Preventing Dementia and Blood Pressure Control

 

A paper came out last week (1) that showed blood pressure control was an effective way to prevent dementia.  One of the most effective ways to prevent stroke is to control blood pressure.  Elevated blood pressure also causes blood vessel damage that can lead to dementia – even in the absence of a clearcut stroke. In one of my clinics, we assessed people with various forms of dementia and it was striking how many people had these kinds of changes on their CT or MRI scans and were unaware of them. In some cases, there was a history of uncontrolled blood pressure like eclampsia during pregnancy that probably resulted in brain changes seen decades later that was not investigated at the time.  Substance use problems, undiagnosed forms of transient hypertension, and substance use problems with intoxication and withdrawal associated hypertension are other possibilities.

The study in question was an interventional study across 163 villages in China and a total of 33,995 research subjects. Inclusion criteria into the study was ≥40 years of age with a mean untreated SBP ≥140 mm Hg and/or a DBP ≥90 mm Hg (or ≥130 mm Hg and/or ≥80 mm Hg among those with clinical CVD, diabetes or chronic kidney disease) or a mean treated SBP ≥130 mm Hg and/or a DBP ≥80 mm Hg, based on six measurements taken on two different days. Additional details are available in the paper on online supplementary information.  Patients were treated across the study by physician supervised non-physician community healthcare providers (NPCHPs).  Research subjects were randomized into treatment as usual (TAU) or non-protocol-based treatment for hypertension and protocol-based care. In the protocol-based care patients received first line antihypertensives like angiotensin converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), calcium channel blockers (CCBs), and diuretic or diuretic-like medications. The treatment group also got free blood pressure medication, lifestyle coaching, and home blood pressure monitors but the TAU group did not.

The primary outcome measures for this intervention study were the presence of dementia and cognitive impairment no dementia (CIND).  Both diagnoses were made by expert panels of neurologists using standardized criteria.  Screening tests were administered at clinic visits to assess cognition, instrumental activities of daily living, and symptoms of dementia in a standard way. 

On the main outcome measures the blood pressure intervention group had a 15% lower risk of dementia and a 16% lower risk of CIND compared with the TAU group.  Those numbers are consistent with an additional meta-analysis done by the authors of similar trials and a previous meta-analysis of blood pressure interventions to prevent dementia.

Strokes are the usual obvious consequences of blood pressure problems and they come in two forms – hemorrhagic and ischemic. Hemorrhagic strokes generally occur through a ruptured blood vessel in the substance of the brain or the subarachnoid space.  Because blood is under very high pressure in the brain that jet can cause additional damage.  In many cases clots form and they can be associated with edema and pressure in the brain. Symptoms can vary from an intense headache to signs of cerebral edema or coma and death.  Ischemic strokes consist of blood vessel occlusion or reduced blood flow to the point that there is inadequate blood supply to neurons. This can occur as the result of ruptured plaques, emboli, or mechanical disruption of the blood vessel.  The emboli can be the result of plaque formation in blood vessels as well as blood clots due to other diseases like atrial fibrillation.  Atrial fibrillation can also be caused by hypertension.

During my teaching seminars on dementia and vascular subtypes – I generally taught about vascular subtypes as cortical or parenchymal infarctions due to major blood vessels (yellow areas on the above diagram), lacunar infarctions due to damage to long perforating arteries to the striatum (pink area), and small vessel ischemic disease or Binswanger’s Disease (BD) due to deep arterioles supplying the subcortical white matter (blue area).  Although BD was described in 1895 it has been a controversial diagnosis that has not been clarified by modern brain imaging and the presence of white matter changes ofet referred to as “white matter ischemic changes” by radiologists.  The diagnosis is also complicated by the fact that many patients has features of both Alzheimer's Disease (AD) and BD and in some cases AD, BD, and small infarctions at autopsy.  If there is any confusion about the diagnosis, a history of hypertension, previous treatment for hypertension, a review of all previous brain imaging, and the clinical pattern of changes in cognition and functional capacity should all be described.   

