Acute post-infective peripheral neuropathy (Guillain–Barré syndrome)

2012 ◽  
pp. 276-277
Author(s):  
Steve Yentis ◽  
Surbhi Malhotra
Keyword(s):  
Peripheral Neuropathy ◽  
Guillain Barre Syndrome ◽  
Guillain Barré Syndrome ◽  
Guillain Barré

scholarly journals Zika virus infection causes temporary paralysis in adult mice with motor neuron synaptic retraction and evidence for proximal peripheral neuropathy

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
John D. Morrey ◽  
Alexandre L. R. Oliveira ◽  
Hong Wang ◽  
Katherine Zukor ◽  
Mateus Vidigal de Castro ◽  
...  
Keyword(s):  
Peripheral Neuropathy ◽  
Virus Infection ◽  
Motor Neurons ◽  
Zika Virus ◽  
Acute Flaccid Paralysis ◽  
Flaccid Paralysis ◽  
Guillain Barre Syndrome ◽  
Zika Virus Infection ◽  
Guillain Barré Syndrome ◽  
Guillain Barré

AbstractClinical evidence is mounting that Zika virus can contribute to Guillain-Barré syndrome which causes temporary paralysis, yet the mechanism is unknown. We investigated the mechanism of temporary acute flaccid paralysis caused by Zika virus infection in aged interferon αβ-receptor knockout mice used for their susceptibility to infection. Twenty-five to thirty-five percent of mice infected subcutaneously with Zika virus developed motor deficits including acute flaccid paralysis that peaked 8-10 days after viral challenge. These mice recovered within a week. Despite Zika virus infection in the spinal cord, motor neurons were not destroyed. We examined ultrastructures of motor neurons and synapses by transmission electron microscopy. The percent coverage of motor neurons by boutons was reduced by 20%; more specifically, flattened-vesicle boutons were reduced by 46%, and were normalized in recovering mice. Using electromyographic procedures employed in people to help diagnose Guillain-Barré syndrome, we determined that nerve conduction velocities between the sciatic notch and the gastrocnemius muscle were unchanged in paralyzed mice. However, F-wave latencies were increased in paralyzed mice, which suggests that neuropathy may exist between the sciatic notch to the nerve rootlets. Reversible synaptic retraction may be a previously unrecognized cofactor along with peripheral neuropathy for the development of Guillain-Barré syndrome during Zika virus outbreaks.

A Case of Peripheral Neuropathy Combined with Leukoencephalopathy after Injection with Intrathecal Methotrexate and Vincristine.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4348-4348
Author(s):  
Hae-sang Lee ◽  
Hyun Joo Jung ◽  
Jun Eun Park
Keyword(s):  
Peripheral Neuropathy ◽  
Acute Lymphocytic Leukemia ◽  
Deep Tendon Reflex ◽  
Lymphocytic Leukemia ◽  
Guillain Barre Syndrome ◽  
Sensory Loss ◽  
Intrathecal Methotrexate ◽  
Gradual Improvement ◽  
Guillain Barré Syndrome ◽  
Guillain Barré

Abstract Vincristine and methotrexate are the anchor drugs in the treatment of acute lymphocytic leukemia. The neurological complications caused by either vincristine or methotrexate have been well documented. A 10 year-old girl diagnosed acute lymphocytic leukemia without central nervous involvement and treated with CCG 1882 based therapy. She suffered from ascending paralysis from lower extremities without seizure or mental change three days after the fifth dose of vincristine and the fifth dose of intrathecal methotrexate during consolidation chemotherapy composed of 3-drug(vincristine, methotrexate, and L-asparaginase). Two days later, she developed dysarthria and respiratory discomfort. Her neurological examination showed a symmetric, flaccid, quadriparesis with loss of deep tendon reflex. But, she did not have sensory loss. We thought Guillain-Barre syndrome as first impression and carried out diagnostic evaluation. Viral study revealed no abnormality and cerebrospinal fluid study was not consistent with Guillain-Barre syndrome or infectious disease. Diffusion weighted magnetic resonance imaging showed a well-demarcated area of moderately high signal intensity in the white mater of the both parietal lobes. Neuromuscular conduction test revealed severe amplitude reduction in motor nerve action potential meaning on peripheral polyneuropathy. These findings were corresponded with drug-induced peripheral neuropathy and chemotherapy-related leukoencephalopathy that was detected incidentally. She did not receive further doses of vincristine and intrathecal methotrexate during the consolidation phase. There was gradual improvement of the weakness in the both lower and upper limbs for 3 months. She was recovery to walk with minimal support. We report peripheral neuropathy combined with subclinical leukoencephalopahty after injection with intrathecal methotrexate and vincristine.

scholarly journals Immune-Related Neurological Toxicities of PD-1/PD-L1 Inhibitors in Cancer Patients: A Systematic Review and Meta-Analysis

