Amantadine Withdrawal Research Articles

Neuroleptic Malignant Syndrome in Patients With Dementia: Experiences of A Single Memory Clinic.

Neuroleptic malignant syndrome (NMS) is a life-threatening condition that occurs as an adverse reaction to antipsychotic and antiemetic agents or sudden withdrawal of dopaminergic medications. Given the metabolic and functional reserves and the comorbidities in older adults, NMS may show an atypical course. The medical records of patients with neurodegenerative diseases leading to dementia between 2013 and 2020 were reviewed for the diagnosis of NMS. Demographic and clinical characteristics of the patients were obtained from the records of laboratory parameters, management, and length of stay. Fifteen older adults (19 episodes) diagnosed with NMS were included. The median age was 76 years, and 5 were female. Ten of 15 NMS patients were atypical. Most of them had an infection accompanying NMS. Neuroleptic malignant syndrome was caused by antidopaminergic agents (5 antipsychotics, 1 metoclopramide) in 6 episodes and discontinuation of a dopaminergic agent, l -DOPA, in 12 episodes. In 1 patient, it was associated with simultaneous use of domperidone and amantadine withdrawal. Rigidity in NMS due to l -DOPA discontinuation was higher than in those due to antipsychotic use ( P = 0.027). Two of our patients needed intensive care, and 1 died. This study highlights the high frequency of atypical NMS and the importance of early recognition of this potentially fatal syndrome, which can accompany neurodegenerative diseases and infections in older adults.

Abruptly Stopping an Adamantane Management for Fatigue in an Elderly Multiple Sclerosis Patient Provoked Acute Withdrawal Symptoms (AWS); A Case Report

Introduction: Health care workers are continuously being burdened with acute conditions especially with the current pandemic of Covid-19. Staying home and feeling trapped can be particularly detrimental to patients with history of depression or psychotic as well as multiple sclerosis. We present a case of a 63-year-old patient with Multiple Sclerosis whose condition is being managed with mainly dopamine agonists. Withdrawal symptoms arose acutely after abrupt cessation of Amantadine; a dopamine agonist. Amantadine is thought to work by raising the amount of dopamine available to brain cells. The purpose of this research is to report a case of a 63-yearold Multiple Sclerosis patient who presented with Acute Withdrawal Syndrome (AWS) after being managed with Amantadine for two years and abruptly stopping the medication. Case Presentation: A 63-year-old woman with past medical history of stroke and multiple sclerosis reported symptoms of AWS after abruptly stopping amantadine use for multiple sclerosis. The patient was on cyclobenzaprine for spasticity, gabapentin and lamotrigine for neuropathic pain and seizure disorder respectively. She also had a history of hypertension and hyperlipidemia and presented with 1-week history of nausea and vomiting followed by visual hallucination, tremor, slurred speech and lethargy. On presentation, the patient was afebrile and hemodynamically stable. This patient denies blurred vision and severe fatigue with bathing or exercise. Upon further evaluation, patient did not report electrical sensation down her limbs or back especially with neck flexion. The initial labs were remarkable for hemoglobin of 8.5mg/dL and hypokalemia of 3.2mmol/L. We suspected vasculitis of CNS. One of the proposed pathophysiology for this is the extensive inflammatory damage to the blood brain barrier, allowing inflammatory cell recruitment into the CNS. The patient was admitted for acute altered mental status with waxing and wanning symptoms. Her acute delirium symptoms lead to the withdrawal of amantadine and cyclobenzaprine. Within about 48-70 hours later, patient developed severe agitation requiring emergent intubation. EEG showed generalized medium voltage delta, theta, and fast activity throughout indicative of diffuse cerebral dysfunction, but no lateralized or epileptic activity was seen. CT brain was negative for acute stroke or bleed. The patient underwent lumbar puncture, and was started on empiric coverage with IV acyclovir, vancomycin, and ceftriaxone for possible meningoencephalitis along with methylprednisolone for possible multiple sclerosis flare vs autoimmune encephalitis. MRI showed stable extensive white matter T2 hyperintense lesions. CSF was negative for infectious processes, and vancomycin, ceftriaxone, and acyclovir were discontinued. The patient continued to require sedation for severe agitation. The severe agitation was suspected to be due to discontinuation of her home medications, one of which was amantadine. The amantadine was resumed with improvement of her mental status within 24 hours. Patient was extubated within 48 hours of initiation of amantadine and was transferred to the floor for continuity of care and eventually discharged home after 15 days of hospitalization. Conclusion: Acute Withdrawal Syndrome (AWS) symptoms are often as a result of abrupt cessation of a medication(s) particularly central acting agents like clonidine, beta adrenergic antagonists as well as diuretics but Amantadine is starting to be a strong culprit since it is also thought to act centrally as a dopamine agonist. Clinicians should always be mindful of AWS especially from patients on long term central acting medications that have been abruptly stopped.

