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Autonomic Nervous System Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Alpha antagonists: ephedrine and methylphenidate hydrochloride (Ritalin) have been largely replaced by midodrine, an alpha-adrenergic agonist which acts by improving arterial and venous constriction in response to standing.9 The initial starting dose is 5 mg/day, and it should only be used during upright hours because of the risk of supine hypertension. Supine hypertension may require short-acting antihypertensive agents (e.g. beta-blocker) but can be minimized by elevating the head of the bed.
Alpha Adrenergic Modulation of Impulse Initiation in Normal and Ischemic Cardiac Fibers
Published in Samuel Sideman, Rafael Beyar, Analysis and Simulation of the Cardiac System — Ischemia, 2020
We then considered the response of fibers to alpha adrenergic stimulation during ischemia at high (10.8 mM) and normal (2.7 mM) [Ca2+]o.35 We found that at both [Ca2+]o, automatic rhythms ceased during ischemia (control rate of 17 ± 2 beats per minute). On reperfusion, the automatic rates remained significantly higher in the high Ca2+ than the low Ca2+ environment. Addition of an alpha adrenergic agonist in the presence of either low or high Ca2+ ischemia again reduced the rate of the dominant automatic rhythm to 0. On reperfusion, however, there was a more rapid return to normal maximum diastolic potential and control automatic rates in the Ca2+ = 2.7 than in the high Ca2+ setting. Hence, in the setting of reperfusion, alpha adrenergic stimulation was “protective”, returning membrane potential and rhythm more rapidly to control values than would otherwise have been the case.
Treatment Of Alzheimer’s Disease
Published in Zaven S. Khachaturian, Teresa S. Radebaugh, Alzheimer’s Disease, 2019
Lina Shihabuddin, Kenneth L. Davis
There is ample evidence demonstrating that multiple neurotransmitter systems are involved in Alzheimer’s disease; thus a combined treatment strategy is likely to be more efficacious than cholinergic monotherapy. Animal research shows that noradrenergic brain lesions negate cholinomimetic enhancement of memory in hypocholinergic animals (Haroutunian et al., 1985). Administration of alpha adrenergic agonist clonidine in turn restores the efficacy of cholinomimetic treatment in animals with a large noradrenergic and modest cholinergic lesions (Haroutunian et al., 1990). The alpha adrenergic antagonist idazoxan, which enhances locus cereleus firing and norepinephrine turnover, has been shown to improve memory in rodents (Sara et al., 1989). Moreover, post-mortem studies showed major neurotransmitter losses of the noradrenergic systems in Alzheimer’s disease patients. All these findings support the use of a combination of cholinergic and noradrenergic agents to treat AD.
Management of Pregabalin Use Disorder: A Case Series
Published in Journal of Psychoactive Drugs, 2022
Lisa Langlumé, Céline Eiden, Sophie Roy, Floriane Taruffi, Julien Gambier, Hélène Donnadieu-Rigole, Hélène Peyrière
In this series of patients, management of withdrawal was based, for some anxious patients, on the short-term use of diazepam with a programmed dose reduction. Importantly, the diazepam dose should be adapted in patients with a history of benzodiazepine abuse and/or current use. At the time of the study, the long-term effectiveness of this adjuvant treatment was unknown. However, two patients who took diazepam relapsed and restarted pregabalin consumption. One of the limitations is the risk of the shift of dependence from pregabalin to diazepam or another substance (Gahr et al. 2015). Clonidine (used in patient no. 8) might be another possible option to manage pregabalin-related withdrawal symptoms. Clonidine is an alpha-adrenergic agonist used off-label for the management of opioid withdrawal (Toce et al. 2018). Clonidine helps to reduce the signs and symptoms of excessive autonomic activity (e.g. anxiety, chills, piloerection, tachycardia, and hypertension). Clonidine has been previously used for pregabalin withdrawal management outside the context of pregabalin use disorder and was effective on agitation (Barrett, Kittler, and Singarajah 2015).
Brimonidine tartrate for the treatment of glaucoma
Published in Expert Opinion on Pharmacotherapy, 2019
Daniel J. Oh, Judy L. Chen, Thasarat S. Vajaranant, Mark S. Dikopf
The third-generation alpha adrenergic agonist, brimonidine tartrate, has the addition of a quinoxaline bicyclic ring and bromine substitution at the chlorine site, increasing alpha-2 selectivity and further reducing lipophilicity[14]. In 1996, brimonidine was approved by the FDA for the treatment of OHTN and glaucoma.
Orthostatic intolerance in post-concussion patients
Published in The Physician and Sportsmedicine, 2022
Sara J. Gould, Graham D. Cochrane, Jarvis Johnson, Camden L. Hebson, Mohamed Kazamel
Identifying patients with OI after a concussion is important, as treatment is straightforward and well-within the scope of the general practitioner and specialist alike [25]. Specific recommendations on increasing daily water and salt intake often help direct patients toward functional recovery. A graduated exercise plan, satisfactory for both recovery from the concussion but also directed toward building back muscle tone in the legs, has been shown to improve OI symptoms over time [8,26]. Compression garments and counterpressure maneuvers are practical and risk-free additions as well, and have been shown to improve cerebral perfusion during standing, and presyncopal symptoms [27,28]. Fludrocortisone is a synthetic mineralocorticoid that mimics aldosterone, acting on the nephron distal tubule to promote sodium retention. It has been shown in a randomized, placebo-controlled trial to reduce the recurrence of vasovagal syncope two weeks after dose stabilization [4]. It is also a fairly benign medicine, and in our experience, does not require frequent monitoring in young patients with normal kidneys, especially for short-term use. Low doses of nonselective ß-blockers may also be beneficial in controlling symptoms of OI. The mechanism of action involves preventing sympathetic overactivity of the Beta-adrenergic receptors, resulting in peripheral vasoconstriction and decreased heart rate. A third medication that is routinely used in OI is midodrine, a prodrug that gets metabolized into its active metabolite, desglymidodrine, with a strong alpha-adrenergic agonist activity. Hence, it constricts arterioles and decreases venous pooling via reducing venous capacitance [16]. Of course, individual providers will have different levels of comfort in implementing these treatments. For more involved patients, discerning what subtype of OI is present, medication choices, and counseling are all more complex and referral to a specialist is warranted [12]. We therefore propose the included algorithm for screening, diagnosis, and management of potential cases of post-concussive OI (Figure 2) to be implemented in clinics taking care of such a patient population.