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Clinical and Experimental Emergency... Jan 2024We hypothesized that the administration of amantadine would increase awakening of comatose patients resuscitated from cardiac arrest.
OBJECTIVES
We hypothesized that the administration of amantadine would increase awakening of comatose patients resuscitated from cardiac arrest.
METHODS
We performed a prospective, randomized controlled pilot trial, randomizing subjects to amantadine 100mg twice daily or placebo for up to 7 days. The study drug was administered between 72-120 hours after resuscitation and patients with absent N20 cortical responses, early cerebral edema, or ongoing malignant electroencephalography patterns were excluded. Our primary outcome was awakening, defined as following two-step commands, within 28 days of cardiac arrest. Secondary outcomes included length of stay, awakening, time to awakening, and neurologic outcome measured by Cerebral Performance Category (CPC) at hospital discharge. We compared the proportion of subjects awakening and hospital survival using Fisher's exact tests and time to awakening and hospital length of stay using Wilcoxon rank sum tests.
RESULTS
After 2 years, we stopped the study due to slow enrollment and lapse of funding. We enrolled 14 subjects (12% of goal enrollment), 7 in the amantadine arm and 7 in the placebo arm. The proportion of patients who awakened within 28 days after cardiac arrest did not differ between amantadine (n=2, 28.57%) and placebo groups (n=3, 42.86%) (p = 1.00). There were no differences in secondary outcomes. Study medication was stopped in three (21%) subjects. Adverse events included a recurrence of seizures (n=2; 14%), both of which occurred in the placebo arm.
CONCLUSION
We could not determine the effect of amantadine on awakening in comatose survivors of cardiac arrest due to small sample size.
PubMed: 38286499
DOI: 10.15441/ceem.23.158 -
Journal of Clinical Medicine Jan 2024Traumatic brain injury (TBI) is one of the most common causes of death and an important burden to the worldwide healthcare system and society. There is a lack of...
INTRODUCTION
Traumatic brain injury (TBI) is one of the most common causes of death and an important burden to the worldwide healthcare system and society. There is a lack of guidelines for types of monitoring or neuroprotective therapy. The aim of this pilot study was to assess its feasibility and, furthermore, to evaluate the impact of Cerebrolysin on the following clinical outcomes: length of stay, Glasgow Outcome Scale (GOS) and mortality.
METHODS
A cohort of 56 patients was included in this non-randomised, real-time, pre-post-interventional study. The patients were assessed with the Glasgow Coma Scale (GCS) and divided into two groups: severe (GCS < 8) and non-severe (GCS > 8). After the radiological examination (CT scan), the patients were qualified for an immediate neurosurgical procedure if needed. The patients were admitted to the intensive care unit, where a standardised protocol for TBI treatment was implemented. Additional neuromonitoring was applied.
RESULTS
There were 56 patients (19 females; 33.9%), of which 41 were considered severe cases; the patients were allocated to the Cerebrolysin ( = 25) or control groups ( = 31). In a generalised linear model (GLM) approach, the use of Cerebrolysin was associated with a decrease in the probability of death in non-severe patients (by 0.333 (standard error (SE) = 0.157, = 0.034)) but not in severe patients (estimate (Est.) = -0.115, SE = 0.127, = 0.364). Patients who received Cerebrolysin and who were neuromonitored had favourable outcomes and better survival rates.
CONCLUSIONS
A multimodal treatment approach with monitoring and Cerebrolysin may have a beneficial effect on patients with less severe TBIs; however, the present study has multiple limitations, and further research is needed.
PubMed: 38256487
DOI: 10.3390/jcm13020353 -
Neuropediatrics Apr 2024The risk factors for respiratory insufficiency in children with Guillain-Barré syndrome (GBS) are poorly known. This study aimed to investigate the factors associated...
OBJECTIVE
The risk factors for respiratory insufficiency in children with Guillain-Barré syndrome (GBS) are poorly known. This study aimed to investigate the factors associated with respiratory insufficiency in children with GBS.
METHODS
This retrospective study included children diagnosed with GBS by pediatric neurologists and admitted at the Wuhan Children's Hospital and other hospitals from January 2013 to October 2022. The patients were divided into the respiratory insufficiency and nonrespiratory insufficiency groups according to whether they received assist breathing during treatment.
RESULTS
The median (interquartile range) age of onset of 103 patients were 5 (3.1-8.5) years, 69 (67%) were male, and 64 (62.1%) had a history of precursor infection. Compared with the nonrespiratory insufficiency group, the respiratory insufficiency group showed more facial and/or bulbar weakness ( = 0.002), a higher Hughes Functional Grading Scale (HFGS) at admission ( < 0.001), and a shorter onset-to-admission interval ( = 0.017). Compared with the acute motor axonal neuropathy (AMAN) subtype, the acute inflammatory demyelinating polyneuropathy (AIDP) subtype showed longer days from onset to lumbar ( = 0.000), lower HFGS at admission ( = 0.04), longer onset-to-admission interval ( = 0.001), and more cranial nerve involvement ( = 0.04). The incidence of respiratory insufficiency between AIDP and AMAN showed no statistical difference ( > 0.05).