Amantadine withdrawal syndrome masquerading as COVID-19 encephalopathy: a case report and review of the literature

ABSTRACTAmantadine withdrawal syndrome (AWS) is a rare but recognized cause of severe and persistent altered mental status sometimes with co-occurring extrapyramidal symptoms. First described in a case series from 1987, its clinical manifestations have been characterized along a spectrum ranging from profound hypoactive delirium to hyperactive delirium with hallucinations. Risk factors for withdrawal include abrupt medication discontinuation, prolonged use, older age and underlying dementia.Herein we describe a case of a 52-year-old woman who presented with confusion, hallucinations, and coronavirus disease-2019 infection. She subsequently developed a prolonged hypoactive delirium after her amantadine was tapered and held. Her hypoactive delirium entirely resolved with resumption of amantadine confirming the diagnosis of AWS. This case illustrates the importance of slowly tapering dopaminergic medications and being aware of rare pharmacologic side effects.

Amantadine withdrawal

Amantadine withdrawal

Amantadine and the Risk of Dyskinesia in Patients with Early Parkinson's Disease: An Open-Label, Pragmatic Trial.

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 withdrawal

Amantadine withdrawal

Amantadine withdrawal

Amantadine withdrawal

Study on the abuse of amantadine in tissues of broiler chickens by HPLC-MS/MS.

To evaluate the residual target tissues for better monitoring of amantadine abuse in broiler chickens, 22-day-old commercial Arbor Acres broiler chickens were, respectively, fed with 10, 20, and 40mg/kg of amantadine for five consecutive days. Plasma, breast, and liver tissue samples from the chickens were collected 0, 4, 16, 24, 48, 96, 144, and 312h after amantadine withdrawal. The high-performance liquid chromatography-tandem mass spectrometry method was used to detect the concentrations of amantadine. The highest concentration was found in the chicken liver and it took the longest time for amantadine to vanish by metabolism. In the high-dose group, amantadine residues were still detected 312h after amantadine withdrawal. As the amantadine dose increased, amantadine residues in the chicken liver were more slowly to disappear than in other tissues. Even if approximately the same concentration of amantadine residues was found in chicken breast and plasma samples, it took a shorter time before the residues were eliminated. In the medium- and high-dose groups, the concentrations of amantadine residues in chicken liver samples were substantially higher than those in chicken breast and plasma samples, and it took more time to eliminate them. Therefore, the chicken liver can be used as a target tissue to detect illegal use of amantadine.

Reduction in Parkinson’s Disease Therapy Improved Punding But Not Feeling of Presence

Reduction in Parkinson’s Disease Therapy Improved Punding But Not Feeling of Presence

Amantadine withdrawal

Amantadine withdrawal

Dropped Head Associated With Amantadine in Parkinson Disease

The antiviral agent amantadine has been used to manage Parkinson's disease or levodopa-induced dyskinesias for nearly 5 decades. Amantadine is often associated with hallucinations as an adverse effect, but a long-term study reported no serious motor complications. We describe an unusual patient who had Parkinson's disease with dropped head syndrome (DHS) caused by amantadine. When the patient, who had DHS while receiving only 2 kinds of antiparkinsonian drugs, was rechallenged with amantadine, DHS developed, accompanied by increased muscle tone in the neck muscles on surface electromyogram. The DHS resolved after the withdrawal of amantadine. Moreover, an intravenous infusion of levodopa did not alter the DHS. These findings collectively suggest that the DHS in our patient was most likely caused directly by amantadine. Our findings suggest that amantadine may carry the risk of augmenting dystonic syndrome in humans.