I am restricting my comments in this post to how hypertension results in dementia so I will not comment on the differential diagnosis of stroke.  Elevated blood pressure can also cause blood vessel damage that is not due to a rupture or embolism.  Prolonged hypertension can cause inflammation in long blood vessels supplying the striatum and periventricular white matter in the brain.  The specifics of that process are being actively studied at this point but damaged is hypothesized to occur because of endothelial cel dysfunction as well as compromise of elastin a connective tissue protein in blood vessels leading to inflammation and narrowing or expansion of blood vessels.  The inflammatory process can lead to further changes and result in a compromised blood-brain barrier and progressive narrowing of those blood vessels.  Eventually the circulation is compromised resulting in the death of neurons visualized as volume loss and white matter changes on imaging studies.   

There seems to be very little work done on the actual pressure signaling at the level of the blood vessel.  Many physiological studies and reviews are focused on overall blood pressure effects and the effect of pressure waves within the vascular system. There are other determinants of endothelial dysfunction including the effects of aging, toxins like tobacco smoke, intercurrent diseases, and metabolic/nutritional factors like blood glucose, lipids, and uric acid.  Epidemiological data supports resting blood pressure and pulse pressure as being significant factors leading to endothelial dysfunction and atherosclerosis.

The modern approach to treating the problem of endothelial dysfunction leading to cardiovascular and cerebrovascular disease is to address all the risk factors.  Hypertension, smoking, diabetes mellitus, metabolic syndrome and obesity, dyslipidemia, and substance use including alcohol all need to be addressed. Many psychiatrists might see this as a primary care problem – but given the way health care is rationed these days a psychiatrist may be the only physician that the patient is seeing on a regular basis.    

That provides the opportunity to collect data like weight, blood pressure and pulse, as well as metabolic parameters if needed. One of my previous posts discusses the issue of blood pressure parameters and white coat effect, and white coat hypertension. The previous thinking was that a lot of people get hypertensive just from the stress of being in a physician’s office.  Some research backed that up showing no difference in outcomes. That research had the same design problems as research about the safety of alcohol.  The control group contained people with cardiovascular diseases and treatment for hypertension. The practical way to address this issue is to advise the patient to check their blood pressure at home with an approved device. Many of these devices can download data into a smartphone app for easy storage.  Home blood pressure monitoring is also useful to detect Transient blood pressure increases due to physical or emotional stress. Although it has not been well studied – this kind of blood pressure reactivity probably needs to be addressed since acute and chronic increases irrespective of etiology are a problem.  

Age is one of the most significant risk factors for dementia. As the incidence of dementia increases with more survivors into old age – there are early interventions that can prevent it from happening.  Good blood pressure control happens to be one of them. 

George Dawson, MD, DFAPA

Supplementary on Binswanger:

Otto Binswanger (1852-1929) was a Swiss physician.  Like many brain specialists of the day he was variously described as a psychiatrist, neurologist, and neuropathologist. He identified as being a psychiatrist primarily but in those days before board certification psychiatry was a much broader field. Both Freud and Meyer had similar qualifications. He is sometimes confused with his nephew Ludwig Binswanger (1881-1966) who was one of the leading researchers of the existential psychiatry movement.  He described “encephalitis subcorticalis chronica progressive” while attempting to differentiate types of dementia from dementia caused by tertiary syphilis that was called general paresis of the insane or GPI at the time.  GPI was a very common reason for institutionalization at the time accounting for 20% of admission and 34% of the death in asylums in the 19^th and early 20^th century before the advent of antibiotics.

Binswanger’s description was controversial up to modern times and I will try to capture that in the graphic below.  The original description was published in 3 issues of a trade paper rather than a medical journal.  It is often critiqued as being long, rambling, and not publishable by today’s standards.  I think that criticism has the benefit of the retroscope since most papers at the time would have similar difficulties.  

Supplemental references on the Binswanger graphic according to those dates:

1894:  Blass JP, Hoyer S, Nitsch R. A translation of Otto Binswanger's article, 'The delineation of the generalized progressive paralyses'. 1894. Arch Neurol. 1991 Sep;48(9):961-72. doi: 10.1001/archneur.1991.00530210089029. PMID: 1953422.

