A Primer for School Psychologists and Counselors
By Peter R. Breggin, M.D.
Dr. Peter Breggin, M.D., is a psychiatrist on the Division of Education faculty at John Hopkins University, Editor-in-chief of Ethical Human Sciences and Services: An International Journal of Critical Inquiry, and was selected by NIH to serve as the expert presenter on “Risks and Mechanisms of Actions of Stimulants” at the November 1998 “NIH Consensus Development Conference on Diagnosis and Treatment of ADHD.” He is author of numerous books and articles on stimulant medication and the drug treatment of children, including Toxic Psychiatry (1991) and Talking Back to Ritalin (1998).
School psychologists and counselors can play a pivotal role in decisions about appropriateness of prescribing stimulant medication to children. Advocates of stimulant medication frequently try to “educate” school mental health professionals to make them more enthusiastic about diagnosing Attention Deficit/Hyperactivity Disorder (ADHD) and encouraging medication. Most recommendations for stimulant drugs originate in schools. School psychologists and counselors therefore need a thorough understanding of the mechanism of action of stimulants, as well as their many adverse effects.
Until recently, most of the information has been generated by individuals with strong vested interests in what may be called the “ADHD/stimulant lobby.” As a psychiatrist, my own research into the mechanism of action and adverse effects of drugs dates back several decades. I first wrote extensively about ADHD and stimulant drugs in Toxic Psychiatry (1991) and then again inTalking Back To Ritalin (1998). In November of this year I was invited by NIMH and NIH to be the scientific expert on “Risks and Mechanism of Action of Stimulant Drugs” at the “Consensus Development Conference on ADHD and its Treatment,” sponsored by the two government agencies. This paper draws on the research presented in my books and at that conference (Breggin, 1999, in press). In addition to my clinical work, it also draws on my faculty position at the Johns Hopkins University Department of Counseling in the Division of Education.
Based largely on double-blind placebo-controlled clinical trials and on animal laboratory research, this paper will focus on the emotional and behavioral effects of dextroamphetamine (e.g., Dexedrine, Adderall), methamphetamine (Desoxyn, Gradumet) and methylphenidate (Ritalin). Emphasis will be placed on two relatively ignored areas: the mechanism of action that enforces specific behaviors and adverse drug effects on the central nervous system, mental life and behavior of the child. An overview of all adverse reactions will also be provided.
The Mechanism of Action: Effects on Animals
Stimulant drugs lend themselves readily to suppressing behaviors that are unwanted in the classroom or highly controlled family situations, and for enforcing obsessive-compulsive behaviors that adults desire in the classroom or the controlled family. Animals, like children, have spontaneous tendencies to move about, to explore, to innovate, to play, to exercise and to socialize. Dozens of studies have shown that stimulant drugs suppress all of these spontaneous tendencies, sometimes completely inhibiting them (Arkawa, 1994; Hughes, 1972; Randrupt & Munkvad, 1967; Schiorring, 1971, 1981; Wallach, 1974). In effect, the animals lose their “vitality” or “spirit.” They become more docile and manageable.
Animals, like children, resist boring, routine, rote or meaningless tasks. Stimulant drugs enforce these behaviors in animals, producing what is called stereotypy or perseveration in animal research (Bhattacharyya et al., 1980; Costall & Naylor, 1974; Koek & Colpaert, 1993; Kuczenski & Segal, 1997, Mueller, 1993; Randrup & Munkvad, 1967; Rebec & Segal, 1980; Rebec & Bayshore, 1984; Segal, 1975; Segal et al., 1980; early studies reviewed in Wallach, 1974 and Schiorring, 1979). In human research, it is called obsessive-compulsive or over-focused behavior (see below). For example, instead of struggling to escape a cage, the animal will sit relatively still carrying on rote, useless behaviors, such as compulsive grooming, chewing on its paws or staring in the corner. If the drugged animal does move about, it will pace a constricted area in a purposeless manner.
In summary, in animals stimulant drugs (1) suppress spontaneous and social behaviors, rendering them more submissive and manageable, and (2) enforce perseveration or obsessive-compulsive over-focusing.
