Emotional and behavioral disorders/biophysical

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The Biophysical Model of Emotional and behavioral disorders[edit]

Mental illnesses used in this model: Autism and Schizophrenia.

The definition of the Biophysical model identifies with the view of emotional disturbance and behavior in its actual affliction to "organic and/or environmental influences." Research on the biological causes of EBD have been divided into three parts: genetic, bio/neurological, and temperament factors.


Genetic factors are being researched under the Human Genome Project. The three major research sources being used are:

Genetic Mapping: locating sequences of genes on chromosomes that may indicate traits and/or disorders.

Physical Mapping: a complicated process of further identifying specific genes.

Sequence Mapping: creating a sequence map of all three-billion DNA bases of the human genome so that specific genes can be identified.

Bio/Neurological factors are also being researched under three major resources:

1. Studies of the neurotransmitter, which include chemicals in the brain that deliver neural impulses from one neuron to another

The 40 year search for neurotransmitter abnormalities in Autism has no firm conclusion.[1] The only constant result across numerous neurotransmitter studies involving children with Autism has been the finding of elevated Serotonin levels in peripheral blood in about a fourth of the individuals studied. A biochemical cause for Schizophrenia also has been suspected for over a century with no single neurotransmitter being identified. A single neurotransmitter hypothesis of Schizophrenia has been rejected as evidence for the involvement of multiple neurotransmitters has increased.[2] Serotonin deficiency has been found to be connected to obesity, obsessive-compulsive disorder, eating disorders, social phobias, premenstrual syndrome, anxiety and panic, migraines, and even extreme violence.[3] However, most brain functions appear to result from the multiple influences of several different neurotransmitters.[4]

2. Organic causes, which include structural abnormalities in the brain

A variety of organic etiologies for Autism, Depression, and Schizophrenia have been proposed. Organic causes for Autism were concluded by some of the earliest researchers in studying this certain population of children.[5] Even though definitive neurological abnormalities have not been demonstrated, there is considerable evidence that the etiology of Autism resides in the operation of a neurological factor or factors. Individuals with Autism are more likely to demonstrate neurological "soft signs," persistent primitive reflexes, abnormalities on an EEG and a brain scan, and an increased likelihood of Seizures.[6] Neurological dysfunction has also been found in patients suffering from Depression, indicating a biophysical attendant of Depression that has yet to be specified. The main structural findings appear to be enlarged lateral ventricles and decreased volume in the frontal lobe and part of the subcortical structures. More recent research supports this conclusion, and suggests that Depression results from a complex interaction of brain structure, brain function, metabolic activity, and environmental factors.[7]

3. Studies of Metabolism

Phenylketonuria (PKU) is one of the many disorders that highlight the importance of the metabolic system in the mediation of learning and behavior. PKU is a recessive genetic disorder that causes the body to be unable to metabolize the protein phenylalanine. When uncontrolled by diet, this disorder is characterized by severe intellectual disability, convulsions, and behavioral problems, among other symptoms.[8] Benjamin Feingold, a pediatric allergist from California, developed the concept of food allergies as a causative factor of ADHD. Becoming interested in allergies after treating adverse reactions to aspirin, he and his associates began to suspect widespread allergic reactions to salicylates, a natural compound that is contained in many fruits and has a structure very similar to aspirin. With this hypothesis, Feingold came up with a strict diet, Feingold Diet, that he claimed should be successful in decreasing symptoms in "about 50% of hyperkinetic-learning disabled children," or ADHD.[9]

Temperament factors refer to a certain behavioral style that is an inborn tendency but also highly influenced by the environment the child grows and lives in. It emerges primarily from a longitudinal study that began in 1965 by Alexander Thomas, Stella Chess, Herbert G. Birch, Margaret Hertzig and Sam Korn to follow a sample of over a hundred children from infancy to adulthood. Thomas and his colleagues identified nine characteristics of temperament that were stable and endured through maturity. They include: activity level, regularity (of biological functions), adaptability, threshold of responsiveness, intensity of reaction, mood quality, distractibility, persistence, and attention span. From these nine characteristics, three major patterns emerged that accounted for 65% of the children: the easy child, accounting for 40% of the sample, the difficult child, account for 10% of the sample, and the slow-to-warm-up child, which accounted for 15% of the sample. The remaining 35% showed no consistent temperament patterns.


Developmental histories

  1. Prenatal and perinatal conditions: problems and/or unusual conditions associated with pregnancy and/or birth.
  2. Developmental milestones: ages at which the child walked, was toilet-trained, talked, etc.
  3. Physical development: severe illnesses, diseases, and/or accidents; unusual eating habits, sleep patterns, or other behaviors; general activity level.
  4. Social development: relationships with peers; indications of emotional tension or stress; effective discipline methods and child's reaction to discipline.
  5. General health: overall physical condition; special health conditions requiring medication; asthma, allergies, diabetes, heart condition.
  6. Family history: number and age of siblings; divorce and remarriage issues; health or education,; problems experienced by parents or siblings; mental health problems of relatives.

