Where OCD Leads My Mind
- Cecelia Ky-Lan Do
- 2 days ago
- 14 min read
by Artemis Christoforatos
art by Luciana Piro

I am eating almonds when I realize that this bowl has been touched before. If the bowl has been touched, it has been contaminated. Did the hand I am using to eat, my clean hand, touch the bowl, or just the almonds? If my hand has touched the bowl, then it has been contaminated. Did it touch my lips in the process of putting the almond to my mouth? If my hand has touched my lips, then my lips are contaminated. Did my tongue touch my lips while placing the almond in my mouth? If my tongue has touched my lips then my tongue is contaminated, which makes my mouth contaminated, which makes my saliva contaminated, which makes my esophagus contaminated, which makes my stomach and intestines contaminated, and I can feel it spreading, I can feel it oozing through my mouth to my bloodstream, from my arms to my fingers, and I can almost smell my body, a stinking mass of rotting flesh. I put the almonds down. Gangrene in my legs and sepsis in my liver and poison in my blood and maggots crawling through my brain. Did it touch the bowl or not? I am retracing my movements, clean hand to almonds, dirty hand on the bowl, I am putting my fingers down, I don’t remember, I can’t remember, I think I did, I feel it, I feel the place my finger touched like a bruise, I definitely did. I get up. I am never going to get over this, I am always going to feel contaminated and this feeling is not going to go away and it was daring enough using a dirty bowl but now things are out of control and there are maggots in my brain or there will be soon enough if I keep going like this and I will be more careful about the bowls and I will wash them myself every time beforehand. I pull out my mouthwash. I wash my hands. I wash the handle and close the faucet. I wash another bowl. I transfer the almonds. I wash my hands again. I wash the first bowl. By then, I’m not even hungry anyways, and the almonds taste like paste. I don’t think I remember what they felt like in the first place.
Those who research and treat obsessive compulsive disorder don’t really know where intrusive thoughts, like the images of maggots in my brain or my hand being “contaminated,” come from. They do know that everyone experiences random intrusive thoughts, such as wondering whether the stove was turned off or the urge to push someone off the subway platform (without actually wanting to do so) [1, 2]. However, those with OCD seem to find these thoughts more distressing, and respond to them more intensely. The intrusive thoughts may be random originally, but someone with OCD would have environmental triggers that lead to reactive recurrence of the thoughts (for example, my hand maybe touching my lips leading to intrusive thoughts of my body rotting or feeling contaminated) [1, 2]. Intrusive thoughts in OCD are ego-dystonic, meaning they go against your values: someone with OCD who worries that they may have harmed someone, for example, is actually less likely to have harmed someone than a member of the general population, and their strong reaction to the thought is likely partly driven by their strong moral opposition to the idea [3, 4]. Because of the high prevalence of intrusive thoughts in the non-clinical population, it is believed that the issue with OCD is not necessarily the presence of obsessions, but the reaction to them: the compulsions [1, 5].
Therefore, although scientists don’t know why I responded so reactively to the possibility of contaminated hands, they would be able to say with more confidence that as I ate the almonds, my responses to my intrusive thoughts—my tracing of previous steps, my self-reassurance, my eventual physical “undoing” of contamination—happened because of dysfunction in a circuit of neurons that make decisions about behavior. This circuit consists of neural pathways through the cerebral cortex, striatal areas, thalamus, and back to the cortex, hence its name: the cortico-striato-thalamo-cortical (CSTC) circuit. Connections between the implicated brain regions modulate goal-directed behavior, particularly movement-related and attentional allocation behaviors [6, 7]. Broadly, the circuit helps us judge if we should do something, whether that be cognitive or physical: do I continue eating the almonds, or wash my hands? And, is it worth it to continue to spend time thinking about whether I touched the bowl or my mouth with my hands? Every one of these thoughts is a decision that the CSTC circuit would approve, even decisions to engage in cognitive activities like reassurance that then feed into other compulsions.

