Nonepileptic attacks in patients with brain tumor-related epilepsy.

Epileptic seizures are well recognized as a presenting symptom in patients with brain tumors, however much less is known about coexisting nonepileptic attack disorder (NEAD) in this population. Establishing a diagnosis of NEAD can be challenging, especially in those with concomitant epilepsy. Nonepileptic attack disorder is associated with a high rate of morbidity, often due to coexisting psychological factors which may require the input of multiple services. In an era where early aggressive management of tumors is enabling patients to live longer, the associated psychological impact of adjusting to physical disease is increasingly apparent. In this case series, we present a narrative summary of 9 patients referred to neurology with brain tumor-related epilepsy (BTRE) over a five-year period (2015-2020) who also experienced NEAD. We describe their tumor characteristics, treatment course, and factors potentially contributing to their presentation. We conducted a case note review of patients presenting to the epilepsy service with BTRE, in whom NEAD was diagnosed based on clinical features and correlation with their EEG. Patients ranged in age from 26 to 63 years. Two patients were diagnosed with grade 1, three with grade 2 and four with grade 3 tumors. Tumors localized to frontal or temporal regions in seven cases. All patients presented initially with BTRE and developed nonepileptic seizures subsequently. Four patients developed NEAD within 1 month of their tumor diagnosis. One patient developed NEAD 79 months following diagnosis. The diagnosis of NEAD was established in 8 patients by direct visualization of attacks (two during concomitant EEG recording). In the remaining patient, diagnosis was based on history (patient and witness). Six patients were diagnosed with concomitant low mood and/ or anxiety and three were commenced on antidepressant medication. At the time of last review, the predominant attacks were nonepileptic in all but one patient.

Acute-onset polyradiculoneuropathy after SARS-CoV2 vaccine in the West and North Midlands, United Kingdom.

INTRODUCTION/AIMS: We aimed to determine whether specific severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) vaccines may be associated with acute-onset polyradiculoneuropathy and if they may result in particular clinical presentations. METHODS: We retrospectively reviewed records of all persons presenting with acute-onset polyradiculoneuropathy from January 1, 2021, to June 30, 2021, admitted to two Neuroscience centers, of the West and North Midlands, United Kingdom. We compared subjects with previous SARS-CoV2 vaccine exposure with a local cohort of persons with acute-onset polyradiculoneuropathy admitted between 2005 and 2019 and compared admission numbers for the studied time frame with that of the previous 3 years. RESULTS: Of 24 persons with acute-onset polyradiculoneuropathy, 16 (66.7%) presented within 4 weeks after first SARS-CoV2 vaccine. Fourteen had received the AstraZeneca vaccine and one each, the Pfizer and Moderna vaccines. The final diagnosis was Guillain-Barré syndrome (GBS) in 12 and acute-onset chronic inflammatory demyelinating polyneuropathy in 4. Among AstraZeneca vaccine recipients, facial weakness in nine persons (64.3%), bulbar weakness in seven (50%), and the bifacial weakness and distal paresthesias GBS variant in three (21.4%), were more common than in historical controls (P = .01; P = .004, and P = .002, respectively). A 2.6-fold (95% confidence interval: 1.98-3.51) increase in admissions for acute-onset polyradiculoneuropathy was noted during the studied time frame, compared to the same period in the previous 3 years. DISCUSSION: Despite a low risk, smaller than that of SARS-CoV2 infection and its complications, exposure to the first dose of AstraZeneca SARS-CoV2 vaccine may be a risk factor for acute-onset polyradiculoneuropathy, characterized by more common cranial nerve involvement.

Primary leptomeningeal lymphoma masquerading as infectious tubercular meningitis.

Primary central nervous system lymphoma (PCNSL) is infrequent and often poses diagnostic conundrums due to its protean manifestations. We present the case of a South Asian young man presenting with raised intracranial pressure and a lymphocytic cerebrospinal fluid (CSF) with pronounced hypoglycorrhachia. Progression of the neuro-ophthalmic signs while on early stages of antitubercular treatment led to additional investigations that produced a final diagnosis of primary leptomeningeal lymphoma. Treatment with chemoimmunotherapy (methotrexate, cytarabine, thiotepa and rituximab (MATRix)) achieved full radiological remission followed by successful autologous transplant. This case highlights the difficulties and diagnostic dilemmas when PCNSL presents as a chronic meningeal infiltrative process. While contextually this CSF is most often indicative of central nervous system tuberculosis and justifies empirical treatment initiation alone, it is essential to include differential diagnoses in the investigation work-up, which also carry poor prognosis without timely treatment. High suspicion, multidisciplinary collaboration and appropriate CSF analysis were the key for a correct diagnosis.