All of these stimuli are processed in the central nervous system.Adrenocorticotropic hormone (ACTH) and the sympathetic nervous system stimulate the synthesis of adrenaline precursors by enhancing the activity of tyrosine hydroxylase and dopamine β-hydroxylase, two key enzymes involved in catecholamine synthesis. ACTH also stimulates the adrenal cortex to release cortisol, which increases the expression of PNMT in chromaffin cells, enhancing adrenaline synthesis. This is most often done in response to stress. The sympathetic nervous system, acting via splanchnic nerves to the adrenal medulla, stimulates the release of adrenaline. Acetylcholine released by preganglionic sympathetic fibers of these nerves acts on nicotinic acetylcholine receptors, causing cell depolarization and an influx of calcium through voltage-gated calcium channels. Calcium triggers the exocytosis of chromaffin granules and, thus, the release of adrenaline (and noradrenaline) into the bloodstream. For noradrenaline to be acted upon by PNMT in the cytosol, it must first be shipped out of granules of the chromaffin cells. This may occur via the catecholamine-H+ exchanger VMAT1. VMAT1 is also responsible for transporting newly synthesized adrenaline from the cytosol back into chromaffin granules in preparation for release.Unlike many other hormones, adrenaline (as with other catecholamines) does not exert negative feedback to down-regulate its own synthesis. Abnormally adrenaline levels can occur in various conditions, such as surreptitious adrenaline administration, pheochromocytoma, and other tumors of the sympathetic ganglia. Its action is terminated with reuptake into nerve terminal endings, some minute dilution, and metabolism by monoamine oxidase and catechol-O-methyl transferase.
An example of this can be from an accident, which can cause damage to the orbitofrontal cortex area of the brain.Cerebrovascular disease may cause a stroke in the frontal lobe. Tumours such as meningiomas may present with a frontal lobe syndrome. Frontal lobe impairment is also a feature of Alzheimers disease, and frontotemporal dementia. Pathogenesis
The pathogenesis of frontal lobe disorders entails various pathologies, some are as follows:

Anatomy and functions
The frontal lobe contains the precentral gyrus and prefrontal cortex and, by some conventions, the orbitofrontal cortex. These three areas are represented in both the left and the right cerebral hemispheres. The precentral gyrus or primary motor cortex is concerned with the planning, initiation and control of fine motor movements dorsolateral to each hemisphere. The dorsolateral part of the frontal lobe is concerned with planning, strategy formation, and other executive functions. The prefrontal cortex in the left hemisphere is involved with verbal memory while the prefrontal cortex in the right hemisphere is involved in spatial memory. The left frontal operculum region of the prefrontal cortex, or Brocas area, is responsible for expressive language, i.e. language production. The orbitofrontal cortex is concerned with response inhibition, impulse control, and social behaviour. Diagnosis
The diagnosis of frontal lobe disorder can be divided into the following three categories:

Clinical historyFrontal lobe disorders may be recognized through a sudden and dramatic change in a persons personality, for example with loss of social awareness, disinhibition, emotional instability, irritability or impulsiveness. Alternatively, the disorder may become apparent because of mood changes such as depression, anxiety or apathy.