Homeless Scholar Blog ~ RESILIENCE

“Although meant to counteract preoccupations in psychology with such characteristics as low self-esteem and assertiveness and high depression, anxiety and anger, the emphasis on happiness [in positive psychology] is problematic in that it does not fully appreciate the inherently stressful nature of living well.” – Salvatore Maddi, “Hardiness: The Courage to Be Resilient”

The concepts of resilience and hardiness are obviously related, but a title search of Pub Med for each shows much more research interest in the former. Hardiness is a presumed characteristic of an individual, whereas resilience is more of a behavioral outcome, a description of the tendency to rebound quickly from the  adverse effects of stress. An important research question is the extent to which people can cultivate resilience capability psychologically, thereby controlling susceptibility to mental disorders and even physical illness. Outcomes associated with high resilience include strong coping skills, a strong support network, and lower rates of depression. Positive physical outcomes include independence in daily activities, faster cardiovascular recovery, and lower mortality risk (MacLeod, 2016). Biomedically, the construct of resilience can be expressed as “physiological reserve” or “intrinsic capacity.”

There are numerous instruments for testing resilience, at least 15, of which the Connor-Davidson Scale, the Resilience Scale for Adults, and the Brief Resilience Scale have received the best psychometric ratings. A 2011 methodological review found no current “gold standard” (Windle, 2011). In Connor and Davidson’s original paper on their scale, 25 descriptors of the construct are listed, for example: “Able to adapt to change; not easily discouraged by failure; think of self as strong person; humor in the face of stress; strong sense of purpose; know where to turn for help….” The authors conclude that “the scale demonstrates that resilience is modifiable and can improve with treatment.”

An early study of a 25-item resilience scale using principal components factor analysis with 810 community-dwelling older adults as sample boiled down to “personal competence” and “acceptance of self and life”. The results supported the internal consistency reliability and concurrent validity of the scale for the measure of resilience (Wagnill & Young, 1993).

A more recent study of the Resilience Scale is critical, but still asserts that its use “can help identify older adults low in resilience and expose these individuals to interventions to improve resilience and facilitate successful aging” (Resnick & Inquito, 2011). The authors recommend the use of more qualitative studies.

Applications of the resilience concept have been fairly wide in both medical and psychological literature. For example, a recent article investigated the relationship between psychological hardiness and resilience with depression in women with breast cancer, concluding that there is a need for training courses and counseling services for these women in order to improve their mental health status. Research into burnout, especially among nurses, continues to be of interest to researchers. A 2016 study of resilience and burnout status among oncology nurses using the RS Scale for Adults and Maslach’s Burnout Inventory, states that information on the relationship between burnout and resilience can be used to plan interventions supporting these workers. A 2018 investigation of the moderating effects of resilience on the relationship between emotional labor and burnout among hospital workers in geriatrics in South Korea urged that management interventions should be developed based on the recognition that emotional labor should be seen as a significant mental health issue. Another 2018 study focused on  resilience among the homeless population and still another on how engagement in creative art was associated with high resilience among Holocaust survivors.

The American Psychological Association has published an information sheet on resilience, including ten ways to build it, viz., making social connections; avoiding seeing crises as insurmountable problems; accepting that change is a part of living; moving toward one’s goals; taking decisive actions; looking for opportunities for self-discovery; nurturing a positive view of oneself; keeping things in perspective (big picture); maintaining a hopeful outlook; and general self-care.

A British work earlier this year synthesized the available evidence on interventions designed to improve individual resilience, assessing the methodological rigor of each included study. Programs were stratified into one of three categories: (a) cognitive-behavioral-based interventions; (b) mindfulness; (c) a combinations of the two. A meta-analysis led to the conclusion that resilience interventions based on a combination of the two techniques had a positive impact on individual resilience.

Being mindful of maladaptive cognitions leading to emotions which reinforce a self-defeating response to the environment can lead to engendering the courage required to build ongoing resilience.

~ Wm. Dray, Ph.D., CPhT – November 2018


MacLeod, S. et al. (2016). The impact of resilience among older adults. Geriatric Nursing, 37: 266-272.

Windle, G. et al. (2011). A methodological review of resilience measurement scales. Health & Quality Life Outcomes, 9:8.

Connor, K.M. & Davidson, J.R. (2003). Development of a new resilience scale: the CD-RISC. Depression and Anxiety, 18: 76-82.

Resnick, B.A., Inquito, P.L. (2011). The Resilience Scale: Psychometric properties and clinical applicability in older adults. Archives of Psychiatric Nursing, 25 (1): 11-20.

Joyce, S., Shand, F. et al. (2018). Road to resilience: A systematic review and meta-analysis of resilience training programmes and interventions. BMJ Open, 8: e017858.




“The problem of anxiety is the nodal point of many important issues. By solving this problem, you can reveal the whole mental life of a human.” – Sigmund Freud

Anxiety may be functional or pathological, and the latter type comes in various forms: social, panic, obsessive-compulsive, post-traumatic stress, and so on. Generalized anxiety disorder (GAD) was originally viewed as a residual construct, but today it is more often considered distinctive. The central feature of the disorder is worry, but unlike ordinary worry, the worry of GAD is uncontrollable, pervasive, i.e., free-floating. (Secondary symptoms include restlessness, fatigue, sleep disturbances, and difficulty concentrating.)

Freud conceived of the precursor of the syndrome, “anxiety neurosis,” back in  1894, and the term was standard until 1980 when the radical DSM-III was published. In the DSM-II, GAD was still referred to as “anxiety neurosis”. A power struggle in psychiatry came to a head with the publication of the third edition, with the result that Dr. Robert Spitzer & Co. had managed to purge psychoanalytic/psychodynamic theory from the tome in the interests of being “atheoretical”. This meant, of course, that unconscious mental forces are left out of the picture, obviously good for the cognitive-behavioral therapists, among others. (However, this assumed that no cases of such anxiety required depth psychology which, in my opinion, was presumptuous. From the empirical work of Howard Shevrin to the Implicit Association Test, there is evidence of unconscious mental processes, and that should have been taken into account in later revisions of the manual. In the DSM-V, for example, there is no mention made of the unconscious mind as a potential source of anxiety, generalized or otherwise.)

In addition to worry, avoidance has been posited as a key feature of GAD. Borkovec’s Avoidance Model asserts that worry is a verbal activity which inhibits vivid mental imagery and associated somatic and emotional activation. This prevents the emotional processing of fear. Insecure attachment from childhood may also play a part in the maintenance of the disorder.

Compared to depression, there is poor physician recognition of generalized anxiety disorder. Among people with GAD, there is high health care utilization, and these patients often present with pain, insomnia, and other physical symptoms, including cardiac and gastrointestinal. (Obviously, though, in the latter cases, a clinician cannot afford to assume psychogenic causation for fear of missing serious heart and gut conditions.) To deal with the problem of GAD in the primary care setting, Roy-Byrne and Wagner (2004, p. 20) have stated, “The collaborative care approach is designed to overcome [treatment] barriers. With this approach, the patient is provided with additional educational materials, physicians are supported by physician extenders [nurses, social workers, or expert consultants) who provide case-based feedback, follow-up, extra visits, and telephone calls to patients.”