In the simplest representation of the CSTC circuit, neural communication, between brain areas like the cortex and striatum, occurs via direct or indirect pathways [8, 9].
In the direct pathway, each step of the circuit amplifies another, leading to a net excitatory effect. First, neurons in the cortex, where higher brain functions such as judgment and decision-making originate, release the excitatory neurotransmitter glutamate to signal the striatum, a subcortical area within the basal ganglia [10]. This is where the “obsession” part of OCD comes in: a distressing thought happens, and the decision to either perform or resist a compulsion follows. To decide what that response should be, the cortex figuratively asks other parts of the brain for their opinion.
The striatum is the second stop in the pathway. Along with other basal ganglia regions, the striatum communicates with the thalamus, where information from sensory neurons about what you see, feel, or hear converges [8]. The striatum, when excited, causes less dopamine release to the thalamus [8, 11]. Dopamine usually dampens thalamic activity, but in the direct pathway, the now active thalamus can provide environmental input that can strengthen the cortex’s original thoughts on conditions in the environment, such as information about what my hands may have touched, or information that might help the thought transition to action, like how far I would need to walk to get to a sink to wash my hands [6].
Should I have suppressed my hand-washing or body-checking impulses, a different, indirect loop would be responsible for giving my cortex “negative feedback” [6]. The indirect pathway shares steps with the direct loop, but has a key detour: after the cortex excites the striatum, more dopamine is produced, which inhibits the thalamus and gives the cortex less information [8]. Thus, the activation of the indirect path tells the brain to “apply the brakes” to whatever compulsion it wants to do.
The complexity of decision-making arises because direct and indirect pathways are activated simultaneously: many different cortical thoughts can trigger a path [8]. It is the interplay of these continuous manipulations of excitation and inhibition that makes the circuit effective in a world where decisions are made by bringing together scores of different information, from personal desire to outside consequences to motor ability. This also means that differences in any stop of either loop of the circuit may lead to excessive obsessive and compulsive behavior [12].
When I was seventeen, I participated in a handful of MRI studies that sought to add to an existing body of literature about how OCD appears in the brain. Functional and structural magnetic resonance imaging (fMRI and sMRI) are often used to study structural and functional presentations of brain-based conditions in subjects with diagnoses like OCD, schizophrenia, or depression in comparison to neurotypical participants. Such studies have revealed that different areas in the CSTC circuit may inform different types of behavior and judgments [13, 14]. Researchers aim to elaborate on the general CSTC circuit framework to identify clearer individual routes that shed light on the factors that can play into compulsive acts: emotion, memory, reward, movement, and sensory input [14–16]. Each route runs through cortical and striatal areas as expected, but because each differs slightly from the other, distinguishing them can be useful.

For example, the “affective” route makes judgments based on emotion and reward through the anterior cingulate cortex (ACC) and the ventromedial prefrontal cortex (vmPFC) [17]). The ACC acts like a judge, interrogating its environment to gain evidence and make decisions, while the vmPFC acts like a translator, interpreting social and emotional cues from its surroundings [18, 19]. fMRI shows that the affective circuit pathway makes an additional stop at the nucleus accumbens, which evaluates whether actions will lead to positive or negative outcomes [20, 21]. Likewise, the dorsal cognitive circuit implicates working memory to inform decision making: it starts in the vmPFC and loops through the caudate nucleus, which assesses environmental stimuli based on previous memories [14, 22].
These sub-circuits all happen concurrently or in quick succession, more like a mixing board of inputs than a singular switch: the anxious element, the motor excitation, and the habitual and memory-based knowledge responses all influence a behavior, or, in the case of OCD, a compulsion [12].
The possibility of the almond bowl is scary, and last time I washed my hands things turned out okay, and I am used to washing my hands whenever a scary thought pops up, and I can sort of feel the contamination, so it must be real, and with all these elements coming together to convince me, without even realizing I have a choice, I find myself at the sink again and again.
