Amantadine Enhancement of Arousal and Cognition After Traumatic Brain Injury

Sawyer, Elizabeth; Mauro, Laurie S.; Ohlinger, Martin J.

doi:10.1345/aph.1k284

Cited by 110 publications

(77 citation statements)

References 15 publications

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“…TBI is associated with reduction in the levels of catecholamines such as dopamine. The dopaminergic pathway is thought to regulate cognition and awareness (6,8). Amantadine has been found to improve neurocognitive function and arousal after TBI due to its dopaminergic effect (7,23).…”

Section: Discussionmentioning

confidence: 99%

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

Akçıl

Dilmen

Vehid

et al. 2018

Turk J Anaesth Reanim

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Objective: Aneurysmal subarachnoid haemorrhage (SAH) may have devastating effects on patients. Motor and neurocognitive impairments may arise depending on the location and grade of the SAH. Although the effects of amantadine on neurocognitive function after traumatic brain injury have been widely studied to the best of our knowledge, their effects on recovery from SAH in humans have not been studied. The present study aimed to evaluate how amantadine influences improvement in neurocognitive function in patients with aneurysmal SAH over a period of six months. Methods: This preliminary study included 12 patients with aneurysmal SAH who were admitted to the neurointensive care unit of Cerrahpasa Faculty of Medicine. Patients in Group A (n=5) received the standard treatment for SAH and amantadine for 30 days after admission, and those in Group C (n=7) received only the standard treatment. Neurocognitive function was evaluated using the Coma Recovery Scale-Revised and Disability Rating Scale on the first and fifth days and at the third and sixth months after admission. The primary endpoint of the present study was to compare the effects of amantadine in combination with the standard treatment to those of the standard treatment alone on the neurocognitive function of patients with SAH for over 6 months. Results: Compared to the standard treatment alone, amantadine administration with the standard treatment during the early period of SAH may improve recovery. Conclusion: Amantadine along with the standard treatment can ameliorate neurocognitive function after SAH. Keywords: Amantadine, subarachnoid haemorrhage, neurocognitive functions Amaç: Anevrizmalara bağlı subaraknoid kanamalarda, kanamanın yeri ve derecesine göre motor ve nörokognitif fonksiyonlar değişik derecelerde etkilenebilmektedir. Travmatik beyin hasarı sonrası amantadinin nörokognitif fonksiyonlar üzerine etkisi geniş olarak çalışılmış olsa da, bildiğimiz kadarıyla insanlarda sunaraknoid kanama sonrası iyileşmeye etkisi çalışılmamıştır. Bu çalışmanın amacı, amantadinin anevrizmaya bağlı subaraknoid kanamalarda kanamadan sonraki 6 ay süresince nörokognitif fonksiyonları nasıl etkilediğini değerlendirmektir. Yöntemler: Bu ön çalışma anevrizmal sunaraknoid kanama tanısıyla Cerrahpaşa Tıp Fakültesi nöroyoğun bakım ünitesine kabul edilen 12 hastayı içermektedir. Grup A'da (n=5) standart subaraknoid kanama tedavisinin yanında 30 gün boyunca amantadin verilirken, Grup C'de sadece standart tedavi uygulandı (n=7). Nörokognitif fonksiyonlar; amantadin başlandığında, beşinci günde, üçüncü ve altıncı ayda "coma recovery scale-revisited" ve "disability rating scale" ile değerlendirildi. Bu çalışmanın primer sonlanım noktası, anevrizmaya bağlı subaraknoid kanaması olan hastalarda, standart tedaviye amantadin eklenmesinin kanama sonrası 6 ay süresince nörokognitif fonksiyonlardaki iyileşme üzerine olan etkilerini standart tedaviyle karşılaştırmaktır. Bulgular: Bu çalışma, anevrizmaya bağlı subaraknoid kanaması olan hastalarda, standart tedaviye amantadin eklendiğinde, ...

