The outcome of patients with severe head injuries treated with amantadine sulphate

Sániová, Beata; Drobný, M; Knéslová, L; Minarik, Milan

doi:10.1007/s00702-004-0112-4

Cited by 67 publications

(68 citation statements)

References 4 publications

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“…This study was also limited by its retrospective design. In addition, this study differed from that of Saniova et al 39 While Saniova et al initiated amantadine therapy 3 days following the injury, Hughes et al 40 did not initiate the drug until approximately 6 weeks after TBI. The duration of treatment also differed.…”

Section: Discussionmentioning

confidence: 86%

“…Therefore, it is possible that the patient's improvement was due to amantadine, spontaneous recovery in the acute period following injury, or a combination of these factors. Saniova et al 39 reported an improvement in outcome GCS scores and mortality in patients receiving amantadine. However, this study was limited by its small patient population and retrospective design, which did not allow for control in the treatments used.…”

Section: Discussionmentioning

confidence: 98%

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Amantadine Therapy in Traumatic Brain Injury Patients

Villareal

2007

Journal of Pharmacy Technology

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s VOLUME 23 s J PHARM TECHNOL 95Each year, 1.4 million Americans experience a traumatic brain injury (TBI). Consequently, 1.1 million Americans require treatment in an emergency department, 235,000 require hospitalization, 80,000-90,000 develop a permanent disability, and 50,000 die as a result of their injury. 1-2 The Centers for Disease Control and Prevention estimates that 2% of the US population requires assistance to perform daily activities due to a TBI. 2 These disabilities, which include cognitive, behavioral, sensory, and motor impairments, have a profound impact on the rehabilitation and future quality of life of patients with TBI. 2, 3 Cognitive impairments may affect 20-80% of patients with TBI, the most common being memory loss. Other types of cognitive impairments may include attention, language, and executive disturbances. Language disturbances may include problems with word-finding and expressing ideas. Patients affected with executive disturbances may exhibit difficulty with functions related to planning and organizing. These patients may display impulsivity, as well as lack of initiation and motivation. 4Many patients with TBI also experience behavioral impairments. Mood disorders, which include major depression and bipolar disorder, may affect 6-77% and 3-9% of patients, respectively. Anxiety, apathy, and psychosis have also been observed. 4 Finally, 11-50% of patients with TBI may experience posttraumatic agitation. 5 These patients may display excessive behaviors, including aggression, akathisia, poor impulse control, disinhibition, impaired attention, and emotional lability. 5-9The pathophysiology of the acute phase of TBI is characterized by neuronal depolarization and neurotransmitter release. During this period, the opening of potassium channels results in the release of excitatory neurotransmitters, including glutamate. 10 Glutamate then activates N-methyl-D-aspartate (NMDA) channels. This results in an influx of sodium and calcium into the cell, causing a variety of pathological changes that may ultimately result in cell death. 11-14 During this phase, there is also a release of acetylcholine and catecholamines including norepinephrine and dopamine. The chronic phase of TBI begins approximately 24 hours following injury and may continue for several weeks. Unlike the acute phase, the pathophysiology of the chronic phase of TBI is characterized by decreased cerebral metabolism and decreased concentrations of excitatory neurotransmitters, acetylcholine, norepinephrine, and dopamine. 15 Decreased Objective: To review literature on amantadine therapy in patients with traumatic brain injury (TBI). were searched to identify papers on the clinical outcomes of patients with TBI treated with amantadine. A bibliographic search was also performed. Study Selection and Data Extraction:Papers were excluded if they were not published in English, if they included patients less than 16 years old, or if they included patients in whom the effects of multiple medications, rather than amantadine alone, were ...

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Section: Discussionmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 98%

Amantadine Therapy in Traumatic Brain Injury Patients

Villareal

2007

Journal of Pharmacy Technology

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“…53,64 In addition to its actions as a dopamine agonist, amantadine is also thought to act as a direct NMDA receptor antagonist, which may reduce glutamate-induced excitotoxicity and associated brain swelling after TBI. 82,83 Thus, early treatment with amantadine may improve arousal by simultaneously minimizing disruptions to dopamine levels in the brain and by reducing excitotoxicity and associated brain swelling.…”

Section: Discussionmentioning

confidence: 99%

Impact of Early Pharmacological Treatment on Cognitive and Behavioral Outcome After Traumatic Brain Injury in Adults

Wheaton

Mathias²,

Vink³

2009

Journal of Clinical Psychopharmacology

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Early pharmacological treatment has the potential to reduce some of the disabling cognitive and behavioral problems that result from traumatic brain injury (TBI). Although a large number of treatments have been developed, clinical research has yielded inconsistent findings with respect to the effectiveness of these pharmacological treatments on cognitive and behavioral outcomes. Furthermore, their relative efficacy has not been evaluated, thereby hindering advances in the treatment of TBI. A meta-analysis of research that examined the impact of pharmacological treatments on cognitive and behavioral outcomes in the early stages after TBI between January 1980 and May 2008 was therefore undertaken. The PubMed and PsycINFO databases were searched using 35 terms. All articles were screened using detailed inclusion criteria. Weighted Cohen's d effect sizes, percent overlap statistics, and fail-safe N statistics were calculated for each pharmacological agent. Studies that used different experimental designs were examined separately. Eleven pharmacological treatments were investigated by 22 clinical studies, comprising 6472 TBI patients in the treatment groups and 6460 TBI controls. One dopamine agonist (amantadine) and 1 bradykinin antagonist (CP-0127 [Bradycor]) produced marked treatment benefits (d > or = 0.8) for a single measure of arousal (Glasgow Coma Scale). Notably, drug dosage and the measure chosen to assess outcome influenced the probability of finding a treatment benefit.

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“…fluoxetine, amitriptyline, sertraline) [19][20][21], dopaminergic (e.g. methylphenidate, amantadine) [22,23] and cholinergic agents (e.g. donepezil, physostigmine-lecithin combination treatment) [ [24][25][26][27].…”

Section: Discussionmentioning

confidence: 99%

Effects of low-dose milnacipran on event-related potentials and neuropsychological tests in persons with traumatic brain injury: A preliminary study

et al. 2015

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The outcome of patients with severe head injuries treated with amantadine sulphate

Abstract: In the group of patients with severe brain injuries treated with standard therapy plus amantadine sulphate the outcome GCS was higher and the case fatality rate lower than in the group treated with standard therapy alone.

Cited by 67 publications

References 4 publications

Amantadine Therapy in Traumatic Brain Injury Patients

Amantadine Therapy in Traumatic Brain Injury Patients

Impact of Early Pharmacological Treatment on Cognitive and Behavioral Outcome After Traumatic Brain Injury in Adults

Effects of low-dose milnacipran on event-related potentials and neuropsychological tests in persons with traumatic brain injury: A preliminary study

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