Amir Babak Ghaemmaghami, MD
One of the challenges facing behaviorally orientedneurologists is that many patients' symptoms fallbeyond the scope of a physical neurological evaluation.Frequently, patients with neurodegenerative disease,particularly in the early stages, present with intactcranial nerves, reflexes, eye movements, and sensory-motor function. Accordingly, clinicians need tools to formally assess the cognitive, psychiatric and behavioral abnormalities that define many dementing disorders.
Amir Babak Ghaemmaghami, MD
Accumulating evidences from experimental, epidemiologic and clinical studies support the potential linkage between poor vitamin D status and the risk of developing Multiple Sclerosis (MS), as well as, an adverse disease course.
Neurogenic orthostatic hypotension is a disorder of noradrenergic neurotransmission. It’s most familiar presentation is lightheadedness or even syncope on standing. We know that the basic mechanism is impaired norepinephrine release from postganglionic sympathetic nerve terminals, resulting in a decrease in blood pressure (BP) and reduced blood flow to vital organs, especially the brain, when one stands. Orthostatic hypotension (OH) is defined as a fall in systolic BP of at least 20 mm Hg or in diastolic BP of at least 10 mm Hg within 3 minutes of standing. Symptoms may include lightheadedness, dizziness, weakness, fatigue, vision changes, poor concentration, head and neck pain, and difficulty standing. It could be due to an underlying neurologic condition or other factors. To get the conversation going, Billy, what are the non-neurologic causes of OH?Continue reading: http://www.medscape.org/viewarticle/835650
The use of statins in neurocardiovascular conditions has widely increased over the decades. Based on extension of indications major side effects of statin therapy became evident. In 1 of 10,000 treated persons per year, statins cause toxic muscle weakness and creatine kinase (CK) level elevation. A novel finding is that in some patients the statin-induced myopathy is caused by an autoimmune-mediated treatable myopathy by the presence of autoantibodies against 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (anti-HMGCR). At present its frequency is 2 to 3 in 100.000 patients treated with statins. This neuromuscular phenotype encompasses a proximal symmetric weakness, and a persisting more than 10 times the upper limit of the normal range elevated CK levels. EMG presents an active myopathy with an increased spontaneous activity while muscle MRI shows muscle edema.
Encephalitis is a severe inflammatory disorder of the brain with many possible causes and a complex differential diagnosis. Advances in autoimmune encephalitis research in the past 10 years have led to the identification of new syndromes and biomarkers that have transformed the diagnostic approach to these disorders. However, existing criteria for autoimmune encephalitis are too reliant on antibody testing and response to immunotherapy, which might delay the diagnosis. We reviewed the literature and gathered the experience of a team of experts with the aims of developing a practical, syndrome-based diagnostic approach to autoimmune encephalitis and providing guidelines to navigate through the differential diagnosis. Because autoantibody test results and response to therapy are not available at disease onset, we based the initial diagnostic approach on neurological assessment and conventional tests that are accessible to most clinicians.