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Other Neurologic Diseases in Pregnancy
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Loralei L. Thornburg, Meredith L. Birsner
Guillain–Barré syndrome is a clinical diagnosis, and many of the presenting symptoms can be initially subtle before progressing to rapidly progressive paralysis. The differential is wide, and in the event of new symptoms, a throughout workup of a CNS disorders, acute neuropathies, etc., is warranted. Once the diagnosis has been established, the safety and effectiveness of plasmapheresis (aka plasma exchange) and/or IVIG to treat GBS is clear and are considered first-line therapy for this diagnosis. Both of these are safe during pregnancy. Timely immunotherapy and comprehensive support are critical to improving recovery [43]. Inpatient monitoring with close monitoring of respiratory status is necessary, as respiratory failure and dysautonomia are common [44]. While most patients will improve, prognosis is variable and mortality 2–10% [45]. If acute Guillain–Barré syndrome occurs in late pregnancy, preterm labor has been reported [46]. Delivery or pregnancy termination does not alter the course or prognosis of the disease, and should be reserved for obstetrical indications. For those with respiratory failure in late pregnancy, delivery may help to reduce physiology changes/pressures on the diaphragm, but will not alter the course of GBS disease.
Case 12
Published in Andrew Solomon, Julia Anstey, Liora Wittner, Priti Dutta, Clinical Cases, 2021
Andrew Solomon, Julia Anstey, Liora Wittner, Priti Dutta
Although Guillain–Barré syndrome is a clinical diagnosis, there are supportive tests which may be useful.Lumbar puncture shows high protein levels with normal cell counts. This is known as cytoalbuminaemic dissociationRepeated spirometry is required to assess for deterioration in lung functionNerve conduction studies are abnormal in 85% of patientsTesting for antiganglioside antibodies: anti-GM1, anti-GD1b, anti-GT1a, anti-GD1a and anti-GQ1b may all be positive. There is some evidence to suggest that different antibodies are associated with different subtypes of the disease and may reflect prognosis
Examine the lower limbs
Published in Hani TS Benamer, Neurology for MRCP PACES, 2019
Q: What is the treatment of Guillain–Barré syndrome? Regular monitoring of forced vital capacity, as the patient is at risk of respiratory failure.Regular monitoring of blood pressure and heart rhythm, as the patient is at risk of autonomic neuropathy.Low-dose subcutaneous heparin to prevent venous thrombo-embolism.Intensive-care support, as ventilation may be needed.Intravenous immunoglobulin.Neurorehabilitation.
Nervous system involvement in SARS-coronavirus infection: a review on lessons learned from the previous outbreaks, ongoing pandemic and what to expect in the future
Published in International Journal of Neuroscience, 2022
Atiq ur Rehman Bhatti, Jad Zreik, Yagiz Ugur Yolcu, Mohammed Ali Alvi, Kingsley Abode-Iyamah, Alfredo Quinones-Hinojosa, Mohamad Bydon
Given the increasing evidence of neurological manifestations secondary to COVID-19, understanding the potential mechanisms of this association may aid treatment efforts. Recent reports have identified patients developing sensory loss such as smell and taste. It has been hypothesized that these symptoms are the result of inflammation in the central nervous system (CNS) such as the medulla oblongata or olfactory bulb [17–19]. However, this is largely unsupported by epidemiological evidence due to the difficulty in differentiating the pathway in the midst of a systemic infection. Another potential mechanism includes over-stimulation of the immune system in response to acute infection to the point where nerve cells are unintentionally targeted [20]. This may explain the recent reports of Guillain-Barre syndrome presenting in COVID-19 patients, but it should also be noted that the mechanism of this specific association has not yet been studied. Reports of encephalitis have also suggested direct viral injury of nervous tissue [21]. Overall, while potential mechanisms have been cautiously deduced, further studies are necessitated to better our understanding of the mechanisms by which neurological complications are manifested.
Men and COVID-19: the aftermath
Published in Postgraduate Medicine, 2020
There has also been significant neurological morbidity as a result of the virus, both as a result of direct neuro-invasion through the high ACE2 expression within the nervous system allowing the virus to cross the blood-brain barrier and direct entry via the olfactory bulb and vagus nerve [79,80]. The symptoms can include stroke, seizures, headache, dizziness, delirium, hypogeusia, and hyposmia [81,82,83]. There have also been 11 confirmed cases of Guillain-barre syndrome [83]. In a prospective study in Italy that explored subjective neurological symptoms (sNS) in 103 hospitalized patients 54 out of 59 men (91.5%) and 40 out of 44 women (90.9%) reported at least one sNS [84]. The most frequent symptoms were sleep impairment (51/103; 49.51%); dysgeusia (48/103; 46.60%), headache (40/103; 38.83%), hyposmia (40/103; 38.83%), and depression (39/103; 37.86%).
The immunotherapy of Guillain-Barré syndrome
Published in Expert Opinion on Biological Therapy, 2018
Paula Restrepo-Jiménez, Yhojan Rodríguez, Paulina González, Christopher Chang, M. Eric Gershwin, Juan-Manuel Anaya
In 1916, three physicians, Guillain, Barré, and Strohl described a syndrome of acute peripheral neuropathy with cerebrospinal fluid (CSF) analysis showing a typical albumino-cytological dissociation and nerve conduction studies with mild alterations. They described two patients presenting with motor symptoms and abolition of deep tendon reflexes, but with preserved cutaneous reflexes and paresthesias without an objective sensory loss [1]. Guillain–Barré syndrome (GBS) has since been described as an acute neuropathy characterized by a rapidly progressive and self-limited weakness [2] which can be quite severe, and can lead to respiratory failure; in many cases with paresthesias and pain, among other complications. That´s why we consider it now a disabling neuromuscular disorder and not a ‘benign’ form of limb weakness as it was described initially [3].