Free Neurology CME

Target Audience: Neurologists

Fabry disease is characterized by a deficiency of the glycoside hydrolase enzyme alpha galactosidase A, resulting in the accumulation of the glycolipid globotriaosylceramide throughout the body, particularly prominently in the blood vessels. A defect in the enzyme alpha galactosidase A results in glycosphingolipid accumulation, ultimately leading to multi-organ dysfunction and the patient’s premature death. Early symptoms, which occur during childhood, involve pain and may include Raynaud phenomenon, paresthesias, and arthralgia in the extremities and proximal limbs, as well as impaired gastrointestinal emptying, resulting in abdominal pain, diarrhea, early satiety, postprandial bloating, nausea, and vomiting. In adulthood, the disease’s impact spreads beyond and begins to affect the cardiac and renal systems.

Target Audience:

The following healthcare professionals: cardiologists, nephrologists, pediatricians, and primary care physicians; physician assistants, nurse practitioners, nurses, and pharmacists; and any other healthcare professionals with an interest in or who may clinically encounter patients with Fabry disease.

By the end of the session the participant will be able to:

• Describe the pathophysiology of Fabry disease diagnosis and treatment.
• Describe the challenges associated with diagnosis of Fabry disease.
• List present and emerging treatment options for Fabry disease and apply them to patient cases using evidence-based medicine.
• Describe the benefits and any applicable risks of therapeutic approaches to Fabry disease and take them into account when formulating a treatment plan for patients.

Alzheimer Disease (AD) is a degenerative disease that most commonly affects the elderly, although it is occasionally detected as early as middle age. AD accounts for over half of all diagnosed dementia, the prevalence of which is increasing. Once there is a diagnosis of probable AD, one must determine which pharmacotherapy, if any, is most appropriate for treatment of the patient. The literature suggests that gaps in care on the part of healthcare professionals exist. While some physicians continue to use the antiquated, nonspecific term “senile dementia” as a descriptive diagnosis of AD, perhaps suggesting a lack of understanding of the gravity of the disease state or its associated pathophysiology, other report feeling uncertain at times about now to best diagnosis of the disease, particularly in its very early stages. Moreover, a number of different practice guidelines have been updated recently, and HCPs are often unable to keep up with the publishing of literature and evolution of clinical practice.

Target Audience:

Healthcare professionals specializing in: neurology, gerontology, internal medicine, palliative care, or those who otherwise commonly care for patients with AD or who frequently encounter them or their caregivers in practice.

By the end of the session the participant will be able to:

• Describe what is presently known about the pathophysiology of AD.
• Describe the challenges associated with diagnosis and treatment of ADDiscuss the neuropathophysiology of AD and how it relates to presently available AD treatments mechanisms.
• Identify the present treatment options currently available for management of AD and apply them to patient cases using evidence-based medicine.
• Describe emerging drug therapies in the treatment of AD.
• Evaluate a treatment plan for a specific patient based on degree of AD to optimize safety and efficacy, suggesting modifications for improvement.

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 is passed to offspring through autosomal dominant inheritance, whereas the wild type variant occurs independently of genetic mutations. 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.

By the end of the session the participant will be able to:

• Describe the epidemiology of ATTR, including its subtypes.
• Compare and contrast invasive and non-invasive methods in the diagnosis of ATTR’s complications.
• Describe challenges in the management of ATTR, including under-diagnosis and challenges patients face in understanding the diagnosis and treatment of ATTR.
• Describe available and emerging therapies for ATTR and design an appropriate therapeutic plan including active patient involvement.

Migraine headache is the leading condition of recurrent cephalalgias of moderate or severe intensity. It is the most common type of headache presented by patients that seek medical treatment, and the World Health Organization (WHO) has ranked migraine in the top fifteen most disabling medical conditions. The condition has been identified as one of the most common neurological disorders, and in the United States, its prevalence in the general population is approximately 12%. In children, the prevalence ranges from 1% to 4% and does not present more commonly in either sex. However, after menarche, its prevalence in females (18%) is approximately three times higher than in males.

Moreover, professional guidelines relating to the classification, diagnosis, prophylaxis, and treatment of migraine headaches have been updated recently, and communicating related information to healthcare professionals in a timely manner is a demonstrated need. The literature suggests that practicing healthcare professionals are often times unable to keep up with the steady publishing of literature and evolution of clinical practice, and awareness of professional guidelines is no exception. Recently published guidelines therefore also inherently suggest a gap in medical practice and justify the need for educational programming. Generalists may be at particular risk for missing updates in standards relating to migraine subtypes like menstual and abdominal migraines.

Target Audience:

Neurologists and any other healthcare professionals who otherwise come into regular clinical contact with and provide care for patients with migraine.

By the end of the session the participant will be able to:

• Recall the pathophysiology and clinical presentation of headache in patients with COVID-19.
• Describe migraine basic science, epidemiology, outcomes, and therapy findings presented at the American Headache Society (AHS) Virtual Annual Scientific Meeting of 2020.
• Categorize new therapies and those in development based on data presented.
• Synthesize overall presentation material from the AHS CME meeting for further clinical application.

Treatment Updates on Chronic Inflammatory Demyelinating Polyneuropathy emphasizes the use of IVIg in the treatment of Chronic Inflammatory Demyelinating Polyneuropathy.

The presentation consists of a single lecture, Treatment Updates on Chronic Inflammatory Demyelinating Polyneuropathy, with discussion by Roy L. Freeman, MD, Richard J. Barohn, MD and Kenneth C. Gorson, MD.

After viewing Treatment Updates on Chronic Inflammatory Demyelinating Polyneuropathy, you will be better able to :
• Conduct a thorough and timely evaluation and differential diagnosis of patients with chronic inflammatory demyelinating polyneuropathy.
• Devise appropriate treatment regimen for the effective management of chronic inflammatory polyneuropathy based on guidelines and clinical evidence.

Target Audiences:
This program is intended for US-based neurologists, immunologists, physician assistants, nurse practitioners, and nurses who manage, or have an interest in managing patients with immune-mediated neuropathies.

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.

ScientiaCME Neuropsychiatry – Neurology contains 2 lectures:

• Highlights from the 2014 American Academy of Neurology Annual Meeting: Take-Aways, Emerging Practice Changes, and Barriers to their Implementation in Multiple Sclerosis (MS) (1 hr CME)
• Multiple Sclerosis (MS) in a Primary Care Setting: Employing Strategies for Appropriate Diagnosis and Improved Patient Outcomes (1 hr CME)

Target Audience: Neurologists

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.