2020 ◽  
Vol 11 ◽  
Author(s):  
Yuan Tian ◽  
Aiqin Gao ◽  
Qing Wen ◽  
Shuyun Wang ◽  
Shuisheng Zhang ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Peripheral Neuropathy ◽  
Cancer Patients ◽  
Meta Analysis ◽  
Sensory Neuropathy ◽  
Guillain Barre Syndrome ◽  
Peripheral Sensory Neuropathy ◽  
Guillain Barré Syndrome ◽  
Guillain Barré ◽  
Peripheral Sensory

BackgroundSystematic assessment of PD-1/PD-L1 inhibitor-related neurological toxicities is important for guiding anti-PD-1 and anti-PD-L1 immunotherapy. Therefore, we conducted this meta-analysis to reveal the relationship between PD-1/PD-L1 inhibitors and neurological toxicities among cancer patients.MethodsClinical trials investigating PD-1/PD-L1 inhibitors in cancer patients were identified by a systematic search of PubMed. The random-effect model was used to synthesize individual studies. Neurological toxicities, including all-grades and grades 3–5, were taken into account for the final comprehensive meta-analysis. The Newcastle Ottawa Scale (NOS) was used to assess the quality of included trials.ResultsThirty-one clinical trials containing data of neurological toxicities were included. Compared with chemotherapy, the risk of all-grade neurological toxicities caused by PD-1/PD-L1 inhibitors was much lower in terms of peripheral neuropathy [OR = 0.07, 95%CI:(0.04, 0.13)], peripheral sensory neuropathy [OR = 0.07, 95%CI(0.04, 0.12)], dysgeusia [OR = 0.26, 95%CI:(0.19, 0.35)], paraesthesia [OR = 0.23, 95%CI:(0.14, 0.36)], and polyneuropathy [OR = 0.12, 95%CI:(0.01, 0.94)]. However, for grades 3–5, the statistically significant results were only seen in peripheral neuropathy [OR = 0.15, 95%CI:(0.07, 0.34)] and peripheral sensory neuropathy [OR = 0.13, 95%CI:(0.04, 0.40)]. No statistically significant difference regarding the risk of headache, dizziness, and Guillain–Barré syndrome was found between PD-1/PD-L1 inhibitors and chemotherapy. For PD-1/PD-L1 inhibitors plus chemotherapy, the risk trends of the above-mentioned neurological toxicities, especially grades 3–5 peripheral neuropathy [OR = 1.76, 95%CI:(1.10, 2.82)] was increased compared to chemotherapy alone.ConclusionOur comprehensive analysis showed that PD-1/PD-L1 inhibitors alone exhibited lower neurological toxicities than chemotherapy. However, the risk of headache, dizziness, and Guillain–Barré syndrome was similar between PD-1/PD-L1 and chemotherapy. For PD-1/PD-L1 inhibitors plus chemotherapy, the incidence trend of neurological toxicities would be increased, especially for peripheral neuropathy of grades 3–5.

scholarly journals Acute Brucellosis with a Guillain-Barre Syndrome-Like Presentation: A Case Report and Literature Review

2021 ◽  
Vol 13 (1) ◽  
pp. 1-10
Author(s):  
Ali Alanazi ◽  
Sara Al Najjar ◽  
Jnadi Madkhali ◽  
Yaser Al Malik ◽  
Athal Al-Khalaf ◽  
...  
Keyword(s):  
Peripheral Neuropathy ◽  
Literature Review ◽  
Guillain Barre Syndrome ◽  
Serological Tests ◽  
Brucella Infection ◽  
Guillain Barré Syndrome ◽  
History Of ◽  
Guillain Barré ◽  
Age Range ◽  
Spine Mri

Introduction: Brucellosis is a zoonotic disease that can affect the central and peripheral nervous system and it has variable neurological manifestation. However, brucellosis infection that presents with acute peripheral neuropathy mimicking Guillain-Barre syndrome (GBS) is rarely reported in the literature. Objective and method: We report a 56-year-old man who was initially diagnosed with GBS, and then he was confirmed to have acute Brucella infection. We also did a systematic literature review to study the natural history and management of previously reported cases of brucellosis that presented with manifestations consistent with GBS. Results: We found 19 (including our patient) cases of brucellosis that presented with GBS-like manifestations. The age range was 9–62 years. Eight (42.1%) patients had a history of fever. Seven (36.8%) patients had no constitutional symptoms. Five (26.3%) patients had splenomegaly. Brucella serological tests were positive in all patients, while blood Brucella culture was positive in three (37.5%) out of eight patients. Albuminocytological dissociation was present in nine (64.3%) out of 14 patients. Nerve conduction studies and electromyography were consistent with demyelination polyneuropathy in eight (42.1%) patients, with axonal polyneuropathy in six (31.6) patients, and with mixed axonal and demyelinating polyneuropathy in one (5.3%) patient. Spine MRI showed root enhancement in three (42.9%) patients. Conclusion: In regions endemic with brucellosis, acute peripheral neuropathy presentation may warrant investigations for Brucella infection.

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