CONCLUSION
In conclusion, facial and/or bulbar weakness, HFGS at admission, and onset-to-admission interval were associated with respiratory insufficiency and might be useful prognostic markers in children with GBS.
Topics: Child; Humans; Male; Child, Preschool; Female; Guillain-Barre Syndrome; Retrospective Studies; Hospitalization; Respiratory Insufficiency; Amantadine
PubMed: 38253279
DOI: 10.1055/s-0043-1777767 -
Biosensors Dec 2023Amantadine (AMD) is an antiviral drug that is prohibited for use in livestock and poultry. In this study, carboxyl-modified magnetic nanoparticles (MNPs) were...
Amantadine (AMD) is an antiviral drug that is prohibited for use in livestock and poultry. In this study, carboxyl-modified magnetic nanoparticles (MNPs) were synthesized using the solvothermal method in one step with harmless and inexpensive regents, and they were used to label monoclonal antibodies (mAbs) of AMD in microwells with electrostatic adsorption. Then, a magnetic immunochromatography assay (MICA) method was successfully established. Under optimal conditions, the MICA showed a good performance, with a linear range of 0.2~10.0 µg/L. The limit of detection (LOD) was 0.068 µg/L with the instrument, and the visual LOD (vLOD) was 0.5 µg/L. There was no cross-reaction with rimantadine and ribavirin. The vLOD in real samples was 1.0 µg/kg. The developed MICA has the advantages of convenience, speed, and sensitivity, which make it suitable for the on-site rapid detection of AMD residues in chicken tissues and eggs.
Topics: Amantadine; Antiviral Agents; Chromatography, Affinity; Nanoparticles; Static Electricity
PubMed: 38248400
DOI: 10.3390/bios14010023 -
Nigerian Journal of Physiological... Dec 2022L-DOPA, the gold standard for managing Parkinson's disease (PD) is fraught by motor fluctuations termed L-Dopa-Induced Dyskinesia (LID). LID has very few therapeutic...
L-DOPA, the gold standard for managing Parkinson's disease (PD) is fraught by motor fluctuations termed L-Dopa-Induced Dyskinesia (LID). LID has very few therapeutic options. Hence, the need for preclinical screening of new interventions. Cholecalciferol (VD3) treatment reportedly improves motor deficit in experimental Parkinsonism. Therefore, the novel anti-dyskinetic effect of VD3 and its underlying mechanisms in LID was investigated. Dyskinesia was induced by chronic L-DOPA administration in parkinsonian (6-OHDA- lesioned) mice. The experimental groups: Control, Dyskinesia, Dyskinesia/VD3, and Dyskinesia/Amantadine were challenged with L-DOPA to determine the abnormal involuntary movements (AIMs) score during 14 days of VD3 (30 mg/kg) or Amantadine (40 mg/kg) treatment. Behavioral Axial, Limb & Orolingual (ALO) AIMs were scored for 1 min at every 20 mins interval, over a duration of 100 mins on days 1,3,7,11 and 14. Using western blot, striatum was assessed for expression of dopamine metabolic enzymes: Tyrosine Hydroxylase (TH) and Monoamine Oxidase-B (MAO-B); CD11b, BAX, P47phox, and IL-1β. Cholecalciferol significantly attenuated AIMs only on days 11 & 14 with maximal reduction of 32.7%. Expression of TH and MAO-B was not altered in VD3 compared with dyskinetic mice. VD3 significantly inhibited oxidative stress (P47phox), apoptosis (BAX), inflammation (IL-1β) and microglial activation (CD11b). VD3 showed anti-dyskinetic effects behaviorally by attenuating abnormal involuntary movements, modulation of striatal oxidative stress, microglial responses, inflammation, and apoptotic signaling; without affecting dopamine metabolic enzymes. Its use in the management of dyskinesia is promising. More studies are required to further evaluate these findings. Keywords: Cholecalciferol; L-DOPA-Induced Dyskinesia; Parkinson's Disease; Microglial; Oxidative stress; Inflammation.
