Several factors contribute to the neuropsychiatric course of patients with MS, including the impact of the patient accepting a chronic and incurable diagnosis, the toll of progressive neurologic/physical disability and subsequent decline in functioning, and the availability of a support system.2 As opposed to disorders such as Parkinson’s disease, where disease progression is relatively more predictable, the culture of MS involves the obscurity of symptom fluctuation, both from the patient’s and/or clinician’s viewpoint. Psychiatric and neurologic symptoms may be difficult to predict, leading to speculation and projection as to the progression of the disease. The diagnosis of psychiatric conditions, such as depression, can be complicated by the fact that MS and psychiatric disorders share presenting symptoms; for example, disturbances in sleep and concentration may be seen in both conditions.
While studies have examined the neurobiology of MS lesions and their effects on mood symptoms, there has been no clear consensus of specific lesion distributions, although lesions in the superior frontal lobe and right temporal lobe regions have been identified in depressed MS patients.8 Lesions in the left frontal lobe may also have some contribution; studies have shown hyperintense lesion load in this area, which was found to be an independent predictor of MDD in MS.9 This, in turn, coincides with the association of left frontal cortex involvement in modulating affective depression, evidenced by studies that have associated depression severity with left frontal lobe damage in post-stroke patients10 as well as the use of transcranial magnetic stimulation of the left prefrontal cortex for treatment-resistant MDD.11 Lesions along the orbitofrontal prefrontal cortex have similarly been connected to mood lability and impulsivity, which are characteristics of bipolar disorder.8 Within the general population, bipolar disorder is associated with areas of hyperintensity on MRI, particularly in the frontal and parietal white matter, which may provide clues as to the role of MS demyelinating lesions in similar locations, although research concerning the relationship between MS and bipolar disorder remains limited.12
EVALUATION No exacerbation of MS
Upon admission, Ms. A’s lability of affect is apparent as she quickly switches from being tearful to bright depending on the topic of discussion. She smiles when talking about the hobbies she enjoys and becomes tearful when speaking of personal problems within her family. She denies suicidal ideation/intent, shows no evidence of psychosis, and denies any history of bipolar disorder or recollection of hypomanic/manic symptoms. Overall, she exhibits low energy and difficulty sleeping, and reiterates her various psychosocial stressors, including her family history of depression and ongoing marital conflicts. Ms. A denies experiencing any acute exacerbations of clinical neurologic features of MS immediately before or during her admission. Laboratory values are normal, except for an elevated thyroid stimulating hormone (TSH) value of 11.136 uIU/mL, which is expected given her history of hypothyroidism. Results of the most recent brain MRI scans for Ms. A are pending.
The authors’ observations
Although we considered a diagnosis of bipolar disorder–mixed subtype, this was less likely to be the diagnosis considering her lack of any frank manic/hypomanic symptoms or history of such symptoms. Additionally, while we also considered a diagnosis of pseudobulbar affect due to her current mood swings and past trial of dextromethorphan/quinidine, this diagnosis was also less likely because Ms. A’s affect was not characterized by uncontrollable outbursts of emotion but was congruent with her experiences and surroundings. For example, Ms. A smiled when talking about her hobbies and became tearful when speaking of conflicts within her family.
Given Ms. A’s mood dysregulation and lability and her history of depressive episodes that began to manifest after her diagnosis of MS was established, and after ruling out other etiologic psychiatric disorders, a diagnosis of mood disorder secondary to MS was made.
Continue to: TREATMENT Mood stabilization