The Mechanism of Action: Emotional and Behavioral Effects on Children
The effects of stimulants on children are identical to those in animals. This is not surprising since the basic biochemical or neurological impact is the same. Similarly, the effects on children are the same regardless of the child’s mental state or diagnosis.
Drawing on double-blind studies, Table 1 (insert section) lists the adverse drug reactions (ADRs) of stimulant drugs that lend themselves to being easily mistaken for improvement in the child. The chart is divided into three categories of stimulant ADRs: (1) Obsessive-compulsive ADRs, such as over-focusing, cognitive perseveration, inflexibility of thinking and stereotypical activities; (2) social withdrawal ADRs, such as social withdrawal and isolation, reduced social interactions and responsiveness, and reduced spontaneity and behaviors that are subdued, depressed, apathetic, lethargic and bland.
Firestone et al. (1998) found that 0.5mg/kg of methylphenidate caused marked “deterioration” compared to placebo in several variables, including “sad/happy” (69% of children) and “uninterested in others” (62%). Mayes et al. (1994) found that 18.5% of children on methylphenidate became “lethargic,” displaying symptoms such as “tired, withdrawn, listless, depressed, dopey, dazed, subdued and inactive.” Barkley et al. (1990) found an increased proneness to crying in 10% of children on a low dose of methylphenidate. Schachar et al. (1997) documented that more than 10% of children dropped out due to methylphenidate-induced ADRs, including serious behavioral aberrations such as “sadness and behavior deterioration, irritability, withdrawal, lethargy, violent-behavior,” “withdrawal and mild mania,” and “withdrawal and dysphoria.” Stimulants commonly cause obsessive-compulsive behaviors, including over-focusing, that are similar to stereotypy in animals. In a study of single small doses of methylphenidate on the day of the experiment, Solanto and Wender (1989) found “cognitive perseveration” (over-focusing) in 42% of children. Castellanos et al. (1997) found that 25% of children on methylphenidate developed obsessive-compulsive ADRs. In the most thorough study of the subject, Borcherding et al. (1990) found that 51% of children taking methylphenidate and dextroamphetamine developed obsessive-compulsive ADRs. Some children exhausted themselves raking leaves or playing the same game over and over again. The authors note that these behaviors were sometimes considered improvements in the classroom.
These data in this section, derived from several controlled clinical trials, further confirm the emotional and behavioral suppression caused by stimulant drugs.
More Extreme Emotional and Behavioral Effects
Swanson et al. (1992) reviewed “cognitive toxicity” produced by methylphenidate. They summarize the more extreme effects on children:
In some disruptive children, drug-induced compliant behavior may be accompanied by isolated, withdrawn, and over-focused behavior. Some medicated children may seem “zombie-like” and high doses, which make ADHD children more “somber,” “quiet,” and “still” may produce social isolation by increasing “time spent alone” and decreasing “time spent in positive interaction” on the playground. (p.15)
Arnold and Jensen (1995) also comment on the “zombie” effect caused by stimulants:
The amphetamine look, a pinched, somber expression, is harmless in itself but worrisome to parents, who can be reassured. If it becomes too serious, a different stimulant may be more tolerable. The behavioral equivalent, the “zombie” constriction of affect and spontaneity, may respond to a reduction of dosage, but sometimes necessitates a change of drug. (p.2307)
The “zombie” effect is mentioned by a number of other investigators (e.g., Fialkov & Hasley, 1984, p. 328; Swanson et al., 1992, p. 15). It is a more extreme manifestation of the supposedly “therapeutic” effect that makes a child more compliant, docile and easier to manage. When a child seems more compliant in class or seems to attend more readily to boring, rote activities, the child is experiencing an adverse drug reaction. The seeming “improvement” is an expression of a continuum of drug toxicity with the zombie effect at one extreme. The toxicity is considered “therapeutic” unless it becomes so extreme that the child seems bizarre or disabled.
Excitatory Adverse Effects
As already described in detail, routine stimulant doses given to children or adults commonly cause ADRs that seem paradoxical, such as depression, lethargy and apathy (Tables 1 and 2; see insert). It is uncertain why stimulants at clinical doses so commonly cause these suppressive effects. Stimulants also cause more classic signs of over-stimulation or excitation, such as anxiety, agitation, aggression and insomnia, as well as manic psychoses the more suppressive effects, as in a mixture of agitation and depression.
