Autism regression around aged 9-18 years old – is it catatonia?

 

From the title of today’s post you can see that this is one for parents of older children and indeed some adults. I should add that personally I am not a fan of observational diagnoses like catatonia, because I am interested in the biological cause of the unwanted behaviors, as a means to find effective therapy. Catatonia is a very broad term, but in current psychiatry that is what we have.

I was recently contacted by a mother whose adolescent son had regressed severely and she wanted to know what she had done wrong. She had not done anything wrong of course. Now she has to figure out what triggered the changes and how to reverse them. Catatonia is one possibility and it has not been covered in this blog.

The word catatonic drifted into casual English. Today, people use it informally to describe anyone who is completely unresponsive, frozen, or motionless.

As a medical term a diagnosis of catatonia is typically confirmed when an individual displays three or more of the following features:

Stupor & Mutism. Profound unresponsiveness to the outside world, along with a lack of, or severely reduced, speech.

Catalepsy & Waxy Flexibility. The tendency to passively hold bizarre, fixed postures against gravity or to maintain a position exactly as it is set by someone else.

Negativism. An active or passive resistance to instructions or movement.

Posturing. The spontaneous holding of unnatural, active postures for long periods.

Stereotypy & Mannerisms. Repetitive, non-goal-directed movements (such as rocking or pacing) or odd caricatures of normal actions.

Excitement/Agitation. Frenzied or purposeless motor activity that does not seem influenced by external stimuli.

Echolalia & Echopraxia. The involuntary mimicking of someone else's speech or movements.

 

Catatonia often occurs in people with schizophrenia, bipolar, or major depressive disorders. It can also be triggered by autoimmune diseases, brain injuries, or even severe infections. About 10% of people with autism will develop symptoms of catatonia. It can affect any level of autism.

Puberty can be the trigger for catatonia, but it can also develop much later in adulthood. 

Diagnosing catatonia looks different depending on the patient's age. For instance children are much more likely to present with refusal to eat or drink and mutism, which caregivers sometimes mistake for stubbornness or behavioral issues.

Autism-related catatonia can manifest differently than it does in non-autistic populations. It is often characterized by a distinct pattern of gradual, late regression rather than a sudden, acute physical freeze.

The "Late Regression" Timeline

While autism is usually diagnosed in early childhood, catatonia typically hits during adolescence or early adulthood.

The Early Warn Signs (Ages 10–14) Before full-blown catatonia develops, young teens with autism often exhibit a gradual increase in obsessive-compulsive routines, extreme physical slowness, or brief episodes of "freezing".

Full Onset (Ages 15–19) Full-syndrome catatonia typically solidifies during the peak of pubertal development. It is rare to see the full syndrome in autistic children under the age of 15.

Unique symptoms in autistic individuals

Because symptoms overlap with common autistic traits, catatonia can be difficult to recognize.

Loss of Function (Severe Regression). A sudden or progressive inability to complete daily activities they previously mastered (e.g., getting dressed, bathing, or using utensils).

Severe "Freezing" and Stuckness. Getting physically stuck mid-motion—such as freezing in a doorway or holding a cup halfway to their mouth for minutes.

The "Shutdown" Phenomenon. Severe passivity where the individual stops talking (mutism), avoids all eye contact, and refuses to eat or drink.

Hyperactive and Self-Injurious Behaviors. Rather than just freezing, autistic individuals frequently display hyperactive catatonia, which includes repetitive, automatic, and severe self-injury (like severe head-banging) that is unrelated to communicative distress.

Fluctuation Symptoms are notoriously variable—an individual may seem heavily affected or locked in place in the morning but move relatively normally by evening.

 

Why does it happen?

In autism, catatonia is frequently triggered by extreme environmental stress, major life transitions (like leaving school), trauma, severe anxiety, or co-occurring mood disorders.

