Amantadine is a prescription medication used to manage Parkinson’s disease and related movement disorders. It helps address symptoms like stiffness and tremors by influencing dopamine activity in the brain. Historically, it was also an antiviral agent for influenza A, but this use is now uncommon due to viral resistance. While effective, amantadine can become toxic if its concentration rises to unsafe levels, which occurs when the drug accumulates beyond what the body can safely handle.
Causes of Amantadine Toxicity
Amantadine accumulation can happen through several pathways. The most direct cause is an overdose, which can be accidental or intentional. An accidental overdose may occur if a patient is confused about their dosing schedule, a situation more common in elderly individuals managing multiple prescriptions, as taking more than the prescribed amount can overwhelm the body’s ability to process the medication, leading to toxic effects.
A more frequent cause of toxicity is impaired kidney function. The body relies on the kidneys to filter amantadine from the blood. In individuals with chronic kidney disease, this clearance process is slowed. As a result, the drug can build up to dangerous concentrations even when the person is taking a standard, medically appropriate dose.
Drug interactions are another potential cause, though less common than renal impairment. Certain medications can interfere with the body’s handling of amantadine, increasing its concentration. For this reason, a patient’s entire medication list is reviewed when prescribing amantadine to avoid unintended accumulation.
Symptoms of Poisoning
The signs of amantadine poisoning are mainly neurological and psychiatric. Patients may experience a sudden onset of confusion, disorientation, agitation, and visual hallucinations, alongside delirium where perception of reality is altered. The nervous system’s overstimulation can also cause myoclonus, which is involuntary muscle twitching. In severe cases, neurotoxicity can progress to seizures or a coma.
Cardiovascular functions are also affected. The drug can interfere with the heart’s electrical signaling, leading to arrhythmias and unstable blood pressure that can become dangerously high or low. A specific life-threatening event is Torsades de Pointes, a rapid heartbeat that can be identified on an electrocardiogram (EKG) and may lead to cardiac arrest.
Many symptoms are also anticholinergic, occurring because the drug blocks the neurotransmitter acetylcholine. This leads to a predictable set of physical signs. These include:
- A persistently dry mouth
- Blurred vision
- Noticeably dilated pupils
- Flushed skin
- Urinary retention (inability to empty the bladder)
Diagnosis in a Clinical Setting
When amantadine poisoning is suspected, diagnosis begins with a patient history and physical examination. Clinicians will ask about all medications, dosages, and the timing of the last dose to establish a timeline. Information about underlying health conditions, especially any history of kidney problems, is important. The physical exam focuses on assessing for characteristic neurological and anticholinergic signs.
Specific laboratory tests are ordered to confirm the diagnosis. Blood tests measuring creatinine and blood urea nitrogen (BUN) are performed to evaluate kidney function. While direct measurement of amantadine in the blood is possible, these tests are not available for rapid analysis in most hospitals. Therefore, the diagnosis is made based on the patient’s clinical presentation and history, rather than waiting for a specific drug level.
An electrocardiogram (EKG) is used to monitor the heart’s electrical activity for dangerous arrhythmias. Clinicians look for abnormalities like a prolonged QT interval, which indicates amantadine is affecting the heart. Continuous EKG monitoring allows the medical team to watch for the development of severe rhythms like Torsades de Pointes.
Medical Treatment for Overdose
The first step in managing amantadine poisoning is to discontinue the drug immediately. This action prevents any further absorption and halts the progression of toxicity. All sources of the medication are stopped while the body begins the slow process of elimination.
The foundation of treatment is supportive care to manage symptoms and maintain stability. This includes intravenous (IV) fluids for hydration and blood pressure support. If a patient is highly agitated or has seizures, benzodiazepines like lorazepam are used to calm the central nervous system. Vital signs are continuously monitored throughout treatment.
If the overdose was recent, gastrointestinal decontamination with activated charcoal may be considered. Activated charcoal binds to the drug in the stomach, preventing it from being absorbed into the bloodstream. Its effectiveness is limited by the time that has passed since ingestion.
There is no specific antidote for amantadine poisoning. Hemodialysis is also not effective for removal, as the drug’s chemical properties cause it to distribute widely into body tissues rather than remaining in the bloodstream, making it difficult for dialysis to filter out. Management continues to focus on controlling cardiac and neurological symptoms until the patient’s own kidneys can gradually excrete the drug.