Introduction:
Obsessive Compulsive Disorder (OCD) is a devastating behavioural and mental illness that can start as early as early teens, and is not limited to washing and cleaning, but obsessions about tidiness, orderliness, checking, rechecking and more. Obsession is a repetitive anxiety provoking thought that something is not clean, tidy, organized, in order, not right, etc. that will not leave the inflicted individual alone. Then the person feels obliged to do something to stop the burdening thought (compulsion) that leads to “compulsive act” that is washing, cleaning, ordering, tidying, checking and rechecking until feels satisfied that is hard to reach. Associated or underlying this chain of thought (obsession), urge to act (compulsion) and the act (compulsive act) are, “doubt” and “superstition” that things are not clean or right the way should be, and if not act upon, some harms will befall on the individuals or beloved ones. Then rituals will come to play, and the person in the eyes of others could appear not anymore as a clean, tidy, or a “perfectionist”, but as totally insane who has lost his touch with reality and cannot be convinced by others. The cases that come to medical attention, are usually more than a mere perfectionism and consists of all the above, that makes it very hard to treat.
The big question is that what causes OCD, specially from an early age. Is it a personality that is labeled “obsessive compulsive personality”, or is it rooted in “perfectionism”, or in anxiety-ridden subjects, or is it genetic and familial? The fact is that many of OCD patients, have had no obsessive compulsive personality, or perfectionism, no history of previous anxiety and none of their other family members suffer the same. The etiology is still unknown, hence the treatment is incomplete and failure in many instances and prevention is not in agenda as nobody knows how!
Did it really all start from a sore throat?!
All the above OCD behaviours and tic disorders could have earlier started from a sore throat that is a very common and recurrent infection in childhood world-wide and mostly caused by streptococcal bacteria, specially group A of Streptococcus (Strep. A), that is also the cause of skin infections, pneumonia and meningitis, responsible for over half a million deaths per year globally. Two common latent damages of Strep A infections are Rheumatic Fever and post-streptococcal glomrulonephritis, both occur about 1-4 weeks after a sore throat infection, pharyngitis or skin infection. These damages are the earliest after an acute infection, so they are well known in medicines, among physicians and the cause and effects are un-debatable. Rheumatic Fever which is a very serious and severe inflammation of the heart, inflicting children world-wide, later on migrates to affect joints and even brain. The damage to the heart could be permanent, causing Rheumatic heart disease that is damages to the heart valves, currently affecting more than 18 million victims world-wide. Post-streptococcal glomerulonephritis is inflammation of the kidneys, leading to damages to this vital organ, high blood pressure, renal failure and has caused 19,000 deaths in 2013.
A later latent impact of Strep A infection is a neurological movement disorder, Sydenham’s Chorea that can occur months after the initial attack, causing jerky involuntary movements, muscle weakness, slurred speech, and personality changes, again mostly in children. PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections) syndrome is similar to Sydenham’s Chorea, but without motor dysfunctions, and instead with tics and/or psychological/behavioural symptoms, e.g. OCD and occurs much earlier, days to weeks after strep A infection. The common occurrence of tics, Tourette syndrome (a vocal tic disorder with occasional inappropriate and obscene vocal exclamations) and obsessive, repetitive and compulsive behaviours among children, a period after infections, specially sore-throats with commonly Strep A have caused some suspicions among researchers over the past two decades for the infective causation of OCD. So researchers have found evidence of some auto-immune changes in OCD subjects, for example significant levels of antibody for somatostatin-28, and negligible reactivity for several other peptides including beta-endorphin and corticotropin in OCD subjects compared with normal controls and a few other psychiatric and neurologic disorders. Also researchers have noticed that some infections with group A beta-hemolytic streptococci among others, may trigger autoimmune responses that cause or exacerbate some cases of childhood-onset obsessive-compulsive disorder (OCD) or tic disorders (including Tourette’s syndrome). Some of these children have responded well to the treatment with plasma exchange, intravenous immunoglobulin, and immunosuppressive doses of prednisone, which all are immunotherapies.
But the obsessive-compulsive and tic symptoms of post-strep infections or PANDAS are characterized by acute and dramatic onset with a relapsing-remitting course and significant psychiatric comorbidities, e.g. emotional lability, separation anxiety, nighttime fears and bedtime rituals, cognitive deficits, oppositional behaviors, and motoric hyperactivity. Immunotherapy has been ineffective in non-infectious childhood-onset obsessive-compulsive disorder and also they differ from the infectious type, neuro-anatomically. The size of basal ganglia in the brain has been corresponded with higher anti-streptococcal antibody titers and is an anatomical indication of infectious origin of OCD and tic symptoms. Obviously not everyone infected with Strep A will develop PANDAS, as this condition is rare beyond age 14, with only 1%, also not everyone with this autoimmune condition, will develop OCD, but about 37% and 14% develop tic disorders, ans 81% of the subjects had prior infection with Strep A. These statistic facts will lead us to the existence of a probable genetic or immunity susceptibility as more than half of first-degree relatives of PANDAS subjects have been estimated to suffer from full clinical or subclinical OCD and obsessive-compulsive personality, and about 40% have history of motor or vocal tics. Moreover there is an increased rate of immune-related symptoms and syndromes among primary OCD adult patients in comparison to other anxiety and mood disorder groups. Therefore it could be plausible that some other immune compromise (s) may be responsible for the causation of adolescence and adult onset OCD.
Is OCD different than PANDAS?
OCD is perhaps the most heterogeneous psychiatric disorder, not only in symptomatic presentations, but association with other non-obsessive symptoms such as different motoric or vocal tics in some, different age of onset and the course and progression of the illness. The childhood onset with a more acute onset and exacerbations, though may run a chronic course, is principally associated with tics and tic disorders. The late onset that could start in adolescence and young adulthood run a slower onset and course of illness and is not associated with tics and tic disorders, may run a short or long course. The childhood onset as outlined here so far seems to be definitely an autoimmune disorder with a probable infectious origins, e.g. streptococcal, viral and others. The only homogeneity in OCD seems o be the relative early onset of the illness across its spectrum of any types, so makes it rare to have an onset after the second decade of life, and equality of prevalence between males and females Therefore DSM-5’s clamping all OCD spectrums together as “OCD and its related disorders” will not help to identify the etiology of these disorders so to find the efficient treatments and hopefully one day its prevention. The teen and early adult onset types do not seem to harbor a clear cause such as offending microbial causes, but they may be a byproduct of latent infection(s), long before in childhood, perhaps not severe enough to cause any symptoms then, but later in life. The proof of this may not be shown only by probing for antibodies of the offending agents, but by following any autoimmune traces of the original insults, or genetic mutations that makes this disorder across its spectrum very inheritable.
The candidate genes in adult onset OCD span across different but specific brain regions and neurotransmitters, including “glutamate”, “serotonin”, “dopamine” and else. To this day, no genetic studies including large genome wide association, pooled genetic analysis and metanalytic studies, have been conclusive in identifying the genetic trace of this disorder, despite of its high heritability. Therefore it is prudent as discussed in the case of other sophisticated psychiatric disorders such as schizophrenia and neurodevelopmental disorders to search for genetic mutations such as SNPs (single nucleotide polymorphisms) and CNVs (copy number variations) caused environmentally mostly by microbial invasions.
Dr.Mostafa Showraki, MD, FRCPC Lecturer, School of Medicine, University of Toronto,Author: “ADHD:Revisited” Book/ “adhdrevisited.com”/”medicinerevisited.com”