Instead of “hypochondriasis”, the DSM-V utilizes the terms, Somatic Symptom Disorder and, in a minority of cases, Illness Anxiety Disorder (“if the patient has extensive worries about health but no or minimal somatic symptoms”).

The propensity to react negatively to everyday uncertainties has been associated with generalized anxiety, obsessive-compulsive disorder, social anxiety and panic disorders, depression, and anorexia/bulimia. This tendency has been referred to as Intolerance of Uncertainty.

GAD has as its defining feature a “free-floating” worry that can affix to almost anything. Thus, it is distinguished from specific obsessions. This worry is not necessarily irrational, just “amplified” out of proportion to what would normally be considered appropriate. In the case of everyday ambiguity, a GAD sufferer will fixate on this as a disturbing aspect of life and wonder why others are nonchalant about such maddening uncertainty. Attachment theory has explanatory value here in that one can easily see how a small child who was insecurely attached to its parents could develop to see the uncertainty as distressing, even threatening. A good example is ACOA: the child of alcoholic parents often does not know what to expect from them from day to day or sometimes even hour to hour. “If parental responses are unstable or inconsistent, a child may not learn to adequately regulate distress,” writes Canadian psychologist Magdalena Zdebik (2017). “Insecurely attached children are more likely to process or interpret ambiguous information or situations as threatening, hostile, or negative than securely attached children.” Frank personality changes in the parent are especially psychically disruptive and, if the situation is severe or prolonged, could actually make the child entertain thoughts of “body-snatching”.

The standard treatment for GAD is the combination of counseling/psychotherapy and an appropriate medication. Until recently, the favored drug was a benzodiazepine–and some physicians still prefer benzos for their fast-acting effectiveness–but this choice has fallen out of favor due to the addiction potential. Sometimes, buspirone is used in its place, but more often the substitute is a selective serotonin reuptake inhibitor (SSRI). (For a skeptical view of this off-label practice, see Healy (2004, p. 281). When supportive therapy is deemed inadequate, cognitive behavioral therapy (CBT) is the usual choice. However, in a minority of cases, a better method would be psychodynamic (derived from psychoanalysis), which can be done as brief therapy. This would be for those patients who have deeper issues generating the anxiety, unconscious conflicts which CBT is too superficial to address.

It seems that Freud is not quite dead yet.

~ Wm. Doe, Ph.D., October 2018


E. Behar et al (2009). Current theoretical models of generalized anxiety disorder. J Anx Disord, 23: 1011-1023.

Healy, D. (2004). Let Them Eat Prozac: The Unhealthy Relationship Between the Pharmaceutical Industry and Depression. New York: NYU Press.

Roy-Byrne, P. & A. Wagner (2004). Primary care perspectives on generalized anxiety disorders. J Clin Psychiatry: 65 [suppl 13]: 20-26.

Zdebik, M.A. (2017). Childhood attachment and behavioral inhibition: Predicting intolerance of uncertainty in adulthood. In Development and Psychopathology. Cambridge University Press.

Homeless Scholar Blog ~ FORENSIC ENTOMOLOGY

“The absence of significant numbers of blowfly larvae and lack of evidence of their feeding in the natural orifices or gunshot wounds on the corpse suggested that the body had been kept elsewhere, probably indoors, for several months and only recently placed on the site where it was found…Subsequent confession by the murderer established that the victim had been shot and kept in a sauna room for five months, then dumped at the edge of the woods where the body was found.” – K.G.V. Smith (1986)

The use of insects in death investigations goes back as least as far as the 13th century when one Sung Tzu (also known as Song Ci) described a homicide in which flies landing on a sickle retaining invisible traces of blood, indicated that it was the murder weapon and led to the perpetrator’s capture. The first formal case documentation, though, is that of a Dr. Bergeret who, in an autopsy of a child found hidden in the wall of a house in 1850, discovered flesh-fly larvae deposits that had to have occurred in 1848, the year before the occupants in question moved in. Another interesting case–hard to choose as there are so many worth nothing–involved a Hungarian ferryboat captain in the 1960s who arrived at work one September evening at 6 p.m., shortly after which the body of postmaster was found on board. The captain, protesting that he was innocent, was sentenced to life imprisonment for murder. Eight years later, the case was re-opened. A forensic entomologist noted the fact that no sarcophagous flies, such as were found in the autopsy the following day, are active in Hungary at 6 p.m. in the month of September. This and other insect data from the entomologist’s experiments, led to the conclusion that the flies’ eggs must have been laid before 6 p.m. on the day of the crime, i.e., before the captain even boarded the vessel. The data on oviposition were verified, and the captain was exonerated.

Why use insects in medicolegal investigations? Several reasons: First, they are usually the earliest creatures to find a decomposing corpse, and their reproduction information can serve as the basis for estimating the post-mortem interval (PMI), i.e., the time between death and corpse discovery. Second, there is predictability in  the changes and succession of arthropod fauna in and around the body. Also, arthropods in the general vicinity can provide valuable data which is sometimes ignored by investigators.

“Not only do insects swarm over an exposed corpse in great numbers,” writes physician K. V. Iverson in a morbid but informative and entertaining volume, “but they also arrive in a very precise sequence, depending upon the body’s location and condition. British Columbia scientists, for example, have found a markedly different insect succession than has been reported for other areas….”

Flies arrive first, then are replaced by beetles, which are replaced in turn by spiders, mites, and millipedes. The flies and beetles are necrophages, feeding on the corpse tissue per se. Parasites and predators eat not only that, but the necrophages as well. Omnivores will eat, in addition to corpse tissue, any flies or beetles still around as well as ants and wasps. Finally, there are incidentals (e.g., spiders and centipedes) which use the dead body as an extension of their environment.

(A quick definition of terms: Strictly speaking, insects are a class of the phylum Arthopoda and characterized by 3 distinct body divisions, 3 pairs of jointed legs, tracheas, and usually two pairs of wings. Arthropoda also include crustaceans, arachnids, and similar forms. It is the largest animal phylum, containing over 900,000 species.  Instar refers to any one of the various stages of insect development; and myiasis is basically the infestation by the larvae (maggots) of flies.)

Many techniques have recently been developed for FE use. Scanning electron microscopy (SEM) can identify key morphological features in eggs and maggots and distinguish species on the basis of shape and length as well as the presence or absence of anastomosis (connected blood vessels).

However, the high cost of the SEM equipment is a disadvantage, as is the time it takes to use; thus, it is not optimal for field study. A faster, less expensive technique is potassium permanganate staining. Slides can be used with any light microscope and can demonstrate key morphological differences for species identification. When structural differences prove difficult to descry, the mitochondrial DNA method can be used to identify characteristics at certain life stages.