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Section: Discussionmentioning

confidence: 99%

“…Amantadine, a NMDA receptor antagonist, has been widely studied in patients with traumatic brain injury (TBI), and its efficacy on neurocognitive improvement after TBI has been demonstrated (6)(7)(8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

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

Akçıl

Dilmen

Vehid

et al. 2018

Turk J Anaesth Reanim

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“…Another pharmaceutical mediator which manipulates dopamine in the brain and was remarkably effective on improving aphasia, is amantadine strong agonists of dopamine and norepinephrine receptors as well as a weak antagonist of glutamatergic NMDA receptor. This drug improves cognitive and motivation deficits by increasing the release of dopamine and norepinephrine in neural terminals of mesolimbic and mesocortical pathway (103). Studies report on the recovery of sensory and motor transcortical aphasia by this drug (104).…”

Section: Drugs Acting On Catecholaminergic Systemmentioning

confidence: 99%

Pharmacotherapy to Improve the Acquired Aphasia following Brain Damages: A Review Study

Ramezani

Reihanian

Yousefzadeh-Chabok

et al. 2015

IrJNS

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Background & Aim: Using pharmaceutical agents in treatment of aphasia has caught the attention of many neurologists and neuroscientists. This short review study has sought the role of pharmacotherapy in treatment of aphasia, a linguistic impairment after acquired brain lesions. The pharmacological principles and mechanisms related to the effects of drugs used in aphasia rehabilitation are pointed. Then, some evidence of clinical trials on different drugs in this field is presented. Methods & Materials/Patients:A comprehensive search in databases including MEDLINE, Cochrane, PubMed, Scopus, EMBASE, Science Direct on experimental studies and clinical trials associated with pharmacotherapy of aphasia after neurological damages was performed.

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“…Many studies have demonstrated that amantadine in dose of 100-400 mg/d may increase the arousal and improve cognitive function when given within 12 wk after the TBI. 37,42 Erythropoietin (EPO). EPO is a secreted glycoprotein with a molecular weight of 30-kD.…”

mentioning

confidence: 99%

Traumatic Brain Injury: Current Treatment Strategies and Future Endeavors

2016

Cell Transplant

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Traumatic brain injury (TBI) presents in various forms ranging from mild alterations of consciousness to an unrelenting comatose state and death. In the most severe form of TBI, the entirety of the brain is affected by a diffuse type of injury and swelling. Treatment modalities vary extensively based on the severity of the injury and range from daily cognitive therapy sessions to radical surgery such as bilateral decompressive craniectomies. Guidelines have been set forth regarding the optimal management of TBI, but they must be taken in context of the situation and cannot be used in every individual circumstance. In this review article, we have summarized the current status of treatment for TBI in both clinical practice and basic research. We have put forth a brief overview of the various subtypes of traumatic injuries, optimal medical management, and both the noninvasive and invasive monitoring modalities, in addition to the surgical interventions necessary in particular instances. We have overviewed the main achievements in searching for therapeutic strategies of TBI in basic science. We have also discussed the future direction for developing TBI treatment from an experimental perspective. Keywords traumatic brain injury, management, intracranial hypertension, treatment strategies Epidemiology of Traumatic Brain Injury (TBI)TBI continues to plague millions of individuals around the world on an annual basis. According to the Centers for Disease Control, the total combined rates for TBI-related emergency department visits, hospitalizations, and deaths have increased in the decade 2001-2010. 1 However, taken individually, the number of deaths related to TBIs has decreased over this same period of time likely secondary in part to increased awareness, structuralizing management and guidelines, and significant technological advancements in current treatment regimens. We should also acknowledge that there is a certain percentage of TBIs that never reach medical care, hence, the overall rates for TBIs are likely underreported. 2The highest rates of TBI tend to be in a very young agegroup (0-4 y) as well as in adolescents and young adults (15-24 y). There is another peak in incidence in the elderly (>65 y). The 2 leading causes of TBI overall are falls and motor vehicle accidents.3 As a result of an overall increased number of TBIs, but lower rate of related deaths, we have a growing population of individuals living with significant disabilities directly related to their TBI. Pathophysiology of TBITBI pathogenesis is a complex process that results from primary and secondary injuries that lead to temporary or permanent neurological deficits. The primary deficit is related directly to the primary external impact of the brain. The secondary injury can happen from minutes to days from the primary impact and consists of a molecular, chemical, and inflammatory cascade responsible for further cerebral damage. This cascade involves depolarization of the neurons

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Amantadine Enhancement of Arousal and Cognition After Traumatic Brain Injury

Abstract: At doses of 200-400 mg/day, amantadine appears to safely improve arousal and cognition in patients with TBI. Additional prospective controlled studies with homogeneous patient populations will better define the role of amantadine for early arousal.

Cited by 110 publications

References 15 publications

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

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

Pharmacotherapy to Improve the Acquired Aphasia following Brain Damages: A Review Study

Traumatic Brain Injury: Current Treatment Strategies and Future Endeavors

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