Amantadine withdrawal

Amantadine withdrawal

Case files of the Program in Medical Toxicology at Brown University: Amantadine withdrawal and the neuroleptic malignant syndrome

A sixty-one-year old woman with a history of depression and idiopathic dystonia presented to the emergency department (ED) with fever, nausea, muscle rigidity, and redness in her extremities. The patient had seen various specialists for her dystonia during the preceding year and had tried multiple medication regimens, including benztropine and tizanidine. The patient described her home medications as tizanidine 2 mg three times daily, diazepam 2.5 mg daily, escitalopram 100 mg daily, rosuvastatin 10 mg daily and bupropion 300 mg nightly. At ED presentation her vital signs were: temperature 37.5°C (99.5F), blood pressure 157/76 mmHg, heart rate 105 beats per minute, respirations 24 per minute, and oxygen saturation of 100% on room air. Her physical examination was significant for diaphoresis, tachycardia, diffuse flushing, tremors in her upper and lower extremities, muscle rigidity, and hyperreflexia in the upper and lower extremities. The tremors were low amplitude and worse with intention, while the rigidity had cogwheeling features and was more notable in her lower extremities. Initial laboratory evaluation was significant for a creatine phosphokinase (CPK) of 1146 IU/L. Her electrocardiogram showed sinus tachycardia with normal QRS and QT intervals, and no evidence of acute ischemia. Two months earlier, the patient’s neurologist had started her on amantadine 100 mg twice daily for dystonia. Three days prior to ED presentation, the patient abruptly stopped taking her amantadine on the advice of a pharmacist, secondary to bilateral lowerextremity edema. The following day, the patient presented to her primary care physician complaining of nausea, tremors, and diffuse flushing. The physician treated her for an allergic reaction with oral steroids and diphenhydramine. The patient’s symptoms worsened over the next day with increasing tremors and rigidity, low-grade fever, nausea, and flushing, which prompted her presentation to the ED.

Syndrome of Inappropriate Antidiuretic Hormone Secretion Possibly Associated With Amantadine Therapy in Parkinson Disease

To report a patient who developed a syndrome of inappropriate antidiuretic hormone secretion (SIADH) related with amantadine therapy. A 66-year-old woman, diagnosed with Parkinson disease, developed asthenia, anorexia, weight loss, lethargy and feeling of muscle weakness, and severe hyponatremia, with diagnostic criteria for SIADH, after exposure to amantadine. After amantadine withdrawal, these symptoms disappeared, and sodium levels reached normal values gradually. The SIADH should be taken into account among the possible side effects of amantadine.

Amantadine withdrawal

Amantadine withdrawal

A Case of Temporary Finger Tremors Due to Amantadine Withdrawal

A Case of Temporary Finger Tremors Due to Amantadine Withdrawal

A Case of Temporary Finger Tremors Due to Amantadine Withdrawal

A Case of Temporary Finger Tremors Due to Amantadine Withdrawal

Amantadine withdrawal

Amantadine withdrawal

Amantadine withdrawal

Amantadine withdrawal

Psychosis in parkinson's disease: Diagnosis and treatment

1. 1. This article reviews the prevalence, diagnosis, pathophysiology and management of psychosis in Parkinson's disease. 2. 2. Psychosis in Parkinson's disease has been associated with all antiparkinsonian medications. The most common symptoms are vivid disturbing dreams, visual hallucinations and paranoid delusions. 3. 3. The emergence of psychosis reduces the patient's functional capacity and increases caregiver burden. It also poses a therapeutic dilemma because effective treatment of psychotic symptoms may result in worsening of motor symptoms and vice versa. 4. 4. Increased physician awareness is essential for proper diagnosis and management. Withdrawal of anticholinergic medications and amantadine followed by levodopa dose adjustment is effective in many patients. 5. 5. Atypical neuroleptics, in low doses, may be successful when other measures have failed. However, these agents are not approved for treating Parkinsonian psychosis and must be considered as investigational therapies.