David Hsu, MD

Vascular surgeons, internists, and neurologists all exist-but why aren’t there any vascular psychiatrists? There certainly is a need.

[[{"type":"media","view_mode":"media_crop","fid":"25918","attributes":{"alt":"vascular dementia","class":"media-image","id":"media_crop_2314432812163","media_crop_h":"0","media_crop_image_style":"-1","media_crop_instance":"2442","media_crop_rotate":"0","media_crop_scale_h":"0","media_crop_scale_w":"0","media_crop_w":"0","media_crop_x":"0","media_crop_y":"0","title":"","typeof":"foaf:Image"}}]]Cardiovascular syndromes yield the highest morbidity and mortality of all diseases.

 In daily practice, psychiatrists commonly encounter vascular syndromes, such as vascular depression,

 Surgeons, internists, and neurologists can obtain subspecialty training in vascular disorders, but at this time, psychiatrists who are interested in this area are encouraged to pursue either psychosomatic medicine or geriatric psychiatry fellowships. Many psychiatrists who publish in vascular psychiatry are in one of those subspecialties. Therefore, vascular psychiatry at this time could be considered a sub-subspecialty.

Imagine a psychiatrist who is hubbed in a cardiovascular center clinic with cardiologists and vascular surgeons and who provides consultation on psychopharmacology or preoperative assessment. Or a psychiatrist who rounds in the cardiac ICU to evaluate depression, delirium, and dementia. Or a psychiatrist who rounds with the stroke team to evaluate cognitive impairment and provide psychotropic recommendations. These examples serve as innovative ways to collaborate and integrate care. Comorbidity of psychiatric syndromes, such as depression, and vascular diseases has already been firmly established. This has led to joint consensus guidelines from the American Heart Association, American Stroke Association, American Psychiatric Association, American Academy of Neurology, and the Alzheimer’s Association.

 There is no other area of medicine that has this high degree of collaboration.

Last year, the Royal College of Psychiatrists 

 titled “Vascular psychiatry: the interface between vascular disease and mental disorders, and its clinical relevance.”

 Certainly, a similar conference could be held in the US. The specialty most closely related to vascular psychiatry at this time is probably vascular neurology,

 and it is already part of the American Board of Psychiatry and Neurology. 

, it states that vascular neurology is a “subspecialty that involves the evaluation, prevention, treatment, and recovery from vascular diseases of the nervous system.”

 Just substitute “the mind” for “the nervous system,” and vascular psychiatry would be defined.

If a training fellowship for vascular psychiatry were to begin, I imagine that it would definitely have to be interdisciplinary. A central educational goal of a true “collaborative” fellowship would be to work with psychiatrists, cardiologists, neurologists, and surgeons. The fellow would be expected to go to didactics and rounds for all of these specialties and provide consultation on anything related to vascular psychiatry. Research would be cross-disciplinary, and grants could help to establish centers of excellence for vascular psychiatry, just like for geriatric psychiatry or depression. Interestingly, if a Society for Vascular Psychiatry were to be established, the initials would be “SVP,” which also stands for “systemic venous pressure.”

Dr Hsu is the Alzheimer’s Disease Research Fellow in the departments of psychiatry and neurology at Massachusetts General Hospital and Brigham and Women’s Hospital, Boston. An Instructor of Psychiatry through Harvard Medical School, he is a staff geriatric psychiatrist and internist. Dr Hsu evaluates subjects in clinical trials for Eli Lilly and Eisai.

 Go AS, Mozaffarian D, Roger VL, et al; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics-2013 update: a report from the American Heart Association. 

 Taylor WD, Aizenstein HJ, Alexopoulos GS. The vascular depression hypothesis: mechanisms linking vascular disease with depression. 

 Gorelick PB, Scuteri A, Black SE, et al; American Heart Association Stroke Council, Council on Epidemiology and Prevention, Council on Cardiovascular Nursing, et al. Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. 

 Lichtman JH, Bigger JT Jr, Blumenthal JA, et al; American Heart Association Prevention Committee of the Council on Cardiovascular Nursing, American Heart Association Council on Clinical Cardiology, American Heart Association Council on Epidemiology and Prevention, et al. Depression and coronary heart disease: recommendations for screening, referral, and treatment. 

 Royal College of Psychiatrists. Vascular psychiatry: the interface between vascular disease and mental disorders, and its clinical relevance. 

http://www.rcpsych.ac.uk/traininpsychiatry/conferencestraining/conferences/oldagewinter13presentation.aspx

 American Board of Psychiatry and Neurology. Vascular neurology. 

Articles

Vascular Psychiatry: A New Specialty?

“When am I going home?”
“We’re just trying to arrange the transportation.”

“When is my husband going to visit?”
“He’s away on business for a few days.”

“Why can’t I go over there?”
“Because you will fall into a bottomless black pit.”

