Lobe functions

Egan, M. F., Goldberg, T. E., Kolachana, B. S. etal. Effect of COMT Vall08/158 Met genotype on frontal lobe function and risk for schizophrenia. Proc. Natl Acad. Sci. U.S.A. 98 6917-6922, 2001. 

Mattson DT, Berk M, Lucas MD. (1997). A neuropsychological study of prefrontal lobe function in the positive and negative subtypes of schizophrenia. J Genet Psychol. 158(4) 487-94. 

Beers, S.R., Rosenberg, D.R., Dick, E.L., Williams, T., O Hearn, K.M., Birmaher, B., and Ryan, C.M. (1999) Neuropsychological study of frontal lobe function in psychotropic-naive children with obsessive-compulsive disorder. Am J Psychiatry 1S6-J77-779. 

Additional studies suggest relationships between diminished frontal lobe function and poorly modulated aggression. Using MRl, Raine et al., (2000) found an 11 % reduction in the prefrontal gray matter volume in 21 subjects with ASP, compared to 34 healthy controls, 26 substance abusers, and 21 psychiatric controls. Thus, it appears that ASP with violent behavior is associated with reduced frontal lobe volume. 

Despite the documented efficacy and safety of the psychostimulants, their mechanism of action is not fully understood. Stimulants affect central nervous system (CNS) dopamine (DA) and norepinephrine (NE) pathways crucial in frontal lobe function. The stimulants act by causing release of catecholamines from the DA axons and blocking their reuptake. Methylphenidate releases catecholamines from long-term stores, so its effects can be blocked by pretreatment with reserpine. Amphetamines, on the other hand, release catecholamines from recently formed storage granules near the surface of the presynaptic neuron, so their action is not blocked by reserpine. In addition, the stimulants bind to the DA transporter in striatum (see Figures 2.6 and 2.7) and block the reuptake of both DA and NE. This action reduces the rate that catecholamines are removed from the synapse back into the axon and leads... 

Mindus P, Rasmussen SA, Dndquist C Neurosurgical treatment for refractory obsessive-compulsive disorder implications for understanding frontal lobe function. J Neuropsychiatry 6 467-477, 1994... 

A minimal basis set of STO (expanded in Gaussian lobe functions) was used, and the least-energy pathway determined, assuming fixed values for some of the parameters. The complete optimization is not practicable for systems of this size and most surface studies make physically reasonable approximations to reduce the number of variables. The computed pathway is a non-least-motion rearrangement. The implications of the results with respect to the stability of F2NOF relative to F3NO were also discussed. 

Stuss, D. T., and Knight, R. T. (2002). Principles of Frontal Lobe Function. Oxford University Press, New York, NY. 

Moreover, according to Fiddle et al. (2000), after six weeks treatment with risperidone, the decreases in frontal lobe metabolism were more extensive. In other words, the risperidone produced a progressive chemical lobotomy with suppression of frontal lobe function. 

Some degree of spellbinding is characteristic of any compromise of frontal lobe function. Beer et al. (2006) noted that orbitofrontal damage is associated with objective inappropriate social behavior. The patients were aware of social norms of intimacy but they were unaware that their task performances violated these norms. The authors call this an impairment of self-monitoring and self-insight. Bach and David (2006) pointed out that self-awareness deficits are very common in patients with traumatic brain injury and key to the development of behavior disturbances Our research found that lack of social self-awareness predicts behavioural disturbance in acquired and traumatic brain injury independent of cognitive and executive function. ... 

Further support for frontal and/or parietal lobe dysfunction in deficit patients has come from neuropsychological testing. An early study found that deficit and nondeficit patients perform less well on measures of frontal, parietal, and temporal lobe-related tasks compared with healthy controls, and deficit patients have further impairment on measures of frontal and parietal function (but not temporal lobe function) when compared with nondeficit patients (Buchanan et al., 1994b). However, subsequent studies have not confirmed the specificity of this pattern rather, the deficit group appears to have very broad and anatomically nonspecific cognitive impairment compared to nondeficit patients (Cohen et al., 2007). 

Lange KW, Robbins TW, Marsden CD, James M, Owen AM, Paul GM (1992) L-dopa withdrawal selectively impairs performance in tests of frontal lobe function in Parkinson s disease. Psychopharmacology 707 394-404. 

More recently, PBT2, an 8-hydroxy quinoline with increased blood-brain barrier permeability has been developed (Adlard et al., 2008) and in a 12-week phase-IIa clinical trial of AD subjects reversed frontal lobe functional deficits and significantly decreased APi 42 levels in CSF (Lannfelt et al., 2008). Together, these data suggest modulation of Zn may be an effective potential therapeutic target in AD. 

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