The Homeless Scholar Blog: NEURAL EFFICIENCY and the IDEA of INTELLIGENCE

“Ultimately, it would certainly be desirable to have an algorithm for the selection of an intelligence, such that any trained researcher could determine whether a candidate’s intelligence met the appropriate criteria. At present, however, it must be admitted that the selection (or rejection) of a candidate’s intelligence is reminiscent more of an artistic judgment than of a scientific assessment.” – Howard Gardner, educational psychologist

A while back, I wrote a post on general intelligence, noting that experts disagree as to what it actually is and emphasizing a broad conceptual analysis of the idea. Yet, for some reason, I kept having nagging doubts: “Why not keep this simple? An intelligent person is simply one with greater neural efficiency. Measure that factor correctly and you will have a quantification of this concept.” Perhaps a more efficient nervous system is more “fluid”, more adaptable, and thus more fit and functional in general. Raymond Cattell had two divisions of intelligence: Fluid and Crystallized, the latter being our acquired knowledge and skills. But the former is about a more “basic” sort of intelligence, how we process information without relying on a storehouse of previously acquired knowledge , but instead using abstract reasoning, pattern recognition, and general problem solving ability. Thrown into an unfamiliar situation with a requirement to think fast, all that stuff we’ve picked up over the years might avail us little or nothing. As Cattell put it, “It is apparent that one of these powers…has the ‘fluid’ quality of being directable to almost any problem.” Fluid intelligence (FI) is measured using a non-verbal, multiple choice picture completion test called the Raven Progressive Matrices, which focuses on detecting relationships among images.(Also used are the Cattell Culture Fair Test and the performance subscale of the Wechsler Adult Intelligence Scale (WAIS).

Peter Schonemann, who studied under Cattell, stated that the g factor (the letter standing for general/basic smarts) does not exist, and that those who emphasized it, like Arthur Jensen, were distorting the original findings of Charles Spearman with the effect, intentional or not, of putting racial minorities at a disadvantage in terms of policy decisions based on pro-hereditarian research. Canadian psychologist, Keith Stanovich argues that IQ tests, or their proxies (e.g., the SAT), do not effectively measure cognitive functioning, because they fail to assess real-world skills of judgement and decision-making. But he does not say the tests should be abandoned, just revised to encompass measurement of the aforementioned skills. Going back to the basic semantic question, Australian educational psychologist, R. W. Howard breaks intelligence down into three categories: Spearman’s g; a property of behavior; and a set of abilities. ‘Each concept,’ he writes, ‘contains different information, refers to a different category, and should be used in different ways…A concept is never right or wrong, but is only more or less useful.’ Matching a given use of the term, ‘intelligence’, with its appropriate category would eliminate much confusion. Furthermore, recent research on IQ testing suggests that at least part of what is being measured is motivation.

Brighter individuals display lower brain energy expenditure while performing cognitive tasks: this is the neural efficiency hypothesis in a nutshell. Such expenditure can be measured using PET scans with cortical glucose metabolic rate used as a correlate of abstract reasoning and attention. Considering “reconfiguration” to reflect said expenditure, recent research has found that “brain network configuration at rest was always closer to a wide variety of task configurations in intelligent individuals. This suggests that the ability to modify network connectivity efficiently when task demands change is a hallmark of high intelligence (Shultz and Cole, 2016). Dix et al (2016) have noted that high fluid intelligence and learning cause fast, accurate analogical reasoning. Yet,”for low FI, initially low cortical activity points to mental overload in hard tasks [and that] learning-related activity increases might reflect an overcoming of mental overload.” Swanson & McMurran (2017) conclude from a randomized control study that “improvement in working memory, as well as the positive transfer in learning outcomes, are moderated by fluid intelligence.” On the other hand, Neubauer and Fink (2009) note that, as opposed to moderate-difficulty tasks, when the more able individuals have to deal with very complex ones, they will invest more cognitive resources. “It is not clear,” write the authors, “if this reversal of the brain activation-intelligence relationship is simply due to brighter individuals’ volitional decision to invest more effort as compared to the less able ones, who might have simply ‘given up’ as they experience that the task surpasses their ability.” It is concluded that new study designs are necessary to explore this volitional factor of cortical effort.

While Howard Gardner’s multiple intelligence scheme seems to stretch the concept too far, a unitary notion centering on neural efficiency as an operational definition seems problematic due to limited explanatory force. Despite the compelling evidence for the NE hypothesis, the semantic issue remains. There is no fact of the matter which determines the “proper” use of the concept of intelligence. Nevertheless, in the light of more recent research (from neuroimaging, especially), the opponents of NE reductionism are clearly on the defensive today.

