American Academy of Neurology Telehealth Position Statement.

Telehealth services complement in-person neurologic care. The American Academy of Neurology supports patient access to telehealth services regardless of location, coverage for telehealth services by all subscriber benefits and insurance, equitable provider reimbursement, simplified state licensing requirements easing access to virtual care, and expanding telehealth research and quality initiatives. The roles and responsibilities of providers should be clearly delineated in telehealth service models.

Telemedicine in neurology: Telemedicine Work Group of the American Academy of Neurology update.

PURPOSE: While there is strong evidence supporting the importance of telemedicine in stroke, its role in other areas of neurology is not as clear. The goal of this review is to provide an overview of evidence-based data on the role of teleneurology in the care of patients with neurologic disorders other than stroke. RECENT FINDINGS: Studies across multiple specialties report noninferiority of evaluations by telemedicine compared with traditional, in-person evaluations in terms of patient and caregiver satisfaction. Evidence reports benefits in expediting care, increasing access, reducing cost, and improving diagnostic accuracy and health outcomes. However, many studies are limited, and gaps in knowledge remain. SUMMARY: Telemedicine use is expanding across the vast array of neurologic disorders. More studies are needed to validate and support its use.

CSF Cytokines in Aging, Multiple Sclerosis, and Dementia.

Inflammation is a common process involved in aging, multiple sclerosis (MS), and age-related neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease (PD), but there is limited evidence for the effects of aging on inflammation in the central nervous system. We collected cerebrospinal fluid (CSF) from 105 healthy control subjects representing a wide age range (23-86), and analyzed levels of cytokines associated innate immunity (TNF-α) and different T-helper subtypes: interferon-gamma induced protein 10 (IP-10) for Th1, interleukin-10 (IL-10) for Th2, and interleukin 8 (IL-8/CXCL8) for Th17. We show that CSF levels of TNF-α, IP-10, and IL-8 all increased linearly with age, but levels of IL-10 demonstrated a U-shaped relationship with age. We further found greater age-related increases in TNF-α, IL-10, and IL-8 relative to increases in IP-10 levels, consistent with a shift from Th1 to other inflammatory phenotypes. Finally, when we analyzed the same four cytokines in people with neurological disorders, we found that MS and AD, but not PD or dementia with Lewy bodies, further accentuated the age-related shift from Th1- to non-Th1-related cytokines. We propose that CSF cytokine levels represent powerful surrogates of brain inflammation and aging, and some, but not all, neurological disorders accelerate the shift away from Th1 phenotypes.

Propranolol therapy for Tardive dyskinesia: A retrospective examination.

OBJECTIVE: To examine the tolerability and effectiveness of propranolol in treating tardive dyskinesia (TD). BACKGROUND: TD is a disabling, often irreversible, movement disorder that results from chronic therapy with dopamine receptor blocking drugs. There are no treatments currently approved for this disorder. Propranolol, a ß-adrenergic blocker, has been reported to alleviate TD in case series and reports. METHODS: Retrospective database search of the Emory movement disorder clinic for TD patients treated with propranolol. All patients identified with at least one follow-up evaluation had records reviewed and responsiveness assessed. Logistic regression analysis examined for predictors of response. RESULTS: Forty-seven patients were analyzed, mean age 63 years. Neuroleptics were discontinued in all patients and duration of TD at the time propranolol was initiated 17 months. Mean severity of TD, based on a 0-3 scale (0 = none, 1 = mild, 2 = moderate, 3 = severe) was 2.2. Mean response, based on a 0-3 scale (0 = no response, 1 = mild response, 2 = moderate response, 3 = complete or near-complete response) was 1.4. Propranolol resulted in improvement in 64% and 77% of those had a moderate to complete or near-complete response. Mean daily dose was 69 mg and duration of therapy 14 months. Three patients stopped the propranolol due to adverse effects: hypotension (2), nightmares (1). Severity of TD and duration of propranolol therapy were associated with response. CONCLUSION: Low dose propranolol appears to be well tolerated and effective in treating TD. A prospective randomized trial is warranted.

Association between polychlorinated biphenyls and Parkinson's disease neuropathology.

Polychlorinated biphenyls (PCBs) are synthetic chemicals primarily used as coolants and insulators in electrical equipment. Although banned for several decades, PCBs continue to exist in the environment because of their long half-life, continued presence in items produced before the ban, and poor disposal practices. Epidemiological and experimental studies have identified exposure to PCBs as a potential risk factor for Parkinson's disease, perhaps more so in females. The objective of this work was to examine the association between PCB levels in post-mortem human brain tissue and the diagnosis of Parkinson's disease, as well as the degree of nigral depigmentation. We also sought to determine if this association was more significant when patients were stratified by sex. Post-mortem brain samples from control patients and those diagnosed with Parkinson's disease were obtained from the Emory University Brain Bank and from the Nun Study. Concentrations of eight prevalent PCB congeners were extracted from post-mortem brain tissue and analyzed using gas chromatography-mass spectrometry. PCB congeners 153 and 180 were significantly elevated in the brains of Parkinson's disease patients. When stratified by sex, the female Parkinson's disease group demonstrated significantly elevated concentrations of total PCBs and specifically congeners 138, 153, and 180 compared to controls, whereas PCB concentrations in males were not significantly different between control and Parkinson's disease groups. In a separate population of women (Nun Study) who had no clinical signs or symptoms of PD, elevated concentrations total PCB and congeners 138, 153 and 180 were also observed in post-mortem brain tissue exhibiting moderate nigral depigmentation compared to subjects with mild or no depigmentation. These quantitative data demonstrate an association between brain PCB levels and Parkinson's disease-related pathology. Furthermore, these data support epidemiological and laboratory studies reporting a link between PCB exposure and an increased risk for Parkinson's disease, including greater susceptibility of females.