Obsessive-compulsive disorder (OCD) is a relatively common disorder that can be traced historically, cross-culturally, and across a broad social spectrum. The earliest descriptions of OCD can be found in religious literature, where obsessional fears around religion were commonplace.

In the 14th century, Jean Charlier de Gerson, a French scholar, educator, reformer, and Chancellor of the University of Paris, was concerned with scrupulosity¹ . The term “scrupulosity” referred to obsessive concern with one’s own sins and compulsive performance of religious devotion, where in earlier centuries it encompassed all types of obsessions and compulsions. The term is derived from the Latin “scrupulum,” a sharp stone, implying a stabbing pain on the conscience . The use of the term dates back centuries, with several historical and religious figures suffering from doubts of “sin”, and expressing their obsessional suffering¹.

During the 17th century, fixations and compulsions were frequently characterized as manifestations of religious melancholy. In his comprehensive work, the Anatomy of Melancholy (1621), Oxford Don Robert Burton documented a case stating, “If he be in a silent auditory, as at a sermon, he is afraid he shall speak aloud and unaware, something indecent, unfit to be said.²”

In 1660, Jeremy Taylor, the Bishop of Down and Connor in Ireland, discussed obsessive doubting, using the term “scruples”: “[A scruple] is trouble where the trouble is over, a doubt when doubts are resolved.²” What we now know as OCD was thus then known as scrupulosity.

In a sermon on religious melancholy in 1691, John Moore, the Bishop of Norwich in England, spoke of individuals haunted by “naughty and sometimes blasphemous thoughts [which] start in their minds while they are exercised in the worship of God [despite] all their endeavors to stifle and suppress them… the more they struggle with them, the more they increase².”

In the seventeenth century, obsessions and compulsions were also described as symptoms of melancholy¹. However, the name OCD did not come into being until the 20th century . The first systematic description of OCD was provided by the French psychiatrist Esquirol in 1838³ . In the late 19th century, the German psychiatrist Emil Kraepelin described OCD as a subtype of anxiety disorder⁴ . In the early 20th century, Sigmund Freud proposed that OCD was a defense mechanism against unconscious impulses⁵ .

In the nineteenth century, OCD was recognized as a neurotic illness where the insight was preserved and was distinguished from delusions where insight is absent.

After Esquirol’s (Esquirol, 1772-1840) description of OCD as a form of Monomania, or partial insanity, Dagonet (1823-1902) described that impulsions violentes irresistibles overcomes the will and manifests as obsessions or compulsions. Morel (1809-1837), considered OCD as diseases of the emotions, “delire emotif”, and thought OCD was originating from a pathology of Autonomic Nervous System.

Westpahal in 1877 used the term Zwangsvorstellung (compelled presentation or idea). In Britain the term Zwangsvorstellung was translated as “obsession” and in US it became “compulsion” and the term “Obsessive-compulsive Disorder” emerged as a terminology.

Freud gradually evolved a conceptualization of OCD that influenced and then drew upon his ideas of mental structure, mental energies, and defense mechanisms. In Freud’s view, the patient’s mind responded maladaptively to conflicts between unacceptable, unconscious sexual or aggressive id impulses and the demands of conscience and reality. It regressed to concerns with control and to modes of thinking characteristic of the anal-sadistic stage of psychosexual development: ambivalence, which produced doubting, and magical thinking, which produced superstitious compulsive acts. The ego marshalled certain defenses: intellectualization and isolation (warding off the affects associated with the unacceptable ideas and impulses), undoing (carrying out compulsions to neutralize the offending ideas and impulses) and reaction formation (adopting character traits exactly opposite of the feared impulses). The imperfect success of these defenses gave rise to OCD symptoms: anxiety; preoccupation with dirt or germs or moral questions; and, fears of acting on unacceptable impulses.⁶

In the early 20th century, Sigmund Freud proposed that Obsessive-Compulsive Disorder (OCD) was a defense mechanism against unconscious impulses. According to Freud’s theory of personality, the mind has three dueling forces: the id (unconscious and primitive urges for food, comfort, and sex), the ego (the conscious self that mediates between the id and the superego), and the superego (the internalized moral compass that represents societal norms and values)⁷. Defense mechanisms are unconscious strategies that people use to protect themselves from anxious thoughts or feelings. They become problematic when applied too frequently or for too long.

One such defense mechanism is isolation of affect, which involves detaching emotion from an idea and rendering it unconscious, leaving the idea bland and emotionally flat. It is especially important in OCD, and in non-disordered people, it most often occurs following a traumatic experience⁸.

Obsessive-compulsive disorder (OCD) and obsessive-compulsive-related disorder (OCRD) conditions ( i.e., trichotillomania, hoarding disorder, body dysmorphic disorder, excoriation disorder, Tourette’s syndrome) are psychiatric conditions that are relatively common, distressing to the patient and their family, and negatively impact the functionality and quality of life ⁹, ¹⁰.

In the 1960s and 1970s, behavioral and cognitive-behavioral therapies emerged as effective treatments for OCD ². In the 1980s, the introduction of selective serotonin reuptake inhibitors (SSRIs) revolutionized the treatment of OCD ². Since then, advances in neuroimaging and genetics have led to a better understanding of the neurobiological basis of OCD ².

