OCD: General Neurological Abnormalities and Possible Treatment Options

Obsessive-compulsive disorder (OCD) is a neuropsychiatric disorder. As the name provides, it has two components: obsessiveness or repeated thoughts and compulsiveness or repeated behavior. These two components seem to work together to form this disorder; obsessiveness may stem from high anxiety levels and to reduce this type of stress, repetitive behavior or action is done to reduce the anxiety and reduce the obsessiveness (Sun, et al., 2019). This disorder is known to possibly be genetic, as some evidence shows that people with first degree OCD relatives have a higher risk of contriving OCD themselves (“Obsessive-Compulsive Disorder. (n.d.)”). Like many other disorders, OCD can be subdivided into different types: contamination and washing; doubts about accidental harm and checking; symmetry, arranging, and counting; and unacceptable taboo thoughts and mental rituals (“Symptoms of OCD”. (n.d.). Because there are so many types of different OCDs, the underlying neurological reasons are not clear but there are some theories regarding the general neurological abnormalities that might be the root of this disorder. In this paper, mechanistic theories and neurological abrasions/ abnormality patterns, will be discussed, some experiments based on this order will be discussed and finally, some possible medications that may alleviate the symptoms of OCD will be discussed.

Much of the noninvasive neurological imaging of people with OCD show abnormal patterns in the CSTC loops or corticostriatal-thalamocortical (CSTC) loops. These circuits including the orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), ventral striatum, and mediodorsal (MD) thalamus. First, let’s discuss the OFC. The orbitofrontal cortex (OFC) is located in the prefrontal cortex of the frontal lobe. The (OFC) seems to control cognitive behavior, meaning, the ability to combine emotions, thoughts and motor responses to create a goal-motivated action (Torregrossa, et al.,2008). Lesions to the OFC are known to cause a reversal-learning deficit, meaning, it causes learning from experiences to happen slowly, and cause repetitive behaviors or habits even when there is no reward from them (Torregrossa, et al., 2008). The Anterior cingulate cortex (ACC) lies near the front of the corpus callosum. It connections the prefrontal cortex to the limbic system, in other words, the cognitive information with the emotional information. There are three major portions of ACC: the emotional or limbic component, cognitive component, and motor component. This might explain why people with OCD may also have been triggered due to trauma thus this emotional factor is showcased through behavior or actions (Yücel, et al. 2003.). The ventral striatum connects the frontal orbital region to the basal ganglia. In people without OCD, the OFC and ACC give input and control striatal activity by a balance of excitatory input and inhibitory input. Medium spiny neurons (MSNs) are excitatory and (PV)-positive interneurons keep them inhibited and controlled. In people with OCD, when their striatum has some deficit, both ACC, OFC and striatal regions are hyperactive. This may be because of the decrease in the number or function of PV interneurons that usually inhibit these Medium spiny neurons from excitation, and because it is a loop from ACC and OFC to the striatum to the thalamus and back, activity is heightened in all regions (Burguière, et al., 2015). Some experiments have been done that show that SAPAP3 is a gene located at the postsynaptic density or PDS at the excited synapses (Ting & Feng, 2011). It was found that this gene was the only family member gene strongly shown in the striatum. The study found that deleting this genetic allele in mice has them develop behavioral problems due to heightened anxiety which caused them to repetitive groom themselves to the point of facial hair loss and skin abrasions around those over groomed areas. These mice without the SAPAP3 gene were also, evidently, were found to have problems with glutamate transmission at cortico-striatal synapses or where the OFC/ACC meet the striatum in the loop (Ting & Feng, 2011). This specific problem regarding the neurotransmission of glutamate was solved when this gene was put in specifically back to the striatum. This shows how sensitive this entire circuitry is structured. The other problem, the overgrooming problem and high anxiety were alleviated with repeated administration of fluoxetine, a common SSRI (Selective Serotonin Re-uptake Inhibitor) (Ting & Feng, 2011). How this works will be discussed later in the paper. The mediodorsal (MD) thalamus seems to be involved with memory and the limbic system which includes the amygdala. The medial, lateral prefrontal and orbitofrontal (OFC) cortices, gives information to the MD and the MD gives information back to the medial prefrontal cortex (Mitchell, et al., 2013).