Frequently stimulants cause tachycardia and cardiac arrhythmias and can even weaken heart muscle (Ishiguro & Morgan, 1997; Henderson et al., 1994). The FDA has received many reports of methylphenidate-induced heart attack (Food and Drug Administration, 1997).
The overall list of stimulant ADRs is much too extensive for inclusion in this paper. Table 2 (insert) draws on several independent sources to present an overview. More detail and further documentation for all of the adverse drug effects mentioned in this paper can be found in my reviews (Breggin, 1998; 1999, in press). Many doctors seem unaware of the varied nature of stimulant ADRs. Often they mistake these drug reactions for the surfacing of new psychiatric disorders in the child and mistakenly increase the dose or add further medications, instead of stopping the stimulants.
Gross and Irreversible Brain Dysfunction
In addition to the many serious central nervous system ADRs that are apparent in the child’s behavior, stimulants also cause gross brain dysfunction. Methylphenidate, for example, in routine doses caused a 23%-30% drop in blood flow to the brain in volunteers (Wang et al., 1994). All stimulants directly disrupt at least three neurotransmitter systems (dopamine, norepinephrine and serotonin). There is strong evidence that stimulant-induced biochemical changes in the brain can become irreversible, especially in regard to amphetamine and methamphetamine, which can cause permanent neurotransmitter system changes and cell death (Battaglia et al., 1987; Melega et al. (1997a, b; Wagner et al., 1980). One study demonstrated that adults can develop atrophy of the brain after being treated with stimulants as children (Nasrallah et al., 1986). These potentially disastrous irreversible effects have been ignored in most reviews (see details in Breggin, 1998; updated in 1999, in press).
Through a combination of anorexia and disruption of growth hormone, stimulants also inhibit growth, including the growth of the brain (reviewed in Breggin, 1998; 1999, in press; Dulcan, 1994; Jacabvitz et al., 1990). Bathing a child’s growing brain in toxic chemicals must ultimately impair its development.
Stimulants are highly addictive. The U.S. Drug Enforcement Administration (DEA) places methylphenidate, amphetamine and methamphetamine into Schedule II along with cocaine and morphine as the most addictive drugs used in medicine. The DEA and the International Narcotics Control Board have both issued warnings about the danger of widespread stimulant prescription in North America (Drug Enforcement Administration, 1995; International Narcotics Control Board have both issued warnings about the danger of widespread stimulant prescription in North America (Drug Enforcement Administration, 1995; International Narcotics Control Board, 1996; 1997). The United States uses 90% of the world’s methylphenidate. Typical of addictive drugs, they often cause withdrawal or rebound. Rebound commonly occurs after only one or two doses in normal children, and it can last many hours and even more than a day (Rapport et al., 1978). During rebound, the child’s original ADHD-like symptoms may become worse than before the drug was ever taken, including hypomania and mania. Even when children do not become addicted to stimulants, they sometimes give them away or sell them to friends who abuse them.
Stimulants commonly cause tics and other abnormal movements, and sometimes these become irreversible (Lipkin et al., 1994). Often the tics occur along with obsessive-compulsive symptoms. Too often, drug-induced ADRs lead mistakenly to the prescription of other psychiatric drugs rather than to the termination of the stimulant.
ADHD and the Rationalization of Stimulant Effectiveness
The concept of ADHD was developed to rationalize a pre-existing motivation with medicine and psychology to use stimulant drugs to control the behavior of children. From the beginning, the focus was on classroom settings in which one-to-one attention is not available. ADHD as a diagnosis evolved as a convenient list of various behaviors that tend to disrupt a classroom and to require additional or special attention from teachers or other adults (Armstrong, 1995; Johnson 1998). Almost every behavior that tries a teacher’s ability or patience, or drains a teacher’s energy and attention, has been put into the diagnosis.
