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Clinical NeuropharmacologyAcute traumatic brain injury is one of the most common causes of death and disability. Reduction in the level of consciousness is a significant complication that can...
OBJECTIVES
Acute traumatic brain injury is one of the most common causes of death and disability. Reduction in the level of consciousness is a significant complication that can impact morbidity. Glasgow Coma Scale (GCS) is the most widely used method of assessing the level of consciousness. Neurostimulants such as amantadine and modafinil are common pharmacologic agents that increase GCS in patients with brain trauma. This study aimed to compare the effectiveness of these 2 drugs.
METHODS
This systematic review obtained articles from Google Scholar, PubMed, Scopus, Embase, and MEDLINE databases. Extensive searches were conducted separately by 4 individuals in 3 stages. Ultimately, 16 clinical trials, cohort studies, case reports, and case series articles were obtained after reading the title, abstract, and full text and considering the exclusion criteria. The data of the final article were entered into the analysis table. This study was registered with PROSPERO (registration number CRD42022334409) and conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines.
RESULTS
Amantadine seems to be associated with a higher overall response rate. In contrast, modafinil is associated with the most remarkable change in GCS score during treatment. However, the number of clinical trials with high quality and sample size has not been satisfactory to compare the effectiveness of these 2 drugs and their potential side effects.
CONCLUSIONS
The authors recommend additional double-blind clinical trials are needed to be conducted with a larger sample size, comparing amantadine with modafinil to delineate the efficacy and adverse effects, both short and long term.
Topics: Humans; Modafinil; Consciousness; Brain Injuries, Traumatic; Amantadine; Brain Injuries; Randomized Controlled Trials as Topic
PubMed: 37962310
DOI: 10.1097/WNF.0000000000000577 -
Journal of Oncology Pharmacy Practice :... Jul 2022Approximately 50-90% of brain metastatic patients who receive radiation therapy (RT) exhibit cognitive decline which may affects the quality of life of cancer survivors.... (Review)
Review
OBJECTIVE
Approximately 50-90% of brain metastatic patients who receive radiation therapy (RT) exhibit cognitive decline which may affects the quality of life of cancer survivors. Hence preservation of cognitive functions in brain metastatic patients becomes important. This review aims to evaluates the pathology or mechanism of cognitive function impairment after brain irradiation and strategies available to preserve cognitive function after radiation therapy.
DATA SOURCES
Published articles evaluating the pathology behind radiation induced cognitive impairment and strategies to resolve or preserve cognitive impairment were searched for in scientific databases (eg: PubMed, Scopus, Cochrane database, Google scholar) using keywords including memantine, brain metastases, radiation therapy, pathophysiology, pathogenesis, mechanism and prevention.
DATA SUMMARY
Several hypotheses have been offered to explain the mechanism of radiation induced cognitive decline. Among them, vascular hypotheses play a significant role. Some pharmacological agents have been also tested in patients receiving radiotherapy, memantine was found beneficial based with the reference to existing data.
CONCLUSION
Future studies are required to evaluate the impact of memantine in different types of radiation therapy procedures and its effects on quality of life of brain metastatic survivors.
Topics: Humans; Memantine; Quality of Life; Brain; Cognition; Brain Neoplasms
PubMed: 35112915
DOI: 10.1177/10781552221077037 -
Neurologia 2022Guillain-Barré syndrome (GBS) is an acute-onset, immune-mediated disease of the peripheral nervous system. It may be classified into 2 main subtypes: demyelinating... (Review)
Review
INTRODUCTION
Guillain-Barré syndrome (GBS) is an acute-onset, immune-mediated disease of the peripheral nervous system. It may be classified into 2 main subtypes: demyelinating (AIDP) and axonal (AMAN). This study aims to analyse the mechanisms of axonal damage in the early stages of GBS (within 10 days of onset).
