No abstract available.
Amantadine* ; Benztropine* ; Double-Blind Method*

Catatonia is a pathological condition in which the patient shows inappropriate motor, behavioral and affective responses to external stimuli. Catatonia can be observed in major depressive disorder, bipolar disorder, schizophrenia, and other conditions. Although the overall prevalence of catatonia has decreased dramatically, nearly 10% of schizophrenic inpatients still exhibit catatonic symptoms that are divided into immobility, abnormal repetitive behaviors and extreme emotional responses. Although numerous pharmacotherapies have been investigated for catatonia, benzodiazepine remains the treatment of choice. NMDA receptor antagonists such as amantadine and memantine have emerged as promising alternatives. As an effort to explain catatonia, 'GABA-NMDA collaboration model' has been proposed. According to this model, functional impairment of GABA-ergic orbitofrontal cortex can lead to disinhibition of subcortical motor system which utilize NMDA as neurotransmitter. This model was able to explain many aspects of catatonia.
Amantadine ; Benzodiazepines ; Bipolar Disorder ; Catatonia ; Cooperative Behavior ; Depressive Disorder, Major ; gamma-Aminobutyric Acid ; Humans ; Inpatients ; Memantine ; N-Methylaspartate ; Neurotransmitter Agents ; Prevalence ; Schizophrenia

Seven novel derivatives of aminoadamantane with 1-aminosubstituted group were synthesized from amantadine or memantine individually in order to find new neuroprotective agent. Six of them are amides of two precursors, one is a 1-amino derivative of memantine substituted with 2-hydroxy propyl. Their chemical structures were confirmed by 1H NMR and HRMS. The neuroprotective activity in vitro was evaluated primarily with 500 micromol x L(-1) glutamate damaged SY5Y cell by measurement of MTT metabolic rate and LDH leakage rate. Glutamate reduced MTT metabolic rate, but increased LDH leakage rate significantly. The addition of new derivatives elevated the MTT value with their certain concentration, reduced cell death rate. Especially as for 3d and 4c, they fully normalized LDH leakage rate with concentration of 20 micromol x L(-1) during LDH measurement. These data indicated that 3d and 4c have significant protective effect on nerve cell against glutamate injury, deserved to be further tested and maybe helpful for treatment of neurodegenerative disease.
Amantadine ; analogs & derivatives ; chemical synthesis ; pharmacology ; Cell Death ; drug effects ; Cell Line, Tumor ; Glutamic Acid ; toxicity ; Humans ; L-Lactate Dehydrogenase ; metabolism ; Memantine ; chemistry ; Neuroblastoma ; metabolism ; pathology ; Neuroprotective Agents ; chemical synthesis ; pharmacology

We describe a 73-year-old Parkinson's disease patient with bilateral pleural effusion after receiving a prescription of L-dopa and amantadine. Although, the mechanism is unknown, the occurrence of bilateral pleural effusion following the administration of amantadine and improvement after the cessation of amantadine suggests a possible relationship between amantadine and pleural effusion.
Aged ; Amantadine* ; Humans ; Levodopa ; Parkinson Disease ; Pleural Effusion* ; Prescriptions

OBJECTIVE: The objective of this study was to evaluate incidence and risk factors of seizure development during amantadine therapy for the patients with brain injury and stroke. METHOD: Thirty subjects (15 subjects with traumatic brain injuries and 15 subjects with strokes) who received a 4-week trial of amantadine from 100 mg/day to 400 mg/day were included. Control group, 40 patients (20 subjects with traumatic brain injuries and 20 subjects with strokes), did not take any brain stimulant. There were no differences in number, age, lesion area, and cognitive levels between two groups. Incidence of seizure in two groups was evaluated. RESULTS: Seizure occurred in 9 subjects in therapy group (30%) and in 1 subject in control group (2.5%). There was higher incidence of seizure in the group treated with amantadine than in the control group. In therapy group, most of the seizures occurred in high dose of 400 mg/day. CONCLUSION: Amantadine in high dose appeared to be associated with higher incidence of seizure. This study suggested that administration of amantadine in high dose in management of brain injury and stroke should be accompanied with careful monitoring of seizure.
Amantadine* ; Brain Injuries* ; Brain* ; Humans ; Incidence ; Risk Factors ; Seizures* ; Stroke*

