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Non ketotic hyperglycemia is a metabolic disorder which can induce various hyperkinetic disorders. We report the case of a 74-year old woman admitted to hospital because of choreo-ballic movements of her left hemibody. Laboratory tests revealed non-ketotic hyperglycemia. CT scan showed an increased density in the right putamen and head of caudate. Magnetic resonance imaging disclosed a hyperintense signal involving the right putamen on T1-weighted images. On T2-weighted images, there was a slight hyperintensity in the right putamen and head of caudate. Correction of the underlying hyperglycemia led to complete resolution of abnormal movements. Pathophysiology of this clinicoradiologic syndrome is briefly discussed.

We report a biopsy proven case of cerebral giant cell angiitis associated with cerebral amyloid angiopathy. Clinical history and radiological lesions were rapidly progressive. The patient recovered with corticosteroid treatment. The pathogenesis relationship between angiitis and amyloid angiopathy are discussed.

Due to the motor evoked potentials recorded in limb muscles after transcranial and spinal magnetic stimulation, conduction in the central motor pathways can now be evaluated safely and painlessly in man. The central motor conduction time obtained includes the time required for transmission, along the fast pyramidal fibres, from the cortex to the spinal motoneurons, the synaptic transmission to motoneurons and the conduction on a short segment of the motor nerve root. Lengthening of this time almost always reflects dysfunction of the central motor pathways. The abnormalities observed are not specific of any particular cause, and they must be interpreted in relation to the context. The usefulness of this new electrophysiological technique is being tested by radiological and anatomico-clinical correlations in various diseases of the central nervous system (e.g. disseminated sclerosis, cerebral infarction, spinal cord injury) and the locomotor apparatus (e.g. cervical myelopathy, radiculopathy).

We examined a 29-year-old woman who had language disturbances and memory impairment after a left thalamic infarction. MRI showed injury that was limited to the tuberothalamic artery territory. Beside reduced voice volume and verbal memory trouble, she presented with aspontaneity, loss of psychic self-activation and affective drive. Considering thalamic lesions, this loss of psychic self-activation or 'athymhormie' was found in a left thalamic infarct and could not be considered as an exclusive characteristic of bithalamic infarctions. The disappearance of the neurobehavioral disturbances within 15 days after the onset of the troubles was associated with the decreasing of the mass lesion found by MRI.

Concentrations of beta-endorphin in the cerebrospinal fluid were measured in 21 painless subjects and 37 patients with chronic pain. Statistical analysis of the results showed no significant difference between the two groups. This lack of correlation between beta-endorphin concentrations in the CSF and the presence of chronic pain highlights the difficulties and limitations encountered when trying to determine the role of endogenous opioid systems with this method.

A case of Joseph's disease characterized by spasticity in all 4 limbs, dystonia and disorders of ocular motility was considerably improved by cotrimoxazole, which confirms a recently published case. Further studies are required to establish this therapeutic effectiveness.

A multicentre controlled trial was conducted on 383 patients to compare the effectiveness of flurbiprofen (100 mg/day) and an ergot derivative in preventing cerebral infarction. The end-point of the trial was recurrence within 3 years of treatment with one or the other drug of a fatal or non-fatal cerebral infarction. Only those patients who had already experienced an established and disabling ischaemic accident in the carotid or vertebro-basilar territory were included; 88% of these entered the trial less than 6 weeks after the accident. Sixty-one patients had recurrent cerebral infarction during the 3-year observation period: 22 in the flurbiprofen group and 39 in the ergot derivative group (p less than 0.02 log rank test adjusted by centre). The actuarial recurrence rates in the two groups were 13% and 21% respectively. These results concur with those of other trials involving aspirin to demonstrate the value of antiplatelet aggregation drugs in the secondary prevention of atherothrombotic cerebral infarction.

In a double-blind survey carried out versus a placebo, the action of isaxonine was examined with 42 patients suffering from peripheral facial paralysis, most often a frigore. The statistical analysis of the clinical and electrophysiological results shows a significantly higher improvement for the isaxonine group, both in quality and speed of recovery of the nervus facialis functions. Clinical and biological tolerance posed no particular problem.

Recognition of the neurological symptoms and signs of the acquired immunodeficiency syndrome (AIDS) since 1982 has demonstrated the involvement of the nervous system in approximately one third of the cases. Certain opportunistic infections or tumors had been previously described in the course of immunodeficiency states of other origins: cerebral toxoplasmosis, cryptococcosis, progressive multifocal leukoencephalopathy, atypical mycobacteriosis and cerebral lymphoma. Other disorders such as subacute encephalitis raise specific etiopathogenic questions. Several of these affections can be associated or succeed each other and this is the natural course in AIDS. The detection of those conditions that are curable, among which toxoplasmosis, is of primary importance.

Both thresholds of nociceptive flexion reflex and pain sensation were studied in 6 normal subjects and in 6 patients with typical thalamic pain. In these patients, on the painful side, these thresholds were found increased (98 p. 100; 89 p. 100 respectively) compared to the normal side. Values obtained in this latter did not significantly differ from those observed in normal subjects. After 8 days of indalpine treatment, the nociceptive reflex threshold was furthered increased in the painful side while the pain threshold was not modified by this drug. In the normal side, changes observed after indalpine were similar to that obtained in normal subjects. All the indalpine-induced modifications were reversed by naloxone in both patients and normals. These results are discussed in the context of the possible mechanisms of thalamic hyperpathia.

