Journal of Geriatric Mental Health

: 2020  |  Volume : 7  |  Issue : 1  |  Page : 11--20

Depression and somatic symptoms in dementia: A narrative review

Shiva Shanker Reddy Mukku, Geetha Desai, Santosh K Chaturvedi 
 Department of Psychiatry, NIMHANS, Bengaluru, Karnataka, India

Correspondence Address:
Dr. Shiva Shanker Reddy Mukku
Department of Psychiatry, NIMHANS, Bengaluru, Karnataka


Dementia is an irreversible progressive degenerative disease with cognitive impairment. Cognitive impairment eventually leads to impaired activities of daily living and premature mortality. Apart from cognitive symptoms, nearly two-thirds of dementia patients have behavioral problems commonly known as behavioral and psychological symptoms of dementia (BPSDs). Depression and dementia have a complex relationship. Depression is a risk factor, prodrome and as well as a BPSD symptom in dementia. Depression in dementia is known to cause decreased quality of life and poor outcomes. Depression though common in dementia it is often under-recognized and treated. Somatic symptoms are further less studied BPSD in dementia. With the changes in nosology and criteria for somatic symptoms disorders in the classificatory system, there is renewed interest in somatic symptoms in dementia. In this article, we discuss about depressive and somatic symptoms in patients with dementia along with assessment and management.

How to cite this article:
Reddy Mukku SS, Desai G, Chaturvedi SK. Depression and somatic symptoms in dementia: A narrative review.J Geriatr Ment Health 2020;7:11-20

How to cite this URL:
Reddy Mukku SS, Desai G, Chaturvedi SK. Depression and somatic symptoms in dementia: A narrative review. J Geriatr Ment Health [serial online] 2020 [cited 2020 Aug 13 ];7:11-20
Available from:

Full Text


Dementia is a progressive neurodegenerative condition commonly presenting in late life. Dementia causes progressive cognitive decline and ultimately leads to dependency for activities of daily living.[1] Apart from cognitive symptoms, dementia patients have behavioral problems commonly termed as behavioral and psychological symptoms of dementia (BPSDs). BPSDs are one of the most distressing symptoms of dementia. Often, BPSDs are the reason for caregiver distress and early institutionalization.[2],[3] BPSDs commonly include apathy, depression, agitation, psychotic symptoms, sleep disturbances, emotional lability, somatic symptoms, and disinhibition.[4] Depression is one of the common BPSDs associated with dementia. Nearly 80% of dementia patients have depressive symptoms over a course of 5 years. In that 10%–20% of patients present with a major depressive disorder.[5] The relation between depression and dementia is well known.[6] Depression presenting in mid-life or late life is a known risk factor for dementia.[7],[8] Depression can present as prodrome of dementia in late-life [9] or it could be one of the BPSDs in an established dementia.[10] Depression in dementing illness is known to have a bearing on the course and quality of life of a patient.[11],[12] Though depression is common in patients with dementia, it is often underrecognized and treated. This is due to various barriers associated with health professionals as well as caregivers of dementia.

Another less studied BPSDs seen in dementia patients are somatic or bodily symptoms or somatization. These symptoms include headache, sensory and pain symptoms, gastrointestinal symptoms, and fatigue.[13],[14] These symptoms are associated with excess somatic preoccupation and distress. Somatization is traditionally considered as nonspecific physical symptoms that persist despite the absence of medical illness.[15] The recent classificatory system have changed the understanding of somatization, that it can be diagnosed even in the presence of medical illness if the preoccupation and distress is excess than expected in the individual.[16] The available literature considering the prevalence of somatization in dementia patients is still emerging. Somatization is considered an expression or idiom of distress presenting in the form of physical symptoms.[17] In continuation of the above, the concept of alexithymia, which means unable to express one's feeling remerged. Studies have reported on the association between alexithymia and somatic symptoms.[18] In case of neurodegenerative conditions presenting with somatization, apart from the psychological explanations, there are also evolving neurobiological processes happening in the brain as a part of the illness. In this way, dementia might provide further insights into the neurobiological understanding of somatoform disorder. From the above prelude, it is clear that comorbid depression and somatization in dementia play an important role in the outcome and quality of life in these patients. The objective of this article is to discuss about depression and somatization in patients with dementia along with recent advances in evaluation and management.


The articles related to dementia, somatic symptoms, and depression were searched in PUBMED and GOOGLE SCHOLAR websites. A search using terms “Dementia” combining with other terms “depression,” “assessment of depression,” “Evaluation of depression” and “Management,” “somatisation,” “Somatic symptoms,” “vague pain symptoms.” We have chosen the articles related to the topic that are published in the English language.

 Depression in Dementia

Dementia and depression in the elderly are the important causes of morbidity and mortality in late life. There is a complex relation between depression and dementia. As it was discussed earlier depression is a proven risk factor for dementia, it could be a prodrome of dementia when it occurs in late life or it can be a BPSD.[6],[19] In the recent Lancet Commission on dementia, depression contributes to 4% out of 35% total potential modifiable risk factors.[20] There is also overlap in clinical features and to certain extant shared genetics such as ApoE4 allele.[21],[22],[23] Depression is one of the most common behavioral symptoms in dementia. Studies have reported depression further reduces the quality of life in patients with dementia.[24],[25] Here, we discuss the prevalence, neurobiology, evaluation, and management of depression in dementia.

 Prevalence of Depressive Symptoms in Dementia

Depression/depressive symptoms are highly prevalent psychiatric morbidity in dementia. In a study done on 98 patients with Alzheimer's dementia (AD)/vascular dementia (VaD) attending psychiatry unit in Moscow, the prevalence of depression was 87% using DSM-IV criteria and Geriatric Depression Scale (GDS).[24] The prevalence of depression in dementia from low- and middle-income countries from the 10/66 study data was 12.4%.[26] In the 10/66 study depression was assessed using Geriatric mental status examination. Compared with Alzheimer's disease (AD), diffuse lewy body dementia (DLBD) (odds ratio [OR]: 2.75 [95% confidence interval [CI]: 1.40–3.72]) and VaD (OR: 2.35, [95% CI: 1.49–3.72]) were associated with a higher risk of depression.[26] In a meta-analysis done in 2015 which included 63 studies reported 12.7% as prevalence of depression in dementia as per DSM-IV criteria and 42% using specific instruments in dementia.[27] The Cache County Study reported a 30-day prevalence of depressive symptoms in 29.9% of participants with dementia and in 16.9% of participants with cognitive impairment that did not meet criteria for dementia, and 4.9% in cognitively normal individuals.[28] The prevalence of depression in the elderly without dementia from two studies with larger samples conducted in rural part of north India and south India were 7.5% and 12.7%, respectively.[29],[30] A recent meta-analysis reported the prevalence of depression in elderly from published Indian studies as 34.4%.[31] The prevalence of depression in dementia is higher compared to that in the elderly without dementia from the available literature. However, there were no comparative studies from India. The variability in the prevalence of depression in dementia across the studies could be due to differences in the instrument used for assessing depression, setting, severity, and type of dementia. Depression is also relatively persistent in dementia, as several studies have shown about half of dementia patients with depression remain depressed even after 1 year.[32]