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In summary, possible problems to the corticostriatal-thalamocortical (CSTC) circuits that can cause OCD or OCD like behaviors include the imbalance of serotonin, dopamine, and glutamate. A person without OCD would have their corticostriatal-thalamocortical (CSTC) circuits follow in the following order. First, glutamate is transmitted from the cortex area which consists of the OFC and ACC to the striatum which has the medium spiny neurons (MSNs) and (PV)-positive interneurons. Second, GABA affects the basal ganglia and then information is projected to thalamic regions. Finally, glutamate is projected back to the thalamus which goes back to the back to the cortex (Ahmari, et al., 2015). However, people with OCD showcase problems in any area of this pathway. Although much evidence supports that problems to the corticostriatal-thalamocortical (CSTC) circuits cause OCD, new evidence shows something more specific. Human OCD imaging findings show that some early models of basal ganglia circuitry may propose that the high activity of the orbitofrontal-subcortical loops, may be caused by a disruption in the balance of activity through these opposing ganglia pathways (Ting & Feng, 2011).

Most people with OCD are prescribed with SSRIs or Selective serotonin reuptake inhibitors as their first line of medication alongside with Cognitive Behavioural Therapy (CBT). This medication, in simple terms, increases the effectiveness of natural serotonin by blocking reuptake from occurring at the presynaptic neuron head. There are different types of SSRIs but the one most used on humans with OCD is called Fluoxetine (Prozac). SSRI are usually used for people with anxiety, depression and panic disorders. This may be the first line of medication for OCD patients as it can reduce the anxiety component of the disorder which stems from mainly the limbic system. Unfortunately, SSRIs do not have a high success rate as only 40-60% of patients respond poorly to this treatment. This may be due to the fact that there are various types of OCDs and that also may play a part in how impactful this treatment might be the specific OCD patient. However, the future for OCD treatment is not bleak, some evidence shows some promising results regarding glutamate neurotransmission within the CSTC pathways. The drawback here is that there is not enough specific evidence on where exactly the glutamate transmission problem area is located. Knowing this could help scientists find a way to reduce compulsive actions or behaviors (Pittenger & Bloch, 2014). Some new evidence was found regarding glutamic neuronal transition which suggests that the amygdala, specifically the basolateral amygdala (BLA), might be the place to focus on in order to reduce especially compulsive or repetitive behaviors. Data from this specific study claims that the BLA consists of about 90% of glutamatergic neurons. Thus, this might be the next area to focus on to reduce the compulsive component of OCD (Sun, et al. 2019).

Overall, obsessive-compulsive disorder (OCD) seems to have two overbearing components: obsessiveness, which is more emotion and anxiety based and compulsiveness, which are the repetitive motor/behavioral actions done to alleviate the anxiety. For the Obsessive component, SSRIs along with CBT seems to work best with the knowledge existing about OCD, for the compulsive component however; glutamate transmission seems to be the more promising answer for that component. Further studies on OCD can pave the path to more treatments with higher success rates. The key to this may be to target not one but both of these components.

References

1. Ahmari, S. E., & Dougherty, D. D. (2015, August). DISSECTING OCD CIRCUITS: FROM ANIMAL MODELS TO TARGETED TREATMENTS. Retrieved November 25, 2019, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4515165/.
2. Burguière, E., Monteiro, P., Mallet, L., Feng, G., & Graybiel, A. M. (2015, February). Striatal circuits, habits, and implications for obsessive-compulsive disorder. Retrieved November 25, 2019, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4293232/.
3. Mitchell, A., S, A., Chakraborty, A., & Subhojit, A. (2013, July 17). What does the mediodorsal thalamus do? Retrieved November 25, 2019, from https://www.frontiersin.org/articles/10.3389/fnsys.2013.00037/full.
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6. Sun, T., Song, Z., Tian, Y., Tian, W., Zhu, C., Ji, G., … Zhang, Z. (2019, February 26). Basolateral amygdala input to the medial prefrontal cortex controls obsessive-compulsive disorder-like checking behavior. Retrieved November 25, 2019, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6397577/.
7. Symptoms of OCD. (n.d.). Retrieved November 25, 2019, from https://www.ocdtypes.com/ocd-symptoms.php.
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