Wm. Doe, Ph.D., February, 2017


A. Dix et al (2016). The role of fluid intelligence in analogical reasoning: How to become neurally efficient? Neurobiology of Learning and Memory, 134B, 236-247.

D.H. Schultz, M.W. Cole (2016). Higher intelligence is associated with less task-related brain network reconfiguration. J. Neurosci., 36 (33).

H.L. Swanson, M. McMurran (2017). The impact of working memory on near and far transfer measures: Is it all about fluid intelligence? Child Neuropsychology, online pub 2/1/2017.

A. C. Neubauer, A. Fink (2009). Intelligence and neural efficiency. Neuroscience and Biobehavioral Reviews, 33; 1004-23.


“The thought that I might kill myself formed in my mind as coolly as a tree or flower.” – Sylvia Plath

Conflicting attitudes toward suicide can be traced at least as far back as ancient Greece, where convicted criminals could take their own lives, but in Rome, attitudes became more restrictive because of too many slaves (valuable property) doing themselves in. In general, suicide is condemned by Christianity, Judaism, and Islam,, but is tolerated by the Brahmans of India. Buddhist monks and nuns have, in social protest, set fire to themselves, and the Japanese hara-kiri and Kamikaze customs were considered acceptable in that society. After the Middle Ages, in Western countries, legal code expressed a more permissive attitude. Physician-assisted suicide, though, continues to be more condemned than condoned.

With the empirical work of sociologists, especially Emile Durkheim, suicide, in the words of one academic, “was increasingly viewed as a social ill reflecting widespread alienation, anomie, and other attitudinal byproducts of modernity.” Thus, in many European countries in the late 19th and early 20th century, the act came to be thought of as “caused by impersonal or [social] forces rather than by the agency of individuals.” Writing in the 1890s, Durkheim listed four types of suicide: altruistic, fatalistic, egoistic, and anomic. The best known is the latter, referring to the quality of “anomie”, a sense of personal normlessness, disconnection from society. Economic decline may figure into this, especially for middle-aged, male Protestants who have been laid off. Durkheim’s findings are generally considered still valid today, but psychologically-oriented researchers tend to be critical of them. This points up the conflicting orientations between the two disciplines in attempting to understand the same social phenomena.

Nearly a million suicide deaths occur worldwide each year. Associated with increased suicide rates are the global financial crisis, natural disasters, and air pollution. Risk is increased at the individual level by past self-harm, parental loss or separation, and younger age relative to classmates. Korea’s suicide rate ranks first in the world with the most favored method being hanging, followed by the distant second and third of falls and poisoning. Of the many medical conditions that confer risk for suicide, stroke is prominent. Patients frequently develop a  post-stroke depression. A recent study examining the association between suffering from stroke and subsequent risk for suicide and suicidal ideation notes that suffering from a stroke increases the risk of dying by suicide and developing suicidal ideation, particularly in young adults and women. Also, though it is a rare phenomenon, murder-suicide has been associated with a “pathological” expression of masculinity, i.e., rigid ideas of manhood fostered by a hypercompetitive, patriarchal society. A recent study of the phenomenon revealed three themes: domestic desperation; workplace injustice; and school retaliation. It is argued that murder-suicide is an extreme end-product of “failed manhood” at work, school, and/or within family family milieux. This is encapsulated by the term, “aggrieved entitlement”.

An interesting aspect of this subject is the mischaracterization by police of murders as suicides. Such is often the intent of the deceased or a perpetrator. A homicide detective has published his idea of common mistakes in suicide investigation, which boil down to an automatic presumption of suicide in a case labeled as such by a call. “All death inquiries should be conducted as homicide investigations until the facts prove differently.” Failure to apply three basic considerations can throw an investigation off the track: The presence of the weapon or means of death at the scene; injuries of wounds that are obviously self-inflicted; existence of a motive or intent on the part of the victim to take his or her own life. Pertinent detail: “Family members have been known to conceal weapons and/or suicide notes in order to collect on an insurance policy.” Also of interest are his questions about the suicide note: “Was it written by the deceased? Was it written voluntarily? Does the note indicate suicidal intent?”