The symptoms of OCD
Obsessive-compulsive disorder (OCD) and obsessive-compulsive-related disorder (OCRD) conditions are psychiatric conditions that are relatively common, distressing to the patient and their family, and negatively impact the functionality and quality of life.

OCD is characterized by repetitive actions that seem impossible to stop, while OCRD conditions include trichotillomania, hoarding disorder, body dysmorphic disorder, excoriation disorder, and Tourette’s syndrome.

Symptoms of OCD can be either obsessions or compulsions, or both. Symptoms can be mild and gradually progress in severity. Stress worsens the symptoms. Persistent, repeated, and unwanted thoughts, urges, or images that are intrusive, and compulsive or ritualistic behavior to get rid of the thoughts are some of the symptoms of OCD.

The exact cause of OCD is not completely understood, but it may be associated with changes in the chemistry and functioning of the brain, family history, environmental factors such as certain infections, stressful events in life, other mental illness such as depression or anxiety, and substance or alcohol abuse.

If untreated after a prolonged period, OCD may lead to complications such as contact dermatitis from frequent hand-washing, inability to attend work, school, or social activities due to repetitive actions, troubled family and social relationships, poor quality of life, and suicidal thoughts and behavior.

Treatment options for OCD aim at reducing symptoms and may include psychotherapy or medications. Cognitive-behavioral therapy helps a patient to control the symptoms. Exposure and response prevention exposes the patient to the feared object.

 Obsessive Compulsive Disorder: The signatures in the brain
According to Stanford Medicine’s OCD page, a number of researchers have contributed to the hypothesis that OCD is caused by a malfunction in a neuronal loop that runs from the orbital frontal cortex to the cingulate gyrus, striatum (caudate nucleus and putamen), globus pallidus, thalamus, and back to the frontal cortex. Organic damage to these regions can lead to obsessive and compulsive symptoms. The results of neurosurgical treatment of OCD provide strong support for this hypothesis ⁶

Cingulotomy interrupts this loop at the anterior cingulate cortex, thereby disrupting frontal cortical input into the Papez circuit and limbic system, which are believed to mediate anxiety and other emotional symptoms.⁶

Anterior capsulotomy and subcaudate tractotomy are two neurosurgical procedures that can interrupt the fronto-thalamic fibers, which are believed to mediate the obsessive and compulsive components of OCD. According to Baxter et al. in 1992, the hyperactivity observed in this neuronal loop arises due to impaired caudate nucleus function. The impairment allows “worry inputs” from the orbitofrontal cortex to excessively inhibit the inhibitory output from the globus pallidus to the thalamus. The resulting excess in thalamic output then impinges on various brain regions involved in the experience of OCD symptoms, including the orbital frontal region, thus reinforcing hyperactivity in the neuronal loop. ⁶

 Neuropsychological functions in OCD have been extensively investigated. Despite some common findings across studies indicating deficient test performance across cognitive domains with small to medium effect sizes, results remain inconsistent and heterogeneous¹¹. However, recent meta-analyses suggest that these factors may not account for the persistent unexplained variability¹¹. Other potential factors—some of which are unique to neuropsychological testing—received scarce research attention, including definition of cognitive impairments, specificity and selection of test and outcome measures, and their limited ecological validity¹¹. Other moderators, particularly motivational aspects, and metacognitive factors (e.g., self-efficacy) were not previously addressed despite their potential association to OCD, and their documented impact on cognitive function¹¹ .

The neuropsychology of OCD is complex and involves multiple brain regions and neural pathways. Some of the key brain regions and neural pathways that have been implicated in OCD include:

• Cortico-striato-thalamo-cortical (CSTC) circuit: The CSTC circuit is a neural pathway that connects the cortex, basal ganglia, and thalamus. This circuit is involved in the regulation of motor behavior, cognition, and emotion. Dysfunction in the CSTC circuit has been implicated in the pathophysiology of OCD¹².
• Orbitofrontal cortex (OFC): The OFC is a region of the prefrontal cortex that is involved in decision-making, reward processing, and emotional regulation. Dysfunction in the OFC has been implicated in the pathophysiology of OCD ¹³.
• Anterior cingulate cortex (ACC): The ACC is a region of the prefrontal cortex that is involved in cognitive control, emotion, and pain processing. Dysfunction in the ACC has been implicated in the pathophysiology of OCD¹³.
• Basal ganglia: The basal ganglia are a group of nuclei located deep within the cerebral hemispheres. They are involved in the regulation of voluntary motor movements, procedural learning, and cognition. Dysfunction in the basal ganglia has been implicated in the pathophysiology of OCD¹⁴.

CNS and The Pathways in OCD

OCD is a disorder that is characterized by intrusive thoughts and repetitive behaviors. The neurobiology of OCD is still being studied, but it is believed that the disorder is associated with changes in the brain’s circuitry. Specifically, the orbitofrontal cortices and basal ganglia (caudate nucleus) are the most commonly reported areas of structural and functional abnormalities in OCD patients¹⁵, ¹⁶

The cortico-striato-thalamic pathways are believed to be involved in the development of OCD. These pathways are responsible for the regulation of motor and cognitive functions, and they are thought to play a role in the development of compulsive behaviors⁶.

