NEURON STRUCTURE OF THE GANGLION PLEXUSES IN THE LARGE INTESTINE

Aim of the study: The aim of the work: to study the syncytial connections in the ganglia of the nerve plexuses of the large intestine. Material and research methods: The work was carried out on 30 sexually mature Wistar rats at the age of 3–4 months, having a mass of 180–320 g by the beginning of the experiment. The study used a universal method of impregnation, based on classical impregnation methods: intravascular — Rannier–Goyer and immersion — Bilshovsky–Gros. The study was conducted in 2019–2020. Results: According to our data, the large intestine has intraorgan ganglia located in the intermuscular and submucosal plexuses. The intermuscular plexus (Auerbach) of the large intestine has the form of a network with cells of various shapes and consists of nerve nodes containing cells of types I and II of Dogiel, however, the latter are numerically significantly predominant (20–25 cells or more). Syncytial connections of neurons in the autonomic ganglia of the intestine were constantly detected. These were syncytial connections of processes and bodies of two neurocytes. Protoplasmic processes of nerve cells diverge in different directions, go to meet similar branches, joining them, form a narrow or wide-looped network. Syncytial connections between the bodies of neurons and peripheral processes form closed annular anastomoses. Interfiber cytoplasmic bonds are formed by membrane syncytial fusion. Conclusion. The large intestine has intraorgan ganglia located in the intermuscular and submucosal plexuses. Syncytial connections of neurons in the autonomic ganglia of the intestine were constantly detected. Interfiber cytoplasmic bonds are formed by membrane syncytial fusion.

PARAGANGLIOMA OF LUMBAR SPINE – A RARE CASE REPORT

Paragangliomas are neuroendocrine neoplasm. These neoplasms originate from specialized neural crest cells and have association with segmental or collateral autonomic ganglia. Spinal paraganglioma is rare tumor. We are presenting a case of spinal paraganglioma in a 58 years old male presented with low back pain, his MRI spine showed extramedullary intradural tumor at the level of L1-L2 vertebra .Tumor was excised and patient was discharged after uneventful stay at hospital. Paragangliomas are WHO grade I slow growing tumor, radiologically paraganglioma resembles other lesions, such as schwannomas, ependymomas, meningiomas. Gross total resection of tumor is treatment of choice .Prognosis is good with very rare recurrence rate.

Acute Sensory and Autonomic Neuronopathy: A Devastating Disorder Affecting Sensory and Autonomic Ganglia

Acute-onset and severe sensory and autonomic deficits with no motor dysfunction, typically preceded by a febrile illness, with poor recovery, and often fatal outcome are the hallmark features of acute sensory and autonomic neuronopathy (ASANN). Pathologically and electrophysiologically, ASANN is characterized by an extensive ganglionopathy affecting sensory and autonomic ganglia with preservation of motor neurons. Consequently, patients, usually children or young adult, develop acute-onset profound widespread loss of all sensory modalities resulting in automutilations, as well as autonomic failure causing neurogenic orthostatic hypotension, neurogenic underactive bladder, and gastroparesis and constipation. The diagnosis is clinical with support of nerve conduction studies and autonomic testing, as well as spinal cord magnetic resonance imaging showing characteristic posterior cord hyperintensities. Although the presumed etiology is immune-mediated, further studies are required to clarify the physiopathology of the disease. We here performed a systematic review of the epidemiology, pathophysiology, diagnosis, and management of ASANN, with three representative cases that recently presented at our clinic. All three patients had the typical clinical manifestations of ASANN but in different combinations, illustrating the variable phenotype of the disorder. Immunosuppression is seldom effective. Management options are limited to supportive and symptomatic care with the goal of minimizing complications and preventing death.

Japanese Encephalitis Virus Infects the Thalamus Early Followed by Sensory-Associated Cortex and Other Parts of the Central and Peripheral Nervous Systems

Japanese encephalitis (JE) is a known CNS viral infection that often involves the thalamus early. To investigate the possible role of sensory peripheral nervous system (PNS) in early neuroinvasion, we developed a left hindlimb footpad-inoculation mouse model to recapitulate human infection by a mosquito bite. A 1–5 days postinfection (dpi) study, demonstrated focal viral antigens/RNA in contralateral thalamic neurons at 3 dpi in 50% of the animals. From 4 to 5 dpi, gradual increase in viral antigens/RNA was observed in bilateral thalami, somatosensory, and piriform cortices, and then the entire CNS. Infection of neuronal bodies and adjacent nerves in dorsal root ganglia (DRGs), trigeminal ganglia, and autonomic ganglia (intestine, etc.) was also observed from 5 dpi. Infection of explant organotypic whole brain slice cultures demonstrated no viral predilection for the thalamus, while DRG and intestinal ganglia organotypic cultures confirmed sensory and autonomic ganglia susceptibility to infection, respectively. Early thalamus and sensory-associated cortex involvement suggest an important role for sensory pathways in neuroinvasion. Our results suggest that JE virus neuronotropism is much more extensive than previously known, and that the sensory PNS and autonomic system are susceptible to infection.

Herpes Simplex Virus 2 in Autonomic Ganglia: Evidence for Spontaneous Reactivation

ABSTRACTHerpes simplex virus 2 (HSV-2) can be transmitted in the presence or absence of lesions, allowing efficient spread among the general population. Recurrent HSV genital lesions are thought to arise from reactivated latent virus in sensory cell bodies of the dorsal root ganglia (DRG). However, HSV-2 has also been found latent in autonomic ganglia. Spontaneous reactivation or a low level of chronic infection could theoretically also occur in these peripheral nervous tissues, contributing to the presence of infectious virus in the periphery and to viral transmission. Use of a recently described, optimized virus with a monomeric mNeonGreen protein fused to viral capsid protein 26 (VP26) permitted detection of reactivating virus in explanted ganglia and cryosections of DRG and the sacral sympathetic ganglia (SSG) from latently infected guinea pigs. Immediate early, early, and late gene expression were quantified by droplet digital reverse transcription-PCR (ddRT-PCR), providing further evidence of viral reactivation not only in the expected DRG but also in the sympathetic SSG. These findings indicate that viral reactivation from autonomic ganglia is a feature of latent viral infection and that these reactivations likely contribute to viral pathogenesis.IMPORTANCEHSV-2 is a ubiquitous important human pathogen that causes recurrent infections for the life of its host. We hypothesized that the autonomic ganglia have important roles in viral reactivation, and this study sought to determine whether this is correct in the clinically relevant guinea pig vaginal infection model. Our findings indicate that sympathetic ganglia are sources of reactivating virus, helping explain how the virus causes lifelong recurrent disease.