[[{"type":"media","view_mode":"media_crop","fid":"23938","attributes":{"alt":"","class":"media-image media-image-right","id":"media_crop_6095069651","media_crop_h":"0","media_crop_image_style":"-1","media_crop_instance":"2003","media_crop_rotate":"0","media_crop_scale_h":"0","media_crop_scale_w":"0","media_crop_w":"0","media_crop_x":"0","media_crop_y":"0","style":"width: 150px; height: 186px; float: right;","title":" ","typeof":"foaf:Image"}}]]Asked by a reader of 

 about the ethics of placing black floor mats in front of exits to deter demented nursing home residents from dangerous wandering, ethicist Chuck Klosterman

 acknowledged that this behavioral intervention is based on deception. On balance, however, he expressed support for a maneuver that might be preferable to more restrictive alternatives, such as chemical or physical restraints. From an ethical standpoint, he considered the mats a way of maximizing independence. He saw no “downside that isn’t purely theoretical.” As clinicians who work with geriatric patients, we’d like to explore the possible downside, even though it may be only theoretical.

Therapeutic lies, or fiblets, are often used to reduce stress and manage the anxieties and disruptive behaviors of demented inpatients, long-term–care residents, or the elderly who are cared for at home, who are not reassured by simple distraction or redirection. When an inpatient or long-term–care resident tries to leave a facility, sometimes with the intent of returning to a home that no longer exists, a fiblet can reduce suffering and offer comfort. An agitated widow seeking her deceased husband high and low in a nursing home may feel much less distress if told that staff will help her look for her husband later but in the meantime she is needed to help set the table for dinner. When “later” arrives, the urgency that drove the woman’s search may have waned considerably. The first two interactions at the start of this article are accepted commonplace, anxiety-reducing fiblets. The third, a verbal interpretation of the visual deception created by a black mat, is a threat rather than a distraction.

Demented patients’ avoidance of dark mats, tiles, or even lines on the floor has long been observed-and sometimes exploited clinically-although we could not locate any studies of the effectiveness and safety of this maneuver. Patients avoid the dark mat because they visually misinterpret the blackness as a drop-off, the socalled visual cliff. Experimental observations of behaviors associated with the visual cliff in infants and in animals shed light on how we might understand the experience of a demented person faced with an unexpected chasm where floor had been expected.

At 5 months of age, infants placed near a visual cliff explore it more or less boldly, but by 9 months a fear reaction is seen.

 The heart rate acceleration associated with this experience may represent fear, although alternative explanations have been proposed. Unambiguous fear reactions have been documented in animals subjected to this experience. Kittens and goats placed atop the deep side of a visual cliff displayed freezing and limb tensing.3 Rhesus monkeys placed on the deep side of the cliff showed crouching, distress vocalizations, self-clasping, and rocking behavior.

Cognitively impaired older adults are not infants or animals, of course, but in some respects their cognitive functions have retrogressed to a stage in which analytic thinking is more limited and catastrophic reactions are more likely than with cognitively intact adults. That persons with dementia might react fearfully to a visual cliff should not surprise us, when we think about the subjective experience of a disoriented person who may also have gait and balance problems and difficulty with visual contrast and interpretation. Many of our cognitively impaired patients also have had terrifying experiences with previous falls. Phobic anxiety, with or without insight, may remain as an emotional response.

In some long-term–care facilities, the concealment of doors by curtains or pictures has reduced exit-seeking behavior. Other doors, visible to patients, can lead to a garden or circular path suitable for walking. A dark mat blocking an exit, however, differs from concealment of an exit or from the technique of redirection with an arrow or a “Do Not Enter” sign on the door. The mat is a visual deception that, we might imagine, could evoke fear in a cognitively impaired person. In principle, though more gently, an apparent pit in front of a door serves the same purpose that we might have achieved by posting a holographic image of a charging rhinoceros on a door’s center panel. Why do we avoid using the ostensibly harmless rhino?

One of my colleagues, a dementia unit nurse director whose office sports a dark blue carpet, has observed the timidity and apprehension with which patients step into her room. An unsteady gait could be further destabilized in such a situation. Less likely but more frighteningly, what might happen to a demented person whose exit has been blocked by a dark floor covering in the event of a fire? Would he or she balk at taking the apparent risk required in order to exit safely?

Lies that reduce suffering and stress in patients unable to fully appreciate the cause of distress can be beneficial. Clinicians sanction their use in dementia care and see them as a manifestation of the ethical imperatives of beneficence and non-malfeasance.

 Whether the use of dark mats is a benign alternative of this sort or whether it might inadvertently invoke a fear reaction can easily be tested. Until such testing provides evidence of safety and effectiveness, the use of these mats for behavioral control should be regarded as an intervention of unproven acceptability.

Dr Ellison is Director of the Geriatric Psychiatry Program at McLean Hospital in Belmont, Mass. Dr Hsu is a Clinical Fellow in the Partners Geriatric Psychiatry Fellowship Program in Boston. They report no conflicts of interest concerning the subject matter of this article.

 Schwartz AN, Campos JJ, Baisel EJ Jr. The visual cliff: cardiac and behavioral responses on the deep and shallow sides at five and nine months of age. 

