title: [Pharmacotherapy of the cognitive sequelae secondary to traumatic brain injury].
abstract: OBJECTIVE
  To review and correlate the most common cognitive disorders secondary to traumatic brain injuries (TBI), the neurobiology of these deficits and their possible modulation by neuropharmacological means.
  
  
  METHODS
  As of a complex cascade of injuries to the brain, patients with TBI may experience alterations that affect the cognitive domain on different levels and to varying degrees, the most common being alteration of the level of alertness; slowing of the speed at which information is processed; attention, memory and learning deficits; language and communication disorders; and impaired executive functions. Brain damage may be caused by a range of pathological mechanisms, such as focal bruising, diffuse axonal damage, cytotoxic damage and neurotransmitter excitotoxicity. Certain pharmacological agents have an effect on the cognitive functions. Pharmacological agents that improve cognitive performance include dopaminergic agents, psychostimulants, some antidepressants and cholinesterase inhibitors.
  
  
  CONCLUSIONS
  Studies into the pharmacological neuromodulation of the cognitive disorders secondary to TBI are currently in the early stages. The information we have available on the neurochemical bases of cognition and cognitive disorders due to TBI suggest that the most important goals of pharmacological intervention in this group of patients are the stimulation of the catecholaminic and cholinergic functions.
authors.affiliation: Institut de Neurorehabilitacio Guttmann, Badalona, España. silvia.riosrom@hotmail.com
authors.forename: S
authors.initials: S
authors.lastname: Riós-Romenets
authors.forename: B
authors.initials: B
authors.lastname: Castaño-Monsalve
authors.forename: M
authors.initials: M
authors.lastname: Bernabeu-Guitart
mesh_terms: D000818:Animals; D000927:Anticonvulsants / Q000009:adverse effects; D000928:Antidepressive Agents / Q000009:adverse effects / Q000627:therapeutic use; D001925:Brain Damage, Chronic / Q000188:drug therapy / Q000209:etiology; D001930:Brain Injuries / Q000150:complications*; D002395:Catecholamines / Q000502:physiology; D000697:Central Nervous System Stimulants / Q000627:therapeutic use*; D002800:Cholinesterase Inhibitors / Q000627:therapeutic use*; D003072:Cognition Disorders / Q000188:drug therapy* / Q000209:etiology; D003244:Consciousness Disorders / Q000188:drug therapy / Q000209:etiology; D018491:Dopamine Agonists / Q000627:therapeutic use*; D006801:Humans; D007806:Language Disorders / Q000188:drug therapy / Q000209:etiology; D007859:Learning Disabilities / Q000188:drug therapy / Q000209:etiology; D008569:Memory Disorders / Q000188:drug therapy* / Q000209:etiology; D018377:Neurotransmitter Agents / Q000502:physiology; D011619:Psychotropic Drugs / Q000009:adverse effects; D016032:Randomized Controlled Trials as Topic / Q000706:statistics & numerical data
chemical_list: D000927:Anticonvulsants; D000928:Antidepressive Agents; D002395:Catecholamines; D000697:Central Nervous System Stimulants; D002800:Cholinesterase Inhibitors; D018491:Dopamine Agonists; D018377:Neurotransmitter Agents; D011619:Psychotropic Drugs