Outside the box: Medications worth considering when traditional antiepileptic drugs have failed

Turner, Adrian L.; Perry, Matthew

doi:10.1016/j.seizure.2017.06.022

Cited by 17 publications

(16 citation statements)

References 112 publications

(162 reference statements)

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“…Amantadine has been safely administered to patients with epilepsy since the mid-1980's [30], but caution is still required. Many patients had multiple other reasons for potential adverse effects (i.e., confusion potentially caused by amantadine or modafinil, urinary tract infection, steroids, vasospasm, hydrocephalus, or hypernatremia).…”

Section: Discussionmentioning

confidence: 99%

Amantadine and Modafinil as Neurostimulants Following Acute Stroke: A Retrospective Study of Intensive Care Unit Patients

et al. 2020

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Background/Objective: Neurostimulants may improve or accelerate cognitive and functional recovery after intracerebral hemorrhage (ICH), ischemic stroke (IS), or subarachnoid hemorrhage (SAH), but few studies have described their safety and effectiveness in the intensive care unit (ICU). The objective of this study was to describe amantadine and modafinil administration practices during acute stroke care starting in the ICU and to evaluate safety and effectiveness. Methods: Consecutive adult ICU patients treated with amantadine and/or modafinil following acute non-traumatic IS, ICH, or SAH were evaluated. Neurostimulant administration data were extracted from the electronic medication administration record, including medication (amantadine, modafinil, or both), starting dose, time from stroke to initiation, and whether the neurostimulant was continued at hospital discharge. Patients were considered responders if they met two of three criteria within 9 days of neurostimulant initiation: increase in Glasgow coma scale (GCS) score ≥ 3 points from pre-treatment baseline, improved wakefulness or participation documented in caregiver notes, or clinical improvement documented in physical or occupational therapy notes. Potential confounders of the effectiveness assessment and adverse drug effects were also recorded. Results: A total of 87 patients were evaluable during the 3.7-year study period, including 41 (47%) with ICH, 29 (33%) with IS, and 17 (20%) with SAH. The initial neurostimulant administered was amantadine in 71 (82%) patients, modafinil in 13 (15%), or both in 3 (3%) patients. Neurostimulants were initiated a median of 7 (4.25, 12.75) days poststroke (range 1-27 days) for somnolence (77%), not following commands (32%), lack of eye opening (28%), or low GCS (17%). The most common starting dose was 100 mg twice daily for both amantadine (86%) and modafinil (54%). Of the 79 patients included in the effectiveness evaluation, 42 (53%) were considered responders, including 34/62 (55%) receiving amantadine monotherapy and 8/24 (33%) receiving both amantadine and modafinil at the time they met the definition of a responder. No patient receiving modafinil monotherapy was considered a responder. The median time from initiation to response was 3 (2, 5) days. Responders were more frequently discharged home or to

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Section: Discussionmentioning

confidence: 99%

Amantadine and Modafinil as Neurostimulants Following Acute Stroke: A Retrospective Study of Intensive Care Unit Patients

et al. 2020

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“…This medication is a diuretic which mechanism of action is to inhibit the carbonic anhydrase enzyme used to reduce the intraocular pressure, edema, and as an anticonvulsant [9]. It is indicated by the Food and Drug Administration (FDA) for centrencephalic epilepsy, such as absence seizures, myoclonic, atonic; but, this drug had shown good results for treatment for other types of epilepsy, such as generalized tonicclonic and mixed seizures [10]. The first report of the use of this drug for this goal was in 1956 by Anssel et al [11] when 26 patients with different idiopathic epilepsy were treated with 1-14mg/kg of acetazolamide taken in two doses a day.…”

Section: Discussionmentioning

confidence: 99%

Case Report: Follow Up of a Patient with De Novo Mutation at Kcna2 Gene Leading to Ataxia and Epileptic Encephalopathy

Vbs

2020

AICS

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Background:The KCNA2 gene codifies a protein of the Kv1.2 potassium channel. Most of the last are express in the central nervous system, where they have an important role in the release of neurotransmitters and neural excitability. A mutation on this gene leads to a drastic over function with the permanent opening of the referred channel.Case presentation: A 13-year-old male child, was diagnosed in 2014 with a mutation on the KCNA2 gene during the investigation of ataxia and epileptic encephalopathy, discovering a new cause of neurodevelopmental disorder. A detailed description of the symptoms of the patient was obtained during his lifetime until the publication of this article. Conclusion:A new cause of neurodevelopmental disorder was found during an investigation of the epileptic encephalopathy and ataxia-the mutation in the KCNA2 gene-, as a detailed evolution of this syndrome.

