OCD is characterised by the presence of recurrent obsession or compulsions (APA, 2000). Obsession are persistent ideas, thoughts, or experiences that are experienced as intrusive and inappropriate, while compulsions are repetitive thoughts (i.e., praying, counting, repeating words silently) or behaviours (such as hand washing, checking, ordering or adjusting things), the goal of which is to reduce anxiety or distress (APA, 2000).
The symptoms of OCD need to be distinguished from the phenomenon of "organic orderliness" associated with TBI. Brain-injured individuals often tend toward increased rigidity in their behaviour and to intolerance of the disruption of their routines (Williams et al., 2003) following injury. This requirement for order is perhaps not too difficult to understand as a means of coping with the neuropsychological and psychological deficits encountered following a TBI including memory disorders and problems with planning and categorization. The notion of the reestablishing some form of control in a world that has spun out of control as a result of the effects of the injury also probably underlies this type of response.
OCD following traumatic brain injury tends to be relatively rare in the literature, but at least 57 cases have so far been described: 5 cases (Lewis, 1942); 7 cases (Anderson, 1942); 1 case (Adler, 1945); 14 cases (Hilbom, 1960); 2 cases (Lish-man, 1968); 4 cases (McKeon, McGuffin, & Robinson, 1984); 1 case (Khanna, Narayan, Sharma, & Mukundan, 1985); 1 case (Kettl & Marks, 1986); 1 case (Jen-ike & Brandon, 1988); 1 case (Drummond & Gravestock, 1988); 1 case (Laplane, Boulliat, Baron, Pillon, & Baulac, 1988); 1 case (Lewis & Rosenberg, 1990); 1 case (Donovan & Barry, 1994); 1 case (Max et al., 1995); 4 cases (Childers, Holland, Ryan, & Rupright, 1998); 1 case (Khouzam & Donnelly, 1998); 10 cases (Berthier, Kulisevsky, Gironell, & Lopez, 2001); and 1 case (Williams et al., 2003).
In the large sample assembled by Berthier et al. (2001), they noted that the patterns of OCD symptomatology (e.g., contamination, somatic symptoms, requirement for symmetry, cleaning, and checking) were well specified and associated with cognitive deficit and MRI evidence of disruption of the frontal-subcortical circuitry.
The time when obsessive compulsive behaviours are observed following the traumatic brain injury varies considerably in the published literature spanning from days to years following the impact, and often worsening over time (Etcharry-Bouyx &
Dubas, 2000). Following head injuries the duration with which these problems can emerge may be as little as 24 hours (McKeon et al., 1984) to three or more years after the injury (Khanna et al., 1985).
The mechanism by which OCD develops following TBI has been a matter of considerable speculation in the literature. Baxter and colleagues (1992) have found significant correlations between the activity of the orbital prefrontal cortex with that of both the caudate nucleus and the thalamus in those individuals who received treatment for their OCD, but not following treatment in those who responded. They also found that changes in metabolic rate as measured by cerebral blood flow in the head of the caudate on the right directly correlated with successful treatment. Rauch, Jen-ike, Alpert, and colleagues (1994) found an increase in relative cerebral blood flow during an OCD symptomatic state in the right caudate nucleus when compared with the resting state. These patients also featured activation of the left anterior cingulate cortex and the bilateral orbital frontal cortex.
These findings support the neuroanatomical theory of OCD (Insel, 1992a, 1992b) that suggests the involvement of a reverberating circuit consisting of increased glu-taminergic neurotransmission from the orbitofrontal and cingulate cortices, the caudate nucleus and the ventral striatum followed by increased GABAergic inhibitory neurotransmission to the globus pallidus followed by decreased inhibitory neurotransmission to the thalamus.
Based on this theory it is expected that only lesions of the pallidum, striatum, and thalamus are necessary to produce OCD. However, there is clear evidence to support the notion of frontal lobe pathology variously in the development of this condition (Donovan & Barry, 1994; Eslinger & Damasio, 1985). In support of the organic basis of this diagnosis, it should be noted that individuals who develop OCD following brain injury tend to have a negative family history for the condition and a later age of onset of the condition than do noninjured control subjects with the diagnosis (Berthier, Kulisevsky, Gironell, & Heras, 1996).
My previous work with the condition (McLaren & Crowe, 2003), supports the notion of a number of predisposing psychological factors to the emergence of OCD in susceptible individuals. In both a clinical and nonclinical sample the development of OCD-like symptomatology occurs in the context of a significant uncontrolled stressful life event in association with the individual's previous disposition to demonstrate the overly sensorious constraint on internal cognitions labelled thought suppression. This is best illustrated by of the example of requesting an individual not to think of a white bear, which in most cases produces the opposite effect. Clearly the constellation of factors that occur following head injury constitute a marked uncontrollable stressful life event, and the suggestion arising from our previous investigation would indicate that a predisposing tendency towards thought suppression would result, indeed, in the individual demonstrating OCD-like symptomatology if they had this predisposition.
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