In a meta-analysis of functional neuroimaging studies using inhibitory control tasks, patients with OCD exhibited underactivation in several brain areas, including the rostral and ventral anterior cingulate cortices, bilateral thalamus/caudate, right anterior insula/frontal operculum, supramarginal gyus, and orbitofrontal cortex¹⁷.

It has been suggested that the faulty wiring of the anterior cingulate cortex (ACC) responsible for reward anticipation, decision-making, impulse control, and autonomic functions has been partially responsible for OCD development¹⁸.

In conclusion, OCD is a complex disorder that involves changes in the brain’s circuitry. The orbitofrontal cortices and basal ganglia (caudate nucleus) are the most commonly reported areas of structural and functional abnormalities in OCD patients. The cortico-striato-thalamic pathways are believed to be involved in the development of OCD, and the faulty wiring of the anterior cingulate cortex (ACC) has been suggested to be partially responsible for OCD development ¹²³.

References:

1. The history of OCD | OCD-UK. Accessed November 22, 2023. https://www.ocduk.org/ocd/history-of-ocd/
2. The Anatomy of Melancholy: how Robert Burton helped shape our understanding of the mind. HistoryExtra. Accessed November 22, 2023. https://www.historyextra.com/period/renaissance/robert-burton-anatomy-melancholy-impact-understanding-mind/
3. Berrios GE. Obsessive-compulsive disorder: Its conceptual history in France during the 19th century. Compr Psychiatry. 1989;30(4):283-295. doi:10.1016/0010-440X(89)90052-7
4. Ebert A, Bär KJ. Emil Kraepelin: A pioneer of scientific understanding of psychiatry and psychopharmacology. Indian J Psychiatry. 2010;52(2):191-192. doi:10.4103/0019-5545.64591
5. History. Obsessive-Compulsive and Related Disorders. Accessed November 22, 2023. https://med.stanford.edu/ocd/treatment/history.html
6. Understanding OCD. Obsessive-Compulsive and Related Disorders. Accessed November 22, 2023. https://med.stanford.edu/ocd/about/understanding.html
7. Defense Mechanisms | Psychology Today. Accessed November 22, 2023. https://www.psychologytoday.com/us/basics/defense-mechanisms
8. J Strachey, Freud A. Inhibitions, symptoms and anxiety. In: The Standard Edition of the Complete Psychological Works of Sigmund Freud. The Hogarth Press; 1926:77-175.
9. Brock H, Hany M. Obsessive-Compulsive Disorder. In: StatPearls. StatPearls Publishing; 2023. Accessed November 22, 2023. http://www.ncbi.nlm.nih.gov/books/NBK553162/
10. Storch EA, Lewin AB, eds. Clinical Handbook of Obsessive-Compulsive and Related Disorders: A Case-Based Approach to Treating Pediatric and Adult Populations. Springer International Publishing; 2016. doi:10.1007/978-3-319-17139-5
11. Kashyap H, Abramovitch A. Neuropsychological Research in Obsessive-Compulsive Disorder: Current Status and Future Directions. Front Psychiatry. 2021;12. Accessed November 22, 2023. https://www.frontiersin.org/articles/10.3389/fpsyt.2021.721601
12. Brand J, Reid JM, McKay D. Neuropsychological Assessment of Obsessive–Compulsive Disorder. In: McKay D, Storch EA, eds. Handbook of Assessing Variants and Complications in Anxiety Disorders. Springer; 2013:43-61. doi:10.1007/978-1-4614-6452-5_4
13. Abramovitch A, Abramowitz JS, Mittelman A. The neuropsychology of adult obsessive–compulsive disorder: A meta-analysis. Clin Psychol Rev. 2013;33(8):1163.
14. Fineberg NA, Day GA, Koenigswarter N de, et al. The neuropsychology of obsessive-compulsive personality disorder: a new analysis. CNS Spectr. 2015;20(5):490-499. doi:10.1017/S1092852914000662
15. Exploring the Neurobiology of OCD: Clinical Implications. Accessed November 22, 2023. https://www.psychiatrictimes.com/view/exploring-neurobiology-ocd-clinical-implications
16. Robbins TW, Vaghi MM, Banca P. Obsessive-Compulsive Disorder: Puzzles and Prospects. Neuron. 2019;102(1):27-47. doi:10.1016/j.neuron.2019.01.046
17. Norman LJ, Taylor SF, Liu Y, et al. Error Processing and Inhibitory Control in Obsessive-Compulsive Disorder: A Meta-analysis Using Statistical Parametric Maps. Biol Psychiatry. 2019;85(9):713-725. doi:10.1016/j.biopsych.2018.11.010
18. Vassena E, Deraeve J, Alexander WH. Surprise, value and control in anterior cingulate cortex during speeded decision-making. Nat Hum Behav. 2020;4(4):412-422. doi:10.1038/s41562-019-0801-5