Can Amantadine Ameliorate Neurocognitive Functions After Subarachnoid Haemorrhage? A Preliminary Study

Akçıl, Eren Fatma; Dilmen, Özlem Korkmaz; Vehid, Hayriye Ertem; Tunalı, Yusuf

doi:10.5152/tjar.2018.20280

Cited by 12 publications

(6 citation statements)

References 27 publications

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“…Recently, Akcil et al ( 2018 ) studied the effects of amantadine on neurocognitive function recovery from subarachnoid hemorrhage (SAH) over 6 months. A group of five patients received the standard-of-care plus amantadine for 30 days, while the other seven patients received the standard treatment only on the first and fifth days and at the third and sixth months after admission.…”

Section: Preclinical and Clinical Evaluation Of Amantadine’s Non-canomentioning

confidence: 99%

“…A group of five patients received the standard-of-care plus amantadine for 30 days, while the other seven patients received the standard treatment only on the first and fifth days and at the third and sixth months after admission. The data suggested that adding amantadine to the standard treatment during the early period of SAH may improve neurocognitive function recovery evaluated using the Coma Recovery Scale-Revised (CRS-R) and Disability Rating Scale (DRS) (Akcil et al 2018 ).…”

Section: Preclinical and Clinical Evaluation Of Amantadine’s Non-canomentioning

confidence: 99%

“…Cognitive battery baseline scores for the treatment group were higher, increasing the group’s susceptibility to ceiling effects. At day 28, the mean change for the placebo group was greater Stroke Barrett and Eslinger ( 2007 ) Stroke (3), postoperative injury Case Series N = 4 Aphasia (Controlled Oral Word Association test) 100 mg BID Patients with transcortical motor aphasia performed better on Controlled Oral Word Association test during the 6 days when given amantadine Akcil et al ( 2018 ) Stroke (due to aneurysmal subarachnoid hemorrhage) RCT N = 12 (amantadine N = 5) Coma Recovery Scale-Revised (CRS-R), Disability Rating Scale (DRS) 200 mg/day or 100 mg BID At both 5 days and 6 months after intensive-care unit admission, patients (who suffered aneurysmal subarachnoid hemorrhage) who were given amantadine had higher CRS-R and lower DRS scores Khasanova et al ( 2009 ) Stroke (atherothrombotic or cardioembolic, acute period) N = 40 (amantadine (PK-Merz) = 20, magnesium sulfate control) Consciousness, neurological deficits 200 mg (in 500 ml) i.v. infusion Patients treated with amantadine sulfate exhibited the more significant restoration of consciousness and better dynamics (regress) of neurological deficit with the most intensive restoration of neurological deficit in the first day that allows to recommend the use of amantadine sulfate in the first hours of ischemic stroke and for the prevention of reperfusion damage in recanalisation therapy of ischemic stroke Krivonos et al ( 2010 ) Acute ischemic stroke (within 24–48 h of onset) N = 33 (amantadine N = 23) 10 patients in the control group received standard-of-care treatment Severity of Neurological Deficit on the National Institutes of Health Stroke Scale (NIHSS), the modified Rankin scale, and the Bartel Daily Living Index 200 mg (500 ml) i.v.…”

Section: Preclinical and Clinical Evaluation Of Amantadine’s Non-canomentioning

confidence: 99%

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Amantadine: reappraisal of the timeless diamond—target updates and novel therapeutic potentials

et al. 2021

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The aim of the current review was to provide a new, in-depth insight into possible pharmacological targets of amantadine to pave the way to extending its therapeutic use to further indications beyond Parkinson’s disease symptoms and viral infections. Considering amantadine’s affinities in vitro and the expected concentration at targets at therapeutic doses in humans, the following primary targets seem to be most plausible: aromatic amino acids decarboxylase, glial-cell derived neurotrophic factor, sigma-1 receptors, phosphodiesterases, and nicotinic receptors. Further three targets could play a role to a lesser extent: NMDA receptors, 5-HT3 receptors, and potassium channels. Based on published clinical studies, traumatic brain injury, fatigue [e.g., in multiple sclerosis (MS)], and chorea in Huntington’s disease should be regarded potential, encouraging indications. Preclinical investigations suggest amantadine’s therapeutic potential in several further indications such as: depression, recovery after spinal cord injury, neuroprotection in MS, and cutaneous pain. Query in the database http://www.clinicaltrials.gov reveals research interest in several further indications: cancer, autism, cocaine abuse, MS, diabetes, attention deficit-hyperactivity disorder, obesity, and schizophrenia.

