“Our results motivate a paradigm shift to challenge how ASD, ADHD, and OCD are currently defined, diagnosed, and treated. In particular, this paper adds to the evidence that these diagnoses may not exist as uniquely-defined diagnostic constructs, and highlights the need to discover other groupings that may be more closely aligned with biology and/or response to treatment.”
So, this study by Kushki et al 2019 is by no means simple. However, the results support our clinical experience of the overlap and common features seen in practice. We see similar overlap is the assessment data we gather, particularly when we SIPT our clients with these diagnoses. The study uses state of the art technology and research methodologies, statistical calculations, and techniques I had never heard of. I had to look them up. However, the research appears to support what we see in clinical practice. I look forward to reading more by these researchers in Canada.
“…we used a data-driven, diagnosis-agnostic approach to examine overlap across three neurodevelopmental disorders (ASD, ADHD, and OCD)…we observed that differences in the domains primarily affected in these disorders may exist along a continuum that includes typical development.”
“The majority of the data-driven clusters contained participants from multiple diagnostic categories, highlighting shared phenotypes and neurobiologies among the diagnostic groups.”
“Social difficulties and inattention are commonly reported as shared features of ASD, ADHD, and OCD….our results support the emerging recognition that the existing behaviorally-defined diagnostic labels may not capture etiologically, biologically, and phenomenologically homogeneous groups.“
“…our results are consistent with the notion that that the ASD-like features, and to some extent inattention traits, exist across a continuum that includes typical development”
These guidelines were first published in May 2018 following several meetings between the PANS Physicians’ Network UK (PPNUK) and the Charity PANS PANDAS UK. Based on the US treatment guidelines originally written by the US PANDAS Physicians’ Network, these guidelines have been modified to adapt to UK medical practice, GP’s are strongly encouraged to start treatment and investigations early as early treatment is likely to improve the long term outcome of these patients.
“There is gradually accumulating evidence that there are some children who experience sudden onset of a neuropsychiatric disorder (usually obsessive-compulsive disorder (OCD) or tics) following a Group A beta-haemolytic streptococcal infection (GABHS). The acronym PANDAS was first cited in 1998 to describe this group of patients.However, neurological sequelae of streptococcal infection have been well recognised (eg, Sydenham’s chorea described by William Osler in 1894).
Doubt remains about the aetiology of the condition and whether it can be considered an independent disease entity.
More recently the term PANS (paediatric acute-onset neuropsychiatric syndrome) has been suggested, as it captures both the sudden onset and uncertainty about the aetiology.”
PANS (Pediatric Acute-onset Neuropsychiatric Syndrome) is when an infectious trigger, environmental factors, and other possible triggers create a misdirected immune response results in inflammation on a child’s brain. In turn, the child quickly begins to exhibit life changing symptoms such as OCD, severe restrictive eating, anxiety, tics, personality changes, decline in math and handwriting abilities, sensory sensitivities, and more.
PANS was introduced in 2012 by Dr. Susan Swedo in the paper From Research Subgroup to Clinical Syndrome: Modifying the PANDAS Criteria to Describe PANS (Pediatric Acute-onset Neuropsychiatric Syndrome).
The PANS Criteria
PANS is a clinical diagnosis. The following is the “working criteria” as listed Dr. Swedo’s paper on PANS:
Abrupt, dramatic onset of obsessive-compulsive disorder or severely restricted food intake.
Concurrent presence of additional neuropsychiatric symptoms, with similarly severe and acute onset, from at least two of the following seven categories: Anxiety Emotional lability and/or depression, Irritability, aggression and/or severely oppositional behaviors, Behavioral (developmental) regression, Deterioration in school performance, Sensory or motor abnormalities, Somatic signs and symptoms, including sleep disturbances, enuresis or urinary frequency
Symptoms are not better explained by a known neurologic or medical disorder, such as Sydenham’s chorea, systemic lupus erythematosus, Tourette disorder or others.
The hallmark trait for PANDAS is sudden acute and debilitating onset of intense anxiety and mood lability accompanied by Obsessive Compulsive-like issues and/or Tics in association with a streptococcal-A (GABHS) infection that has occurred immediately prior to the symptoms. In some instances, the onset will be 4 to 6 months after a strep infection because the antibiotics did not fully eradicate the bacteria. Many pediatricians do not know the latent variability of strep – Rheumatologists and Streptococcal Experts do.
The acute onset means a Y-BOCS (Yale Brown Obsessive-Compulsive Scale) score of >20 and or a Chronic Tic Disorder YGTSS (Yale Global Tic Severity Scale) often with multiple tics. Below is the symptom criteria for PANDAS. Additional symptoms may be present.
A clinical diagnosis of PANDAS is defined by the following criteria:
Presence of significant obsessions, compulsions, and/or tics
Abrupt onset of symptoms or a relapsing-remitting course of symptom severity
Interestingly no one asked for evidence of Sydenham’s Chorea, which has been well documented for much longer. Perhaps because it has a very physical presence that is clinically easier to diagnose, especially as the condition progresses to full-blown ataxic movement patterns, as well as the neuropsychiatric symptoms.