 Etiology of Depression in Dementia

The causes of depressive symptoms in dementia can be understood by classifying into two broad categories viz., psychological and biological. The psychological factors contribute especially in earlier stages of dementia for depression. In the initial stages of mild cognitive impairment and mild dementia, patients have cognitive decline but are able to perform usual activities. In this stage, factors that contribute for depression are becoming consciously aware of cognitive decline, reduced: functional ability, excessive worry about their own health, preoccupation about their role, anxiety due to word-finding difficulty, difficulty in recalling names of relatives in social gatherings and stigma. The collusion that often exists between the families and physicians under the premise that patient does not remember the information shared also creates anxiety in the patients.[33]

The structures involved in the regulation of emotions and mood are the prefrontal cortex and limbic structure.[34] The prefrontal structures more specifically dorsolateral and ventromedial areas are known to be implicated in producing depression.[35] Along with above said structures, the corticostriatal circuits connecting the prefrontal basal ganglia and limbic structures are the networks regulating the mood and behavior.[36] Any condition that causes disruption of these circuits leads to depression. Dementia being a neurodegenerative condition causes disruption of corticostriatal circuits and affect prefrontal regions thus increases the risk for depression.[37],[38] In VaD, the involvement of subcortical structures and deep white matter are implicated in depression.[39],[40] Another important factor that increases the risk of depression in dementia is the involvement of the serotonergic system. In AD and synucleopathies (Parkinson's disease [PD], DLBD), the degenerative process involves raphe nucleus is and implicated in the loss of serotonergic neurons.[41] There is also evidence from postmortem studies of patients with dementia which report decreased levels of serotonin and its metabolite 5-hydroxyindoleacetic acid in cerebrospinal fluid and cortex.[42],[43] A study on postmortem brain sample of AD patients compared the neurotic plaques (NPs) and neurofibrillary tangles (NTs) and Geriatric Depression Scores (GDS). The study reported no association of GDS scores with NP and NF in patients with AD.[44]

 Risk Factors for Depression in Dementia

Reported risk factors for depression in dementia include earlier age at onset of dementia, female gender, lower education, previous history of depression, greater severity of neuropsychiatric symptoms, benzodiazepine use, history of transient ischemic attack and recent losses.[44],[45],[46] Psychosocial factors such as financial burden, dependency, change in the family setup and poor social support increase the risk of anxiety and depression in patients with dementia.[47] However, factors such as the severity of cognitive impairment, insight, NPs, and NTs are poorly correlated with depression in dementia.[44],[45],[48],[49]

 Impact of Depression on Dementia

In a patient with a dementing illness, comorbid depression has severe repercussion in the course and quality of life. Depression increases inactiveness, lead to decreased physical activity, poor sleep and decreased appetite. During depression, patients may not comply with routine activities, regular medication, and physician consultations. All these will lead to further cognitive decline and progression of illness. Depression decreases the quality of life of a patient and increases mortality.[12] This also lead to increase in the caregiver burden and distress in them.[50] More serious consequences of depression in dementia many include refusal of food and suicidal attempts. All these issues in a patient with dementia and comorbid depression will increase morbidity and early institutionalization.[51],[52] There is also increased health-care utilization and family burden.[53],[54]

 Bidirectional Relationship between Depression and Dementia

Depression and dementia are two mental illnesses that are commonly seen in the elderly. Depression and dementia manifest at different time points in life which is the common scenario or depression can present as a prodrome of dementia or coexist together. Apart from higher dual existence in the elderly, they also increase the risk of each other. Several retrospective and prospective studies (Framingham Heart Study, Rotterdam Scan Study, Women's Health Initiative Memory Study) have reported that depression irrespective of the age of onset increases the risk for dementia.[7],[19],[55],[56] There are reports that besides depression being a risk factor for dementia, it can be an early symptom or prodrome of dementia.[9],[57] Few neurobiological hypothesis have been put forward regarding this, such as glucocorticoid neurotoxicity, comorbid cerebral vascular disease, higher prevalence of Apoε 4 in elderly with depression which are known risk factors for dementia.[58],[59],[60]


It is a standard practice for patients presenting with depressive illness in late life to screen and evaluate for cognitive impairment and dementia. Similarly, in patients with established dementia, screening, and enquiry for depressive symptoms are advised at every patient visit. It is not as straight forward to diagnose depression in dementia as in healthy young individuals. There are few challenges in diagnosing depression in dementia such as patient inability to comprehend the physician words, unable to express due to word-finding difficulty and hearing and visual impairment in elderly are other issues that compound the matters further during the psychiatric interview. All these could lead to interviewing the caregivers and getting circumstantial evidence about the patient's well-being and psychological issues. This might not give accurate information all the time. Sometimes if caregivers are not keen observers, it leads to underreporting and missing the depression.[61] There is also an overlap of certain symptoms such as apathy, poor concentration and sleep/appetite changes which can occur in depression as well as dementia. These symptoms may often be overlooked thus under recognizing the depression.[62]

Here are a few pointers that could be useful in routine clinical practice to diagnose depression in dementia. Depression in dementia patient should be suspected if there is (1) unexplained acute cognitive worsening from the previous level of functioning; (2) if there are new behavioral problems such as agitation, withdrawn behavior, decreased spontaneous speech and decreased sleep at night, decreased food intake and uncooperativeness for routine activities; and (3) symptoms such as anxiety, loss of energy, irritability, delusions and hallucinations may all be are more common in depression with dementia. All these should be enquired with caregivers or staff of residential care facility during the physician visit. Always spend time with the patient to get his perspective on depressive symptoms. Observation of patient behavior will also reveal signs of depression such as psychomotor retardation or agitation, crying spells and appearing withdrawn. It is advisable to review patients and reach a diagnosis on prospective observation than cross-sectional examination especially when one suspect medico-legal issues. Few standard scales are recommended for use to screen for depression in dementia.[62],[63] One of the popular and widely used scales is the GDS.[64] It is a self-rated 30 item rated on binary response (yes or no) scale. It is a validated tool to screen depression in the elderly. The shortened 15 item version is more frequently used in the clinical setting. A score above 5 indicate possible depression and score above 10 more probable depression. Another scale used to screen depression in moderate to severe stage of dementia is Cornell scale for depression in dementia (CSDD).[65] It is a 19 item scale, scored from the informant interview about the patient and direct observation of the patient. Each item is rated for severity on a scale of 0–2 (0 = absent, 1 = mild or intermittent, and 2 = severe). Scores above 10 indicate a probable major depression. Scores above 18 indicate a definite major depression. These two scales are useful in busy clinics to find elderly patients who are likely to have underlying depression thus they can be interviewed further for clinical diagnosis. In patients in whom depression is not evident from single consultation, regular follow-up is suggested. In patients with severe depression expressing suicidal ideas or suicidal attempts needs to be admitted to a safer place for further intensive management. It is advisable to review the medical history and medication to prevent any drug interactions.


