[11 cases of neuropathy induced by almitrine, of which one had optic neuropathy]. / Onze cas de neuropathie à l'almitrine, dont un avec neuropathie optique.

The only etiologic factor retained in 11 patients with sensory or sensory-motor neuropathy was almitrine therapy. In one patient there was in addition an optic neuropathy. The reduction in visual acuity in this patient coincided with the onset of the sensory-motor neuropathy of lower limbs after treatment with 100 mg/day of almitrine over a 2-year period. No other metabolic, inflammatory, toxic, vascular or immunologic cause was found. There was a moderate chronic respiratory insufficiency. Visual recuperation started one month after the arrest of almitrine treatment and was satisfactory 7 months later. The other 10 patients had neuropathy of limbs without visual disorders. Neuromuscular biopsy in one case showed lesions to be of the axonal type.

[Guillain-Barré syndrome with favorable outcome in a case of recent human immunodeficiency virus infection]. / Syndrome de Guillain et Barré d'evolution favorable dans un cas d'infection récente par le virus de l'immunodéficience humaine.

An acute polyradiculoneuropathy occurred in a 30 years homosexual male. E.L.I.S.A. test and Western Blot showed recent infection by H.I.V. Besides, endogenous reinfestation by cytomegalovirus was found: high concentrations of specific IgG antibodies and presence of the virus in the blood. T4 helper cells were severely reduced, without any other sign of cellular immunity failure. None of the two viruses was found in the nervous biopsy. This Guillain-Barre syndrome with a subsequent cellular reaction in the CSF, is probably to be related to an immunoallergic mechanism. Brief increase of antibodies specific for HBsAg and Borrelia Burgdorferri and the beneficial effect of plasmapheresis, supported this view. Two months later, the patient showed superficial lymph nodes hyperplasia, without any other symptom of pre-Acquired Immuno-Depression Syndrome.

[Immunohistochemical study of the basic lesions of Alzheimer's disease]. / Etude immunohistochimique des lésions élémentaires de la maladie d'Alzheimer.

Alzheimer's disease is characterized by the presence of two argentophilic histopathologic brain lesions: neurofibrillary tangles (NFT) and senile (neuritic) plaques (SP). NFT consist of large perikaryal masses of abnormal cytoplasmic fibers, most of which have the ultrastructural appearance of pairs of intermediate-sized (10 nm) filaments wound into a double helix and named Paired Helical Filaments (PHF). PHF also occur within the degenerating neurites of SP. The insolubility of PHF in strong detergents is turned to account for their isolation. We have isolated these structures from an Alzheimer brain and raised antibodies against PHF. The anti-PHF antibodies detected specifically NFT and SP on nervous tissue sections of Alzheimer brains, and also NFT in the hippocampus of normal aged brains. The stainings of NFT and SP by the anti-PHF or the classical Bodian silver staining technique were compared. The immunohistochemical method is more precise, more reproducible, more specific and will be of great interest for the quantification of these structures, specially when they are in minor quantities particularly in the atypical disease. Furthermore, the anti-PHF antibodies did not visualize neurofilament containing structures, and did not react with neurofilament protein subunits on immunoblots. These results are compared to those reported in the literature.

Observation of morphological relationships between angiopathic blood vessels and degenerative neurites in Alzheimer's disease.

Two main techniques are used to stain the three types of brain lesions characteristic of Alzheimer's disease: Neurofibrillary tangles (NFT), senile plaques (SP) and congophilic angiopathy. Thioflavine-S is an histochemical marker of the amyloid substance located essentially in the central core of senile plaques and in the walls of the pathological blood vessels. Specific antibodies against Paired Helical Filaments (PHF), the ultrastructural elements of NFT, reveal neuron cell bodies with NFT and numerous dystrophic neurites, mostly around neuritic plaques. Using simultaneous histochemical and immunohistochemical labellings on the same tissue sections of Alzheimer cortex (association cortex and hippocampus), the different lesions were stained with great sensitivity and specificity. Moreover, an unusual morphological relationship between two types of lesions was detected in two Alzheimer brains with prominent congophilic angiopathy: we observed a well marked concentration of dystrophic neurites, immunolabelled with anti-PHF, around blood vessels with Thioflavine-S stained amyloid angiopathy. These lesions were distributed like a sleeve around 1/10 of dyshoric or congophilic blood vessels. The significance of such lesions is unknown but they probably represent a step of the pathogenesis of Alzheimer brain lesions and may explain the general mechanism of lesion formation in Alzheimer's disease.

Anti-PHF antibodies: an immunohistochemical marker of the lesions of the Alzheimer's disease. Characterization and comparison with Bodian's silver impregnation.

An immune serum raised against paired helical filaments (PHF) was able to stain senils plaques (SP) and neurofibrillary tangles (NFT) specifically, the two characteristic lesions of the dementia of Alzheimer-type. This polyclonal antibody against PHF was characterized by immunochemistry and also compared with the classical Bodian silver staining. NFT and SP were observed where they were expected: in the fronto-temporal neo-cortex and hippocampus of Alzheimer-type patients, and also in hippocampus of non-demented elderly subjects. The pattern of SP visualized by the two methods was identical whereas NFT were not detected specifically by silver salts, specially in the nervous tissue where NFT were in discrete quantities. Since the preparation of the antigen is very easy and the resulting antibodies are specific, we conclude that this technique will be of considerable interest for routine neuropathological diagnosis. Finally, the properties of our anti-PHF antibody are compared with those reported in the literature. This antibody will probably be a good tool for the identification of the chemical nature of PHF components.