EPITOMES-PHYSICAL MEDICINE AND REHABILITATION
664
Serial examinations of these patients showed that phenytoin use had acute adverse effects on cognition in those with the most severe brain injuries. Despite these findings, there is no evidence that the adverse effects of phenytoin use exceed those of other anticonvulsants. In studies of patients with other forms of epilepsy, the cognitive effects of various anticonvulsants have been found to be subtle and overlapping. The greatest impairments are seen with timed tasks; these worsen with increasing serum drug levels, even within the therapeutic range. A comparative evaluation of anticonvulsants is needed because these patients differ from those with other forms of epilepsy who have more stable cognition. The implications of these studies for clinical practice are as follows. Long-term phenytoin prophylaxis after traumatic brain injury is no longer warranted in the absence of a clinically definable seizure disorder. Prophylaxis during the first week after injury can suppress early seizures at a time when brain metabolism and blood flow may be compromised. After a week, phenytoin prophylaxis should be discontinued. If seizures do develop, many factors need to be considered, including ways to enhance compliance and to minimize cognitive side effects, especially during rapid phases of recovery. Regardless of which drug is chosen, the lowest dose necessary to control seizures should be used to minimize cognitive side effects. TERESA L. MASSAGLI, MD
Seattle, Washington REFERENCES Dikmen SS, Temkin NR, Miller B, Machamer J, Winn HR: Neurobehavioral effects of phenytoin prophylaxis of posttraumatic seizures. JAMA 1991; 265:12711277 Massagli TL: Neurobehavioral effects of phenytoin, carbamazepine, and valproic acid: Implications for use in traumatic brain injury. Arch Phys Med Rehabil 1991; 72:219-226 Meador KJ, Loring DW, Huh K, Gallagher BB, King DW: Comparative cognitive effects of anticonvulsants. Neurology 1990; 40:391-394 Temkin NR, Dikmen SS, Wilensky AJ, Keihm J, Chabal S, Winn HR: A randomized, double-blind study of phenytoin for the prevention of posttraumatic seizures. N Engl J Med 1990; 323:497-502
Neurobehavioral and Family Functioning Following Traumatic Brain Injury in Children TRAUMATIC BRAIN INJURY is a major cause of morbidity in children and accounts for more than 100,000 admissions to hospital per year. Children who survive moderate and severe head trauma are at risk for immediate and lasting neurobehavioral sequelae that can interfere with their reintegration into school, affect peer relations, and cause family dysfunction. Recent studies have identified useful early predictors of outcome and have provided evidence that the magnitude of neuropsychological impairment is directly related to the severity of the brain injury. The immediate consequences of traumatic brain injury depend on a number of factors, including the severity of the brain injury and the presence of extracranial injuries, particularly cardiac, chest wall, and intra-abdominal ones. The lower the initial Glasgow Coma Scale score and the longer the duration of coma, the greater the risk of permanent neurologic and cognitive impairment. Favorable prognostic indicators include the absence of early hypoxemia and a prolonged elevation of intracranial pressure, a Glasgow Motor Scale score of 4 to 6 at 72 hours, a coma of less than 24 hours, and posttraumatic amnesia of less than 2 weeks. Children with mild traumatic brain injury-initial Glasgow Coma Scale score of 13 to 15-account for more than 80% of
all pediatric head injuries, but they generally have no serious compromise of educational function. A recent investigation compared the early neuropsychological and academic outcome of a cohort of children with traumatic brain injury with that of controls individually matched on various premorbid characteristics. The assessments on these patients aged 6 to 15 years were undertaken three weeks after full orientation was achieved. The pattern of greater performance decline with increasing severity of brain injury was consistent for measures assessing intelligence, memory, speeded motor performance, adaptive problem solving, and academic performance. Moderately (Glasgow Coma Scale 9 through 12) and severely (Glasgow Coma Scale 3 through 8) injured patients performed at normal to low-normal levels in reference to standardized intellectual norms, but they showed substantial impairment when compared with their matched controls. Striking early deficits in the rate of information processing, speeded motor performance, and graphomotor dexterity have particular educational implications. The same investigators examined the effects of injury severity on family functioning and determined preinjury factors that