Free Neurology CME

In this brief 15-minute activity, you will:

– Follow the case of a patient who presents with foot drop and no other medical conditions
– Choose optimal management approaches by answering nongraded questions within the activity (answers are collected for informational purposes only and used to assess the effectiveness of this educational activity)
– See how your answers compare with those of your peers
– View video clips providing expert insights

In this online, self-learning activity:

Cervical dystonia is the most common focal dystonia, characterized by involuntary muscular contractions resulting in abnormal head, neck, and shoulder movements in addition to posture that can cause tremor and pain. Early-onset dystonia can begin in infancy, childhood, or adolescence, and it generally progresses from focal to generalized. Adult-onset dystonia usually affects the upper part of the body; the origin of the dystonia determines the risk of spread. Cervical dystonia may appear as torticollis, laterocollis, anterocollis, or retrocollis. It may be distinguished from nondystonic hand tremor and essential tremor by the absence of limb tremor and the manner of neck movement. However, it is more difficult to distinguish from pseudodystonias, resulting in misdiagnosis, inappropriate treatment, and treatment delay.

Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) is a demyelinating, autoimmune condition affecting the central nervous system. MOGAD is characterized by the presence of autoantibodies directed against the MOG protein located on the surface of myelin sheaths surrounding nerve fibers in the CNS. The disease course may be monophasic or relapsing, and a progressive course is extremely rare, making the mortality rate fairly low (2.1%) compared to other neuroinflammatory diseases. It is a relatively new addition to the category of demyelinating diseases, and approximately 10,000 cases of MOGAD are estimated within the U.S.

Activity Description / Statement of Need:

In this online, self-learning activity:

Thymidine kinase 2 deficiency (TK2D) is an ultrarare mitochondrial disease caused by recessive mutations in the TK2 gene and manifesting as a form of mitochondrial DNA depletion/deletion syndrome (MDDS) and mitochondrial myopathy. Under normal conditions, the TK2 gene encodes for the thymidine kinase enzyme present in the mitochondria, which is responsible for the phosphorylating of pyrimidine nucleosides, deoxythymidine, and deoxycytidine. These are the first steps in mitochondrial DNA synthesis, and researchers speculate that TK2 mutations affect muscle tissue because its higher energy demands make it most susceptible to mitochondrial impairment. Mutational analyses of patients with MDDS have found that approximately 15% have TK2 mutations, which may be extrapolated to about 600 to 2,700 individuals in the US.

Target Audience:

HCPs including but not limited to: neurologists, pediatric neurologists, pediatricians, primary care providers, pulmonologists, gastroenterologists, and medical geneticists; physician assistants, nurse practitioners, pharmacists, and nurses who practice in the aforementioned areas of specialty; and any other HCPs with an interest in or who may clinically encounter patients with TK2D.

In this online, self-learning activity:

Dravet syndrome (DS) is a rare form of early-onset epilepsy syndrome affecting between 1:16,000 and 1:46,000 and is associated with pleomorphic seizure activity, cognitive decline, motor, and behavior abnormalities. Sudden unexpected death in epilepsy is the cause of death in nearly half of the deaths in patients with DS, with the mean age of death 8.7 years old and 73% of deaths occurring before age 10. Seizures typically begin in the first year of age, with most occurring between months 5 and 8, and it is usually a prolonged, tonic-clonic (accounting for 52% of first seizures) or hemiclonic (35%) seizure. Environmental triggers or events, such as fever, acute stress, and physical exercise may precipitate seizures, and at least 85% of those who are clinically diagnosed with DS have variations in the SCN1A gene. Unfortunately, diagnosis is not uncommonly delayed until a patient 3 years of age or older, prior to which antiseizure medication selection may be suboptimal or ineffective, which may lead to seizure exacerbation, an increased risk of status epilepticus, and worse cognitive outcomes.

In this online, self-learning activity:

Generalized myasthenia gravis (gMG) is an autoimmune neuromuscular junction disorder marked by fluctuating, fatigable weakness that can involve ocular, bulbar, limb, and respiratory muscles. In a U.S. claims-based analysis, diagnosed prevalence in 2021 was 37.0 per 100,000 and incidence was 3.1 per 100,000, underscoring a clinically meaningful population at risk for disability and episodic deterioration. Reviews describe persistent symptom burden and functional consequences that extend beyond clinic-based strength testing. Real-world observational data link higher disease severity to greater impairment in activities of daily living, including reduced independence with self-care and mobility. International consensus guidance recommends stepwise management with early steroid-sparing intent and timely adjustment when treatment targets are not met. Higher severity is also associated with worse work productivity and activity impairment, amplifying socioeconomic burden.