low rate of stimulation (below 0.25 Hz). In contrast this relationship is not verified for higher stimulation rates. These data are discussed with respect to their implication in pain research.
The subjective sensations and late components of the cortical somatosensory evoked potential (SEP) have been correlatively studied when elicited by stimulation parameters which were selected in order to activate selectively, either the largest afferent fibers (train of shocks of 10 mA, with a 0.05-0.2 msec duration for each shock) or the several groups of fibers (A alpha beta; A delta and C) of the cutaneous branches of the median nerve (single shock, 1 msec duration; 20 mA). In both cases, a good correlation was found between the quality and intensity of sensations and the amplitude of the late component N150-P220-N400 of the SEP. However, it was also found that this relationship was not linear and suggested that it is possible to saturate the cortical integrative system responsible for the SEP. A selective blockage of the largest fibers (compression) or of the finest ones (lidocaine) have shown that there is no specific involvement of a particular type of peripheral fiber in the genesis of the N150-P220-N400 components. Moreover, these late components could also be recorded with similar latencies when cutaneous stimulations were applied in any part of the body.
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During the last few years the list of drugs capable of inducing a iatrogenic neuropathy has been considerably lengthened. Drug toxicity to peripheral nerves may be discovered at the experimental stage, but it is usually recognized after the drug has been launched on the market, hence the importance of pharmacovigilance. The responsibility of a drug for the occurrence of neuropathy may be difficult to prove, particularly when the drug is used in the treatment of a disease which, by itself, may be responsible for a lesion of the peripheral nervous system. Iatrogenic neuropathies are usually axonal, but some drugs produce a primary disorder in the myelin-Schwann cell couple. Schwann cell diseases may be induced by drugs, such as perhexiline maleate, amiodarone or chloroquine, which inhibit lysosomal enzyme activity. In such cases inclusions representing fat-loaded lysosomes can be detected in various tissues, and particularly in Schwann cells. In certain patients, notably those treated with gold salts, an immune mechanism might be responsible for neuropathy. Most drug-induced neuropathies are due to a primary lesion of the neuron which is more often an axonopathy than a neuronopathy. It is usually a retrograde distal axonopathy the occurrence of which is attributed to a disorder of the fast retrograde axonal flow. In a few cases, the finding of a biochemical mechanism perturbing the axonal flow may help in preventing the occurrence of a iatrogenic neuropathy.
Static and dynamic equilibrium (posture and gait) is indispensable for a normal behavior in human. Its mechanisms are nearly the same in superior species and in man, but humans are the only ones to have acquired exclusively biped upright position and gait. Equilibrium is a sensory function involving 3 sub systems: visual, vestibular and sensori-motor (proprioceptive), controlled by cerebellum and cerebral structures. Information coming from those 3 sub systems must be concordant. In case of discordance, the patient is in a state of sensory conflict. This conflict can induce disequilibrium or true vertigo. After a recall on equilibrium, the authors report the results of an epidemiologic study upon 5298 patients suffering of balance disorders and treated by an alpha-blocker: nicergoline (30 mg/day during 6 months).