Nonpharmacological interventions

The nonpharmacological intervention should be the first line of treatment in the management of depression in dementia especially when the severity of depression is mild to moderate. These interventions could be as simple as initiating daily physical activities to start with. Physical activities/exercises have been found to be effective in reducing depressive symptoms along with multiple physical benefits.[66] Reminiscence therapy using patients old pictures, videos, personal objects and making patients to connect to the past events and promote a positive mood in them is another method.[67] Another behavioral intervention by Lewisohn's based on 'Pleasant Events model' known as behavioral programming. This model is based on the assumption that a person's behavior is related to how he or she feels. This technique involves identifying pleasant and negative events in the patient's daily life.[68] This model along with physical exercise has been evaluated in AD patients and found to have a positive effect in depression.[69] Cognitive behavioral therapy targeting the negative automatic thoughts and cognitive distortion could be useful in mild stage of dementia.[70],[71] Another behavioral intervention that has been studied is problem solving therapy.[72],[73] It was found to be effective for caregivers of dementia.[74] Few other innovative interventions such as art therapy,[75] animal-assisted therapy,[76] music therapy,[77],[78] and multisensory stimulation (snoezelen)[79] can be tried in certain patients but these are not well studied in the Indian setting. Aromatherapy and massage/touch therapy has been tried with a positive effect on agitation in patients with dementia, but, there is limited evidence for depression.[80],[81] Though nonpharmacological interventions are useful and should be tried first especially in mild to moderate severity of depression there are certain limitations. First is the patient's cooperativeness and acceptability of these interventions. Another important limitation is the time that needs to be spent by caregivers or paid professionals with patients. It is a major challenge in low- and middle-income countries, where the care is provided by mostly informal (family members). The last limitation is many of these interventions we have discussed were not been vigorously tested in methodologically proven ways.


Pharmacological interventions should be considered if psychological/behavioral interventions have not resulted in an optimal response or not feasible in patients with dementia. Medication can be tried in severe depression either alone or along with psychological interventions wherever feasible. The response to medication in patients with dementia is suboptimal compared to the younger population. The reasons include elderly age, higher medical comorbidities which will alter the pharmacokinetics and pharmacodynamics of the psychotropics. Medical comorbidities often limit reaching a therapeutic dose leading to low response rates. The degenerative condition itself causes changes in brain microenvironment leading to treatment-resistance. There are relatively less vigorous methodological studies on use of antidepressants in dementia. There is a low to moderate level of evidence for medication in the treatment of dementia with depression. Guidelines for the management of BPSD in dementia formulated by National Institute for Health and Care Excellence,[82] American Psychiatric Association guidelines,[83] Australian guidelines for depression in dementia [84] and Clinical Practice Guidelines-Indian Psychiatric Society [85] are recommended.

Antidepressants in depression

Antidepressants are broadly classified into tricyclic antidepressants (TCA), selective serotonin reuptake inhibitors (SSRIs) and newer antidepressants such as mirtazapine, bupropion venlafaxine etc., Many of these drugs have been studied in dementia patients with dementia with comorbid depression. The evidence for antidepressants in dementia with depression found only modest effect which was not statistically significant compared to placebo.[86],[87] SSRIs are the preferred first choice of medication followed by mirtazapine and trazodone.[88] Concerns with SSRI in the elderly include sedation, risk of falls, osteoporosis, fractures, hyponatremia, and risk of gastrointestinal (GIT) bleeding. Any elderly patient who requires SSRI trial needs to be investigated thoroughly with blood investigation (serum electrolytes, RFT, LFT, and FBS), electrocardiogram, and history of GIT bleeding and falls. Antidepressants should be titrated slowly to their effective dose, monitoring simultaneously for adverse effects periodically. TCAs are preferably be avoided in patients with dementia due to their higher cardiotoxicity and anticholinergic burden.[89]

Acetylcholinesterase inhibitors and memantine

Cholinesterase inhibitors and memantine are commonly prescribed medication in AD. These drugs are known to preserve the functioning for longer duration and delay the time to institutionalization. Limited studies that have looked at the effect of Acetylcholinesterase inhibitor (ACEI) and memantine on BPSD found their usefulness.[90],[91] Though depression was not specifically studied, there was reduction in behavioral problems and neuropsychiatry inventory scores with ACEI.[92],[93],[94]


Valproate, carbamazepine and lamotrigine have been used for behavioral problems with modest efficacy.[95],[96] There are studies that found decreased GABA level in cortical regions and hypothesized to have a causative role in BPSD.[97] Anticonvulsants by increasing the GABA level were proposed to be helpful in BPSD. There is little direct evidence for anticonvulsants for depression in dementia. These can be used after the failed trial of SSRI and other newer antidepressants.

Brain stimulation methods

Electroconvulsive therapy (ECT) is a proven and effective treatment for depression in cognitively healthy patients. ECT was investigated as a treatment for depression in dementia in few studies. The studies have shown positive results in studies on dementia with depression.[98] The risk of worsening of cognitive symptoms such as post-ECT confusion, the presence of medical comorbidities often limits its acceptability in elderly and even more so in patients with dementia.[99] There is recent emerging evidence on the tolerability of ECT in patients with dementia for various indications.[98],[100] At this point, ECT can be considered as an option when other treatment methods fail in moderate to severe dementia patients. Pre-ECT evaluation for fitness, education of family members, and monitoring for any cognitive worsening regularly after ECT will ensure safe and effective use of ECT.[101] Repetitive transcranial magnetic stimulation (rTMS) has been tried in patients with AD primarily for cognitive symptoms.[102] In two studies involving smaller samples, rTMS led to improvement in comorbid depression in patients with AD.[103],[104] Transcranial direct current stimulation (tDCS) is another noninvasive modality with literature limited to its usefulness for apathy in dementia. There is an ongoing randomized controlled trial evaluating the effectiveness of tDCS for depression in dementia.[105]

 Somatic Symptoms in Dementia

The 1-year prevalence rate of somatoform disorders in the elderly in the community is 3.8% compared to 11%–20% in a younger individual.[106],[107] Most studies reported low prevalence of somatoform disorders in late life. This is due to various limitations in the methodology of the studies along with difficulties in assessing elderly for somatoform disorders. Elderly patients often have comorbid medical illnesses that are known to cause pain and other physical symptoms. They generally present to a physician with these complaints rather than to mental health professionals, thus leading to less enquiry and recognition of somatoform in elderly.[108] As per the ICD-10 diagnostic criteria, somatization disorder is defined as the presence of vague, multiple physical symptoms for at least 2 years with excessive preoccupation and distress. These symptoms should not be explained by any other medical condition.[15] After two decades these criteria were changed in DSM-5, and the condition is called somatic symptom disorder. It is now defined as a condition with persistent somatic symptoms that are accompanied by abnormal thoughts, feelings and behaviors. Another major change from ICD-10 was somatic symptom disorder can be diagnosed even in the presence of the medical condition.[109] There is well-established evidence for the occurrence of somatic symptoms as individual symptoms or as comorbid condition in depressive disorders and anxiety disorders in the elderly. Somatic symptoms are considered to represent psychological distress presenting as physical symptoms. The underlying concept which explains the presence of somatic symptoms is alexithymia. Alexithymia is an enduring characteristic trait in which a person is unable to express his emotions due to genetic and environmental factors.[110] There are reports on the occurrence of somatic symptoms in neurodegenerative condition such as dementia. More than half a century ago, Robertson published detailed clinical descriptions of 3 cases with Pick's disease where somatic complaints and generalized hyperalgesia were the prominent clinical symptoms.[111] This is followed by Gustafson who made similar observations in frontotemporal dementia (FTD) and possible neuroanatomical structures involved.[112]