 

Biological drivers

While psychological and environmental stress (such as extreme anxiety, bullying, or major routine changes) frequently act as the spark, catatonia is ultimately a neurological breakdown. The primary biological triggers, chemical imbalances, and genetic factors that cause the brain to enter a catatonic state include:

1.     Neurotransmitter imbalances

The most widely accepted biological explanation for catatonia is a sudden, severe imbalance of chemical messengers in the brain circuits that control movement and behavior:

·        GABA Deficit: GABA is the brain's primary calming/inhibitory neurotransmitter. In catatonia, there can be a sudden drop in GABA-A receptor activity. Because the brain loses its ability to regulate or slow down signals, motor pathways lock up. This explains why benzodiazepines (which increase the sensitivity to a given amount of GABA) can often rapidly reverse the condition.

·        Glutamate Overdrive: Glutamate is an excitatory chemical. A spike in glutamatergic activity, specifically involving NMDA receptors, can overstimulate the brain's motor networks, forcing the body into fixed, rigid postures.

·        Dopamine Drop: A sudden drop in dopamine activity—specifically at D2 receptors—paralyzes the brain’s reward and movement centers. This mimics the chemical state seen in Parkinson's disease, creating severe physical slowness or total immobility.

 

2.     Neuroimmune and autoimmune triggers

The immune system can directly attack the brain, causing acute neuroinflammation that triggers catatonia.

·        Autoimmune Encephalitis: Conditions like anti-NMDA receptor encephalitis occur when the body mistakenly produces autoantibodies that attack NMDA receptors in the brain. Catatonia is a primary symptom in up to 70% of these cases.

·        Systemic Infections: In medically vulnerable or autistic individuals, severe underlying infections (like a urinary tract infection, pneumonia, or a severe viral illness) can trigger a massive cytokine response. This inflammation breaches the blood-brain barrier, disrupting motor circuits and inducing catatonic behavior.

 

3.     Structural brain differences

Neuroimaging studies show that catatonia often stems from communication failures within specific brain loops (the cortico-striato-thalamo-cortical circuits) which govern motor planning.In autistic individuals with catatonia, MRI scans frequently reveal abnormally small cerebellar structures. Because the cerebellum is responsible for fine-tuning motor actions and smooth coordination, these structural differences make the motor loop highly vulnerable to completely breaking down under stress.

4.     Genetic susceptibility

Catatonia can have a hereditary link. Genetic studies on families with a vulnerability to periodic catatonia have identified specific genetic alterations. Interestingly, susceptibility regions on chromosomes 15 and 22 are heavily implicated in both autism and catatonia, suggesting a shared genetic architecture that primes certain individuals for the condition.

5.     Medication effects & withdrawal

Abrupt biological shifts caused by pharmaceutical substances can paralyze the motor system:

·        Dopamine Blockers: Exposure to strong antipsychotic medications can sometimes block dopamine receptors so aggressively that it induces catatonia .

·        Sedative Withdrawal: Suddenly stopping medications that calm the central nervous system (such as benzodiazepines or barbiturates) causes a rebound biological shock, stripping away the brain’s chemical brakes and inducing a catatonic freeze. Always taper the dosage.

  

Mainstream therapy for catatonia 

The treatment goal is to resolve any physical freezing first, then address the underlying psychiatric or medical cause.

Clinicians use a strict, stepped protocol ranging from medications to medical procedures. The first-line medication is Lorazepam (Ativan), a benzodiazepine. Lorazepam increases GABA-A activity, restoring the brain's missing chemical brakes. Intravenous Lorazepam is given to confirm the diagnosis if symptoms improve rapidly.

Electroconvulsive therapy (ECT) is the definitive treatment for severe cases. ECT is deployed if a patient shows no improvement after intensive Lorazepam trials. ECT is performed safely in a hospital setting under general anesthesia and muscle relaxants.

Maintenance Therapy: Long-term, periodic ECT may be required for individuals with chronic conditions.