Scientists in Germany (Zoologische Staatsammlung Munchen) have established a DNA reference library of potentially forensic relevant arthropod species, essentially using a form of barcoding. “DNA barcoding,” they write, “uses a short genetic sequence of the mitochondrial cytochrome c oxidate 1 gene (CO1-5′) as a unique identifier to differentiate between species.” Also, mock crime scenes using pig carcasses have been used frequently in the training of entomologists. The carcass serves as a surrogate for a human body and is used to illustrate various environmental effects relevant to crime investigation with insects. Finally, there are gene expression studies, in which the age of an egg is determined based on the expression of particular genes. Sometimes developmental stages are not evident by changes in size of the egg or pupa. The use of such genetic analysis can determine size changes, which data can then render the PMI more accurate.

Although this subfield of forensic pathology has powerful investigative methods, there are certain pitfalls and limitations to this approach. The post-mortem interval can easily be underestimated in numerous ways. For example, the wrapping of the corpse, low temperature, rain, burial, or the inactivity of most flies at night can lead to a delay in colonization, and hence, inaccurate measurements. Where the body is discovered might not be the scene of death. Also, infestations on a body might have begun before, not since, death. Drugs and toxins which affect maggots might be overlooked. Variations in the developmental biology of local populations could throw things off. All in all, the calculation of insect activity as it relates to the cadaver can be quite complex and fraught with pitfalls. However, despite these concerns, forensic entomology remains “the most reliable method for establishing the minimum time since death in the first weeks post-mortem” (Amendt & Richards, 2011).

~ Wm. Doe, PhD, CPhT – September 2018


Kenneth G.V. Smith (1986). A Manual of Forensic Entomology. London: The Trustees of the British Museum (Natural History). [opening quote: pp. 66-7]

E.P. Catts & M. L. Goff (1992). Forensic entomology in criminal investigations. Annu Rev Entomol, 37: 253-272.

J. Amendt & C.S. Richards (2011). Forensic entomology: Applications and limitations. Forensic Sci Med Pathol, 7: 379-392.

C. Chimeno, J. Moriniere, et al. (2018). DNA barcoding in forensic entomology–Establishing a reference library of potentially forensic-relevant arthropod species. J. Forensic Sci. [online]

K. V. Iserson (2001). Death to Dust: What Happens to Dead Bodies. Tucson, AZ: Galen Press; p. 388



Homeless Scholar Blog ~ SUDDEN DEATH

“Although the vast majority of these deaths may be ascribed to coronary atherosclerosis, there are many other potential causes of sudden cardiac death, such as cardiomyopathies, which are more frequently encountered in people aged less than 35 years.” – Oliva & Pascali, (2010), “Sudden Death in Forensic Pathology,” p. 108

A while back, I wrote a general article on the electricity of heart function, but in this post I am focusing on the specific problem of sudden cardiac death (SCD), news of which often comes as a surprise, especially when it occurs in the young and apparently healthy.

A widely accepted definition of SCD is: “A natural death due to cardiac causes heralded by abrupt loss of consciousness, within one hour after the onset of acute symptoms, or an unwitnessed, unexpected death of someone seen in a stable medical condition less than 24 hours previously with no evidence of a non-cardiac cause.” The term, “non-sudden cardiac death” would be used if resuscitation is initially effective but the patient dies somewhat later (Koene, 2017).

In younger individuals, such incidents are usually related to athletic activity. The leading cardiac causes of sudden death in athletes are cardiomyopathies, coronary artery abnormalities, myocarditis, channelopathies (muscle diseases causes by congenital defects in the cell membrane proteins that move ions in and out of the cell), valvulopathies, coronary artery disease, and aortic stenosis. (But there are also NON-cardiac causes: hypothermia (including heat stroke), use of illicit drugs, acute pulmonary diseases, acute cerebral diseases (including stroke), sickle cell disease, and rhabdomyolysis (an acute, sometimes fatal disease characterized by destruction of skeletal muscle).

For the general population, in industrialized countries, myocardial ischemia from advanced atherosclerosis is the most common cardiac cause of sudden death. The non-arrhythmic forms of SCD include aortic dissection, pulmonary embolism, cardiac tamponade (accumulation of excess fluid in the pericardium), and atrial myxoma (tumor in an upper chamber of the heart). An important warning symptom of SCD following syncope (fainting) is dyspnea, exceeded in risk only by a history of prior lifetime syncope or presyncope.

Sudden cardiac death accounts for 50% of all cardiovascular deaths. Key factors are atherogenesis, plaque destabilization, onset of ischemia and arrhythmias. Current estimates for out-of-hospital SCDs are 390,000 per year in the U.S.; in-hospital: 200,000. Ventricular tachycardia accounts for about two-thirds of all SCD attributed to arrhythmias. (Other causative arrhythmias are ventricular fibrillation, Torsade de Pointes (very rapid ventricular tachycardia that may turn into ventricular fibrillation), and pulseless electrical activity, including bradyarrhthmias.) But sudden death is not always mediated by arrhythmias. One of the greatest risk factors for out-of-hospital cardiac arrest is congestive heart failure. Contributing pathological factors of SCD in heart failure fall into two categories: endogenous (so-called “substrate development”: hypertrophy; left ventricle dilation/remodeling: scar formation/fibrosis; conduction pathway changes): and acute environmental triggers (electrolyte imbalances; sympathetic activation; ischemia; hemodynamic changes) (Weeks, 2016).

For decades, cardiovascular scientists have been trying to identify vulnerable atherosclerotic plaque in patients, with the hope of preventing disaster. Rupture of such plaque can be detected in victims of sudden death with the use of post-mortem CT coronary angiography (Moss, 2018). However, although rupture-prone plaques have been visualized even in living patients, risk prediction has been disappointing. In fact, it has been argued that the concept of vulnerable plaque is a “myth” hindering future research and that the focus should be not on individual plaques, but on arteriosclerotic disease burden (Arbab-Zadeh & Fuster, 2015).

The contingency of the human condition is such that any recommendation for prevention of SCD, especially in vulnerable individuals, must needs be a matter of probability. Nevertheless, certain factors can be mentioned based on documented medical cases. (Despite the earlier emphasis on young athletes, most people who suffer sudden cardiac death have a history of coronary heart disease.) Modifiable risk factors include cholesterol intake, smoking, glucose intolerance, hypertension, and obesity. The standard medical interventions are antiarrhythmic agents and implantable cardioverter-defibrillators. But public access to automated external fibrillators (AED) is hampered by the public’s limited ability to locate them quickly. Most people do not recognize the international sign and do not know what AED stands for. An American cardiologist has suggested that a better, more uniform sign design be employed and perhaps a better name as well (Otto, 2016). Also important for prevention is the exercise stress test, which can assess both ischemia and susceptibility to sustained ventricular tachyarrhythmias.

~ Wm. Doe, PhD, CPhT – August 2018


Koene, R. J. et al. (2017). Syncope and the risk of sudden cardiac death: Evaluation, management, and prevention. Journal of Arrhythmia, 33.

Brugada, R. (Ed.) (2010). Clinical Approach to Sudden Cardiac Death Syndrome. London: Springer-Verlag.

Moss, A.J. et al. (2018). Vulnerable plaque detection in sudden cardiac death: Post-mortem CT coronary angiography. BMJ Heart, 104 (Suppl. 5).