Regarding this distinction, Lemoyne Snyder, in his classic book on homicide investigation, has observed that “a murderer is more likely to fire several bullets into the victim to make sure that he is dead before leaving the scene. A suicide, on the other hand, frequently shoots himself but survives the fatal wound for a considerable period of time. Therefore, other factors being equal, a period of survival following the fatal wound favors suicide as the cause of death.” Elsewhere, he notes that “occasionally a person will shoot himself twice in [the temple]. These wounds are not always immediately fatal. It is not at all uncommon for a person to live for several hours or even days after a wound of this kind, and occasionally they will even recover. One should always look with great suspicion on wounds of entrance on other parts of the head, because they are much more likely to be due to murder.” [original emphasis]

“In the psychological sciences,” notes the Stanford Encyclopedia of Philosophy, “many suicidologists view suicide not as an either/or notion, but as a gradient one, admitting of degrees based on individuals’ beliefs, strength of intentions, and attitudes. The Scale for Suicidal Ideation is perhaps the best example of this approach.” There are 19 items in the scale, for example: “Wish to live; wish to die; reasons for living/dying; deterrents to active attempt; method (specificity or planning of contemplated attempt; availability or opportunity for contemplated attempt); sense of ‘capability’; final acts in anticipation of death,” and so on. These items are calculated on a scale of 0 to 2.

“They tell us that suicide is the greatest piece of cowardice,” wrote Schopenhauer, “that suicide is wrong; when it is quite obvious that there is nothing in the world to which every man has a more unassailable title than to his own life and person.” Many people might criticize this sentiment as outrageously selfish, thinking of family situations of dependence on a suicidal individual. But at what point do these considerations become secondary to a rational self-destructive imperative? Such is the ethical ambiguity inherent in this issue.

~ Wm. Doe, Ph.D. – January 2017


“Emile Durkheim on Suicide”.

Lemoyne Snyder (1977). Homicide Investigation (3rd Ed.). Springfield, Ill.: Charles Thomas        Publishers

M. Sinyor (2017). Global trends in suicide epidemiology. Curr Opin Psychiatry; 30(1).

M. Pompili (2012). Do stroke patients have an increased risk of developing suicide ideation        or dying by suicide? CNS Neurosci Ther, 18(9).


“Cognitive distortions are not an inevitable feature of depressive thinking nor unheard of among nondepressed people…[My theoretical writings] have sometimes implied a generality of depressive distortion and (implicitly) nondepressed accuracy that probably cannot be sustained.” – Aaron Beck, psychiatrist and founder of cognitive therapy

“The absence of comprehensive and reliable evidence for risks, perceived industrial interests of clinicians, as well as publication bias, which is well known to any author of systematic reviews, have in some quarters, eroded public faith in the drug treatment of depression and its regulation.” – K.P. Ebmeier et al (2006). “Recent developments and current controversies in depression”.  Lancet, vol. 367, Jan. 14

The holiday season seems an appropriate time to write a few words about depression, since many people have that experience around now (although it may be construed as “seasonal affective disorder”.) There are numerous theories about depression, with an ongoing conflict between those championing  the medical model vs. those favoring a more psychological approach. My view is that both have merit but that medical explanations have been oversold, especially in the period from the mid-1990s through most of the following decade, with an overemphasis on putative deficiencies of neurotransmitters, most notably serotonin. I’ll spare the reader the usual litany of DSM criteria for Major Depression, the most important being, after the mood itself, anhedonia. And of course, it is well known that the risk of suicide for those so diagnosed is high. A psychiatry textbook notes that “no single symptom is present in all depressive syndromes…[and] even a depressed mood is not universal.” (R. Waldinger (1997) Psychiatry for Medical Students, p. 103)

Dorothy Rowe, the British psychologist, is a good example of a theorist/clinician who rejects biological explanations for depression. Coming out of Personal Construct Theory, she believes that this particular form of mental distress develops when one’s world view, and by extension, sense of self, is upset. The depression is seen by Rowe as a maladaptive defense against such an attack on one’s “constructed” identity, leading to a sort of emotional paralysis. Her psychotherapeutic approach was centered on applying perpectivism to the crisis and convincing the depressed person that numerous interpretations of such life events are possible.

The biological view, however, has a certain intellectual appeal, especially when propounded by a charming expert like Eric Kandel, Columbia University psychiatrist and Nobel laureate in Medicine, who, surprisingly, also advocates psychoanalysis. (He got the prize for showing how short-term memories are chemically converted into long-term ones.) In a controversial 1998 paper entitled “A New Intellectual Framework for Psychiatry,” Kandel wrote (not addressing depression specifically, but psychopathology in general), “The future of psychoanalysis, if it is to have a future, is in the context of an empirical psychology, abetted by imaging techniques, neuroanatomical methods, and human genetics. Embedded in the sciences of human cognition, the ideas of psychoanalysis can be tested, and it is here that these ideas can have their greatest impact.” Thus, the therapeutic future belongs to cognitive neuroscience.