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“…Therefore, for many years it has been deployed as a treatment option for cardiovascular diseases, such as hypertension (Lewis et al, 1978;Midtbø et al, 1986), supraventricular tachyarrhythmias (Schamroth et al, 1972;Krikler & Spurrell, 1974), and angina pectoris (Livesley et al, 1973;Parodi et al, 1979). Remarkably, verapamil has been also used as a drug option for the treatment of hypertrophic and keloid scars (Ahuja and Chatterjee, 2014;Verhiel et al, 2015), obesity-associated autophagy defects and fatty liver pathologies (Park and Lee, 2014), osteoarthritis (Matta et al, 2015), cluster headache (Meyer and Hardenberg, 1983;Tfelt-Hansen and Tfelt-Hansen, 2009;Leone et al, 2017;Petersen et al, 2019), bipolar disorders (Wisner et al, 2002;Cipriani et al, 2016;Dubovsky, 2018), type 2 diabetes (Yin et al, 2017;Carvalho et al, 2018;Carnovale et al, 2019), chronic rhinosinusitis (Miyake et al, 2018), Peyronie's disease (Russo et al, 2018), tuberculosis (Rayasam and Balganesh, 2015;Song and Wu, 2016), epilepsy (Nicita et al, 2016;Turner and Perry, 2017), and reversible cerebral vasoconstriction syndrome (Cappelen-Smith et al, 2017). However, verapamil has expressed ambiguous effects in Parkinson's disease (Garcıá-Albea et al, 1993;Pasternak et al, 2012) and dementia (Maxwell et al, 1999;Yaser et al, 2005;Nimmrich and Eckert, 2013).…”

Section: Introductionmentioning

confidence: 99%

Verapamil and Alzheimer’s Disease: Past, Present, and Future

et al. 2020

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Verapamil is a phenylalkylamine class calcium channel blocker that for half a century has been used for the treatment of cardiovascular diseases. Nowadays, verapamil is also considered as a drug option for the treatment of several neurological and psychiatric disorders, such as cluster headache, bipolar disorders, epilepsy, and neurodegenerative diseases. Here, we review insights into the potential preventive and therapeutic role of verapamil on Alzheimer's disease (AD) based on limited experimental and clinical data. Pharmacological studies have shown that verapamil has a wide therapeutic spectrum, including antihypertensive, anti-inflammatory, and antioxidative effects, regulation of the blood-brain barrier function, due to its effect on P-glycoprotein, as well as adjustment of cellular calcium homeostasis, which may result in the delay of AD onset or ameliorate the symptoms of patients. However, the majority of the AD individuals are on polypharmacotherapy, and the interactions between verapamil and other drugs need to be considered. Therefore, for an appropriate and successful AD treatment, a personalized approach is more than necessary. A well-known narrow pharmacological window of verapamil efficacy may hinder this approach. It is therefore important to note that the verapamil efficacy may be conditioned by different factors. The onset, grade, and brain distribution of AD pathological hallmarks, the time-sequential appearances of AD-related cognitive and behavioral dysfunction, the chronobiologic and gender impact on calcium homeostasis and AD pathogenesis may somehow be influencing that success. In the future, such insights will be crucial for testing the validity of verapamil treatment on animal models of AD and clinical approaches.

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Outside the box: Medications worth considering when traditional antiepileptic drugs have failed

Cited by 17 publications

References 112 publications

Amantadine and Modafinil as Neurostimulants Following Acute Stroke: A Retrospective Study of Intensive Care Unit Patients

Amantadine and Modafinil as Neurostimulants Following Acute Stroke: A Retrospective Study of Intensive Care Unit Patients

Case Report: Follow Up of a Patient with De Novo Mutation at Kcna2 Gene Leading to Ataxia and Epileptic Encephalopathy

Verapamil and Alzheimer’s Disease: Past, Present, and Future

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