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ABSTRACT & COMMENTARY
By Nitin K Sethi, MD
Assistant Professor of Neurology, Weill Cornell Medical College
Dr. Sethi reports no financial disclosures relevant to this field of study.
This article originally appeared in the July 2014 issue of Neurology Alert. It was edited by Matthew E. Fink, MD, and peer reviewed by M. Flint Beal, MD. Dr. Fink is Professor and Chairman, Department of Neurology, Weill Cornell Medical College and Neurologist-in-Chief, New York Presbyterian Hospital, and Dr. Beal is Anne Parrish Titzel Professor, Department of Neurology and Neuroscience, Weill Cornell Medical Center. Dr. Fink is a retained consultant for Procter & Gamble, and Dr. Beal reports no financial relationships relevant to this field of study.
SYNOPSIS: In this large prospective study of trauma patients, the most important factor associated with post-traumatic seizures was the presence of alcohol intoxication.
SOURCE: Vaaramo K, et al. Predictors of new-onset seizures: A 10-year follow-up of head trauma subjects with and without traumatic brain injury. J Neurol Neurosurg Psychiatry 2014;85:598-602.
Recent reports indicate that both civilian and military cases of traumatic brain injury (TBI) are on the rise. An estimated 1.5-2.5 million civilian TBI cases occur per year in the United States. Mild TBI has also been recognized as the "signature injury" of America’s global war on terrorism in Iraq and Afghanistan. Seizures are a long-recognized sequela of head injury, especially when complicated by moderate-to-severe TBI. While seizures occur soon after head trauma in immediate and early post-traumatic epilepsy (PTE), epilepsy can be a delayed consequence with seizures occurring as far out as 5-20 years. Penetrating head trauma, brain contusion, subdural hematoma, epidural hematoma, intracranial hemorrhage, and depressed skull fracture all increase the risk of PTE. Other predictors include age 65 years or older, Glasgow Coma Scale (GCS) of 3-8, loss of consciousness (LOC) > 30 minutes, and post-traumatic amnesia (PTA) lasting more than 24 hours.
The authors investigated risk factors for new-onset seizures in a cohort of 739 trauma patients. There were 362 trauma patients without TBI (GCS score of 15, no LOC, no PTA); 297 with mild TBI (GCS scores from 13-15, LOC < 30 minutes or PTA < 1 hour, no traumatic intracranial findings on CT/MRI); and 80 with moderate-to-severe TBI (GCS < 13, evidence of traumatic injury on CT/MRI). Those with a prior history of seizures, dementia, stroke, and other neurological disease were excluded. Out of 42 patients who developed new-onset seizure(s), alcohol-related seizures occurred in 19 (45.2%), most commonly among those with no TBI. Seventeen of these 19 patients (89.5%) with alcohol-related new-onset seizures were intoxicated at the time of the index trauma. Moderate-to-severe TBI patients had higher mortality and were more likely to develop PTE. Alcohol-related head injury, moderate-to-severe TBI, and preceding psychiatric disease were all found to be independent predictors of new-onset seizure.
One of the sequelae of trauma with TBI, in both the civilian and military setting, is the emergence of seizures and development of PTE, which may occur as far out as 5 years following head injury. While the severity of head trauma is the main predictor for the emergence of PTE, active alcohol and drug abuse at the time of the index injury predisposes to new onset seizures via a complex and multifaceted interaction. Alcohol impairs reaction time, hand-eye coordination, judgment, and driving skills, predisposing one to trauma and TBI. It further lowers the seizure threshold via its effects on glutamate NMDA and GABA receptors.1 Chronic alcoholics are prone to electrolyte and glucose imbalance and seizures may occur both in the setting of binge drinking (rum fits) as well as abrupt cessation (alcohol withdrawal seizures and delirium tremens). Patients may at times present with new onset status epilepticus. All patients with head trauma should be screened for alcohol and drug abuse and effective intervention strategies should be implemented if abuse is identified. These patients remain at risk for post-traumatic seizures and should be kept under observation. While benzodiazepines such as lorazepam are efficacious for primary and secondary prevention of recurrent seizures in the alcoholic patient, long-term anticonvulsant therapy may not be needed in abstinent patients or those with mild TBI.2,3
1. Hillbom M, et al. Seizures in alcohol-dependent patients: Epidemiology, pathophysiology and management. CNS Drugs 2003;17:1013-1030.
2. McMicken DB, Freedland ES. Alcohol-related seizures. Pathophysiology, differential diagnosis, evaluation, and treatment. Emerg Med Clin North Am 1994;12:1057-1079.
3. Bråthen G, et al. EFNS Task Force on Diagnosis and Treatment of Alcohol-Related Seizures. EFNS guideline on the diagnosis and management of alcohol-related seizures: Report of an EFNS task force. Eur J Neurol 2005;12:575-581.