Various studies show structural and functional differences in cortical areas such as the ACC and vmPFC in patients with OCD, suggesting that the processes in the above subcircuits may require more or less sensory or emotional input than average to occur. As a result, obsessive and compulsive symptoms feel more intense or happen faster than in the general population [23–25]. While everyone, therefore, can have intrusive thoughts, the “stickiness” of those thoughts in the vmPFC or OFC might be what makes compulsive responses more likely to occur in OCD.
It may be that my anterior cingulate cortex, my putamen, my ventromedial prefrontal cortex, and my thalamus stacked the odds against me, odds that got worse and worse as I gave in to my compulsions more and more. But that is not the end of my story.
Fifty years ago, Eric Kandel poked a sea slug (Aplysia) again and again until it stopped caring and stopped moving, thus introducing a phenomenon called “habituation” to the field of neuroscience. The first time Kandel and colleagues applied a tactile stimulus to the siphon in the underbelly of the slug, its gills retracted strongly in defensive reflex, but as the stimulus continued, they moved less and less [26]. Recordings of the cells of the slug’s neurons demonstrated that in each session, the sensory neurons activated simply had less neurotransmitter to release to a postsynaptic motor neuron; the neuron physically could not be stimulated at the same strength indefinitely, which Kandel termed short-term depression [26].
I don’t know where my OCD came from. Was it a faulty brain? Was it genetics? One of the simplest ways to study fear consolidation in the lab is to shock a mouse repeatedly while playing a tone, until they freeze every time the tone is played. Like a lab mouse, was it simple fear conditioning guiding my actions, developing a false association between doing a compulsion and safety from a feared outcome [27]? For whatever reason, my intrusive thoughts stuck, and I found my life turned into an endless spiral of compulsions. But just as the slug stopped engaging its defense mechanisms, a mouse in a lab can go through fear extinction, where the more a tone is played without consequence, the less it freezes [27]. When Kandel poked the slug, he showed that with increasing exposure to a stimulus, your neurons will fire less in frequency and intensity [28]. He also demonstrated that by not engaging in the compulsions that guide your every day, habituation will extend beyond the training sessions in which your neurons are prodded to exhaustion, and even the first time a stimulus is administered, they will reduce their firing rate and strength [29]. All the learning you first did to associate a trigger with a compulsion strengthens the related neural synapses for that compulsion to make it almost automatic, but updating this information, changing these associations, challenges that response [30]. Your brain cannot remain in active engagement of the sympathetic nervous system long-term, and its guard will begin to fall [31].
This is the principle of exposure and response prevention (ERP) therapy. ERP tells you, paradoxically, that to face your fears in a way that makes you as distressed as possible is the fastest way to stop being scared. The more exposure without the compulsive response to alleviate your fear, the less powerful that fear will be [32, 33]. Various pharmacological methods can be implemented to alleviate the anxiety from the stimulus exposure, to ease the plausibility of intrusive or illogical thoughts, or to encourage and increase the brain’s plasticity. Antidepressants such as serotonin reuptake inhibitors (SRIs) and antipsychotics are often used, and there have even recently been experimental studies on ketamine and psilocybin, a psychedelic mushroom compound [34, 35]. But ultimately, the treatment for OCD involves veering off the pathways your compulsive responses have developed over time, pushing your neurons to branch past their worn out paths.

And that is how I find myself staring at a toilet lid, a timer facing away from me on the sink, my hands pressed against off-white porcelain. There are toilet germs from when the toilet was flushed, they sprayed everywhere, and people touched this toilet lid after being exposed to urine and feces, and so you are exposed too. They are sinking through your hands up your skin and into your bloodstream, and you cannot undo this. The toilet was cold at first, but I’ve been here long enough that I don’t notice it anymore. I do notice the firmness of the material, the pressure of my hands against the seat, and the soreness in my back from bending over. There is a lump in my throat, making it hard to breathe. You are not allowed to wash your hands after touching this toilet. You will touch other things, and you will spread the feces across the unit, and people will die, and it will be your fault. My chest is tight. The timer makes an almost imperceptible clicking noise. There are people talking outside. Someone flushes another toilet. You will die. They will die. You will never be able to concentrate on anything ever again except the fact that you have feces on your hands and you are spreading biohazardous material everywhere. It is chilly in here. You are making the world a dangerous place. My throat hurts, but not as much, and my chest is okay. When I am sure (but not too sure) that my anxiety has fallen by half, I straighten up, stop the timer, and touch my clothes to spread the germs.