Second-line options include glutamate antagonists like Amantadine or Memantine, if first-line choices fail. Alternative GABA agents like Zolpidem (Ambien) are sometimes utilized to break treatment-resistant freezing. Medications to Avoid: Traditional dopamine-blocking antipsychotics (like haloperidol) are generally not useful. Antipsychotics can worsen the motor paralysis or trigger Neuroleptic Malignant Syndrome.

 

Peter’s thought’s on mainstream therapy

The 30+% of level 3 autism who respond to bumetanide would have an extreme negative (paradoxical) reaction to Lorazepam (Ativan). They would get very aggressive and “go nuts.”

In most countries ECT is highly regulated. It clearly is effective for some people, but it looks a rather crude therapy to me.

The mainstream therapies look very “thin” to me. I think much more should be possible.  

I think the term catatonia is much too vague and you need to know why these changes have occurred, then you can figure out a therapy.

PANS can trigger the symptoms of catatonia. In many counties PANS is still not recognized as a diagnosis. PANS (Pediatric Acute-onset Neuropsychiatric Syndrome) would not respond to a benzodiazepine drug like Lorazepam, but would instead require immunotherapy, which is completely different.

As usual we come back to getting an observational like catatonia, autism or trendy new ones like ARFID (picky eating) is just the first step in the process. Then you need to find out why? What biological or behavioral factors are driving these symptoms. Then you can figure out how to treat them, or indeed choose not to treat them, if you are so inclined.

  

Could it be OCD rather than catatonia?

One reason catatonia can be difficult to recognize in autism is that several of its symptoms overlap with severe obsessive-compulsive disorder (OCD). In fact, some studies have found that obsessive-compulsive symptoms are very common in autistic individuals who later develop catatonia.

Parents often report that their child begins:

• Writing the same words repeatedly
• Talking about the same topics over and over
• Performing increasingly rigid rituals
• Becoming distressed when routines are interrupted
• Withdrawing socially

These symptoms may point to OCD, catatonia, or a combination of both.

The key distinction is that OCD is driven by obsessions and compulsions, whereas catatonia is characterized by a loss of initiative and a decline in function. An autistic teenager with OCD may be extremely active in performing rituals, while a teenager with catatonia may become progressively slower, less spontaneous, and increasingly "stuck."

Questions that may help distinguish the two include:

• Does the person become anxious if prevented from performing the behavior?
• Are they physically slower than before?
• Do they need prompting to start everyday activities?
• Have they lost skills they previously mastered?
• Are they spending long periods inactive or frozen?

The two conditions can coexist. In some cases, severe OCD may precede the development of catatonia.

Investigations

When a child, teenager, or adult with autism experiences a significant regression after years of relative stability, it is worth looking beyond the autism diagnosis itself.

One investigation I would seriously consider is an EEG (electroencephalogram). Epilepsy or "just" abnormal electrical activity in the brain can sometimes present as:

• Regression
• Social withdrawal
• Changes in communication
• Cognitive decline
• Repetitive behaviors
• Episodes of staring or unresponsiveness

Several studies have reported higher rates of epilepsy among autistic individuals who develop catatonic symptoms.

An EEG may not identify the cause of the regression, but it is a relatively straightforward way to investigate an important and potentially treatable neurological contributor.

Other investigations may include:

• Sleep assessment
• Review of medications
• Assessment for OCD and anxiety disorders
• Evaluation for depression
• Screening for autoimmune or inflammatory conditions where clinically indicated

The important point is that autism itself is not usually a progressive condition. When someone loses skills after years of stability, it is worth asking what has changed and whether there is a treatable condition contributing to the decline.

 

From PANS to PANDAS? Another Problem Solved

 

Source: EpiphanyASD

 

There is a lot written about PANS (Pediatric Acute-onset Neuropsychiatric Syndrome) and PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections) which is a subset of PANS; however they are still not fully recognized as medical conditions.

