Functional seizures: The patient's perspective of a diagnostic and treatment odyssey.

Functional seizures can be challenging to properly diagnose, often leading to delays in treatment. The etiology of functional seizures is multifactorial, with psychological factors identified in many, but not all cases. Misdiagnosis may occur due to clinical features mimicking other medical conditions. Once a correct diagnosis is reached, delivery of definitive, evidence-based treatment may be challenging due to limited availability of specialized resources. Research shows psychological education and cognitive behavioral therapy (CBT) have the greatest efficacy. However, individual differences, including acceptance of the diagnosis, therapeutic alliance, duration of symptoms, comorbidities, and access to care may influence outcomes. There is a critical need for reports that can help identify barriers to effective diagnosis and treatment. We present the diagnosis and treatment of a woman who visited the emergency room after an attack of predominant left-sided paralysis, speech dysfunction and altered awareness. Following multiple daily episodes and visits to multiple medical practitioners, testing led to a diagnosis of functional seizures. While the patient was recommended to undergo a variety of therapeutic interventions, including CBT, she ultimately terminated treatment. In a subsequent interview, the patient revealed her personal experience with perceived limitations of acute management strategies. We explore the complexities of diagnosing and treating individuals with functional seizures.

Using Patient-Centered Clinical Neuroscience to Deliver the Diagnosis of Functional Neurological Disorder (FND): Results from an Innovative Educational Workshop.

OBJECTIVES: Psychiatry training is lacking examples of neuroscience education that translates neuroscience literature into accessible clinically oriented concepts. The authors created a teaching activity using patient-centered neuroscience education that focused on delivering the diagnosis of functional neurological disorder (FND). This study aimed to (i) develop a workshop modeling a clinician-patient interaction, (ii) provide a modern neuroscience perspective of FND, and (iii) evaluate the change in clinicians' perceptions of FND. METHODS: A total of six workshops (each 1 h long and consisting of a video, PowerPoint slides, and pre and post questionnaires) were conducted. Paired t tests were used to measure the change. RESULTS: Forty-seven clinicians participated. After completing the workshop, nearly all endorsed that functional symptoms are "real" (95%) and that treatment is helpful (100%). Participants also reported a greater comfort level with discussing FND diagnosis (46% vs 85%, p < 0.001), an overall increase in understanding the disorder (33% vs 82%, p < 0.001), assessing need for tests (33% vs 66%, p < 0.001), understanding treatment options (26% vs 89%, p < 0.001), and recognition that treatment can help control these symptoms (81% vs 100%, p < 0.01). In addition, learners were more likely to report that patients with FND are truthful (75% vs 95%, p < 0.001) and less likely to be manipulative (48% vs 80%, p < 0.001). CONCLUSIONS: A brief, educational intervention using neuroscience-based content was found to significantly improve clinicians' perception and confidence when delivering the diagnosis of FND.

Detection of seizure-like movements using a wrist accelerometer.

Caregivers of people with epilepsy are commonly concerned about unwitnessed seizures causing injury and even death. The goal of this study was to determine if a wrist-worn motion detector could detect tonic-clonic seizures. Individuals admitted for continuous video/EEG monitoring wore a wristwatch-size device that was programmed to detect rhythmic movements such as those that occur during tonic-clonic seizures. When such movement was detected, the device sent a Bluetooth signal to a computer that registered the time and duration of the movements. Recorded detections were compared with the routinely recorded video/EEG data. Six of 40 patients had a total of eight tonic-clonic seizures. Seven of the eight seizures were detected. Nonseizure movements were detected 204 times, with opportunity for canceling transmission by the patient. Only one false detection occurred during sleep. In principle, this device should allow caregivers of people with tonic-clonic seizures to be alerted when a seizure occurs.

Therapeutic brain stimulation for epilepsy.

DBS has been a possible therapy for epilepsy for more than 30 years, and now it is moving to the point of clinical utility. Animal models have shown efficacy of DBS at several brain regions, although not all animal studies have shown efficacy. Clinically, an array of sites have been explored, including the cerebellum, anterior nucleus of the thalamus, CM nucleus, hippocampus, subthalamic nucleus, brainstem, and corpus callosum; direct stimulation of the cortex has also been explored. Interest in evaluating these sites for treatment of epilepsy has been enhanced by the success of vagus nerve stimulation for epilepsy and DBS for movement disorders. Literature consists of mostly small and uncontrolled studies that are subject to limitations in interpretation. A pivotal large, double-blind controlled trial of anterior nucleus of the thalamus has recently been completed, and it showed efficacy for partial seizures with or without secondary generalization.28 A controlled trial for RNS is underway.57 In addition, pilot studies of hippocampal stimulation 41,43 are expected to lead to more definitive trials of this site.Brain stimulation for epilepsy holds several challenges for the future. Mechanisms of DBS are poorly understood, although investigations are actively being pursued. Little is known about optimal stimulation parameters. DBS has been little examined in cases of intractable generalized epilepsy. Because DBS carries some risk, mainly of hemorrhage and infection, clinicians will need to develop an effective method of identifying the best candidates. DBS is palliative rather than curative, but experience suggests that this relatively new therapy may be of benefit to some people with otherwise untreatable epilepsy.

Stiff-person syndrome.

Classic stiff-person syndrome (SPS) is a clinically diagnosed disease characterized by axial and often appendicular rigidity with lumbar hyperlordosis and painful spasms. Supportive data include increased glutamic acid decarboxylase autoantibody titers more than 20 nmol/L, a needle electromyography with continuous motor unit activity in at least one axial muscle, and normal MRI and cerebrospinal fluid studies. Variants of SPS include those with focal limb dysfunction (stiff-limb syndrome), encephalomyelitis ("SPS plus"), and those associated with paraneoplastic autoantibodies. Although the precise mechanism is unknown, an autoimmune etiology for SPS is proposed, based on its association with autoantibodies and other autoimmune diseases and its response to immunomodulatory therapy. The cornerstone of treatment consists of symptomatic care with benzodiazepines and/or baclofen. Other neuromodulators include antiepileptic medications and muscle relaxants. Continued disability despite first-line therapy should prompt consideration of agents aimed at immunomodulation and immunosuppression. Intravenous immunoglobulin is one of the few agents to be evaluated in a double-blind, randomized controlled trial. Other options include steroids, plasma exchange, and chemotherapy agents.