were most predictive of family outcome three months and one year following injury. Overall global family functioning was well maintained a year after injury in families of children with mild and moderate traumatic brain injuries. Families of children with severe traumatic brain injuries, however, showed substantially higher levels of stress and strained family relationships at follow-up. Functioning of the family before injury consistently emerged as the single most important predictor of family outcome. These studies identify those children and families at greatest risk for sequelae after childhood traumatic brain injury. Families at risk for future problems can be identified at the time of injury and provided with ongoing support and referral services as early as possible. Targeting those children with moderate and severe traumatic brain injuries for early multidisciplinary rehabilitative support and careful follow-up of neuropsychological, psychosocial, and educational progress may minimize long-term morbidity. Studies of the consequences of head injuries should be interpreted with caution if carefully and appropriately matched control groups are not included. Without the use of properly selected controls, it is difficult to distinguish between postinjury deficits caused by premorbid characteristics versus those caused by the brain injury per se. In addition, a child's actual deficits may be masked and valuable services withheld if postinjury performance is considered only in the context of population-based norms. CRAIG M. McDONALD, MD
Sacramento, California KENNETH M. JAFFE, MD Seattle, Washington
REFERENCES Bijur PE, Haslum M, Golding J: Cognitive and behavioral sequelae of mild injury in children. Pediatrics 1990; 86:337-344 Jaffe KM, Fay G, Polissar L, et al: Severity of pediatric traumatic brain injury and early neurobehavioral outcome: A cohort study. Arch Phys Med Rehabil 1992; 73:540547 Kraus JF, Rock A, Hemyari P: Brain injuries among infants, children, adolescents, and young adults. Am J Dis Child 1990; 144:684-691 Michaud L, Rivara FP, Grady MS, Reay DT: Predictions of survival and severity of disability following severe brain injury in children. Neurosurgery 1992; 31:254-264 Rivara JM, Fay GC, Jaffe KM, Polissar NL, Shurtleff HA, Martin KM: Predictors of family functioning one year following traumatic brain injury in children. Arch Phys Med RehabilI992; 73:899-910
664
Serial examinations of these patients showed that phenytoin use had acute adverse effects on cognition in those with the most severe brain injuries. Despite these findings, there is no evidence that the adverse effects of phenytoin use exceed those of other anticonvulsants. In studies of patients with other forms of epilepsy, the cognitive effects of various anticonvulsants have been found to be subtle and overlapping. The greatest impairments are seen with timed tasks; these worsen with increasing serum drug levels, even within the therapeutic range. A comparative evaluation of anticonvulsants is needed because these patients differ from those with other forms of epilepsy who have more stable cognition. The implications of these studies for clinical practice are as follows. Long-term phenytoin prophylaxis after traumatic brain injury is no longer warranted in the absence of a clinically definable seizure disorder. Prophylaxis during the first week after injury can suppress early seizures at a time when brain metabolism and blood flow may be compromised. After a week, phenytoin prophylaxis should be discontinued. If seizures do develop, many factors need to be considered, including ways to enhance compliance and to minimize cognitive side effects, especially during rapid phases of recovery. Regardless of which drug is chosen, the lowest dose necessary to control seizures should be used to minimize cognitive side effects. TERESA L. MASSAGLI, MD
Seattle, Washington REFERENCES Dikmen SS, Temkin NR, Miller B, Machamer J, Winn HR: Neurobehavioral effects of phenytoin prophylaxis of posttraumatic seizures. JAMA 1991; 265:12711277 Massagli TL: Neurobehavioral effects of phenytoin, carbamazepine, and valproic acid: Implications for use in traumatic brain injury. Arch Phys Med Rehabil 1991; 72:219-226 Meador KJ, Loring DW, Huh K, Gallagher BB, King DW: Comparative cognitive effects of anticonvulsants. Neurology 1990; 40:391-394 Temkin NR, Dikmen SS, Wilensky AJ, Keihm J, Chabal S, Winn HR: A randomized, double-blind study of phenytoin for the prevention of posttraumatic seizures. N Engl J Med 1990; 323:497-502