OBJECTIVE: Weight gain is a commonly encountered problem associated with atypical antipsychotics, especially olanzapine. To investigate the weight reducing effect of amantadine, we conducted an prospective open label study. METHODS: We started amantadine treatment in outpatients who had gained weight during olanzapine treatment (mean dose of 11.94 mg/day, mean weight gain of 6.33 kg). Data were collected at St. Mary's Hospital, College of Medicine, The Catholic University of Korea. The add-on treatment of amantadine was given at a mean dose of 161.9 mg/day with mean duration of administration for 110.2 day. Brief Psychiatric Rating Scale (BPRS), Extrapyramidal Symptom Scale were checked to evaluate the tolerability of amantadine. RESULTS: Before administration of amantadine, the mean dose of olanzapine was 11.94+/-4.58 mg and mean duration of administration was 123.1+/-174.6 days. Body weight and BMI during this period was significantly increased mean 6.33+/-4.45 kg (Z=-3.839, p<0.001), 4.94+/-0.75 (Z=-3.724, p<0.001) respectively. Amantadine was administered mean dose of 161.90+/-58.96 mg for mean 110.2+/-78.7 days. Body weight and BMI was decreased mean 0.96+/-3.44 kg, 0.71+/-2.7, respectively. There was no deterioration in psychiatric symptoms, as shown in BPRS score decrement and no adverse effects were reported. CONCLUSION: The present data suggests that amantadine does not significantly decrease weight gain experienced by some patients during olanzapine treatment and does not worse psychotic symptoms. Randomized placebo-controlled trial should be needed to confirm these findings.
Amantadine* ; Antipsychotic Agents ; Body Weight ; Brief Psychiatric Rating Scale ; Humans ; Korea ; Outpatients ; Prospective Studies ; Weight Gain*

Kleine-Levin syndrome is a rare disorder which usually affects adolescent males and is characterized by periodic hypersomnia, hyperphagia and abnormal behavior. This is an unexplained clinical syndrome for which several etiologies have been entertained with no standard treatment is yet available. A 18-year old woman began suffering from recurrent hypersomnia, hyperphagia, and behavioral disturbances such as irritability, derealization, and amnesia. She was normal between the episodes and diagnosed as Kleine-Levin syndrome. In the course of about two years she had 11 episodes and the mean interval between the episodes was 52.8+/-16.7 days. After application of amantadine, there were two mild episodes and then she had no episodes for more than 6 months. This case suggests the possible role of amantadine in the treatment of Kleine-Levin syndrome.
Adolescent ; Amantadine* ; Amnesia ; Depersonalization ; Disorders of Excessive Somnolence ; Female* ; Humans ; Hyperphagia ; Kleine-Levin Syndrome* ; Male

BACKGROUND: Drug-induced Parkinsonism(DIP) is the second commonest cause of Parkinsonism, after idiopathic Parkinson's disease(IPD). DIP is frequently produced by antipsychotic drugs. But the clinical characteristics of DIP did not get attention by neurologist. So we studied the clinical profiles of DIP patients. METHODS: We studied the clinical profiles of thirthone patients who showed parkinsonism after antipsychotic drug treatment. We compared the score of motor part of the Unified Parkinson's Disease Rating Scale(UPDRS) between trihexyphenidyl(n=15) & amantadine(n=16) monotherapy group(initial & 4 week after treatment). RESULTS: The mean age of patients was 45 years. Bradykinesia was the 1st symptom in 26 patients(94%), tremor in 5 patients(6%). In 25 patients(81%), the first symptom appeared within 1 week after sntipsychotic treatment. There was a statistical significant negative correlation between the dosage of antipsychotic drug and the symptom-onset interval following treatment with antipsychotic drugs(simple correlation analysis, p>0.01). Bradykinesia and rigidity were appeared in all DIP patients, symmetric distribution was more common(94%, 87%) Tremor occurred in 27 patients (87%). In patients with tremor, postural or action tremor was dominant in 15 patients(56%) asymmetric distribution was more common(16/27, 59%). There are no statistical difference in motor score of UPDRS between trihexyphenidyl & amantadine monotherapy group(student t-test, p<0.05) CONCLUSIONS: Bradykinesia was the most common 1st symptom in DIP patients. Asymmertrical postural or action tremor was relativelly common in DIP. Amantadine showed the same efficacy in the treatment of DIP compared to anticholinergics.
Amantadine ; Antipsychotic Agents ; Cholinergic Antagonists ; Humans ; Hypokinesia ; Parkinson Disease ; Parkinsonian Disorders* ; Tremor ; Trihexyphenidyl