Then there is the school of Depressive Realism which has it that at least some depressed people, usually those with milder cases, may not be distorting anything, but may actually be more accurate in their assessments than non-depressed types who are operating under ‘positive illusions’. In 1979, researchers Lauren Alloy and Lyn Abramson published a key study on depressive and nondepressive perception, which opened up a can of nematodes vis-a-vis this concept of “cognitive distortion” of reality. 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 times 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 with a rosy glow. A crucial question is whether depression itself leads people to be ‘realistic’ or whether realistic people are more vulnerable to depression than other people.”

Depression can become an outright psychosis, but this is quite rare (less than 1% of depressed people). It may also take the form, according to some experts (e.g., Hagop Akiskal and Theodore Millon), of a personality disorder. (Millon has posited colorful subtypes: Ill-humored (passive-aggressive), voguish (histrionic/narcissistic), self-derogating (dependent), morbid (masochistic), and restive (avoidant). This last is the subtype “most likely to commit suicide in order to avoid all the despair in life.” (It should be noted, though, that not all those with a depressive disorder will conform to a subtype description.) Or, it can be less severe but more chronic, as with Persistent Depressive Disorder (formerly called Dysthymia). Advocates of psychopharmacology think antidepressants (usually selective serotonin re-uptake inhibitors) are, more often than not, beneficial for treatment of most forms of depression, especially Major. Fans of Peter (“Listening to Prozac”) Kramer will sometimes rage at critics of the drugs, saying that SSRIs “saved my life”. The critics, like Peter Breggin and David Healy, will point to the evidence linking these drugs to suicide. Last year, Healy wrote, “In the 1990s…no one knew if SSRIs raised or lowered serotonin levels; they still don’t know. There was no evidence that treatment corrected anything. The role of persuading people to restore their serotonin levels to ‘normal’ fell to the newly obligatory patient representatives and patient groups.” [Emphasis added] (In case you’re wondering, Dr. Healy is not anti-drug treatment. For severe depression, though, he prescribes tricyclic antidepressants instead.)

There are also physical treatments: ECT (electroconvulsive shock therapy), transcranial magnetic stimulation, and near-infrared laser. The latter seems especially promising. For example, a 2015 study at the Massachusetts General Hospital showed that patients receiving 6 sessions of NIR treatment had significantly decreased scores on the Hamilton Depression assessment. The procedure was well tolerated, with no adverse effects.

Mild to moderate depressions may need no explanation on the biological level, but if severe cases do, what is the nature of the bodily derangement? Serotonin deficiency appears to be more an article of faith and Big Pharma propaganda than an empirically verifiable phenomenon. But there may be other possibilities (e.g., abnormal neurotransmission of chemicals not yet studied, raised cortisol or, as noted, magnetic and/or radiant energy factors). Among the possible take-homes, I will choose the importance of noting the limits of the science on this so far, and of separating it from commercially-driven presumption.

Finally, here’s hoping you are spared a Blue Christmas.

~ Wm. Doe, Ph.D., December 20, 2016


P. Cassano et al (2015). Near-infrared transcranial radiation for major depressive disorders. Psychiatry Journal. Article ID 352979.

R.A. Friedman & A.C. Leon (2007). Expanding the black  box – Depression, antidepressants, and the risk of suicide. NEJM, 356: 2343-6.

D. Healy (2015). Serotonin and depression. BMJ 350: h1771.

J. Herbert (2013). Cortisol and depression. Psychol. Med. 43(3).






“Borderline Personality Disorder – dreadful/meaningless term we tried to change in DSM-IV, but no consensus substitute.” – Allen Frances, MD, head of the DSM-IV task force, Twitter, 30 March 2016

“Expressively spasmodic, interpersonally unpredictable, cognitively capricious” – this is a partial description of the aforementioned syndrome (BPD) by prominent personality psychologist, Theodore Millon, the first descriptor comprising recurrent suicidal and self-mutilating behavior. According to the DSM-5, “The essential feature of BPD is a pervasive pattern of instability of interpersonal relationships, self-image, and affects, and marked impulsivity that begins by early adulthood and is present in a variety of contexts.” Among the current diagnostic criteria are inappropriate, intense anger; frantic efforts to avoid real or imagined abandonment; identity disturbances; chronic feelings of emptiness; and recurrent suicidal or self-mutilating behavior. This construct was originally proposed by Otto Kernberg in the 1960s and later developed by Robert Spitzer during the task force planning for DSM-III in 1980, which caused some confusion since the adjective was often applied to mild schizophrenia. The new denotation was meant to refer to a condition that is neither psychotic nor neurotic, although some clinicians have noted transient psychotic breaks in such patients. “The borderline patient,” wrote one psychiatrist in a textbook for medical students, “is easily overwhelmed by anger and frustration and generally acts impulsively when feeling become intolerable. This usually involves repeated self-destructive acts (e.g., wrist-slashing, overdoses, car crashes) and may also include drug abuse, sexual promiscuity, and abrupt changes in job and living situation (Waldinger, 1997). It is estimated that 2% of adults in the U.S. are diagnosed with the disorder (NAMI, 2008).

