Thursday, April 27, 2006

The Wilbarger Approach: How patient should we be?

I received an email today regarding a parent who was interested in finding training on how to implement a 'brushing' program on their five year old child. The child's therapist allegedly encouraged the parents to research it themselves - which seemed a little odd to me. This got me thinking: perhaps there is a population of therapists who just can't find resources on the Wilbarger Approach.

I can understand the frustration. There has been very little published in the literature about this approach - perhaps the two most-cited references of the authors themselves are Wilbarger and Wilbarger (1991) and Wilbarger and Wilbarger (2002). These are not research studies; they are just descriptions and theoretical ideas about the concept of sensory defensiveness. There are studies that have been published by others but they have been single subject designs or they have been published in newsletters. The Sensory Defensiveness website (allegedly sponsored by Patricia Wilbarger) has promised answers to frequently asked questions since sometime in the mid to late 1990s. I think it is an abandoned site.

For many years (going back to the early 1990s) I recall that the Wilbarger Protocol was a hot topic in the occupational therapy continuing education world. How many OTs attended those training sessions? Is it possible that 3,500 therapists paid for this training? At a hypothetical cost of $300 for a conference, is it possible that over $1 million dollars has been spent on learning about this intervention? That is an interesting question.

I was hard pressed to find a training session for the Wilbarger Protocol today. You can order a VHS tape for $30 at Professional Development Products. Is there no more demand in the OT market for the product that it has been relegated to the discount bin in the continuing education world?

Well for an intervention that was virtually ignored by researchers the Wilbarger Protocol certainly had some legs. It still does, if you use Google as any indicator of popular interest in a topic.

Lucy Miller made an extremely cogent argument about the need to "promote research that leads to better diagnoses and effective interventions" as opposed to making "unequivocal and emotional statements." I agree with her argument completely, but as the title of this entry implies - how long are we supposed to wait for this research to be done? The approach was developed and many people were trained. There were promises made that 'research is coming soon,' but I haven't seen it.

While surfing around tonight I think I found a potential source of very useful information - and I think we might be able to thank Ruth Segal. I believe that I met her a couple years ago at an SSO conference, and I wish I knew then that she was interested in this topic. Anyway, an old web page from NYU states that one of her research projects was on "The perspectives of children, caregivers, and therapists of the brushing and compression program for sensory defensiveness." I haven't been able to find out if this has been published, so if anyone knows I would be interested. The point here is that she thought this research might help us to "understand the phenomenon of embracing or rejecting new interventions." In my opinion, this really represents the 'bottom line' on this entire discussion. Why do OTs embrace these interventions - and why do OTs hold on to them in the absence of supporting research?

Most importantly, have we served the public interest by creating a 'demand' for a service that we have never supported with research and that we no longer even train therapists in?


References:

Miller, L.J. (2003). Empirical evidence related to therapies for sensory processing impairments. Communique’, 31(5), 34-37. Response to: Shaw, S.R. (2002). A school psychologist investigates sensory integration therapies: Promise, possibility, and the art of placebo. Communique’, 31(2), 5-6.

Wilbarger, P., & Wilbarger, J. L. (1991). Sensory defensiveness in children aged 2 - 12. Santa Barbara, CA: Avanti Educational Programs.

Wilbarger, J.L. & Wilbarger, P.L. (2002). Wilbarger approach to treating sensory defensiveness and Clinical Application of the Sensory Diet. Sections in Alternative and Complementary Programs for Intervention, Chapter 14. In Bundy, A.C., Murray, E.A., & Lane, S. (Eds.). Sensory Integration: Theory and Practice, 2nd Ed. F.A. Davis, Philadelphia, PA.

Monday, April 24, 2006

Contributing to the cause

April is OT month. It seems that every group, movement, or cause has a Day or Month. Still, April has always been OT Month in my mind, long before I found out that it was also Autism Awareness Month, Cesarean Awareness Month, Child Abuse Prevention Month, National Humor Month, National Welding Month, National Garden Month, etc... you get the point.

In the past I have done public service announcements on radio, radio interviews, spent money on advertising, endured a promotional cable-access 4 part series, (think Wayne's World meets OT), and of course there are the standard guest lectures in front of highschoolers that could care less, giveaways at college job fairs, and the perennial poster presentation in the employee workroom/cafeteria/front hallway.

This year I decided to do something of more substance. This website remains an ongoing project to support the cause, as is this other website. (Shameless method for generating more web traffic).

Then there was my real television debut today: Caroline and I did a segment on AM Buffalo . It was definitely less painful than the Wayne's World experience - and hopefully a more effective medium for transmitting a message.

This really raises the bar for next year though. Maybe we should try skywriting.

What did you do for OT Month?

Wednesday, April 19, 2006

Occupational therapy and Horner syndrome

This entry is relatively esoteric, but I spent time researching Horner Syndrome so if the information can help even one more person I suppose that posting it here is worthwhile. This is truly the benefit of the Internet: things that waste space on my hard drive may be a treasure trove of information to someone in the world. Here's hoping.

