Neurology CME

Convenient, Comprehensive Neurology and PM&R CME

Designed for neurologists and physical medicine & rehabilitation doctors, residents, and fellows, this continuing medical education program covers all diagnostic and management approaches to both inherited and acquired neuromuscular conditions.

The 41 lectures in Electrodiagnostic Medicine and Neuromuscular Disorders — each just 30 and 45 minutes in length — delve into basic techniques and clinical applications of electrodiagnosis and ultrasound, as well as generalized disorders, motor neuron diseases, polyneuropathies, neuromuscular junction disorders, and myopathies. Key take-home points from this online CME program include:

• Basics of Needle EMG: Voluntary Activity. Motor unit potential waveform reflects the change in motor unit architecture due to disease processes, while the interference pattern provides information about the number of motor units and their activation.
• Neuropathies Associated with Systemic Disease and Cancer. Countless systemic disorders — metabolic, nutritional, inflammatory, infectious, neoplastic, and others — can cause neuropathy and accordingly, neuropathy can take many forms. Carefully characterizing the phenotype of neuropathy can help narrow down the relevant causes.
• Muscle Channelopathies. For a patient with a personal and family history of muscle stiffness and pain, consider genetic testing for myotonic disorders.
• And more…

Activity Description / Statement of Need:

In this online, self-learning activity:

Transthyretin amyloidosis (ATTR) is a progressive, multisystem, life-threatening disorder characterized by the extracellular deposition of misfolded, insoluble amyloid fibrils. The role of the TTR protein is to transport thyroxine and retinol-binding proteins, and it is vital for cognition, nerve regeneration, and axonal growth. TTR itself is innately amyloidogenic even without the presence of genetic mutations, which may account for wild-type ATTR (wtATTR), while a hereditary form of ATTR (hATTR) may be passed to offspring through autosomal dominant inheritance. Left untreated, the average life expectancy of ATTR is 3 to 15 years from symptom onset.

This accredited educational activity would identify the critical components of the management process and offer solutions to close gaps in diagnosis and care, with the ultimate goals being the improvement of ATTR management, treatment adherence when applicable, and health and cost outcomes. 

Target Audience:

The following HCPs: neurologists, cardiologists, and hematologists; physician assistants, nurse practitioners, and pharmacists in the aforementioned areas of specialty; and any other HCPs with an interest in or who may clinically encounter patients with ATTR.

Activity Description / Statement of Need:

In this online, self-learning activity:

Transthyretin amyloidosis (ATTR) is a progressive, multisystem, life-threatening disorder characterized by the extracellular deposition of misfolded, insoluble amyloid fibrils. As TTR is a protein present in human serum, and its role is to transport thyroxine and retinol-binding proteins, it is vital for behavior, cognition, nerve regeneration, and axonal growth. TTR itself is innately amyloidogenic even without the presence of genetic mutations. The familial variant of the disease (hATTR) is ATTR that is passed to offspring through autosomal dominant inheritance, whereas the wild type variant (wtATTR) refers to ATTR that occurs independently of genetic mutations. hATTR may present as late as mid-adulthood, but its symptoms usually start between the ages of 2 and 10 years. Left untreated, the average life expectancy of ATTR is 3 to 15 years from symptom onset.

Target Audience:

The following HCPs: neurologists, cardiologists, and hematologists; physician assistants, nurse practitioners, nurses, and pharmacists in the aforementioned areas of specialty; and any other HCPs with an interest in or who may clinically encounter patients with ATTR.

Activity Description / Statement of Need:

In this online, self-learning activity:

Pompe disease (PD) is a progressive, often fatal, autosomal recessive, neuromuscular disorder caused by mutations of the α-glucosidase gene on chromosome 17. PD is characterized by glycogen accumulation in skeletal, cardiac and smooth muscles due to a deficiency in α-glucosidase (GAA), an important lysosomal enzyme responsible for glycogen catabolism. PD is categorized into three groups based on symptoms and age of onset. The classic infantile form presents in the first year of life, usually in the first two months, with hypertrophic cardiomyopathy. The non-classic infantile form presents later in the first year of life, without or with less severe cardiomyopathy. The late onset form of PD presents any time after one year of life, usually without cardiac complications.

PD is rare, with one study estimating the incidence in the U.S. to be 1 in 22,000 births. The biggest risk factor for the disease is genetics; at conception, each sibling of an affected individual has a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and a 25% chance of being not a carrier. Nonspecific diagnostic findings for PD may include abnormal EMG, elevated serum creatine kinase, elevated transaminases and elevated lactate dehydrogenase. A definitive diagnosis for PD involves a dried blood spot test to determine GAA enzyme activity level; reduced GAA activity (less than 40% of normal) is indicative of a positive diagnosis. A gene mutation analysis, or another GAA enzyme test using a different area of tissue, is recommended to confirm the diagnosis. The disease is not uncommonly undiagnosed or is misdiagnosed, representing one practice gap that continued HCP education may address, particularly given that earlier treatment may minimize rapid and irreversible disease progression.

Target Audience:

The following HCPs: Neurologists, pediatricians, and primary care physicians; physician assistants and nurse practitioners in those areas of specialty; pharmacists who practice in specialty pharmacies that treat patients with rare diseases; and any other HCPs with an interest in or who may clinically encounter patients with PD.

Activity Description / Statement of Need:

In this online, self-learning activity:

Insomnia is characterized by the dissatisfaction of sleep quality or quantity characterized by having difficulty falling asleep, staying asleep, waking too early, or a combination of these. It is the most common general complaint in medical practice, and it is designated chronic if the condition persists for three months, despite the opportunity for sleep or eradication of external stimulus.Insomnia affects people of all ages, though the likelihood of developing insomnia increases with age: one-third of the adult population reports having been affected by at least one symptom of insomnia. Several factors may contribute to the condition. Poor sleep may develop spontaneously, be influenced by genetics, occur in response to stress or other psychological triggers, arise due to endogenous neurochemical dysregulation, or a combination of any of those factors. Insomnia puts patients at a higher risk of developing mood disorders such as anxiety and depression, and cardiovascular disease. The condition is liable for patients spending $2,000 per year and the U.S. $63 billion annually, encompassing the cost of reduced productivity – including absences, work-related accidents, and health care resources.

Target Audience:

The following HCPs: neurologists, psychiatrists, sleep medicine specialists, and primary care physicians; physician assistants, nurse practitioners, and pharmacists who practice in the aforementioned areas of specialty; and those who otherwise have an interest in or commonly care for or clinically encounter patients with chronic insomnia.