Ischemic stroke in 455 COVID-19 patients.

There is increasing evidence that COVID-19 can be associated with ischemic stroke (COVID-stroke). The frequency and pathogenesis of COVID-stroke, however, remains largely unknown. This narrative review aimed at summarizing and discussing current knowledge about frequency and pathogenesis of COVID-stroke in 455 patients collected from the literature. COVID-stroke occurs in all age groups and predominantly in males. The anterior circulation is more frequently affected than the posterior circulation. COVID-stroke is most frequently embolic. The severity of COVID-stroke ranges from NIHSS 3 to 32. Cardiovascular risk factors are highly prevalent in patients with COVID-stroke. COVID-stroke occurs simultaneously with the onset of pulmonary manifestations or up to 40 days later. Clinical manifestations of COVID-19 are most frequently mild or even absent. The majority of patients with COVID-stroke achieve complete or partial recovery, but in one-quarter of patients, the outcome is fatal. In conclusion, the frequency of ischemic stroke has not increased since the outbreak of the SARS-CoV-2 pandemic. COVID-stroke predominantly affects males and the anterior circulation. COVID-stroke is multifactorial but predominantly embolic and more frequently attributable to cardiovascular risk factors than to coagulopathy.

Consider differentials before diagnosing COVID-19 associated polyradiculitis.

Evidence is accumulating that SARS-CoV-2 infections and SARS-CoV-2 vaccinations can induce Guillain-Barre syndrome (GBS). More than 400 GBS cases after SARS-CoV-2 infection respectively vaccination have been reported as per the end of 2021. GBS is usually diagnosed according to the Brighton criteria, but also the Besta criteria or Hadden criteria are applied. The diagnosis can be supported by MRI with contrast medium of the cranial or spinal nerves showing enhancing nerve roots. As GBS can be complicated by autonomic dysfunction such as pupillary abnormalities, salivatory dysfunction, reduced heart rate variability, bowel disturbance (constipation, diarrhea), urinary hesitancy, urinary retention, or impotence, it is crucial to investigate GBS patients for autonomic involvement. Before diagnosing GBS various differentials need to be excluded, including neuropathy as a side effect of the anti-SARS-CoV-2 medication, critical ill neuropathy in COVID-19 patients treated on the ICU, and compression neuropathy in COVID-19 patients requiring long-term ventilation.

Discussion of the Brazilian neurologists about sudden unexpected death in epilepsy.

OBJECTIVE: This study aimed to evaluate the concept of health professionals affiliated with the Brazilian League of Epilepsy on whether or not to inform patients about the risk factors related to the occurrence of sudden unexpected death in epilepsy. METHODS: A descriptive research of inquiry was conducted with direct survey on the Brazilian neurologist's view, regarding medical behavior in the health area to report or not about the risk of sudden unexpected death in epilepsy. Data collection consisted of a structured questionnaire available online. RESULTS: The study population consisted of a sample of 44 Brazilian League of Epilepsy members who answered the questionnaire, of which 25 (56.8%) were men and 19 (43.2%) were women. Among the analyzed questionnaires, 79.5% reported that they were aware of the risk factors for sudden unexpected death in epilepsy and 18.2% admitted not knowing the potential risk factors for sudden unexpected death in epilepsy. Notably, 59.1% of these professionals thought that an early discussion with the patient about sudden unexpected death in epilepsy must be considered. The majority (70%) felt that the neurologist should do this, and 22% believed that the subject should be discussed with psychologists. It was noted that 84.1% of respondents did not discuss or discussed only with some of their patients about the risk factors for sudden unexpected death in epilepsy. CONCLUSIONS: There is a need for encouraging early discussion of sudden unexpected death in epilepsy with epilepsy patients if the patient asks about the risks related to epilepsy and its treatment, when treatment adherence is low, in cases of intractable epilepsy with strong indication for surgical treatment, and when polytherapy is needed.

Peripheral neuropathy in COVID-19 is due to immune-mechanisms, pre-existing risk factors, anti-viral drugs, or bedding in the Intensive Care Unit.

BACKGROUND: This mini-review aims to summarize and discuss previous and recent advances in the clinical presentation, pathophysiology, diagnosis, treatment, and outcome of SARS-CoV-2-associated peripheral neuropathies. METHODS: Literature review. RESULTS: Altogether, 105 articles about SARS-CoV-2-associated neuropathy describing 261 patients were retrieved. Peripheral neuropathy in patients with COVID-19 is frequent and predominantly due to immune mechanisms or neurotoxic side effects of drugs used to treat the symptoms of COVID-19 and, to a lesser extent, due to the compression of peripheral nerves resulting from prolonged bedding in the Intensive Care Unit (ICU) and pre-existing risk factors such as diabetes. SARS-CoV-2 does not cause viral neuropathy. Neurotoxic drugs such as daptomycin, linezolid, lopinavir, ritonavir, hydro-chloroquine, cisatracurium, clindamycin, and glucocorticoids should be administered with caution and patients should be appropriately bedded in the ICU to prevent SARS-CoV-2-associated neuropathy. Patients with Guillain-Barré syndrome (GBS) benefit from immunoglobulins, plasma exchange, and steroids. CONCLUSIONS: Neuropathies of peripheral nerves in patients with COVID-19 are frequent and mostly result from immune mechanisms or neurotoxic side effects of drugs used to treat the symptoms of COVID-19 and, to a lesser extent, from the compression of peripheral nerves due to prolonged bedding on the ICU. SARS-CoV-2 does not cause infectious neuropathy.