A simple reminder about the official criterion for ADHD in the Diagnostic and Statistical Manual (American Psychiatric Association, 1994, p. 84) should make clear how the list focuses on behaviors that interfere with an orderly, quiet, controlled classroom. The first criterion under hyperactivity is “often fidget with hands or feet or squirms in seat” and the second is “ often leaves seat in classroom or in other situations in which remaining seated is expected.” The first criterion under impulsivity is “ often blurts out answers before questions have been completed” and the second is “ often has difficulty awaiting turn.” Under inattention the first criterion is “often fails to give close attention to details or makes careless mistakes in schoolwork, work, and other activities.”
None of the ADHD criteria are relevant to how the child feels . Mental and emotional symptoms, such as anxiety or depression, are not included. All of the behaviors in the ADHD diagnosis are commonly displayed by children in groups where they are frustrated, anxious, bored or receive too little attention. Individually, each of the behaviors represents normal developmental stages. Of course, the behaviors can become exaggerated. A child can become extremely hyperactive, impulsive or inattentive. These behaviors, even when extreme, do not constitute a syndrome—-a consistent pattern of symptoms related to a specific cause.
In Talking Back to Ritalin , I have catalogued dozens of “causes” for ADHD-like behavior. Most commonly it is the expression of a normal child who is bored, frustrated, frightened, angry, emotionally injured, undisciplined, lonely, too far behind in class, too far ahead of the class or otherwise in need of special attention that is not being provided. More rarely, the child may be suffering from a genuine physical disorder, such as a head injury or thyroid disorder, that requires special medical attention rather than stimulant medication.
ADHD as Conflict
ADHD-like behaviors in a child almost always indicate a conflict between the child and adults in the child’s life, especially adult expectations for submissive, conforming or compliant behavior. But instead of being used as a signal for the need for conflict resolution, the diagnosis is used as a justification for drugging the diagnosed member of the conflict, the powerless child.
With more concern for the child, the very same behaviors in any child could be used to focus attention on the need for change in the behavior of the adults in the conflict. The seemingly exaggerated hyperactivity, impulsivity or lack of attentiveness in the child can and should become a signal for the adults in the child’s life to find, identify and respond to the child’s genuine needs for rational discipline, unconditional love, play, exercise and engaging education. An effective teacher, parent or coach would do exactly that. Signs of hyperactivity, impulsivity and inattention in a youngster are used to indicate the need for greater, more focused attention to the child.
Stimulant drugs, as we have seen, flatten the child’s behavioral signal system. The child literally becomes neurologically unableto express feelings of boredom, frustration, distress or discomfort by displaying hyperactivity, impulsivity or inattention. Adults can then feel justified in teaching the class or managing the group without attending to the child’s individual and often varied needs.
Evidence for Effectiveness
Reviews by stimulant drug advocates routinely demonstrate that stimulants have no positive long-term effects whatsoever on any aspect of a child’s behavior. Short-term (a few weeks or months), they can suppress behavior, but they do not improve academic performance or learning. Based on the most extensive review in the literature, Swanson (1993) concluded:
Long-term beneficial effects have not been verified by research. Short-term effects of stimulants should not be considered a permanent solution to chronic ADD symptoms. Stimulant medication may improve learning in some cases but impair learning in others. In practice, prescribed doses of stimulants may be too high for optimal effects on learning to [to be achieved] and the length of action of most stimulants is viewed as too short to affect academic achievement. (p. 44)
Swanson (1993) defined “short-term” as 7-18 weeks. He also summarized:
No large effects on skills or higher order processes— Teachers and parents should not expect significantly improved reading or athletic skills, positive social skills, or learning of new concepts.
No improvement in long-term adjustment— Teachers and parents should not expect long-term improvement in academic achievement or reduced antisocial behavior. [italics in original] (p. 46)
Swanson is not alone in his conclusions. Popper and Steingard (1994) state:
Stimulants do not produce lasting improvement in aggressivity, conduct disorder, criminality, education achievement, job functioning, marital relationships, or long-term adjustment. (p. 745)
Richters et al. (1995) from NIMH conclude: “The long-term efficacy of stimulant medication has not been demonstrated for anydomain of child functioning” (italics in original, p. 991). They conclude that there is no evidence for even short-term positive effects on academic performance.
