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Displacement, stereotypies, frustration, and perseveration

A stereotypy is a fixed-action pattern out of control. Stereotypies are unvarying, repetitive, patterned behaviors that have become unmoored from their original sign stimulus. They are out of context and irrelevant to the situation in which they occur. They usually occur when an animal is frustrated or restrained in some way. The animal, unable to SEEK what it needs, displaces frustration with some other behavior pattern that can be carried through to completion. For example, when a sheet of glass prevents a thirsty dove from getting to its water bowl, the dove will peck at the ground nearby or preen itself. So what starts out as simple displacement activity becomes a stereotypy under continuing stressful conditions. It should be noted here that in creating this description, Aubrey Manning's and Marian Stamp Dawkins's An Introduction to Animal Behaviour (1992) are referenced .

Understanding ADHD, OCD, PTSD, and Tourette syndrome

The form stereotypies take depends of the animal's species. In Animals in Translation, Temple Grandin and Catherine Johnson write:

Highly social animals such as dogs and horses need the companionship of other animals or people. Grazing animals such as horses and cattle need hay or grass. Burrowing animals such as rodents need materials to burrow and hide in. Animals that walk long distances such as polar bears and tigers need room to roam. The nervous system of young animals reared in barren kennels or laboratory cages may be damaged because the growing nervous system needs varied sensory input to develop normally. Some of the most abnormal behaviors that occur in barren environments are performed when the animal is undisturbed by people. When people enter the animals stop doing the abnormal behavior.

Bird biting cage bars

So how do various frustrated animals displace their motivation to SEEK necessary resources and stimulation? Parrots that lack social companionship will pull out their feathers. Horses will engage in cribbing (repetitively biting on a fence). Sows in gestation cages, where there is no straw for chewing and no dirt for rooting, will bite the cage bars until their gums bleed. John J. McGlone, in Current Status of Housing and Penning Systems for Sows, (2002), provides the image at left (links to source). Dogs compulsively lick a paw, a condition known as acral lick dermatitis. As Grandin and Johnson discuss above, the abnormal behavior most often occurs when frustrated animals are left alone with little stimulation. In primates, stereotypies often play out in self-directed behaviors, such as grooming. Chimpanzees caged in laboratories sometimes compulsively pluck their own body hair. In Love at GOON Park, Deborah Blum recounts how some of the first members of People for the Ethical Treatment of Animals (PETA) exposed laboratories where macaque monkeys were housed in isolation. The monkeys "paced, rocked, clasped themselves, and—introducing injury anyway—chewed on themselves."

What we often fail to realize is that the same animal brain circuitry that generates stereotyped behavior in animals under stressful conditions can also generate stereotyped behavior in humans under stressful conditions. Human stressors exacerbate ADHD, OCD, PTSD, Tourette syndrome, and compulsive grooming symptoms. In Why Zebras Don't Get Ulcers: The Acclaimed Guide to Stress, Stress-Related Diseases, and Coping (2004), Robert M. Sapolsky writes: "When it comes to what makes for psychological stress, a lack of predictability and control are at the top of the list of things you want to avoid."

In humans, perseveration can sometimes be confused with compulsivity. It is important to differentiate between the two because different neurotransmitters are involved and that means different medicines might be employed to treat symptoms. In his video course, Biology and Human Behavior: The Neurological Origins of Individuality, Robert M. Sapolsky discusses how humans who suffer from early dementia, when they cannot complete a cognitive task, will sometimes fall back on more easily enacted behaviors. He notes that patients with frontal cortex damage or deterioration will resort to something called perseveration and intrusion. He points out that the frontal cortex helps you focus on what the task is right now. So when you ask early state dementia patients to count backward from 20, they will sometimes start the task but then revert to reciting something over learned and more firmly established in memory, such as the months of the year. Instead of doing the cognitively harder thing via the frontal cortex, the patient reverts to a previous, easier task. In finding and using substitute language and facts, these patients are resorting to perseveration, accessing information that has been learned through life experience. Regarding fixed-action patterns and stereotypies, it is pattern generators genetically inculcated in subcortical structures over generations that dictate behavior. Out-of-control dopamine activation of these pattern generators is more likely the cause of compulsions. This is not to say, however, that there are not situations where compulsion and perseveration combine to create what would be extremely problematic symptoms.

Perseveration (ADHD) or compulsion (OCD)?

Regarding fixed-action patterns and stereotypies, it is our subcortical nuclei—that part of our human brains so similar to the brains of other mammals—that are most prominently in control. The transmission of dopamine to subcortical areas that in turn connect to areas of our neocortex, sending movement messages to this or that muscle, is the mechanism responsible for this automatic-like behavior. According to Jaak Panksepp in Affective Neuroscience, in animal experiments where the cortex is removed from an animal's brain, the decorticate animal is hyperactive, prone to "jump rapidly from one activity to another." Panksepp observes that without cortical processing to shape subcortical motivation, these animals display symptoms similar to those impulsive symptoms seen in children suffering extreme attention deficit hyperactivity disorder (ADHD). The neurotransmitter most at work in shaping dopamine-driven subcortical motivation once it reaches the cortex is norepinephrine (see Norepinephrine action, synthesis, and pathways). So when either dopamine or norepinephrine levels are out of whack, some kind of symptoms will occur.