 Prevalence of Somatic Symptoms in Dementia

There were few studies that have evaluated the prevalence of somatic symptoms along with other behavioral problems in dementia. One of the initial studies by Bathgate et al. compared the prevalence of somatic symptoms in FTD, AD and VaD using a semi-structured questionnaire. The study found the somatic symptoms in the form of hyperalgesia was 33% in FTD, 42% in AD and 26% VaD.[113] Another cross-sectional study by Chan et al., reported somatic symptoms in 35% FTD patients with right predominant temporal lobe atrophy.[114] A larger retrospective study by Landqvist Wald et al. in 97 FTD patients reported somatic symptoms in 40.2%. The study also compared the relation between somatic symptoms in tau-positive and tau-negative FTD patients. However, no significant correlation was found between various pathological types and somatic symptoms.[13] The latest study on somatic symptoms by Gan et al. compared the prevalence of somatic symptoms in semantic dementia and AD. The prevalence was higher in Semantic dementia (SD) (41.5%) compared to AD (11.2%) with an odd ratio of 6:1. The common symptoms were misidentification, preoccupation with normal bodily sensation such as hunger, bladder filling, borborygmi, rhinorrhea, and reflux.[115] Among the very few prospective studies, the one by Onofrij et al. compared prevalence of somatic symptoms in PD with other degenerative conditions (DLBD, AD, FTD, Progressive Supranuclear Palsy [PSP], and Multisystem Atrophy [MSA]). The study found prevalence of 7% in PD, 12% in DLBD, 1% in AD, 2.5% in PSP and 0% in FTD and MSA. Within the diagnostic groups, there was a difference between those with somatic symptoms and those without in demographic and clinical features.[116] However, in patients with PD, the cognitive decline was higher in those with somatic symptoms.[116] In elderly without dementia a study from north India using “Schedule for Clinical Assessment in Neuropsychiatry” reported prevalence of somatization as <2%.[29] Similar study from south India using “Patient Health Questionnaire-15” reported somatization in 40% of the elderly.[117] The frequency of somatization is higher in dementia compared to the elderly without dementia, but there is heterogeneity among the studies. Few limitations of these studies such as most of them being cross-sectional or retrospective in nature, hospital-based and no structured assessment used in most studies, which limits the generalizability of the results [Table 1].{Table 1}

 Neurobiological Aspects of Somatization in Dementia

Patients with somatoform disorder are thought to have certain abnormalities in the sensory processing in the brain. These patients often exhibit a heightened focus on their own bodies, perceiving their bodily complaints quicker as illness than healthy people do.[118] Central sensitization is another concept that has recently been used to describe a neurobiological abnormality. According to this concept, it is assumed that somatic symptom onset is associated with a hyper-responsive neural network. Patients with somatization are also known to rate normally innocuous stimuli as painful stimulation due to an alteration of the central network.[119] A meta-analysis of 10 studies reported major differences in the premotor and supplementary motor cortex, middle frontal gyrus, anterior cingulate cortex, insula and posterior cingulate cortex in somatoform disorder patients compared to healthy individuals.[120] Similar to these findings, somatization in dementia could also be due to abnormalities in central pain processing networks.[121],[122] Studies have reported somatic symptoms more commonly in semantic FTD and behavioral variant FTD and to a lesser extent in AD.[113] FTD formed a prototype in understanding the origin of somatic symptoms in dementia. The initial finding reported that midline frontal and anterior cingulate which are part of pain processing are affected in FTD.[123] This could be one reason for somatization in FTD. Later studies using neuroimaging in FTD patients with somatic symptoms revealed grey matter loss in posterior thalamus, posterior insula and anterior temporal cortex. These areas are known to be part of central pain processing. In the case of SD, there is another perspective for somatization. It is known that in SD there is loss of object knowledge, single-word comprehension with relatively spared episodic memory. Apart from the inability to make meaning of the external world, they have difficulty in interpreting normal physiological sensation described as “alexisomia”. This leads to excessive preoccupation and misinterpreting these stimuli which manifest as somatic symptoms.[115] There is also a genetic basis to the somatic symptoms in FTD particularly those with C9ORF72 mutations reported to have a higher rate of somatic symptoms.[124] It is well known that somatization is often associated with depression and anxiety, but contrary to this, study by Landqvist Wald et al. found no such association.[13]

 Challenges in the Evaluation of Somatic Symptoms in Elderly and Dementia

Evaluation of somatic symptoms in the elderly is challenging. To begin with, late life is associated with increased prevalence of medical and surgical conditions. Conditions such as osteoarthritis, peripheral neuropathy, osteoporosis, tumors, diabetes, ischemic heart disease and their complications are well known to cause pain and other physical symptoms. These are difficult to differentiate from somatoform disorder in routine consultation with a physician.[125] The somatic symptoms are often treated as physical condition and treated in that manner. There is also a tendency for physicians to overlook the diagnosis of somatoform in elderly compared to that in the younger patients. Another challenge faced among the elderly is excessive worry regarding their physical changes associated with ageing and health-related issues. The preoccupation about their health, associated safety measures and frequent physician consultations will make them more likely receive a diagnosis of anxiety disorder or depression than a somatoform disorder.[108] Further, lack of office-based and easy to use screening tools also lead to under-recognition of this disorder. In the case of dementia, the issues are even more complex. The cognitive impairment in dementia become a major barrier in interviewing the patients. In a patient with dementia cognitive impairment, medical comorbidity and disruptive behavioral problems are the major issues for caregivers and physicians. In these scenarios, somatic symptoms are overlooked and often never get evaluated.

