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A 68-year-old patient suffered for 8 years from radicular S1 pain on the left side, which was aggravated by walking. After an increased effort, he experienced a violent dorsal pain and sensitive troubles in the left T1 and T2 territories. Low back pain and painful paresthesiae of right leg came on next. Physical examination revealed proprioceptive symptoms on the left, a left pyramidal syndrome and a sacral pilonidal sinus. MRI showed on level of L2 vertebra, a spinal cord duplication in a unique dural tube, corresponding to diplomyelia or split cord malformation (SCM) type II. The patient had low conus medullaris anchored on L3-L4 level. A syringomyelia surmounted this medullar dysraphia. Split cord malformations, SCM type I (diplomyelia) or SCM type II (diastematomyelia), are usually revealed in infancy or early childhood. They are very rarely discovered late in the life. With progress in noninvasive spinal cord imaging, such diagnoses will undoubtedly be made more often in adults.

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Sarcoidosis is a multisystem granulomatous disease mostly involving the chest. Sarcoid optic neuropathy is an uncommon but serious manifestation that requires long-term corticosteroid treatment. We report here the case of a 50-year-old black patient complaining of a recent blurred vision on his left eye. The ophthalmologic examination was normal. Goldmann visual field and visual evoked potentials confirmed the diagnosis of retrobulbar optic neuropathy. Sarcoidosis was presumed on a chest radiography and computed tomography and confirmed with a transbronchial biopsy. Symptoms disappeared with intravenous bolus of corticosteroids. Three months later, without treatment, a right inferior eyelid tumor was observed. Magnetic resonance imaging (RMI) showed two orbital masses and multiple meningeal lesions enhancing with contrast suggesting neurosarcoidosis which decreased with a long-term high-dose corticosteroid therapy (1 mg/kg/d). Optic neuropathy is a rare manifestation of neurosarcoidosis, mostly accompanied by optic-disc involvement with papillary lesions. Chest roentgenogram and computed tomography give a presumption of sarcoidosis. But biopsy is mandatory to confirm the diagnosis demonstrating the histologic lesion of a non caseating granulomatous. Corticosteroid therapy is dramatically efficient but sometimes several months treatment is required.

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Hepatitis C is frequently associated with immune-mediated diseases, such as cryoglobulinemia. Guillain-Barré syndrome is an acute demyelinating neuropathy of probable immune pathogenesis. We describe two patients with Guillain-Barré syndrome, and associated chronic hepatitis C, the second one previously treated with interferon. The link between both conditions may be hepatitis C being the trigger of this immune polyneuropathy. Guillain-Barré syndrome should be added to the list of conditions associated with hepatitis C.

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A 29-year-old Haitian man had a sore throat with a marked tonsillar exudate followed by the onset of increasingly blurred vision with swallowing difficulties and, then, a diffuse acute demyelinating neuropathy. Cerebrospinal fluid showed moderate pleiocytosis and elevated protein content. Serological testing for diphtheria, but not for tetanus and poliomyelitis, was markedly positive. Other tests including HIV1 and 2, HTLV1 and Lyme disease were negative. Diphtheritic neuropathy should be considered in the differential diagnosis of Guillain-Barré syndrome in nonvaccinated patients.

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The authors report the case of a 26 year old non-migrainous man who presented over a 5 week period with a cluster of classical migrainous attacks associated with CSF lymphocytosis. The association of this type of CSF response with attacks of migraine is unusual; in migraine the CSF is normal or may show an isolated increase in protein content (with the exception of the very rare familial hemiplegic migraine). In the reported case, other conditions liable to give rise to migraine and CSF lymphocytosis having been excluded (acute DLE, brucellosis...), this association corresponded to a benign and spontaneously regressive condition, possibly a migraine symptomatic of benign acute lymphocytic meningitis. The authors suggest that a primary meningeal inflammation may have been the cause of the cluster of migraine attacks which in this case were more accompanied perhaps because they induced a wave of depression of cortical activity.

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Thirty patients with previous cerebral ischaemic accident were explored by both computerized tomography (CT) and radionuclide tomography after injection of 123I-labelled N-isopropyl-iodo-amphetamine. All lesions that were visible at CT were also visible at radionuclide tomography. However, in 7 patients with normal CT results the latter method showed areas of cerebral activity anatomically correlated with neurological signs or vascular lesions. Cerebellar diaschisis was observed in 50% of established lesions in the carotid territory. Radionuclide tomography therefore appears as a very sensitive method to be used in ischaemic pathology with transient or regressive accidents.

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The clinical history and postmortem neuropathologic findings of a case of cerebral lymphoma revealed by a typical parkinsonian syndrome are reported. The clinical symptoms initially improved with dopa therapy. The tumor was classified as a diffuse, non-cleaved, large-cell lymphoma of B-cell origin producing monoclonal lambda light chains. The substantia nigra was infiltrated by the tumor and showed neuronal loss and extraneuronal pigment. The most striking histological feature was the presence of neuronophagic-like nodules composed of lymphomatous cells both in the locus niger and in the left thalamus. No tumoral mass effect and no histological stigmata of other etiologies of parkinsonian syndromes were observed. A hypothesis is that the neuronophagic-like nodules may reflect a neuronotoxic activity of the lymphoma and may be considered at the origin of parkinsonism.

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Two cases of tuberculous meningitis showed that there is a delay between the C.T. images and the clinical signs. The computed tomography which was still normal one and two months after the first clinical signs did not permit an early diagnosis of the tuberculous meningitis. It did not give either, at least in the beginning, a good appreciation of the results of the treatment, since most of the C.T. images appeared and/or increased while the patient's conditions had already been improving under treatment for several days or weeks. In a long range, however, the C.T. images usually disappear.

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