Stimulant drugs have two basic effects on animals and children regardless of their mental status. First, stimulants reduce all spontaneous and social behavior. This makes the child more docile, submissive and manageable (compliant). Second, stimulants enforce perseverative, obsessive-compulsive or over-focused behavior. This makes the child more easily led or compelled to do rote, boring activities. These twin toxic effects are readily misinterpreted as “improved behavior” in highly structured or controlled environment where children are given insufficient or inappropriate attention and where their genuine needs are being ignored. As a result of toxicity, stimulants suppress a child’s behavior in a global fashion that has nothing to do with any diagnosis or disorder.
Stimulant drugs also produce a wide variety of other adverse effects. By causing anorexia and by disrupting growth hormone, they suppress the growth of the body, including brain size and development. They cause severe biochemical imbalances in the developing brain that can become permanent. They often worsen ADHD-like symptoms and can cause psychoses.
The ADHD diagnosis is tailored to justify the use of stimulants for the behavioral control of children in groups. It enumerates behaviors that healthy children often display in structured-over-controlled groups in which their individual needs are unmet.
Ultimately, by suppressing emotional and behavioral signals of distress and conflict, stimulants allow adults to ignore the needs of children in favor of creating a controlled environment. Meanwhile, stimulants do not improve academic performance and provide no long-term improvement in any aspect of a child’s behavior or life.
School psychologists and counselors should strongly discourage the use of stimulant drugs for treating “ADHD” and other emotional or behavioral problems that surface in the classroom. Instead, more effort should be made to identify and to address the genuine individual needs of the children in our schools whether or not they are signaling their distress or conflict with ADHD-like behaviors.
Borcherding, B.V., Keysor, C.S., Rapoport, J.L., Elia, J., Amass, J. (1990). Motor/vocal tics and compulsive behaviors on stimulant drugs: Is there a common vulnerability? Psychiatric Research , 33, 83-94
Breggin, P.R. (1998). Talking back to Ritalin . Monroe, ME: Common Courage Press
Breggin, P.R. (1999, May, in press). Psychostimulants in the treatment of children: Risks and mechanism of action. Ethical Human Sciences and Services, 1 (1).
Firestone, P., Musten, L.M.,Pisterman, S., Mercer, J., & Bennett, S. (1998). Short-term side effects of stimulant medications in preschool children with attention-deficit/hyperactivity disorder. A double-blind placebo-controlled study. Journal of Child and Adolescent Psychopharmacology, 8, 13-25.
Melega, W.P., Raleigh, M.J., Stout, D.B., Huang, S.C., & Phelps, M.E. (1997a). Ethological and 6-fluoro-L-DOPA-PET profiles of long-term vulnerability to chronic amphetamine. Behavioural Brain Research , 84, 258-268.
Melega, W.P., Raleigh, M.J., Stout, D.B., Lacan, G., Huang, S.C., & Phelps, M.E. (1997b). Recovery of striatal dopamine function after acute amphetamine- and methamphetamine-induced neurotoxicity in the vervet monkey. Brain Research , 766, 113-20.
Nasrallah, H., Loney, J., Olson., S., McCalley-Whitters, M., Kramer, J., & Jacoby, C. (1986). Cortical atrophy in young adults with a history of hyperactivity in childhood. Psychiatry Research , 17, 241-246.
Schiorring, E. (1981). Psychopathology induced by “speed drugs”. Pharmacology Biochemistry & Behavior , 14, Suppl. 1, 109-122.
Swanson, J.M., Cantwell, D., Learner, M., McBurnett, K., Pfiffner, L & Kotkin, R. (1992, fall). Treatment of ADHD: Beyond medication. Beyond Behavior 4, 13-16 and 18-22.
Wang, G-J, Volkow, N., Fowler, J., Ferrieri, R., Schlyer, D., Alexoff, D., Pappas, N., Lieberman, J., King, P. Warner, D., Wong, C., Hitzemann, R., & Wolf, A. (1994). Methylphenidate decreases regional cerebral blood flow in normal human subjects. Life Sciences , 54, 143-146.