Arbab-Zadeh, A. & V. Fuster (2015). The myth of the “vulnerable plaque.” J. Am. Coll. Cardiol., 65 (8).

Weeks, P.A., A. Sieg, et al. (2016). The role of pharmacotherapy in the prevention of sudden cardiac death in patients with heart failure. Heart Fail Rev, 21.

Otto, C.M. (2016). Heartbeat: Prevention of sudden cardiac death. Heart, 102: 729-30.

Homeless Scholar Blog ~ MEDICAL UNCERTAINTY

“Although physicians are rationally aware when uncertainty exists, the culture of medicine evinces a deep-rooted unwillingness to acknowledge and embrace it.” – Simpkin & Schwartstein, “Tolerating Uncertainty,” NEJM, 11/3/2016

“Medicine is a science of uncertainty and an art of probability.” – William Osler

Intolerance of uncertainty is often cited as a symptom of generalized anxiety disorder, and given the existence of medical uncertainty, some intolerance of it is bound to be present also in medicine. This may lead to cognitive bias as a defense against anxiety, which can lead to serious negligence on one hand, and on the other, unnecessary, and sometimes harmful, treatment decisions.

If we assume a physician’s competent management of uncertainty, there is still the issue of communicating to patients the harms and benefits of treatment. Five types of uncertainty have been differentiated; (1) risk about future outcomes; (2) ambiguity regarding the strength of validity of evidence about risk; (3) uncertainty about the personal significance of particular risks; (4) uncertainty arising from complexity in risk information (e.g., instability of risks and benefits over time); (5)uncertainty resulting from ignorance. (Politi & Han, 2007). (Speaking of ignorance, there appears to be no clear best practice for presenting uncertainty. The old cliche about more research needing to be done definitely applies to this problem.)

Another aspect of this issue is the factor of medical tests. The matter of radiology reports is a case in point. (The overuse of CT scans is an important side issue.) In these reports, whether intentionally or not, the level of uncertainty is poorly defined, and diagnostic possibilities are listed in a haphazard way. One group of radiologists recommends that “when a short list of differential diagnoses is given, the items be rank-ordered by their probability and accompanied by a simple explanation of the radiologist’s thoughts, just as if we were speaking with the clinician in person in the reading room. An example of proper diction is: “The appearance suggests diagnosis X, which is felt to the most likely possibility; however, diagnosis Y must also be considered, though it is thought to be less likely because….” (Bruno et al, 2017). Also, it has been noted that certain words and phrases carry different meanings for radiologists and clinicians. To address this problem, a standardization called structured programming has become more prevalent.

Since uncertainty is inherent in prognosis, the matter of prognostic indices is obviously relevant, but the “punctilious quantification of the amorphous,” as one M.D. puts it, is unlikely to ever yield satisfying clarity. However, a framework of three central tasks has been proposed to help patients and families manage uncertainty: (1) normalization of the uncertainty; (2) addressing patients’ emotions about uncertainty; (3) helping patients and families manage the effect of uncertainty on their ability to live in the here and now. Many clinicians have trouble with this prognostic uncertainty. As Smith et al (2013) observe, “Some react by not being willing to talk to the patient about the future at all (commonly expressed as ‘We have to wait and see’ or ‘No one can tell’). Others, ignoring that uncertainty built into prognostication, do more and more tests in a futile hope of being able to predict the future. Physicians need to recognize their reactions to uncertainty and how these reactions may influence their conversations with patients.”

The late pathologist, William B. Ober, in an essay on medical education, wrote that too many pre-medical students “choose to study the sciences at the expense of the humanities.” This adversely affects “the total ability of the physician to deal with the complex equation that is represented by the individual patient’s illness,” as partially reflecting psychological and social stresses. And another part of this complexity is an ability to recognize uncertainty and to deal with it honestly.

One group of physician critics has said that changes in the medical curriculum reflecting more humanities and biopsychosocial models “seems too general to address issues related to intolerance of ambiguity.” Failure to do so has adverse effects on the general patient population and in particular, on the underserved whose poverty presents medical and psychosocial complications which heighten the ambiguity.

~ Wm. Doe, PhD, CPhT – July 2018


S. Wayne, D. Dellmore (2011). The association between intolerance of ambiguity and decline in medical student attitudes toward the underserved. Acad. Med. 86(7).

A.K. Smith, D.B. White et al. (2013, June 27). Uncertainty: The other side of prognosis. New Eng J Med, 368 (26): 2448-2450.

W. B. Ober (1987). Bottoms Up!: A Pathologist’s Essays on Medicine and the Humanities. Carbondale, Ill. So. Ill. Univ. Press.

M. C. Politi, P.K.J. Han (2007). Communicating the uncertainty of harms and benefits of medical intervention. Medical Decision Making, Sep/Oct.

M. A. Bruno et al. (2017). Communicating uncertainty in the radiology report. Am. J. Roentgenol., 209.

B. Lee, M.T. Whitehead (2017). Radiology reports: What you think you’re saying and what they think you’re saying. Curr Prob Diag Rad, 46: 186-195.







“These emotional lessons are so potent and yet so difficult to understand from the vantage point of adult life because…they are stored in the amygdala as rough, wordless blueprints for emotional life. Since these earliest emotional memories are established at a time before infants have words for their experience, when these emotional memories are triggered in later life, there is no matching set of articulated thoughts about the response that takes us over….” – Daniel Goleman, Emotional Intelligence 

Alcoholism (or Alcohol Use Disorder, to be up-to-date and official) has been talked and written about to death, but I’ve brought it up here as an example of the application of a subfield of abnormal and developmental psychology called developmental psychopathology. (Also relevant is the discipline of affective neuroscience.) It no longer concerns me greatly if the syndrome is considered a “disease” or a “disorder”, or what the merits of A.A. (if any) might be. Here, I’m interested in the psychosocial matrix of the pathology, especially the familial influences, above and beyond any genetic predisposition that may be at play. Some children are resilient enough to resist such influences, but many are not; and in general, the younger a child is, the more susceptible it is to such dynamics, especially because the brain structures (most notably, the limbic system) are in a formative stage such that a sort of environmental shaping may occur, literally. (Such a focus has additional relevance in the current context of immigrant children taken by the U.S. government from their parents and put in cages. This point was brought up the other day by the president of the American Association of Pediatrics.)

A cross between developmental psychology and child psychiatry, the field of developmental psychopathology (DP) developed in the 1970s. The key figure in the discipline is generally considered to be Harvard scientist Dante Cicchetti, who sought to bring empirical rigor to clinical study of problematic behaviors of childhood. This subfield examines developmental pathways of both normal and abnormal behaviors, including consideration of individual differences, biological and social factors. DP can identify at-risk children and effect timely interventions to interrupt maladaptive behavioral processes. The main reason why more was not done earlier on in this area is “a widespread attitude among academic psychologists that any research that was not basic research could not be scholarly and scientifically rigorous [and also that] clinicians….have sometimes tended to underestimate the importance of academic research, not only for advancing psychology, but also for solving everyday clinical problems.” Several key questions guide DP: What are the similarities and differences of individuals as they grow older and some take maladaptive paths? Why do some individuals experience differences in psychological functioning over time? What consequences do personal histories have on their subsequent mental health? A propos, human neuroimaging and animal studies have shown that early and persistent alterations in amygdala circuitry and function follow early-life stress, effects that are not reversed when the stressor is removed. Such findings connect developmental psychology with affective neuroscience.

