Current Issues in Psychopharmacology: Attention-Deficit Hyperactivity Disorder

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Table of Contents

Attention-deficit hyperactivity disorder
Behavior regulation
Primary transmitters
References

Attention-deficit hyperactivity disorder

ADHD (Attention-deficit hyperactivity disorder) is described as a developmental disorder that is concerned with neurological behavior (Lerner & Wigal, 2008). ADHD appears to affect between 3 and 5 percent of the population of children, and its symptoms manifest themselves before such children have reached the age of 7 years. DHD is distinguished by constant inattention and impulsiveness patterns and these patterns may or may not be accompanied by a hyperactivity component (National Institute of Mental Health, 2008).

Statistics indicate that boys are twice as much likely to suffer from ADHD, in comparison to girls (Lerner & Wigal, 2008) although several studies have indicated that this could be a result of subjective bias (Murphy & Barkley, 2005). With maturity, adolescents, as well as adults suffering from ADHD, have a higher likelihood of experiencing a mechanism to scope, as a way of compensating for the impairment that they exhibit. Besides, a genetic element is often thought to be at play, with regard to ADHD (Lerner & Wigal, 2008). Treatment methods for ADHD often entail a modification of behavior, medication, counseling, and a change of lifestyle (Murphy & Barkley, 2005).

Impulsiveness entails a behavior in which individual tends to act without a prior thought of the ensuing consequences of their actions, disorganization and interruption tendencies during a conversation with other people (Martin, 2006). On the other hand, hyperactivity is characterized by restlessness tendencies, squirminess, and fidgeting, as well as restless sleeping episodes. ADHD may also be characterized by episodes of inattention in which the victims are distracted too easily, have a tendency to daydream, and have difficulties in listening, or completing assignments (Murphy & Barkley, 2005).

Behavior regulation

The inhibitory and excitatory postsynaptic potentials, as well as the transmitters and synaptic transmission, are actively involved in the generation and control of various behaviors. In this regard, a postsynaptic potential refers to an alteration of the ‘resting potential’, following a presynaptic cell stimulus. According to Wickens (2005), a positive postsynaptic excitatory potential comes about as a result of positive cells.

On the other hand, if the cell turns out to be negative, then a negative postsynaptic excitatory potential ensues. Wickens (2005) further opines that neurotransmission comes about following a nerve impulse accumulation at the axon hillock, located inside a neuron. As a result of these nerve impulses accumulating, neurotransmission (otherwise referred to as synaptic transmission) occurs. It is this synaptic transmission, therefore, that enables the various neurons to communicate.

Primary transmitters

There are about four transmitters that are often termed primary transmitters. These include dopamine, serotonin, acetylcholine, and GABA.

Serotonin

Serotonin production within the brain is associated with the occipital brain lobes located next to the brain’s rear. This is the area that is charged with the responsibility for vision control as well as a regulation of one’s brain’s ability to go to ‘resynchronize’ and go to rest (Murphy & Barkley, 2005). All of this is made possible thanks to the generation of serotonin together with its accompanying delta waves in the brain. At a time when the levels of serotonin in an individual are quite well balanced, such an individual makes rational thoughts, and they also tend to enjoy deep sleep.

An overproduction of serotonin may lead to paranoid and nervous individuals. Besides, excessive serotonin levels could also result in inferiority and inadequacy feelings, thereby leading to depression, sadness, depression, and anger. It has also been shown that the inception of serotonin deficiencies is often exhibited by such early signs of warning that indicate a disengagement between, on the one hand, the body and on the other hand, the mind (Wickens, 2005). A number of these symptoms thus entails hallucinations, hypertension, depression, palpitation, loner behavior, allergies, pain and aches in the muscles, urinary frequencies, codependency, restlessness, loss of memory, phobias, shyness, and perfectionism.

Acetylcholine

This is used in reference to the neurotransmitter that is generated by neurons located at the brain’s parietal lobes. There is a correlation between acetylcholine and the brain’s alpha waves, responsible for regulating the speed of the brain. The neuron acetylcholine acts as a lubricant, in effect ensuring that brain cells always remain in a moist state, thereby enabling an easier passage of information and energy through cells (Wickens, 2005). In addition, acetylcholine functions as a building block of myelin, responsible for insulating the body, as well as nerve protection.

A balance acetylcholine level results in a confident and creative individual. It has been documented that virtually all the deficiencies of acetylcholine result in dehydration. Some of the other diseases and symptoms that may come about due to its deficiency include anxiety, Alzheimer’s disease, inflammatory disorders, osteoporosis, mood swings, bipolar disorder, memory disturbances, and disorders of learning (National Institute of Mental Health, 2008).

Dopamine

This refers to those waves of the brain that are responsible for the alertness exhibited by individuals. These brain waves get created from dopamine-producing neurons, in the brain’s frontal lobes. Dopamine plays the role of a natural amphetamine, thereby facilitating energy control, motivation as well as excitement (Martin, 2006). In addition, dopamine is responsible for controlling metabolism, voluntary movements, blood pressure, digestion, setting of goals, intelligence, production of adrenaline, abstract thoughts, and also facilitates in making long-term plans.

On the other hand, its deficiency often results in anemia, a loss in bone density, pain in the joints, disorders of the thyroid, depression, mood swings, anger, forgetfulness, elevated blood pressure, instability in blood sugar, and hyperactivity. Hormones or medications are usually used in treating severe deficiencies of dopamine.

GABA

This transmitter is responsible for the production of calmness, and also plays a role in the endorphins production. An individual that exhibits a balanced level of GABA is often characterized by a sense of reliability and stability (Martin, 2006). On the negative side, however, GABA levels in excess may lead to individuals abandoning their personal needs, and instead, opt to let the plight of others take center stage. A deficiency of the GABA transmitters, at the early stage, may entail irritability and nervousness, or even feelings of anxiety. At times, individuals exhibiting these deficiencies may even start experiences feelings of being stressed out, overwhelmed even, as well as light-headedness, allergies, and aching muscles.

The deficiency of GABA, just like the rest of the neurotransmitters of the brain, influences the key functional domains of the brain. Personality, memory, physical, as well as attention issues, could also manifest themselves as a result of a deficiency of GABA (National Institute of Mental Health, 2008). Such issues may include chronic pain, headache, backache, loss of muscle, palpitations, constipation, insomnia chronic pain, urinary frequency, restlessness, rage, incoherent flows of thoughts, and difficulties in paying attention.

References

Lerner, M., & Wigal, T. (2008). “Long-term safety of stimulant medications used to treat children with ADHD”. Pediatric annals 37 (1): 37–45.

Martin, G.N. (2006). Human Neuropsychology (2^nd Ed.). Harlow: Pearson.

Murphy, K. R & Barkley, R. A. (2005). Attention-Deficit Hyperactivity Disorder. (3^rd edition). New York: The Guilford Press

National Institute of Mental Health (2008). “Attention Deficit Hyperactivity Disorder (ADHD)”. Web.

Wickens, A. (2005). Foundations for biopsychology. (2^nd edition). London: Prentice Hall.

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