Yesterday was just a little easier than last week, this morning was better than yesterday, and so an hour later, with hands on the toilet, timer in the background, I’m back.
REFERENCES:
1. Berry, L.-M., & Laskey, B. (2012). A review of obsessive intrusive thoughts in the general population. Journal of Obsessive-Compulsive and Related Disorders, 1(2), 125–132. https://doi.org/10.1016/j.jocrd.2012.02.002
2. Rachman, S., & de Silva, P. (1978). Abnormal and normal obsessions. Behaviour Research and Therapy, 16(4), 233–248. https://doi.org/10.1016/0005-7967(78)90022-0
3. Audet, J.-S., Aardema, F., & Moulding, R. (2016). Contextual determinants of intrusions and obsessions: The role of ego-dystonicity and the reality of obsessional thoughts. Journal of Obsessive-Compulsive and Related Disorders, 9, 96–106. https://doi.org/10.1016/j.jocrd.2016.04.003
4. Cervin, M. (2023). Obsessive-Compulsive Disorder: Diagnosis, Clinical Features, Nosology, and Epidemiology. Psychiatric Clinics of North America, 46(1), 1–16. https://doi.org/10.1016/j.psc.2022.10.006
5. Radomsky, A. S., Alcolado, G. M., Abramowitz, J. S., Alonso, P., Belloch, A., Bouvard, M., … Wong, W. (2014). Part 1—You can run but you can’t hide: Intrusive thoughts on six continents. Journal of Obsessive-Compulsive and Related Disorders, 3(3), 269–279. https://doi.org/10.1016/j.jocrd.2013.09.002
6. Calzà, J., Gürsel, D. A., Schmitz-Koep, B., Bremer, B., Reinholz, L., Berberich, G., & Koch, K. (2019). Altered Cortico–Striatal Functional Connectivity During Resting State in Obsessive–Compulsive Disorder. Frontiers in Psychiatry, 10, 319. https://doi.org/10.3389/fpsyt.2019.00319
7. Zhu, Y., Jiang, X., & Ji, W. (2018). The Mechanism of Cortico-Striato-Thalamo-Cortical Neurocircuitry in Response Inhibition and Emotional Responding in Attention Deficit Hyperactivity Disorder with Comorbid Disruptive Behavior Disorder. Neuroscience Bulletin, 34(3), 566–572. https://doi.org/10.1007/s12264-018-0214-x
8. Ahmari, S. E., & Dougherty, D. D. (2015). Dissecting Ocd Circuits: From Animal Models to Targeted Treatments. Depression and Anxiety, 32(8), 550–562. https://doi.org/10.1002/da.22367
9. Karas, P. J., Lee, S., Jimenez-Shahed, J., Goodman, W. K., Viswanathan, A., & Sheth, S. A. (2019). Deep Brain Stimulation for Obsessive Compulsive Disorder: Evolution of Surgical Stimulation Target Parallels Changing Model of Dysfunctional Brain Circuits. Frontiers in Neuroscience. https://doi.org/10.3389/fnins.2018.00998
10. Chantranupong, L., Beron, C. C., Zimmer, J. A., Wen, M. J., Wang, W., & Sabatini, B. L. (2023). Dopamine and glutamate regulate striatal acetylcholine in decision-making. Nature, 621(7979), 577–585. https://doi.org/10.1038/s41586-023-06492-9
11. Rocha, G. S., Freire, M. A. M., Britto, A. M., Paiva, K. M., Oliveira, R. F., Fonseca, I. A. T., … Cavalcanti, J. R. L. P. (2023). Basal ganglia for beginners: the basic concepts you need to know and their role in movement control. Frontiers in Systems Neuroscience, 17, 1242929. https://doi.org/10.3389/fnsys.2023.1242929
12. Lee, S. W., Song, H., Jang, T. Y., Cha, H., Kim, E., Chang, Y., & Lee, S. J. (2022). Aberrant functional connectivity of neural circuits associated with thought-action fusion in patients with obsessive–compulsive disorder. Psychological Medicine, 52(11), 2106–2115. https://doi.org/10.1017/S0033291720003980
