Cranial Sensory Ganglia Research Articles

Neural crest lineage in the protovertebrate model Ciona.

Neural crest cells are multipotent progenitors that produce defining features of vertebrates such as the 'new head'1. Here we use the tunicate, Ciona, to explore the evolutionary origins of neural crest since this invertebrate chordate is among the closest living relatives of vertebrates2-4. Previous studies identified two potential neural crest cell types in Ciona, sensory pigment cells and bipolar tail neurons5,6. Recent findings suggest that bipolartail neurons are homologous to cranial sensory ganglia rather than derivatives of neural crest7,8. Here we show that the pigment cell lineage also produces neural progenitor cells that form regions of the juvenile nervous system following metamorphosis. Neural progenitors are also a major derivative of neural crest in vertebrates, suggesting that the last common ancestor of tunicates and vertebrates contained a multipotent progenitor population at the neural plate border. It would therefore appear that a key property of neural crest, multipotentiality, preceded the emergence of vertebrates.

Fibroblast growth factor 8 promotes in vitro neurite outgrowth of placode-derived petrosal and nodose ganglia to varying degrees

Fibroblast growth factors (FGFs) are required for the specification and formation of the epibranchial placodes, which give rise to the distal part of the cranial sensory ganglia. However, it remains unclear whether FGFs play a role in regulating the neurite outgrowth of the epibranchial placode-derived ganglia during further development. Previous studies have shown that Fibroblast growth factor 8 (FGF8) promotes neurite outgrowth from the statoacoustic ganglion in vitro. However, these studies did not distinguish between the neural crest- and placode-derived components of the sensory ganglia. In this study, we focused on the petrosal and nodose ganglia as representatives of the epibranchial ganglia and investigated their axonal outgrowth under the influence of FGF8 signaling protein in vitro. To precisely isolate the placode-derived ganglion part, we labeled the placode and its derivatives with enhanced green fluorescent protein (EGFP) through electroporation. The isolated ganglia were then collected for qRT-PCR assay and cultured in a collagen gel with and without FGF8 protein. Our findings revealed that both placode-derived petrosal and nodose ganglia expressed FGFR1 and FGFR2. In culture, FGF8 exerted a neural trophic effect on the axon outgrowth of both ganglia. While the expression levels of FGFR1/2 were similar between the two ganglia, the petrosal ganglion exhibited greater sensitivity to FGF8 compared to the nodose ganglion. This indicates that the placode-derived ganglia have differential responsiveness to FGF8 signaling during axonal extension. Thus, FGF8 is not only required for the early development of the epibranchial placode, as shown in previous studies, but also promotes neurite outgrowth of placode-derived ganglia.

Distribution and anti-nociceptive function of endomorphin-1 in the rat cranial sensory ganglia.

Distribution of endomorphin-1 (EM-1) was immunohistochemically investigated in the rat cranial sensory ganglia. Small to medium-sized neurons in the trigeminal (TG), petrosal (PG), and jugular ganglia (JG) expressed EM-1-immunoreactivity. However, EM-1-immunoreactive (-ir) neurons were infrequent in the nodose ganglion. In the brainstem, EM-1-ir varicose fibers were detected in the superficial layer of the medullary dorsal horn and the caudal part of the nucleus tractus solitarius. By trichrome immunofluorescence analysis, approximately 70% of EM-1-ir neurons were also immunoreactive for transient receptor potential vanilloid 1 (TRPV1) in all the examined ganglia. Additionally, 56.8% of EM1-ir TG neurons and approximately 30% of EM-1-ir PG and JG neurons showed calcitonin gene-related peptide (CGRP)-immunoreactivity. By a retrograde tracing method, several TG, PG, and JG neurons innervating the facial and external ear canal skin expressed EM-1-immunoreactivity. However, EM-1-ir neurons innervating the tooth pulp, circumvallate papilla, and pharynx were relatively rare. Thus, EM-1 expression and its coexistence with TRPV1 and CGRP in the cranial sensory neurons may depend on their various peripheral targets. EM1-ir neurons probably project to the superficial layer of the medullary dorsal horn and caudal part of the nucleus tractus solitarius. EM-1 may be involved in nociceptive transmission from the skin.