 Instruments to Assess Somatic Symptoms in Elderly

There are many instruments for assessing somatic symptoms with only few studied in the elderly population. Somatic Symptom Index is one of the earliest scales for identifying somatoform disorder. It has 35 items and validated in many epidemiological studies.[126] Brief Symptom Screen is a self-rated 10 item scale developed for elderly people. Symptoms included are shortness of breath, feeling tired or fatigued, problems with balance or dizziness, perceived weakness in legs, constipation, daily pain, stiffness, poor appetite, anxiety, and anhedonia.[127] Patient Health Questionnaire (PHQ-15) is a self-administered somatic symptoms subscale, derived from the full Patient Health Questionnaire. PHQ-15 specifically assesses somatic symptom severity and the potential presence of somatization and somatoform disorder. The PHQ-15 has good reliability, construct, and criterion validity.[128] Few other instruments include Scale for Assessment of Somatic Symptoms,[129] Subjective Health Complaints Inventory,[130] and Somatic Symptom Scale-8.[131] Details regarding these instruments are given in [Table 2].{Table 2}


BPSD is an important symptom domain which determines the quality of life and caregiver burden in dementia care. BPSD presenting as depression and somatization are often underdiagnosed and undertreated. Depression has a unique relation with dementia in terms of shared risk factors, shared genetics and few symptom overlap. These features make identifying depression in dementia a diagnostic challenge. Collateral information from multiple caregivers, behavioral observation and using appropriate standard scales helps in early identification of depression in dementia. The management of depression in dementia should always begin with behavioral and psychological interventions. In a situation where behavioral interventions are not feasible or not effective, medication should be considered. Antidepressants should be considered only after weighing the risk and benefits or as a first choice in those with severe depression. The effectiveness of antidepressants in dementia with depression is poor in randomized control trails. ECT can be considered in refractory depression in patients with dementia or in whom medication has caused significant adverse effects. Somatic symptoms/somatization in dementia are less explored domain compared to other BPSDs. They are commonly reported in FTD and its variants. There is emerging literature of neurobiology of somatic symptoms in SD. Somatization further needs to be investigated in other subtypes of dementia.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Scott KR, Barrett AM. Dementia syndromes: Evaluation and treatment. Expert Rev Neurother 2007;7:407-22.
2Müller-Spahn F. Behavioral disturbances in dementia. Dialogues Clin Neurosci 2003;5:49-59.
3Feast A, Orrell M, Charlesworth G, Melunsky N, Poland F, Moniz-Cook E. Behavioural and psychological symptoms in dementia and the challenges for family carers: Systematic review. Br J Psychiatry 2016;208:429-34.
4Cerejeira J, Lagarto L, Mukaetova-Ladinska EB. Behavioral and psychological symptoms of dementia. Front Neurol 2012;3:73.
5Milwaukee W. IPA Complete Guides to Behavioral and Psychological Symptoms of Dementia (BPSD). New South Wales, Australia: International Psychogeriatric Association; 2010.
6Muliyala KP, Varghese M. The complex relationship between depression and dementia. Ann Indian Acad Neurol 2010;13:S69-73.
7Saczynski JS, Beiser A, Seshadri S, Auerbach S, Wolf PA, Au R. Depressive symptoms and risk of dementia: The Framingham Heart Study. Neurology 2010;75:35-41.
8Schweitzer I, Tuckwell V, O'Brien J, Ames D. Is late onset depression a prodrome to dementia? Int J Geriatr Psychiatry 2002;17:997-1005.
9Brommelhoff JA, Gatz M, Johansson B, McArdle JJ, Fratiglioni L, Pedersen NL. Depression as a risk factor or prodromal feature for dementia? Findings in a population-based sample of Swedish twins. Psychol Aging 2009;24:373-84.
10Kitching D. Depression in dementia. Aust Prescr 2015;38:209-11.
11Meeks TW, Vahia IV, Lavretsky H, Kulkarni G, Jeste DV. A tune in “a minor” can “b major”: A review of epidemiology, illness course, and public health implications of subthreshold depression in older adults. J Affect Disord 2011;129:126-42.
12Mehta KM, Yaffe K, Langa KM, Sands L, Whooley MA, Covinsky KE. Additive effects of cognitive function and depressive symptoms on mortality in elderly community-living adults. J Gerontol A Biol Sci Med Sci 2003;58:M461-7.
13Landqvist Waldö M, Santillo AF, Gustafson L, Englund E, Passant U. Somatic complaints in frontotemporal dementia. Am J Neurodegener Dis 2014;3:84-92.
14Brown FW. Somatization disorder in progressive dementia. Psychosomatics 1991;32:463-5.
15ICD-10 Classification of Mental and Behavioral Disorders. Geneva, Switzerland: World Health Organization; 1992.
16Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Washington, DC: American Psychiatric Association; 2013.
17Desai G, Chaturvedi SK. Idioms of distress. J Neurosci Rural Pract 2017;8:S94-7.
18Mattila AK, Kronholm E, Jula A, Salminen JK, Koivisto AM, Mielonen RL, et al. Alexithymia and somatization in general population. Psychosom Med 2008;70:716-22.
19Barnes DE, Yaffe K, Byers AL, McCormick M, Schaefer C, Whitmer RA. Midlife vs. late-life depressive symptoms and risk of dementia: Differential effects for Alzheimer disease and vascular dementia. Arch Gen Psychiatry 2012;69:493-8.
20Livingston G, Sommerlad A, Orgeta V, Costafreda SG, Huntley J, Ames D, et al. Dementia prevention, intervention, and care. Lancet 2017;390:2673-734.
21Corsentino EA, Sawyer K, Sachs-Ericsson N, Blazer DG. Depressive symptoms moderate the influence of the apolipoproteine epsilon4 allele on cognitive decline in a sample of community dwelling older adults. Am J Geriatr Psychiatry 2009;17:155-65.
22Qiu WQ, Zhu H, Dean M, Liu Z, Vu L, Fan G, et al. Amyloid-associated depression and ApoE4 allele: Longitudinal follow-up for the development of Alzheimer's disease. Int J Geriatr Psychiatry 2016;31:316-22.
23Leyhe T, Reynolds CF 3rd, Melcher T, Linnemann C, Klöppel S, Blennow K, et al. A common challenge in older adults: Classification, overlap, and therapy of depression and dementia. Alzheimers Dement 2017;13:59-71.
24Winter Y, Korchounov A, Zhukova TV, Bertschi NE. Depression in elderly patients with Alzheimer dementia or vascular dementia and its influence on their quality of life. J Neurosci Rural Pract 2011;2:27-32.