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Section: Preclinical and Clinical Evaluation Of Amantadine’s Non-canomentioning

confidence: 99%

Section: Preclinical and Clinical Evaluation Of Amantadine’s Non-canomentioning

confidence: 99%

Section: Preclinical and Clinical Evaluation Of Amantadine’s Non-canomentioning

confidence: 99%

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Amantadine: reappraisal of the timeless diamond—target updates and novel therapeutic potentials

et al. 2021

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“…While amantadine was found not beneficial at all for overall cognition in traumatic brain injured patients in a multisite, randomized, controlled trial, published in September 2018, 5 it was found effective in enhancing neurocognitive function after TBI in another prospective, randomized controlled trial taking place in Turkey and published in the same year. 6 Systematic reviews discussing the effectiveness of amantadine in TBI were not easily done because the definition of TBI is not consistent across research. It changes according to specialties and circumstances.…”

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confidence: 99%

“…However, conflicting findings from clinical trials regarding its effectiveness for reducing cognitive and behavioral problems have hindered advances in justifying this hypothesis. While amantadine was found not beneficial at all for overall cognition in traumatic brain injured patients in a multisite, randomized, controlled trial, published in September 2018, 5 it was found effective in enhancing neurocognitive function after TBI in another prospective, randomized controlled trial taking place in Turkey and published in the same year 6 …”

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Assessment of the effect of amantadine in patients with traumatic brain injury: A meta-analysis

Mohamed

Sayed

Zaki

et al. 2021

J Trauma Acute Care Surg

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BACKGROUND:Traumatic brain injury is a global burden. We aimed to perform a meta-analysis to determine the efficacy of amantadine for cognitive performance after traumatic brain injury. METHODS:The systematic review was prospectively registered on the International Prospective Register of Systematic Reviews website under the registration number CRD42017080044. We used Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines to report the steps of meta-analysis. The search included electronic databases (PubMed, PsycINFO, Embase, Cochrane Library databases, CENTRAL, ProQuest and ClinicalTrials.gov trial registry). Critical care medicine journals and clinical neurology specialty were searched using www.scimagojr.com. There was no publication date restriction. Two authors assessed studies' relevance and extracted data. Studies were assessed for quality using the Cochrane risk of bias tool. Data were analyzed using Comprehensive Meta-analysis Program versions 2.0 and 3.0. RESULTS:Twenty-six studies out of 3,440 records were included in the systematic review, of which only 14 clinical trials and 6 observational studies were included in the meta-analysis. Amantadine significantly enhanced the cognitive function relative to control group (mean difference [MD], 0.50; 95% confidence interval [CI], 0.33-0.66; p < 0.001, 16 studies, 1,127 participants, low certainty evidence). Consistent significant difference in favor of amantadine relative to control group was found (MD of 0.79 [95% CI, 0.34-1.24], very low certainty evidence, for cohort studies vs. MD of 0.40 [95% CI, 0.25-0.56], moderate certainty evidence, for RCTS). Starting amantadine in the first week after TBI had a significant effect on improving cognitive function (MD, 0.97; 95% CI, 0.45-1.49; 16 studies, 1,127 participants, low certainty). Amantadine showed a better effect when administered for less than 1 month (MD, 0.83; 95% CI, 0.56-1.11; low certainty) and to patients below 18 years of age (MD, 0.66; 95% CI, 0.32-0.99; low certainty) or to patients with less severe traumatic brain injury (MD, 0.40; 95% CI, 0.18-0.62; low certainty). No statistically significant difference existed between amantadine and the control concerning the adverse events (OR, 1.74; 95% CI, 0.88-3.44; p = 0.11, moderate certainty). Metaregression of the different clinical parameters, which are onset of treatment, age, and severity of traumatic brain injury, showed a statistically significant relation between onset of treatment and the effect size of amantadine. The relation between the other two parameters and the effect size of amantadine showed a marginal statistical significance. CONCLUSION:Amantadine may improve the cognitive function when used after TBI. Further research with high validity is needed to reach a solid conclusion about the use of amantadine in traumatic brain injury.

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Pharmacological Treatments

Szymkowicz,

Alnagger,

Seyfzadehdarabad

et al. 2023

Coma and Disorders of Consciousness

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Can Amantadine Ameliorate Neurocognitive Functions After Subarachnoid Haemorrhage? A Preliminary Study

Cited by 12 publications

References 27 publications

Amantadine: reappraisal of the timeless diamond—target updates and novel therapeutic potentials

Amantadine: reappraisal of the timeless diamond—target updates and novel therapeutic potentials

Assessment of the effect of amantadine in patients with traumatic brain injury: A meta-analysis

Pharmacological Treatments

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