I prefer to see PANS/PANDAS in the broader context of autoimmune encephalitis, a collection of related conditions in which the body's immune system mistakenly attacks the brain, causing inflammation. The immune system produces antibodies that mistakenly attack heathy receptors in the brain.  Depending on which types of receptors are targeted, you will get different symptoms, plus you will get symptoms from the inflammation.

If they are NMDA receptors, you may have hallucinations and appear to have developed schizophrenia overnight.

It has been suggested that the definition of PANS is too narrow and a broader term called CANS was proposed.  CANS is not exactly the same as PANS.  PANS is the popular term in the US.

“A 2011 paper by Singer proposed a new, "broader concept o childhood acute neuropsychiatric symptoms (CANS)", removing some of the PANDAS criteria in favor or requiring only acute-onset. Singer said there were "numerous causes for CANS", which was proposed because of the "inconclusive and conflicting scientific support" for PANDAS, including "strong evidence suggesting the absence of an important role for GABHS, a failure to apply published [PANDAS] criteria, and a lack of scientific support for proposed therapies".”

Moving from PANDAS to CANS (pay-walled)

I do not see why the focus is always on children, because we know that adults can also be affected.

In children and adults with autism it seems that quite often they may suddenly develop verbal or motor tics, as the obvious symptom of autoimmune encephalitis.  These tics gradually disappear when treated with a short course of oral steroids.

One point emphasized by the likes of Susan Swedo, at the US National Institute of Mental Health, is that PANS/PANDAS is not autism.

Non-autistic children can develop PANS/PANDAS, but so can autistic people.

A non-autistic child with untreated PANS/PANDAS would appear to most people as autistic, so similar are the symptoms.

An adult with NMDA receptors encephalitis will very likely be diagnosed as schizophrenic.

The autistic person who develops PANS/PANDAS appears like an autistic person who has encountered a regression. Many of the symptoms of PANS/PANDAS are common symptoms of autism, so the onset of PANS/PANDAS may just look like the already present symptoms have gotten worse.

Susan Swedo has commented that there is nothing to suggest PANS/PANDAS is more common in children with autism. She states that PANS/PANDAS is a condition of onset in early childhood, which is likely to reoccur when re-exposed to the same trigger, but reoccurrence is much less of a risk after 21 years old.

I think most cases of PANS/PANDAS in people with severe autism are never diagnosed and so never treated.  It is just put down as an autistic regression.  How many of those adults with severe autism and extremely challenging behaviors fall into this category?  Given the enormous cost, up to half a million dollars a year, to house this type of person in a care facility with 24-hour support, you would think a little bit more effort should be given to early diagnosis and treatment.

 

A Sceptical World

One of our neurologist readers commented in this blog about how she successfully treated her child’s PANS episode, even though in her country PANS does not exist as a diagnosis and her colleagues at work had no idea how to treat it. Quick intervention required only minor treatment.

In some countries with free universal healthcare, you only get to diagnose and treat PANS if you go outside that system and pay extra.

In the US there are some pretty expensive tests proposed for PANS and CANS.

In mainstream medicine PANS/PANDAS are not generally accepted as conditions and yet Stanford University has had a PANS/PANDAS clinic for a decade.

https://med.stanford.edu/pans/about.html

 

Time for detective work

 

The usual issue I have to manage in spring/summer is what I call summertime raging and dumber in the summer.  Note that a cognitive regression is a very common symptom of PANS/PANDAS.

My solution to summertime raging and dumber in the summer revolves around allergy, mast cells and reducing pro-inflammatory cytokines.

This year some new symptoms developed after summer:

·        Sensory amplification, in the form of sound sensitivity

·        Clinginess to Mum/Mom and separation anxiety

·        Hair twirling, using fingers to twist hair

·        Nail picking, the medical term is Onychotillomania

·        General anxiety

·        Increased urinary frequency, not due to a UTI (urinary tract infection)

·        Aggression and reactive rage (as opposed to predatory rage)

·        Mood disorder, crying for no apparent reason at school and home 

All the above symptoms can be passed off as autism.

