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A Look at Obsessive Compulsive Disorder (OCD)

1.1. Introduction:

Kalat (2003) defines anxiety as an escape emotion. Anxiety causes physiological arousal, which according to Weiten (2001) is a natural and common reaction to threatening or stressful situations. When anxiety becomes excessive it can become maladaptive and detrimental (Ungar & Shear, 2004)

From an evolutionary perspective anxiety probably evolved because it enhanced a persons vigilance for various sources of threat. Evolutionists note that when the anxiety becomes chronic regarding multiple situations it is an evolutionary dysfunction (Weiten, 2001). This maladaptive anxiety is known as an anxiety disorder.

The National Institute of Mental Health (2004) cites; generalised anxiety disorder; obsessive compulsive disorder; panic disorder; post traumatic stress disorder and social anxiety disorder as the five major types of anxiety disorders. These anxiety disorders do not always occur in isolation. For example a person with obsessive compulsive disorder may also suffer from panic disorder (Watkins, 2001). This essay will only concentrate on obsessive-compulsive so that it is possible to discuss this disorder in greater detail.

2. Obsessive-Compulsive Disorder (OCD):

2.1.Defining OCD:

Obsessive-compulsive disorder (OCD) is defined as the persistent uncontrollable intrusions of unwanted thoughts (obsessions) and to engage in senseless rituals (compulsions) to relieve the anxiety of these thoughts (Weiten, 2001). The mean age of onset of OCD ranges from 22 to 36 years of age (Jenike, 2004) and is equally prevalent in men and women (World Health Organisation, 1992). The Anxiety Disorders Association of America (2004) notes that although less frequent OCD can occur in childhood.

According to Watkins (2001) OCD was believed to be fairly rare, however research in the last decade has indicated that it is much more prevalent than previously thought. Jenike (2004) adds that OCD continues to be underdiagnosed and undertreated. This is due partly to the myth that surrounds OCD, that it is a result of a weak or unstable personality (Obsessive-Compulsive Foundation, 1998) as well as the tendency of persons suffering from OCD to be ashamed of their behaviour and attempt to hide it from others.

2.2. Symptoms:
OCD usually involves having both obsessions and compulsions, the Obsessive-Compulsive Foundation does however note that a person may sometimes have only one or the other (1998). Mentally healthy people are sometimes able to recognise some of the symptoms of OCD such as checking if the house is locked, however for people with OCD these compulsions interfere with daily life and are very distressing (National Institute of Mental Health, 2004).

OCD symptoms include a wide variety of obsessive thoughts occurring over and over again, such as the fear that something terrible may happen to a loved one, or the fear of being contaminated by dirt or germs. These obsessions are often followed by compulsions such as excessively washing or repetitive checking. These rituals and thoughts are recognised as senseless by the person and yet they are unable to resist the compulsion to perform them (Dumont, 1996).

The World Health Organisation (1992) notes that these symptoms must be present on most days for at least two weeks and be a source of distress as well as interfering with daily activities. Lastly, it is important to note that the symptoms cited above can occur in conjunction with signs of depression or other anxiety disorders and these are no bar to diagnoses.

3. What Causes OCD?

3.1. Nature vs. Nurture and OCD:

Psychodynamic theory classified OCD as a psychoneurosis (Watkins, 2001). Freud suggested that the roots of OCD came from a disturbance in the sexual life or development of the child. To support this is evidence from a study using a meta-analysis of twin and family studies to explore the role of genetic and environmental factors, which showed that the largest proportion of variance liability accounted for environmental factors as a cause (Hettema, Neale & Kendler, 2001).

Weiten (2001) points to research that suggests anxiety sensitivity to explain the interaction between genes and the environment. This notion explains that people are born with genes that cause them to be highly sensitive to the internal physiological symptoms of anxiety, which can be set off by the environment.

