Pharmacotherapy of the cognitive sequelae secondary to traumatic brain injury
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. As of a complex cascade of injuries to the brain, patients with TBI may experience alterations that...
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Veröffentlicht in: | Revista de neurologiá 2007-11, Vol.45 (9), p.563 |
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creator | Riós-Romenets, S Castaño-Monsalve, B Bernabeu-Guitart, M |
description | 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.
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.
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. |
doi_str_mv | 10.33588/rn.4509.2007279 |
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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.
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.</description><identifier>ISSN: 0210-0010</identifier><identifier>DOI: 10.33588/rn.4509.2007279</identifier><identifier>PMID: 17979087</identifier><language>fre ; spa</language><publisher>Spain</publisher><subject>Animals ; Anticonvulsants - adverse effects ; Antidepressive Agents - adverse effects ; Antidepressive Agents - therapeutic use ; Brain Damage, Chronic - drug therapy ; Brain Damage, Chronic - etiology ; Brain Injuries - complications ; Catecholamines - physiology ; Central Nervous System Stimulants - therapeutic use ; Cholinesterase Inhibitors - therapeutic use ; Cognition Disorders - drug therapy ; Cognition Disorders - etiology ; Consciousness Disorders - drug therapy ; Consciousness Disorders - etiology ; Dopamine Agonists - therapeutic use ; Humans ; Language Disorders - drug therapy ; Language Disorders - etiology ; Learning Disorders - drug therapy ; Learning Disorders - etiology ; Memory Disorders - drug therapy ; Memory Disorders - etiology ; Neurotransmitter Agents - physiology ; Psychotropic Drugs - adverse effects ; Randomized Controlled Trials as Topic - statistics & numerical data</subject><ispartof>Revista de neurologiá, 2007-11, Vol.45 (9), p.563</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17979087$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Riós-Romenets, S</creatorcontrib><creatorcontrib>Castaño-Monsalve, B</creatorcontrib><creatorcontrib>Bernabeu-Guitart, M</creatorcontrib><title>Pharmacotherapy of the cognitive sequelae secondary to traumatic brain injury</title><title>Revista de neurologiá</title><addtitle>Rev Neurol</addtitle><description>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.
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.
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.</description><subject>Animals</subject><subject>Anticonvulsants - adverse effects</subject><subject>Antidepressive Agents - adverse effects</subject><subject>Antidepressive Agents - therapeutic use</subject><subject>Brain Damage, Chronic - drug therapy</subject><subject>Brain Damage, Chronic - etiology</subject><subject>Brain Injuries - complications</subject><subject>Catecholamines - physiology</subject><subject>Central Nervous System Stimulants - therapeutic use</subject><subject>Cholinesterase Inhibitors - therapeutic use</subject><subject>Cognition Disorders - drug therapy</subject><subject>Cognition Disorders - etiology</subject><subject>Consciousness Disorders - drug therapy</subject><subject>Consciousness Disorders - etiology</subject><subject>Dopamine Agonists - therapeutic use</subject><subject>Humans</subject><subject>Language Disorders - drug therapy</subject><subject>Language Disorders - etiology</subject><subject>Learning Disorders - drug therapy</subject><subject>Learning Disorders - etiology</subject><subject>Memory Disorders - drug therapy</subject><subject>Memory Disorders - etiology</subject><subject>Neurotransmitter Agents - physiology</subject><subject>Psychotropic Drugs - adverse effects</subject><subject>Randomized Controlled Trials as Topic - statistics & numerical