Particularly relevant to the clinical assessment of older adults, depending on the location of neurodegeneration, disinhibited behavior can be a symptom of Alzheimer’s disease [12] or vascular dementia [13]. Disinhibition is also one of the core symptoms of the behavioral variant of frontotemporal dementia (bvFTD) [14]. According to the recent International Consensus criteria for bvFTD, at least 3 of the 6 core symptoms of behavioral disinhibition-apathy, stereotyped or compulsive behavior, loss of empathy, hyper-orality, and executive deficits are needed to make the diagnosis [14]. Neuroimaging and cerebrospinal fluid (CSF) biomarkers may help in possibly understanding potential cause of dementing illness [15, 16]; however, the differential diagnosis for FTD currently relies on clinical judgment. Frontal lobe syndrome, a positive history of psychiatric illness, male gender, a relative absence of stereotypy, and presence of depressive symptoms are predictive for psychiatric origin symptoms rather than bvFTD [17].

A possible link between bipolar disorder and bvFTD has also been suggested by case reports of patients presenting with manic symptoms as a first manifestation of bvFTD [18, 19] and patients with a lifetime diagnosis of bipolar disorder evolving into bvFTD [20, 21]. This large clinical overlap in social cognition, executive disturbances, and behavioral profiles might be explained by the involvement of common functional neuro-anatomical networks [22–24]. A proportion of bvFTD patients have a slow course with relatively normal neuroimaging, particularly those carrying a C9orf72 repeat expansion [25]. This repeat expansion has been found in patients with bipolar disorder preceding FTD [26, 27]; however, this mutation was not detected in a cohort of 206 patients with bipolar disorder [28].

The condition fulfilling criteria for possible bvFTD failing to convert to probable bvFTD over time is labeled the benign bvFTD phenocopy syndrome [29, 30]. These patients exhibit behavioral and functional impairments consistent with a frontal lobe syndrome but fail to progress over time and have no frontal or anterior temporal atrophy or hypo-perfusion at follow-up. Although an alternative explanation is generally lacking in these cases, it is possible that this could be an end-stage manifestation of bipolar disorder.

Although far less common than depression, mania can occur in 1 % of stroke patients, in 2–12 % of patients with movement disorders such as Huntington’s disease, in patients with epilepsy or infections of the brain [31]. Tumors, neurosurgery, and traumatic head injury can result in manic symptoms [10], occasionally with a delay of up to 12 months before the manic symptoms develop [32, 33]. Focal brain lesions in the right hemisphere have been associated with mania [34]. Steffens and Krishnan [35] proposed criteria for vascular mania and depression subtype specifiers, and their concept of vascular mania appears to have some overlap with the neurological disinhibition syndrome. Late-life mania may occur in patients with non-symptomatic vascular brain damage.

Differentiating between frontal disinhibition and bipolar mania can be challenging. While many symptoms are overlapping between the two conditions, bipolar mania may be more characterized by elevated mood and decreased need for sleep, rather than disturbed sleep. The presence of a positive family history of affective disorder may indicate that a somatic cause resulted in mania by triggering an existing bipolar predisposition [8].

In general, medical comorbidities are a substantial burden in older age bipolar disorder patients [36, 37]. A retrospective chart review of 73 patients over age 65 admitted for a manic episode revealed that 86.3 % had medical comorbidity [38]. Clinical emphasis on maintaining optimal physical health and avoiding polypharmacy may optimize the likelihood for better outcomes.

Standardized rating scales have been critical for studying bipolar disorder and a number of these scales are useful in an office setting for both evaluating and monitoring patients. In research, assessment of bipolar disorder and psychiatric comorbidities can be done through a semistructured diagnostic interview, as the Mini-International Neuropsychiatric Interview Plus (MINI) [75] or Structured Clinical Interview for DSM Disorders (SCID) [76]. Several scales are available to rate comorbid symptoms, such as the Beck Anxiety Inventory (BAI) [77] and Hamilton Anxiety Rating Scale (HAM-A) [78] for anxiety symptoms, or Alcohol Use Disorders Identification Test (AUDIT) [79] for alcohol use. A major function of rating scales, particularly in clinical trials, is to assess bipolar symptom severity. Some of the briefer rating scales, especially those that are self-rated tools such as the Quick Inventory of Depressive Symptomatology (QIDS) and the Beck Depression Inventory (BDI), can be used in clinical settings. Commonly used bipolar symptom rating scales, including those that can be self-rated by patients, are summarized in Table 2.3. In the era of growingly sophisticated information technology, electronic self-monitoring instruments using computers, personal digital assistants, Web interfaces, and smartphones have recently been explored. A recent review by Fauholt-Jepsen et al. [80] suggested that electronic self-monitoring of depression is more robust than that of mania and that more rigorous studies on its benefits and harm are needed.