Coronavirus disease-2019 (COVID-19) has caused a pandemic that has recently affected every aspect of life. Fortunately, many vaccines with high safety and efficacy profiles were developed timely to face this pandemic. In a very short time, billions of people were vaccinated. In the meantime, a wide range of neurological syndromes are being reported. Guillain-Barré syndrome (GBS) which is a rare immune-mediated post-infectious peripheral neuropathy was reported after both the COVID-19 infection itself and many types of its vaccines. We are reporting a case of post-AstraZeneca vaccine GBS and reviewing the literature of all reported post-COVID-19 vaccines GBS till July 2021. 29 adult patients were reported. Of them 58.6% were males. Their mean age is 58.2 years. The median time to clinical onset after vaccine administration was 13.2 days. 86.2% of patients had their symptoms following immunization with the 1^st dose of AstraZeneca vector-based covid vaccine. Facial palsy was the most predominant single symptom in 75.8% of patients. Guillain-Barré syndrome is a well-recognized but still rare adverse event following vaccination against COVID-19. Although preliminary data incriminates viral vector-based vaccines more than the other types, active post-vaccination surveillance and more powerful statistics are mandatory to reach a solid conclusion regarding the presence of a causal relation.

During the era of the Coronavirus disease 2019 (COVID-19) pandemic, various neurological syndromes were reported during or after the infection. Fortunately, efforts were made to successfully develop various vaccines with high efficacy and safety. Despite the promising results of those vaccines, they are too novel to be fully understood. Here we are shedding light on a neurological case presentation that may be attributed to one of the COVID-19 vaccines. A 23-year-old male patient with no prior comorbidities presented with quadriparesis and numbness that were clinically and electrophysiologically consistent with Guillain-Barré Syndrome (GBS). The condition started 10 days after the first dose of the AstraZeneca vaccine. Moreover, MRI of the brain and spinal cord has shown evidence of non-specific central demyelination. Despite the radiological finding, the patient is not fulfilling the diagnosis of a known demyelination disorder and the lesions regressed on follow-up. Since no better explanation or trigger could be found, a post-vaccination immune-mediated reaction was considered. We still cannot assume the certainty of the causality association between the vaccine and the neurological presentation. Meanwhile, we suggest vigilance for cases of GBS or myelitis following vaccination for Covid-19 and that post-vaccination surveillance programs ensure a statistically significant tool to prove or dispsrove the causality.

Background: Cytotoxic lesion of the corpus callosum (CLOCC) is a magnetic resonant image (MRI) finding that could be triggered by anti-seizure medications, viral encephalitis, malignancies, metabolic disturbances, altitude sickness and migraine with aura. Its association with the cerebrospinal fluid (CSF) pressure or volume is not established. Case presentation: A 22-year-old female patient presented with a headache with features suggestive of idiopathic intracranial hypertension (IIH). The MRI head revealed CLOCC as a rounded lesion in the splenium of the CC with restricted diffusion. The CSF pressure was 26 cmH2O, and its analysis showed only a mild increase in mononuclear cells. The patient was diagnosed with IIH and commenced acetazolamide. The follow-up MRI after 6 weeks revealed a complete disappearance of the CLOCC. Conclusion: CLOCC, although very rare, could be present after an increase in the CSF pressure in patients with IIH. The lesion was restricted to the splenium and reversible after controlling the CSF pressure. Its presence could be associated with good prognosis.

Acute hemorrhagic leukoencephalitis (AHLE) is a rare, hyperacute inflammatory disorder of the central nervous system that is usually diagnosed on clinical and radiological grounds when tissue is unavailable. We report a previously healthy, unvaccinated 19-year-old woman with a 5-day febrile respiratory illness and a nasopharyngeal real-time reverse transcription polymerase chain reaction test positive for influenza A. Within approximately 12 h of admission, she progressed from full consciousness to coma with signs of brainstem dysfunction and developed shock requiring vasopressors. Brain magnetic resonance imaging showed bilateral confluent white-matter lesions with vasogenic edema, symmetric thalamic restricted diffusion, midbrain and pontine involvement, and petechial hemorrhages within the pons on susceptibility-weighted imaging. Cerebrospinal fluid showed elevated protein and mild lymphocytic pleocytosis. Despite intravenous methylprednisolone, intravenous immunoglobulin, oseltamivir, and intensive care, she died approximately 36 h after admission. The diagnosis of AHLE was clinicoradiological because neuropathological examination was not performed, and the symmetric thalamic and brainstem involvement overlapped with influenza-associated acute necrotizing encephalopathy (ANE). This case illustrates the fulminant course that influenza A-associated hemorrhagic encephalopathy can take in young adults, the value of early multisequence imaging, and the difficulty of distinguishing AHLE from ANE without neuropathological confirmation.