Various twin studies have suggest a weak genetic predisposition to anxiety disorders (Weiten, 2001). Research has been done with regards to specific genes, and a number of possible links have become evident. Kalat (2001) notes an oddity that anxiety researchers noticed with regards to anxiety disorders (including OCD). The researchers found that most people with anxiety disorders inherited a condition called joint laxity. The symptoms from this condition are unrelated to those of anxiety disorders. However the genes that control anxiety disorder and joint laxity occur on chromosome 15. For people with anxiety disorders, a section on chromosome 15 is unstable and occurs three times instead of two.

There has been some controversy over the 5HT1D^sub^beta receptor gene. This receptor is involved in the regulation of serotonin release (Hilton, 2002), which as will be discussed further is an important factor with regards to OCD. In a study conducted by Mundo, Richter, Sam, Macciardi, and Kennedy (2000) results indicated a significant linkage between 5HT1D^sub^beta receptor gene and OCD. A further study however, conducted by Di Bella, Cavillini and Bellodi (2002) concluded that their data (from a study group of 79 nuclear families) did not support the role for the 5HT1D^sub^beta receptor gene in conferring susceptibility to OCD.

Two other genes have been implicated with regards to OCD. A study carried out by Lin, Vance, Smith, and Shaw (2004) showed evidence that a mutation of the SGCE gene may play a part in OCD. Lin et al (2004) explain that this single pair-based mutation leads to a loss of amino acids from the 3' end of the protein which may cause the individual to be susceptible to OCD. The second was noted by Hall and her colleagues in a study which linked a neurotrophic factor gene to OCD (Genomics & Genetics Weekly, 2003). The brain-derived neurotrophic factor (BDNF) showed significant evidence of association with OCD.

It is important to note that although these genes have been linked to OCD, none of the evidence presented points to genes, or the environment as a cause of OCD. Rather it is suggested that genes, environmental factors or both may increase susceptibility to the disorder.

3.2. Streptococcal Infection and OCD:

Although it is more common for OCD to begin in adulthood, OCD symptoms sometimes present in children. According to Bower (2000), as well as many other scholars, these symptoms (and symptoms of other disorders) often develop shortly after a streptococcal infection. Researchers call these cases PANDAS (Paediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus). Research has further confirmed this link by studies pointing to a group A beta-haemolytic Streptococcus (GABHS) as a cause for the neuropsychiatric symptoms (Stephenson, 2002).

It is important to note that streptococcal infection is not completely accepted as a cause and remains a yet-unproven phenomenon (Kurlan & Kaplan, 2004).

4. The Brain and OCD

4.1. Basal Ganglia and Prefrontal Areas of the Brain:

One of the most supported theories regarding the cause of OCD relates to brain activity. More specifically the basal ganglia, it has in numerous studies been linked to OCD. The basal ganglia refers to a group of large nuclei lying in the centre of the brain including; the caudate nucleus; putamen and the globas pallidus (Kalat, 2004). It's function is to receive and modify information from the cerebral cortex (Dale, 2003). The basal ganglia plays important roles in movement, behaviour and emotion.

Using PET scans (Positron-emission tomography) researchers are able to look at patterns of brain activity and are able to compare the patterns of OCD sufferers with people of no mental illness. PET scans have shown significant differences between the two. PET scans have presented evidence that people with OCD use different brain circuitry than people without the disorder while tackling cognitive tasks (National Institute of Mental Health, 2004). Added to the abnormalities found in the basal ganglia functioning, abnormalities have also been isolated in prefrontal areas of the brain (Leocani, Locatelli, Bellodi and Fornara, 2001). EEG studies have confirmed these findings.

Put simply, this research all suggests that one part of the brain has trouble communicating with the other part. These two brain structures use the chemical messenger (neurotransmitter) serotonin. It has been postulated that the insufficient levels of serotonin in OCD persons are prominently involved in OCD. A study conducted by Peterson, Thomas, Kane and Scahill (2003) showed an association between OCD and significantly smaller volumes of the putamen. While other studies indicate a reduction in the left caudate volume and increased metabolic activity in the prefrontal cortex (Presta, Marazziti, Dell'Osso & Pfanner, 2003). It remains yet incomplete or unknown exactly what the dysfunction is with/in the basal ganglia and/or the prefrontal areas of the brain.