A recent study has posited three subtypes for the syndrome; affect dysregulation; rejection sensitivity; and so-called mentalization failure (predictive of PTSD),which refers to an inability to make sense of one’s own and others’ mental states (Lewis & Caputi, 2012). Millon identified four different subtypes: Discouraged (codependent, with anger close to the surface); Impulsive; Petulant (ambivalent, defiant, resentful, unpredictable); and Self-destructive. A factor analysis by Sanislow (2000) came up with three factors: again, the affect dysregulation (affective instability, inappropriate anger, and efforts to avoid abandonment); disturbed relatedness; and behavioral dysregulation. As is evident from the above, BPD is rather controversial among experts. In a 2007 study, Rebekah Bradley and colleagues identified three problems with the diagnosis, centering around heterogeneity, categorical quality, and overlap with other PDs. Regarding heterogeneity, the authors write, ” Two patients may both be diagnosed with it while sharing only one symptom in common. This has important clinical implications because subtypes of BPD seem to exist that do not reflect random variation among criteria but rather meaningful, patterned heterogeneity, such as internalizing and externalizing subtypes.” As to the categorical point, personality research consistently supports dimensionality as a more reliable way to conceptualize personality disorders than to see them as discrete categories. Finally, the overlap between borderline and other PDs is so extensive that it tends to undermine the validity of the former as a clearly defined taxon.

The therapeutic modality most often associated with BPD is dialectical behavior therapy (DBT), a modification of cognitive-behavioral, which was developed by University of Washington psychologist, Marsha Linehan. DBT includes components of biosociality, dialectical social philosophy, and Zen Buddhist psychology. “The biosocial theory of BPD,” writes Linehan and colleagues, “asserts the client’s emotional and behavioral dysregulation are elicited and reinforced by the transaction between an invalidating rearing environment and a biological tendency toward emotional vulnerability. (Lynch, 2007, p. 183). In dialectical terms, a behavior, such as self-injury, can be both functional and dysfunctional; functional as a short-term stress reducer, but dysfunctional because of the obvious negative effects, including suicide risk. The synthesis involves “validating the need to relieve distress while helping the client utilize skills that function to reduce stress.” This dialectical approach is deemed to be consonant with the philosophy of Zen. The core problem in BPD is thought to be affect dysregulation, and the goal of therapy is to increase functional behavior even in the presence of intense negative emotion. J.F. Clarkin of the Personality Disorders Institute at Cornell writes that “results from…naturalistic follow-up of patients in DBT showed variable maintenance of treatment effects and ongoing impairment of functioning in patients who initially experienced symptom relief.” (Clarkin et al, 2004, p.54)

Psychological treatment has been shown to be more effective than any pharmacological intervention, but concerns about cost have limited use of psychotherapy. Also, the chronicity of the disease demands studies in long-term effects, and it is uncertain that DBT, despite its successes, can deliver such effects as well as a psychodynamic approach, especially transference-focused psychotherapy (TFP), which is based on the idea of object relations which unlike the Freudian insistence on pleasure-seeking, asserts that humans are primarily relationship-seeking. Object relations, according to psychologist, Thomas Klee, refers to “the self-structure we internalize in early childhood which functions as a blueprint for establishing future relationships.” Unlike a focus on behavioral regulation per se, TFP focuses on these self-structures which in BPD have been pathologically damaged in early development and require a sort of “mental archaeology” to resolve self-destructive patterns engendered by traumatic relational internalizations.

As for a substitute name, a commenter on Dr. Frances’ Twitter thread suggested Complex Trauma Disorder, which is as good as any other I’ve heard.

~ Wm. Doe, PhD – November 21, 2016


T. Millon (1995). Disorders of Personality: DSM-IV and Beyond (New York: Wiley)

R. Bradley, C.Z. Conklin, D. Westen (2007). Borderline Personality Disorder. In Personality Disorders: Toward the DSM-V. (Thousand Oaks, CA: Sage Publications)

K.L. Lewis, P. Caputi (2012).Borderline personality disorder subtypes: A factor analysis of the DSM-IV criteria. Personality and Mental Health, 6(3).

