You Mean I'm Not Lazy, Stupid or Crazy?!: The Classic Self-Help Book for Adults With Attention Deficit Disorder Read Online Free PDF
Author: Kate Kelly
from various parts of the body and from the outside world. Italso regulates and controls behavior.
The messenger system of the CNS consists of millions of nerve cells. These are cell bodies with long, thin projections called axons and dendrites . Impulses are carried along the length of a nerve cell and jump from one cell to another in much the same way electricity travels through a wire.
“The Brain’s Postal System”
Messages are first received by receptors in the nerve cell’s dendrite. The message, in the form of an electrical impulse, travels from the dendrite through the cell body and the axon. At the end of the axon is a synapse, a gap between the nerve cells. The electrical impulse, or message, is conducted across the synapse by chemical messengers called neurotransmitters . These chemicals carry the message across the gap from one cell’s axon to another’s dendrite.
You might be familiar with some of these neurotransmitters. Endorphins are the pain-relieving neurotransmitters that act as the body’s own morphine. An outpouring of endorphins during vigorous exercise causes the marathon runner’s “high.” This increase protects his body from feeling the pain of stressedmuscles and joints—an athlete is often unaware of an injury until he rests. Epinephrine , better known as adrenaline, is the neurotransmitter that mobilizes the reaction to danger. This activates the fight-or-flight response. The heart beats rapidly and the breathing passages become wider so one can either run or fight an enemy.
That wasn’t too bad, was it? Now let’s use this information as weconsider some theories that have emerged from research.
Current Theories About the Key Players in ADD
Since the command center is so complex, it isn’t surprising that there are conflicting theories about the causes of ADD. Although there isn’t consensus, many researchers agree that this interrelated system is dysregulated in some fashion. The following discussion examines some of the theoriesabout this dysregulation as well as an assortment of other proposed theories.
Neurotransmitters
Researchers have used indirect drug response research to conclude that an insufficient supply of the neurotransmitter dopamine plays an important role in ADD. It is known that thestimulant drugs used to treat ADD increase dopamine levels. Of course, any problem in the brain is far too complex tobe the result of a single neurotransmitter malfunction. At the very least, the interaction of multiple neurotransmitters is suspected, with the most likely culprits being dopamine, norepinephrine and serotonin .
Brain Structures
Using an MRI to scan the brains of children with ADD, researchers found that four brain regions were smaller than those in children without ADD—the frontal lobes , the corpus callosum , the basal ganglia and the cerebellar vermis . When we look at the functions of these brain parts, it makes sense that they may play a role in the symptoms of ADD. The frontal lobes are critical to many of the brain’s executive functions, including planning, initiative and the ability to regulate behavior. We also know that actual frontal lobe brain damage causes impulsivity, moodswings, disinhibited behavior and sometimes hyperactivity.
The cerebellum (the vermis is part of this structure) is responsible for balance and motor coordination. The basal ganglia serves as a connector between the cerebellum and the cerebrum (which includes the frontal lobes). It also helps to regulate moods and control impulsive behavior. The corpus callosum is basically a collection of nervefibers that connect the left and right frontal lobes, allowing them to communicate.
Is it the actual brain structures or the connections between them that cause our ADD symptoms? Is it the fault of those tiny messengers, the neurotransmitters? Likely, the answer is all of the above. Despite a significant increase in research since we wrote the first edition of this book, scientists
The messenger system of the CNS consists of millions of nerve cells. These are cell bodies with long, thin projections called axons and dendrites . Impulses are carried along the length of a nerve cell and jump from one cell to another in much the same way electricity travels through a wire.
“The Brain’s Postal System”
Messages are first received by receptors in the nerve cell’s dendrite. The message, in the form of an electrical impulse, travels from the dendrite through the cell body and the axon. At the end of the axon is a synapse, a gap between the nerve cells. The electrical impulse, or message, is conducted across the synapse by chemical messengers called neurotransmitters . These chemicals carry the message across the gap from one cell’s axon to another’s dendrite.
You might be familiar with some of these neurotransmitters. Endorphins are the pain-relieving neurotransmitters that act as the body’s own morphine. An outpouring of endorphins during vigorous exercise causes the marathon runner’s “high.” This increase protects his body from feeling the pain of stressedmuscles and joints—an athlete is often unaware of an injury until he rests. Epinephrine , better known as adrenaline, is the neurotransmitter that mobilizes the reaction to danger. This activates the fight-or-flight response. The heart beats rapidly and the breathing passages become wider so one can either run or fight an enemy.
That wasn’t too bad, was it? Now let’s use this information as weconsider some theories that have emerged from research.
Current Theories About the Key Players in ADD
Since the command center is so complex, it isn’t surprising that there are conflicting theories about the causes of ADD. Although there isn’t consensus, many researchers agree that this interrelated system is dysregulated in some fashion. The following discussion examines some of the theoriesabout this dysregulation as well as an assortment of other proposed theories.
Neurotransmitters
Researchers have used indirect drug response research to conclude that an insufficient supply of the neurotransmitter dopamine plays an important role in ADD. It is known that thestimulant drugs used to treat ADD increase dopamine levels. Of course, any problem in the brain is far too complex tobe the result of a single neurotransmitter malfunction. At the very least, the interaction of multiple neurotransmitters is suspected, with the most likely culprits being dopamine, norepinephrine and serotonin .
Brain Structures
Using an MRI to scan the brains of children with ADD, researchers found that four brain regions were smaller than those in children without ADD—the frontal lobes , the corpus callosum , the basal ganglia and the cerebellar vermis . When we look at the functions of these brain parts, it makes sense that they may play a role in the symptoms of ADD. The frontal lobes are critical to many of the brain’s executive functions, including planning, initiative and the ability to regulate behavior. We also know that actual frontal lobe brain damage causes impulsivity, moodswings, disinhibited behavior and sometimes hyperactivity.
The cerebellum (the vermis is part of this structure) is responsible for balance and motor coordination. The basal ganglia serves as a connector between the cerebellum and the cerebrum (which includes the frontal lobes). It also helps to regulate moods and control impulsive behavior. The corpus callosum is basically a collection of nervefibers that connect the left and right frontal lobes, allowing them to communicate.
Is it the actual brain structures or the connections between them that cause our ADD symptoms? Is it the fault of those tiny messengers, the neurotransmitters? Likely, the answer is all of the above. Despite a significant increase in research since we wrote the first edition of this book, scientists
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