Prevalence of OCD and PTSD has been most extensively studied amongst war veterans and victims. Morina et al. (2016) conducted a study of civilian surviving victims of the Kosovo War searching for evidence of OCD and PTSD symptoms as well as the interconnectedness of these two diseases. They found that 39% were showing symptoms of stress, fear and anxiety and a significant number of subjects tested for either disorder were also predisposed to carry the symptoms of the other. Compared to the general population, a PTSD brain is 47% more likely to develop OCD and patients with obsessive compulsions had an up to 52% likeliness of having had a traumatic event in their life prior to developing OCD. Researchers conducted a Posttraumatic Diagnostic Scale (PDS) questionnaire, an Obsessive-Compulsive Inventory (OCI-R) questionnaire and a Hopkins Symptom Checklist to test for signs of depression. Gender was found to play a significant role in the likeliness of developing obsessive-compulsive symptoms, with 47% of women with a traumatic past event likely to also experience obsessive compulsions, while only one out of four men reported the same. Type and number of traumatic events as well as depression were found not to significantly impact the development of PTSD with either gender. Education was negatively correlated to mental health issues.

Though multiple studies have confirmed the co-occurrence of PTSD and OCD, it is important to remember that as much as these two debilitating mental diseases co-exist or aggravate each other’s symptoms, there are differences scientists and therapists must observe both for accurate diagnosis, as well as for the purpose of applying the adequate medicinal and psychotherapeutic treatments. PTSD and OCD are both characterized by intrusive negative thoughts that may range from absent mindedness, through depressive outlook to the world to aggression towards oneself or others. Both conditions are experienced as an inability to take control of one’s life, thoughts and emotions, triggering erratic, unusual behaviour and mood swings. In both cases, the onset of the symptoms may be sudden, may develop gradually with the early symptoms going unnoticed both for the subject and their family and they may get triggered and activated much later, for example as a delayed response to childhood trauma (McFarlane, 2010b) making it difficult to identify what may have caused them. 

In terms of differences, it was found that the focus of an OCD brain is on a future behaviour or experience, while a PTSD subject is taken back compulsively to the past, reliving over and over the details of their trauma. This directional difference is largely the driver behind the behaviours. OCD patients establish rituals as a means of preventing an imagined threat from happening, despite intellectually being aware that the repetition on its own will not bring the desired outcome or remove the threat. The compulsion however outlaws rationale. Avoidance of triggering circumstances may also be present as a means of sustaining a sense of control. PTSD patients on the other hand avoid situations and people that remind them of the experienced trauma, even when consciously they may be aware of the lack of any connection to the pain they suffered in the past. The repetitive behaviour as such is directed at diminishing and eliminating circumstances and conditions that may take them back to the experience of their trauma. Given the comorbidity of PTSD and OCD and the lifetime prevalence of PTSD ranging from 1% to over 9% in lower-middle to upper-middle income countries (Sareen, 2014) it is perhaps of no surprise that OCD is sometimes developed as a coping mechanism for someone suffering from past trauma they have not been able to overcome (Dinn, Harris and Raynard, 1999).  

The aforementioned study by Cheng et al. (2015) has conducted MRI scans on 3 groups, 30 PTSD subjects, 29 with OCD and 20 with SAD against 30 healthy controls (HC). Brain alterations have been identified in all 3 groups, however in different brain areas and to different degrees.

With the use of VBN technique (Nemoto, 2017) they have examined focal brain differences. That is to say, even though no two brains are exactly the same, healthy brains have the same anatomy, same volume of areas proportionate to the total brain mass, same neurocircuitry and so on. Images obtained with VBN allowed them to see which areas of the brain showed neuroanatomical alterations compared to a healthy brain, the OCD brain vs the PTSD and SAD brain, as well as compared to the rest of the subjects’ own brain. Researchers found that age played no role in the differentiation of the 4 groups. Some of the most evident differences have been observed in the left hypothalamus and left inferior parietal lobule (IPL). The hypothalamus in conjunction with the pituitary gland plays a key role in a number of functions, such as hormone release, temperature control of the body, regulation of emotional response to external and internal stimuli (Flament-Durand, 1980). When damaged, a dysfunction of these roles alone is sufficient to throw off the immune system, cause irregular body temperature and neuroinflammation and alter the patient’s ability to assess and apply appropriate emotional response.