Clinical profile of herpes zoster in human immunodeficiency virus infected at a rural-based tertiary care center

Background: Due to the reactivation of the varicella-zoster virus, which had lainissed within sensory ganglions, herpes zoster (HZ) is typified by unilateral radicular pain and grouped vesicular eruption that is typically restricted to the dermatome innervated by a single spinal or cranial sensory ganglion. It is widely known that reactivation of varicella-zoster virus infection as HZ can cause morbidity in a human immunodeficiency virus (HIV)-positive host. Aims and Objectives: The aim of this study was to describe the clinical profile of HZ among HIV-positive patients in a rural tertiary care center. Materials and Methods: A prospective hospital-based study was conducted in a rural tertiary care hospital in Karnataka for duration of 24 months. All patients attending the outpatient department (OPD) of dermatology with clinical features of HZ and post-herpetic complications irrespective of their age and gender were included in the study. Data collection done in a semi-structured questionnaire on patient particulars as well as pre-existing co-morbidities was documented. Results: A cross-sectional study included 75 HZ patients attending OPD. Among the total 75 HZ patients, 11 were found to be seropositive for HIV infection. Seroprevalence among HZ was 14.6%. Among seropositive patients, the maximum belonged to the age group 41–60 years (63.3%). In the seropositive group, maximum cases (36.4%) occurred during summer while it was in the post monsoon season (39%) in the seronegative group. Conclusion: It is known that multidermatomal and severe pain is more commonly seen in HIV-infected patients than in the normal population. Many HIV-positive patients can present with a typical presentation of zoster as seen in our study.

The Neuroanatomical Basis of Unfamiliar Presentations of Herpes Zoster: A Review and A Case Report

Herpes zoster (HZ, shingles) is caused by reactivated varicella zoster virus, that travels along the peripheral branches from its dormant location in neurons of spinal and cranial sensory ganglia. HZ is well known for its skin vesicular eruptions and severe sensory neuropathy. Over the years, reports have described the occurrence of segmental paresis of skeletal muscles and the involvement of the large and small intestine, clinically resembling intestinal obstruction.

Current scenario and future applicability of antivirals against herpes zoster.

Herpes zoster (HZ) is a common disease in the aging population and immunocompromised individuals, with a lifetime risk of 20%-30% that increases with age. HZ is caused by reactivation of the varicella-zoster virus (VZV), which remains latent in the spinal dorsal root ganglia and cranial sensory ganglia after resolution of the primary VZV infection. The main focus of HZ management is rapid recovery from VZV infection as well as the reduction and prevention of zoster-associated pain (ZAP) and postherpetic neuralgia (PHN). The use of antivirals against VZV is essential in the treatment of HZ. However, limited antivirals are only licensed clinically for the treatment of HZ, including acyclovir, valacyclovir, famciclovir, brivudine, and amenamevir. Fortunately, some new antivirals against different types of Herpesviridae have been investigated and suggested as novel drugs against VZV. Therefore, this review focuses on discussing the difference in efficacy and safety in the currently licensed antivirals for the treatment of HZ, the applicability of future novel antivirals against VZV, and the preventive or therapeutic effects of these antivirals on ZAP or PHN.

Human stem cell models to study placode development, function and pathology.

Placodes are embryonic structures originating from the rostral ectoderm that give rise to highly diverse organs and tissues, comprising the anterior pituitary gland, paired sense organs and cranial sensory ganglia. Their development, including the underlying gene regulatory networks and signalling pathways, have been for the most part characterised in animal models. In this Review, we describe how placode development can be recapitulated by the differentiation of human pluripotent stem cells towards placode progenitors and their derivatives, highlighting the value of this highly scalable platform as an optimal in vitro tool to study the development of human placodes, and identify human-specific mechanisms in their development, function and pathology.