Sound sensitivity is a common problem in autism, but Monty was getting so sensitive to sounds that he could not tolerate sitting next to someone eating at home. At school, where it is very noisy, this was not a problem.

Clinginess to Mum/Mom rather merged with the aggression and reactive rage symptoms.  Aggression is a very common problem in severe autism and it is usually directed mainly at Mum.  This time it was not just behaviors, but talking in advance about potential aggressive behaviors, this was new and got worse and worse.

Hair twirling has occurred before and is a common expression of anxiety, which then just becomes a habit, like a stim or tic.  This was previously resolved by a haircut.  This time the short hair did not solve the issue.

Nail picking (Onychotillomania) is when use your index finger to pick at the cuticle on your thumb and end up tearing the skin. This is rather like compulsive hair pulling (Trichotillomania) which is a common feature of OCD (obsessive compulsive disorder).  NAC is used to treat Trichotillomania. 

Anxiety is nearly always an issue in all levels of autism. 

The urinary symptoms of PANS/PANDAS are something that I had not paid attention to earlier. 

We covered polydipsia, drinking too much water, in a special post. This is a big problem for some readers of this blog. 

Thirst – Too much or too little (Polydipsia and Hypodipsia) Vasopressin and Angiotensin

People taking Bumetanide for autism will drink a lot, but should do so only in the few hours after taking the therapy, not all day long.

Autistic people with polydipsia are at risk of death due to low sodium levels (hyponatremia).

Monty was drinking so much I was giving him additional sodium and potassium.

Children with autism often use toilet breaks as an escape from whatever task they have been given.  Monty’s assistant had commented on how he seemed to be trying to escape from her.

The mood disorder was very marked and on one occasion Monty cried at school; his classmates were worried about him and did their best to comfort him.  This had never happened before and there was no apparent trigger. The same thing happened at home a few times, normally in the evening.

After a gradual worsening of the above symptoms, Monty had a viral infection, and he informed us that he had a sore throat. Behaviors then got significantly worse and he had a week off school, more for the behaviours than for the mild flu-like symptoms.  Having then announced that his ear was hurting, we took him to the Ear Nose and Throat doctor. To get to see the doctor you first have to go and get a negative Covid test. The diagnosis was a mild ear infection that might not need an antibiotic, but if it got worse take the antibiotic (Cefpodoxime). This is a β-lactam antibiotic. 

We did cover the non-antibiotic properties of this class of antibiotic in a dedicated post, since many antibiotics have profound anti-inflammatory and other effects not related to killing bacteria.  You can never know with 100% certainty which effect is giving you the benefit.

 

Autism and Non-Antibiotic Properties of Common Beta-lactam Antibiotics

 

 

For anyone interested in trivia. The aerobic mold which forms the basis of this antibiotic, cephalosporin C, was found in the sea near a sewage outfall by Cagliari harbour in Sardinia, by the Italian pharmacologist Giuseppe Brotzu in July 1945. 

If you like sandy beaches like Monty, Sardinia is a great place to visit. Cagliari is in the south, the famous part of Sardinia is Costa Smeralda, on the northern coast, where the celebs go to be seen.

Since Monty’s problem was more behavioral than due to pain in his ear, we started the antibiotic without delay.

Over 5 days, the behaviors began to improve and on day 6 the hair twirling vanished entirely for a day, so clearly something new was going on in his brain.

The mood disorder switched to occasional extreme laughter/happiness, rather than the previous tears.

The behavioral regression started well before the viral infection and ear infection, so it is not just a simple case of a sore throat and a strep infection.

Are all the above symptoms due to PANS/PANDAS?

There actually is a 100% overlap between Monty’s recent symptoms and a list of possible PANS/PANDAS symptoms. Every symptom I listed is on the doctor’s checklist below: -

 

Description of PANS Symptoms

 

Description of PANS Symptoms

1) OCD

Traditional OCD presents with mild obsessions and compulsions that become more involved and burdensome over time. In traditional OCD, symptoms tend to be persistent with minor variance in symptoms (often referred to as a waxing and waning). In contrast, PANS OCD presents with a sudden onset typically from mild or no symptoms to debilitating in an abrupt amount of time. Often, parents recall the exact date of symptom onset, and frequently report “it just came on out of the blue.”