13. Perera, M. P. N., Gotsis, E. S., Bailey, N. W., Fitzgibbon, B. M., & Fitzgerald, P. B. (2024). Exploring functional connectivity in large-scale brain networks in obsessive-compulsive disorder: a systematic review of EEG and fMRI studies. Cerebral Cortex (New York, NY), 34(8), bhae327. https://doi.org/10.1093/cercor/bhae327
14. Tomiyama, H., Murayama, K., Nemoto, K., Hasuzawa, S., Mizobe, T., Kato, K., … Nakao, T. (2022). Alterations of default mode and cingulo-opercular salience network and frontostriatal circuit: A candidate endophenotype of obsessive-compulsive disorder. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 116, 110516. https://doi.org/10.1016/j.pnpbp.2022.110516
15. Liu, R., Zhang, F., Wang, P., Luo, J., Liu, Y., Huang, K., … Li, Z. (2025). Unveiling anomalies in visual processing regions in obsessive-compulsive disorder: evidence from gray matter volume and functional connectivity analyses. Brain Imaging and Behavior. https://doi.org/10.1007/s11682-025-01039-0
16. Zhao, Q., Xu, T., Wang, Y., Chen, D., Liu, Q., Yang, Z., & Wang, Z. (2021). Limbic cortico-striato-thalamo-cortical functional connectivity in drug-naïve patients of obsessive-compulsive disorder. Psychological Medicine, 51(1), 70–82. https://doi.org/10.1017/S0033291719002988
17. Hiser, J., & Koenigs, M. (2018). The multifaceted role of ventromedial prefrontal cortex in emotion, decision-making, social cognition, and psychopathology. Biological psychiatry, 83(8), 638–647. https://doi.org/10.1016/j.biopsych.2017.10.030
18. Monosov, I. E., Haber, S. N., Leuthardt, E. C., & Jezzini, A. (2020). Anterior cingulate cortex and the control of dynamic behavior in primates. Current biology : CB, 30(23), R1442–R1454. https://doi.org/10.1016/j.cub.2020.10.009
19. Schneider, B., & Koenigs, M. (2017). Human lesion studies of ventromedial prefrontal cortex. Neuropsychologia, 107, 84–93. https://doi.org/10.1016/j.neuropsychologia.2017.09.035
20. Iyer, E. S., Vitaro, P., Wu, S., Muir, J., Tse, Y. C., Cvetkovska, V., & Bagot, R. C. (2025). Reward integration in prefrontal-cortical and ventral-hippocampal nucleus accumbens inputs cooperatively modulates engagement. Nature Communications, 16, 3573. https://doi.org/10.1038/s41467-025-58858-4
21. Zhou, K., Xu, H., Lu, S., Jiang, S., Hou, G., Deng, X., … Zhu, Y. (2022). Reward and aversion processing by input-defined parallel nucleus accumbens circuits in mice. Nature Communications, 13, 6244. https://doi.org/10.1038/s41467-022-33843-3
22. Nakagawa, K., Cheong, Y., Lee, S., Habata, K., Kamiya, T., Shiotsu, D., … Jung, M. (2023). Region-based analysis of sensory processing using diffusion tensor imaging. PLOS ONE, 18(4), e0284250. https://doi.org/10.1371/journal.pone.0284250
23. Ahmari, S. E., & Rauch, S. L. (2022). The prefrontal cortex and OCD. Neuropsychopharmacology, 47(1), 211–224. https://doi.org/10.1038/s41386-021-01130-2
24. Apergis-Schoute, A. M., Bijleveld, B., Gillan, C. M., Fineberg, N. A., Sahakian, B. J., & Robbins, T. W. (2018). Hyperconnectivity of the ventromedial prefrontal cortex in obsessive-compulsive disorder. Brain and Neuroscience Advances, 2, 2398212818808710. https://doi.org/10.1177/2398212818808710
25. Long, J., Luo, L., Guo, Y., You, W., Li, Q., Li, B., … Gong, Q. (2021). Altered spontaneous activity and effective connectivity of the anterior cingulate cortex in obsessive–compulsive disorder. Journal of Comparative Neurology, 529(2), 296–310. https://doi.org/10.1002/cne.24948
