Obsessive-Compulsive Disorder James Lindesay

CLINICAL FEATURES

Diagnostic Criteria

OCD is characterized by intrusive, persistent obsessive thoughts, images or impulses and/or compulsive behaviours that are a significant source of distress, or interfere with the patient’s personal or social functioning. The current diagnostic criteria, as set out in DSM-IV⁵ and ICD-10⁶, apply to all patients, irrespective of age. The limited evidence available indicates that the clinical features of OCD in elderly patients are very similar to those of younger adults. In their comparative study, Kohn et al.⁷ found that concerns about symmetry, need-to-know and counting rituals were less common in elderly patients, and hand-washing and fear of having sinned were more common, but otherwise there were few differences in clinical features compared with younger OCD patients. Extreme ego-syntonic religiosity has been proposed as a variant of OCD that may be more common in older patients⁸.

Differential Diagnosis

Unpleasant, intrusive thoughts and abnormal stereotyped behaviours occur in other mental disorders, and OCD is not diagnosed if their content is exclusively related to another disorder, for example guilty preoccupations in depression, worries in generalized anxiety, concern with illness in hypochondriasis, weight control in anorexia or avoidance in phobic disorders⁵. It should be borne in mind that conditions such as depression, generalized anxiety and substance abuse may be co-morbid with OCD. In elderly patients, increased anxious orderliness may be a prodrome of dementia; however, this behaviour is not resisted or associated with the tension that occurs in OCD. The compulsive behaviours of OCD resemble the stereotyped behaviours that occur in certain other disorders, such as Tourette’s syndrome, Sydenham’s chorea, encephalitis and partial complex seizures. Tourette’s syndrome and OCD commonly cooccur⁹, and patients with OCD may have a history of Sydenham’s chorea in childhood¹⁰. There is currently some debate as to whether conditions such as OCD, body dysmorphic disorder, trichotillomania and hypochondriasis might form an obsessive-compulsive ‘spectrum of disorders’.

Despite its similar name, obsessional personality disorder is quite distinct from OCD. It is characterized not by obsessions and compulsions, but by a preoccupation with orderliness, perfection and control dating back to early adulthood⁵. Individuals who are unable to discard personal possessions may present as the so-called ‘senile squalor’ syndrome after a lifetime of accumulating rubbish. This syndrome overlaps both obsessional personality disorder and OCD¹¹.

Not all patients with OCD have insight into the irrationality and inappropriateness of their obsessions and compulsions. If the obsessional thoughts are held with delusional intensity, an additional diagnosis of delusional disorder may be warranted. The ruminative delusions and stereotypies of schizophrenia are usually not ego-dystonic, and therefore would not be regarded as OCD⁵.

Clinical Assessment

An effective treatment plan for OCD requires a detailed clinical assessment. What exactly are the main problems? What, if anything, exacerbates or improves the symptoms? How long has the condition been present, and how has it evolved since its onset? What treatments, if any, have been tried in the past? What other symptoms or disorders are present? Any concomitant depression, mania, psychosis or alcohol dependency will require specific management before behavioural treatments for OCD can be effective. If the patient is cognitively impaired, this will have implications for the choice of treatment; for example, some behavioural strategies will not work if information cannot be retained or recalled. In elderly patients with OCD of recent onset, it is important to investigate carefully for any underlying cerebral disease. Late-onset cases are associated with frontal dysfunction¹², which may be caused by a variety of focal and generalized disorders, including cerebrovascular disease, tumours and primary neurodegenerative dementias. Late-onset OCD may also be the result of external factors, such as adverse life events and exposure to trauma, that weaken an elderly individual’s resistance to long-standing subclinical obsessionality¹³.

EPIDEMIOLOGY

Most of our knowledge about the epidemiology of OCD in old age derives from the US National Institute for Mental Health (NIMH) Epidemiologic Catchment Area (ECA) Program. Overall, the one-year prevalence for those aged 65 years and older was 0.85% (men 0.75%, women 0.93%), as opposed to 1.65% for the sample as a whole¹⁴. A more detailed analysis of the elderly population at the Eastern Baltimore site found prevalence rates of 1.3% for those aged 65–74 years and 0.6% in those aged 75+¹⁵. Following the second wave of the ECA, annual incidence rates were estimated. In males aged 65+, the incidence rate of OCD was one-third of that for males of all ages, but in females there was a non-significant upturn in the incidence rate after age 65¹⁶. In common with a number of other psychiatric disorders, the lifetime prevalence of OCD decreased with age in this study. The reason for this is unclear, but it may be the result of cohort effects, differential mortality or age-specific differences in symptom ascertainment and recall. A rather higher overall one-year prevalence rate of 1.5% in over-65-year-olds has been reported in a more recent community study in Quebec, greater than that found for major depression (1.1%)¹⁷.

AETIOLOGY

OCD is familial; it occurs in 40–50% of parents, 19–39% of siblings and 16% of children of probands with the disorder¹⁸. Just what is inherited is not clear; other anxiety disorders are also more common in the families of OCD probands¹⁹. At least part of this familiality is due to genes, and most of the studies that have been carried out have focused on candidate genes in the serotonergic and dopaminergic neuronal pathways²⁰. However, to date most of these studies have been too small to establish linkage with an acceptable level of significance, and apart from the glutamate transporter gene, there has been no replication of findings. It is not known how the expression of any genetic susceptibility to OCD may vary across the life span.

Most of the evidence from clinical, neuropsychological and neuroimaging studies implicates the basal ganglia and their connections with the thalamus and the cerebral cortex in the aetiology of OCD²¹. Specifically, it has been proposed that there are structural and functional abnormalities in a neuronal circuit involving the orbitofrontal cortex, the basal ganglia, the substantia nigra and the ventrolateral pallidum²². Recent developments in imaging, such as voxel-based morphometry and multivoxel analyses have confirmed abnormality of the orbitofrontal-striatal areas in OCD, but indicate that other regions such as the dorsolateral and ventrolateral pre-frontal and parietal areas are also involved²³. The specific response of OCD to serotonin (5-HT) re-uptake-inhibiting drugs (see below) suggests that serotonergic neuronal systems are involved, directly or indirectly. In the cognitive behavioural model of OCD, obsessions and compulsions result from pathological, anxiety-provoking over-control of normal intrusive cognitions²⁴.

TREATMENT

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