***

Introduction

Horner syndrome, also identified as Horner-Bernard syndrome or oculosympathetic paresis, is a constellation of symptoms including miosis, ptosis, apparent enophthalmos, anhidrosis, and reddening of the conjunctiva (Adams &Victor, 1985, p. 208). This condition was described through observations of animals by the French physiologist Claude Bernard. Additionally, some of his co-workers were American surgeons who described this condition in a Civil War soldier who had a cervical sympathetic nerve injury (Kisch, 1951). However, Johann Friedrich Horner, a Swiss ophthalmologist, is generally credited with the first full description of this condition in 1869 despite the earlier publications of the other physicians (Bell, Atweh, Ivy, & Possenti, 2001).

The most notable visual symptoms include miosis, ptosis, and apparent enopthalmos. Miosis is a term for pupillary constriction. In Horner syndrome it is common for one pupil to be more constricted than the other pupil. Under normal conditions, the pupils remain equal at all times in all levels of light. Most references that I scanned indicate that there are no functional implications of anisocoria (having differently sized pupils). However, MacMillan, Cummins, Heron, & Dutton (1994) describe a simultaneous interocular brightness sense test that was sensitive for anisocoria. Additionally, Grossberg & Kelly (1999) describe how binocular brightness sensitivity assists in perception of surface brightness and contour. The functional impact of these issues on everyday vision is not clear, although the same authors have also written about how this process is important for figure ground perception (Kelly & Grossberg, 2000).

Ptosis is drooping of an eyelid. This has an obvious impact on cosmesis but there are also functional considerations. The muscle that is involved by sympathetically-mediated ptosis is the Müller muscle (Adams & Victor, 1985). Ptosis that occurs in the developmental period may have an impact on functional visual acuity as well as visual field (Dray & Leibovitch, 2002).

Enophthalmos is posterior displacement of the eye. In Horner syndrome the narrowing of the interpalpebral fissure, combined with subtle ptosis, causes the appearance of enopthalmos (Lepore, 1983). There are no apparent functional deficits associated with apparent enopthalmos other than the impact on cosmesis.

Etiology

Horner syndrome is caused by an interruption of the oculosympathetic pathway, which is a three neuron pathway. The first order neuron originates in the hypothalamus and descends to the upper thoracic cord where it synapses with second order neurons. These travel over the lung and enter the sympathetic chain in the neck, and synapse in the superior cervical ganglion. Here, third order neurons project postganglionic axons to the eye to innervate the dilator of the iris. Postganglionic sympathetic fibers also innervate the Müller muscle. Postganglionic sympathetic fibers, responsible for facial sweating, follow the external carotid artery to the sweat glands of the face. Interruption at any location along this pathway (preganglionic or postganglionic) will induce an ipsilateral Horner's syndrome (Amonoo-Kuofi, 1999).

Horner syndrome can be caused by damage to first order neurons by conditions including Arnold-Chiari malformation, basal meningitis, basal skull tumors, cerebral vascular accidents, demyelinating diseases, intrapontine hemorrhage, neck trauma, pituitary tumor, and syringomyelia (Bardorf, Van Stavern, & Garcia-Valenzuela, 2001).

Horner syndrome can be caused by damage to second order neurons by conditions including Pancoast tumor, birth trauma with injury to lower brachial plexus, cervical rib, aneurysm/dissection of aorta, subclavian or common carotid artery, central venous catheterization, trauma/surgical injury, chest tubes, lymphadenopathy, mandibular tooth abscess, lesions of the middle ear, and neuroblastomas (Bardorf, Van Stavern, & Garcia-Valenzuela, 2001).

Horner syndrome can be caused by damage to third order neurons by conditions including internal carotid artery dissection, Raeder syndrome, carotid cavernous fistula, cluster/migraine headaches, and herpes zoster (Bardorf, Van Stavern, & Garcia-Valenzuela, 2001).

Additionally, Horner syndrome can be caused by many medications and injuries; the literature is replete with single case studies of esoteric Horner syndrome etiology.


Medical and therapeutic interventions

There are several medical and therapeutic interventions for Horner syndrome. Initially, pharmacologic testing is used to determine the presence of Horner syndrome as well as the possible location of the lesion. The use of 4-10% cocaine eye drops versus 1% Hydroxyamphetamine can help to distinguish between second and third order Horner syndrome. In general, a sympathetically denervated pupil will not dilate to cocaine, regardless of the level of the sympathetic interruption because there is a decreased amount of norepinepherine. Hydroxyamphetamine stimulates the norepinepherine release, so an eye with Horner syndrome with damaged postganglionic fibers (third-order neuron lesions) does not dilate as well as the normal pupil after hydroxyamphetamine drops (Bardorf, Van Stavern, & Garcia-Valenzuela, 2001). Because of the sensitivity of using cocaine in a pediatric population, some authors have advanced the use of 1% apraclonidine for pharmacologic testing, but this does not distinguish pre- or post- ganglionic lesion sites (Bacal & Levy, 2004).

Most of the interventions for Horner syndrome are primarily focused on the cause of the syndrome (disease, injury). However, there are interventions to correct the symptoms of the syndrome. Surgical procedures to correct ptosis have been described in the literature (Glass, Putterman, & Fett, 1990). Interventions for miosis could be made by a referral to an ophthalmologist or optometrist who could fully evaluate the functional impact that the miosis is having on vision.