Topics: Rats; Mice; Animals; Levodopa; Parkinson Disease; Dopamine; Microglia; Cholecalciferol; bcl-2-Associated X Protein; Rats, Sprague-Dawley; Dyskinesia, Drug-Induced; Amantadine; Inflammation; Disease Models, Animal
PubMed: 38243560
DOI: 10.54548/njps.v37i2.3 -
Scientific Reports Jan 2024Many COVID-19 survivors experience lingering post-COVID-19 symptoms, notably chronic fatigue persisting for months after the acute phase. Despite its prevalence, limited... (Randomized Controlled Trial)
Randomized Controlled Trial
Many COVID-19 survivors experience lingering post-COVID-19 symptoms, notably chronic fatigue persisting for months after the acute phase. Despite its prevalence, limited research has explored effective treatments for post-COVID-19 fatigue. This randomized controlled clinical trial assessed the impact of Amantadine on patients with post-COVID-19 fatigue. The intervention group received Amantadine for two weeks, while the control group received no treatment. Fatigue levels were assessed using the Visual Analog Fatigue Scale (VAFS) and Fatigue Severity Scale (FSS) questionnaires before and after the trial. At the study's onset, VAFS mean scores were 7.90 ± 0.60 in the intervention group and 7.34 ± 0.58 in the control group (P-value = 0.087). After two weeks, intervention group scores dropped to 3.37 ± 0.44, significantly lower than the control group's 5.97 ± 0.29 (P-value < 0.001). Similarly, FSS mean scores at the trial's commencement were 53.10 ± 5.96 in the intervention group and 50.38 ± 4.88 in the control group (P-value = 0.053). At the trial's end, intervention group scores decreased to 28.40 ± 2.42, markedly lower than the control group's 42.59 ± 1.50 (P-value < 0.001). In this study, we report the safety, tolerability, and substantial fatigue-relieving effects of Amantadine in post-COVID-19 fatigue. The intervention demonstrates a statistically significant reduction in fatigue levels, suggesting Amantadine's potential as an effective treatment for this persistent condition.
Topics: Humans; Multiple Sclerosis; COVID-19; Amantadine; Treatment Outcome; Surveys and Questionnaires
PubMed: 38228731
DOI: 10.1038/s41598-024-51904-z -
Qatar Medical Journal 2023Parkinsonism-hyperpyrexia syndrome (PHS) is a potentially life-threatening condition that occurs due to the abrupt withdrawal or significant dose reduction of...
BACKGROUND
Parkinsonism-hyperpyrexia syndrome (PHS) is a potentially life-threatening condition that occurs due to the abrupt withdrawal or significant dose reduction of antiparkinsonian medications. It presents similarly to neuroleptic malignant syndrome (NMS) and is characterized by severe rigidity, fever, autonomic instability, and altered mental status.
CASE
A 62-year-old male with a 10-year history of Parkinson's disease (PD) underwent laparoscopic mesh repair for a left-sided diaphragmatic and large hiatus hernia. His antiparkinsonian medications included levodopa/carbidopa, amantadine, pramipexole, and benzhexol. Medications were withheld as part of the nil per os (NPO) status. Postoperatively, he developed withdrawal features, including tremors, difficulty speaking, tachycardia, hypertension, fever, and sweating. PHS, resulting from the withdrawal of antiparkinsonian medications, was diagnosed. The patient was transferred to the intensive care unit (ICU), intubated, and his antiparkinsonian medications were reintroduced. The patient's condition improved gradually, and he was discharged home on the 15th postoperative day.
DISCUSSION
The abrupt discontinuation of antiparkinsonian medications precipitated PHS in our patient. Recognizing the clinical picture of PHS and differentiating it from other possible conditions, such as neuroleptic malignant syndrome and malignant hyperthermia, is pivotal. Management involves resuming medications and providing supportive care. Early recognition and prompt reintroduction of the antiparkinsonian medications are essential for the patient's recovery.
CONCLUSION
PHS is a rare but potentially life-threatening condition that occurs due to the withdrawal of antiparkinsonian medications, leading to an acute hypodopaminergic state. Our case emphasizes the importance of careful perioperative management of antiparkinsonian medications and early recognition and management of withdrawal symptoms in patients with Parkinson's disease undergoing surgery.
PubMed: 38204562
DOI: 10.5339/qmj.2023.34 -
BMJ Open Jan 2024Fatigue is one of the most disabling symptoms of multiple sclerosis (MS), and effective treatments are lacking. Amantadine is one of the most used treatments, although...
Amantadine and/or transcranial magnetic stimulation for fatigue associated with multiple sclerosis (FETEM): study protocol for a phase 3 randomised, double-blind, cross-over, controlled clinical trial.
INTRODUCTION
Fatigue is one of the most disabling symptoms of multiple sclerosis (MS), and effective treatments are lacking. Amantadine is one of the most used treatments, although its efficacy is under debate. Transcranial magnetic stimulation (TMS) is a promising intervention that has shown positive effects in some preliminary investigations. We aim to investigate the effect of 6 weeks of amantadine and/or TMS in fatigue due to MS.