Hmx gene conservation identifies the origin of vertebrate cranial ganglia.

The evolutionary origin of vertebrates included innovations in sensory processing associated with the acquisition of a predatory lifestyle1. Vertebrates perceive external stimuli through sensory systems serviced by cranial sensory ganglia, whose neurons arise predominantly from cranial placodes; however, the understanding of the evolutionary origin of placodes and cranial sensory ganglia is hampered by the anatomical differences between living lineages and the difficulty in assigning homology between cell types and structures. Here we show that the homeobox transcription factor Hmx is a constitutive component of vertebrate sensory ganglion development and that in the tunicate Ciona intestinalis, Hmx is necessary and sufficient to drive the differentiation programme of bipolar tail neurons, cells previously thought to be homologues of neural crest2,3. Using Ciona and lamprey transgenesis, we demonstrate that a unique, tandemly duplicated enhancer pair regulated Hmx expression in the stem-vertebrate lineage. We also show notably robust vertebrate Hmx enhancer function in Ciona, demonstrating that deep conservation of the upstream regulatory network spans the evolutionary origin of vertebrates. These experiments demonstrate regulatory and functional conservation between Ciona and vertebrate Hmx, and point to bipolar tail neurons as homologues of cranial sensory ganglia.

Elucidating the Role of N‐cadherin during Trigeminal Gangliogenesis

Cadherin‐based adhesion is critical to the formation of multicellular tissues, including the cranial sensory ganglia of the peripheral nervous system. Initial assembly of the cranial trigeminal ganglion, which houses the cell bodies for the trigeminal nerve, relies on the coalescence of N‐cadherin (N‐cad)‐expressing placode cell‐derived neurons and Cadherin‐7‐expressing neural crest cells. The trigeminal ganglion has a role that is primarily sensory, transmitting information on pain, touch, and temperature from different facial regions back to the central nervous system. Proper survival and differentiation of trigeminal neurons relies, in part, upon binding of neurotrophic and other growth factors secreted from target tissues to their cognate receptors found on peripheral axons. These complexes are then trafficked to neuronal cell bodies, resulting in the activation of downstream signaling pathways. Prior studies have shown that N‐cad internalization and trafficking are required for proper neuronal outgrowth. Moreover, N‐cad knockdown in chick trigeminal placode cells leads to early defects in trigeminal ganglion assembly by increasing placodal neuron dispersal. Later functions for N‐cad in chick trigeminal gangliogenesis, however, remain obscure. We hypothesize that N‐cad controls trigeminal ganglion development through the regulation of multiple signaling pathways. To address this, we performed morpholino‐mediated knockdown of N‐cad in chick trigeminal placode cells followed by immunohistochemistry and biochemistry to evaluate trigeminal gangliogenesis. Our preliminary data show that N‐cad depletion has a sustained negative impact on the trigeminal ganglion through cell and non‐cell autonomous effects, resulting in decreased ganglion size, aberrant nerve outgrowth and branching, and reduced levels of Cadherin‐7, neurotrophins and their receptors, and Smad family members. Future studies will aim to elucidate the mechanisms by which N‐cad controls trigeminal ganglion development via these molecules and pathways, including experiments designed to examine protein trafficking in trigeminal neurons. Taken together, our findings reveal potential adhesion‐dependent and ‐independent functions for N‐cad in the trigeminal ganglion, which will aid in the understanding of its tissue‐specific roles. This knowledge will shed light on the etiology of disorders characterized by abnormal neural crest cell and placode cell development and those affecting the peripheral nervous system.