1910:  Dening TR.  Stroke and other Vascular Disorders – Clinical Section.  In: A History of Clinical Psychiatry. Berrios G, Porter R (eds). New Brunswick.  The Athlone Press. 1995: 72-85.

1910:  Nicolson M.  Stroke and other Vascular Disorders – Social Secition. In: A History of Clinical Psychiatry. Berrios G, Porter R (eds). New Brunswick.  The Athlone Press. 1995: 86-94

1986:  Esiri MM, Oppenheimer DR.  Diagnostic Neuropathology. Blackwell Scientific Publications, London, 1896.

1994:  Hansen LA. Pathology of Other Dementias.  In:  Alzheimer Disease.  Terry RD, Katzman R, Bick KL (eds). New York. Raven Press. 1994: 167-196.

The discussion of neuropathology in this text and the subsequent edition is superior to what is seen in general pathology texts and some neuropathology texts.

Román GC, Tatemichi TK, Erkinjuntti T, Cummings JL, Masdeu JC, Garcia JH, Amaducci L, Orgogozo JM, Brun A, Hofman A, et al. Vascular dementia: diagnostic criteria for research studies. Report of the NINDS-AIREN International Workshop. Neurology. 1993 Feb;43(2):250-60. doi: 10.1212/wnl.43.2.250. PMID: 8094895. 

2025:  Bir SC, Khan MW, Javalkar V, Toledo EG, Kelley RE. Emerging Concepts in Vascular Dementia: A Review. J Stroke Cerebrovasc Dis. 2021 Aug;30(8):105864. doi: 10.1016/j.jstrokecerebrovasdis.2021.105864. Epub 2021 May 29. PMID: 34062312.

 

References:

1:  He J, Zhao C, Zhong S, Ouyang N, Sun G, Qiao L, Yang R, Zhao C, Liu H, Teng W, Liu X, Wang C, Liu S, Chen CS, Williamson JD, Sun Y. Blood pressure reduction and all-cause dementia in people with uncontrolled hypertension: an open-label, blinded-endpoint, cluster-randomized trial. Nat Med. 2025 Apr 21. doi: 10.1038/s41591-025-03616-8. Epub ahead of print. PMID: 40258956.

2:  Supplementary Information for Reference 1 (see Supplementary Table 7. Meta-Analysis of Randomized Controlled Trials of Antihypertensive Treatment on Dementia) for results of 5 additional RCTs of hypertension treatment in dementia.  https://www.nature.com/articles/s41591-025-03616-8#Sec23

3:  Franklin SS, Thijs L, Hansen TW, O'Brien E, Staessen JA. White-coat hypertension: new insights from recent studies. Hypertension. 2013 Dec;62(6):982-7. doi: 10.1161/HYPERTENSIONAHA.113.01275. Epub 2013 Sep 16. PMID: 24041952.

4:  Lockhart SN, Schaich CL, Craft Set al. Associations among vascular risk factors, neuroimaging biomarkers, and cognition: Preliminary analyses from the Multi-Ethnic Study of Atherosclerosis (MESA). Alzheimers Dement. 2022 Apr;18(4):551-560. doi: 10.1002/alz.12429. Epub 2021 Sep 5. PMID: 34482601; PMCID: PMC8897510.

Dementia Prevention And Substance Use Disorders

Dementia from Addictive Compounds

As a geriatric psychiatrist and an addiction psychiatrist, what I see happening in both professional literature and lay literature is mind boggling.  There is a clear bias advocating for the benign and even therapeutic effects of alcohol and addicting drugs.  What most articles omit is that the health effects of alcohol are limited to no more than two standard drinks per day for men and one drink per day for women.  The drinks cannot be all taken on the same day.  The limits are per day not per week.  Most of the evidence also suggests that the alcoholic beverage should be wine rather than beer or distilled spirits.  Recent studies suggest that of the 70% of Americans who drink - about 1/3 of them are probably drinking in excess of those amounts.  Doing the arithmetic that amounts to about 56 million people.  Even a low percentage of brain injury will result in a significant number of cases od dementia. Moderate to heavy drinking (3-12+ drinks/day) carries the associated risks of high carbohydrate intake and sedentary life style.  It is very common to find that moderate to heavy drinkers stop their usual outdoor activities and exercise and spend a lot of time watching television.  This can lead to obesity, glucose intolerance and dyslipidemia and in the worst case scenario metabolic syndrome.  All of those consequences lead to increased risk of cardiovascular and cerebrovascular disease.  

