Annals of Indian Academy of Neurology最新文献

Stroke remained the second leading cause of death globally in 2019. The antiplatelet drug clopidogrel is used to keep blood clots from forming in people who have experienced a stroke. Although most people find clopidogrel to be safe and beneficial, there is inevitably a range in how each patient responds. The review covers about Clopidogrel resistance in stroke patients, their risk factors and the methods to identify it. Clopidogrel resistance is characterized as the drug's inability to prevent the target enzyme from acting. The prognosis of patients with ischemic stroke and the responsiveness to clopidogrel are significantly impacted by the various genetic polymorphism CYP2C19 genotypes. The two primary mutant alleles, CYP2C19 *2 and CYP2C19 *3, have been found to be the most prevalent genotypes. Better mRS scores six months after treatment showed a higher response rate in patients without these CYP2C19 variant alleles. Other factors are drug-drug interaction (proton pump inhibitors), demographics (age, sex, social history), comorbid conditions, etc. Blood samples for testing platelet reactivity were drawn one month after discharge from a peripheral blood sample. Several methods are used to identify the clopidogrel resistance. Some of them are ADP-Induced platelet aggregation, Platelet Reactivity Index VASP, Verify Now Assay, TEG Analyzer, Plasma microRNA-223. Drugs that are not prodrugs and whose metabolism is not dependent upon CYP2C19 can be selected as a superior alternative in case of CR. Ticagrelor is one such effective substitute. Proton pump inhibitors and clopidogrel should only be used concurrently in patients with reliable clinical indications.

Paraneoplastic neurologic syndromes are cancer-associated, immune-mediated neurologic manifestations that may involve any part of the nervous system. They usually present with characteristic neurologic features and should be considered in high-risk phenotypes such as limbic encephalitis, encephalomyelitis, rapidly progressive cerebellar syndrome, opsoclonus-myoclonus, sensory neuronopathy, enteric neuropathy, and Lambert-Eaton myasthenic syndrome. The diagnosis is made by antibody positivity in the serum or cerebrospinal fluid, in the presence of an appropriate clinical phenotype. Findings on antibody testing by immunoblot should always be verified by immunofluorescence. We report a rare case of sensory neuronopathy with triple paraneoplastic antibody positivity (anti-Hu, anti-collapsing response-mediator protein 5, and anti-amphiphysin) on immunoblot but only anti-Hu positivity on immunofluorescence. The presence of lower facial dyskinesias should raise the possibility of an immune-mediated neurologic syndrome in the appropriate clinical context.

Autoimmune autonomic disorders encompass a spectrum of disorders mediated by immune responses directed against the autonomic nervous system, including the peripheral and central autonomic pathways. While centrally mediated autoimmune autonomic disorders primarily can cause autonomic hyperactivity, peripherally mediated disorders are more common and can cause either locally confined or global autonomic failure. These disorders are often underrecognized owing to vague and varied clinical signs and symptoms. The discovery of specific autoantibodies in the past decade has caused a growing recognition of autoimmune causes for these disorders. The management is also complex, as these disorders often manifest with generalized symptoms, are difficult to diagnose, invoke challenges involving robust establishment of an autoimmune syndrome, and are rare. This article presents an overview of autonomic disorders that have a suspected autoimmune etiology, as well as recent advancements in their diagnosis and management.

Background and objectives: Magnetoencephalography (MEG) could be a valuable tool in the presurgical evaluation of drug-resistant epilepsy (DRE), especially when the initial evaluation is inconclusive. In this retrospective study, we describe the profile of MEG in patients with DRE and normal magnetic resonance imaging (MRI).

Methods: We included patients with focal epilepsy and normal MRI who underwent presurgical evaluation for DRE. MEG profiles of these patients, including the frequency of spikes, density of clusters, number of clusters, and concordance with video electroencephalography (VEEG), were analyzed.

Results: Of the 73 patients included, magnetic source imaging (MSI) provided localizing information in 51 (69.9%) patients. Among patients with localizing MEG findings, localizing information on VEEG too was noted in 42 (57.5% of the whole cohort). Thirty-one (42.5%) patients had concordant findings with region-specific localization, six (8.2%) patients had partial concordance, and five (6.8%) subjects showed discordant findings. There was a moderate agreement for the presumed epileptogenic zone in comparing findings derived from MEG and VEEG (kappa value of 0.451, P < 0.001). The agreement was lower when MEG localized to the frontal lobe (kappa value of 0.379, P = 0.001) than the temporal lobe (kappa value 0.442, P = 0.002).

Conclusions: MEG can provide localizing information in most patients with a normal MRI. A moderate degree of agreement between localization by MEG and VEEG was noted. These findings highlight the usefulness of MSI in the presurgical evaluation of MRI-negative DRE.

Immune-mediated epilepsy (IME) constitutes a substantial proportion of drug-refractory epilepsies. Rapid diagnosis and prompt immunosuppression are required along with antiseizure medications (ASMs). Here we report three unrelated children who presented with fever, encephalopathy, and refractory epilepsy and subsequently tested positive for rare intraneuronal and surface receptor antibodies, namely, contactin-associated protein like 2 (CASPR2), glutamic acid decarboxylase (GAD65), and paraneoplastic antigen Ma2 (PNMA2). In all of them, brain magnetic resonance imaging (MRI) was noncontributory. Electroencephalography showed nonspecific interictal epileptic discharges. F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) brain scan revealed abnormality in metabolic pattern with hypermetabolism in basal ganglia, thalami, frontotemporal cortices, and cerebellar hemispheres, consistent with autoimmune encephalitis. Immunosuppression was initiated along with ASMs. Complete seizure freedom was achieved in GAD65 antibody IME and >50% seizure reduction in CASPR2 and PNMA2 antibody IME. A variable degree of behavioral problems persisted in all. Early immunosuppression is warranted in IME, but does not universally guarantee a complete response.