The DP approach has been able to integrate theories and findings that had previously been in isolation from one another. Regarding alcohol use studies, DP has offered a more complex and nuanced analysis of relevant transitions and multiple etiological pathways underlying the disorder. Advances in quantitative methods (especially multilevel and structural equation modeling) have enabled a greater correspondence between statistics and theory. In terms of developmental vulnerability, Chassin et al. (2013) note in their review, “The apparent sensitivity of the adolescent brain to alcohol-related insult is though to be associated with neurodevelopmental vulnerability to disruption of the extensive remodeling of the brain that takes place in adolescence.” Additionally, they note that “rodent models allow molecular analysis of mechanisms underlying neurotoxic effects that appear heightened in adolescence and could presage enhanced susceptibility to addiction.”

Alcohol use disorder is a subject of interest for DP since insight into the condition can be gained by looking at the way the addicted person reacted to a difficult early environment in which “set-ups” for maladaptive coping emerged, with or without the presence of parents who were struggling with the same problem. Some outcomes of this particular situation can be seen in the Internet forums for Adult Children of Alcoholics (ACOA).

A related field is affective neuroscience, which examines the neural circuitry involved in the experience and expression of emotion, integrating research from animal models with that of human behavior. This research suggests a cross-species commonality of neural circuitry involved in emotional regulation. It is important to appreciate the plasticity and anatomical development of the human central nervous system when considering adverse early impact of the environment. As Joseph LeDoux, prominent NYU neuroscientist (referenced by Goleman (1995)) has put it, “Early experiences are etched into the amygdala as wordless emotional blueprints for adult life.” The structure most involved in such memories, the amygdala, is developed before the neocortex and hippocampus, areas responsible for explicit memory, are fully formed.

The implications for future substance abuse are clear. A favorite expression in A.A. is “Cunning, baffling, powerful!” to describe the effects of the drug on biopsychologically vulnerable individuals. But it’s not so baffling when one considers how a deformed limbic system leading to deranged frontal circuitry could produce a brain susceptible to a marked soothing effect from an anesthetic sedative like ethanol.

~ Wm. Doe, Ph.D. – June 2018


Banks, S.J., K.T. Eddy, et al. (2007). Amygdala-frontal connectivity during emotional regulation. SCAN, 2: 303-312.

Cicchetti, D. (1984). The emergence of developmental psychopathology. Child Development, 55 (1), Feb.

Chassin, L., K.J. Sher, et al. (2013). The developmental psychopathology of alcohol use and alcohol disorders: Research achievements and future directions. Dev. Psychopathol., 25, Nov.

Goleman, D. (1995). Emotional Intelligence. New York: Bantam Books.


“For my part, whatever anguish of spirit it may cost, I am willing to know the whole truth; to know the worst and provide for it.” – Patrick Henry

“To succeed, one cannot afford to be a realist.” – Albert Bandura

Was the debate over the validity of depressive realism ever resolved? Not that I can see, although it has proven to be a more complex topic than I originally thought.

For those not familiar with the term, it basically refers to a putative tendency of mild to moderately depressed individuals to see reality more accurately than those who are not depressed, the latter being prone to “positive illusions”. Based on a classic 1979 study by Lauren Alloy and Lyn Abramson, essentially involving how much control depressed and non-depressed experimental subjects reported having over whether a light came after they pushed a button under various conditions.

Contrary to the conventional wisdom of the time that mentally healthy individuals should be accurate in their assessment of reality, the findings of Alloy and Abramson suggested just the opposite: that nondepressed subjects overestimated their degree of control, and depressed subjects exhibited accuracy across all experiments. Anticipating later work on so-called “positive illusions”, the authors summarize similar findings by stating that “taken together”, these studies suggest that at time depressed people are “sadder but wiser” than nondepressed people. Nondepressed people succumb to cognitive illusions that enable them to see both themselves and their environment en rose. A crucial question is whether depression itself leads people to be “realistic” or whether realistic people are more vulnerable to depression than other people.

Martin Seligman, prominent psychologist and mentor to the authors, naturally felt obliged to explain his students’ disturbing results. “As a therapist,” he wrote in his book Learned Optimism, “I was trained to believe that it was my job to help depressed patients both to feel happier and to see the world more clearly…but maybe truth and happiness antagonize one another.” In speculating on why pessimism and depression have had such evolutionary staying power, Seligman opines that as creatures of the Pleistocene , our evolutionary makeup has been shaped by an era of catastrophic climate changes and, to survive, our ancestors had to expect the worst. But the modern world does not suffer from the type of environmental threat and calamity that characterized that earlier period, so, the reasoning goes, we are stuck with an “old-fashioned” brain, a vestige of a bygone era. To his credit, Seligman, at least in this book, proffers a more nuanced version of positive psychology (PoPsy) than some of its adherents. (Unfortunately, there are problems with falling back on evolutionary psychology (EP), which discipline Noam Chomsky has described as “philosophy of mind with a little science thrown in.” But one does not have to take so dim a view of the field to acknowledge that there are problems with many of its theories, which have been critiqued by Stephen Jay Gould, David Buller, Kenan Malik, and other. EP is too often invoked as a non-problematic solution to the theoretical problems arising from research in social and abnormal psychology.)

If the sociobiological/EP argument to explain the persistence of pessimism is not viable, perhaps the issue can be framed in other terms. Recent research suggests a helpful distinction between a global or dispositional pessimism and what psychologist Julie K. Norem terms “defensive pessimism”, a pro-active stance wherein possible problems are anticipated and dealt with in advance, thus decreasing anxiety and optimizing performance. That is, from being a “negative”, self-handicapping mindset, this is a highly adaptive approach that looks for things that could go wrong and prepares for them, rather than assuming in a cockeyed optimistic fashion that it will all somehow out in one’s favor.

“Defensive pessimism,” wrote Norem, “is a strategy that helps us work through our anxious thoughts rather than denying them so that we may achieve our goals…Defensive pessimism is emphatically not about leading anxious people into depression; quite the contrary–it can actually aid our efforts toward self-discovery and enhance our personal growth.”

According to Norem, the picture of human psychology is more complicated than the current American positivity Zeitgeist might lead one to believe. Actually, it could be argued that defensive pessimism is a sophisticated form of PoPsy, as it is a proactive way of coping with anxiety. It may seem counterintuitive, but the performance of defensive pessimists is impaired by the ‘imposition’ of a positive mood, which interferes with their overall troubleshooting strategy.