There are addiction risks with alcohol consumption apart from atherosclerotic heart disease. Alcohol is proarrhythmic and doubles the risk for arrhythmia.  In one large Danish study (11) they noted that alcohol intake and a history of atrial fibrillation was a risk factor for ventricular fibrillation.  Some authors view alcohol use a risk factor in preventable atrial fibrillation.  In clinical practice it is very common to interview patients with atrial fibrillation who notice that during times of heavy alcohol use they can sense that they are in atrial fibrillation and they spontaneously convert to sinus rhythm as their blood alcohol levels drop.  Atrial fibrillation is a causative mechanism for embolic stroke and associated cognitive disorders.

The direct toxic effect of alcohol on the brain has been debated for years. Amnesia from Wernicke-Korsakoff syndrome is a known diagnostic entity related to thiamine deficiency associated with excessive alcohol use.  It is probably underdiagnosed in most populations compared with postmortem diagnoses of the specific lesions consistent with Wernicke-Korsakoff syndrome (WKS).  A large number of people with alcohol use problems have demonstrable cognitive effects on testing as well as structural and functional brain imaging brain imaging studies suggest some effect on brain structure.  The lack of a pathological lesion has led some to suggest that this is a non-specific effect, but it is very likely that there are several variants of cognitive dysfunction related to alcohol use that are not associated with WKS (12).  On a clinical basis it is very common to see patients with subjective cognitive impairment that typically involves working memory, declarative memory, and executive function.  In treatment setting where abstinence from alcohol is assured many of these problems seem to clear up after about 60 days of abstinence.  But there are also populations of people with varying degrees of anterograde and retrograde amnesia that is not as dense as expected with full WKS.  Many of these patients are seen in treatment settings and never referred for comprehensive assessments of their cognitive disorder.  To my knowledge there have been no studies looking at the issue of whether or not partial amnestic states correlate with WKS lesions at autopsy.        

The problems with recognizing and treating cognitive disorders associated with substance use problems are exemplified in the first few paragraphs about alcohol.  They are no less important for other commonly abused substances.  In the case of stimulants, amphetamine analogues are known neurotoxins.  Studies by Volkow and others have shown persistent changes in dopaminergic neurons up to 15 months after the last use.  This may correlate with a persistent attentional deficit that leads patients to conclude that they now have attention deficit disorder.  Additional brain insults from hemorrhagic strokes and cardiovascular problems associated with long term stimulant use are common.  Stimulants are well known precipitants of acute myocardial ischemia and brain complications from hypoperfusion and emboli.  Acute hypertension and tachycardia are part of the acute intoxication syndrome that can lead to hypertension and hemorrhagic stroke.  This recurrent cycle leads to commonly observed complications of cardiomyopathy in the 4th and 5th decades of life and heightened risk of ventricular arrhythmias and cardiac arrest.

The graphic at that top of this post is not exhaustive - but point out some significant acute and chronic complications of drug use that can lead to permanent brain injury.  These mechanisms cannot be overlooked as avoidable causes of dementia.  I will be trying to elaborate on this graphic in the future to look at developing a review in this area.  Any acute acre and addiction psychiatrist is probably more aware of these syndromes and complications because they are encountered in clinical practice.  I have not seen any formal estimates of the fraction of dementia cases are preventable by avoiding these compounds.  The largest fraction of dementia cases would likely be attributable to the most commonly used drugs - tobacco and alcohol.  Drugs that kill more people acutely on a proportional basis like stimulants and opioids probably leave fewer survivors with dementia as a complication.  

Contrary to the conventional wisdom these days - avoiding dementia is another strong argument for a sober life style.