Neurological and neuropsychological assessment

A lot of unusual and bizarre behaviors are said to have neurological bases which is why neurological assessment is a very important aspect of the biophysical evaluations. Most that have neurological effects are repetitive speech and mannerisms, abnormal motor function, and overreaction to sensory stimuli such as loud noises or flickering lights. However, these assessments are not a regular routine when it comes to identifying children who have emotional/behavioral disorders. A doctor will first try a simple test you may have been asked to do yourself; touching your nose and identifying the number being traced in the palm of your hand is a way to test mental and neurological alertness. If these tests show problems, the doctor may choose to do an electroencephalogram (EEG).[10] The Halstead-Reitan Neuropsychological Test Battery is used with three different versions for three different age levels (5–8 years, 9–14 years, and 15-adult). This test is the most used when it comes to identifying children with brain injuries. Another common test used is the Luria-Nebraska Neuropsychological Battery - Children's Revision created by Alexander Luria. Two more recent tests are Dean-Woodcock Neuropsychological Assessment System and Woodcock-Johnson Tests of Cognitive Abilities.

Educational applications[edit]

Genetic technologies

The specific role of the special educator during treatments for genetic disorders is to apply effective instruction given what is known about certain disorders. Robert Hodapp and D.J. Fidler recommended four guiding principles for special educators relative to etiologically based approaches:

  1. Environment interventions can help to improve functioning for individuals, regardless of their genetic constitution.
  2. Individual differences exist within any group of individuals with a specific genetic disorder.
  3. All behaviors result from many factors, although a genetic disorder may alert professionals to potential maladaptive behaviors.
  4. Children with genetic disorders change as they get older.

The key for special educators is to link specific behaviors with more effective intervention outcomes. Bruce F. Pennington cautions that "the etiology of a disorder does not necessarily dictate its treatment." Psychosocial interventions can be highly effective with highly heritable disorders such as autism, while medications may be very effective for disorders that are primarily environmental, such as post traumatic stress disorder.


In the late 1990s, more children and adolescents were taking prescription drugs than ever before; Prozac and Zoloft being commonly used for more older children while younger youth took prescription drugs for a diagnosis of ADHD.[11] In 2004 the U.S. Food and Drug Administration (FDA) issued the Black Box Warning. The warning posted on prescriptions all around the country gave information regarding risk of suicidal thoughts, hostility, and agitation, mostly common on antidepressant packages. The most common diagnosis' that would end up with a child having prescriptions drugs are ADHD, ODD, and conduct disorder. More than half of these children are also on some type of psychotropic medication. Children receiving any type of special education are three times likely to be on some type of medication. After many studies and research done at the Centers for Disease Control and Prevention (CDC), Steven Forness and Kenneth Kavale suggested that the Biophsyical model be integrated with the Behavioral model. The recommendation includes: collaborating with teachers of learning disabled students on detecting EBD, assisting special education and related professionals in recognition of comorbid disorders, collaborating with medical professional regarding psychopharmacological treatment, and helping parents and early childhood teachers to recognize early signs of psychopathology.

Commonly prescribed drugs for students with EBD

Type Brand Name FDA-approved Indications Absolute Contraindications Known Side-Effects
Stimulants: Ritalin, Cylert, Dexedrine ADHD, Narcolepsy Liver problems (for Cylert) Insomnia, decreased appetite, GI pain, irritability, increased heart rate, worsening of symptoms
Antidepressants: Tricyclic: Imipramine, Elavil, Desipramine, Tofranil Enuresis Pregnancy, prior hypersensitivity reaction Psychosis, cardiac complications, impulsivity, mania, seizures, confusion, high blood pressure, rash, tics, tremors, uncoordination,anxiety, insomnia and/or nightmares
SSRIs: Prozac, Zoloft, Paxil None Known hypersensitivity reactions, pregnancy, liver disease, using other antidepressants GI problems, decreased appetite, nervousness, weight loss (for Prozac), anxiety, sweating, insomnia, motor restlessness, dry mouth
Lithium Bipolar disorder Allergic drug reaction, pregnancy, kidney disease, thyroid disease, heart disease GI problems, tremors, decreased white blood cells, malaise
Antipsychotics: (neuroleptics, major tranquilizers) Thorazine, Mellaril, Prolixin, Serentil, Stelazine, Trilafon, Compazine Psychosis, ADHD mania, aggressive behavior, nonpsychotic anxiety, Tourette's syndrome Hypersensitivity to neuroleptics, other central nervous system depressants being used, pregnancy, low white cell count Cardiac arrhythmia, sedation, affective blunting, cognitive dulling, social withdrawal, tardive dyskinesia, liver toxicity, death
Clozaril, Risperdal Not currently FDA approved for use under age 12, but promising results Minimal side effects
Anticonvulsants: Tegretol, Dilantin, Depakene Epileptic seizures, bipolar disorder, alcohol withdrawal, chronic pain due to nerve injury Known hypersensitivity, pregnancy, bone marrow depression, use of other antidepressants Differs with specific drug, but common; problems with motor coordination,tremor, drowsiness, GI upset, skin rashes

Nutrition therapy

Some children may be put on the recently discussed Feingold diet. The Feingold diet eliminates certain foods with preservatives BHT and BHA, artificial colors and flavorings, and natural salicylates. Children aren't usually put on this diet for a long time; they eventually resume eating certain foods, but the artificial additives are never reinstated in the diet.