 

Many compulsions are either mental rituals (and therefore difficult to observe) or appear as extremes of an acceptable behavior (e.g., compulsive handwashing). Common OCD rituals in children include: washing/grooming, checking (locks, door), counting, ordering/symmetry, hoarding, restrictive eating, and repetitive questioning.

 

Emerging research suggests different treatment options are available for children with PANS OCD than for children with non-PANS OCD. Understanding the difference between the two forms of OCD allows appropriate interventions to be implemented.

 

2) Eating Restriction

PANS children describe various reasons for not eating normally or adequately, such as: fear of vomiting, sensitivity to taste, smell, and texture, fear food is spoiled, or fear of being poisoned. In some cases, the restricted eating is directly related to body image distortions, including concerns about being overweight (even when the child is normal weight and was previously satisfied with their body habitus.)

 

3) Anxiety

Anxiety frequently presents as constant, generalized anxiety or age-inappropriate separation anxiety.

 

4) Sensory Amplification

PANS children may become uncharacteristically and intensely bothered by smells, tastes, sounds, and textures, causing difficulties with daily routines, such as brushing teeth, riding in a car, eating, and dressing.

 

5) Motor Abnormalities

PANS children may exhibit motor and vocal tics, handwriting changes and/or clumsiness.

 

6) Behavioral Regression

PANS children may display regressed behaviors, such as: baby talk, refusal to carry out age-appropriate grooming activities, tantrums, clinginess, and/or separation anxiety.

 

7) Deterioration in School Performance

Psychological testing of children with PANDAS, a subset of PANS where strep is the infectious trigger, has found impairments on a visual-spatial recall test, on measures of executive function, and on a dexterity test. PANS children may also experience a decreased processing speed, memory issues, and/or difficulty in math and calculation.

 

8) Mood Disorder

Depression, mania, irritability, hypersexuality, emotional lability, and rage have been noted during a PANS exacerbation. Moods may change from happy to sad to angry in moments. Reactive rage (as oppose to predatory rage) may start instantaneously and stop as quickly, leaving the child remorseful and confused.

 

9) Urinary Symptoms

An initial complaint may be urinary frequency. A careful history will often expose additional symptoms. PANS children may develop polyuria (up to many times per hour), frequent urges to urinate, and/or day and night secondary enuresis. These urinary symptoms are not due to UTI, anxiety or OCD type worries.

 

10) Sleep Disturbances

Polysomnography has demonstrated a variety of sleep abnormalities in children with PANS, including initial and middle insomnia, REM behavior disorder, parasomnias, and/or sleep phase shifting. 

 

Since I did introduce the term CANS, here is a comparison of PANDAS, PANS and CANS from a recent Italian paper:- 

CANS: Childhood acute neuropsychiatric syndromes

 

Table 1 - Criteria for PANDAS, PANS, and CANS 

 

PANDAS

1. Presence of OCD and/or a tic disorder

2. Pediatric onset (Symptoms of the disorder first become evident between 3 years of age and the puberty.)

3. Episodic course of symptom severity Abrupt onset of symptoms or dramatic symptom exacerbations. Often, the onset of a specific symptom exacerbation can be assigned to a particular day or week, at which time the symptoms seemed to ‘‘explode’’ in severity. Symptoms usually decrease significantly between episodes and occasionally resolve completely between exacerbations.

