4. 4 ORGANIC MOOD DISORDER
Abnormalities of mood and affect are
among the most common neuropsychiatric disturbances. Many medications,
drugs of abuse, and neurological and medical conditions have been
associated with mood disorders. However, establishing a causal
relationship between depressive symptoms and a specific medical condition
is difficult, and the percentage of those coexisting symptoms that can be
called secondary remains unknown (Caine and Lyness, 2000). ICD-10
specifies that the affective disorder must be judged not to represent an
emotional response to the patient’s knowledge of having a concurrent brain
disorder.
Epidemiology
Depression in the medically ill
appears to be equally prevalent by sex, or possibly slightly higher in men
(Caine and Lyness, 2000). Patients with secondary mania are more likely to
have negative family and personal histories of mood disorder (Evans et
al., 1995).
Etiology
Conditions reported to produce
depression include cortical degenerations like Alzheimer’s disease and
frontotemporal dementias, extrapyramidal disorders like Parkinson’s
disease and Huntington’s disease, cerebrovascular diseases, cerebral
neoplasms, cerebral trauma, CNS infections like viral encephalitis,
epilepsy, endocrine disorders like hyperthyroidism and hypothyroidism, and
inflammatory disorders like systemic lupus erythematosus (Cummings and
Mega, 2003). Lesion-deficit and functional imaging studies of depressed
neurological patients have consistently identified involvement of frontal
and temporal cortices and striatum (Mayberg et al., 2002). These common
abnormalities have been interpreted as evidence of disease-specific
disruption of known neurochemical pathways involving
frontal-striatal-thalamic and basotemporal limbic circuits (Alexander et al., 1990).
Secondary mania is much less
prevalent in most neurological illnesses, with the exceptions of multiple
sclerosis and possibly Huntington’s disease. Patients with mania
originating in late life are more likely to have an underlying organic
disturbance. Secondary mania also occurs at an unexpectedly higher
prevalence following closed head injury, and relatively frequent
occurrence of irritability, aggression and hypersexuality has important
implications for management of these patients. The major neuroanatomic
correlate of mania after TBI is the presence of anterior temporal lesions
(Robinson et al., 2000). Infectious processes, including HIV infection,
may also be an important risk factor for the development of secondary
mania, and it has been suggested that mania occurring late in HIV
infection is likely the result of HIV effects on the CNS, while mania that
occurs early in asymptomatic HIV seropositive patients may be more
etiologically related to genetic predisposition (Evans et al., 1995).
Clinical features
It has been observed that depression
is underrecognised and undertreated in patients with neurological
conditions. Presence of a neurological disorder may make the recognition
of depression more difficult and may modify the manifestations of the
disorder. For e.g., patients with Parkinson’s disease may have slowed
movements and vocal changes similar to depression, without any
corresponding mood abnormality. Assessment of the core psychological
features of depression, including sadness, feelings of guilt,
worthlessness, hopelessness and helplessness, is critical in recognizing
depression in patients with neurological disorders (Cummings and Mega,
2003).
Management
Nortriptyline and trazodone have been
found effective in treating poststroke depression (Lipsey et al., 1984;
Reding et al., 1986). Desipramine and sertraline have been found useful in
treating depression in TBI (Wroblewski et al., 1996; Fann et al., 2000).
Organic mania is often difficult to
treat. Although the correction of the underlying organic factors may
effectively reverse the manic presentation, many organic factors (for
e.g., trauma, stroke and aging) are not reversible, and the presence of
these etiologic factors may complicate traditional antimanic treatments
(Jorge et al., 1993). Unfortunately, treatable causes of secondary mania,
like vitamin B12 deficiency, are often overlooked. It is often difficult
to determine which patients will improve solely with the correction of the
underlying organic abnormality and which patients also require antimanic
pharmacotherapy. Therefore, in many patients, pharmacotherapy is initiated
along with the treatment of the underlying secondary causes of mania.
Lithium may be effective in some patients, but adverse effects limit its
use in this group of manic patients (Evans et al., 1995). Clonidine,
valproate, carbamazepine and antipsychotics have been found to be
effective in treating secondary mania (Bakchine et al., 1989; Starkstein
et al., 1991) |