Distribution of alpha-synuclein in the rat cranial sensory ganglia, and oro-cervical regions

BackgroundAlpha-synuclein (Syn), an unfolded soluble cytosolic protein, is known as a disease-associated protein in the brain. However, little is known about distribution of this protein in the peripheral nervous system. In this study, expression of Syn was investigated in the sensory ganglia of the cranial nerves V, IX and X. MethodsTo analyze distribution of Syn and its co-expression with calcitonin gene-related peptide (CGRP) or the transient receptor potential cation channel subfamily V member 1 (TRPV1), immunohistochemical techniques were used in the rat cranial sensory ganglia and their peripheral tissues. ResultsSyn-immunoreactive (-ir) neurons were abundant in the sensory ganglia of the petrosal (56.7%), jugular (28.3%) and nodose ganglia (82.5%). These neurons had small to medium-sized cell bodies (petrosal, mean ± S.D. = 667.4 ± 310.8 μ m2; jugular, 625.1 ± 318.4 μ m2; nodose, 708.3 ± 248.3 μ m2), and were distributed throughout the ganglia. However, the trigeminal ganglion was mostly free of Syn-ir neurons. By double and triple immunofluorescence staining, Syn-ir neurons co-expressed CGRP and TRPV1 in the petrosal and jugular ganglia. Syn-immunoreactivity was expressed by nerve fibers in the epithelium and taste bud of oral and cervical viscerae. These nerve fibers were abundant in the naso-pharynx, epiglottis and laryngeal vestibule. Some taste bud cells were also immunoreactive for Syn. In addition, Syn-ir nerve fibers were detected in the vicinity of macrophages, dendritic cells and Langerhans cells. ConclusionsSyn was abundant in the visceral sensory neurons but not in somatic sensory neurons. This protein may play a role in nociceptive and chemosensory transduction in the glossopharyngeal and vagal sensory ganglia. It is possible that Syn has a function about the immune mechanism of the upper air way.

Eya2 expression during mouse embryonic development revealed by Eya2lacZ knockin reporter and homozygous mice show mild hearing loss.

Eya2 expression during mouse development has been studied by in situ hybridization and it has been shown to be involved skeletal muscle development and limb formation. Here, we generated Eya2 knockout (Eya2- ) and a lacZ knockin reporter (Eya2lacZ ) mice and performed a detailed expression analysis for Eya2lacZ at different developmental stages to trace Eya2lacZ -positive cells in Eya2-null mice. We describe that Eya2 is not only expressed in cranial sensory and dorsal root ganglia, retina and olfactory epithelium, and somites as previously reported, but also Eya2 is specifically detected in other organs during mouse development. We found that Eya2 is expressed in ocular and trochlear motor neurons. In the inner ear, Eya2lacZ is specifically expressed in differentiating hair cells in both vestibular and cochlear sensory epithelia of the inner ear and Eya2-/- or Eya2lacZ/lacZ mice displayed mild hearing loss. Furthermore, we detected Eya2 expression during both salivary gland and thymus development and Eya2-null mice had a smaller thymus. As Eya2 is coexpressed with other members of the Eya family genes, these results together highlight that Eya2 as a potential regulator may act synergistically with other Eya genes to regulate the differentiation of the inner ear sensory hair cells and the formation of the salivary gland and thymus.

The Pathology of the Vestibular System in CANVAS.

To describe the site of lesion responsible for the severe, bilateral, symmetrical, selective loss of vestibular function in Cerebellar Ataxia with Neuronopathy and Vestibular Areflexia Syndrome (CANVAS), an adult-onset recessively-inherited ataxia, characterized by progressive imbalance due to a combination of cerebellar, somatosensory, and selective vestibular impairment with normal hearing. Histologic examination of five temporal bones and the brainstems from four CANVAS patients and the brainstem only from one more, each diagnosed and followed from diagnosis to death by one of the clinician authors. All five temporal bones showed severe loss of vestibular ganglion cells (cell counts 3-16% of normal), and atrophy of the vestibular nerves, whereas vestibular receptor hair cells and the vestibular nuclei were preserved. In contrast, auditory receptor hair cells, the auditory ganglia (cell counts 51-100% of normal), and the auditory nerves were relatively preserved. In addition, the cranial sensory ganglia (geniculate and trigeminal), present in two temporal bones, also showed severe degeneration. In CANVAS there is a severe cranial sensory ganglionopathy neuronopathy (ganglionopathy) involving the vestibular, facial, and trigeminal ganglia but sparing the auditory ganglia. These observations, when coupled with the known spinal dorsal root ganglionopathy in CANVAS, indicate a shared pathogenesis of its somatosensory and cranial nerve manifestations. This is the first published account of both the otopathology and neuropathology of CANVAS, a disease that involves the central as well as the peripheral nervous system.

