[Chronic alcohol-tobacco poisoning: towards an early detection of optic neuropathy]. / Intoxication alcoolo-tabagique chronique: vers un dépistage précoce de la neuropathie optique.

Forty-two patients (33 men, 9 women) with normal visual acuity admitted to an alcoholism rehabilitation programme were evaluated for colour vision using the automatized Fransworth-Munsell test (ChromopsR) and for central visual field using Friedmann's analyser. An early colour blindness without axis, i.e. a lack of colour discrimination, was often found. At the same time, in the more intoxications perimetric defects appeared in the 30 degrees area first centrally, then followed by arcuate superior scotomas.

Axonal regeneration is compromised in NFH-LacZ transgenic mice but not in NFH-GFP mice.

To investigate neurofilament (NF) dynamics during the cytoskeleton reorganization in regenerating axons, and their electrophysiological and histological consequences, we used two transgenic lines of mice: neurofilament high (NFH)-LacZ and NFH-green fluorescent protein (GFP). In NFH-LacZ mice, NFs are retained in cell bodies and deficient in axons (Eyer and Peterson, 1994), while in NFH-GFP mice the fluorescent fusion protein is normally transported along axons (Letournel et al., 2006). Following a crush of the sciatic nerve, conduction recovery in NFH-GFP mice is similar to wild-type (wt) mice, but it is reduced in NFH-LacZ mice. Moreover, changes of axonal calibres following regeneration are similar between NFH-GFP and wt mice, but they are systematically reduced in NFH-LacZ mice. Finally, the axonal transport of NFH-GFP fusion protein and NFs is re-initiated after the crush as evidenced by the fluorescent and immunolabelling of axons distal from the crushed point, but NFs and the fusion protein are not transported along axons during regeneration in NFH-LacZ mice. Together, these results argue that the absence of axonal NFs in NFH-LacZ mice compromises the axonal regeneration, and that the NFH-GFP reporter fusion protein represents an efficient model to evaluate the NF dynamics during axonal regeneration.

[Spinal cord potentials evoked by stimulation of cutaneous afferents in the cat spine (evidence of an N3 wave)]. / Potentiels de moelle dorsale évoqués par stimulation des afférences cutanées chez le chat spinal (évidence d'une onde N3Y.

Negative intermediary cord potentials evoked by low threshold cutaneous afferents were recorded from the surface of the lumbosacral spinal cord. In addition to the N1, N2 waves classically described, it is possible to distinguish a third one names here N3 wave. The characteristics and longitudinal distribution of this wave are different from those of N1 or N2.

Neural generator of P14 far-field somatosensory evoked potential studied in a patient with a pontine lesion.

Somatosensory evoked potentials (SEPs) to electrical stimulation of the right and the left median nerves were studied in a patient with a pontine lesion. At first there was mainly right medial lemniscus involvement. Four months later the left medial lemniscus was found to be also involved. SEPs to stimulation of the right median nerve had normal wave forms and latencies while N20 was lacking and P14 was abnormal after stimulation of the left median nerve in the first SEP record. N20 and P14 were absent with preservation of P9 and P11 after stimulation of both left and right median nerves in the second SEP record. Therefore the P14 component has been found abnormal, then absent, in a patient with a pontine lesion.

[Dorsal root potentials evoked by stimulation of cutaneous afferents in the spinal cat (study of the N3 wave)]. / Potentiels de moelle dorsale évoqués par stimulation des afférences cutanées chez le chat spinal (etude d'une onde N3).

The comparative study, when stimulation is increased, of the amplitude changes shown by the negative waves of dorsal root potentials, indicates that the N1 and N2 waves are evoked by A alpha cutaneous afferent, whereas N3 wave is due to A alpha, A beta and perhaps A delta cutaneous afferents. On the other hand, a possible inhibitory action of N1, N2 negative complex on N3 wave is postulated.

Central sympathetic dysregulation and immunological abnormalities in a case of progressive facial hemiatrophy (Parry-Romberg disease).

A case of hemifacial atrophy (Parry-Romberg disease) is discussed. Electrophysiological and immunological studies were performed. Electromyography, blink reflex and trigeminal evoked potential abnormalities indicate that the brain stem may be implicated in the aetiology of the disease. Immunological evidence favoured this possibility and demonstrated possible involvement of the noradrenergic system. Hyperactivity of the brain stem sympathetic centres, possibly caused by an autoimmune process, may be the primary cause of the cutaneous and subcutaneous atrophy in Parry-Romberg disease.