The inferior parietal lobule (IPL) located in the left hemisphere of the brain carries a multimodal property in the sense that it acts as a point of junction and translator of different stimuli, such as visual, sensorimotor, auditory, language, etc. and our brain’s ability to classify and organize things, as well as maintain focus on the task at hand are largely dependent on it (Singh-Curry and Husain, 2009). When damaged, we damage an area responsible for perspective thinking. Arora et al. (2015) argued, that when faced with the need of changing our perspective about something, whether that need is triggered by internal thoughts or external stimuli, due to their exogenous nature these stimuli should prompt an activation of IPL. In case of neural degeneration of this area, the ability to identify thoughts and behaviour that serve the individual may be lost. While an OCD brain is typically able to recognize harming or unwanted behaviour and its main challenges lie in its inability to control it or prevent acting on it, for a PTSD subject the difficulty is in gaining perspective of the entirety of their life and the person is instead consumed by the details and impact of the trauma they suffered.

Hori and Kim’s study (2019) postulates that:

Epidemiological studies have demonstrated that PTSD is associated with significantly increased rates of physical comorbidities in which immune dysregulation is involved, such as metabolic syndrome, atherosclerotic cardiovascular disease, and autoimmune diseases. In line with this, a number of blood biomarker studies have reported that compared to healthy controls, individuals with PTSD exhibit significantly elevated levels of proinflammatory markers, such as interleukin-1β, interleukin-6, tumour necrosis factor-α, and C-reactive protein (p. 143).                                  

It was further proposed that PTSD is connected to physical diseases apparently non-related to the brain, such as obesity, diabetes, autoimmune disease and cardiovascular diseases. These conditions however are known to have inflammatory properties. Interleukin-6 (IL-6) acts both as a pro and anti-inflammatory interleukin, which in this case further complicates matters (Tanaka, Narazaki and Kishimoto, 2014). Patients with PTSD have consistently shown increased levels of pro-inflammatory markers, however the IL-6 in combination with other biomarkers have also generated inflammatory markers below the control groups. Temporality between the occurrence of PTSD and inflammation offers an additional source of debates and poses the need for further research. If inflammation aids the dysregulation of the immune system as well as the development of stress, depression, lack of clarity of thought, etc. it becomes easy to understand how it can also be a contributing factor to the onset of PTSD. Other studies however conducted on women with PTSD have not been able to identify conclusive evidence that there may have been significant differences in the levels of pro-inflammatory markers in those who have been diagnosed with the disease and the healthy control groups.

A study by the Centre for Addiction and Mental Health (CAMH) may be the first to showcase evidence of the relationship between OCD and inflammation, specifically that certain brain areas function differently in OCD (O’Malley, 2017). This poses the inevitable question of how the brain in its entirety works. That is to say, is there a predetermined set of rules and regulations that warrant a healthy normal functioning of this important organ and diseases are the cause of glitches in the system, or is it the alteration from the norm that makes room for diseases to develop? In a case-control study by Attwells et al. (2017b) researchers examined the presence of neuroinflammation in the basal ganglia. The basal ganglia is closely connected to a number of brain areas, including the thalamus. Besides its role in motoric functions, the basal ganglia also play an important role in the regulation of emotions and cognitive functions (Lanciego, Luquin and Obeso, 2012). The thalamus and hypothalamus are part of the diencephalon, which acts as a relay of sensory information and connects the nervous system and endocrine system. When dysregulated or under attack, the affected areas appear to produce an autoimmune-like response to infection. Positron emission tomography (PET) radioligands have been connected to translocator protein (TSPO) with the aim of finding evidence that neuroinflammation causes an increased translocation protein density at the point of microglial activation. Microglial cells act as mediators in the central nervous systems’ (CNS) immune response to infections and inflammations. Though certain limitations have been identified in the use of PET scans and the interpretation of the data, the results have shown clear evidence that when microglial cells are activated, symptoms of OCD, such as distress and anxiety levels have also increased in concordance with greater TSPO distribution volume (V_T) in the orbitofrontal cortex (Setiawan, et al., 2015).      