It is easy to see that the rather mild claims of defensive pessimism could be accommodated by the theory of self-efficacy, but Norem told me several years ago in an e-mail that in a discussion with Bandura, he said he’d have none of it. Depressive realism, however, is more controversial, and strong criticisms have been made over the years, especially concerning its ecological validity. A 2012 meta-analysis–the first for DR–looked at 75 studies from five countries and came up with an assessment that is mixed at best, reporting a large degree of variability in experimental responses. “The question for future research then becomes,” wrote Michael T. Moore and colleagues, “under what circumstances and for which groups of people is depressive realism valid.”

But the critics of DR do not necessarily “win” the debate, and that is partially because, in the bigger picture, we are at a “metaphysical block.” Psychologist Colin Feltham, in his recent book on the subject, focused on a “dark” existentialism, influenced, among others, by Schopenhauer and Leopardi, suggesting that DR has a philosophical legitimacy that cannot be totally psychologized.

Cognitive hard-liners would do well to note that even Aaron Beck nuanced his position on DR, writing in a 1995 article, “…cognitive distortions are not an inevitable feature of depressive thinking nor unheard of among nondepressed people,” adding that his theoretical writings “have sometimes implied a generality of depressive distortion and (implicitly) nondepressive accuracy that probably cannot be sustained…In view of the losses, marital disruptions and personal rejections often experienced by depressed people, it is important to acknowledge that their negative thinking will sometimes not strike detached observers as farfetched or absolutely incorrect.” (Haaga & Bedck, 1995; p. 45)

So, in prescriptive terms, can there be a meaningful heuristic indicative of when positive thinking is advisable, and when not? Broadly speaking, in ambiguous situations, when action informed by optimism does not seem as hazardous or self-defeating as action dictated by pessimism, then the former option should probably be taken. It is difficult to generalize about this, but for a person whose predicament is constrained by adverse physical and financial factors, it may be, more often than not, realistic to conclude that “it won’t work out, so why gamble away precious resources (mental, physical, financial)?” However, sometimes this is a self-defeating, kneejerk mode that should be challenged. What determines whether it should be challenged is the intensity of the ambiguity and perceived differential harm for the choice. That is, one should ass, “Is it irrational to be pessimistic in this context? How certain is an unsafe or miserable outcome?” Compelling research suggests that mild-to-moderately depressed people do indeed see things accurately (hence the term, “depressive realism”), but there is often a perception of ambiguity and uncertainty involved. The ambiguity brings a sort of interpretive latitude into play which may occasionally justify a “strategically optimistic” choice. But this is not the same as a “global”, or dispositional behavioral change in attitude: this space opened up for competing, reasonable interpretations is contingent upon the ambiguity and risk calculus, and is thus not an across-the-board challenge to “positive thinking”.

~ Wm. Doe, Ph.D. – May, 2018


Alloy, L.A. & Abramson, L.Y. (1979). Judgment of contingency in depressed and nondepressed students. J Exp Psychol Gen, 108 (4): 441-485.

Haaga, D.A. & Beck, A.T. (1995). Perspectives in depressive realism: Implications for cognitive therapy of depression. Beh Res Ther, 33 (1): 41-48.

Moore, M.T. et al (2012). Depressive realism: A meta-analytic review. Clin Psychol Rev, 32 (6).

Norem, J.K. & Chang, E.C. (2002). The positive psychology of negative thinking. J Clin Psycho, 58 (9): 993-1001.

Homeless Scholar Blog ~ HYPOCHONDRIASIS (or whatever they’re calling it when you read this)

“It sometimes happens that a man who, up until now, has believed himself to be gifted with perfect health, opens a medical book, either by chance or to pass the time, and on reading the pathological descriptions of an illness, recognizes that he is afflicted by it; enlightened by a fateful flash of insight, he feels at every symptom mentioned some obscure organ shuddering within him, or some hidden fiber of whose role in the body he had been unaware, and he pales as he realized that a death he thought was still a long way off is so imminent.” – Theophile Gautier

“Oscar Levant couldn’t be here tonight as he is feeling well.” – Milton Berle

Personal disclosure: I have a history of being, as doctors call it, a “crock” — i.e., a “hypochondriac,” one afflicted with what, until recently, was officially labeled “hypochondriasis”. More popularly referred to without the “sis” and meaning exaggerated concern about health not based on real medical pathology, but on unrealistic interpretations of physical symptoms or sensations. (The previous version of the DSM included an umbrella category, “Somatoform disorders,” psychiatric syndromes that assume the form of somatic illness. These were categorized as Somatization, Undifferentiated Somatoform, Conversion, Pain (Disorder), Hypochondriasis, and Body Dysmorphic Disorder. This scheme has since been swept into the psychiatric trash can of history. But more on that presently.) I’m better about this than I used to be, but it still flairs up occasionally, and I try not to berate myself for it. Over the years, people’s reactions to my neurotic propensity have fallen into three categories: empathy (infrequent), amusement, and contempt.

But enough about me — Is there a consensus finally on what causes this anxious formation? Well, not exactly. Theories range from sensory amplification to fear of death (including psychoanalytic, behavioral, and familial (genetic predisposition activated by symptom(s) plus social reinforcement)). One dogmatic friend was accusatory about the death anxiety theory. To this, I advanced the objection that hypochondriasis, in my case, could merely be a gearing up to be proactive so as to avoid a possibly worse outcome than if it had been ignored or reacted to avoidantly.

The idea of death anxiety being at the root of hypochondriasis comes out of existentialism, and has been developed to the hilt by terror management theory, which is based on the writing of cultural anthropologist, Ernest Becker. Basically TMT proposes that control of this anxiety is the primary function of society and the main motivation of human behavior. Both self-esteem and cultural worldviews/institutions are seen as mass psychological defenses. TMT has considerable empirical support especially in the social psychology literature. However, there have been numerous criticisms of the theory; for example, that some elements of it can be equally well explained by other theories, there is no accounting for personal growth and acceptance of death, and that the case is weak that the organism’s chances of survival are increased by terror management processes. “It simply does not follow that a motive for self-preservation,” write two critics, “will lead organisms to minimize the perceived severity of threats to their survival as the theory suggests.” Relevance of theory possibly varies with individuals, as with depression: for some, CBT is adequate because cognitive distortion sometimes really is the problem; for others, psychodynamic or even existential–sometimes in combination (although exploration of “castration anxiety” is probably unnecessary.)

My sense is that the somatic amplification theory likely had the widest applicability. According to its best-known proponent, psychiatrist Arthur J. Barksy, it refers to “the tendency to experience bodily sensation as intense, noxious, and disturbing [and] includes an individual’s disposition to focus on unpleasant sensations and to consider them as pathological rather than normal.” There is a self-report questionnaire for it, called the Somatosensory Amplification Scale, which assesses the repondent’s perceived sensitivity to 10 uncomfortable bodily sensations. Also it has been shown that cortical-evoked potentials and changes in skin conductance produced by auditory stimuli are enhanced in somatization disorder patients. Among Barksy’s suggestions for managing patients with somatic preoccupation are: focusing on functioning and refraining from attempts to eliminate symptoms completely; reviewing old records before ordering tests; validating the patient’s distress; providing a diagnosis and describing the amplification process with specific examples; cautiously reassuring.

