Pharmacological treatment of neurobehavioural sequelae of traumatic brain injury.

Abstract

Neurobehavioural sequelae of traumatic brain injuries require an appropriate/effective pharmacological response in that they represent an important cause of disability. In this field, there is no evidence that reaches the level of a standard: there are guidelines on the use of methylphenidate, donepezil and bromocriptine for the treatment of cognitive disturbances, for the non-use of phenytoin and for the use of beta-blockers for controlling aggressiveness. Resolving a single symptom is not relevant in a rehabilitation project if it is not in the context of a more complex picture of neurobehavioural recovery, in which the positive and negative effects of every therapeutic choice are considered. For example, phenytoin could be used for the positive control of epileptic crises but is not advised since it impedes the recovery of cognitive functions in general. Analogous effects not yet identified may concern benzodiazepine, neuroleptics and other sedatives usually prescribed in cases of cranial trauma. Psychotropic drugs are considered to be able to influence the neuronal plasticity processes. Studies on animals have shown that the administration of D-amphetamine combined with sensorial-motor exercise produces the steady acceleration of motor recovery, which acts as a catalyst to the neurological recovery process. On the other hand, alpha1-NA receptor antagonist drugs produce negative effects; these include clonidine (antihypertension) and haloperidol (neuroleptic). Studies need to be carried out to evaluate the effectiveness of particular drugs. These studies need to focus not only on the disappearance of symptoms but also on the positive and negative effects on overall rehabilitation and on the neurobiological recovery of the patient.