Clinical Study on Outcome of Treatment for Herpes Zoster

Introduction: Herpes Zoster (HZ) is caused by reactivation of Varicella Zoster Virus (VZV). It is characterised by occurrence of grouped vesicles on erythematous base which involves the entire dermatome innervated by a single spinal or cranial sensory ganglion and is associated with radicular pain. Antivirals (Acyclovir, Famciclovir and Valacyclovir) started within 72 hours of onset of lesions are the agents of choice. Aim: To study the clinical manifestations, comorbidities, efficacy and safety of Acyclovir, complications and sequelae associated with HZ. Materials and Methods: A 3-year longitudinal cohort study was conducted in 212 adult patients (>18 years of age) suffering with HZ in the Department of Dermatology, Dhiraj General Hospital, Pipariya, Gujarat, India. In this study 212 patients with HZ were prescribed oral Acyclovir in a dose of 800 mg 5 times a day for 7 days. All patients were analysed in terms of clinical manifestations, pre-existing co-morbidities and incidence of complications. The clinical history and findings were recorded in a prestructured proforma. All patients were subjected to cytological examination (Tzanck smear) and Human immunodeficiency viruses (HIV) testing Enzyme-Linked Immunosorbent Assay (ELISA). Diagnosis was made primarily on the basis of clinical findings and presence of multinucleated giant cells in Tzanck smear. All the patients were treated with Oral Acyclovir. Cases were followed-up fortnightly for six weeks and evaluated for relief of symptoms, treatment outcome and complications/sequelae. Results: Two hundred and twelve cases were studied. One hundred and forty-two cases were in the 4th and 5th decades of life. Sixty-three cases had comorbidities like diabetes mellitus in 31, autoimmune diseases like pemphigus vulgaris, systemic lupus erythematosus, rheumatoid arthritis and inflammatory bowel disease in 19 and AIDS in 8 cases. Five cases had malignancy/lymphomas and were receiving chemotherapy for the same. In the majority, HZ occurred de novo without any comorbidities. The most common dermatomes involved were cervical and thoracic. Out of 212 cases Oral Acyclovir 800 mg was well tolerated by 74. Most common complication was Postherpetic Neuralgia (PHN), seen in 80 cases. Conclusion: The treatment of HZ with Oral Acyclovir 800 mg 5 times a day for 7 days is efficacious for healing of skin lesions and also reduces the chances of PHN if instituted within 72 hours.

Insights Into the Early Gene Regulatory Network Controlling Neural Crest and Placode Fate Choices at the Neural Border.

The neural crest (NC) cells and cranial placodes are two ectoderm-derived innovations in vertebrates that led to the acquisition of a complex head structure required for a predatory lifestyle. They both originate from the neural border (NB), a portion of the ectoderm located between the neural plate (NP), and the lateral non-neural ectoderm. The NC gives rise to a vast array of tissues and cell types such as peripheral neurons and glial cells, melanocytes, secretory cells, and cranial skeletal and connective cells. Together with cells derived from the cranial placodes, which contribute to sensory organs in the head, the NC also forms the cranial sensory ganglia. Multiple in vivo studies in different model systems have uncovered the signaling pathways and genetic factors that govern the positioning, development, and differentiation of these tissues. In this literature review, we give an overview of NC and placode development, focusing on the early gene regulatory network that controls the formation of the NB during early embryonic stages, and later dictates the choice between the NC and placode progenitor fates.