George Dawson, MD, DFAPA


References:

1: de Gaetano G, Costanzo S, Di Castelnuovo A, Badimon L, Bejko D, Alkerwi A,Chiva-Blanch G, Estruch R, La Vecchia C, Panico S, Pounis G, Sofi F, Stranges S, Trevisan M, Ursini F, Cerletti C, Donati MB, Iacoviello L. Effects of moderate beer consumption on health and disease: A consensus document. Nutr Metab Cardiovasc Dis. 2016 Jun;26(6):443-67. doi: 10.1016/j.numecd.2016.03.007. Epub 2016 Mar 31. Review. PubMed PMID: 27118108.

Moderate consumption is defined as 1 drink per day in women and 2 drinks per day  for men in a non-binge drinking pattern. J-shaped dose-response curve

2: Fernández-Solà J. Cardiovascular risks and benefits of moderate and heavy alcohol consumption. Nat Rev Cardiol. 2015 Oct;12(10):576-87. doi: 10.1038/nrcardio.2015.91. Epub 2015 Jun 23. Review. PubMed PMID: 26099843.

U-Shaped dose-response curve

3: Matsumoto C, Miedema MD, Ofman P, Gaziano JM, Sesso HD. An expanding knowledge of the mechanisms and effects of alcohol consumption on cardiovascular disease. J Cardiopulm Rehabil Prev. 2014 May-Jun;34(3):159-71. doi: 10.1097/HCR.0000000000000042. Review. PubMed PMID: 24667667.

4: Graff-Iversen S, Jansen MD, Hoff DA, Høiseth G, Knudsen GP, Magnus P, Mørland J, Normann PT, Næss OE, Tambs K. Divergent associations of drinking frequency and binge consumption of alcohol with mortality within the same cohort. J Epidemiol Community Health. 2013 Apr;67(4):350-7. doi: 10.1136/jech-2012-201564. Epub 2012 Dec 12. PubMed PMID: 23235547.

5: Weyerer S, Schäufele M, Wiese B, Maier W, Tebarth F, van den Bussche H,Pentzek M, Bickel H, Luppa M, Riedel-Heller SG; German AgeCoDe Study group (German Study on Ageing, Cognition and Dementia in Primary Care Patients). Current alcohol consumption and its relationship to incident dementia: results from a 3-year follow-up study among primary care attenders aged 75 years and older. Age Ageing. 2011 Jul;40(4):456-63. doi: 10.1093/ageing/afr007. Epub 2011 Mar 2. PubMed PMID: 21367764.

6: Bathla M, Singh M, Anjum S, Kulhara P, Jangli S IIIrd. Metabolic syndrome indrug naïve patients with substance use disorder. Diabetes Metab Syndr. 2016 Sep 3. pii: S1871-4021(16)30183-7. doi: 10.1016/j.dsx.2016.08.022. [Epub ahead of print] PubMed PMID: 27618517

Alcohol was the main substance used by patients meeting WHO criteria for Metabolic Syndrome.

7: Vancampfort D, Hallgren M, Mugisha J, De Hert M, Probst M, Monsieur D, Stubbs B. The Prevalence of Metabolic Syndrome in Alcohol Use Disorders: A Systematic Review and Meta-analysis. Alcohol Alcohol. 2016 Sep;51(5):515-21. doi: 10.1093/alcalc/agw040. Epub 2016 Jun 23. Review. PubMed PMID: 27337988. 

1 person in 5 with alcohol use disorder has metabolic syndrome.

8: Wakabayashi I. Frequency of heavy alcohol drinking and risk of metabolicsyndrome in middle-aged men. Alcohol Clin Exp Res. 2014 Jun;38(6):1689-96. doi: 10.1111/acer.12425. Epub 2014 May 12. PubMed PMID: 24818654.

Positive correlation between heavy drinking and metabolic syndrome.

9: Yousefzadeh G, Shokoohi M, Najafipour H, Eslami M, Salehi F. Association between opium use and metabolic syndrome among an urban population in Southern Iran: Results of the Kerman Coronary Artery Disease Risk Factor Study (KERCADRS). ARYA Atheroscler. 2015 Jan;11(1):14-20. PubMed PMID: 26089926; PubMed Central PMCID: PMC4460348.

