Nerve biopsy in T-cell lymphoma with neurolymphomatosis: where and when.

Peripheral T-cell lymphomas are rare heterogeneous haematological malignancies that may also involve peripheral nerves in a very small subset of cases. We report a patient with a diagnostically challenging cutaneous T-cell lymphoma and multifocal mononeuropathies in whom a targeted nerve biopsy identified lymphomatous infiltration of nerves and expedited combination treatment with chemotherapy and an autologous stem cell transplant. She showed an excellent response with a complete metabolic response on positron emission tomography imaging and significant clinical improvement, maintained 5 years post-treatment.

Improving liaison neurology services.

Liaison neurology (consulting with inpatient ward referrals) is the main way that most patients admitted with neurological disease will access neurology services. Most liaison neurology services are responsive, seeing referrals on request, but they also can be proactive, with a regular neurology presence in the acute medical unit. Fewer than half of hospitals in England have electronic systems, yet these can facilitate the process-allowing electronic responses to advise on investigations before seeing the patient, and arranging follow-up after-as well as prioritising referrals and documenting the process. In this time of COVID-19, there are additional benefits in providing prompt remote advice. Improving the way liaison neurology is delivered can improve patient outcomes and save money by shortening admissions. This hidden work of the neurologists needs to be recorded and recognised.

Posterior reversible encephalopathy syndrome complicating diabetic ketoacidosis; an important treatable complication.

Development of acute neurological symptoms secondary to cerebral oedema is well described in diabetic ketoacidosis (DKA) and often has a poor prognosis. We present the clinical and radiological data of a 17-yr-old girl who developed cortical blindness, progressive encephalopathy, and seizures caused by posterior reversible encephalopathy syndrome (PRES) that developed after her DKA had resolved. Vasogenic oedema in PRES resolves if the underlying trigger is identified and eliminated. In this case, hypertension was identified as the likely precipitating factor and following treatment her vision and neurological symptoms rapidly improved. We suggest how recent DKA may have contributed to the development of PRES in this patient.

Bifacial weakness with paresthesias: Serial nerve conduction studies indicate diffuse demyelinating neuropathy.

INTRODUCTION: Bifacial weakness with paresthesias is a rare subtype of Guillain-Barré syndrome (GBS), characterized by facial diplegia in the absence of any other cranial neuropathies, limb weakness, or ataxia. Frequently, patients also complain of distal limb paresthesias before or at the time they develop facial weakness. METHODS: We describe a man who developed post-infective isolated symmetric facial diplegia associated with distal paresthesias. Nerve conduction studies were conducted at 4 time-points over 6 months. RESULTS: A monophasic disease course and presence of cerebrospinal fluid albuminocytological dissociation supported a diagnosis of bifacial weakness with paresthesias. Serial nerve conduction studies demonstrated an evolving demyelinating neuropathy with evidence of distal and proximal demyelination without conduction block, which partially resolved over time. Despite complete resolution of facial weakness within weeks, distal paresthesias persisted beyond 6 months. CONCLUSIONS: This study suggests that neuropathy in patients with bifacial weakness and paresthesias is demyelinating and diffuse.

Bell's palsy syndrome: mimics and chameleons.

In this article we will explore the mimics and chameleons of Bell's palsy and in addition argue that we should use the term 'Bell's palsy syndrome' to help guide clinical reasoning when thinking about patients with facial weakness. The diagnosis of Bell's palsy can usually be made on clinical grounds without the need for further investigations. This is because the diagnosis is not one of exclusion (despite this being commonly how it is described), a lower motor neurone facial weakness where all alternative causes have been eliminated, but rather a positive recognition of a clinical syndrome, with a number of exclusions, which are described below. This perhaps would be more accurately referred to a 'Bell's palsy syndrome'. Treatment with corticosteroids improves outcome; adding an antiviral probably reduces the rates of long-term complications.