National Association of School Psychologists Psychostimulant Effects on Children
Peter R. Breggin, 1998
Table 1: Adverse Drug Reactions From Stimulants
Mistakenly Identified As “Beneficial.”
Data From 20 Controlled Clinical Trials
|Obsessive Compulsive ADRs||Social Withdrawal ADRs||Behaviorally Suppressive ADRs|
|Stereotypical activities (1,3)Obsessive-compulsive behavior (1,3,7,17)Cognitive perseveration (7)Inflexibility of thinking (9) Over-focusing or excessive focusing (7, 9)||Social withdrawal and isolation (3, 12, 14)General dampening of social behavior (19)Reduced social interactions, talking, or sociability (3, 8, 10*, 15*, 18**, 19)Decreased responsiveness to parents & other children (10*, 18**, 19)Increased solitary play (4, *8)Diminished play (15*)||Compliance, especially in structured environments (4*, 8*, 10*, 11*)Reduced curiosity (7)Somber (2)Subdued (3)Apathetic; lethargic: “tired, withdrawn, listless, depressed dopey, dazed subdued and inactive” (3; also 12, 20)Bland, emotionally flat, affectless (5, 16)Depressed, sad, easy/frequent crying (3, 4, 12, 13, 18**, 20)|
Little or no initiative or spontaneity (5)
Diminished curiosity, surprise, or pleasure (5)
Humorless, not smiling (5)
Social inhibition—passive and submissive behaviors (6)
*Considered positive or therapeutic by the source
** Considered possibly positive or therapeutic by source
1. Borcherding et al. (1990) 11. Cotton and Rothberg (1988)
2. Tannock et al. (1989) 12. Schachar et al. (1997)
3. Mayes et al. (1994) 13. Barkley et al. (1990)
4. Schleifer et al. (1975) 14. Handen et al. (1990)
5. Rie et al. (1976a) 15. Barkley and Cunningham (1979)
6. Granger et al. (1993) 16. Whalen et al. (1989)
7. Solanto and Wender (1989) 17. Castellanos, et al. (1997)
8. Cunningham and Barkley (1978) 18. Firestone, et al (1998)
9. Dyme et al. (1992) 19. Buhrmestar, et al. (1992)
10. Barkley et al. (1985) 20. Gittelman-Klein et al. (1976)
Table 2: Adverse Effects Caused by Methylphenidate and Amphetamines
|Cardio- Vascular||Central NervousSystem||Gastro- Intestinal||Endocrine/ Metabolic||Other||Withdrawal & Rebound|
|Psychosis with hallucinations(skin crawling or visions)[mania]Excessive CNS stimulation[convulsions]Drowsiness, “dopey,”less alert|
Agitation, anxiety, irritability, nervousness [hostility]
Dysphoria (esp. at higher doses)
Impaired cognitive test performance (esp. at higher doses)
Dyskinesias, tics, Tourette’s
Nervous habits (e.g. picking at skin, pulling hair)
Stereotypy and compulsions
Depression, emotional oversensitivity, easy crying
Decreased social interest
Zombielike constriction of affect and spontaneity*
Amphetamine look (pinched, somber expression)**
|AnorexiaNauseaVomitingStomach ache, crampsDry mouth|
|pituitary dysfunction, including growth hormone and prolactin]Weight lossGrowth suppressionGrowth retardationDisturbed sexual function****|
|Blurred vision HeadacheDizzinessHypersensitivityReaction with rash,|
conjunctivitis, or hives[hair loss]***
|InsomniaEvening crashDepressionOveractivity and irritabilityRebound ADHD Symptoms|
Sources Combination of Dulcan (1994. table 35-6. p. 1217). Arnold and Jensen (1995. Table 38-5. p. 2306). Maxman and Ward (1995. pp 365-6). And Drug Enforcement Administration (1995B. p 23) Any additional material indicated by brackets
*”Zombie” references from Arnold and Jensen (1995. Table 38-5. p 2306. Table 38-7. p 2307. and column 2. p 2307).
Swanson. et al. (1992. p 15). Fialkov and Hasley (1984. p 328)
**Arnold and Jensen (1995)
***For methylphenidate only
****For dextroamphetamine only