Several articles in the literature describe physical or occupational therapy intervention for facial paralysis in general, although most of these refer specifically to Bell’s palsy (Beurskens & Heymans, 2003; Cronin & Steenerson, 2003). Some of these methods may be interesting to investigate regarding rehabilitation of muscles of facial expression as they relate to Horner syndrome.

Impact on occupational performance

Horner syndrome may have an impact on occupational performance. Although there is no description of Horner syndrome in the occupational therapy literature, several areas of potential difficulty can be inferred.

One significant area that could be affected includes completion of personal care and grooming occupations because of the cosmetic changes associated with Horner syndrome. Horner syndrome causes unilateral miosis, ptosis, and apparent enopthalmos. These all can physically alter an individual’s appearance and can cause the individual to be self conscious and can cause others to view the individual negatively (Bullock, Warwar, Bienenfeld, Marciniszyn, & Markert, 2001). For this reason alone it is important to address the symptoms of this disorder.

As mentioned previously, visual dysfunction including amblyopia and perhaps visual perceptual problems could develop as a result of uncorrected ptosis and miosis. Visual function has a broad impact on all areas of occupational performance so deficits in these areas could lead to many functional difficulties with participating in preferred occupations.

Another area to potentially consider in the impact of a dysfunctional sympathetic nervous system could have on an individual. Many different conditions cause Horner syndrome, and it is possible that there are other sympathetic nervous system difficulties that are associated with the underlying cause. Occupational therapists are well-trained in understanding sympathetic nervous system functioning and could evaluate this system if needed to determine any impact on occupational performance.

Occupational therapy assessments

Occupational therapy assessments that would be appropriate for an individual who has Horner syndrome include occupation-based assessments that would address issues relating to participation in personal care and the meaning that these occupations have for the individual. The Canadian Occupational Performance Measure (Law, Baptiste, McColl, Opzoomer, Polatajko, & Pollock, 1990) is an individualized outcome measure designed to detect change in a client's self-perception of occupational performance over time. This assessment would be helpful to elicit information from the individual regarding the impact that the Horner syndrome is having on their self-image.

If the individual is a child aged five through nine, The Visual Skills Appraisal (Richards & Openheimer, 1999) could be useful to measure ocular efficiency. There are six subtests that evaluate pursuit, scanning, alignment, locating movements, eye-hand coordination, and fixation unity.

The Motor Free Visual Perception Test (Colarusso & Hammill, 2003) could be a useful test to determine if there are any visual perceptual difficulties. This test measures visual perceptual skills with stimulus items of increasing difficulty or complexity in each of the areas, normed on ages from 4 to adult. The test is used to identify lags in visual processing of spatial relationships, visual closure, and visual memory, which may adversely affect an individual’s functioning.

General observations of the individual completing functional tasks would also be helpful in determining if there are any functional vision deficits associated with the Horner syndrome.

Occupational therapy interventions

Occupational therapy interventions that would be appropriate for an individual who has Horner syndrome include working on self care occupations that could improve the individual’s sense of control over their appearance. This is also an area where it would be interesting to see if any facial exercise programs (Beurskens & Heymans, 2003; Cronin & Steenerson, 2003) would have any impact on the paralysis associated with Horner syndrome.

In addition to the cosmetic impact of ptosis and attempts to strengthen denervated muscles, the individual could learn to compensate for any functional visual field loss by training in scanning techniques (Quintana, 1995, p. 529). These would be particularly helpful for the superior visual field that could be occluded because of eyelid drooping.

If it was determined that the individual had any associated visual perceptual deficits due to loss of figure ground perception, associated perceptual training could be attempted. This training could take the form of remediation or compensatory techniques.

Summary

Horner syndrome is a rare condition that can be caused by a number of medical conditions, many of which themselves can cause visual system dysfunction. Very little is published about Horner syndrome, and most of the available literature discusses esoteric etiology and treatment of the underlying cause of the symptoms. However, the symptoms can not be ignored as they can have a significant impact on a person’s occupational performance.

As very little has been published in the literature on the impact that these symptoms have on function, this makes choosing assessment instruments and interventions a very difficult task. There is still a lot to learn about these symptoms and how they relate to function. There is also a lot to learn regarding the systemic impact of sympathetic denervation, the possible perceptual deficits that can develop associated with uncorrected anisocoria or ptosis, and the role of different intervention techniques to address these deficits. Occupational therapists could help contribute to the body of knowledge regarding this syndrome.


References:

Adams, R.D. & Victor, M. (1985). Principles of neurology, 3rd ed. New York: McGraw-Hill.

Amonoo-Kuofi, H.S. (1999). Horner's syndrome revisited: with an update of the central pathway, Clinical Anatomy. 12, 345-361

Bacal, D.A. & Levy, S.R. (2004). The use of apraclonidine in the diagnosis of Horner syndrome in pediatric patients. Archives of Opthalmology, 122, 276-279.

Bardorf, C.M., Van Stavern, G., & Garcia-Valenzuela, E. (2001, June 26). Horner Syndrome. Retrieved February 15, 2005, from http://www.emedicine.com/oph/topic336.htm

Bell, R.L., Atweh, N., Ivy, M.E., & Possenti, P. (2001). Traumatic and iatrogenic Horner’s syndrome. Case reports and review of the literature. Journal of Trauma, 51, 400-404.