A comparative electromyographic study was carried out in normal subjects (group I) and in alcoholics without clinical evidence of polyneuropathy (group II). -The H reflex of the extensor digitorum brevis muscle (E.D.B.), the electromyogram of EDB, the conduction velocity of the fasted motor fibers of the peroneal nerve (PN), the sensory conduction velocity and amplitude of the evoked potential of the cutaneous fibers of PN, the H reflex of the soleus muscle. -Two kinds of changes were observed in group II: --a significant increase in the latent period of H respones in EDB, in particular the latent period of responses provoked by distal stimulation of PN (+25 PER CENT); --A SIGNIFICANT DECREASE IN THE AMPLITUDe of the sensory potential of the PN(--46 per cent). The other parameters studied in group II did not show any significant difference in comparison with the control group. These results indicate that PN is involved early in a complex fashion in latent alcoholic neuropathies. They confirm that the distinction between axonal neuropathy and segmental demyelination is rarely absolute.

The effects of a repetitive stress (expectation of severe pain) on the threshold of a nociceptive flexion reflex of the lower limb (Rlll, Bi) were investigated in normal subjects. A progressive and significant rise of the Rlll, Bi Threshold was observed as the stress was repeated several times over a 60 to 90 minutes' period. This effect was entirely reversed by naloxone, with fall of the threshold below initial values. In a double-blind test, the injection of a placebo had no significant effect on the reflex threshold when compared with control values. These results are in agreement with those reported in animals. They provide experimental evidence for an involvement of endogenous opiate systems in the mechanism of stress in normal subjects.

The various evaluation scales available to study the clinical courses of Alzheimer-like dementias are controverted, and the practical aspects of a controlled trial are being considered. A tentative protocol has been designed, in which multiple individual assessments are combined with several validated scales and tests. This protocol would lend itself to a multicentre study, as it only includes evaluation tools that are easy to handle and do not require too much time. It should make it possible to select a relatively homogeneous group of patients and provide an opportunity to quantify the course of Alzheimer's disease over one year. In the discussion, emphasis is laid upon the foreseeable difficulty to evaluate a therapeutic benefit in our present imperfect knowledge of the natural history and prognostic factors of the disease.

The cumulative effects of a repetitive stress induced by anticipation of pain (noxious foot shock) were studied on the threshold of a nociceptive flexion reflex of the lower limb. The threshold of the nociceptive reflex progressively increased with the repetition of the stress. This effect was reversed by naloxone, which even produced hyperalgesia, since a rapid and significant decrease in this threshold, below the initial values, was noted. Tha data provide evidence for involvement of endogenous opioids in the phenomenon of stress-induced analgesia in normal man.

Electrophysiological studies of the nociceptive reflex (R3) were carried out in eight normal subjects, and one patient with congenital insensitivity to pain, in order to compare the effects of naloxone and a placebo. No significant variation in the reflex threshold was seen in the normal subjects. Two electrophysiological abnormalities were observed in the patient: a 350 per cent spontaneous elevation in the R3 threshold compared to the control group; a rapid and large drop (67 per cent) in the threshold lasting for about ten minutes after the injection of Naloxone. These results suggest that in this particular case the insensitivity to pain could be related to the permanent hyperactivity of a morphine-like inhibitory system.

Electrophysiological studies of the cutaneous reflexes during avoidance reaction of the arms demonstrate more particularly the presence of facilitation of late reflex responses and stimultaneous activation of flexor and extensor muscles. The avoidance reaction is not the inverse electrophysiological image of pathological prehension, as it produces, at least in one of its aspects, a much more fundamental modification of the segmental reflex systems of muscle contraction regulation. This motor disorganization is rarely observed, and could result from a disequilibrium between proprioceptive sensitivity and skin sensitivity: the loss of proprioceptive control would facilitate contact reactions.

Spontaneously elevated nociceptive threshold levels were markedly diminished after Naloxone injections in 4 patients with congenital insensitivity to pain. This finding suggested the hypothesis of a relation between congenital insensitivity to pain and permanent hyperfunction of an endomorphinic system. Radio-immunoassay of CSF beta-endorphin was performed in all 4 cases. The normal or only slightly elevated levels cannot explain electrophysiologic findings, but as a function of the multiplicity of endogenous opioid systems, hyperactivity of another endomorphinic system cannot be excluded. Other hypotheses may also be proposed.

A review of experimental studies concerning acupuncture gives a current indication as to the neurophysiological mechanisms of its hypoalgesic effects. In man, these effects are demonstrated by study of the nociceptive flexion reflex. Other methods for the study of pain threshold have revealed a hypoalgesic action in man and in the animal. The authors analyse the pathways and structures necessary to analgesia: peripheral afferent pathway, ascending pathways, suprasegmental controls. The inhibitory mechanisms activated by acupuncture appear to be identical to those involved in analgesia by morphine and by central stimulation.