25Shaji KS, George RK, Prince MJ, Jacob KS. Behavioral symptoms and caregiver burden in dementia. Indian J Psychiatry 2009;51:45-9.
26Andreasen P, Lönnroos E, von Euler-Chelpin MC. Prevalence of depression among older adults with dementia living in low- and middle-income countries: A cross-sectional study. Eur J Public Health 2014;24:40-4.
27Chi S, Wang C, Jiang T, Zhu XC, Yu JT, Tan L. The prevalence of depression in Alzheimer's disease: A systematic review and meta-analysis. Curr Alzheimer Res 2015;12:189-98.
28Peters ME, Rosenberg PB, Steinberg M, Tschanz JT, Norton MC, Welsh-Bohmer KA, et al. Prevalence of neuropsychiatric symptoms in CIND and its subtypes: The Cache County Study. Am J Geriatr Psychiatry 2012;20:416-24.
29Tiwari SC, Srivastava G, Tripathi RK, Pandey NM, Agarwal GG, Pandey S, et al. Prevalence of psychiatric morbidity amongst the community dwelling rural older adults in northern India. Indian J Med Res 2013;138:504-14.
30Rajkumar AP, Thangadurai P, Senthilkumar P, Gayathri K, Prince M, Jacob KS. Nature, prevalence and factors associated with depression among the elderly in a rural south Indian community. Int Psychogeriatr 2009;21:372-8.
31Pilania M, Yadav V, Bairwa M, Behera P, Gupta SD, Khurana H, et al. Prevalence of depression among the elderly (60 years and above) population in India, 1997-2016: A systematic review and meta-analysis. BMC Public Health 2019;19:832.
32Garre-Olmo J, López-Pousa S, Vilalta-Franch J, Turon-Estrada A, Hernàndez-Ferràndiz M, Lozano-Gallego M, et al. Evolution of depressive symptoms in Alzheimer disease: One-year follow-up. Alzheimer Dis Assoc Disord 2003;17:77-85.
33Ganguli M. Depression, cognitive impairment and dementia: Why should clinicians care about the web of causation? Indian J Psychiatry 2009;51 Suppl 1:S29-34.
34Naismith SL, Norrie LM, Mowszowski L, Hickie IB. The neurobiology of depression in later-life: Clinical, neuropsychological, neuroimaging and pathophysiological features. Prog Neurobiol 2012;98:99-143.
35Koenigs M, Grafman J. The functional neuroanatomy of depression: Distinct roles for ventromedial and dorsolateral prefrontal cortex. Behav Brain Res 2009;201:239-43.
36Drevets WC, Price JL, Furey ML. Brain structural and functional abnormalities in mood disorders: Implications for neurocircuitry models of depression. Brain Struct Funct 2008;213:93-118.
37Lopez OL, Zivkovic S, Smith G, Becker JT, Meltzer CC, DeKosky ST. Psychiatric symptoms associated with cortical-subcortical dysfunction in Alzheimer's disease. J Neuropsychiatry Clin Neurosci 2001;13:56-60.
38Hirono N, Mori E, Ishii K, Ikejiri Y, Imamura T, Shimomura T, et al. Frontal lobe hypometabolism and depression in Alzheimer's disease. Neurology 1998;50:380-3.
39Rensma SP, van Sloten TT, Launer LJ, Stehouwer CD. Cerebral small vessel disease and risk of incident stroke, dementia and depression, and all-cause mortality: A systematic review and meta-analysis. Neurosci Biobehav Rev 2018;90:164-73.
40Brookes RL, Herbert V, Lawrence AJ, Morris RG, Markus HS. Depression in small-vessel disease relates to white matter ultrastructural damage, not disability. Neurology 2014;83:1417-23.
41Lanctôt KL, Herrmann N, Mazzotta P. Role of serotonin in the behavioral and psychological symptoms of dementia. J Neuropsychiatry Clin Neurosci 2001;13:5-21.
42Arai H, Kosaka K, Iizuka R. Changes of biogenic amines and their metabolites in postmortem brains from patients with Alzheimer-type dementia. J Neurochem 1984;43:388-93.
43Bråne G, Gottfries CG, Blennow K, Karlsson I, Lekman A, Parnetti L, et al. Monoamine metabolites in cerebrospinal fluid and behavioral ratings in patients with early and late onset of Alzheimer dementia. Alzheimer Dis Assoc Disord 1989;3:148-56.
44McCutcheon ST, Han D, Troncoso J, Koliatsos VE, Albert M, Lyketsos CG, et al. Clinicopathological correlates of depression in early Alzheimer's disease in the NACC. Int J Geriatr Psychiatry 2016;31:1301-11.
45Rosness TA, Barca ML, Engedal K. Occurrence of depression and its correlates in early onset dementia patients. Int J Geriatr Psychiatry 2010;25:704-11.
46Savva GM, Zaccai J, Matthews FE, Davidson JE, McKeith I, Brayne C, et al. Prevalence, correlates and course of behavioural and psychological symptoms of dementia in the population. Br J Psychiatry 2009;194:212-9.
47Orrell M, Bebbington P. Psychosocial stress and anxiety in senile dementia. J Affect Disord 1996;39:165-73.
48Verkaik R, Nuyen J, Schellevis F, Francke A. The relationship between severity of Alzheimer's disease and prevalence of comorbid depressive symptoms and depression: A systematic review. Int J Geriatr Psychiatry 2007;22:1063-86.
49Carpenter BD, Xiong C, Porensky EK, Lee MM, Brown PJ, Coats M, et al. Reaction to a dementia diagnosis in individuals with Alzheimer's disease and mild cognitive impairment. J Am Geriatr Soc 2008;56:405-12.
50Watson LC, Lewis CL, Moore CG, Jeste DV. Perceptions of depression among dementia caregivers: Findings from the CATIE-AD trial. Int J Geriatr Psychiatry 2011;26:397-402.
51Feng L, Scherer SC, Tan BY, Chan G, Fong NP, Ng TP. Comorbid cognitive impairment and depression is a significant predictor of poor outcomes in hip fracture rehabilitation. Int Psychogeriatr 2010;22:246-53.
52Lavretsky H, Zheng L, Weiner MW, Mungas D, Reed B, Kramer JH, et al. Association of depressed mood and mortality in older adults with and without cognitive impairment in a prospective naturalistic study. Am J Psychiatry 2010;167:589-97.
53Grover S, Malhotra N. Depression in elderly: A review of Indian research. J Geriatr Ment Health 2015;2:4.
54Bock JO, Luppa M, Brettschneider C, Riedel-Heller S, Bickel H, Fuchs A, et al. Impact of depression on health care utilization and costs among multimorbid patients–from the MultiCare Cohort Study. PLoS One 2014;9:e91973.
55Goveas JS, Espeland MA, Woods NF, Wassertheil-Smoller S, Kotchen JM. Depressive symptoms and incidence of mild cognitive impairment and probable dementia in elderly women: The Women's Health Initiative Memory Study. J Am Geriatr Soc 2011;59:57-66.
56Geerlings MI, den Heijer T, Koudstaal PJ, Hofman A, Breteler MM. History of depression, depressive symptoms, and medial temporal lobe atrophy and the risk of Alzheimer disease. Neurology 2008;70:1258-64.
57Ganguli M, Du Y, Dodge HH, Ratcliff GG, Chang CC. Depressive symptoms and cognitive decline in late life: A prospective epidemiological study. Arch Gen Psychiatry 2006;63:153-60.