Note: If you are interested in ADHD symptoms and have not yet read Attention, Learning, and Memory: The VIGILANCE System in Part 2 of, then It is urged that you do so.

According to the Merck Manuals Online Medical Library, there are three types of ADHD. The first is characterized as predominantly inattentive. The second is characterized as predominantly hyperactive-impulsive. And a third type is characterized as being a combination of inattentiveness and hyperactivity-impulsiveness. It is important to consider whether these different symptom pictures represent distinctly different imbalances in brain neurotransmitters.

As we discuss above, perseveration can occur in ADHD as well as in dementia. In addition to symptoms of speech and cognition, perseveration can also present as more of a physical-type behavior or movement. Perseveration can be defined as repetitive movement or repetitive speech that focuses on one idea or task, thereby overlooking more significant stimuli that would normally prompt a behavior change. Perseverative behavior often has a compulsive quality to it so you can see how perseveration might be mistaken for compulsion and thus labeled as inappropriate. As we discuss in Norepinephrine action, synthesis, and pathways, it is norepinephrine—transmitted in long, branching axons from loci coerulei in the pons of the brain stem to the left and right cortical areas—that enables the cortex to register the consequence of incoming stimuli and determine which stimulus is most worthy of immediate attention. So inadequate norepinephrine contributes to perseveration while excessive dopamine contributes to compulsions. And again, it is probably not always an either-or situation. Sometimes, imbalances may exist in both norepinephrine and dopamine pathways.

The role of norepinephrine and dopamine in ADHD and OCD

In Affective Neuroscience, Panksepp explains that "with excessive DA [dopamine] activity, animals begin to exhibit repetitive behavior patterns known as stereotypies; with low NE [norepinephrine] activity, they tend to perseverate on a task despite changes in stimulus contingencies (presumably because of attentional deficits)." Panksepp cites research to conclude: "Existing evidence suggests that NE promotes sensory arousal, while DA promotes motor arousal. As we would expect from such functional considerations, NE terminals are concentrated in sensory projection areas of the cortex, while DA terminals are more prominent in motor areas."

In regard to human illnesses such as OCD and ADHD, then, it may therefore be appropriate to say that excessive dopamine often drives compulsions whereas inadequate norepinephrine and/or inadequate dopamine often drives perseveration.

Researchers have suggested that high levels of dopamine transporters are associated with ADHD. During some of the research on dopamine, a 2006 report is found titled "High Dopamine Transporter Levels Not Correlated with ADHD." The U.S. Department of Energy's Brookhaven National Laboratory, in collaboration with Mount Sinai School of Medicine in New York, produced the report. Researchers used positron emission tomography (PET) technology to study dopamine transporters in the brain. PET scan images such as the ones below (link to source) show that patients in the study with ADHD had lower levels of dopamine transporters in the nucleus accumbens when compared to control subjects. (We will discuss the nucleus accumbens in greater detail later in this narrative.)

Causes of ADHD disease

The authors of the study, including Nora Volkow, Director of the National Institute on Drug Abuse, and Gene-Jack Wang, from Brookhaven, speculate that rather than having high levels of dopamine transporters in the brain, as others have suggested, ADHD patients suffer inattentive symptoms due to lower levels of dopamine release. Volkow reports: "These findings suggest that an additional variable in conjunction with dopamine transporters would be required to account for the severity of the symptoms of inattention in ADHD." Volkow goes on to say: "We speculate that this other variable may be lower levels of dopamine release in ADHD subjects." If the Brookhaven study findings are correct, then these circumstances help explain why psychostimulants, which make dopamine more available, help improve attention in some patients.

During our discussion of the VIGILANCE system in Part 2 of, in a subsection titled Stress, attention, learning, memory, and ADHD, we discuss Amy F.T. Arnsten's work. In Norepinephrine Has a Critical Modulatory Influence on Prefrontal Cortical Function," (2000), she reports that "NE [norepinephrine] cells of the locus ceruleus [also spelled locus coeruleus] increase their firing in response to behaviorally relevant stimuli. Selective depletion of NE in the forebrain makes animals more distractible." Arnsten cites dysfunction in the prefrontal cortex as a fundamental component of ADHD. Arnsten explains that the prefrontal cortex "uses working memory to intelligently guide behavior, inhibiting inappropriate impulses or distractions and allowing us to plan and organize effectively." Arnsten notes that it is both norepinephrine and dopamine that accomplishes attentiveness in the prefrontal cortex.