The DSM-5 is highly controversial and the controversy extends to the new diagnostic replacements for “hypochondriasis”: Somatic Symptoms Disorder and Illness Anxiety Disorder. “If the individual has extensive worries about health but no or minimal somatic symptoms, it may be more appropriate to consider Illness Anxiety Disorder…” In contrast [with SDD], individuals with IAD have minimal somatic symptoms and are primarily concerned with the idea that they are ill. Furthermore, there are two modes: care-seeking and care-avoidant (wherein medical care is rarely sought). The DSM-5 argues that the old scheme was confusing and that the new one recognizes overlap by reducing the total number of disorders. A group of German researchers (Bailer et al, 2016), using a case-control study, attempted to validate the new diagnoses and concluded that their results do not support the proposed splitting of health anxiety/hypochondriasis into two diagnoses.

“Psychometric data purporting  to show that hypochondriasis increases in the elderly,” write gerontologists at the National Institute of Aging, “are confounded by real health changes with age, and evidence from longitudinal studies shows that where health complaints increase, they probably reflect veridical reports of changing health status.” A website on geriatric hypochondriacs notes that “Complaints of ill health among the elderly are most commonly centered on the discomforts and restrictions of physical decline, or, in hospital jargon, ‘the dwindles’…” This charming little term at least suggests that the problem is not all in their minds. Which is resonant with the insightful personal remark from an old friend who was complaining about the longstanding crockish ways of an associate, but then added: “On the other hand, he’s getting old now, so things are less imaginary.”

~ Wm. Doe, Ph.D. – April 2018


American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders, 5th Edition. Washington, D.C.: APA Press

J. Bailer et al (2016). Health anxiety and hypochondriasis in the light of DSM-5. Anxiety, Stress, and Coping, 29 (2).

M.R. Leary & L.S. Schreindorfer (1997). Unresolved issues with terror management theory. Psychological Inquiry, i.1

A.J. Barsky (1992). Amplification, somatization, and the somatoform disorders. Psychosomatics, 33 (1).

P.T. Costa & R.R. McCrae (1985). Hypochondriasis, neuroticism, and aging. American Psychologist, 40 (1).

Alternatives for Seniors (7/3/2015). “How to Handle a Hypochondriac Senior.”  https://www.alternativesforseniors.com/blog/hypochondriac-senior


Homeless Scholar Blog ~ THE DESTRUCTION of MEMORY

“In everyday life, one is continuously called on to use experiences one has just passed through or passed through the day before, as well as those undergone at various periods of one’s existence. All this knowledge is combined to enable one to deal with the exigencies of a current situation. That the Korsakoff patient is incapable of this type of mental activity explains the poverty and ineffectiveness of his life, for he is unable to reunite the data that a new situation demands, especially it if is a complex one.” – Jacques Barbizet, Human Memory and its Pathology

“The progressive destruction of memory follows a logical order…It begins at the most recent recollections which, barely repeated and…having no permanent associations, represent organization in its feeblest form.” – Theodule Ribot, 1882 (Kopelman, 2002)


RECENTLY, A FRIEND OF MINE OF MINE ENDED UP in the the ER as a result of his heavy chronic alcohol consumption. The diagnosis was severe encephalopathy. Since he has been out, he has resumed drinking and shows the typical symptoms of Korsakoff’s Syndrome (KS), which often follows from Wernicke’s Encephalopathy (WE): severe anterograde amnesia (impairment of new learning), variable retrograde amnesia (loss of remote memory), and confabulation (filling in memory gaps with fabrication, but without intent to deceive). I stress “typical” since not all KS patients engage in confabulation, and it fades away after four or five years. The root cause of KS, as with WE, is severe thiamine (vitamin B1) deficiency (formerly called beri-beri). Although there are several possible causes for the deficiency (e.g., anorexia, cancer), it is usually seen as the sequela of chronic alcoholism. Massive perenteral infusions of the vitamin usually cures the disorientation, ataxia, and ophthalmoplegia of the encephalopathy, but all too often significant brain damage remains, manifesting itself as the amnesic symptom first described by Sergei Korsakoff in the 1880s. The prognosis for KS: 20% achieve complete recovery within two years of abstinence from alcohol; 60% achieve partial recovery; and the rest are institutionalized or discharged to the streets.

The critical lesion sites for memory disorder have been debated. Among the ones in the literature are: dorsomedial thalamus, mammillary bodies of the hypothalamus, mamillothalamic tract, and hippocampus/medial temporal lobe. The basal forebrain (cholinergic center) and corpus callosum have also been implicated. At present, those arguing for thalamic lesions as the most significant appear to be in the majority. The thalamus, part of the diencephalon and situated just above the brainstem, send information not only to the cortex, but also to the hippocampus and amygdala.) Thus, the notion of the hippocampus as the “memory center” of the brain is shown to be simplistic, although there may be some damage there in KS patients. However, unlike the thalamic damage (in most cases), this is reversible with abstinence.

For comparison, I’m including mention here of three well-known amnesia cases. First, though, it’s worth noting that these amnesic disorders do not involve dementia. Specifically, the difference between KS and dementia is that unlike the former, in which intelligence is basically intact and impairment to memory (and occasionally, some executive function), in dementia, there is a progressive, global impairment of mental ability. The three cases are those of N.A., the victim of an accident in which a miniature fencing foil went up his nose and pierced the thalamus. This led to severe amnesia, but only affecting recall of verbal material; all other cognitive functions remained normal. Then, there is the case of Clive Wearing, a musician and musicologist, whose extreme amnesia developed from herpetic encephalitis. And finally, the most famous case in modern neurology, that of Henry Molaison, who died in 2008 and who, before then, was referred to as H.M. An injury in childhood led to intractable epilepsy and eventually, radical surgery which removed both his hippocampi, leaving him, naturally unbeknownst to the surgeon in advance, with severe amnesia. Psychologist Brenda Milner assessed him, wondering what he was still capable of involving short-term memory. One of her investigations involved a star-tracing task with a mirror, something a bit challenging even for normal people. To her surprise, H.M. was able to improve the quality of his traced stars over a matter of days until it was comparable with that of undamaged subjects, even though he had no recollection of having done any tracing from the day before (and could not even remember Milner from one day to the next). From this, she realized that an implicit/unconscious/procedural memory was at work, governed by parts of the brain other than those controlling explict/conscious memory: these “implict areas” are the striatum and the cerebellum.

Furthermore, Kandel (2006) states that “Milner’s star-tracing experiment with H.M. was the first time a scientist had uncovered the biological basis of psychoanalytic hypothesis. By showing that a person who has no hippocampus (and therefore no ability to store conscious memories) can nonetheless remember an action, she validated Freud’s theory that the majority of our actions are unconscious.”

