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Fifi
Published in Walter J. Hendelman, Peter Humphreys, Christopher R. Skinner, The Integrated Nervous System, 2017
Walter J. Hendelman, Peter Humphreys, Christopher R. Skinner
Fifi has a relatively rapid-onset disease evolving over 48 hours; it is characterized by severe limb, facial and pharyngeal weakness accompanied by distal extremity numbness and paresthesiae. The presence of proximal and distal limb weakness, complete areflexia and flexor plantar responses is consistent with a generalized polyradiculoneuropathy. Given the recent history of a respiratory illness, the most likely diagnosis is an acute inflammatory demyelinating polyneuropathy, otherwise known as Guillain–Barré syndrome.
HIV and AIDS Pain
Published in Mark V. Boswell, B. Eliot Cole, Weiner's Pain Management, 2005
Maurice Policar, Vasanthi Arumugam
Two major forms of demyelinating polyradiculopathy have been reported in HIV-infected patients: acute inflammatory demyelinating polyneuropathy (AIDP) and chronic inflammatory demyelinating polyneuropathy (CIDP). AIDP, also known as Guillain–Barre syndrome (GBS), has been reported in HIV-infected patients, usually occurring at the time of seroconversion or in asymptomatic individuals with CD4 cell counts > 500.
Changes Associated with CNS Infections Caused by the Herpesvirus Varicella Zoster Virus (VZV) and Models of VZV Neurotropism
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
Varicella is also rarely associated with a diagnosis of myelitis, reflecting inflammation of the spinal cord. This causes a range of symptoms from near subclinical acute signs to headache, fever, pain, chronic loss of limb movements or sensation, and bowel dysfunction. Myelitis may reflect VZV spreading from the dorsal root ganglia to the spinal cord at a stage of replication in the ganglia prior to the initiation of latency. It is more commonly associated with zoster and ganglionic replication after reactivation. In most patients, myelitis is mild and recovery is the norm. The eye may become involved in varicella in a rare optic neuritis (Galbussera et al. 2006), and there is linkage of this with a diagnosis of myelitis. Varicella is also associated with rare cases of meningitis and encephalitis in which virus involvement of the brain parenchyma or meninges occurs with inflammation. These can have dramatic clinical symptoms such as reduced levels of consciousness, seizures, headache, and vomiting (Guess et al. 1986). As other viruses and infectious agents cause myelitis, encephalitis, and encephalomyelitis, rapid diagnosis is critical in the management and rapid antiviral treatment of the disease (Ben-Amor et al. 2011). If not managed, sequelae such as paresis, seizures, and mental retardation may follow. Encephalitis has also been encountered in adults with varicella. Acute inflammatory demyelinating polyneuropathy (also called Guillain—Barré syndrome) is a rare complication of varicella, in which a polyradiculopathy occurs, which may be accompanied by cranial nerve palsies that affect facial expression and ocular muscles. Finally, vasculitis and stroke have also been associated with varicella and may underlie a diagnosis of VZV encephalitis (Gilden et al. 2009; Hosseinipour et al. 1998; Nagel et al. 2010).
COVID-19 and MOG-IgG–associated acquired demyelinating polyneuropathy compatible with chronic inflammatory demyelinating polyneuropathy in a previously healthy girl
Published in Baylor University Medical Center Proceedings, 2022
Asra Akbar, Gregory M. Blume, Sean Creeden, Sharjeel Ahmad
COVID-19 can cause general central nervous system manifestations including encephalopathy, seizures, and worsening of autoimmune disease. Peripheral nervous system involvement has been reported in patients with COVID-19 infection.6 The incidence of neurological complications such as acquired demyelinating neuropathy has increased during the SARS-CoV-2 pandemic,7 but the data are limited in the pediatric population. COVID-19 and associated acquired demyelinating and autoimmune neuropathy such as acute inflammatory demyelinating polyneuropathy is documented in adults but has been rarely reported in the pediatric population.8–13 The potential association between SARS-CoV-2 infection and exacerbations of neuroimmunological disorders remains speculative, but is certainly probable.
Headache and intracranial hypertension in Guillain-Barré syndrome: a case report and literature review
Published in International Journal of Neuroscience, 2019
Tong Wang, Zhe Wang, Zhangyu Guo
Guillain-Barré syndrome (GBS), also known as acute inflammatory demyelinating polyneuropathy, is an immune reaction affecting the peripheral nervous system. Most patients have normal cerebrospinal fluid pressure. Headache and increased intracranial pressure in GBS was relatively rare [1]. A majority of the patients have been children. Most of the patients of headache in GBS place it in the context of the posterior reversible encephalopathy syndrome which is in association with dysautonomia-related GBS complication. There are also a few reports of headache in the setting of increased CSF pressure and papilledema [2]. Besides, the etiology and mechanism of headache and increased CSF pressure were still unknown. Here, we describe a female diagnosed as GBS with intracranial hypertension during recovery period and recovered rapidly by lateral ventricle drainage.
Study of total duration of distal compound muscle action potential in demyelinating and axonal Guillain-Barre’ syndrome
Published in Neurological Research, 2023
Federica Ginanneschi, David Cioncoloni, Giorgio Capoccitti, Nila Volpi, Fabio Ferretti, Fabio Giannini, Alessandro Rossi
Diagnosis of Guillain-Barrè Syndrome (GBS) is based on a collection of clinical, biological and electrophysiological criteria. Nerve conduction studies can support the diagnosis and allow defining the subtype (i.e. myelin or axonal) of GBS. Subtyping the GBS is crucial to further unravel the relationship with preceding infections, anti-ganglioside antibodies, prognosis and treatment response. However, in the early phase of GBS, the distinction between acute inflammatory demyelinating polyneuropathy (AIDP) and axonal GBS may be hard in some patients, mainly due to the lack of specificity of electrophysiological criteria for demyelination [1].