Current opioid users had the highest prevalence of metabolic syndrome (39.6%) but the study was confounded by a high baseline rate in the controls (37.2%).

10:   Brunner S, Herbel R, Drobesch C, Peters A, Massberg S, Kääb S, Sinner MF.Alcohol consumption, sinus tachycardia, and cardiac arrhythmias at the Munich Octoberfest: results from the Munich Beer Related Electrocardiogram Workup Study (MunichBREW). Eur Heart J. 2017 Apr 25. doi: 10.1093/eurheartj/ehx156. [Epub ahead of print] PubMed PMID: 28449090.

11: Jabbari R. Ventricular fibrillation and sudden cardiac death during myocardialinfarction. Dan Med J. 2016 May;63(5). pii: B5246. Review. PubMed PMID: 2712702.

12: Ridley NJ, Draper B, Withall A. Alcohol-related dementia: an update of the evidence. Alzheimers Res Ther. 2013 Jan 25;5(1):3. doi: 10.1186/alzrt157. eCollection 2013. Review. PubMed PMID: 23347747.


Supplementary:

The calculation for the following observation:

Recent studies suggest that of the 70% of Americans who drink - about 1/3 of them are probably drinking in excess of those amounts.  Doing the arithmetic that amounts to about 56 million people.

321M(current US population) - 80M (population less than drinking age) x 0.7 (percentage of population that drinks) x 0.3 percentage of excess drinkers = 56 million people.

 

Delirium Reinvented

One of my colleagues posted an article from the The Atlantic on delirium to her Facebook feed a few days ago.  Most of my colleagues in that venue are hospital, consultation-liaison, addiction or geriatric psychiatrists and we diagnose a lot of delirium.  Entitled the Overlooked Danger of Delirium in Hospitals it makes it seem like this is some kind of new and strange diagnostic category.  The article talks about the prevalence, the association with critical illness and advanced age, and the diagnostic overlap of dementia and delirium.  We hear from an Internal Medicine specialist Sharon Inouye, MD about the need to correctly diagnose and prevent delirium.  She mentions that as opposed to a decade ago, physician and nurses are all taught about delirium.  There is mention of the CAM (Confusion Assessment Method) that Inouye developed.  Like all health care articles there are estimates of the massive cost of delirium as well some prevention techniques.  There is also political concern that Medicare will declare delirium a "never" event with penalties for any hospital with cases of delirium.  That would be unfortunate because it makes a mistake that also seems to be made in this article - that delirium is a manifestation of many illnesses, especially the kind of illnesses that patient's are hospitalized for.

The article seemed odd to me because it was written from the perspective that delirium is an iatrogenic preventable event!  Certainly that can be the case. Delirium is a primary feature of hundreds of different disorders and recognizing delirium and those etiologies is potentially life saving.  Delirium can mimic psychiatric conditions due to the presence of hallucinations and delusional thinking.  For example, it is entirely possible to see a patient in the emergency department with apparent paranoid delusions and miss the fact that they happen to be delirious.  Sometimes the only sign is that the patient is inattentive and when vital signs are checked they have an elevated temperature.  This can be a common presentation of viral encephalitis in younger patients or urinary tract infections in the elderly.  It is bad form to miss either of those diagnoses and attribute the symptoms to a psychiatric disorder.  Another common form of delirium that is missed is drug or alcohol intoxication or withdrawal states.  Some intoxicants will render the patient totally unable to care for themselves until they are detoxified.  Other deliriums from alcohol or sedative withdrawal are life threatening and can be associated with seizures and other life-threatening states.  An acute change in a person's mental state resulting in delirium needs to be recognized and assessed as a medical emergency.    