4. Association with Streptococcal infection Symptom exacerbations must be temporally related to Streptococcal infection

5. Association with neurological abnormalities During symptom exacerbations, patients will have abnormal results on neurological examination. Motor hyperactivity and adventitious movements

 

PANS

1. Abrupt, dramatic onset of OCD or severely restricted food intake

2. Concurrent presence of additional neuropsychiatric symptoms, with similarly severe and acute onset, from at least two of the following seven categories

1) Anxiety

2) Emotional lability and/or depression

3) Irritability, aggression and/or severely oppositional behaviors

4) Behavioral (developmental) regression

5) Deterioration in school performance

6) Sensory or motor abnormalities

7) Somatic signs and symptoms, including sleep disturbances, enuresis or urinary frequency.

3. Symptoms are not better explained by a known neurologic or medical disorder (Such as Sydenham's chorea, systemic lupus erythematosus, Tourette disorder, or others).

  

Idiopathic CANS

Acute onset before age 18 of behavioral and motor signs encompassing

1. Primary criterion OCD

2. Secondary criteria

1) Anxiety

2) Psychosis

3) Developmental regression

4) Sensitivity to sensory stimuli

5) Emotional lability

6) Tics

7) Dysgraphia

8) Clumsiness

9) Hyperactivity

3. Mono- or polyphasic cours

Treatment

Susan Swedo advises to treat PANDAS with 3 weeks of antibiotics.

Monty’s 2 previous cases of sudden onset motor/verbal tics were resolved by 5 days of Prednisone.  This is a common therapy for a PANS flare-up.  There is a study from Stanford on its benefit.  The sooner you use this therapy, the greater the benefit.

The most important thing with all forms of autoimmune encephalitis seems to be speedy treatment so the condition does not become chronic.  Then you have to use much more invasive and expensive therapies like IVIG and Plasmapheresis.

It is clear that PANS/PANDAS is likely to reoccur.

In Monty’s case the first two instances were very similar.  They were both acute onset tics. The third instance was very different.

Given that Monty’s antibiotic very obviously had a behavioral benefit, we will follow Swedo’s advice and continue for 3 weeks, which is 2 weeks longer than the standard ear infection therapy.

The short course of Prednisone will hopefully complete the therapy and life will go back to normal.

I recall that our neurologist reader, with those sceptical colleagues, did not even need steroids to resolve her child’s problems, NSAIDs were sufficient.  The sooner you treat the symptoms, the less potent the therapy needs to be and the more effective it seems to be.  Some people commence treatment years after the symptoms emerge.

 

Conclusion

One conclusion to this post might have been along the lines of “My god, whatever next?” as if autism brings never-ending problems.

I rather see it as, why did it take me so long to recognize the symptoms?

The answer to that one is that PANS/PANDAS/CANS, or indeed the broader Autoimmune encephalitis, is a family of conditions.  Just because you saw one set of broad symptoms earlier, does not mean you will not face a different subset of symptoms next time.

The urinary symptoms of PANS were a surprise and worth highlighting.

Autistic regressions should be investigated and treated.

On the one hand, doctors, particularly in the US, do like expensive diagnostic tests.  They want certainly and often struggle to treat ill-defined conditions that they have not been taught about.  They prefer not to tinker around, in fact tinkering is frowned upon.

On the other hand, when very expensive testing is done and it identifies in someone a combination of rare genetic dysfunctions associated with autism, nobody thinks to look up each gene and see how to compensate for the usual loss of function - that does not seem to count as medicine.  The genetic diagnosis is crystal clear, but the therapy would definitely require some tinkering around, to perfect it.  But, such tinkering is so frowned upon that the “specialist” just stands well clear and moves on to the next patient.   

Tinkering around is an essential part of fixing practical problems.

In my case of autism, I have not paid $925 for the Cunningham Panel of PANS/PANDAS tests, or even a strep test, or a urine culture test.

The cost of treating the 2 apparent PANS episodes in previous years was about $5 dollars each time.  The cost of the current episode was more, about $15, plus the cost of a visit to the ENT doctor and the required Covid test.  Our neurologist reader likely spent even less for her NSAIDs.

PANDAS, PANS, CANS or just autoimmune encephalopathy, it does not really matter what you call it, prompt intervention will likely resolve the symptoms.