4.2. Other Findings:

Presta et al (2003) note studies which correlate the thalamus with OCD severity. Added to this in a study conducted by Kwon, Shin, Kim, and Kim (2003) evidence was presented that Hippocampal volume is reduced in OCD patients verses normal patients as well as enlarged amygdala volume.

4.3. Serotonin:

Serotonin is a chemical messenger for the brain - a neurotransmitter - it is released by one nerve and taken up by the same or other nerves at the synapse. The link between serotonin and OCD was made when drugs that increase brain concentration of serotonin showed improvement in OCD symptoms. Weiten (2001) explains that abnormalities in neural circuits using serotonin have been linked to OCD.

Although Serotonin has been implicated as a cause for OCD, the drugs (which will be discussed further) do not always prove effective. This may be due to the fact that the specific receptor subtypes that affect OCD are not known. Studies have been made such as the study by Mundo et al (2000) that pointed to receptor gene 5HT1D^sub^beta. As yet no study has proved conclusive enough in isolating specific receptor subtypes.


5. Treatment:

Treatments for OCD include behaviour therapy and medication and occasionally (usually only in severe cases and non-remitting cases) ECT or neurosurgery are used. ECT or electroconvulsive therapy is a procedure in which current is passed through the brain, which produces controlled convulsions. ECT is believed to act by causing a massive neurochemical release in the brain (MedicineNet, 2003).

There is no simple or single treatment for OCD and at times a combination of treatments is used. The treatment for OCD will depend highly on the patient with regards to their age, severity of the OCD and health of the patient. Young children for example are usually treated only with SRI's. In older patients medication as well as Cognitive Behaviour Therapy has proved most beneficail (March et al, 1997).

5.1. Cognitive Behaviour Therapy:

Cognitive Behaviour Therapy has proved effective for OCD sufferers. PET scans have shown that cognitive behavioural therapy (CBT) produces changes to patterns of brain activity (National Institute of Mental Health, 2004).

CBT involves exposure and response prevention. Exposure to the anxiety producing stimuli should gradually decrease with repeated exposure. Response prevention refers to the blocking of compulsions, this must be coupled with exposure for optimum effectiveness of CBT (Obsessive Compulsive Association, 2004). The cognitive component of CBT assists the patient to challenge their faulty assumptions. This approach assumes that if the patient better understands his/her behaviour and is able to falsify it they will be more enabled to control this behaviour.

5.2. Medication:

As already noted it is clear that serotonin plays a part in OCD, this is because of the effectiveness of serotonin reuptake inhibitors (SRI's). SRI's block the reuptake of serotonin causing more to be produced therefore increasing the concentration of serotonin in the brain.

There are five available SRI's; Clomipramine; Fluoxetine (Prozac); Fluvoxamine; Paroxetine; Sertraline; and Citalopram (Obsessive Compulsive Foundation, 2004). Clomipramine is classified as an SSRI (non-selective SRI) which means it affects many other neurotransmitters, while the others affect only serotonin. For this reason Clomipramine is used in more severe cases or if the other drugs are proving ineffective, as it presents more side effects

At times patients will not respond to an SRI. It is recommended by March et al (1997) to gradually increase the dose to it's maximum (within 4-6weeks) and if there is still no response after 13 weeks to try another SRI. Mundo et al (2000) note that OCD patients resistant to the SRI's have reported improvements after the chronic administration of sumatriptan.      

6. Conclusion:

Recent research on obsessive compulsive disorder has managed to dispel many myths. Such as OCD is a result of a weak personality, purely environmental factors or that it is fairly uncommon. Above all other factors it has emerged that brain activity especially with regards to serotonin probably play the largest part in OCD. It does seem however that the research on OCD is still in it's infancy. Many more studies and much more investigation will have to be conducted before we are able to fully understand this illness it's causes and what treatment we could offer.

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