Ischaemic stroke and SARS-CoV-2 infection: A causal or incidental association? / Ictus isquémico e infección por SARS-CoV-2, ¿asociación casual o causal?

INTRODUCTION: Ischaemic stroke has been reported in patients with COVID-19, particularly in more severe cases. However, it is unclear to what extent this is linked to systemic inflammation and hypercoagulability secondary to the infection. METHODS: We describe the cases of 4 patients with ischaemic stroke and COVID-19 who were attended at our hospital. Patients are classified according to the likelihood of a causal relationship between the hypercoagulable state and ischaemic stroke. We also conducted a review of studies addressing the possible mechanisms involved in the aetiopathogenesis of ischaemic stroke in these patients. RESULTS: The association between COVID-19 and stroke was probably causal in 2 patients, who presented cortical infarcts and had no relevant arterial or cardioembolic disease, but did show signs of hypercoagulability and systemic inflammation in laboratory analyses. The other 2 patients were of advanced age and presented cardioembolic ischaemic stroke; the association in these patients was probably incidental. CONCLUSIONS: Systemic inflammation and the potential direct action of the virus may cause endothelial dysfunction, resulting in a hypercoagulable state that could be considered a potential cause of ischaemic stroke. However, stroke involves multiple pathophysiological mechanisms; studies with larger samples are therefore needed to confirm our hypothesis. The management protocol for patients with stroke and COVID-19 should include a complete aetiological study, with the appropriate safety precautions always being observed.

EARLY-ESLI study: Long-term experience with eslicarbazepine acetate after first monotherapy failure.

PURPOSE: Evaluate real-life experience with eslicarbazepine acetate (ESL) after first monotherapy failure in a large series of patients with focal epilepsy. METHOD: Multicentre, retrospective, 1-year, observational study in patients older than 18 years, with focal epilepsy, who had failed first antiepileptic drug monotherapy and who received ESL. Data from clinical records were analysed at baseline, 3, 6 and 12 months to assess effectiveness and tolerability. RESULTS: Eslicarbazepine acetate was initiated in 253 patients. The 1-year retention rate was 92.9%, and the final median dose of ESL was 800 mg. At 12 months, 62.3% of patients had been seizure free for 6 months; 37.3% had been seizure free for 1 year. During follow-up, 31.6% of the patients reported ESL-related adverse events (AEs), most commonly somnolence (8.7%) and dizziness (5.1%), and 3.6% discontinued due to AEs. Hyponatraemia was observed in seven patients (2.8%). After starting ESL, 137 patients (54.2%) withdrew the prior monotherapy and converted to ESL monotherapy; 75.9% were seizure free, 87.6% were responders, 4.4% worsened, and 23.4% reported ESL-related AEs. CONCLUSION: Use of ESL after first monotherapy failure was associated with an optimal seizure control and tolerability profile. Over half of patients were converted to ESL monotherapy during follow-up.

Antiepileptic treatment in patients with epilepsy and other comorbidities.

BACKGROUND: A high number of patients with epilepsy have comorbidities. The type of comorbidity is an important factor in deciding on the most suitable treatment, including that for acute epileptic seizures and chronic antiepileptic treatment. Evidence-based criteria should guide the selection of the appropriate antiepileptic drugs given specific comorbidities. METHODS: We performed a comprehensive search of the scientific literature on epilepsy treatment in patients with the following comorbidities: heart disease, lung disease, liver disease, kidney disease, porphyria, organ transplantation, thyroid disease, metabolic disorder, infection, mental disability, psychiatric disorder, cognitive impairment, stroke, and brain tumour. RESULTS: Most of the studies were case series and retrospective analyses. No randomised controlled trials specifically designed for this type of clinical situation were identified. The level of scientific evidence to guide clinical decisions is therefore low. CONCLUSIONS: In this review we make recommendations based on the best scientific evidence available for treating epilepsy in patients with other comorbidities, including the treatment of epileptic seizures in acute situations as well as chronic antiepileptic treatment. When no scientific evidence is available, our recommendations are based on pharmacokinetic criteria and tolerability of antiepileptic drugs, using accumulated experience and the consensus of the members of the Andalusian Epilepsy Society.

Second case of neurocysticercosis in a patient with liver transplantation (first case in Spain): a case report.

BACKGROUND: Neurocysticercosis (NCC) is a disorder caused by the Taenia solium larva. It is the most common parasitosis of the central nervous system (CNS). Its distribution is universal, but it is endemic in many developing countries and in the third world. In Spain most patients come from countries where the condition is endemic. However, sporadic cases occur among the population of rural regions. NCC in transplant recipients is uncommon. One renal transplant recipient developed NCC but responded to treatment with praziquantel. Recently, it has been reported to complicate a liver transplantation. CASE REPORT: The patient was a 49-year-old Ecuatorian man who received a cadaveric donor liver graft in June 2001 due to acute liver failure induced by toadstool and was under treatment with FK506. In January 2006, the patient presented with a generalized onset of a tonic-clonic seizure for 1 minute without sphincter incontinence, headache, fever, or previous brain trauma. Neurological evaluation did not show evidence of organic brain dysfunction. The neuroimaging findings (brain) computed tomography scan, magnetic resonance imaging were compatible with NCC: many cystic lesions intra- and extraparenchymatous with a scolex visible in three of them. Serology for cysticercosis in plasma was initially indeterminate but positive afterward. The patient was treated with anticonvulsivants (valproic acid) and albendazole. Systemic steroids were added in order to reduce the edema produced upon death of the cyst. Treatment lasted 3 weeks and it was completed without complications or neurological symptoms. Liver function was not affected. One year later the patient remained asymptomatic. CONCLUSION: NCC is a condition that must be included in the differential diagnosis of patients with CNS involvement and cystic lesions on neuroimaging investigations in transplant recipients, especially patients originating from or traveling to endemic areas. First-line therapy for active cysts includes antiparasitic drugs (albendazole or praziquantel) as well as steroids and anticonvulsivants. In our patient, this therapy was effective.

[Brachial presentation of spinal pseudochoreoathetosis. The result of proprioceptive information being processed in parallel]. / Seudocoreoatetosis espinal de presentación braquial. Resultado del procesamiento paralelo de la información propioceptiva.

INTRODUCTION: The term pseudochoreoathetosis is used to refer to the choreoathetoid movements that are produced by alterations in the proprioceptive sensitivity due to damage it has suffered at some point along its course. Proprioceptive sensitivity is considered to go up as far as the cortex along the posterior cords of the spinal cord, which means that if they are injured in the cervical region there should be a sensory deficit in both the upper (UL) and lower limbs (LL). CASE REPORTS: We describe five cases of transverse myelitis with localised cervical injury that selectively and mainly affected the posterior cords of the spinal cord. In the five patients there was selective involvement of the proprioceptive sensitivity in the UL respecting the LL and pseudochoreoathetoid movements of the limb that has been deafferented for proprioceptive sensitivity. The dissociation between the UL and the LL occurs because the spinocerebellar and spinocervical tracts take the proprioceptive information from the LL in parallel to the posterior cords, which receive the proprioceptive sensitivity from the UL. CONCLUSIONS: At present, the most widely accepted physiopathological mechanism explaining pseudochoreoathetosis consists in a failure in the integration of the sensory-motor afferences in the striatum, which causes faulty sensory-motor integration at this level and gives rise to pseudochoreoathetosis.