Hearing loss in multiple sclerosis.

Hearing loss in an uncommon symptom in multiple sclerosis (MS). In nine patients with MS, seven with unilateral hearing loss and two with bilateral impairment, accompanying symptoms and signs included facial numbness, hemifacial paresis or spasms, ipsilateral limb ataxia, nystagmus, vertigo, tinnitus, and spastic-ataxic gait. Central auditory dysfunction was suggested by audiometric findings and/or by brainstem auditory evoked potentials in all nine patients. Clinical improvement in two was accompanied by return toward normal in the results of audiometric or electrophysiologic studies. Hearing impairment should be sought in patients with MS and appropriate studies pursued.

Spontaneous infarction in pituitary tumors: neurologic and therapeutic aspects.

In addition to progressive endocrine dysfunction and progressive visual loss, pituitary neoplasms may annouce their presence by the more catastrophic alternative of spontaneous tumor infarction. In two patients reported, illness due to the spontaneous infraction of pituitary tumors was heralded by sudden onset of focal headache associated with diplopia. Stupor, confusion, and evidence of increased intracranial pressure occurred without subarachnoid hemorrhage or massive extrasellar extension of tumor. One patient developed inappropriate antidiuretic hormone secretion with spontaneous infarction in a large but clinically silent chromophobe adenoma. In both patients, skull x-rays suggested a long-standing intrasella mass. Both underwent prompt treatment with endocrinologic replacement therapy and subsequent successful transsphenoidal removal of voluminous, infarcted, pituitary masses.

Airborne rabies encephalitis: demonstration of rabies virus in the human central nervous system.

A veterinarian contracted rabies in the course of laboratory work with homogenates of rabid goat brain. Epidemiologic study determined a respiratory mode of transmission. After a fulminant encephalitic illness, formed rabies virions were identified in the synaptic zones of the olfactory glomeruli. Identification, isolation, experimental disease production, and tissue cytopathic effects of virus recovered from the brain fulfilled Koch's postulates in this unusual instance of virus disease of the nervous system.

Baclofen for spasticity in multiple sclerosis. Double-blind crossover and three-year study.

Baclofen is a safe and effective means for treating spasticity associated with multiple sclerosis. We found no toxic effects on hepatologic, hematopoietic, or renal function, acutely or for over 3 years of follow-up. A statistically significant reduction was noted in frequency of spasms, and clonus, and there was improved range of joint movement, which enabled patients to maintain functional status for prolonged periods. For the more disabled patients, treatment with baclofen gave symptomatic relief of painful spasms and made immobility more tolerable. Optimum effect was achieved when baclofen was administered in the early stages of disease, before major disabilities became permanent.

Sensory seizure mimicking a psychogenic seizure.

A patient had episodes of bilateral paresthesias with retained consciousness. The attacks were clinically considered to be psychogenic seizures. Electroencephalography indicated that the attacks were epileptic, perhaps originating from the second sensory area. Electroencephalographic recording of a seizure is essential in differentiating epileptic from psychogenic episodes.

A morphological characterization of the canine area postrema.

The cellular morphology of the dog's area postrema (AP) was demonstrated with the Golgi-Cox technique. Golgi preparations suggested division of the canine AP into three regions: a periventricular mantle zone, a central region, and a junctional zone adjacent to the nucleus tractus solitarii. The distinctive feature of the dog's AP was arrays of periventricular neurons intermixed with glialoid cells. Additional Bodian sections revealed a commissural fiber network connecting the halves of the AP at the obex. The interconnected three-layer structure implies a polysynaptic pathway by which AP stimulation activates central sympathetic outflow.

Quantitative assessment of cutaneous sensory function in subjects with neurologic disease.

Based upon techniques devised for the behavioral study of cutaneous sensation in monkeys, a method has been developed which studies quantitatively cutaneous sensation in man. The techniques is analogous to the von Békésy method of audiometry and employs a subject-operated stimulus and signalling divice. In tests utilizing electrical stimulation of the skin surfaces the subject serves as his own control for comparison of one cutaneous zone with another and from one trial session to another. A permanent, written record of stimulus and nonverbal perceptual response is produced in this instrumental method which permits statistical analysis of responses. The analysis includes determination of cutaneous sensory thresholds, limits of stimulus intensity during detection, duration of perception, detection cycle rates, and persistence indices. This instrumental method of cutaneous sensory assessment is quantifiable, free of verbal bias, and repeatable in terms of defined stimulus strengths. In applied clinical studies, patients with peripheral nerve lesions show elevations of perceptual thresholds, reduced numbers of detection-disappearance cycles per unit time, prolonged, contorted decay slopes, and occasionally persistence of perception in the absence of stimulation. Patients with central lesions have variable threshold abnormalities, but little slowing of cycle rate or perceptual persistence. These quantitative sensation parameters can be evaluated longitudinally during the course of an illness and its treatment. The method has potential use in the investigation of basic aspects of sensation and its interactions with behavior.