Beurskens, C.H. & Heymans, P.G. (2003). Positive effects of mime therapy on sequelae of facial paralysis: stiffness, lip mobility, and social and physical aspects of facial disability. Otology & Neurotology. 24, 677-681.

Bullock, J.D., Warwar, R.E., Bienenfeld, D.G., Marciniszyn, S.L., & Markert, R.J. (2001). Psychosocial implications of blepharoptosis and dermatochalasis. Transactions of the American Ophthalmological Society, 99, 65-71.

Colarusso, R. P., & Hammill, D.D. (2003). The Motor Free Visual Perception Test (MVPT-3). Navato, CA: Academic Therapy Publications

Cronin, G.W. & Steenerson, R.L. (2003). The effectiveness of neuromuscular facial retraining combined with electromyography in facial paralysis rehabilitation. Otolaryngology - Head & Neck Surgery, 128, 534-538.

Dray, J.P. & Leibovitch, I. (2002). Congenital ptosis and amblyopia: a retrospective study of 130 cases. Journal of Pediatric Ophthalmology and Strabismus. 39, 222-225.

Glatt, H.J., Putterman, A.M., & Fett, D.R. (1990). Müller's Muscle-Conjunctival Resection Procedure in the Treatment of Ptosis in Horner's Syndrome. Ophthalmologic Surgery, 21, 93-96.

Grossberg, S. & Kelly, F.J. (1999) Neural dynamics of binocular brightness perception. Vision Research, 39, 3796-3816.

Kelly, F., & Grossberg, S. (2000). Neural dynamics of 3D surface perception: Figure-ground separation and lightness perception. Perception & Psychophysics, 62, 1596-1618.

Kisch, B. (1951). Horner’s syndrome, an American discovery. Bulletin of the History of Medicine, 25, 284-288.

Law, M., Baptiste, S., McColl, M.A., Opzoomer, A., Polatajko, H. & Pollock, N. (1990). The Canadian Occupational Performance Measure: An outcome measure for occupational therapy. Canadian Journal of Occupational Therapy, 57, 82-87.

Lepore, F.E. (1983). Enopthalmos and Horner’s Syndrome. Archives of Neurology, 40, 460.

MacMillan, E.S., Cummins D., Heron, G. & Dutton, G.N. (1994). The simultaneous interocular brightness sense test. A test of optic nerve function. Archives of Opthamlology, 112, 1190-1197.
Quintana, L.A. (1995). Remediating perceptual impairments. In Trombly, C. (Ed.). Occupational therapy for physical dysfunction, 4th ed. Baltimore: Williams & Wilkins.

Richards, R. & Openheimer, G.S. (1999). Visual Skills Appraisal. Novato, CA: Academic Therapy Publications

Monday, April 17, 2006

More on the occupation of collecting

At some risk, I occasionally offer self-reflective entries that explore narrative meaning to childhood occupations. Background for this current self-indulgent essay can be found by reading about the occupation of collecting. In this previous essay I wanted to explore rule making and gamesmanship – now I seek to expand discussion of this occupation into a theme of how environment and context shape the occupational experience. Unstructured neighborhood play is not common today, and it is a significant loss for children. Imagine if I never experienced this:

***

During a recent trip home I visited my parents and noticed all of the things that were changing. I know that they have been changing steadily, but for some reason I recently noticed this more acutely.

The waterfront looked especially good, and as I scanned the rows of new buildings I saw one older but beautifully restored building with a landscaped waterfall alongside it. And I remembered the time that Brian and I found a dead body in that old building.

We were only ten years old or so, and each Saturday morning made our ritualistic trek down to the waterfront to scan the parking lot for beer bottle caps. We collected them, and found great joy in conducting our searches for new and different styles of caps.

The waterfront was kind of run down back then, and there were several old buildings there. I don't know what drew us into those buildings that day - perhaps it was a dare. But we went into these old abandoned buildings to see what was inside of them.

They were barely shells of buildings - I imagine that some fire long long ago had gutted them. The brick framing was still there, the windows were all knocked out and there was scattered debris all over the floor. It was a cold day, and damp, and the rushing of a nearby stream and waterfall made the coldness hang in the air. As we moved from room to room in these old buildings we laughed and joked and did the things that ten-year-old boys do.

When we turned a corner to look into one last room, we saw it. Frozen in our tracks, we saw the body of a middle aged man lying lifeless in the corner. Sometimes no words need to be said. We both looked at each other and ran as fast as we could.

We eventually caught up with each other and tried to catch our breath once outside. We decided that seeing it once was not enough – we needed to be sure of what we saw and we needed to decide what to do about it.

Cautiously, deftly, we tiptoed back through the maze of debris. The air felt a little colder, a little damper. We were SCARED. My heart pounding, I knew I wasn’t about to enter that room again, but we wanted to make sure of what we saw. We stood outside the doorway to the room for a while, trying to see past the darkness. Past the coldness. Past the dampness.

The crumpled human form was lying in the middle of a pile of wooden beams, garbage, and bricks. How would we know it was really a dead body?? Brian got the idea to poke it with a stick, to make sure it was a body. It was so dimly lit in there, and we just wanted to be sure. After heated debate and lots of “I’m not going to go in there” discussions, we decided to do the next best thing.

