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When these processes are chronically activated, they can alter the body and the brain, dysregulate immune function and lead to conditions like asthma, allergies and autoimmune diseases. The scientific literature has confirmed the association between gifted children and an increased rate of allergies and asthma. Big Think Edge For You. Big Think Edge For Business. Preview an Edge video. Videos Space is dead: A challenge to the standard model of quantum mechanics. Videos Sink or swim: How to survive waves of change in a fast-paced industry. Why highly intelligent people suffer from more mental and physical disorders.

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Intellectual disabilities statistics

For instance, they may notice they do not have same skills and abilities as their peers. Adolescents and adults with ID also get depressed. Disturbances in sleep and eating routines, social withdrawal, and anxiousness can indicate depression. Bipolar disorder is another mood disorder.

People with ID are two to three times more likely to be diagnosed with bipolar disorder than the general population. A diagnostic criterion for ID is onset before age If symptoms develop after age 18, the correct diagnosis is neurocognitive disorder formerly dementia. However, a person with ID can receive both diagnoses if a further loss of functioning occurs after age This may be due to a new brain injury e. Alternatively, a progressive brain disease or disorder may develop.

Typically, people with ID are not at greater risk for neurocognitive disorders later in life.

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However, if the ID is caused by Down syndrome, early onset Alzheimer's disease is common. When people with Down syndrome develop Alzheimer's, they usually don't live more than 10 years after diagnosis. The most detailed evidence has come from studies of the somatic sensory system.

The primary somatic sensory cortex contains four separate maps of the surface of the body in four areas in the postcentral gyrus Brodmann's areas 1, 2, 3a, and 3b. These cortical maps differ among individuals in a manner that reflects their use. Moreover, the cortical maps for somatic sensations are dynamic, not static, even in mature animals The distribution of these functional connections can expand and retract, depending on the particular uses or activities of the peripheral sensory pathways.

Since each of us is brought up in a somewhat different environment, exposed to different combinations of stimuli, and we develop motor skills in different ways, each brain is modified in unique ways. This distinctive modification of brain architecture, along with a unique genetic makeup, constitutes the biological basis for individuality.

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Two studies provide evidence for this view One study found that the somatosensory maps vary considerably among normal animals. However, this study did not separate the effects of different experiences from the consequences of different genetic endowment.

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  • Another study was conducted to see whether activity is important in determining the topographic organization of the somatosensory cortex. Adult monkeys were encouraged to use three middle fingers at the expense of two other fingers of the hand to obtain food. After several thousand trials, the area of cortex devoted to the three fingers was greatly expanded at the expense of the area normally devoted to the other fingers figure 3. Practice alone, therefore, may not only strengthen the effectiveness of existing patterns of connections, but also change cortical connections to accommodate new patterns of actions.

    As these arguments make clear, it is intriguing to suggest that insofar as psychotherapy is successful in bringing about substantive changes in behavior, it does so by producing alterations in gene expression that produce new structural changes in the brain.

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    This obviously should also be true of psychopharmacological treatment. Treatment of neurosis or character disorders by psychotherapeutic intervention should, if successful, also produce functional and structural changes.

    We face the interesting possibility that as brain imaging techniques improve, these techniques might be useful not only for diagnosing various neurotic illnesses but also for monitoring the progress of psychotherapy. The joint use of pharmacological and psychotherapeutic interventions might be especially successful because of a potentially interactive and synergistic—not only additive—effect of the two interventions. Psychopharmacological treatment may help consolidate the biological changes caused by psychotherapy.

    One example of this congruence is now evident in obsessive-compulsive disorder OCD. This common debilitating psychiatric illness is characterized by recurrent unwanted thoughts, obsessions, and conscious ritualized acts and compulsions that are usually attributed to attempts to deal with the anxiety generated by the obsessions. Medications that are selective serotonin reuptake inhibitors SSRIs and specific behavioral therapies that use the principles of deconditioning, involving exposure and response prevention, are effective in reducing the symptoms of many patients with OCD.

    Many investigators have postulated a role for the cortical-striatal-thalamic brain system in the mediation of OCD symptoms. OCD is associated with functional hyperactivity of the head of the right caudate nucleus. After effective treatment of OCD with either an SSRI such as fluoxetine alone or with behavioral modification alone with exposure and response prevention techniques , there is a substantial decrease in activity measured as glucose metabolic rate in the head of the right caudate nucleus.

    In one study 29 patients who responded to behavior therapy had a significant decrease in glucose metabolic rate in the caudate nucleus bilaterally compared to those who did not respond to treatment. These arguments suggest that when a therapist speaks to a patient and the patient listens, the therapist is not only making eye contact and voice contact, but the action of neuronal machinery in the therapist's brain is having an indirect and, one hopes, long-lasting effect on the neuronal machinery in the patient's brain; and quite likely, vice versa.

    Intellectual Disability

    Insofar as our words produce changes in our patient's mind, it is likely that these psychotherapeutic interventions produce changes in the patient's brain. From this perspective, the biological and sociopsychological approaches are joined. The biological framework that I have outlined here is not only important conceptually; it is also important practically. To function effectively in the future, the psychiatrists we are training today will need more than just a nodding familiarity with the biology of the brain. They will need the knowledge of an expert, a knowledge perhaps different from but fully comparable to that of a well-trained neurologist.

    In fact, it is likely that in the decades ahead we will see a new level of cooperation between neurology and psychiatry. This cooperation is likely to have its greatest impact on patients for whom the two approaches—neurological and psychiatric—overlap, such as those in treatment for autism, mental retardation, and the cognitive disorders due to Alzheimer's and Parkinson's diseases. It can be argued that an intellectual framework so fully embedded in biology and aligned with neurology is premature for psychiatry.

    In fact, we are only beginning to understand the simplest mental functions in biological terms; we are far from having a realist neurobiology of clinical syndromes and even farther from having a neurobiology of psychotherapy. These arguments have some validity. Thus, the decision for psychiatry revolves around the question, When will the time be optimal for a more complete rapprochement between psychiatry and biology? Is it when the problem is still premature—when the biology of mental illness still confronts us as deep mysteries—or is it when the problem is already postmature—when mental illness is on the way to being understood?

    If psychiatry will join the intellectual fray in full force only when the problems are largely solved, then psychiatry will deprive itself of one of its main functions, which is to provide leadership in the attempts to understand the basic mechanisms of mental processes and their disorders. Since the presumed function of academic psychiatry is to train people who advance knowledge—people who can not only benefit from the insights of the current biological revolution but also contribute to it—psychiatry must take its commitment to the training of biological scientists more seriously.

    It must put its own oars into the water and pull its own weight. If the biology of mental processes continues to be solved by others without the active participation of psychiatrists, we may well ask, What is the purpose of a psychiatric education? While psychiatrists debate the degree to which they should immerse themselves in modern molecular biology, most of the remaining scientific community has resolved that issue for itself. Most biologists sense that we are in the midst of a remarkable scientific revolution, a revolution that is transforming our understanding of life's processes—the nature of disease and of medical therapeutics.

    Most biologists believe that this revolution will have a profound impact on our understanding of mind.