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Obsessive-Compulsive-Disorder; Pathophysiology is Not that Obscure

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Obsessive-Compulsive-Disorder is an anxiety disorder characterized by persistent obsessions (intrusive, repetitive thoughts) and compulsions that are a means to 'resolving' those obsessions and / or reinforcing the significance of them. OCD patients typically have a strong sense of moral obligation and reject immoral ideas and thoughts, as a result of being strict on their beliefs, anxiety after exposure to minor examples of negative implications may provoke intrusive thoughts.

OCD typically gets worse when anticipating the resolution of a problem, thought, or dilemma. OCD can in some cases, be completely debilitating and can appear as social anxiety despite the anxiety not actually residing from social factors and social isolation not being a consequence of unfavorable encounters but rather self-consciousness of the paradigm of persistent intrusive thoughts.

OCD behaviors may be
-cleaning obsessions followed by aggressively or repetitively washing ones hands or the target of the obsession.
-obsessions on sexual morality and recurrent intrusive thoughts which include unfriendly and horrible 'hijacking' of thoughts by one's most hated images and ideas.
-obsessions on things like walking on side-walks without stepping on the cracks, the obsession is the IDEA something bad will happen if one steps on a crack, puddle, mud etc...and the compulsion is to avoid the crack or puddle etc obsessively.

According to these two pubmed entries, OCD is biologically rooted in ELEVATED serotonin levels and possibly this co-occuring with HYPOACTIVITY (not enough activation) of the NMDA glutamate receptor, in OCD subjects, the glutamate hypoactivity is seemingly centralized or specific to that one receptor, whereas at other receptors the level of glutamate may be higher than normal...

The under-activation of the NMDAR in OCD is most likely not as severe as the under-activation seen in schizophrenia, but is bordering on that level...thus there is a thin line to where obsessions and compulsions evolve into psychosis . Caution is advised in OCD subjects taking any anti-glutamate remedy as it may provoke a worsening of symptoms or even psychosis in those with refractory OCD. A better idea would be to take a NMDAR agonist and a serotonin antagonist specific for the 1D receptor which seems to be over-active in OCD.


Eat Weight Disord. 2002 Sep;7(3):221-31.
Is there a common mechanism of serotonin dysregulation in anorexia nervosa and obsessive compulsive disorder?
Barbarich N1.
Author information
Abstract
Numerous studies have documented increased rates of comorbidity in patients with anorexia nervosa (AN) or obsessive compulsive disorder (OCD). The interaction of many possible factors influences this comorbidity, but one possible explanation involves the neurotransmitter serotonin, which is widely distributed in the brain and has been implicated in a number of psychological behaviours. Although low serotonin levels have been found in patients with impulsive and aggressive behaviour, high levels have been correlated with obsessive and compulsive behaviour. In an attempt to further our understanding of this relationship, a large number of studies have measured serotonin levels throughout different stages of illness in both AN and OCD; furthermore, serotonin challenge studies and drug treatment trials have provided further support for this theory. This paper discusses the evidence supporting the view that the obsessive behaviour characteristic of AN and OCD may be partially due to a dysregulation in the serotonergic system.
PMID: 12452254 [PubMed - indexed for MEDLINE]

Psychopharmacology (Berl). 2010 May;210(1):13-24. doi: 10.1007/s00213-010-1808-9. Epub 2010 Mar 19.
The role of NMDA receptors in the signal attenuation rat model of obsessive-compulsive disorder.
Albelda N1, Bar-On N, Joel D.
Author information
Abstract
RATIONALE:
In recent years, an increasing body of evidence points to the involvement of the glutamatergic system and specifically the glutamatergic ionotropic N-methyl-D-aspartate (NMDA) receptor in the pathophysiology of obsessive-compulsive disorder (OCD).
OBJECTIVES:
To test the role of NMDA receptors in compulsive behavior using the signal attenuation rat model of OCD. In this model, 'compulsive' behavior is induced by attenuating a signal indicating that a lever-press response was effective in producing food.
METHODS:
The NMDA antagonist, MK 801 (0.025-0.100 mg/kg) and the partial NMDA agonist, D-cycloserine (3-100 mg/kg) were administered to rats just before assessing their lever-press responding following signal attenuation (Experiments 1 and 2, respectively). Because the effects of signal attenuation are assessed under extinction conditions, drug doses that were effective in Experiments 1 and 2 were also tested in an extinction session of lever-press responding that was not preceded by signal attenuation (Experiment 3).
RESULTS:
Systemic administration of D: -cycloserine (15 mg/kg) selectively decreased compulsive lever pressing, whereas systemic administration of MK 801 did not affect compulsive lever-pressing but dramatically increased resistance to extinction.
CONCLUSIONS:
Activation of NMDA receptors may have an anti-compulsive effect in OCD patients.
PMID: 20238210 [PubMed - indexed for MEDLINE]

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