58Sureshkumar R, Bharath S, Jain S, Prakash O, Purushottam M, Thennarasu K, et al. ApoE4 and late onset depression in Indian population. J Affect Disord 2012;136:244-8.
59Schneider B, Ercoli L, Siddarth P, Lavretsky H. Vascular burden and cognitive functioning in depressed older adults. Am J Geriatr Psychiatry 2012;20:673-81.
60MacQueen G, Frodl T. The hippocampus in major depression: Evidence for the convergence of the bench and bedside in psychiatric research? Mol Psychiatry 2011;16:252-64.
61Pattanayak RD, Sagar R. Depression in dementia patients: Issues and challenges for a physician. J Assoc Physicians India 2011;59:650-2.
62Brown EL, Raue P, Halpert KD, Adams S, Titler MG. Detection of depression in older adults with dementia. J Gerontol Nurs 2009;35:11-5.
63Goodarzi ZS, Mele BS, Roberts DJ, Holroyd-Leduc J. Depression case finding in individuals with dementia: A systematic review and meta-analysis. J Am Geriatr Soc 2017;65:937-48.
64Yesavage JA, Brink TL, Rose TL, Lum O, Huang V, Adey M, et al. Development and validation of a geriatric depression screening scale: A preliminary report. J Psychiatr Res 1982;17:37-49.
65Alexopoulos GS, Abrams RC, Young RC, Shamoian CA. Cornell scale for depression in dementia. Biol Psychiatry 1988;23:271-84.
66Williams CL, Tappen RM. Exercise training for depressed older adults with Alzheimer's disease. Aging Ment Health 2008;12:72-80.
67Bohlken J, Weber SA, Siebert A, Forstmeier S, Kohlmann T, Rapp MA. Reminiscence therapy for depression in dementia. GeroPsych (Bern) 2017;30:145-51.
68Zeiss PM, Lewinsohn AM. Adapting behavioral treatment for depression to meet the needs of the elderly. Clin Psychol 1986;34:98-100.
69Teri L, Gibbons LE, McCurry SM, Logsdon RG, Buchner DM, Barlow WE, et al. Exercise plus behavioral management in patients with Alzheimer disease: A randomized controlled trial. JAMA 2003;290:2015-22.
70Forstmeier S, Maercker A, Savaskan E, Roth T. Cognitive behavioural treatment for mild Alzheimer's patients and their caregivers (CBTAC): Study protocol for a randomized controlled trial. Trials 2015;16:526.
71Walker DA. Cognitive behavioural therapy for depression in a person with Alzheimer's dementia. Behav Cogn Psychother 2004;32:495-500.
72Alexopoulos GS, Raue PJ, Kiosses DN, Mackin RS, Kanellopoulos D, McCulloch C, et al. Problem-solving therapy and supportive therapy in older adults with major depression and executive dysfunction: Effect on disability. Arch Gen Psychiatry 2011;68:33-41.
73Mackin RS, Areán P, Elite-Marcandonatou A. Problem solving therapy for the treatment of depression for a patient with Parkinson's disease and mild cognitive impairment: A case study. Neuropsychiatr Dis Treat 2006;2:375-9.
74Garand L, Rinaldo DE, Alberth MM, Delany J, Beasock SL, Lopez OL, et al. Effects of problem solving therapy on mental health outcomes in family caregivers of persons with a new diagnosis of mild cognitive impairment or early dementia: A randomized controlled trial. Am J Geriatr Psychiatry 2014;22:771-81.
75Rusted J, Sheppard L, Waller D. A multi-centre randomized control group trial on the use of art therapy for older people with dementia. Gr Anal 2006;39:517-36.
76Motomura N, Yagi T, Ohyama H. Animal assisted therapy for people with dementia. Psychogeriatrics 2004;4:40-2.
77Lord TR, Garner JE. Effects of music on Alzheimer patients. Percept Mot Skills 1993;76:451-5.
78Holmes C, Knights A, Dean C, Hodkinson S, Hopkins V. Keep music live: Music and the alleviation of apathy in dementia subjects. Int Psychogeriatr 2006;18:623-30.
79Herrmann N. Some psychosocial therapies may reduce depression, aggression, or apathy in people with dementia. Evid Based Ment Health 2005;8:104.
80Viggo Hansen N, Jørgensen T, Ørtenblad L. Massage and touch for dementia. Cochrane Database Syst Rev 2006;2006:CD004989.
81Ballard CG, O'Brien JT, Reichelt K, Perry EK. Aromatherapy as a safe and effective treatment for the management of agitation in severe dementia: The results of a double-blind, placebo-controlled trial with Melissa. J Clin Psychiatry 2002;63:553-8.
82Pink J, O'Brien J, Robinson L, Longson D, Guideline Committee. Dementia: Assessment, management and support: Summary of updated NICE guidance. BMJ 2018;361:k2438.
83APA Work Group on Alzheimer's Disease and other Dementias, Rabins PV, Blacker D, Rovner BW, Rummans T, Schneider LS, et al. American Psychiatric Association practice guideline for the treatment of patients with Alzheimer's disease and other dementias. Second edition. Am J Psychiatry 2007;164 12 Suppl: 5-56.
84Curran EM, Loi S. Depression and dementia. Med J Aust 2013;199:S40-4.
85Shaji KS, Sivakumar PT, Rao GP, Paul N. Clinical practice guidelines for management of dementia. Indian J Psychiatry 2018;60:S312-28.
86Dudas R, Malouf R, McCleery J, Dening T. Antidepressants for treating depression in dementia. Cochrane Database Syst Rev 2018;8:CD003944.
87Orgeta V, Tabet N, Nilforooshan R, Howard R. Efficacy of antidepressants for depression in Alzheimer's disease: Systematic review and meta-analysis. J Alzheimers Dis 2017;58:725-33.
88Gellis ZD, McClive-Reed KP, Brown E. Treatments for depression in older persons with dementia. Ann Longterm Care 2009;17:29-36.
89Avasthi A, Grover S. Clinical practice guidelines for management of depression in elderly. Indian J Psychiatry 2018;60:S341-62.
90Campbell N, Ayub A, Boustani MA, Fox C, Farlow M, Maidment I, et al. Impact of cholinesterase inhibitors on behavioral and psychological symptoms of Alzheimer's disease: A meta-analysis. Clin Interv Aging 2008;3:719-28.
91Maidment ID, Fox CG, Boustani M, Rodriguez J, Brown RC, Katona CL. Efficacy of memantine on behavioral and psychological symptoms related to dementia: A systematic meta-analysis. Ann Pharmacother 2008;42:32-8.
92Garcia-Alloza M, Gil-Bea FJ, Diez-Ariza M, Chen CP, Francis PT, Lasheras B, et al. Cholinergic–serotonergic imbalance contributes to cognitive and behavioral symptoms in Alzheimer's disease. Neuropsychologia 2005;43:442-9.
93Mowla A, Mosavinasab M, Haghshenas H, Borhani Haghighi A. Does serotonin augmentation have any effect on cognition and activities of daily living in Alzheimer's dementia? A double-blind, placebo-controlled clinical trial. J Clin Psychopharmacol 2007;27:484-7.
94Amara G, Saada W, Ben Nasr S, Ben Hadj Ali B. Cholinesterase inhibitors and depression in the elderly. Encephale 2010;36:77-81.
95Yeh YC, Ouyang WC. Mood stabilizers for the treatment of behavioral and psychological symptoms of dementia: An update review. Kaohsiung J Med Sci 2012;28:185-93.