Feingold has said he made success with a moderate percentage of children with ADHD, although he received an inordinate amount of publicity because parents often reported dramatic behavior changes and established the Feingold Association, a national network of parents.[12]

Teacher's Role for the Biophysical Model

- Making a referral and following up through contacts with the specialists.
- Help monitor the classroom behavior of a child on medication or on a specialized diet.
- Take the initiative to maintain contact with specialists such as physicians.
- Provide parents with materials on the pros and cons of some of the questionable therapies that may not be standard practice in the medical community.

Parents and teachers should be wise to question ANY therapies designed to correct learning and behavior problems that exhibit several of the following characteristics:

  1. They a reportedly based on biochemical or neurophysiological theories that are incongruent with current concepts of the central nervous system.
  2. They are said to be absolutely harmless.
  3. The children with whom they are supposedly effective are a broad, ill-defined group.
  4. The studies cited as supportive research are usually anecdotal and testimonial rather than well-controlled experimental studies.
  5. The therapies have an emotional appeal, and their detractors are attacked defensively.[13]


  1. ^ Pennington, B.F. 2002. The Development of psychopathology: Nature and Nurture. New York: Guilford Press.
  2. ^ Byne, W., Kemether, E., Jones, L., Haroutunian, V. & Davis, K.L. 1999. The Neurochemistry of Schizophrenia. In D.S. Charney, E. J. Nestler, & B. S. Bunney Eds., Neurobiology of Mental Illness. PP. 236-245. New York: Oxford University Press.
  3. ^ Lemonick, M.D. 1997, September 29. The Mood Molecule. Time, PP. 74-82.
  4. ^ Sinacola, R.S., & Peters-Strickland, T.S. 2006. Basic Psychopharmacology for Counselors and Therapists. Boston, MA: Allyn & Bacon.
  5. ^ Asperger, H. 1991. Autistic Psychopathy in Childhood. In U. Frith (Ed. & Trans.), Autism and Asperger Syndrome (pp. 37-92). Cambridge, UK: Cambridge University Press. (Original work published 1944). Bender, L. 1968. Childhood Schizophrenia: A review. International Journal of Psychiatry. 5, 211. Kanner, L. 1943. Autistic Disturbances of Affective Contact. Nervous Child, 2, 217-250. Rimland, B. 1964. Infantile Autism. New York: Meredith. Rutter, M. 1965. The Influence of Organic and Emotional Factors on the Origins, Nature, and Outcome of Childhood Psychosis. Developmental Medicine and Child Neurology. 7, 518-528.
  6. ^ Klin, A., & Volkmar, F.R. 1999. Autism and Other Pervasive Developmental Disorders. In S. Goldstein & C.R. Reynolds Eds., Handbook of Neurodevelopment and Genetic Disorders in Children. pp. 247-274. New York: Guilford Press.
  7. ^ Pennington, B.F. 2002. The Development of Psychopathology: Nature and Nurture. New York: Guilford Press.
  8. ^ Sattler, J.R., & Hoge, R.D. 2006. Assessment of Children: Behavioral, Social, and Clinical Foundations 5th ed. San Diego: Sattler.
  9. ^ Feingold, B.F. 1975. Hyperkinesis and Learning Disabilities Linked to Artificial Food Flavors and Colors. The American Journal of Nursing, 75, 803.
  10. ^ Bigler, E.D., Nielson, D., Wilde, E., Bartholomew, J., Brooks, M., & Bradford, L.W. (1999). Neuroimaging and genetic disorders. In S. Goldstein & C. R. Reynolds (Eds), Handbook of neurodevelopmental and genetic disorders in children (pp. 61-83). New York: Guilford Press.
  11. ^ Webber, Jo., Plotts, Cynthia A. Emotional and Behavioral Disorders Theory and Practice 5th Edition. 2008. Pearson Education: New York, NY. p. 98.
  12. ^ Feingold, B.F. (1975). Hyperkinesis and learning disabilities linked to artificial food flavors and colors. The American Journal of Nursing, 75, 797-803.
  13. ^ Golden, G. (1980). Nonstandard therapies in the developmental disabilities. American Journal of Diseases of Children, 134, 487-491.