The vestibular system is involved in maintaining stable blood pressure and respiration during changes in posture and is essential for eliciting motion sickness-related vomiting. Because the nucleus tractus solitarius (NTS) participates in the regulation of sympathetic and inspiratory outflow and the triggering of emesis, we tested the hypothesis that this region receives vestibular inputs in cats. In one set of experiments, microinjections of the tracer Phaseolus vulgaris leucoagglutinin into the medial and inferior vestibular nuclei labeled projections to the middle and lateral regions of the NTS. In electrophysiological experiments, electrical stimulation of the vestibular nerve modified the firing rates of neurons located in the same regions. Some neurons with vestibular inputs received convergent signals from the abdominal vagus nerve and could potentially mediate motion sickness-related vomiting. Others received convergent baroreceptor inputs and could act as a substrate for some components of vestibulosympathetic reflexes. In contrast, inspiratory neurons in the dorsal respiratory group received little vestibular input, suggesting that vestibulorespiratory reflexes are mediated by cells located elsewhere.
1. The efferent projections of the interstitial nucleus of Cajal (NIC) were studied in the squirrel monkey after iontophoretic injections of biocytin and Phaseolus Vulgaris leucoagglutinin into the NIC. To ensure the proper placement of the tracer, the same pipettes were used to extracellularly record the discharge pattern of NIC neurons. 2. Three projection systems of the NIC were distinguished: commissural (through the posterior commissure), descending, and ascending. 3. The posterior commissure system gave rise to dense terminal fields in the contralateral NIC, the oculomotor nucleus, and the trochlear nucleus. 4. The descending system of NIC projections deployed dense terminal fields in the ipsilateral gigantocellular reticular formation and the paramedian reticular formation of the pons, as well as in the ventromedial and commissural nuclei of the first two spinal cervical segments. It also gave rise to moderate or weak terminal fields in the vestibular complex, the nucleus prepositus hypoglossi, the inferior olive, and the magnocellular reticular formation, as well as cell groups scattered along the paramedian tracts in the pons and the pontine and medullary raphe. 5. The ascending system of NIC projections gave rise to dense terminal fields in the ipsilateral mesencephalic reticular formation and the zona incerta as well as moderate or weak terminal fields in the ipsilateral centromedian and parafascicular thalamic nuclei. It also provided dense bilateral labeling of the rostral interstitial nucleus of the medial longitudinal fasciculus and the fields of Forel, and moderate or weak bilateral labeling of the mediodorsal, central medial, and central lateral nuclei of the thalamus. 6. Models of saccade generation that rely on feedback from the velocity-to-position integrators and include the superior colliculus in their local feedback loop are contradicted because no fibers originating from the NIC traveled to the superior colliculus to deploy terminal fields. 7. Consistent with its morphological and functional diversity, these data indicate that the primate NIC sends signals to a multitude of targets implicated in the control of eye and head movements.
Based on evidence from morphometric studies of PNS, we suggested that acrylamide (ACR)‐induced distal axon degeneration was a secondary effect related to duration of exposure (Toxicol Appl Pharmacol 151 [1998] 211). To test this hypothesis in CNS, the cupric‐silver stain method of de Olmos was used to define spatiotemporal characteristics of nerve somal, dendritic, axonal and terminal degeneration in rat cerebellum. Rats were exposed to ACR at either 50 mg/kg per day (i.p.) or 21 mg/kg per day (p.o.) and at selected times (i.p. = 5, 8 and 11 days; p.o. = 7, 14, 21, 28 and 38 days) brains were removed and processed for silver staining. Results demonstrate that intoxication at the higher ACR dose‐rate produced early (day 5) and progressive degeneration of Purkinje cell dendrites in cerebellar cortex. Nerve terminal degeneration occurred concurrently with somatodendritic argyrophilia in cerebellar and brainstent nuclei that receive afferent input from Purkinje neurons. Relatively delayed (day 8), abundant axon degeneration was present in cerebellar white matter but not in cortical layers or in tracts carrying afferent fibers (cerebellar peduncles) from other brain nuclei. Axon argyrophilia coincided with the appearance of perikaryal degeneration, which was selective for Purkinje cells since silver impregnation of other cerebellar neurons was not evident in the different cortical layers or cerebellar nuclei. Intoxication at the lower ACR dose‐rate produced simultaneous (day 14) dendrite, axon and nerve terminal argyrophilia and no somatic Purkinje cell degeneration. The spatiotemporal pattern of dendrite, axon and nerve terminal loss induced by both ACR dose‐rates is consistent with Purkinje cell injury. Injured neurons are likely to be incapable of maintaining, distal processes and, therefore, axon degeneration in the cerebellum is a component of a “dying‐back” process of neuronal injury. Because cerebellar coordination of somatomotor activity is mediated solely through efferent projections of the Purkinje cell, injury to this neuron might contribute significantly to gait abnormalities that characterize ACR neurotoxicity.
Background In the Autumn of 2016, diplomatic personnel residing in Havana began to present with symptoms of dizziness, ear pain, and tinnitus that emerged after perception of high frequency noise and/or a pressure sensation. Understanding the acute symptoms of this disorder is important for better defining the disorder and developing optimal diagnostic, preventive, and treatment algorithms. Objectives To define the presenting symptoms in a cohort of patients in the acute time period after perceiving a noise/pressure exposure in Havana. Design/Settings/Participants Review of 25 symptomatic individuals who reported a localized sensation of noise/pressure and 10 asymptomatic individuals (roommates of those affected) who did not experience the sound/pressure. Results Immediately after the exposure, the majority of individuals reported intense ear pain in one or both ears and experienced tinnitus. All of the individuals noticed unsteadiness and features of cognitive impairment. On presentation to our center, dizziness (92%) and cognitive complaints (56%) were the most common symptoms. Formal testing revealed that 100% of individuals had an otolithic abnormality and evidence of cognitive dysfunction. Conclusion and Relevance This study focuses on the acute presentation of a phenomenon in which symptoms emerge after perception of a localized noise/pressure and in which the acute symptomology includes the universal nature of vestibular injuries and select cognitive deficits. The findings presented in this acute group of patients begin to provide a better picture of the initial injury pattern seen after this exposure and may allow for more accurate diagnosis of this disorder in future cases. Level of Evidence Retrospective review
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