Brain frontal lobe

Ki values for human brain frontal lobe sites labelled by [ H]-mepyramine... 

Mesocortical A neural pathway that connects the ventral tegmentum to the cortex, particularly the frontal lobes. It is one of the major dopamine pathways in the brain. 

Named for the bones of the cranium under which they lie, the lobes are conspicuously defined by prominent sulci of the cortex, which have a relatively constant position in human brains. Each lobe is specialized for different activities (see Figure 6.3). Located in the anterior portions of the hemispheres, the frontal lobes are responsible for voluntary motor activity, speaking ability, and higher intellectual activities. The parietal lobes, which are posterior to the frontal lobes, process and integrate sensory information. The occipital lobes, located in the posterior-most aspects of the cerebrum, process visual information, and the temporal lobes, located laterally, process auditory information. 

Textbooks on neuroscience often describe the location and function of hundreds of individual brain regions (see references above). However, for current purposes these will be kept to a minimum (Figure 2.1). Anatomically, the brain can be subdivided into the forebrain containing the telencephalon and diencephalon, the midbrain or mesencephalon and the hindbrain (metencephalon and myelencephalon). The telencephalon includes the left and right cerebral hemispheres encompassed by the cerebral cortex (neocortex). Cortex is a translation of the word bark and is so-called because its surface, made up of numerous sulci (grooves or invaginations) and gyri (raised areas), is on the outer surface of the brain like the bark of a tree. Each hemisphere is divided into four lobes, named from the front (rostral) to back (caudal) of the brain frontal, temporal, parietal and occipital. 

Adolescence is a time of novelty seeking related to curiosity and learning skills for survival that maybe part of a natural maturation process. Adolescent brains are not fully mature, especially the frontal lobes, which have to do with problem... 

Cerebral blood flow and glucose metabolism Nicotine increases cerebral blood flow (Hara et al. 1993 Yokoi et al. 1993). Functional MRI of smokers who were administered intravenous nicotine shows increases of cerebral blood flow in several areas of the brain. Corresponding to feelings of mood elevation, nicotine activates the nucleus accumbens, amygdala, cingulate cortex, and frontal lobes. This activation is very consistent with functional systems subserving arousal and reinforcement. 

Multiple-dose arecoline infusions in Alzheimer s disease. Arch Gen Psychiatiy. 45(10) 901-5. Taylor AE, Saint-Cyr JA, Lang AE. (1986). Frontal lobe dysfunction in Parkinson s disease. The cortical focus of neostriatal outflow. Brain. Oct. 109(pt 5) 845-83. 

Combi R, Dalpra L, Tenchini ML, Ferini-Strambi L (2004) Autosomal dominant nocturnal frontal lobe epilepsy A critical overview, J Neurol 251 923-934 Connolly J, Boulter J, Heinemann SF (1992) Alpha 4-2 beta 2 and other nicotinic acetylcholine receptor subtypes as targets of psychoactive and addictive drugs, Br J Pharmacol 105 657-666 Conti-Tronconi BM, Dunn SM, Barnard EA, DoUy JO, Lai FA, Ray N, Raftery MA (1985) Brain and muscle nicotinic acetylcholine receptors are different but homologous proteins, Proc Natl Acad Sci U S A 82 5208-5212... 

Rodriguez-Pinguet NO, Pinguet TJ, Figl A, Lester HA, Cohen BN (2005) Mutations linked to autosomal dominant nocturnal frontal lobe epilepsy affect allosteric Ca + activation of the a4 32 nicotinic acetylcholine receptor. Mol Pharmacol 68 487-501 Romano C, Goldstein A (1980) Stereospecific nicotine receptors on rat brain membranes. Science 210 647-650... 

Injury to certain areas within the brain s frontal lobes may produce a syndrome that resembles depression but without depressed mood or a sad affect. Instead, this apathetic syndrome is marked by a lack of motivation, little emotional response, profound psychomotor slowing, and disengagement from social interaction. Antidepressants, stimulants, and medicines that specihcally boost dopamine activity have been tried when treating apathy after TBI (see Table 12.1). 

As many as 1 in 10 patients experience episodes of mania akin to those seen in bipolar disorder after TBl. Right-sided brain injury, particularly in the frontal lobe or so-called limbic structures, has the greatest potential to produce a secondary mania. The manic symptoms include euphoric or irritable mood, decreased need... 

Kraus MF, Levin HS. The frontal Lobes and traumatic brain injury. In Salloway SP, Malloy PF (eds). The Frontal Lobes and Neuropsychiatric Illness. Washington DC American Psychiatric Publishing, 2001, pp 199-213. 

A global view of consciousness is that it is generated throughout the entire brain, as a result of synchronisation of relevant neural networks. Specific systems or regions—for example the cerebral cortex, brainstem reticular formation and thalamic nuclei—may be key anatomical integrators. Areas with the most widespread interconnections are pivotal, and on this basis the cortex and thalamus are more relevant than cerebellum and striatum for example. Frontal cortex for example connects with every other brain region, both in terms of input and output, with 80% of such connections accounted for by cortico-cortical connections. Thalamic intralaminar nuclei are, in conjunction with the reticular nucleus, reciprocally connected to all cortical areas. By contrast the cerebellum has very few output pathways and striatal-cortical input is (via the thalamus) confined to frontal lobe. 

Neuropsychological deficits exist in children with Asperger s syndrome, nonverbal learning dysfunction and other learning disabilities, mental retardation (MR), frontal lobe and temporal lobe dysfunction, and traumatic brain injury (Filley et al., 2001). 

Fuld P, Katzman R, Davies P, et al Intrusions as a sign of Alzheimer dementia chemical and pathological verification. Ann Neurol 11 155-159, 1982 Fuller RW, Hemiick-Luecke SK Antagonism by tomoxetine of the depletion of norepinephrine and epinephrine in rat brain by ocmethyl-m-tyrosine. Res Commun Chem Pathol Pharmacol 41 169-172, 1983 Fuster JM The Prefrontal Cortex Anatomy, Physiology and Neuropsychology of the Frontal Lobe. New York, Raven, 1989... 

Tariot PN, Cohen RM, Welkowitz JA, et al Multiple-dose arecohne infusions in Alzheimer s disease. Arch Gen Psychiatry 45 901-905, 1988 Taylor AE, Saint-Cyr JA, Lang AE Frontal lobe dysfunction in Parkinson s disease the cortical focus of neostriatal outflow. Brain 109 845-883, 1986 Taylor DP, Smith DW, Hyslop DK, et al Receptor binding and atypical antidepressant drug discovery, in Receptor Binding in Drug Research. Edited by O Brien RA. New York, Marcel Dekker, 1986, pp 151-165 Tejedor-Real P, Mico JA, Maldonado R, et al Effect of mixed (RB 38A) and selective (RB 38B) inhibitors of enkephalin degrading enzymes on a model of depression in the rat. Biol Psychiatry 34 100-107, 1993... 

Brain lesions that produce depression can be divided into structural and biochemical types. Any disease that produces a mass lesion or deficit in the frontal lobes can cause a depressive syndrome. Typically, occurrence and severity are correlated with proximity to the tip of the frontal lobe rather than to the extent of motor function loss. The most extensively studied lesions are strokes, but tumors and plaques related to multiple sclerosis can both produce similar results. 

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