96Suzuki H, Inoue Y. A comparison of lamotrigine or sodium valproate on the efficacy in Alzheimer's disease with behavioral and psychological symptoms of dementia: A retrospective open-label study running title: Efficacy of anticonvulsants for BPSD. J Gerontol Geriatr Res 2015;4:1-5.
97Garcia-Alloza M, Tsang SW, Gil-Bea FJ, Francis PT, Lai MK, Marcos B, et al. Involvement of the GABAergic system in depressive symptoms of Alzheimer's disease. Neurobiol Aging 2006;27:1110-7.
98Oudman E. Is electroconvulsive therapy (ECT) effective and safe for treatment of depression in dementia? A short review. J ECT 2012;28:34-8.
99Nuttall GA, Bowersox MR, Douglass SB, McDonald J, Rasmussen LJ, Decker PA, et al. Morbidity and mortality in the use of electroconvulsive therapy. J ECT 2004;20:237-41.
100Acharya D, Harper DG, Achtyes ED, Seiner SJ, Mahdasian JA, Nykamp LJ, et al. Safety and utility of acute electroconvulsive therapy for agitation and aggression in dementia. Int J Geriatr Psychiatry 2015;30:265-73.
101American Psychiatric Association. Committee on Electroconvulsive Therapy, Weiner RD. The Practice of Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging: A Task Force Report of the American Psychiatric Association. American Psychiatric Association; 2001.
102Rutherford G, Gole R, Moussavi Z. rTMS as a treatment of Alzheimer's disease with and without comorbidity of depression: A review. Neurosci J 2013;2013:679389.
103Ahmed MA, Darwish ES, Khedr EM, El Serogy YM, Ali AM. Effects of low versus high frequencies of repetitive transcranial magnetic stimulation on cognitive function and cortical excitability in Alzheimer's dementia. J Neurol 2012;259:83-92.
104Bentwich J, Dobronevsky E, Aichenbaum S, Shorer R, Peretz R, Khaigrekht M, et al. Beneficial effect of repetitive transcranial magnetic stimulation combined with cognitive training for the treatment of Alzheimer's disease: A proof of concept study. J Neural Transm (Vienna) 2011;118:463-71.
105Narita Z, Yokoi Y. Transcranial direct current stimulation for depression in Alzheimer's disease: Study protocol for a randomized controlled trial. Trials 2017;18:285.
106Dehoust MC, Schulz H, Härter M, Volkert J, Sehner S, Drabik A, et al. Prevalence and correlates of somatoform disorders in the elderly: Results of a European study. Int J Methods Psychiatr Res 2017;26:e1550.
107Hilderink PH, Collard R, Rosmalen JG, Oude Voshaar RC. Prevalence of somatoform disorders and medically unexplained symptoms in old age populations in comparison with younger age groups: A systematic review. Ageing Res Rev 2013;12:151-6.
108Wijeratne C, Brodaty H, Hickie I. The neglect of somatoform disorders by old age psychiatry: Some explanations and suggestions for future research. Int J Geriatr Psychiatry 2003;18:812-9.
109Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Washington, DC: American Psychiatric Association; 2013.
110Karukivi M, Saarijärvi S. Development of alexithymic personality features. World J Psychiatry 2014;4:91-102.
111Robertson EE, Le Roux A, Brown JH. The clinical differentiation of Pick's disease. J Ment Sci 1958;104:1000-24.
112Gustafson L. Frontal lobe degeneration of non-Alzheimer type. II. Clinical picture and differential diagnosis. Arch Gerontol Geriatr 1987;6:209-23.
113Bathgate D, Snowden JS, Varma A, Blackshaw A, Neary D. Behaviour in frontotemporal dementia, Alzheimer's disease and vascular dementia. Acta Neurol Scand 2001;103:367-78.
114Chan D, Anderson V, Pijnenburg Y, Whitwell J, Barnes J, Scahill R, et al. The clinical profile of right temporal lobe atrophy. Brain 2009;132:1287-98.
115Gan JJ, Lin A, Samimi MS, Mendez MF. Somatic symptom disorder in semantic dementia: The role of alexisomia. Psychosomatics 2016;57:598-604.
116Onofrj M, Bonanni L, Manzoli L, Thomas A. Cohort study on somatoform disorders in Parkinson disease and dementia with Lewy bodies. Neurology 2010;74:1598-606.
117Babu AR, Sreedevi A, John A, Krishnapillai V. Prevalence and determinants of somatization and anxiety among adult women in an urban population in Kerala. Indian J Community Med 2019;44:S66-9.
118Kapfhammer HP. Somatoform disorders. Clinical evidence, etiology, pathogenesis, and therapy. Nervenarzt 2008;79:99-115.
119Bourke JH, Langford RM, White PD. The common link between functional somatic syndromes may be central sensitisation. J Psychosom Res 2015;78:228-36.
120Boeckle M, Schrimpf M, Liegl G, Pieh C. Neural correlates of somatoform disorders from a meta-analytic perspective on neuroimaging studies. Neuroimage Clin 2016;11:606-13.
121Fletcher P, Rohrer J, Schott J, Rossor M, Warren J. Abnormal pain and temperature processing in dementia. J Neurol Neurosurg Psychiatry 2015;86:e4.35-e4.
122Waln O, Jankovic J. An update on tardive dyskinesia: From phenomenology to treatment. Tremor Other Hyperkinet Mov (N Y) 2013;3. pii: tre-03-161-4138-1.
123Vogt BA. Pain and emotion interactions in subregions of the cingulate gyrus. Nat Rev Neurosci 2005;6:533-44.
124Landqvist Waldö M, Gustafson L, Nilsson K, Traynor BJ, Renton AE, Englund E, et al. Frontotemporal dementia with a C9ORF72 expansion in a Swedish family: Clinical and neuropathological characteristics. Am J Neurodegener Dis 2013;2:276-86.
125van Driel TJ, Hilderink PH, Hanssen DJ, de Boer P, Rosmalen JG, Oude Voshaar RC. Assessment of somatization and medically unexplained symptoms in later life. Assessment 2018;25:374-93.
126Escobar JI, Rubio-Stipec M, Canino G, Karno M. Somatic symptom index (SSI): A new and abridged somatization construct. Prevalence and epidemiological correlates in two large community samples. J Nerv Ment Dis 1989;177:140-6.
127Ritchie CS, Hearld KR, Gross A, Allman R, Sawyer P, Sheppard K, et al. Measuring symptoms in community-dwelling older adults: The psychometric properties of a brief symptom screen. Med Care 2013;51:949-55.
128Kroenke K, Spitzer RL, Williams JB. The PHQ-15: Validity of a new measure for evaluating the severity of somatic symptoms. Psychosom Med 2002;64:258-66.
129Desai G, Chaturvedi SK, Dahale A, Marimuthu P. On somatic symptoms measurement: The scale for assessment of somatic symptoms revisited. Indian J Psycholo Med 2015;37:17.
130Thygesen E, Lindstrom TC, Saevareid HI, Engedal K. The subjective health complaints inventory: A useful instrument to identify various aspects of health and ability to cope in older people? Scand J Public Health 2009;37:690-6.
131Gierk B, Kohlmann S, Kroenke K, Spangenberg L, Zenger M, Brähler E, et al. The somatic symptom scale-8 (SSS-8): A brief measure of somatic symptom burden. JAMA Intern Med 2014;174:399-407.