C.A. Sanislow et al. (2000). Factor analysis of the DSM-III-R criteria for borderline personality disorder in psychiatric inpatients. Am. J. Psychiatry, 157(10).

T.R. Lynch et al (2007). Dialectical behavioral therapy for borderline personality disorder. Annu. Rev. Clin. Psychol; 3: 181-205.

J.F. Clarkin, O.F. Kernberg et al (2004). The Personality Disorders Insitute randomized clinical trial for borderline personality disorder: rationale, methods, and patient characteristics. J. Pers. Disord. 18(1): 52-72.


Fainting, or syncope, may or may not be serious. Sometimes idiopathic, its causes are numerous, including cardiac arrhythmia, hypoglycemia, otthostatic hypotension, and anemia, as well as stress, heat, pain, and dehydration. Fainting accounts for 6% of hospital admissions, but again, it can occur in otherwise healthy individuals. Lightheadedness, per se, is technically termed presyncope. Both fainting and feeling faint may also be signs of a disorder of the autonomic nervous system known as dysautonomia.

An umbrella term for a group of diseases, dysautonomia, comprises such exotic sounding phenomena as autonomic neuropathy, multiple system atrophy, autonomic failure, postural orthostatic tachycardia syndrome, and the most common, neurocardiogenic syncope. The autonomic nervous system (ANS) is part of the peripheral (as opposed to central) nervous system and regulates involuntary body functions: heart, glands, smooth muscles. The sympathetic division of the ANS speeds up heart rate, raises blood pressure, and constricts blood vessels, while the parasympathetic division is geared for rest and digestion, slowing the heart rate and increasing peristalsis. (Fun fact: the parasympathetic controls erection; the sympathetic, ejaculation.) A glance at a diagram of the ANS will how extensive it is, subserving eyes, salivary glands, trachea, and all organ-points south, including bladder and rectum. Naturally, an autonomic disorder will manifest with more than fainting. Some of the other symptoms are blurred, tunnel, or double vision; dry mouth; difficulty swallowing; rapid heart rate: impotence; incontinence; and constipation. Exercise intolerance may be neither a sign of early heart failure or COPD nor mere deconditioning, but rather an indication of some kind of autonomic dysfunction. Emphasis is often placed on the heriditary, so-called primary, form, but there is also an acquired, secondary dysautonomia, caused by many disorders from Parkinson’s disease, diabetes, multiple sclerosis and AIDS to Lyme disease, spinal cord injury, chronic alcohol misuse, and surgery or injury involving the nerves.

Some cases of vertigo have been linked to underlying autonomic dysfunction. A retrospective review of 113 patients showed that vertiginous individuals who failed to improve with standard treatment had their problem alleviated by an autonomic treatment regimen.Thus, the authors concluded, there is a subgroup of spontaneous vertigo patients who also demonstrate symptoms and findings consistent with poor autonomic regulation (Pappas, 2003). A later, smaller study validated the clinical diagnosis of autonomic dizziness as a cause of chronic, nonvertiginous dizziness that may be exacerbated by physical exertion or orthostatic challenges. Lack of thorough investigation or analysis could overlook an autonomic etiology in some patients with dizziness, with or without syncope.

The following tests are used to evaluate syncope: of course, a through physical examination; ECG; heart monitors (e.g., “Holter monitor”, which records continuously for 24-48 hours); echocardiography; stress test; table tilt test; electrophysiological study for arrhythmia; and, if the situation still seems uncertain, possibly an implantable cardiac monitor.

This article’s focus on a supposedly rare disorder is really more generally about the pitfalls of medical diagnosis. Dysautonomia is often taken for something else, undiagnosed or misdiagnosed, which, of course, leads to additional and preventable suffering for the patient. It is possible that the condition underlies controversial disorders such as irritable bowel disease, fibromyalgia, and chronic fatigue syndrome. “Horses before zebras” is a good general rule, but perhaps the zebras, in this context, need more  attention than is generally given.

~ Wm. Doe, Ph.D.- October 29, 2016


D.S. Goldstein, G. Eisenhofer (2002). Dysautonomias: Clinical disorders of the autonomic          nervous system. Annals of Internal Medicine, Nov. 5.

National Dysautonomia Research Foundation (n.d.). The Autonomic Nervous System.

J.P. Staab, M.J. Ruckenstein (2007). Autonomic nervous system function in chronic dizziness. Otology & Neurotology, 28.