26. Kandel, E. R. (1970). Nerve Cells and Behavior. Scientific American, 223(1), 57–71.
27. Lai, C. S. W., Adler, A., & Gan, W.-B. (2018). Fear extinction reverses dendritic spine formation induced by fear conditioning in the mouse auditory cortex. Proceedings of the National Academy of Sciences, 115(37), 9306–9311. https://doi.org/10.1073/pnas.1801504115
28. Marquez-Legorreta, E., Constantin, L., Piber, M., Favre-Bulle, I. A., Taylor, M. A., Blevins, A. S., … Scott, E. K. (2022). Brain-wide visual habituation networks in wild type and fmr1 zebrafish. Nature Communications, 13(1), 895. https://doi.org/10.1038/s41467-022-28299-4
29. Kohashi, T., Lube, A. J., Yang, J. H., Roberts-Gaddipati, P. S., & Carlson, B. A. (2021). Pauses during communication release behavioral habituation through recovery from synaptic depression. Current Biology, 31(14), 3145-3152.e3. https://doi.org/10.1016/j.cub.2021.04.056
30. Stephenson, C., Philipp-Muller, A., Moghimi, E., Nashed, J. Y., Cook, D. J., Shirazi, A., … Alavi, N. (2025). Effects of cognitive behavioural therapy and exposure–response prevention on brain activation in obsessive–compulsive disorder patients: systematic review and meta-analysis. European Archives of Psychiatry and Clinical Neuroscience, 275(5), 1491–1507. https://doi.org/10.1007/s00406-024-01852-6
31. Olbrich, H., Jahn, I., Stengler, K., Seifritz, E., & Colla, M. (2022). Heart rate variability in obsessive compulsive disorder in comparison to healthy controls and as predictor of treatment response. Clinical Neurophysiology, 138, 123–131. https://doi.org/10.1016/j.clinph.2022.02.029
32. McGuire, J. F., Orr, S. P., Wu, M. S., Lewin, A. B., Small, B. J., Phares, V., … Storch, E. A. (2016). Fear Conditioning and Extinction in Youth with Obsessive-Compulsive Disorder. Depression and Anxiety, 33(3), 229–237. https://doi.org/10.1002/da.22468
33. Trent, E. S., Zhou, R. J., Mammo, L., Goodman, W. K., & Storch, E. A. (2025). High intensity approaches to exposure and response prevention for obsessive-compulsive disorder. Behavioural Brain Research, 481, 115427. https://doi.org/10.1016/j.bbr.2025.115427
34. Beaglehole, B., Glue, P., Neehoff, S., Shadli, S., McNaughton, N., Kimber, B., … Hughes-Medlicott, N. J. (2025). Ketamine for treatment-resistant obsessive-compulsive disorder: Double-blind active-controlled crossover study. Journal of Psychopharmacology, 39(1), 23–28. https://doi.org/10.1177/02698811241301215
35. van Roessel, P. J., Grassi, G., Aboujaoude, E. N., Menchón, J. M., Van Ameringen, M., & Rodríguez, C. I. (2023). Treatment-resistant OCD: Pharmacotherapies in adults. Comprehensive Psychiatry, 120, 152352. https://doi.org/10.1016/j.comppsych.2022.152352


