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Spinal Cord Disease
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Two distinct phenotypes: Acute transverse myelitis: Intramedullary infection and associated inflammation.Not specific to cord tracts or cell types.Acute onset of fever with any combination of neurologic deficits attributable to the spinal cord (sensory disturbance, autonomic dysfunction, weakness with hyper- or hyporeflexia, the latter reflecting either anterior horn involvement or spinal shock).Acute flaccid paralysis: Viral affinity for anterior horn cell (poliovirus model).Prodromal illness with fever and mental status changes.Acute onset of a pure LMN pattern of weakness in one or more limbs without sensory or autonomic dysfunction.
Enteroviruses
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Karen Straube-West, Burk Jubelt
Acute flaccid paralysis usually begins with fever, flu-like symptoms, and sometimes muscle cramps followed by muscle weakness in one or more limbs. The prodromal symptoms may not occur with EV70. Paralysis is usually asymmetrical, flaccid, more proximal than distal, and often patchy [70]. The reflexes are lost as paralysis progresses. Over the next several days, paralysis may develop in other extremities and bulbar involvement with impaired respiration may occur. Extension of paralysis is unlikely to occur after the fifth or sixth day. Paralysis caused by coxsackievirus and ECHO are usually mild compared with that seen with PV, EV70, and EV71. Generally, the weakened muscles regain some strength. The differential diagnosis of paralytic disease should thus include all of the enteroviruses that can cause paralysis (Table 17.4). In addition, several other viruses, e.g., rabies [64], herpes zoster [71], and West Nile virus [72], can occasionally cause acute lower motor neuron paralysis. Other entities in the differential include acute inflammatory polyradiculitis (Guillain–Barré syndrome), botulism, acute toxic neuropathies, acute intermittent porphyria, acute transverse myelitis, and acute spinal cord compression from epidural abscess [73–75].
Guillain–Barré syndrome
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Manual of Neuroanesthesia, 2017
Electrodiagnostic testing: Electrodiagnostic testing is performed to support the diagnosis of flaccid paralysis due to peripheral neuropathy. The features of demyelination include slow conduction velocities, temporal dispersion, and increased latencies.23 Another characteristic of electrodiagnostic testing in patients with GB syndrome is “sural nerve sparing.” The sensory response pattern to the sural nerve is normal, but there is impaired sensory conduction in the upper limb. This pattern is observed within 1 week of illness in half of the patients with GB syndrome.23,24
Acute motor axonal neuropathy following SARS-CoV-2 infection in the third trimester of pregnancy
Published in Baylor University Medical Center Proceedings, 2022
Mohamed M. G. Mohamed, Amar Jadhav, Polo Banuelos, Alexandre Lacasse, Vikas Kumar
GBS is a heterogenous group of disorders characterized by flaccid ascending paralysis.4 It is the most common cause of flaccid paralysis in the US and worldwide.4 GBS is hypothesized to be of autoimmune origin, often preceded by an infectious process. Molecular mimicry appears to play a role in its pathophysiology, with different targets leading to different subtypes.3–5 Since pregnancy is usually associated with a dampened immunological response, GBS is an uncommon disorder in pregnancy.4,6 SARS-CoV-2 infection has also been implicated in patients presenting with GBS.2,3 Although AMAN has been previously reported in pregnant patients,7,8 its diagnosis following SARS-CoV-2 infection has not been widely reported.
The dynamic expression of canonical Wnt/β-catenin signalling pathway in the pathologic process of experimental autoimmune neuritis
Published in International Journal of Neuroscience, 2020
Yin Liu, Shuping Liu, Sijia Pan, Qiaoyu Gong, Jiajia Yao, Zuneng Lu
GBS is an autoimmune disease and an acute inflammation disorder that affects the peripheral nerve system (PNS) and is characterized by rapidly progressive paralysis, loss of deep tendon reflexes in the extremities, absent or mild sensory signs, and variable autonomic dysfunctions [1, 2]. It is currently the most frequent cause of acute flaccid paralysis worldwide and constitutes one of the serious emergencies in neurology. The major histopathological changes in GBS are inflammatory cell infiltration into the PNS with neuroinflammation, demyelination and axonal injury [3]. Experimental autoimmune neuritis (EAN) is a CD4+ T cell-mediated autoimmune disease of the PNS that is used as an animal model of GBS. Both cellular and humoural immune responses are implicated in its pathogenesis [4]. It has been proposed that inflammatory mediators produced in the affected sciatic nerve are involved in the pathogenesis of EAN. In general, an adequate balance between proinflammatory and immune dampening cytokines, i.e. the Th1/Th2 balance, is necessary for a successful immune response, whereas a disturbed balance may lead to disease [5]. Th1 cells are thought to induce cell-mediated autoimmune diseases, whereas Th2 cells suppress such diseases [5, 6]. Th1 cytokines include IFN-γ, TNF-α and IL-1β, Th2 cytokines include IL-4, IL-5, IL-10 and IL-13, and the unbalance of Th1 and Th2 cells has a direct relevance to autoimmune responses. GBS and EAN feature an acute onset and monophasic course of diseases, but the specific mechanism driving the limitation is not yet clear.
Clinical characteristics of children infected with enterovirus D68 in an outpatient clinic and the association with bronchial asthma
Published in Infectious Diseases, 2018
Tsutomu Itagaki, Yoko Aoki, Yohei Matoba, Shizuka Tanaka, Tatsuya Ikeda, Katsumi Mizuta, Yoko Matsuzaki
Our study revealed that EV-D68 infection in children is predominantly associated with upper respiratory tract illness and is accompanied by cough and mild fever, which persist for 1–2 days. Acute flaccid paralysis was observed in one of the 31 EV-D68 cases in 2010 (3.2%). EV-D68 was not detected in a cerebrospinal fluid sample, similar to most cases of acute flaccid paralysis with EV-D68-positive respiratory samples in the USA in 2014 [25]. Although neurological effects are uncommon, EV-D68 might be associated with neurological diseases, including acute flaccid myelitis [25]. However, the CDC reported a large number of acute flaccid myelitis cases in 2016 with minimal EV-D68 detection [38]. Thus, the association between EV-D68 and acute flaccid myelitis, other than a temporal association in 2014, remains unclear.