 Gibson EJ, Walk RD. The “visual cliff.” 

 Rosenblum LA, Cross HA. Performance of neo-natal monkeys in the visual cliff-situation. 

 Culley H, Barber R, Hope A, James I. Therapeutic lying in dementia care. 

 Tuckett AG. The experience of lying in dementia care: a qualitative study. 

Placing black floor mats in front of exits to deter demented nursing home residents from dangerous wandering may pose ethical questions.

A Dark Side of Dementia Care

[[{"type":"media","view_mode":"media_crop","fid":"15961","attributes":{"alt":"subjective cognitive decline","class":"media-image media-image-right","id":"media_crop_9977219366835","media_crop_h":"0","media_crop_image_style":"-1","media_crop_instance":"880","media_crop_rotate":"0","media_crop_scale_h":"0","media_crop_scale_w":"0","media_crop_w":"0","media_crop_x":"0","media_crop_y":"0","style":"float: right; margin: 5px;","title":" ","typeof":"foaf:Image"}}]]The pace of Alzheimer disease (AD) research is fast moving, and the prize of finding the cure seems tantalizingly close. We have the target protein, the antibody to knock out the protein, and the imaging test locating the protein in the brain, but there still remains one problem . . . Who should receive the antibody?

Researchers from around the world came together recently for the 

 International Conference in Boston and presented the latest findings in trying to answer that very question. The conference made headlines in 

 and yielded multiple letters to the editor.

 A group from Germany led by Dr Frank Jessen presented strong evidence that maybe people with “subjective cognitive decline” (SCD) should be the ones to be given the antibody first.

The phenomenon of SCD occurs when patients who do not have cognitive impairment but who nevertheless present to their physician with cognitive concerns. To be clear, these patients score within the normal range of standard cognitive instruments, such as the Folstein 

, and do not have any functional deficits. They also do not fall within the realms of “mild cognitive impairment (MCI).” Persons with SCD just notice that their minds are “not as sharp” as before, which may get in the way of daily tasks (like remembering to buy groceries). Research presented at the Boston meeting also suggests that those with SCD have more build-up of the protein likely to cause AD. Thus far, the Alzheimer research community seems to be excited about the SCD hypothesis and will likely pursue this further.

All this focus on SCD hopes to further define “

.” Studies tell us that beta amyloid, the main protein causing AD, start to accumulate in brains up to 

 The trials last year testing solanezumab and bapineuzumab started too late, although patients had a mild reduction of cognitive symptoms and reduced amyloid. Researchers now want to test patients much earlier (ie, those who have MCI or normal cognition). The first trial to do that has started already in Colombia through Genentech, 

, and the National Institutes of Health, with the antibody crenezumab.

SCD brings up several research questions, as well as potentially complicated ethical questions. Can patients reliably assess their cognitive decline? Findings from Jessen and other groups suggest that the answer is yes. Future studies will need to better assess whether certain cognitive domains are more predictive than others and whether SCD can be reproducible in the lay population. Participants in clinical research are often “cleaner” and do not represent the people who have multiple co-morbidities or come from various socioeconomic backgrounds. What if a 40-year-old man comes into clinic with SCD? Would a doctor order a PET scan and potentially give the antibody? How about someone with Down syndrome, a previous head injury, or a history of stroke?

However, the larger question for me is: What then constitutes normal cognition if SCD can predict AD? One future scenario is for AD to develop in a patient at the “right” age. Her doctor wants to get a PET scan and start the antibody right away. Technically, the doctor would be treating AD as defined as amyloid build-up in the brain. Would she then be deemed to have AD? Should she quit her job or stop driving? Would her health insurance cover treatment for this “disease,” and should she tell her life-insurance company? Would Medicare pay for the antibody as “preventive care,” just like for hypertension and hyperlipidemia? What if the patient were actually undergoing a major depressive episode with cognitive deficits and got better after starting an antidepressant? Should she continue getting the antibody treatment even though her cognition improved?

I guess we’ll just have to cross that bridge when we get there.

Dr Hsu is a Clinical Fellow in Geriatric Psychiatry, Partners HealthCare, Harvard Medical School.

 The above perspective is the opinion of the author and does not necessarily reflect the view of the Partners HealthCare system or Harvard Medical School.

1. Belluck P. Dementia’s signs may come early. 

http://www.nytimes.com/2013/07/18/health/looking-for-early-signs-of-dementia.html

. Accessed August 5, 2013.
2. Ballard C, Gauthier S, Corbett A, et al. 

. Lancet. 2011;377:1019-1013.
3. Sperling RA, Aisen PS, Beckett LA, et al. 

Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease

We have the target protein for Alzheimer, the antibody to knock out the protein, and the imaging test locating the protein in the brain, but there still remains one problem . . . who should receive the antibody?

David Hsu, MD

Articles

Vascular Psychiatry: A New Specialty?

A Dark Side of Dementia Care

Why “Subjective Cognitive Decline” Is Important