In the 1930s, if a doctor saw a patient with chorea, especially if the patient were a child or young woman, it was a reasonable assumption that the diagnosis was Sydenham’s chorea. In western societies today, such a presentation is unlikely to be Sydenham’s chorea and considerable thought must be given to the differential diagnosis. The time course of the chorea is useful diagnostically: most previously healthy children with an acute or subacute chorea have an autoimmune aetiology. Additional causes of childhood choreas include:
Other autoimmune causes, such as seen in systemic lupus erythematosus.
Athetoid cerebral palsy.
Drug-induced causes – metoclopramide, phenothiazines and haloperidol are the most important.
Primary and metastatic brain tumours affecting the basal ganglia.
Metabolic – bilirubin encephalopathy and toxins, especially carbon monoxide, manganese and organophosphate poisoning.
*Genetic Causes can include:
Benign hereditary chorea starts in childhood and is a non-progressive chorea. Inheritance is usually autosomal dominant, although rare cases of autosomal-recessive and X-linked inheritance have been reported.
Wilson’s disease is an autosomal-recessive disorder of copper metabolism.
Ataxia telangiectasia and other related conditions.
Huntington’s disease presents most often between the ages of 35 years and 45 years but it can be younger, especially if inherited from the paternal line. There is usually but not invariably, a family history. A juvenile form exists that should be seen as a variation of the normal form and not a distinct entity.
Our vestibular system is amazing. So many people don’t even know what they do until it isn’t working – like when someone has vertigo and even getting out of bed becomes impossible.
I had no idea how important it was or how much it influenced everyday life.
A tiny organ located in the inner ear, near the cochlea (the hearing organ) the vestibular system tells us about how our head is moving through space, it can detect movement in any plane and can distinguish between acceleration, deceleration rotational and linear movement.
On top of all of this, the vestibular system detects gravity. It tells us which way is up and which is down. The information from the vestibular system is used by the brain to inform all kinds of things, from maintaining balance and posture to stabilising our visual field.
This means that we can stand or sit up straight, know when we are moving and that objects in the distance appear to stay still, even if we are driving, moving or jumping about.
A great explanation of the vestibular system and how it works to help.
Over the last few days, ASI Wise CLASI CASI Module 1 participants have been exploring the neuroscience supporting the theory of Ayres’ Sensory Integration – and how we all need to take in, integrate, adequately process and respond to sensory input to be able to successfully participate in everyday life, throughout our life.
We focussed on developing our understanding of the contribution of the sensory systems to early development and then function across the lifespan. We explored the essential role the senses play in underpinning behaviours and higher-order function. We considered the application in paediatrics, CAMHS, and services for adults and older adults with learning disabilities and/or mental health difficulties.
Module participants present their learning about the BIG 3 Sensory systems:
We considered supporting research and evidence in occupational therapy and in other fields including biology, neuroscience, psychology, sociology, and medicine. We were introduced to patterns of sensory difficulties people with Autism might have.
The module explored the neuroscience that supports our practice as therapists. It is inspiring to hear that the flow of new and emerging research in this field appears almost constant.
The answer to a question on SI4OT, a FB group for OT’s curated by our social media team, includes this interesting article.
This study was focussing on the vestibular system, and the researchers tried to work out the exact amount of vestibular input needed in therapy. The results strongly suggest that it is very individualised and requires direct therapist observation to know. This is exactly in line with Ayres’ teachings. There is no exact amount that can be prescribed
The use of sensory input to support function, health and wellbeing is an art and a science.
The science is knowing for instance that habituation of tactile input to Ruffini nerve ending is usually fairly rapid – eg light touch as we put arms in shirt sleeves while habituation to pain receptors will vary a lot and maybe ongoing after tissue damage we can’t always see.
The art is that our response to sensory input to sensory systems will vary greatly and is very individualised. This response is not just linked to immediate registration and perception of the input – meaning and memory need to be considered too. Think about happy smells and songs that stay in your head all day. Think too about the response to trauma when a person smells their abuser’s perfume.
There is no recipe for how much to give and when. This is the art and science of ASI. So many factors impact on what a person needs and when to have an adaptive response.
This is why sensory input is not just something you can prescribe someone by saying;
“Give Jane 20 mins on a swing 3x a day”
Essential to practice is the person’s response to sensory input – Do they have an adaptive response?
“Ayres (1972b) described the adaptive response as central to praxis intervention. Adaptive responses are purposeful actions directed toward a goal that is successfully achieved, and the production of adaptive responses is thought to be inherently organizing for the brain. Ayres (1972b, 1985) further emphasized that SI intervention was a transaction among client, task, and environment.”
Bundy, A. and Lane, S. , Sensory Integration Theory and Practice, 3rd Edition, [Philadelphia]. Available from: FADavis.
Watching and seeing this response to input, alongside feedback from the parents/family/person is what we do to understand each person’s unique responses and pattern. However, knowing and remembering that many things can impact on this, day to day and even minute by minute is essential.