data</subject><issn>0210-0010</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1jztPwzAURj2AaCnsTMh_IOE6tmN7RBUvqQgGmKsbP6ir5oHjIOXfUwRM50xH30fIFYOSc6n1TepKIcGUFYCqlDkhS6gYFAAMFuR8HPcAggsDZ2TBlFEGtFqS59cdphZtn3c-4TDTPtCjUtt_dDHHL09H_zn5A_6I7TuHaaa5pznh1GKOljYJY0djt5_SfEFOAx5Gf_nHFXm_v3tbPxabl4en9e2mGBg3uQggvRLaONTSyZpr4CCstL4KDgQLwpmAFXhU2hhTC6wbI9HpRorGBwl8Ra5_u8PUtN5thxTb47Dt_y_-DboxT0c</recordid><startdate>20071101</startdate><enddate>20071101</enddate><creator>Riós-Romenets, S</creator><creator>Castaño-Monsalve, B</creator><creator>Bernabeu-Guitart, M</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>20071101</creationdate><title>Pharmacotherapy of the cognitive sequelae secondary to traumatic brain injury</title><author>Riós-Romenets, S ; Castaño-Monsalve, B ; Bernabeu-Guitart, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p139t-f05e7489da85d56380304c5ce2fd041f4d9fa20ea7899964a6b95ad8b54bef503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>fre ; spa</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Anticonvulsants - adverse effects</topic><topic>Antidepressive Agents - adverse effects</topic><topic>Antidepressive Agents - therapeutic use</topic><topic>Brain Damage, Chronic - drug therapy</topic><topic>Brain Damage, Chronic - etiology</topic><topic>Brain Injuries - complications</topic><topic>Catecholamines - physiology</topic><topic>Central Nervous System Stimulants - therapeutic use</topic><topic>Cholinesterase Inhibitors - therapeutic use</topic><topic>Cognition Disorders - drug therapy</topic><topic>Cognition Disorders - etiology</topic><topic>Consciousness Disorders - drug therapy</topic><topic>Consciousness Disorders - etiology</topic><topic>Dopamine Agonists - therapeutic use</topic><topic>Humans</topic><topic>Language Disorders - drug therapy</topic><topic>Language Disorders - etiology</topic><topic>Learning Disorders - drug therapy</topic><topic>Learning Disorders - etiology</topic><topic>Memory Disorders - drug therapy</topic><topic>Memory Disorders - etiology</topic><topic>Neurotransmitter Agents - physiology</topic><topic>Psychotropic Drugs - adverse effects</topic><topic>Randomized Controlled Trials as Topic - statistics & numerical data</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Riós-Romenets, S</creatorcontrib><creatorcontrib>Castaño-Monsalve, B</creatorcontrib><creatorcontrib>Bernabeu-Guitart, M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Revista de neurologiá</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Riós-Romenets, S</au><au>Castaño-Monsalve, B</au><au>Bernabeu-Guitart, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pharmacotherapy of the cognitive sequelae secondary to traumatic brain injury</atitle><jtitle>Revista de neurologiá</jtitle><addtitle>Rev Neurol</addtitle><date>2007-11-01</date><risdate>2007</risdate><volume>45</volume><issue>9</issue><spage>563</spage><pages>563-</pages><issn>0210-0010</issn><abstract>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.
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.
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.</abstract><cop>Spain</cop><pmid>17979087</pmid><doi>10.33588/rn.4509.2007279</doi></addata></record> |
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subjects | Animals Anticonvulsants - adverse effects Antidepressive Agents - adverse effects Antidepressive Agents - therapeutic use Brain Damage, Chronic - drug therapy Brain Damage, Chronic - etiology Brain Injuries - complications Catecholamines - physiology Central Nervous System Stimulants - therapeutic use Cholinesterase Inhibitors - therapeutic use Cognition Disorders - drug therapy Cognition Disorders - etiology Consciousness Disorders - drug therapy Consciousness Disorders - etiology Dopamine Agonists - therapeutic use Humans Language Disorders - drug therapy Language Disorders - etiology Learning Disorders - drug therapy Learning Disorders - etiology Memory Disorders - drug therapy Memory Disorders - etiology Neurotransmitter Agents - physiology Psychotropic Drugs - adverse effects Randomized Controlled Trials as Topic - statistics & numerical data |
title | Pharmacotherapy of the cognitive sequelae secondary to traumatic brain injury |
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