Arnsten explains that the nonselective norepinephrine reuptake blocker, the tricyclic antidepressant desipramine, and the newer, selective norepinephrine reuptake blocker, atomoxetine (a non-stimulant), have been shown to ameliorate ADHD symptoms. Atomoxetine also increases dopamine availability in the brain.

discovering as much as you can about specific symptoms, and the neurotransmitters involved in particular behaviors, can help patients, parents, and doctors make more informed decisions about medications. it is stressed, however, that if dopamine-driven obsessions or compulsions are present, rather than perseveration, then a dopamine agonist—which increases dopamine availability in the brain—might exacerbate OCD symptoms. this caution is provided because later in this narrative, discussion of low-dose dopamine antagonists is included in the treatment of obsessions and compulsions; a dopamine antagonist reduces dopamine availability in the brain. That is why it is so important to differentiate between compulsivity and perseveration.

In researching ADHD medications and their actions, a definition from MedlinePlus Dictionary might be helpful. The term "adrenergic" means "liberating or activated by adrenaline or a substance like adrenaline." Adrenaline and epinephrine are the same biochemical. We discuss epinephrine and ANS—the autonomic nervous system, including the fight-or-flight response, in Part 1 of Stimulants sometimes used to treat ADHD are considered to be adrenergic. Also, remember that we discuss Norepinephrine action, synthesis, and pathways in Part 2 of

Below are a few resources that might be helpful if you are researching medications for ADHD. When these resources were found initially , a direct link is provided for all items. Access to NeuroPsychiatry Reviews has since been removed, for reasons unknown. A librarian, especially if associated with a medical school library, may be able to help you access hard-to-find materials.

Donald E. Greydanus provides a short overview of ADHD drugs in "Psychopharmacology for ADHD in Adolescents: Quo Vadis?" (2003). Although unable to supply a direct link to this article, you may enter the title into Google search to access it. A short advertisement precedes the article.

Peter Doskoch, in NeuroPsychiatry Reviews, addresses use of tricyclic antidepressants such as desipramine and imipramine in "ADHD: What to do When Stimulant Treatment Fails" (2002).

Jessica Dziedzic, in "Defending the Phenotype—Identifying True ADHD" (2008), in NeuroPsychiatry Reviews, provides information that may be helpful in clarifying some ADHD issues.

The link provided here will require you to register (free) with Medscape Today to view "Atomoxetine: The First Nonstimulant for the Management of Attention-Deficit/Hyperactivity Disorder" (2004). Regarding pharmacology, Corman, Fedutes, and Culley state: "Animal models have demonstrated that atomoxetine increases by threefold extracellular norepinephrine and dopamine concentrations in the prefrontal cortex, an area responsible for attention, judgment, self-monitoring, memory, motor sequences, and impulse control, but does not alter serotonin levels."

Regarding the stimulant, dextroamphetamine, Wikipedia notes that the drug can trigger "a cascading release of catecholamines." At the bottom of the Wikipedia entry are included a variety of hyperlinked references. Both norepinephrine and dopamine are catecholamines (also see Monoamines and catecholamines—notes on molecular structures in Part 2 of

Is hoarding related to ADHD?:


In discussing fixed-action patterns, it is easy to correlate the actions of a squirrel hiding nuts with the compulsions of those who hoard possessions. It may not, however, be as simple as activation of a dopamine-driven fixed-action pattern. As we discuss above, inadequate norepinephrine can play a significant role in perseveration, which is sometimes difficult to distinguish from compulsivity. In an editorial titled "Is Compulsive Hoarding a Genetically and Neurobiologically Discrete Syndrome? Implications for Diagnostic Classification," Sanjaya Saxena looks at a variety of studies about compulsive hoarding and defines it as follows: "Compulsive hoarding and saving leads to clutter that can cover living and work spaces, rendering them unusable. Hoarding frequently causes significant impairment in social and occupational functioning. In severe cases, it can produce health risks from infestations, falls, fires, and inability to cook or eat in the home." It is interesting that Saxena cites four studies that have specifically recruited compulsive hoarders and "found that many of them do not have other OCD symptoms (emphasis added)."

When you look behind the result of hoarding—an unmanageable volume of possessions—a symptom picture emerges. Saxena cites several reports indicating that hoarders have significant difficulty making decisions, including "Compulsive Hoarding: Current Status of the Research," in which Steketee and Frost point out that hoarders have "information processing deficits" in attention, organization, memory, and decision-making. In "A Cognitive-Behavioral Model of Compulsive Hoarding," Frost and Hartl have conducted research that indicates compulsive hoarders "are slow in completing tasks; frequently late for appointments; and display circumstantial, overinclusive language." Another way to put it is that hoarders often go on and on and on. This sounds a lot like perseveration. Previously, It is written that perseveration is best defined as repetitive movement or repetitive speech that focuses on one idea or task, thereby overlooking more significant stimuli that would normally prompt a behavior change. It is not saying that dopamine-driven fixed-action patterns do not play any role in hoarding. But it is important to consider whether inadequate norepinephrine in the frontal cortex, the imbalance most associated with ADHD, plays a role in producing hoarding symptoms.

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