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Leprosy (Hansen's Disease)
Published in Scott M. Jackson, Skin Disease and the History of Dermatology, 2023
On the other end of the spectrum is the lepromatous form of the disease, characterized by widespread nodules and plaques, nasal congestion and nosebleeds, loss of eyebrow hair, progressive infiltration of the face with the eventual development of leonine facies, lymph node and internal organ involvement, and nerve damage and resultant neuropathy so severe that ulceration, infection, and amputation of digits—or even limbs—might ensue. Neurological symptomatology is very frequently the first sign of the disease since the organism shows a tendency to thrive in the Schwann cells of peripheral nerves. Ample organisms are seen on the biopsy of these patients' skin lesions because the host response is poor and the organism thrives; another term for this form is multibacillary disease. The most common form of the disease is actually somewhere in the middle of the spectrum between tuberculoid and lepromatous, which has been termed borderline leprosy, as it presents with features of both. Today, HD is an illness that can be treated successfully with antibiotics. Due to the rapid development of antibiotic resistance with single-agent regimens, multi-drug treatment is recommended with rifampin, clofazimine, and dapsone.
Neurologic Diagnosis
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
This follows primary damage of the myelin sheath by a disturbance of Schwann cell metabolism (e.g. some hereditary neuropathies), a direct immune-mediated attack on the myelin or the Schwann cell (e.g. Guillain–Barré syndrome), or toxic damage to the myelin sheath (e.g. diphtheria toxin).
The Opioid Epidemic
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
Glial cells play an important role in creating a neuroinflammatory state. As non-neuronal cells inhabiting the central nervous system and peripheral nervous system, glial cells play a supportive role in maintenance and regulation. Glial cells include oligodendrocytes, astrocytes, ependymal cells, and microglia in the central nervous system. Schwann cells and satellite cells support the peripheral nervous system. Microglia cells are particularly important and serve as resident macrophages in the brain and spinal cord, and as such are active against damaged neurons and infectious agents. At rest, microglia do not typically contribute to the synaptic milieu of neurotransmitters. This is in contrast to astrocytes which play an active function in taking up and releasing neurotransmitters.
Outcome measures and biomarkers in chronic inflammatory demyelinating polyradiculoneuropathy: from research to clinical practice
Published in Expert Review of Neurotherapeutics, 2021
Jeffrey A. Allen, Filip Eftimov, Luis Querol
There is no known biomarker that reliably reflects myelin damage. Plasma levels of the Schwann cell-specific transmembrane protease serine 5 protein (TMPRSS5) were shown to be significantly elevated in Charcot-Marie-Tooth disease [56]; however, its role as a biomarker in acquired demyelinating neuropathies is unknown. There is some evidence that CSF sphingomyelin, a myelin-enriched lipid, may be a useful diagnostic and disease activity biomarker. Diagnostically, sensitivity (80.8%) and specificity (98.8%) in patients with acute and chronic demyelinating polyradiculoneuropathies is favorable. CSF sphingomyelin also has been shown to be higher in patients with active CIDP compared to those with stable disease and compared to axonal controls, suggesting its potential role as a disease activity biomarker [57]. Further study of CSF sphingomyelin in large cohorts of patients at various stages of disease is needed before it can be adopted into routine clinical care.
Therapeutic potential of Mucuna pruriens (Linn.) on ageing induced damage in dorsal nerve of the penis and its implication on erectile function: an experimental study using albino rats
Published in The Aging Male, 2020
Prakash Seppan, Ibrahim Muhammed, Karthik Ganesh Mohanraj, Ganesh Lakshmanan, Dinesh Premavathy, Sakthi Jothi Muthu, Khayinmi Wungmarong Shimray, Sathya Bharathy Sathyanathan
Present study reiterate that myelin through Schwann cells provides important structural, electrical, and trophic support to the nerve. Demyelination or hypomyelination implicated in several diseases and lead to poor action potential propagation and dampen axonal conductivity. In general, the clinical analyses and remediating the conductivity between axon and target organ in the pathological setting is a challenge. Exploring the possibility of myelin repair as an achievable therapeutic target mediated through AR is a bright prospect. With aging there is an increased possibility of DNP disturbance, M. pruriens has shown beneficial effects through AR expression in nerve regeneration and preservation of endothelial function and corpus cavernosum from fibrosis [10,48–50]. However, further study on neuromuscular mechanisms are to be determined. Similarly, analysis of unknown neurotrophins or cytokines may participate in this process and research has recently been initiated in our laboratory to further elucidate these pathways.
Ultrastructural effects of nerve growth factor and betamethasone on nerve regeneration after experimental nerve injury
Published in Ultrastructural Pathology, 2020
Leman Sencar, Mustafa Güven, Dilek Şaker, Tuğçe Sapmaz, Abdullah Tuli, Sait Polat
It is widely accepted that in the distal of the main-injured area following nerve injury, NGF is released from the axons and Schwann cells and taken from nerve terminals and is then transmitted to neuron perikaryon through retrograde axonal transmission, thus stimulating axon regeneration.18,24 It is thought that the Schwann cells also have important roles in peripheral nerve regeneration. Consequently, studies have pointed out that NGF receptors increase in Schwann cells as a result of axonal injury.5 It has been recorded that Schwann cells synthesized cell adhesion molecules and facilitated axonal orientation and regeneration in this way as a result of the injury.16,24 In our study, exogen NGF was given to the rats for 2 weeks in order to compensate for this. Due to the fact that the nerve fibers and cellular structure were relatively maintained in NGF-treated groups and there was more functional recovery than the experimental control group, it can be suggested that Schwann cells probably proliferated and provided axonal regeneration in the injured area with the stimulatory effect of NGF.