Peripheral nerve and neuromuscular disorders.

Mononeuropathies, plexopathies, and radiculopathies may occur with increased incidence during pregnancy and the puerperium. Immunologically mediated disorders of peripheral nerve, neuromuscular junction, and muscle have distinctive management problems when they occur during pregnancy.

Arterial and venous stroke associated with pregnancy.

Pregnancy increases the risk of both arterial and venous strokes. The diverse causes of these strokes warrants a thorough investigation including angiography if needed to secure a diagnosis in order to give the patient the best advice and treatment. The section on arterial stroke reviews the differential diagnosis and highlights how pregnancy influences some conditions causing stroke. The section on cerebral venous thrombosis reviews the clinical scenarios of this unusual condition, the evolving techniques for its diagnosis, and its treatment with anticoagulants.

Neurologic emergencies in pregnancy.

Any one neurologic emergency is rare during pregnancy. As a group, neurologic disorders are a major cause of maternal mortality. Optimal management requires a multidisciplinary approach and ready access to the collective experience of other clinicians. This article discusses the management of status epilepticus, eclamptic hypertensive encephalopathy, stroke, including subarachnoid hemorrhage, myasthenic crisis, porphyric crisis, acute Guillain-Barré syndrome, autonomic hyperreflexia, malignant hyperthermia, chorea gravidarum, and Wernicke's encephalopathy.

Effect of sexual hormones on the electroencephalogram and seizures.

The role of hormones and reproductive function in electroencephalography (EEG) and epilepsy has long intrigued electroencephalographers. In this report, the relationship between the menstrual cycle and pregnancy and EEG changes and seizure frequency is reviewed. These neurophysiologic changes are likely secondary to hormonal effects. The effect of these hormones on experimental animal models is also reviewed.

Prostaglandin release in multiple sclerosis: correlation with disease activity.

Release of prostaglandin E (PGE) was examined in leukocyte cultures from patients with definite MS who had had at least one recent exacerbation, others with chronic progressive or stable MS, and healthy controls. MS patients had higher baseline levels of PGE than did controls. Patients with active symptoms exhibited a sharp increase in PGE release early in or just before the onset of clinical symptoms. Levels dropped early in exacerbation immediately after the burst in PGE synthesis activity. Values gradually increased to control levels and then to preexacerbation levels. Similar rises and falls were not seen in stable MS. MS patients may have a circulating population of activated leukocytes that produce PGE.

Endocrinology of pseudotumor cerebri.

This article will review the endocrine function of obese young women with pseudotumor cerebri and primary empty sella syndrome. The literature can be difficult to interpret. Much of it predates the era of CT scanning. Often, cases of primary and secondary empty sella syndrome are comingled. The author reviews specific endocrinologic disorders that have sometimes been associated with increased intracranial pressure excluding pituitary adenomas.

Lymphocyte adherence to myelinated tissue in multiple sclerosis: correlation with disease activity.

Human peripheral blood T-lymphocytes adhere to myelinated sections of human and nonhuman brain tissue. No lymphocyte adherence is seen to gray matter. Lymphocytes from patients with MS adhere more than control lymphocytes. Lymphocyte adherence in patients with stable MS and in healthy controls did not vary more than 15%. Lymphocyte adherence in MS patients was decreased significantly during exacerbation. Values rose to pre-exacerbation levels in remissions. Results suggest that T cells that adhere to myelin may migrate from the peripheral blood during exacerbation.

Neurologic abnormalities in Lyme disease without erythema chronicum migrans.

The clinical features in eight patients with neurologic abnormalities typical of Lyme disease and elevated titers of antibody to the spirochete, Borrelia burgdorferi, its causative agent, are described. None of the patients had the diagnostic skin lesion, erythema chronicum migrans. Lyme arthritis, the other clinical marker for the disease, developed subsequently in only three. The neurologic abnormalities included aseptic meningitis, encephalitis, cranial neuritis, motor and sensory radiculitis, and myelitis in various combinations. The occurrence of severe encephalitis resulting in dementia in two of these patients and irreversible myelopathy in one enlarges the known spectrum of neurologic abnormalities due to infection with B. burgdorferi. Lyme disease can present with neurologic abnormalities without diagnostic extraneural features, can be suspected on clinical and epidemiologic grounds, and can be diagnosed serologically.

Juvenile multisystem degeneration with motor neuron involvement and eosinophilic intracytoplasmic inclusions.

A case of juvenile multisystem degeneration with motor neuron involvement, possibly of familial type, showing many unusual clinical and pathologic features is reported. Eosinophilic intracytoplasmic inclusions were present in some remaining anterior horn cells and motor nerve nuclei of the brain stem as well as in a few neurons of the reticular activating system, the dorsal vagus nuclei, and the intermediolateral cell column. Smaller eosinophilic inclusions were seen in large neurons of the caudate nucleus and putamen, substantia nigra, and subthalamic nucleus.

Compartmentalized immune responses: antigen-specificity of cerebrospinal fluid T-cell lines maintained in the absence of antigen.

The generation of long-term interleukin 2-dependent T-cell lines from anatomically compartmentalized sites of pathology offers a unique approach to the investigation of certain autoimmune diseases. However, it is generally believed that antigen-specific T-cell lines and clones lose antigen reactivity and specificity when propagated in the absence of antigen. Therefore, the optimal application of this approach to such diseases in which the pathogenetic antigens are unknown may be difficult. In approaching this problem, we have recently demonstrated that a proportion of antigen-specific T-cell lines derived from the peripheral circulation can maintain antigen specificity if propagated with antigen-presenting cells alone or with antigen-presenting cells together with OKT3 antibody, but in either case in the absence of antigen. In this report we describe the use of this approach to maintain the antigen specificity of T cells obtained from an anatomically compartmentalized site of pathology--the cerebrospinal fluid from a patient with tuberculous meningitis. We report here that a proportion of the T-cell lines generated from such cerebrospinal fluid lymphocytes can be maintained as antigen specific in the absence of antigen if propagated with either antigen-presenting cells alone or with antigen-presenting cells and OKT3 antibody. The approach illustrated in this report should now find broad applicability in the investigation of a number of autoimmune disease.