Vertebrate Sensory Ganglia: Common and Divergent Features of the Transcriptional Programs Generating Their Functional Specialization.

Sensory fibers of the peripheral nervous system carry sensation from specific sense structures or use different tissues and organs as receptive fields, and convey this information to the central nervous system. In the head of vertebrates, each cranial sensory ganglia and associated nerves perform specific functions. Sensory ganglia are composed of different types of specialized neurons in which two broad categories can be distinguished, somatosensory neurons relaying all sensations that are felt and visceral sensory neurons sensing the internal milieu and controlling body homeostasis. While in the trunk somatosensory neurons composing the dorsal root ganglia are derived exclusively from neural crest cells, somato- and visceral sensory neurons of cranial sensory ganglia have a dual origin, with contributions from both neural crest and placodes. As most studies on sensory neurogenesis have focused on dorsal root ganglia, our understanding of the molecular mechanisms underlying the embryonic development of the different cranial sensory ganglia remains today rudimentary. However, using single-cell RNA sequencing, recent studies have made significant advances in the characterization of the neuronal diversity of most sensory ganglia. Here we summarize the general anatomy, function and neuronal diversity of cranial sensory ganglia. We then provide an overview of our current knowledge of the transcriptional networks controlling neurogenesis and neuronal diversification in the developing sensory system, focusing on cranial sensory ganglia, highlighting specific aspects of their development and comparing it to that of trunk sensory ganglia.

Neural crest and placode roles in formation and patterning of cranial sensory ganglia in lamprey.

Vertebrates possess paired cranial sensory ganglia derived from two embryonic cell populations, neural crest and placodes. Cranial sensory ganglia arose prior to the divergence of jawed and jawless vertebrates, but the developmental mechanisms that facilitated their evolution are unknown. Using gene expression and cell lineage tracing experiments in embryos of the sea lamprey, Petromyzon marinus, we find that in the cranial ganglia we targeted, development consists of placode-derived neuron clusters in the core of ganglia, with neural crest cells mostly surrounding these neuronal clusters. To dissect functional roles of neural crest and placode cell associations in these developing cranial ganglia, we used CRISPR/Cas9 gene editing experiments to target genes critical for the development of each population. Genetic ablation of SoxE2 and FoxD-A in neural crest cells resulted in differentiated cranial sensory neurons with abnormal morphologies, whereas deletion of DlxB in cranial placodes resulted in near-total loss of cranial sensory neurons. Taken together, our cell-lineage, gene expression, and gene editing results suggest that cranial neural crest cells may not be required for cranial ganglia specification but are essential for shaping the morphology of these sensory structures. We propose that the association of neural crest and placodes in the head of early vertebrates was a key step in the organization of neurons and glia into paired sensory ganglia.

Cell fate decisions during the development of the peripheral nervous system in the vertebrate head.

Sensory placodes and neural crest cells are among the key cell populations that facilitated the emergence and diversification of vertebrates throughout evolution. Together, they generate the sensory nervous system in the head: both form the cranial sensory ganglia, while placodal cells make major contributions to the sense organs-the eye, ear and olfactory epithelium. Both are instrumental for integrating craniofacial organs and have been key to drive the concentration of sensory structures in the vertebrate head allowing the emergence of active and predatory life forms. Whereas the gene regulatory networks that control neural crest cell development have been studied extensively, the signals and downstream transcriptional events that regulate placode formation and diversity are only beginning to be uncovered. Both cell populations are derived from the embryonic ectoderm, which also generates the central nervous system and the epidermis, and recent evidence suggests that their initial specification involves a common molecular mechanism before definitive neural, neural crest and placodal lineages are established. In this review, we will first discuss the transcriptional networks that pattern the embryonic ectoderm and establish these three cell fates with emphasis on sensory placodes. Second, we will focus on how sensory placode precursors diversify using the specification of otic-epibranchial progenitors and their segregation as an example.

