Dopamine neoinnervation in the substantia nigra and hyperinnervation in the interpeduncular nucleus of adult rat following neonatal cerebroventricular administration of 6-hydroxydopamine.

An aberrant network of dopamine axons was found to pervade the rat substantia nigra following neonatal destruction of its dopamine nerve cell bodies and dendrites by cerebroventricular administration of 6-hydroxydopamine. Light-microscopic immunocytochemistry with a primary monoclonal antibody directed against dopamine-glutaraldehyde-protein was used to investigate the time-course of development and the critical period of induction of this ectopic dopamine innervation (neoinnervation). In rats 6-hydroxydopamine-lesioned at postnatal day 3 (P3) and examined at P7, P10, P15, P30 or later, some dopamine fibers were already present in the substantia nigra at P7; their number increased sharply until P15 and only slightly thereafter, assuming a topographic distribution reminiscent of the missing dopamine nerve cell bodies and dendrites. A similar growth of dopamine fibers took place in the substantia nigra after lesions made at P6, P9 and P12, but was less pronounced after lesion at P15 and absent after lesion at P21 or later. Excessive innervation by dopamine axons (hyperinnervation) was concomitantly observed in the nearby interpeduncular nucleus. The sprouting of dopamine axons in both regions was therefore rapid and coincided in time and space with the developmental redistribution of mesencephalic dopamine neurons in normal rat. It is conceivable that these aberrant dopamine innervations play a role in the peculiar behavior and responsiveness to dopaminergic agents manifested by neonatally 6-hydroxydopamine-lesioned rats. It will be of particular interest to investigate the functional consequences of the dopamine neoinnervation in the substantia nigra, where an eventual axonal release might thus be replacing the normal somatodendritic release of this amine.

[Progressive multifocal leukoencephalopathy mimicking multiple sclerosis as the sole clinical manifestation of acquired immunodeficiency syndrome]. / Leucoencéphalopathie multifocale progressive mimant une sclérose en plaques comme seule expression clinique d'un syndrome d'immuno-déficience acquise.

A 38 year-old wife, of belgian origin and residency, suffered from a left retrobulbar optic neuritis in 1973, with as only sequel dyschromatopsia and central scotoma enlargement. In 1985, 12 years later, she complained of a progressive weakness of the right hand, and developed a spastic tetraplegia within four months. The C.T. Scan showed white matter hypodensities, without mass effect or contrast enhancement, first limited to the left centrum semiovale and later on with multifocal character. Somatosensory evoked potentials after stimulation of the right median nerve demonstrated only lemniscus medialis response. Multiple sclerosis was initially suspected. Analysis of lymphocytes subsets however showed a markedly reduced helper population with as a result a very low H/S ratio, and the serology was found positive for HTLV-III-LAV, thus demonstrating the diagnosis of acquired immune deficiency syndrome (AIDS). Visceral autopsy demonstrated only a CMV pneumonia. Autopsy of the brain showed typical lesions of progressive multifocal leukoencephalopathy (PML). This case is compared with 20 previously published observations of PML associated with AIDS and appears rather unusual due to the association of unfrequent clinical peculiarities: previous, probably coincidental, retrobulbar optic neuritis, female patient, lack of risk factor and clinical symptoms of AIDS. The diagnostic difficulties in the present case are emphasized.

Spinal arachnoiditis due to aspergillus meningitis in a previously healthy patient.

A 30-year-old, previously healthy, non-addicted man presented with a chronic spinal meningitis complicated by arachnoiditis and spinal cord compression. Biopsy showed a chronic granulomatous leptomeningitis, in which some cells contained branching septate organisms that were immunostained with an antiserum to Aspergillus fumigatus. Precipitins to A. fumigatus were detected in cerebrospinal fluid (CSF), but not in blood, and aspergillus infection was apparently restricted to the leptomeninges. Clinically successful treatment led to the disappearance of CSF precipitins and oligoclonal bands.