DEVELOPMENT
We analysed histological, electrophysiological, and imaging findings from patients with AIDP and AMAN, and compared them to those of an animal model of myelin P2 protein-induced experimental allergic neuritis. Inflammatory oedema of the spinal nerve roots and spinal nerves is the initial lesion in GBS. The spinal nerves of patients with fatal AIDP may show ischaemic lesions in the endoneurium, which suggests that endoneurial inflammation may increase endoneurial fluid pressure, reducing transperineurial blood flow, potentially leading to conduction failure and eventually to axonal degeneration. In patients with AMAN associated with anti-ganglioside antibodies, nerve conduction block secondary to nodal sodium channel dysfunction may affect the proximal, intermediate, and distal nerve trunks. In addition to the mechanisms involved in AIDP, active axonal degeneration in AMAN may be associated with nodal axolemma disruption caused by anti-ganglioside antibodies.
CONCLUSION
Inflammatory oedema of the proximal nerve trunks can be observed in early stages of GBS, and it may cause nerve conduction failure and active axonal degeneration.
Topics: Amantadine; Animals; Axons; Guillain-Barre Syndrome; Neural Conduction; Peripheral Nerves
PubMed: 35779867
DOI: 10.1016/j.nrleng.2020.08.001 -
Neurologia 2022Guillain-Barré syndrome (GBS) is an acute-onset, immune-mediated disease of the peripheral nervous system. It may be classified into 2 main subtypes: demyelinating... (Review)
Review
INTRODUCTION
Guillain-Barré syndrome (GBS) is an acute-onset, immune-mediated disease of the peripheral nervous system. It may be classified into 2 main subtypes: demyelinating (AIDP) and axonal (AMAN). This study aims to analyse the mechanisms of axonal damage in the early stages of GBS (within 10days of onset).
DEVELOPMENT
We analysed histological, electrophysiological, and imaging findings from patients with AIDP and AMAN, and compared them to those of an animal model of myelin P2 protein-induced experimental allergic neuritis. Inflammatory oedema of the spinal nerve roots and spinal nerves is the initial lesion in GBS. The spinal nerves of patients with fatal AIDP may show ischaemic lesions in the endoneurium, which suggests that endoneurial inflammation may increase endoneurial fluid pressure, reducing transperineurial blood flow, potentially leading to conduction failure and eventually to axonal degeneration. In patients with AMAN associated with anti-ganglioside antibodies, nerve conduction block secondary to nodal sodium channel dysfunction may affect the proximal, intermediate, and distal nerve trunks. In addition to the mechanisms involved in AIDP, active axonal degeneration in AMAN may be associated with nodal axolemma disruption caused by anti-ganglioside antibodies.
CONCLUSION
Inflammatory oedema of the proximal nerve trunks can be observed in early stages of GBS, and it may cause nerve conduction failure and active axonal degeneration.
Topics: Animals; Humans; Guillain-Barre Syndrome; Peripheral Nerves; Neural Conduction; Edema; Amantadine
PubMed: 30057217
DOI: 10.1016/j.nrl.2018.06.002 -
Journal of Neural Transmission (Vienna,... Feb 2021The 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... (Review)
Review
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.
Topics: Amantadine; Diamond; Humans; Huntington Disease; Parkinson Disease; Receptors, N-Methyl-D-Aspartate
PubMed: 33624170
DOI: 10.1007/s00702-021-02306-2 -
Seminars in Neurology Jun 2022Pharmacologic interventions are commonly used to support rehabilitation efforts of patients with disorders of consciousness (DoC). The 2018 practice guidelines recommend...
Pharmacologic interventions are commonly used to support rehabilitation efforts of patients with disorders of consciousness (DoC). The 2018 practice guidelines recommend amantadine in adults with traumatic DoC to promote functional recovery, though several other stimulants are used off-label in clinical practice and trials, such as methylphenidate, bromocriptine, levodopa, and zolpidem. Differences in the mechanisms of action, adverse effects, pharmacokinetics, and drug-drug interactions should be considered when selecting the best agent for each individual patient. Overall, pharmacologic stimulants may provide a safe and inexpensive pathway to increased functionality and participation in rehabilitation. This article provides a concise summary of scientific evidence supporting the use of pharmacologic therapies to stimulate recovery of consciousness in patients with DoC.