Brian had one of the best pitching arms in the school, so we emptied our pockets and found all the pennies. This would be worth losing a few pennies over. As hard as he could, Brian whipped the pennies at the corpse, bouncing them off of the arms, the legs, the torso. Nothing moved. It was dead all right. After the last penny bounced off the dead man’s skull, we both turned and ran again as fast as we could.

We didn’t stop when we got out of the building; we ran all the way straight to the police station. Out of breath, again, we stammered our story to the desk sergeant there. “We found… dead body… waterfront… abandoned building…” I am not sure that we impressed the sergeant, but after having us recount the incident more and more officers gathered around to hear the tale. After some private discussion, they put us into the back of a patrol car and the sergeant drove us down there.

We were released from the vehicle (both terrified and feeling trapped when we realized we couldn’t open the doors from the inside) and walked toward the building. Each time that we went into that building it got a little colder and a little damper and our hearts pounded even farther out of our chests. The sergeant asked us to follow him in and direct him to the body. We followed meekly behind, terrified, as he led the way in with his hand on his holster. I remember thinking that was odd – what was he planning on shooting? A dead body??

As we approached the doorway we knew there was no way in the world we were going into that room again. Like frightened rabbits we huddled outside the doorway and pointed into the corner toward our grisly discovery. The sergeant stepped in slowly, almost crouching, and as he came closer and closer to the body we saw him suddenly stand up stiffly.

In later discussions, Brian and I discovered that we feared the exact same thing at that moment. The sergeant had killed that man! And we found the body, so now he was going to kill us! If we could have run we would have, but we could not move. Could not think. Could not breathe.

The sergeant turned to us and began to yell, “For Christ’s sake…!” and he turned back toward the corpse and kicked it swiftly in the buttocks. “God damn it Murph, get your ass up and out of here you stinking drunk.” With another kick the body rustled, slowly rose, and shambled past us zombie-like – stinking of alcohol and drunkenness.

Walking briskly toward us, the sergeant grabbed us both by the collars and hauled us out into the daylight. We received a long lecture about the dangers of going into abandoned buildings, about wasting police resources with false alarms. But he told us he wouldn’t tell our parents as long as we promised to never go into those buildings again.

Mutely, we both nodded our heads. We finished walking our way down toward the waterfront. The day had gotten off to a strange start, but there were still bottle caps to go searching for..

Tuesday, April 11, 2006

Occupational therapy and attention deficit disorder

Introduction

I am frequently asked - "Does this child have an attention deficit disorder, or is it a sensory integration disorder?" I generally respond that I don't know what either ADHD or sensory integration disorders are.

There is a fundamental problem that we have in diagnostic evaluation: professions have created 'disorders' before there is an understanding of the mechanisms underlying the disorders. This opens up the possibility for criticism because we begin calling 'disorders' by names and then have no basis for backing up our opinions. I still feel relatively comfortable stating that I don't know what ADHD or sensory integration dysfunctions are. This confuses people who are looking for answers but I believe it to be the most honest response that is possible for this question.

I believe that there are multifactorial reasons why children behave the way they do. Some of those reasons are neurologically based and some are behaviorally based. I wanted to focus on the neurobiology of arousal and attention mechanisms as a starting point.

A discussion on the topics of arousal and attention first requires an operational definition of the terms. William James wrote that "Everyone knows what attention is. It is the taking possession by the mind in clear and vivid form, of one out of what seem several simultaneously possible objects or trains of thought...It implies withdrawal from some things in order to deal effectively with others, and is a condition which has a real opposite in the confused, dazed, scatterbrained state." (James, 1890, p. 403). Current theorists are now challenging this perspective on attention and are identifying models of attention that focus on parallel processing or multitasking abilities (Pashler, 1998).

The construct of attention is dependent on the construct of arousal. Arousal is often equated with consciousness, which has also been defined in many different ways. Primary and secondary consciousness, from Edelman and Tononi’s perspective (2000), does not seem to have a single point of residence in the nervous system, but instead is regulated by the interaction of several centers. However, from a more specific and limited definition that has clinical utility, some specific structures can be considered that contribute to arousal level.

Review of the neurological structures governing arousal/attention and their interrelationships.

The reticular activating system is the center for all arousal except for smell (Dodd & Castellucci, 1991, p. 517). Bilateral destruction of the ascending reticular formation projections to the midline and intralaminar nuclei of the thalamus is known to cause coma (Kelly, 1991, pp. 815-816).

The hypothalamus is also important for regulating autonomic responses to arousing stimuli. There are specific and measurable behaviors associated with arousal and orientation toward novel stimuli. These include pupillary dilation, vasoconstriction of the limbs, vasodilation of the head, increased electrodermal activity, and cardiorespiratory regulation (DeGangi & Porges, 1990, pp. 7-8).

The limbic system is also important in the arousal/attention process by coordinating autonomic, somatic, and behavioral systems (p. 15). People who have limbic system damage may have difficulties with qualitative analysis of incoming stimuli causing inattention, overattention, or inability to functionally interpret the meaning or importance of the stimuli.

The reticular activating system, hypothalamus, and limbic systems and their associated functions are closely coordinated in a pattern of inhibition and feedback loops between the cortex and the lower structures (p. 13). A functional overview of the mechanism associated with arousal/attention includes receiving the initial stimulation, regulation of arousal and sensory registration, activation of the alerting and orienting responses, and then selective attention or inattention. All of these functions occur under cortical direction, both directly and indirectly.


