Several studies have suggested Dilantin cerebral atrophy may be prevalent in long-term patients due to the adverse effects of phenytoin toxicity. Dilantin cerebral atrophy can potentially cause permanent moving and speaking problems in patients and should be treated as soon as possible.

Dilantin (phenytoin) has been on the market since 1953 and is used to treat patients with a number of epileptic conditions. This medication works by slowing the electrical signals in the brain to prevent the onset of seizures.

While Dilantin has treated millions of patients, there have also been numerous injury reports submitted to the FDA indicating Dilantin cerebral atrophy. Cerebral atrophy can be either focal or generalized, with symptoms of the condition often being compared to having a stroke.

Cerebral atrophy occurs when brain tissue deteriorates and loses neurological connections ultimately breaking down communication between the brain and the body. General cerebral atrophy affects the entire brain, while focal primarily impacts the cerebellum. When the cerebellum becomes damaged, patients lose their ability to walk and speak properly with those voluntary functions compromised.

Overview of Dilantin Cerebral Atrophy

Dilantin cerebral atrophy has been a concern to scientists since 1994 when researchers found that phenytoin patients had significantly smaller cerebelli compared to non exposed patients. This study was initially conducted to observe how phenytoin affected the brain while preventing seizures. During the study, researchers discovered potential Dilantin cerebral atrophy in diagnostic images.

Later studies found similar results including a case study conducted in 2007 which followed a young woman who reportedly developed Dilantin cerebral atrophy. The woman had been taking phenytoin since she was 18 and was diagnosed with cerebral atrophy at age 31 after doctors analyzed CT scans of her brain. This was one of the first studies to suggest long-term phenytoin exposure increased the risk of developed Dilantin cerebral atrophy.

One of the more recent studies to indicate this correlation was published in a 2013 issue of Neurology Asia.  In the journal, researchers stated that “persistent cerebellar dysfunction with cerebellar atrophy is a well-known complication of long-term phenytoin use.” The case study described a phenytoin patient who reportedly developed Dilantin cerebral atrophy while taking his prescription.

However, during the study researchers noted that acute Dilantin cerebral atrophy rarely causes permanent cerebellar damage. The FDA eventually approved a label change for phenytoin, to state that taking phenytoin could increase the chances of cerebellar atrophy.

At this time, researchers are not sure why phenytoin may be cause cerebral atrophy but believe it may be linked to the patient having adverse reactions to the treatment mechanism.

Additionally, there are a number of other factors that can contribute to the development of cerebral atrophy with some factors being environmental or genetic. This means cerebral atrophy can develop from toxicity exposure to alcohol or other treatment drugs, can form from degenerative disease, or occur as a lasting side effect from traumatic injury. Patients who develop Dilantin cerebral atrophy symptoms should see their doctor as soon as possible, with side effects of including jerky or unsteady movements or slow and slurred speech.