Authors have studied photopic and scotopic flash EPGs for 19 control subjects and 20 patients with Parkinson's disease before and after various anti-Parkinsonian therapy. The following fingings were observed 1. There was no significant difference in implicit time of photopic and scotopic a and b waves between the control and the Parkinsonian groups(P(t)>0.05). 2 Amplitudes of photopic and scotopic a and b-waves were smaller in Parkinsonian group during the pre-medication therapy than in control group(P(t)<0.05) however those of photopic a-and b- waves and scotopic b-wave were normalized with anti-Parkinsonian therapy(P(t)<0.01). 3 Parkinsonian patients treated with dopa preparations showed the significant increases of amplitde of scotopic b wave(P(t)<0.001) but those treated with anticholinergics, Amantadine or Bromocryptine did not(P(t1>0.05). 4. Compared with that of tremor predominant Parkinsonism the amplitudes of photopic and scotopic a-and b-waves were small in patients with akineto-rigidity(P(t)<0.01). Therefore it is concluded that the dopaminergic changes in retinal cells are responsible for producing b wave as well as a wave. So clinically flash EFGs can. Be used beneficially in treating Parkinsonian patients in view of choosing the anti-Parkinsonian drugs and monitoring the effectiveness of therapy.
Amantadine ; Bromocriptine ; Cholinergic Antagonists ; Dihydroxyphenylalanine ; Humans ; Parkinson Disease* ; Parkinsonian Disorders ; Retinaldehyde ; Tremor

OBJECTIVE: We examined whether amantadine can prevent the development of dyskinesia. METHODS: Patients with drug-naïve Parkinson's disease (PD), younger than 70 years of age and in the early stage of PD (Hoehn and Yahr scale < 3), were recruited from April 2011 to December 2014. The exclusion criteria included the previous use of antiparkinsonian medication, the presence of dyskinesia, significant psychological disorders, and previous history of a hypersensitivity reaction. Patients were consecutively assigned to one of 3 treatment groups in an open label fashion: Group A-1, amantadine first and then levodopa when needed; Group A-2, amantadine first, dopamine agonist when needed, and then levodopa; and Group B, dopamine agonist first and then levodopa when needed. The primary endpoint was the development of dyskinesia, which was analyzed by the Kaplan-Meier survival rate. RESULTS: A total of 80 patients were enrolled: Group A-1 (n = 27), Group A-2 (n = 27), and Group B (n = 26). Twenty-four patients were excluded from the analysis due to the following: withdrawal of amantadine or dopamine agonist (n = 9), alternative diagnosis (n = 2), withdrawal of consent (n = 1), and breach in the protocol (n = 12). After exclusion, 5 of the 56 (8.93%) patients developed dyskinesia. Patients in Group A-1 and A-2 tended to develop dyskinesia less often than those in Group B (cumulative survival rates of 0.933, 0.929, and 0.700 for A-1, A-2, and B, respectively; p = 0.453). CONCLUSION: Amantadine as an initial treatment may decrease the incidence of dyskinesia in patients with drug-naïve PD.
Amantadine ; Diagnosis ; Dopamine Agonists ; Dyskinesias ; Humans ; Hypersensitivity ; Incidence ; Levodopa ; Parkinson Disease ; Survival Rate