Hypothesized location of the neurological disorder

The neurological basis of ADHD has been debated for the last several decades. Some researchers hypothesize that the frontal lobes of patients with ADHD may be involved, as this is the site of cortical control over lower brain arousal and orienting functions (Blum & Mercugliano, 1997, p.451). It is thought that catecholamine neurotransmitters such as dopamine and norepinepherine are deficient because stimulant medications that are prescribed for the disorder are known to increase the availability of these neurotransmitters (p. 451). Other studies indicate that size of selected brain structures may be decreased in some children who have ADHD (p. 451). Some researchers have identified that subcortical structures are implicated in the ADHD disorder (Kinomura, Larssen, Gulyas, & Roland, 1996). Some professionals suggest that ADHD is more of a behavioral style than a diagnostic entity with a specified or identifiable location of neurological deficit (Chess & Thomas, 1987). Still other physicians openly question the validity of the diagnosis ADHD, suggesting that there is no such disorder at all (Victoroff, 2000).

Specific symptoms of dysfunction

According to the DSM-IV (APA, 1994) diagnostic criteria for attention deficit hyperactivity disorder include both symptoms of inattention and symptoms of hyperactivity or impulsivity. These symptoms must be present for at least six months and of a degree that is maladaptive and inconsistent with developmental level. Additionally, these symptoms must appear prior to the age of seven, must be present in more than one setting, and not due to any other confounding disorder.

Despite these clear criteria for diagnosing ADHD, many children are not identified with this disorder until they are school-aged. Prior to this time they may be identified as having a regulatory disorder, as described by DeGangi (2000).

Difficulties with maintaining sustained attention are especially problematic when the child enters elementary school. During these early school years the child may have difficulties with complying with classroom rules and routines (Blum & Mercugliano, 1997, p. 450). As children get older, social concerns are more prevalent. In the majority of people who have ADHD, symptoms persist into adolescence and adulthood (p. 450). This causes long term and chronic occupational dysfunction. Children who have attention deficit hyperactivity disorder are more likely to have co-morbid conduct and mood disorders (p. 450).


Etiology of ADHD

Some researchers now believe that ADHD may be a genetic disorder (Todd, 2000). ADHD as defined by DSM-IV criteria includes a clinical spectrum of disorders that may have multiple etiologies. Common to these disorders is the symptom of inattention.

Evidence suggests that attention is a neuropsychological function and that disorders of attention are biologically based. Epidemiological data, the measured effectiveness of selected pharmacological intervention, and neuroimaging all continue to contribute to the current understanding of this disorder. Despite a substantial amount of research and popular attention in the media there is still no commonly agreed on cause of the disorder or universally accepted intervention protocols.


Implications for Occupational Performance

Regulation of attention and arousal is a basic requirement for human function. DeGangi and Porges state that "when a person is actively engaged in voluntary attention, functional purposeful activity and learning can occur" (p. 6). Attention deficit disorder is the most common neurodevelopmental disorder of childhood, with an estimated prevalence of 3%-5% among school-age children and a male to female ratio of 4:1 -9:1 (Blum & Mercugliano, 1997, p. 449).

The disorder has a significant impact on the academic participation of many children. A basic model for understanding the relationship between arousal and performance is described by Lane (2001, p. 133). In this model, performance is most notably decreased in periods of excessively high or excessively low arousal; peak performance is noted during times of moderate arousal. Optimal arousal is necessary for achieving appropriate function for attention getting, attention holding, and attention releasing, as originally described by Cohen (1972).

On the most basic level of development, arousal and attention are best measured by tools such as the Neonatal Behavioral Assessment Scale (Brazelton, 1995). This scale includes measures of arousal, state organization, habituation, and attending. Brazelton (1995) states that certain aspects of infant functioning should only be measured when the child is in an optimal state of arousal and attending.

Similar tools are not readily available to evaluate the impact of arousal and attention on the occupational performance of older children. However, behavioral observations can be made as a part of other standardized tests.




REFERENCES

American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: Author.

Blum, N.J. & Mercugliano, M. (1997). Attention deficit/hyperactivity disorder. In M.L. Batshaw (Ed.). Children with disabilities (4th ed., pp. 449-470). Baltimore: P.H. Brookes.

Brazelton T.B. & Nugent J.K. (1995). Neonatal Behavioral Assessment Scale, 3rd ed. Clinics in Developmental Medicine, 31, London: Cambridge University Press.

Chess, S. and Thomas, A. (1987). Origins and evolution of behavior disorders: From infancy to early adult life. Cambridge, MA: Harvard, 1987.

Cohen, L.B. (1972). Attention-getting and attention-holding processes of infant visual preferences. Child Development, 43, 869-879.

DeGangi, G.A. (2000). Pediatric disorders of regulation in affect and behavior: A therapist's guide to assessment and treatment (Practical resources for the mental health professional). Chestnut Hill, MA: Academic Press.

DeGangi, G. & Porges, S. (1990). Alertness, Attention, and Arousal. In C.B. Royeen Neuroscience Foundations of Human Performance. Rockville, MD: American Occupational Therapy Association Inc.

