[Immunopathology and treatments of Guillain-Barré syndrome and of chronic inflammatory demyelinating polyneuropathy]. / Mécanismes immunitaires et traitements du syndrome de Guillain-Barré et des polyradiculonévrites inflammatoires chroniques.

The concepts of Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP) have changed over the last decade. The spectrum of GBS ranges from acute inflammatory demyelinating polyneuropathy to pure motor, sensory-motor or bulbar variants and the Miller Fisher syndrome. Also CIDP includes different variants in addition to the typical clinical picture with symmetrical proximal and distal weakness, such as a form with predominant distal weakness, a pure sensory form, an asymmetric form and a form with predominant cranial nerve involvement. Detailed immunopathologic features have been described in GBS and CIDP: most current investigations are centered on the hypothesis of molecular mimicry in GBS and together with the pathogenic role of cell-mediated immunity different antibodies have been discovered in GBS which interfere with nerve impulse conduction on neuromuscular transmission. The immunopathogenesis of CIDP remains fragmentary and insufficient for a unified hypothesis. Activated macrophages and T-cells with the participation of T-1 helper cell related cytokines seem to play a fundamental role in demyelination. The nature of antigen presenting cells, T-cell receptors, adhesion molecules and the proinflammatory cytokines need to be explored to design more specific immunotherapies. Established treatments in GBS include intravenous immunoglobulin and plasma exchange. Randomized trials have shown the efficacy of prednisone, intravenous immunoglobulin and plasma exchange in CIDP. New insight in the pathogenetic role of the cytokine-network in CIDP opens new therapeutical possibilities with the modification of the T-1 helper cell reaction with interferon.

[Neurological complications of HIV infection. Review: new diagnostic, therapeutic and prognostic aspects]. / Neurologische Komplikationen der HIV-Infektion. Aktuelle Ubersicht: neue diagnostische, therapeutische und prognostische Aspekte.

About one third of patients with HIV infection show neurological complications with considerable morbidity and high mortality. This is an actualized review of the most important neurological manifestations resulting from primary HIV infection, from secondary opportunistic infections, or as complications of antiretroviral therapy. The primary neurological manifestations, including HIV-associated dementia complex, myelopathies, peripheral neuropathies and myopathies, the more common opportunistic infections, primary central nervous system lymphoma and cerebrovascular diseases, are discussed in the light of new evidence in diagnosis, therapy and prognosis. Cognitive and psychiatric symptoms, visual changes, headache, seizures, dizziness, involuntary movements, gait disturbances, cranial neuropathies and focal deficits are the common neurological symptoms in HIV infection which are described under the aspect of differential diagnosis. It is important to bear in mind that nearly all information available to date on this subject concerns HIV patients in the period before combination therapies (including protease inhibitors). The introduction of highly active antiretroviral therapy (HAART) with protease inhibitors in 1995, and non-nucleoside reverse transcriptase inhibitors, have opened up new therapeutic modalities with a new emphasis on earlier detection and treatment of neurological complications. The prognosis of different HIV-associated neurological diseases has considerably improved, as recently shown in the case, for example, of progressive multifocal leucoencephalopathy.

[Intermittent paraparesis as manifestation of a bilateral chronic subdural hematoma]. / Fluktuierende Paraparese als Manifestation eines bilateralen chronischen Subduralhämatoms.

Chronic subdural haematomas are mainly related to slight or moderate head trauma with consecutive lesion of bridge or cortical veins and bleeding in the subdural space. Further predisposing factors are known impairment of coagulation (coagulopathies, treatment with anticoagulants, alcohol abuse), risk factors for degenerative disease of the arteries (diabetes mellitus, arterial hypertension), and development of pressure gradients (hydrocephalus, epileptic seizures, lumbar puncture, CSF drainage and cerebral atrophy). Chronic subdural haematomas appear bilaterally in 20 to 25% of cases. We report on a 69-year-old male with a 4-day history of intermittent, proximal, painless paraparesis (BMA grade M2-5) without a trigger event. Sensibility was normal in all qualities and vigilance was not disturbed. Computed tomography of the neurocranium revealed a bitemporally located chronic subdural haematoma with extension to parietal on both sides. Trepanation was performed over the tuber parietale and temporoparietally on both sides, with release of 150 ml fluid. The neurologic deficits regressed totally within 12 hours postoperatively. To the best of our knowledge, we are the first to describe the clinical paradox of intermittent, painless paraparesis with preserved sensibility and without disturbances of vigilance, as manifestation of a chronic subdural haematoma possibly leading to impairment of cerebral blood flow in the area of the middle cerebral artery. Small changes in systemic blood pressure lead to changes in cerebral perfusion pressure due to vessel compression by the haematoma, thus explaining the intermittent character of the clinical presentation.

Visual disturbances and transurethral resection of the prostate: the TURP syndrome.

A 73-year-old man with a history of a cerebral and a cardiac vascular disease and atrial flutter developed visual disturbances characterized by vision being dark in both eyes and by seeing as through a color photographic negative immediately after an uncomplicated transurethral resection of the prostate (TURP) for prostatic hyperplasia under spinal anesthesia. There was complete remission of the symptomatology after 2.5 h. A cerebrovascular workup was negative. Considering postoperative hyponatremia and hypoosmality, we discuss the possible role of glycine-induced visual disturbances as described in the TURP reaction syndrome, to our knowledge an entity almost unknown in the neurologic literature. Glycine-induced visual disturbances should therefore be considered in the differential diagnosis of bilateral transient visual loss.