Thus, clinical attempts at mitigating amnesia have focused on procedural memory, which appears to be preserved in Korsakoff patients, as it was with H.M. (Oudman, 2015). In a review of implicit memory studies of KS, Hayes (2012) concludes that specific task parameters and demands are key in revealing intact or impaired performance. These parameters include “timing between stimuli, the specific nature of the stimuli used in a task, and the integrity of supportive cognitive functions necessary for performance. One of the experts in this area, Barbara O. Wilson, notes seven definitions of “recovery” in the rehabilitation literature and stresses limitations regarding brain injury. “We can and do see diminution of impairment in behavioral [and] physiological function over time…Partial recovery of function with considerable substitution…is what most of us in rehabilitation expect to see. Return to normal or near-normal levels of performance is unlikely for most memory-impaired people once past the acute stage.” (p. 18) However, although Wilson makes a few passing references to KS patients, most of her book seems to apply to traumatic brain disorder. My friend’s sister said in an e-mail, “He is not himself anymore,” thus underscoring the essential link between memory and identity. As neurologist Oliver Sacks asks in his book, The Man Who Mistook His Wife for a Hat, “What sort of life (if any), what sort of world, what sort of self, can be preserved in a man who has lost the greater part of his memory and, with this, his past, and his moorings in time?” I’m hoping that, for my friend at least, that question is more than rhetorical.

~ Wm. Doe, Ph.D. – March 2018


Jacques Barbizet (1970). Human Memory and its Pathology. San Francisco: W.H. Freeman & Co.

M.D. Kopelman (2002). Disorders of memory. Brain, 25 (10).

M. Victor et al. (1989). The Wernicke-Korsakoff Syndrome and Related Neurologic Disorders Due to Alcoholism and Malnutrition. (2nd Ed.) Philadelphia: F.A. Davis & Co.

Barbara O. Wilson (2009). Memory Rehabilitation: Integrating Theory and Practice. New York: Guilford Press.

Eric Kandel (2006). In Search of Memory. New York: W.W. Norton.

E. Oudsman, T.C. Nijboer et al. (2015). Procedural learning and memory rehabilitation in Korsakoff’s syndrome. Neuropsychol Rev, 25 (2).

S.M. Hayes, C.B. Fortier et al. (2012). Implicit memory in Korsakoff’s syndrome: a review of procedural learning and priming studies.. Neuropsychol Rev, 22 (6).




Homeless Scholar Blog ~ INTOLERANCE of UNCERTAINTY

“Some poems don’t rhyme, and some stories don’t have a clear beginning, middle, and end. Life is about not knowing, having to change, taking the moment and making the best of it, without knowing what’s going to happen next.” – Gilda Radner

Uncertainty is part of the human condition, but not everyone reacts to this continual ambiguity in the same way. Of course, some uncertain situations are more serious than others, but regardless of the gravity involved, some individuals are just more distressed about it. The propensity to react negatively to everyday uncertainties has been associated with generalized anxiety disorder (GAD), obsessive-compulsive disorder, social anxiety and panic disorders, depression, and anorexia/bulimia. (The most frequent measure is the Intolerance of Uncertainty (IU) scale, a 27-item report which has been made more methodologically sound through its abbreviation into the IUS-12.) Perhaps there are certain genetic vulnerabilities at play with this syndrome, but it seems more fruitful to focus on developmental issues, specifically, what “unhealthy” environment(s) a “strong reactor” was exposed to in childhood?

Intolerance of uncertainty has been conceptually distinguished from three other constructs (Rosen et al., 2014): intolerance of ambiguity (IA), uncertainty orientation (UO), and need for cognitive closure (NCC). IA focuses on the “here and now”, while IU centers on an apprehension about events occurring in the future. NCC and UO are similar in that they appear to have implications for motivation: approach of avoidance. IU and IA tend to foster indecisiveness, a lack of behavioral reaction to the perception of the situation.

On the psychophysiological level, IU has been shown to be related to reward responding and threat amplification, and may be linked to anterior insula response to uncertainty (Gorka, 2016). More recently, and supporting this, IU has been associated with greater insula and amygdala response to uncertainty, with altered event-related potentials regarding rewards and errors, and with deficiencies in safety learning indexed by skin conductance (Tanovic, 2018).

In addition, cross-sectional survey data has shown a high level of rumination in the association between IU and depression symptoms. This data supports rumination as a moderator and mediator in the relation of IU to both depression and anxiety symptoms (Liao & Wei, 2011). High IU is transdiagnostic and has been proposed as a phenotypic case of internalizing psychopathology.

GAD has as its defining feature  a “free floating” worry that can affix to almost anything. Thus, it is distinguished from specific obsessions. This worry is not necessarily irrational, just “amplified”, out of proportion to what would normally be considered appropriate. In the case of everyday ambiguity, a GAD sufferer will fixate on this as a disturbing aspect of life and wonder why others are nonchalant about it. Attachment theory has explanatory value here in that one can easily see how a small child who was insecurely attached to its parents could develop to see the uncertainty as distressing, even threatening. A good example is the ACOA (Adult Children of Alcoholics) syndrome: the child of alcoholic parents often does not know what to expect from them from day to day or sometimes even hour to hour. “If parental responses are unstable or inconsistent, a child may not learn to adequately regulate distress,” writes Canadian psychologist, Magdalena Zdebik (2017). “Insecurely attached children are more likely to process or interpret ambiguous information or situations as threatening, hostile, or negative than securely attached children.”

Frank personality changes in the parent are especially psychically disruptive and, if the situation is severe and prolonged, could actually make the child entertain thoughts of “body-snatching”.

Arguably, uncertainty and ambiguity would be somewhat mitigated in a more enlightened, rational social system, but, still, a residuum is bound to persist even then, as it is essentially part of the human condition. One function of religion is to alleviate the stress from lack of guidance through the vicissitudes of everyday life and especially painful crises when they arise. Cognitive-behavioral therapy is often cited as effective for anxiety in general, but existential psychotherapy can be useful in helping those who have a problem with UI by framing it in terms of coping with the basic anxiety of inescapable freedom to act, and often action is, as noted, given poor guidelines, the ubiquitous uncertainty. Although it may be overstating the case to say, as Sartre did, “We don’t know where we came from, we don’t where we’re going, and we don’t know what we’re doing while we’re here,” in the face of intractable ambiguity, decisions will still have to be made, which includes the decision to do nothing.

~ Wm. Doe, Ph.D., February 2018


N. O. Rosen et al (2014). Differentiating intolerance of uncertainty from three related but distinct constructs.  Anxiety, Stress, & Coping, 27, 1.

M.A. Zdebik et al (2017). Childhood attachment and behavioral inhibition: Predicting intolerance of uncertainty in adulthood. Development and Psychopathology. Cambridge University Press.

S.M. Gorka et al (2016). Intolerance of uncertainty and insula activation during uncertain reward. Cogn Affect Behav Neurosci, 16: 929-39.

E. Tanovic (2018). Intolerance of uncertainty: Neural and psychophysiological correlates of the perception of uncertainty as threatening. Clin Psychol Rev (e-pub). 1/6/2018.

K.Y. Liao & M. Wei (2011). Intolerance of uncertainty, depression, and anxiety: The moderating and mediating roles of rumination. J Clin Psychol, 67 (12).