D.G. Pappas (2003). Autonomic related vertigo. Laryngoscope, 113 (10).



One of my favorite defunct psychiatric diagnoses is Inadequate Personality Disorder, which was characterized in the DSM-II by “ineffectual responses to emotional, intellectual, social, and physical demands despite apparent capabilities to perform in those areas.” It was removed in the controversial third edition of 1980 along with cyclothymic, explosive, and asthenic PDs. Replacements were schizotypal (formerly ‘borderline schizophrenic’), narcissistic, avoidant, dependent, and borderline (meaning, as a personality disorder, emotional instability with self-mutilating tendencies). The “diagnosis” of homosexuality had been dropped in 1973.

Probably a good thing about IPD, although an argument has been made for it by a medical blogger as a manifestation of “frontal lobe syndrome”. This last one is said to be a disturbance of the executive functions: the ability to inhibit, plan, organize, stategize, and maintain goals. Back in 1964, a psychiatrist named Edward Podolsky wrote an article linking the inadequate personality construct with alcoholism, listing 11 traits, among them “inadaptability, ineptness, poor judgment, lack of physical and emotional stamina, and social incapacity; a lack of persistence or continuity of effort or attachment; a low tenacity of purpose,” and so on. Alcohol is used to counter intolerable feelings of inadequacy and inferiority and to engender some semblance of emotional stability. Although the Inadequate Personality PD diagnosis is archaic, a contemporary clinician could, of course, bring it in through the back door by employing the useful category of “Personality Disorder Not Otherwise Specified.”

The 3rd edition of the manual was controversial–indeed, political–because of a feud between Task Force chief Robert Spitzer’s behavioral camp and the supporters of the old guard, that being a psychodynamic/neo-Freudian approach. As Spitzer and his DSM-III task force saw it, “neurosis” was a superfluous, “ideological” concept, an article of dogma stemming from Freud’s misguided theorizing. Scientific clarity and diagnostic accuracy would be removed from official guidelines. Mayes and Horwitz (2005) put it thus: “In revising the DSM [a group of primarily neo-Kraepelians] transformed the little-used mental health manual into a biblical textbook specifically designed for scientific research, reimbursement compatibility, and, by default, psychopharmacology.” (The reference is to German psychiatrist, Emil Kraepelin (1856-1926), considered by some to be the founder of psychopharmacology). And in so doing, they also delegitimized unconscious mental processes which are fundamental to psychoanalysis.

But was this reasonable? Theoretically, there are two aspects to the concept of a psychological unconscious: the cognitive and the psychodynamic. Probably, Spitzer would have permitted the more empirically grounded former as this did not really interfere with his project. (For an overview of the “cognitive unconscious”, see Kihlstrom (1987) below). But as the 20th century drew to a close, more evidence in favor of the existence of unconscious mental processes beyond the mere cognitive was being noted. As psychologist Drew Westen wrote in 1999, “The existence of unconscious cognitive processes is no longer controversial in psychology,” and furthermore, there is substantial experimental and clinical evidence for unconscious affective processes as well. Some of this research even supports a case for some Freudian ideas. For example, psychologist Howard Shevrin has been conducting neurophysiological testing of such mental activity for over half a century. In 2013, using “time frequency” event-related potential data, he published a major report on the subliminal inhibition of conscious symptoms in social phobia subjects. “These novel findings,” he wrote, “constitute neuroscientific evidence for the psychoanalytic concepts of unconscious conflict and repression.” In addition, Dutch psychiatrist Bessel van der Kolk’s studies of PTSD have demonstrated that affective fragmentation which is inaccessible to cognition (thereby pointing up a serious limitation to cognitive therapy). Psychologist Glenn Shean has noted that a depressed patient may be responding at an affective level to inner somatic and outer stimuli that have not been contextualized or organized but represent unrecognized elements of previous experience. Shean believes that psychodynamic, rather than cognitive therapy is appropriate for this population. In his book on emotional intelligence, Daniel Goleman summed up the developmental psychopathology this way: “Early childhood lessons” are stored in the amygdala as “rough, wordless blueprints for emotional life.”

In recent years, controversy has flared up again with the DSM, Allen Frances (task force head of the 4th edition) being quite public in his denunciation of the 5th revision for its medicalization of normality with bogus diagnoses which play into the greedy paws of Big Pharma. Among the harmful changes, he lists the expansion of the notion of Generalized Anxiety Disorders to include ordinary worrying; the restriction of the autism diagnosis, which might adversely affect school services: pathologizing temper tantrums as “Disruptive Mood Dysregulation Disorder”; irresponsible conceptualization of adult attention deficit disorder, which encourages the questionable prescription of stimulants;  and the first time drug users will be thought of as incipient addicts.