Neurobehavioral and Family Functioning Following Traumatic Brain Injury in Children TRAUMATIC BRAIN INJURY is a major cause of morbidity in children and accounts for more than 100,000 admissions to hospital per year. Children who survive moderate and severe head trauma are at risk for immediate and lasting neurobehavioral sequelae that can interfere with their reintegration into school, affect peer relations, and cause family dysfunction. Recent studies have identified useful early predictors of outcome and have provided evidence that the magnitude of neuropsychological impairment is directly related to the severity of the brain injury. The immediate consequences of traumatic brain injury depend on a number of factors, including the severity of the brain injury and the presence of extracranial injuries, particularly cardiac, chest wall, and intra-abdominal ones. The lower the initial Glasgow Coma Scale score and the longer the duration of coma, the greater the risk of permanent neurologic and cognitive impairment. Favorable prognostic indicators include the absence of early hypoxemia and a prolonged elevation of intracranial pressure, a Glasgow Motor Scale score of 4 to 6 at 72 hours, a coma of less than 24 hours, and posttraumatic amnesia of less than 2 weeks. Children with mild traumatic brain injury-initial Glasgow Coma Scale score of 13 to 15-account for more than 80% of
all pediatric head injuries, but they generally have no serious compromise of educational function. A recent investigation compared the early neuropsychological and academic outcome of a cohort of children with traumatic brain injury with that of controls individually matched on various premorbid characteristics. The assessments on these patients aged 6 to 15 years were undertaken three weeks after full orientation was achieved. The pattern of greater performance decline with increasing severity of brain injury was consistent for measures assessing intelligence, memory, speeded motor performance, adaptive problem solving, and academic performance. Moderately (Glasgow Coma Scale 9 through 12) and severely (Glasgow Coma Scale 3 through 8) injured patients performed at normal to low-normal levels in reference to standardized intellectual norms, but they showed substantial impairment when compared with their matched controls. Striking early deficits in the rate of information processing, speeded motor performance, and graphomotor dexterity have particular educational implications. The same investigators examined the effects of injury severity on family functioning and determined preinjury factors that were most predictive of family outcome three months and one year following injury. Overall global family functioning was well maintained a year after injury in families of children with mild and moderate traumatic brain injuries. Families of children with severe traumatic brain injuries, however, showed substantially higher levels of stress and strained family relationships at follow-up. Functioning of the family before injury consistently emerged as the single most important predictor of family outcome. These studies identify those children and families at greatest risk for sequelae after childhood traumatic brain injury. Families at risk for future problems can be identified at the time of injury and provided with ongoing support and referral services as early as possible. Targeting those children with moderate and severe traumatic brain injuries for early multidisciplinary rehabilitative support and careful follow-up of neuropsychological, psychosocial, and educational progress may minimize long-term morbidity. Studies of the consequences of head injuries should be interpreted with caution if carefully and appropriately matched control groups are not included. Without the use of properly selected controls, it is difficult to distinguish between postinjury deficits caused by premorbid characteristics versus those caused by the brain injury per se. In addition, a child's actual deficits may be masked and valuable services withheld if postinjury performance is considered only in the context of population-based norms. CRAIG M. McDONALD, MD
Sacramento, California KENNETH M. JAFFE, MD Seattle, Washington
REFERENCES Bijur PE, Haslum M, Golding J: Cognitive and behavioral sequelae of mild injury in children. Pediatrics 1990; 86:337-344 Jaffe KM, Fay G, Polissar L, et al: Severity of pediatric traumatic brain injury and early neurobehavioral outcome: A cohort study. Arch Phys Med Rehabil 1992; 73:540547 Kraus JF, Rock A, Hemyari P: Brain injuries among infants, children, adolescents, and young adults. Am J Dis Child 1990; 144:684-691 Michaud L, Rivara FP, Grady MS, Reay DT: Predictions of survival and severity of disability following severe brain injury in children. Neurosurgery 1992; 31:254-264 Rivara JM, Fay GC, Jaffe KM, Polissar NL, Shurtleff HA, Martin KM: Predictors of family functioning one year following traumatic brain injury in children. Arch Phys Med RehabilI992; 73:899-910
