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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.

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.

Progressive encephalomyelitis with rigidity and myoclonus (PERM) is an autoimmune condition character- ised by various neurological symptoms associated with the dysfunction of the brain stem and spinal cord. PERM has been recognised as a paraneoplastic syndrome, its effects due mainly to the cross reaction of onconeural antibodies against the tumour also affecting neuronal cells.Interestingly, PERM can also present as an isolated syndrome not linked to malignancy. It must be noted however, that tumours may present much later than the syndrome and the aggressive nature of PERM may lead to patient mortality before the tumour can be identified clinically. Paradoxically, the treatment of malignancy can induce remission of PERM as will be illustrated in this case report.A 45-year-old lady initially presented with paraesthesia in both lower limbs followed by leg spasms. There was also difficulty with voiding and constipation. All the initial investigations were negative and the pos- sibility of functional neurological syndrome was made. Few weeks later, patient was readmitted and on this occasion transferred to the neuroscience centre. The patient had features of increased reflexes (including clonus) and also exhibited features of autonomic dysfunction such as heat intolerance, tachy- cardia, hypertension and bowel and urinary dysfunction.Glycine receptor positive progressive encephalomyelitis with rigidity and myoclonus (PERM) was diagnosed and investigations including PET scan confirmed an underlying breast cancer. Initial improvement with immunotherapy was sustained after cancer chemotherapy and surgery.saiju.jacob@uhb.nhs.uk

Guidelines set by the Association of British Neurologists recommend thymectomy for patients under the age of 45 with positive AChR antibodies or thymoma. Previous literature supports this, as thymectomy had been shown to improve clinical outcomes and reduce the need for immunosuppressive therapy. However, given the advancement of more successful immunosuppressive medicine the need for thymec- tomy can be questioned.Aim- to identify whether thymectomy aids Myasthenia Gravis (MG) management by reducing the need for immunosuppressive medication.Method- A retrospective evaluation identified 173 patients who had thymectomy in the UHB trust in the past 10 years, from which patients who had a primary indication of MG were extracted. Patient records were reviewed to collate data. Relevant trusts departments were contacted to fill the missing data.Results- 36 patients filled the criteria for inclusion. The average dose of prednisolone had an insignificant reduction by 22mg (STD- 10mg). 16 patients (44%) had a lower dose of prednisolone than prior to surgery. The average dose of Azathioprine had an insignificant increase since surgery by 18mg. There was also a reduction in the use of IVIG and plasma exchange.Conclusion- Thymectomy is unlikely to cause a significant reduction in the need for immunosuppressive therapy. Further research may be required to secure a larger sample size over a longer time period.saiju.jacob@uhb.nhs.uk

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.

Tropical diseases are increasingly reported outside their areas of high prevalence.1 Not only that many physicians are unfamiliar with these conditions but also there is the added challenge that it can present in an atypical way thereby remaining elusive for diagnosis. We report the case of a 41-year-old man of Indian origin who presented with swollen left forearm with severe localised pain and erythema (figure 1) simulating a picture of cellulitis, but subsequent examination also …

ObjectiveThe use of immune checkpoint inhibitors (CIs) for malignancies has revolutionised oncological management in the last few years. These agents are known to cause immune-mediated complications in various systemic organs. The neurological complications of these are now being increasingly recognised. The cases managed in our institution where there were neuroimmunological complications following CIs were reviewed. We discuss management strategies for early recognition and treatment, thus minimising morbidity.MethodA joint effort by neurologists and medical oncologists to review clinical practice guidelines for management of neurological adverse effects of checkpoint inhibitors. This was based on a review of several cases reported, as well as experience from all the cases managed in our hospital.ResultsThere are no British guidelines from the neurological perspective for early identification of symptoms. Guidelines are based on expert consensus and also on treatments reviewed from literature.ConclusionRecommendations advice early identification of signs and symptoms followed by grading them as mild, moderate and severe (grades 1, 2, 3). Grade 1 symptoms require continuation of the CIs and symptomatic management. CIs should be stopped temporarily for grade 2 and permanently for grade 3 symptoms. Steroids plasma exchange, IVIg would be the first line of treatment.

A 47 year old with subacute onset of walking difficulties, asymmetric lower limb and facial weakness and areflexia was admitted as a suspected case of Guillain-Barre syndrome. Clinical examination revealed left lower motor neuron facial weakness, right upper limb and lower limb weakness and a suspended area of pain and allodynia at T7. Structural imaging of the brain and spine was normal. CSF protein was elevated with pleocytosis. Nerve conduction studies was suggestive of proximal demyelinating polyradicular neuropathy. The clinical suspicion of neuroborreliosis was confirmed in CSF with Borrelia VlsE antigen positivity and serum Borrelia Burgdorferi IgG EIA positivity. The patient had no recollection of tick exposure but did recall a presumed horsefly bite on the forearm two weeks earlier of uncertain significance. This is a case of Bannwarth syndrome - meningoradiculoneuritis due to neuroborreliosis endemic in Northern Europe. Our patient was treated with Ceftriaxone with rapid improvement of symptoms. This case highlights the importance of careful history taking including ascertainment of travel to Borrelia endemic areas and recognition of this eminently treatable meningoradiculoneuropathy.

Leprosy is an uncommon disease in England and Wales, yet it remains an important disease globally with 2 50 000 cases diagnosed annually. Underreporting is likely in developed countries, where awareness of the clinical phenotypes and presentations of the disease may be lower than in higher prevalence countries. A 44 year old gentleman of Indian origin presented with swollen left forearm and erythematous plaque on the left hand. Clinical assessment revealed wasting of intrinsic muscles in the hypothenar eminence, profound motor and sensory deficit in the ulnar nerve distribution, with clawing of 4th and 5th digits of the left hand. EMG showed complete denervation of the left ulnar nerve. A modified Ziehl-Neelsen stain of the left arm skin biopsy demonstrated numerous, small aggregate bacilli, frequently co-localised within the areas of granulomatous inflammation. The skin biopsy sample identified the presence of bacterial 16 s DNA. Further analysis with 16S DNA sequencing was specific for Mycobacterium Leprae, thereby confirming the diagnosis of leprosy neuropathy.