The study by Nestadt et al. (2010) postulates the existence of genetic contribution to the aetiology of OCD. Besides the biological components (commonality of compulsive behaviour in a number of psychiatric conditions such as Tourette syndrome, schizophrenia, Parkinson’s disease, etc., as well as prevalence of altered metabolic activity in brain areas involved in higher cognition and regulation of emotions) it has been observed that a significant number of OCD subjects had the condition running in the family. Different family studies have produced different results on occurrence of OCD amongst first degree relatives. An earlier research by Lenane et al. (1990) on young subjects reported a 7% to 15% chance of the child developing OCD if they had a parent or a sibling diagnosed with the condition or showing symptoms of the diseases. A later study by do Rosario-Campos et al. (2005) observed a 32.5% ratio. Though the two studies report significantly different ratios, something that could be attributed to questionnaires increasing in precision over time, or to the development of our understanding of the condition by scientific bodies, they are very similar in that onset at an early age is a strong indicator of genetic inheritance. First tests on twins date back to the 1930s (Lewis, 1936) and since then scientists have allocated a special attention to this subgroup, which at an 80% prevalence amongst MZ twins comes to no surprise. Serotonin has been closely linked to OCD, as it plays an important role in the communication between different parts of the brain. When the serotonin transporter called the SERT gene is impacted, it contributes to the breakdown of the communication (Murphy, Lerner, Rudnick, and Lesch, 2004). As such, serotonin studies have been the focal point of research in a context where amongst twins and siblings the serotonin transporter coding variant was suspected to have been increased by the close genetic similarity. Despite of clear evidence of genetic predisposition and inheritance of OCD between close family members and twins, the less than 100% prevalence amongst MZ twins is also an indicator of the role of both nature and nurture, in other words environmental factors also playing an important role in the likeliness of someone developing compulsive disorders (Hemmings and Stein, 2006).  

According to the American Psychological Association (APA), “Trauma is an emotional response to a terrible event like an accident, rape or natural disaster. Immediately after the event, shock and denial are typical” (Berman, 2019). The WHO World Mental Health (WMH) surveyed 24 countries for a total of 29 different types of lifetime and randomly selected traumas with the aim of identifying a link between PTSD and different traumatic event types (Kessler et al., 2017). A total of 68,894 adult subjects were interviewed twice, once for a significant life altering trauma and a second for a random trauma type, evaluated as less likely to mark for lifetime. Over a staggering 70% of the respondents reported having experienced or witnessed a traumatic event and over 30% exposed to four or more. Yet according to the World Health Organization (WHO) statistics, less than 4% of the population of the world suffers from PTSD (WHO, 2013). Though these numbers vary across geographies, genders and cultural groups and statistics change as more data is collected, they pose the question of why and how only a relatively small percentage of people exposed to traumas develop a mental health disorder as their consequence. Research shows that predisposition to anxiety, stress, fear and depression tend to run in the family. Cornelis et al. (2010) points out that while genetics have been long observed to play a role in the development of PTSD, the genetic variants that may act as a root cause are still in question. Much like with OCD, PTSD studies with MZ and DZ twins have shown a 30% to 40% probability of inheritability compared to the general population. Predisposition to PTSD has been tested from the perspective of heritability of PTSD and heritability of traumatic events. Studies have shown that the human body is an active participant in the selection and processing of the environmental stimuli (Kremen, Koenen, Afari, and Lyonse, 2011).  That is to say, in a process called gene-environment covariance (Kendler and Eaves, 1986) the human organism makes choices of what it wants to get exposed to and what stimuli or circumstances will get filtered out. In the 60s psychologists have stressed the importance of a person’s role in shaping their environment, instead of just being a passive receiver of their circumstances. By the 70s the focus has shifted through twin studies to the role of genetics and over the decades an increasing amount of evidence was collected on “the causal mechanisms, which indicate genetic control over environmental exposure” (Jaffee and Price, 2007). As such, heritability of PTSD, similarly to vulnerabilities to other disorders amongst twins has provided and continues to provide scientists areas of research that bring us closer to an understanding of underlying biological and genetic mechanisms of inheritable mental and physical conditions.