Evidence-Based Reviews

Disorders of diminished motivation: What they are, and how to treat them

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These disorders share features of depression, delirium, and catatonia, but key differences have major treatment implications.

AUDIO: Dr. Spiegel discusses etiologies of disorders of diminished motivation, and how to differentiate them from depressive disorders.


 

References

Disorders of diminished motivation (DDM)—including apathy, abulia, and akinetic mutism—are characterized by impairment in goal-directed behavior, thought, and emotion.1 These disorders can be observed clinically as a gross underproduction of speech, movement, and emotional response.

DDM are not classified as disorders within DSM-5, and it remains unclear if they are distinct disorders or symptoms that overlap in other conditions. Some sources support distinct diagnoses, while the traditional position is that DDM are variations along a spectrum, with apathy as the mildest form and akinetic mutism as the most severe form (Figure).1-3 DDM can result from various neurologic, medical, psychiatric, socioeconomic, and drug-induced pathologies, and may represent differing severity of the same underlying pathology.1,4 It is postulated that DDM arise from disruptions in the dopaminergic frontal-subcortical-mesolimbic networks.1,4

We present 2 cases of patients who developed distinct phenotypes within DDM. Despite differences in presentation and symptom severity, both patients showed clinical improvement on methylphenidate (not the only treatment option) as assessed by the Neuropsychiatric Inventory (NPI),5 a scale used to measure dementia-related behavioral symptoms that includes an Apathy/Indifference (A/I) subscale.

CASE 1
Apathy secondary to glioblastoma multiforme

Ms. E, age 59, presents with wound drainage 3 weeks after a repeat right craniotomy for recurrent glioblastoma multiforme (GBM) of the temporal lobe. Her medical history is not believed to have contributed to her current presentation.

On hospital day 2, Ms. E undergoes debridement and reclosure at the craniotomy site. Prior to the procedure, the patient was noted to have anhedonia and flat affect. Her family reports that she seems to get little enjoyment from life and “only slept and ate.” Psychiatry is consulted on hospital day 3 for evaluation and management of a perceived depressed mood.

On initial psychiatric evaluation, Ms. E continues to have a constricted affect with delayed psychomotor processing speed. However, she denies dysphoria or anhedonia. Richmond Agitation-Sedation Scale6 score is 0 (alert and calm) and test of sustained attention (‘Vigilant A’) is intact (ie, based on the Confusion Assessment Method for the Intensive Care Unit [CAM-ICU],7 Ms. E does not have delirium). The NPI A/I frequency score is 15, with a severity score of 3, for a total score of 45, indicating moderate behavioral disturbance on the NPI A/I subsection. A diagnosis of neuropsychiatric apathy due to recurrent GBM or craniotomy is made, although substance-induced mood disorder due to concurrent dexamethasone and opiate use is considered. Methylphenidate, 2.5 mg/d, is started, and Ms. E’s blood pressure remains stable with the initial dose.

Methylphenidate is titrated to 5 mg, twice daily, over a 1-week period. Ms. E’s NPI A/I subscale score improves to 3 (mild behavioral problem), with 3 points for frequency and a multiplier of 1 for mild severity, reflecting an improvement in neuropsychiatric apathy, and she is transferred to a long-term care rehabilitation center.

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