OUTLINING AND EVALUATING THE BIOLOGICAL APPROACH TO EXPLAINING
OCD
The biological approach is also known as the medical model and is based on the fact that mental
abnormal conditions are seen as similar to physical illnesses being caused by abnormal biological
processes.
There are two possible biological explanation to OCD: neural and genetic.
The neural explanations take into consideration various reasons by which an individual may develop
OCD:
• One being associated with high dopamine level. This neurotransmitter is linked to reward
processing in the brain and an unbalanced level of dopamine can result in unfulfilled
expectations causing anxious feelings and an urge to fulfil the unsatisfaction, consequentially
behaving in a compulsive way. (Zohar, 2004)
• One being linked with a breakdown of the immune system indicating that the illness is
associated to damage of neural mechanisms. This onset of the disorder is more often seen in
children than adults, as seen by Pichichero who reported that children with throat infections
often displayed indications of OCD and Tourette syndrome.
• Another explanation has been found through the use of PET scans of the brain revealing a
high level of activity in the thalamus, which is the area of the brain whose functions include
controlling and safety behaviour. An overreactive thalamus would also result in an overactive
orbital frontal cortex (OFC) which is the part of the brain involved in decision making and the
base of our behaviours. This area helps initiate activity after receiving impulses to act and
then to end the activity after the impulse stops. In an OCD subject the OFC can have
difficulties switching off the impulse, consequentially becoming obsession and resulting in
compulsive behaviour.
This happens because the brain’s deeper structure (where the thalamus resides) and the OFC have
complications to communicate. This exchange of information between the two parts happens
primarily through the use of serotonin, so when the level of this neurotransmitter is low, we have a
higher possibility of developing OCD. In support of this theory, in 1990 Pigott found out that
antidepressant drugs (which increase serotonin activity) have been shown to reduce OCD symptoms.
Another research evidence was given by A. R. Gilbert with his study on the decrease in thalamic
volumes of paediatric patients with OCD who are taking paroxetine, which is a drug that increase the
level of serotonin in the brain blocking the reabsorption of it into neurons.
Volumetric MRI images studies were conducted on a group of children with OCD in comparison of a
control group of healthy subjects before and after taking the paroxetine. The results showed a
decreased thalamic volume on OCD patients after having assimilated the medicine to a comparison
level of the control group and a reduction of OCD symptoms.
Even though this research supports the neural explanation, we have to take into consideration that not
every person with OCD has the same abnormalities in the brain so the results of it cannot be
generalised to all cases.
Zohar et al. also conduct a study on the implication of the level on dopamine in OCD patients giving
mCPP (which reduces serotonin levels), finding out that their symptoms were significantly enhanced
in comparison to a healthy control group. This suggests that the OCD subject’s conditions were
related to an abnormal level of serotonin in their brain.
The neural explanation, even if it been supported by many studies, is still in a development phase.
OCD
The biological approach is also known as the medical model and is based on the fact that mental
abnormal conditions are seen as similar to physical illnesses being caused by abnormal biological
processes.
There are two possible biological explanation to OCD: neural and genetic.
The neural explanations take into consideration various reasons by which an individual may develop
OCD:
• One being associated with high dopamine level. This neurotransmitter is linked to reward
processing in the brain and an unbalanced level of dopamine can result in unfulfilled
expectations causing anxious feelings and an urge to fulfil the unsatisfaction, consequentially
behaving in a compulsive way. (Zohar, 2004)
• One being linked with a breakdown of the immune system indicating that the illness is
associated to damage of neural mechanisms. This onset of the disorder is more often seen in
children than adults, as seen by Pichichero who reported that children with throat infections
often displayed indications of OCD and Tourette syndrome.
• Another explanation has been found through the use of PET scans of the brain revealing a
high level of activity in the thalamus, which is the area of the brain whose functions include
controlling and safety behaviour. An overreactive thalamus would also result in an overactive
orbital frontal cortex (OFC) which is the part of the brain involved in decision making and the
base of our behaviours. This area helps initiate activity after receiving impulses to act and
then to end the activity after the impulse stops. In an OCD subject the OFC can have
difficulties switching off the impulse, consequentially becoming obsession and resulting in
compulsive behaviour.
This happens because the brain’s deeper structure (where the thalamus resides) and the OFC have
complications to communicate. This exchange of information between the two parts happens
primarily through the use of serotonin, so when the level of this neurotransmitter is low, we have a
higher possibility of developing OCD. In support of this theory, in 1990 Pigott found out that
antidepressant drugs (which increase serotonin activity) have been shown to reduce OCD symptoms.
Another research evidence was given by A. R. Gilbert with his study on the decrease in thalamic
volumes of paediatric patients with OCD who are taking paroxetine, which is a drug that increase the
level of serotonin in the brain blocking the reabsorption of it into neurons.
Volumetric MRI images studies were conducted on a group of children with OCD in comparison of a
control group of healthy subjects before and after taking the paroxetine. The results showed a
decreased thalamic volume on OCD patients after having assimilated the medicine to a comparison
level of the control group and a reduction of OCD symptoms.
Even though this research supports the neural explanation, we have to take into consideration that not
every person with OCD has the same abnormalities in the brain so the results of it cannot be
generalised to all cases.
Zohar et al. also conduct a study on the implication of the level on dopamine in OCD patients giving
mCPP (which reduces serotonin levels), finding out that their symptoms were significantly enhanced
in comparison to a healthy control group. This suggests that the OCD subject’s conditions were
related to an abnormal level of serotonin in their brain.
The neural explanation, even if it been supported by many studies, is still in a development phase.