One of the first cases of delirium that I ran into after residency was a case of cerebral edema that I was consulted on because of "hysterical behavior".  After that, I worked in and eventually ran a Geriatric Psychiatry and Memory Disorders Clinic for about 8 years.  The majority of people coming to that clinic had dementia of some sort.  They would see me and a neurologist.  We started out with an internist who was also a geriatric specialist, but that turned out to be overkill in terms of the number of medical specialists seeing each person in an outpatient clinic.  We eventually opted for records from the patient's primary care physician.  One of the most valuable functions of that clinic was our ability to follow people with prolonged deliriums.  Once a delirium has been established by a disease state and that state has resolved the delirium can persist for months.  Some of the outliers in that clinic took up to 6 months to clear.  We found that in many cases, the patients were extensively tested for intellectual ability and functional capacity when they were in the delirious state and told that they had dementia.  It was always instructive for the patient and family to get the testing repeated when we were sure the delirium had resolved and find that they had been restored to baseline.  Many people know their full scale IQ score and were relieved to see that they were back to that level of functioning.

A valuable lesson from working in that clinic and in hospital settings was the use of the electroencephalogram (EEG) as a possible test for delirium.   EEGs are commonly viewed as diagnostic tools to determine if a person is having seizures, but they also contain a lot of information about brain metabolism.  EEGs can be difficult to interpret especially if the patient is on a number of medications that affects cerebral metabolism. There are two broad categories of EEG patterns for delirium: one with a predominance of slow frequencies (designated theta and delta) and one with faster frequencies (designated beta).  We found a number of people with very significant cognitive impairment that was thought to be either a psychiatric disorder or a dementia but with a profound degree of slowing more consistent with a delirium.    

Delirium is an augenblick diagnosis for most psychiatrists.  The patient could appear disinterested, apathetic, agitated, or overtly confused.  It occurs in situations where brain physiology is compromised such as post surgical/anaesthesia states, drug intoxication states, drug reaction states, or possible physical illness delirium should be high on the differential diagnosis.  The Atlantic article makes it seem like knowledge about delirium is something very recent, but psychiatrists have been focused on it for a long time.  In the first two iterations of the DSM, delirium was subsumed under the categories of acute and chronic brain syndromes (DSM-I 1952) and organic brain syndromes (DSM-II 1968).  The current diagnostic code and name has been with us since the DSM III in 1980.  One of the early experts in delirium was Zbigniew J. Lipowski, MD, FRCP(C) - a Professor of Psychiatry from the University of Toronto.  His first text on the condition was Delirium: Acute Brain Failure in Man published in 1980.  That was followed by his classic text,  Delirium: Acute Confusional States published in 1990.  A comparable text from a neurological standpoint was Arieff and Griggs Metabolic Brain Dysfunction in Systemic Disorders published in 1992.

Any psychiatrist trained in the past 30 years should be able to diagnose delirium and come up with a differential diagnosis and monitoring or treatment plan.  A significant number of people can be followed on an outpatient basis as long as they are in a safe environment with the appropriate level of assistance.  The main goal of treatment is to make sure that the primary medical illness that led to the problem has been treated.  There are no known medications that will accelerate the resolution of these symptoms and medical management usually involves getting rid of medications that can lead to cognitive problems.  That can include benzodiazepines, antidepressants and antipsychotics but also more common medications like antihistamines and anticholinergic medications that are used for various purposes.  Like most psychiatric interventions in our health care system, clinics with staff interested in doing this work are few and far between generally because they are rationed resources.

There is a current movement underway to train Family Physicians and Internists (like Dr. Inouye) to recognize and prevent delirium.  In the minority of hospitals where psychiatrists work they are also a clear resource.  A delirium in a previously healthy person should signal a fairly comprehensive evaluation to figure out what happened.

And whenever there is a question of whether a person has a delirium or a psychiatric disorder - call a psychiatrist.  Psychiatrists know a lot about delirium and have for decades.



George Dawson, MD, DFAPA



Reference:

Sandra G. Boodman.  Overlooked Danger of Delirium in Hospitals.  The Atlantic.  June 7, 2015.


Supplementary 1:  The graphic is a standard EEG.  I tried to post a slowed EEG seen in delirium, but the publisher wanted what I consider to be an exorbitant fee for a non-commercial blog.  If anyone has a slow anonymous EEG laying around, send me a copy and I will post it.