Projections of the carotid sinus nerve to the medulla in the dog.

The afferent and efferent projections of the carotid sinus nerve were examined within the medulla of the dog with axonal transport of horseradish peroxidase (HRP), and compared with the projections of the glossopharyngeal nerve. The carotid sinus nerve was identified electrophysiologically prior to injection of tracer. Carotid sinus nerve afferent fibers entered the medulla as part of the glossopharyngeal nerve root near the caudal limits of the cochlear nuclei. Labeled axons entered the solitary tract and ran caudally to about 3 mm anterior to the obex, where they began to enter the nucleus tractus solitarii (nTS). Carotid sinus afferent fibers and presumptive terminals were discretely localized within limited portions of the ipsilateral dorsal, medial, and lateral nTS as far as 3 mm caudal to the obex. A few fibers entered the dorsolateral area postrema ipsilateral to HRP injection. Labeled fibers in the commissural nTS crossed the midline and entered the contralateral medial nTS. Efferent neurons were observed only in half of the cases, and were limited to one to three labeled perikarya in the periphery of the retrofacial nucleus. Comparison of the carotid sinus distribution with the previously described vagal afferent projections to the canine nTS revealed partially overlapping, but clearly distinctive patterns, which support a viscerotopic organization of the nTS.

Afferent projections of the cervical vagus and nodose ganglion in the dog.

The distribution within the brain stem of the afferent projections of the cervical vagus and the nodose ganglion was studied with horseradish peroxidase (HRP) and HRP-wheat germ agglutinin conjugate. Two to eight days after application of tracer into the cervical vagosympathetic trunk or the nodose ganglion the brain stems and ganglia were perfused and processed by the tetramethyl benzidine method. Vagal afferent fibers entered the lateral medulla as a distinct bundle spatially separate from the vagal efferent rootlets which were caudal and ventral to the afferents. Labeled axons in the solitary tract began to enter the nucleus tractus solitarii (nTS) 4.5 mm anterior to obex and were seen throughout the ipsilateral nTS as far as 3.5 mm caudal to obex. Label density varied within the nTS, with heaviest labeling in the dorsal and dorsolateral portions. Label was also seen in the ipsilateral area postrema (ap) and dorsal motor nucleus of the vagus. Labeled fibers crossed in the commissural portions of ap and nTS to enter the contralateral ap and nTS.

Brainstem distribution of neurons with efferent projections in the cervical vagus of the dog.

The distribution within the brainstem of cell bodies and efferent fibers projecting in the cervical vagus was studied with retrograde transport of horseradish peroxidase (HRP). Five to eight days after multiple microinjections of HRP into either the cervical vagosympathetic trunk or the nodose ganglion the brainstems and nodose ganglia were perfused and processed by the tetramethyl benzidine method. HRP-positive neurons were found in three brainstem regions: a dorsal cell column comprising the dorsal motor nucleus of the vagus (dmnX), a ventrolateral group in the region of nucleus ambiguus (nA), and scattered cells along a line between these columns. The density of labeled neurons was greatest within dmnX. Axons from cells of the ventrolateral column projected dorsomedially; just ventral to dmnX they turned laterally to exit the medulla in multiple rootlets. Within nA labelled neurons were distributed according to size, with larger cells more medial and smaller ones more lateral. Caudal to nA in nucleus retroambigualis and nucleus dorsalis medialis cell bodies appeared segregated into clusters.

Impact of arterial hypertension on the brain.

Even mild arterial hypertension dramatically increases the risk of vascular brain disease. Cerebral infarction is most commonly attributable to large-vessel thromboembolic disease. Lacunar infarcts, due to lipohyalin degeneration of vessel walls, are a particular hazard in the hypertensive patient. Hypertensive encephalopathy is associated with hypertension from any cause and may occur at any age. Brain hemorrhage is associated with arterial hypertension and is almost always fatal, regardless of treatment. Hypertension plays a major causal or complicating role in all cerebrovascular disease. The decline in the incidence of stroke over the past decade coincides with improving detection and treatment of hypertension.