Dodd, J. & Castelluci, V.F. (1991). Smell and taste: The chemical senses. In E.R. Kandel, J.H.Schwartz, & T.M. Jessell (Eds.), Principles of neural science (3rd ed. pp. 512-529). New York: Elsevier.

Edelman, G.E., & Tononi, G. (2000). A universe of consciousness: How matter becomes imagination. New York: Basic Books.

James, William (1890). Principles of psychology. New York: Holt.

Kelly, D.D. (2001). Disorders of sleep and consciousness. In E.R. Kandel, J.H.Schwartz, & T.M. Jessell (Eds.), Principles of neural science (3rd ed. pp. 805-819). New York: Elsevier

Kinomura,S., Larssen,J., Gulyas, B., Roland, P.E. (1996) Activation by attention of the human reticular formation and thalamic intralaminar nuclei. Science, 271, 512-515

Lane, S.J. (2001). Sensory modulation. In A.C.Bundy, S.J. Lane, & E.A.Murray (Eds.) Sensory integration theory and practice. (2nd ed. pp. 101-122). Philadelphia: F.A.Davis.

Pashler, H. E. (1998). The psychology of attention. Cambridge, MA: MIT Press

Todd, R.D. (2000). Genetics of attention deficit hyperactivity disorder. American Journal of Medical Genetics 96, 241-243.

Victoroff, J. (2000). Does ADHD Exist? Psychiatric Times, 5, 13.

Wednesday, April 05, 2006

a spoon of peas

I received a phone call today from a mother who wanted to ask me a question. “Why is Patrick talking about eating cake or vegetables every time we work on his homework?”

Having been exposed, I had to tell the parent this story:

During a recent therapy session I sat next to 6 year old Patrick while he completed a puzzle. I was watching his strategy for putting the pieces together. As he skillfully interlocked the pieces he announced, “Mr. Chris, this is a piece of cake.”

Seeing that I needed to add some complexity to the activity I replied, “What are you talking about? That’s not a piece of cake. It’s a puzzle.”

Children who have Asperger’s Syndrome sometimes interpret language literally, and as Patrick had a severe difficulty with this I thought I would challenge him a little.

“Why are you saying that the puzzle is a piece of cake? It’s not even a piece of cake – it’s a puzzle of a dinosaur. You don’t make any sense.”

Patrick paused, trying to understand my response. “No, Mr. Chris. It is a piece of cake. But I know it is a puzzle. It is a dinosaur puzzle that is a piece of cake.”

“Well Patrick,” I replied, “now I am really confused, because I thought T-Rex was a meat eater, not a cake eater. I didn’t know that dinosaurs were made of cake.” Patrick’s gears were really turning now, trying to find a way to make sense of my concerns.

Patrick recovered quickly. “Mr. Chris, when something is a ‘piece of cake’ that means that you can do it. And it’s easy so you like to do it.”

I was pleased with his explanation, but persisted anyway, “So if you like to do something and it is easy you call it a ‘piece of cake,’ kind of because eating cake is easy too?”

Patrick was relieved that I was getting his point. “Yes, cake is easy to eat, and dinosaur puzzles are easy to do. So doing a dinosaur puzzle is a piece of cake!”

I needed to throw a wrench back into the conversation, so I added, “What do you call it if something is really hard to do, like writing your name?” Patrick hated handwriting.

Patrick went back to thinking, and then announced “Maybe we should call handwriting something else because it is hard. Handwriting is not a piece of cake. What is something that is hard Mr. Chris?”

“Eating a spoon of peas,” I shot back immediately.

Patrick beamed. “OK, when something is hard, I am going to say that it is a spoon of peas, and when something is easy I can call it a piece of cake!”

This made perfect sense to both of us, and that ended the conversation.

_______________________

The mom was very relieved that her son had a legitimate reason for calling difficult tasks “a spoon of peas.”

Sunday, April 02, 2006

On behavior intervention plans and the carceral archipelago

It is critical for occupational therapists to understand the nature of power relationships and control mechanisms when they are working with children or adults who have disabilities. I understand that I can take steps beyond what I will express here – and begin a discourse on the very nature of identifying the concept of disability – but I want to ignore those larger issues and instead focus on the relationships between those who are already identified as ‘disabled’ and those identified as ‘normal.’ So for the purposes of this discussion, we will overlook the discussion that ‘medicalization’ creates power differentials and supports social control in itself.

I am not an ivory tower academic. I am just a street-level occupational therapist who is trying to do a good job and to appropriately serve the people who ask me for help. I mention this because if anyone reads this I want them to know that my interest is grounded in the tasks I am asked to do everyday. This is very real to me – it is not an academic exercise.

Stories offer us a mechanism for understanding something about experience; they are meant to be both evocative and provocative (Mattingly & Garro, 2000, pp. 10-11). They also are supposed to “offer a powerful way to shape conduct because they have something to say about what gives life meaning… compelling stories move us to see life… in one way rather than another.” Here is the story that brings this to the forefront of my thinking:

Shannon was born with cerebral palsy and she has a mild degree of mental retardation. These conditions cause obvious functional impairments and she has always been eligible for special education services. Murphy (1990) states that being disabled is the same as being relegated to permanent liminality. This is mostly true for Shannon. She could walk and talk – but with a limp and a slur. She didn’t learn as quickly as the other students. She has seen and understood her lack of competence for her entire life. This was reinforced by her placement in special classes and by the lack of inclusion when her age-mates called all the other children in the class to invite them to a birthday party. Shannon stayed home those days, and her mother probably comforted her. This is a common theme for many children who have developmental disabilities.