METHODS AND ANALYSIS
The study is a national, multicentre, phase 3, randomised, double-blind, cross-over, placebo-controlled and sham-controlled clinical trial. Adult patients with relapsing-remitting MS, Expanded Disability Status Scale score of 1.5-4.5 and Fatigue Severity Score>4 are eligible for the trial. Participants will be randomised to one of the sequences of the study. Each sequence consists of four periods of 6 weeks of treatment and three washout periods of 12-18 weeks. All patients will receive all the combinations of therapies. The primary outcome is the Modified Fatigue Impact Scale. The secondary outcomes are the Symbol Digit Modalities Test (cognition), Beck Depression Inventory-II (depressive symptoms) and Short-Survey 12 (quality of life). Safety and cost-effectiveness will also be evaluated. An exploratory substudy including MRI and blood biomarkers will be conducted.
ETHICS AND DISSEMINATION
The study is approved by the Ethics Committee of the Hospital Clinico San Carlos and the Spanish Agency of Medications and Medical Devices. All study findings will be published in scientific peer-reviewed journals and presented at relevant scientific conferences.
TRIAL REGISTRATION NUMBER
EudraCT 2021-004868-95; NCT05809414.
Topics: Adult; Humans; Multiple Sclerosis; Transcranial Magnetic Stimulation; Quality of Life; Amantadine; Double-Blind Method; Fatigue; Treatment Outcome; Randomized Controlled Trials as Topic; Multicenter Studies as Topic; Clinical Trials, Phase III as Topic
PubMed: 38176857
DOI: 10.1136/bmjopen-2023-078661 -
American Journal of Ophthalmology Case... Dec 2023To describe a case of bilateral interface fluid formation 2 years after laser-assisted in situ keratomileusis (LASIK) surgery caused by the side effect of amantadine.
PURPOSE
To describe a case of bilateral interface fluid formation 2 years after laser-assisted in situ keratomileusis (LASIK) surgery caused by the side effect of amantadine.
OBSERVATIONS
A 47-year-old male patient with a history of Parkinson's disease treated with amantadine who had uneventful LASIK surgery in both eyes 2 years ago, presented with a decline in vision over the past 6 weeks. Results: Best corrected vision was 20/200 and 20/400 in the right and left eye respectively. Intraocular pressures were measured within the normal range. Biomicroscopic exam showed bilateral corneal edema. Anterior segment optical coherence tomography (AS-OCT) revealed fluid accumulation within the LASIK flap interface in both corneas. The patient's corneal edema and fluid in the interface began to gradually resolve, and vision improved 2 weeks after discontinuing amantadine.
CONCLUSIONS AND IMPORTANCE
Although there is no previous report, it is possible that amantadine may cause interface fluid formation in patients with LASIK surgery.
PubMed: 38161515
DOI: 10.1016/j.ajoc.2023.101895 -
The Journal of Medicine Access 2023Catatonia is a psychomotor syndrome resulting from an underlying psychiatric or medical disorder commonly observed in inpatient psychiatric units. While benzodiazepines...
Catatonia is a psychomotor syndrome resulting from an underlying psychiatric or medical disorder commonly observed in inpatient psychiatric units. While benzodiazepines and electroconvulsive therapy (ECT) are effective treatment options, the unavailability of ECT in many community psychiatric hospitals in the United States negatively affects patient outcomes. We present a 25-year-old African American male with a psychiatric diagnosis of schizophrenia complicated by malignant catatonia who was admitted to a community psychiatric hospital. He required intensive medical stabilization with supportive management, and transfer requests to ECT-equipped hospitals were initiated. While awaiting transfer for 148 days, the patient's symptoms did not fully remit with lorazepam (even with 36 mg daily in divided doses) and other psychotropic medication trials, including antipsychotics and mood stabilizers. After nearly 5 months of inpatient stay, he was successfully transferred, received ECT treatment, and experienced rapid resolution of catatonia. After discharge, to obtain three monthly sessions of maintenance ECT, he had 5-h one-way ground transportation arranged to an out-of-county ECT-equipped facility. There was no relapse in catatonia by the 2-year follow-up. This report highlights a significant healthcare disparity when attempting to manage severe catatonia within community hospital settings without access to ECT in the United States. Alternative treatments, including antipsychotics, had minimal impact on symptoms and possibly increased morbidity in this case while awaiting ECT. Treatment at our designated safety net hospital still required referral to 14 ECT-equipped hospitals before successful transfer. This case highlights the urgent need for ECT availability in more community hospitals to treat patients with refractory psychiatric conditions, including catatonia. ECT is an essential psychiatric treatment that, for certain conditions, has no appropriate alternatives. We propose that access to ECT be considered in the determination of safety net hospital systems, with improved ability to transfer patients who are suffering from treatable life-threatening mental health conditions.
PubMed: 38144544
DOI: 10.1177/27550834231220504