diagnosis

Attention Deficit Disorder Diagnosis

What are the causes of Attention Deficit disorder?

Although we have known about ADD behaviors for as long as 30 years, we are still not certain as to the exact nature of the cause. Because of the length of experience physicians have had with treating ADD we have narrowed down the possible causes considerably, and we have discovered a number of treatments that provide a significant improvement in the overall mental functioning of the ADD affected person.

History

The term ADD is relativity new. This dysfunction has been known commonly as "Hyperactivity", and prior to that as "Minimal Brain Dysfunction". The current term "Attention Deficit Disorder" is in itself not completely accurate and as we learn more, we find many variations on the effect on the brain's ability to process information and the resulting behaviors.

Brain Function

There is a general consensus that at least two of the brain's major functions, "alertness" and "arousal," are involved with ADD. The medical community generally accepts that the frontal lobe of the brain is also the area most strongly effected by the ADD condition. To understand the functioning of ADD you must understand to some extent the internal "message delivery system" of the human brain. In the following paragraphs I will present some of how this system works.

The human brain is an incredibly complex biological system consisting of billions of brain cells interconnected through a complex system which joins parts of these cells at areas known as the synaptic clefts. (See illustration #2). The Dendrites, as these connecting "arms" are called begin at the brain cell and separate and split to eventually terminate at these synaptic clefts.

The dendrites can be viewed in a variety of ways, not only as extending horizontally, but also vertically (up and down) through at least five layers of the brain. As an extremely sophisticated messaging system, these interconnect all the various areas and functions of the brain. As messages come in from all parts of the body - eyes, tongue, ears, lungs, etc., they are routed through brain cells and across this "neural network" of interconnecting dendrites and collectively allow the brain to perform its various regulating and stimulating functions. The clefts do not actually allow the dendrites to touch but have between themselves a very small gap through which the brain cell must send a chemical "message" across the gap to communicate with the adjacent cell.

The communication at the synaptic cleft is essentially a chemical one which produces a compound known as a neurotransmitter. The neurotransmitters believed to be most strongly involved with ADD are Norepinephrine and Dopamine. Although Serotonin may also be involved, it is not as strongly indicated as being involved with ADD.

Neurotransmitters

A neurotransmitter can typically create two reactions in the brain, the first being stimulating an area of brain cells, the second being repressing the stimulation of brain cells. For a person to pay close, focused attention to an activity, portions of the brain must be stimulated. For a person to control impulsive behaviors, a portion of the brain must be repressed or slowed down. The behaviors of the ADD affected individual often indicate that this process is not taking place as it does in the "normal individual." Current studies are showing that the ADD brain may have only 10 to 25% of the levels of these neurotransmitters present as the "normal" brain. Is not surprising then that the successful ADD individual will have to put 30% to 50% more effort into a task in order to complete it. We also know that stress has a significant impact on the availability of these critical neurotransmitters and may reduce their levels even more than the average 10 to 25%.

Brain Processing

We can also look at the functions of the various parts of the brain and better understand why this creates such a problem. From the frontal lobes of the brain information is passed through this neural network of synapses to a sort of "central processing area" to consider what we should do with it. There it may be compared with past experience, considered and a decision made. It is also routed on from there into our long term memory to be stored for future use. If the messages are not carried to and from these various parts of the brain we can easily misunderstand or misinterpret the events and react in a totally inappropriate manner. Also the information may never get delivered to the long-term memory and we may have no recollection of the events or conversation.

Functionally, we have the problem of being unable to focus the attention due to the reduced amount of Norepinephrine. This means all conversations, activities, sounds and visual input are given equal importance. This is why something trivial or unrelated to the task at hand can seem just as important as the task to the ADD affected person. In terms of impulsive behaviors, the presence of Dopamine at adequate levels appears to be able to "repress" those actions and comments that one might not say if they were able to take the time to really think about the action or comment. The shortage of Dopamine at the synaptic cleft can make it nearly impossible for the ADD affected individual to control the impulse.

Medication

How does the medication work? The stimulant medications are used to increase the production of Norepiniphrine and Dopamine at the synaptic cleft. The anti-depressant medications are used to decrease the "reuptake" of neurotransmitters, and so make more available at the Synaptic Cleft "receptor sites". The effect of these medications on ADD affected individuals is decidedly different than what would occur with a "normal" person. With ADD, these medications allow your brain to more effectively deliver the messages across the neural network and thereby make the better choices that you would be able to make if everything was working properly. It is important to understand that this is not a structural problem within the neural network of the brain, but a chemical dysfunction. It is not to be confused with brain damage or damaged brain cells.

This article is copyrighted to and written by Steven Ledingham. Note: as the person posting this information on the World Wide Web, I do not the not warrant (the accuracy or content) of the information contained herein. This document is provided for informational purposes only and should not be used in the treatment of this disease. See a licensed medical practitioner for actual diagnoses and treatment.

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