Frontal lobe syndrome

Hoehn-Saric, R., Harris, G.J., Pearlson, G.D., Cox, C.S., Machlin, S.R., and Camargo, E.E. (1991) A fluoxetine-induced frontal lobe syndrome in an obsessive compulsive patient. / Clin Psychiatry 52 131-133. 

Deactivation is closely related to the frontal lobe syndrome it describes the affective or emotional component. Adams and Victor (1989) divide the manifestations of frontal lobe syndrome into (a) cognitive and intellectual changes such as loss of abstract reasoning and planning, (b) personality deterioration, and (c) impairment or lack of initiative and spontaneity (p. 333). Deactivation refers to the impairment of initiative and spontaneity, which Adams and Victor call the most common effect of frontal lobe disease. 

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). 

Apathy and frontal lobe-like syndromes. A reversible, dose-related frontal lobe-like syndrome characterized by apathy, indifference, loss of initiative, and/or disinhibition has been reported in adults on SSRI therapy (Hoehn-Saric et al.l990, 1991). Recently, five cases of amotivational syndrome in youths, 10 to 17 years of age, were reported (Garland Baerg, 2001). Symptoms had a delayed onset, were dose related, and were reversible. The authors caution that such presentation may go underrecognized or may be mistakenly attributed to residual depression or to avoidance rather than to a medication side effect. 

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). 

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. 

In summary, negative symptoms have been associated with perturbations in multiple neuroactive chemicals. However, the deficit syndrome has only been investigated with regards to a few of these. The most promising areas of research currently seem to be in the area of decreased DA in the frontal lobes and NMDA receptor dysfunction. 

Keywords Receptors, nicotinic Parkinson s disease Alzheimer s disease Schizophrenia Autism Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) CHRNA5 CHRNA3 Nicotine dependence Tourette s syndrome Down syndrome... 

Clues on the physiological role of neuronal nicotinic receptors come from the identification of a form of human epilepsy that can be caused by mutations in either the a4 or the J32 nicotinic subunits. This rare syndrome, autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE), was the first idiopathic epilepsy to be identified as a monogenic disorder (244), and consists of seizures that occur during light... 

Fig. 7.20 Hyperperfusion syndrome following carotid endarterectomy (CEA). Seventy-nine-year-old female 1 week after CEA with status epUepticus. T2-weighted image demonstrates gray and white matter hypeiintensity in the left frontal lobe, suggestive of acute infarction. There is no decreased diffusion on...

There are many clinical observations (e.g. neglect syndrome) supporting a right frontal dominance in attention capacity. An enlarged right frontal lobe may provide the underlying anatomical substrate for this attention asymmetry in humans. 

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