Topics: Adult; Amantadine; Consciousness; Consciousness Disorders; Humans; Recovery of Function
PubMed: 36100228
DOI: 10.1055/s-0042-1755271 -
Science Advances Dec 2023Cortical spreading depolarization (CSD) is a promising target for neuroprotective therapy in traumatic brain injury (TBI). We explored the effect of NMDA receptor...
Cortical spreading depolarization (CSD) is a promising target for neuroprotective therapy in traumatic brain injury (TBI). We explored the effect of NMDA receptor antagonism on electrically triggered CSDs in healthy and brain-injured animals. Rats received either one moderate or four daily repetitive mild closed head impacts (rmTBI). Ninety-three animals underwent craniectomy with electrocorticographic (ECoG) and local blood flow monitoring. In brain-injured animals, ketamine or memantine inhibited CSDs in 44 to 88% and 50 to 67% of cases, respectively. Near-DC/AC-ECoG amplitude was reduced by 44 to 75% and 52 to 67%, and duration by 39 to 87% and 61 to 78%, respectively. Daily memantine significantly reduced spreading depression and oligemia following CSD. Animals ( = 31) were randomized to either memantine (10 mg/kg) or saline with daily neurobehavioral testing. Memantine-treated animals had higher neurological scores. We demonstrate that memantine improved neurovascular function following CSD in sham and brain-injured animals. Memantine also prevented neurological decline in a blinded, preclinical randomized rmTBI trial.
Topics: Rats; Animals; Memantine; Brain Injuries, Traumatic; Brain; Electrocorticography; Receptors, N-Methyl-D-Aspartate
PubMed: 38091390
DOI: 10.1126/sciadv.adj2417 -
The Lancet. Neurology Jun 2022
Topics: Amantadine; Catatonia; Humans
PubMed: 35568040
DOI: 10.1016/S1474-4422(22)00119-3 -
Polski Merkuriusz Lekarski : Organ... Feb 2021Amantadine and memantine, apart from their action on cholinergic receptors and dopamine secretion, have a significant influence on the inflammatory process, including... (Review)
Review
Amantadine and memantine, apart from their action on cholinergic receptors and dopamine secretion, have a significant influence on the inflammatory process, including the so-called "cytokine storm" and reduction of apoptosis and oxidative stress. Amantadine also inhibits the induction of inflammatory factors such as RANTES, activates kinase p38 of mitogen-activated protein (MAP) and c-Jun-NH2-terminal kinases (JNK), which inhibit viral replication. It also significantly inhibits the entry of SARS-CoV-2 into the bronchial epithelial cell and blocks the viroporin proton channel of the virus. In addition, it has the ability to pass through the membrane of lysosomes into their interior and act as an alkalizing agent, which prevents the release of viral RNA into the cell, which may be a key element in therapeutic management. Memantine also reduces inflammation, mainly in the nervous system, but also acts as a lysosomotropic factor, inhibiting viral replication. However, it is important to bear in mind when undertaking amantadine or memantine therapy with side effects that may overlap with COVID- 19 symptoms, worsening the condition of patients. Currently, the effectiveness of amantadine and memantine in the treatment of patients with COVID-19 symptoms has been demonstrated in a few clinical trials, mainly in patients treated for neurodegenerative diseases. The obtained results are of considerable value, but require confirmation in further studies.
Topics: Amantadine; Anti-Inflammatory Agents; COVID-19; Humans; Memantine; SARS-CoV-2
PubMed: 33713098
DOI: No ID Found -
Neurology India 2023
Topics: Humans; Amantadine; Acetaminophen; Renal Dialysis; Neurotoxicity Syndromes
PubMed: 37322764
DOI: 10.4103/0028-3886.378646