Prefrontal cortex lesions and MAO-A modulate aggression in penetrating traumatic brain injury.
Summary of "Prefrontal cortex lesions and MAO-A modulate aggression in penetrating traumatic brain injury."
This study investigates the interaction between brain lesion location and monoamine oxidase A (MAO-A) in the genesis of aggression in patients with penetrating traumatic brain injury (PTBI).
Brain Injury Research Laboratory, Kessler Foundation Research Center, 1199 Pleasant Valley Way, West Orange, NJ 07052 email@example.com.
This article was published in the following journal.
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/21422455
- DOI: http://dx.doi.org/10.1212/WNL.0b013e318211c33e
Medical and Biotech [MESH] Definitions
The rostral part of the frontal lobe, bounded by the inferior precentral fissure in humans, which receives projection fibers from the mediodorsal nucleus of the thalamus. The prefrontal cortex receives afferent fibers from numerous structures of the diencephalon, mesencephalon, and limbic system as well as cortical afferents of visual, auditory, and somatic origin.
Brain Hemorrhage, Traumatic
Bleeding within the brain as a result of penetrating and nonpenetrating CRANIOCEREBRAL TRAUMA. Traumatically induced hemorrhages may occur in any area of the brain, including the CEREBRUM; BRAIN STEM (see BRAIN STEM HEMORRHAGE, TRAUMATIC); and CEREBELLUM.
Recurrent seizures causally related to CRANIOCEREBRAL TRAUMA. Seizure onset may be immediate but is typically delayed for several days after the injury and may not occur for up to two years. The majority of seizures have a focal onset that correlates clinically with the site of brain injury. Cerebral cortex injuries caused by a penetrating foreign object (CRANIOCEREBRAL TRAUMA, PENETRATING) are more likely than closed head injuries (HEAD INJURIES, CLOSED) to be associated with epilepsy. Concussive convulsions are nonepileptic phenomena that occur immediately after head injury and are characterized by tonic and clonic movements. (From Rev Neurol 1998 Feb;26(150):256-261; Sports Med 1998 Feb;25(2):131-6)
Hearing Loss, Central
Hearing loss due to disease of the AUDITORY PATHWAYS (in the CENTRAL NERVOUS SYSTEM) which originate in the COCHLEAR NUCLEI of the PONS and then ascend bilaterally to the MIDBRAIN, the THALAMUS, and then the AUDITORY CORTEX in the TEMPORAL LOBE. Bilateral lesions of the auditory pathways are usually required to cause central hearing loss. Cortical deafness refers to loss of hearing due to bilateral auditory cortex lesions. Unilateral BRAIN STEM lesions involving the cochlear nuclei may result in unilateral hearing loss.
Evoked Potentials, Auditory, Brain Stem
Electrical waves in the CEREBRAL CORTEX generated by BRAIN STEM structures in response to auditory click stimuli. These are found to be abnormal in many patients with CEREBELLOPONTINE ANGLE lesions, MULTIPLE SCLEROSIS, or other DEMYELINATING DISEASES.
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