Both of Shannon’s parents died when she was just twelve. There were no other relatives who could care for her, so she entered foster care. She lived in a multitude of homes, each placement being less successful than the previous one.

Over time it was determined that in addition to cerebral palsy Shannon also had oppositional defiant disorder. And conduct disorder. And adjustment disorder. And post traumatic stress disorder. There are some others too. Shannon’s behavior was becoming unmanageable.

There was a need to control Shannon’s behavior. Her chart outlined all the concerns, indicating that she could be manipulative and demanding. To control the behaviors a plan was put into place.

Behavior plans are written for the staff who wield ultimate power and provide a panopticistic strategy for managing the people in their charge. By definition they are generally reductionistic and arguably dehumanizing. Shannon’s plan went into detail about her temper tantrums and sexual precocity; it failed to mention that her parents died when she was just entering adolescence. Instead, the plan stated that “behavioral problems seem to be related to the transition from school, the bus ride, and entrance into the high school after attending the morning vocational program.”

Shannon had a reward program where she could earn tokens for positive behavior. She could earn ten tokens a day. Thirty tokens bought her two pencils. Sixty tokens bought her a candy bar. A hundred tokens bought her a fifteen minute conversation with a favored teacher, who she loved. Two hundred fifty tokens bought her a ‘date’ with a favored residential staff member, who would arrange to take her somewhere special.

Yes, the only things she truly valued and loved had to be purchased, coercively, with tokens. Ten days of good behavior bought her a brief nurturing conversation. Twenty five days of good behavior bought her individualized contact with the only semblance of family that was available. Hope is critical for people who face extreme adversity (Spencer, Davidson, & White, 1997). I can’t imagine that anyone could muster up much hope under these circumstances.

I expect that the behavior plan was written with good intentions, but I am very worried that too many professionals with good intentions make horrible mistakes. Occupational therapists should continue to study these stories so that they can develop a deeper understanding of illness experiences and be in a better position to help participate in humane care for people who have developmental disabilities.


References:

Mattingly, C., & Garro, L. C. (2000). Narrative and the cultural construction of illness and healing. Berkley, CA: University of California Press.

Murphy, R. (1990). The Body Silent. New York: W.W.Norton.

Spencer, J., Davidson, H., & White, V. (1997). Helping clients develop hope for the future. American Journal of Occupational Therapy, 51, 191-198.


Related reading:

Foucault, M. (1977). Discipline and punish: The birth of the prison (A. Sheridan, Trans.). New York: Pantheon Books. (original work published 1975).

Saturday, April 01, 2006

April is Occupational Therapy Month!

Occupational Therapy: The Profession that Focuses on Life Skills

For millions of people, the service of occupational therapy is a lifeline. People of all ages receive it to help them participate in the activities of their daily life. Sometimes people need occupational therapy to do things we take for granted, like getting dressed, being productive at school or work, eating unassisted, even socializing.

Occupational therapy doesn't just treat medical conditions, it helps people stay engaged in the activities that give them pleasure or a sense of purpose, despite challenges.

Occupational therapists do this by helping people surmount their disabilities or medical conditions to do everyday things. The nature of the therapy depends on the individual and their environment; occupational therapists consider the whole person when developing a therapy plan. Occupational therapists collaborate with physicians and other professionals to ensure a comprehensive approach.

Children, for instance, sometimes have behavioral or developmental problems that limit their educational progress. Lawmakers believe occupational therapy is so important to the well-being of children, federal law mandates that schools must offer occupational therapy to children who need it.

Occupational therapy is "outcome-oriented," which means therapists help clients work toward achievable performance goals.

In rehabilitation clinics or hospitals, occupational therapists and occupational therapy assistants help adults learn or regain skills that allow them to do meaningful things like working, driving, shopping, or even preparing a meal. All types of people need this kind of help everyday, from a worker injured on the job to a grandparent recovering from surgery or a stroke.

Occupational therapy helps avoid health problems, and makes it easier to live with them.

Consider our growing senior population: Healthier people are living longer lives. Occupational therapy research proves that keeping people active and healthy as they age will improve their quality of life as well as lower their health care costs. That is why there are occupational therapy programs focusing on wellness and prevention—to help seniors stay healthier and remain active in their homes and communities. Trained therapists can make homes safer for people with reduced mobility and failing vision. Occupational therapists can also teach seniors new driving techniques that will keep them behind the wheel longer, as safe drivers.

Occupational therapy addresses one of the most important aspects of rehabilitation and recovery—the return to a normal life.

Occupational therapy has its roots, a century ago, in helping war veterans return to life at home. These days, occupational therapists work in rehabilitation hospitals and on the front lines of combat. Some occupational therapy programs help soldiers recognize and relieve stress. In addition, occupational therapy helps soldiers learn to care for themselves after an injury, including helping them use artificial limbs.

In recognition of all the ways occupational therapy contributes to society's well-being, April has been designated as Occupational Therapy Month.

To find out more about occupational therapy and how it might help you, visit the ABC Therapeutics website.