BDNF and NGF signals originating from sensory ganglia promote cranial motor axon growth.

After exiting the hindbrain, branchial motor axons reach their targets in association with sensory ganglia. The trigeminal ganglion has been shown to promote motor axon growth from rhombomeres 2/3 and 4/5, but it is unknown whether this effect is ganglion specific and through which signals it is mediated. Here, we addressed these questions by co-cultures of ventral rhombomere 8 explants with cranial and spinal sensory ganglia in a collagen gel matrix. Our results show that all cranial sensory ganglia and even a trunk dorsal root ganglion can promote motor axon growth and that ganglia isolated from older embryos had a stronger effect on the axonal growth than younger ones. We found that brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) are necessary and sufficient for this effect. Altogether, our results demonstrate that the promoting effect of sensory ganglia on cranial motor axon growth is stage dependent, but not ganglion specific and is mediated by BDNF and NGF signals.

Extensive apoptosis during the formation of the terminal nerve ganglion by olfactory placode-derived cells with distinct molecular markers

The terminal nerve ganglion (TNG) is a well-known structure of the peripheral nervous system in cartilaginous and teleost fishes. It derives from the olfactory placode during embryonic development. While the differentiation and migration of gonadotropin releasing hormone (GnRH)-expressing neurons from the olfactory placode has been well documented, the TNG has been neglected in birds and mammals, and its development is less well described. Here we describe the formation of a ganglion-like structure from migratory olfactory placodal cells in chicken. The TNG is surrounded by neural crest cells, but in contrast to other cranial sensory ganglia, we observed no neural crest corridor, and olfactory unsheathing cells appear only after the onset of neuronal migration. We identified Isl1 and Lhx2 as two transcription factors that label neuronal subpopulations in the forming TNG, distinct from GnRH1+ cells, thereby revealing a diversity of cell types during the formation of the TNG. We also provide evidence for extensive apoptosis in the terminal nerve ganglion shortly after its formation, but not in other cranial sensory ganglia. Moreover, at later stages placode-derived neurons expressing GnRH1, Isl1 and/or Lhx2 become incorporated in the telencephalon. The integration of TNG neurons into the telencephalon together with the earlier widespread apoptosis in the TNG might be an explanation why the TNG in mammals and birds is much smaller compared to other vertebrates.

VARICELLA-ZOSTER VIRUS CNS DISEASE CLINICAL FEATURES IN UKRAINIAN PATIENTS. PROSPECTIVE STUDY

Introduction: Herpes zoster (HZ), or shingles, is localized disease characterized by unilateral radicular pain and a vesicular rash limited to the area of skin innervated by a single dorsal root or cranial sensory ganglion. Whereas varicella, or chickenpox, results from primary exogenous varicella-zoster virus (VZV) infection, HZ is caused by reactivation of endogenous VZV that has persisted in latent form within sensory ganglia following an earlier episode of chickenpox. The aim: To explore the clinical features, diagnosis, and treatment of CNS injury caused by VZV infection in a prospective single center study from January 2014 to January 2018. Materials and methods: 117 adult patients, among which young women predominated with confirmed VZV infection were analyzed in the study. CSF and blood contents, antibody for herpes zoster M and G classes, and MRI scans have been studied, but the crucial diagnostic sign was the presence of specific viral DNA in the CSF or blood. The main clinical manifestations of the disease were ganglionitis and ganglioradiculoneuritis. Another brain lesion like uveitis, encephalitis and vasculitis were observed also. A clinical case of an unusual course of VZV-infection is given. Results and conclusions: The most common clinical variants of HZ were ganglionitis (69.7%). Cranial localization was observed in 31% of patients, spinal one - in 38.7%, injury to the meninges was found in 16.3% of patients.