Actually, there probably is something to the concept of an inadequate personality, in the sense of repetitive, self-defeating, maladaptive behavior patterns, but in my readings, the psychiatrists have been silent about the macrosocial forces which may come into play here. Is it possible that at least some ineffectual individuals are having trouble coping with a hypercompetitive, irrational society, yet are not limited to the point of official disability? Should they be doomed to a life of poverty, even homelessness, if they cannot run as fast, perform as well, as those who have adapted to a highly questionable social system? A rational, humane society should provide for all of its citizens, regardless of their ability at any given time to keep a hypercapitalist machine humming along. People, as the saying goes, before profits.

~ Wm. Doe, PhD – September, 2016


Susan Keller (2014). Inadequate personality disorder.

R. Hayes, A.V. Horwitz (2005). DSM-III: The revolution in the classification of mental illness.

J.F. Kihlstrom (1987). The cognitive unconscious.

Drew Westen (1999). The scientific status of unconscious processes.

Bessel van der Kolk’s trauma website.

Glenn Shean (2003). Is cognitive therapy consistent with what we know about emotions?

Howard Shevrin (2013). Subliminal unconscious conflict alpha power.

Allen Frances – DSM5 In Distress blog.


At first, it doesn’t seem that frailty would be controversial. It’s a common word that conjures up an image of a weak, fragile, usually elderly individual who is physically compromised due to advanced age, or a person of any age enfeebled by serious illness. “Frailty,” according to the Merck Manual of Geriatrics, “refers to a loss of physiologic reserve that makes a person susceptible to disability from minor stresses.” However, while physicians may agree conceptually on the character of this condition, there is disagreement about its operationalization, which leads to the postponement of its integration in the clinical setting. But before considering the methodological problem, it’s worth noting a few things about the pathogenesis.

Genetic/epigenetic and metabolic factors are potentially involved as are environmental and lifestyle stressors, and acute and chronic disease. Specifically, chronic inflammation in the form of circulating interleukin (IL)-6 has been identified as being associated with the condition in community-dwelling older adults. There is, in general, an inability to effectively regulate the body’s normal inflammatory response. C-reactive protein and tumor necrosis-alpha have also been detected in this population. In addition, there is a problem with processing glucose properly. Frail people secrete more cortisol, a hormone that over time, as with chronic inflammation, also can damage skeletal muscles and the immune system. Compromise of intermediary systems (musculoskeletal, endocrine, cardiovascular,and hematologic) lead to a frailty phenotype comprising weakness, weight loss, low activity, slow performance and exhaustion with the outcomes of falls, disability, dependency, and death.

Multiple frailty measurements exist, with varying levels of quality; there is no international standard. Among the instruments commonly used are Fried’s Phenotype; Rockwood & Mitnitski’s Index: and the Multidimensional Prognostic Index. One group of researchers recently concluded that “the recognition of sarcopenia [skeletal muscle degeneration] as the biological substrate of physical frailty, allows framing an objectively measurable condition to be implemented in standard practice.” (Landi, 2015) Elsewhere, it is concluded that “As the number of false positive values of most available tests is substantial, then frailty scores are of limited value for both screening and diagnostic purposes in daily practice.” (Pijpers, 2012)

However, despite methodological limitations, research clearly shows that recognizing frailty in the primary care setting (and the Emergency Rooms) aids in the management of people who are frail. Especially noteworthy is its being an independent marker for worse outcomes following surgery: complications, length of stay, discharge issues, and mortality. Frailty is one of the leading causes of morbidity and premature mortality in older people, and the failure to identify and note its presence may lead to a substandard level of care, including serious clinical misjudgments.

~ Wm. Doe, PhD – August 2016

Selected References

X. Chen et al (2014). Frailty syndrome: an overview. Clin Interv Aging, 9.

F. Landi, R. Calvani, et al. (2015). Sarcopenia as the biological substrate of physical frailty. Clin Geriatric Med, 31.

E. Pijpers, D.A. Cohen, et al. (2012). The frailty dilemma: review of the predictive accuracy of major frailty scores.  Eur J Internal Med, 23 (2).

Merck Manual of Geriatrics, 3rd Ed. (2000). Whitehouse Station, N.J.: Merck Research Labs.



The progressive deterioration of neuronal structure and/or function which is neurodegeneration is expressed in a number of diseases, and the cause may be genetic or early-developmental. Some of the more prevalent syndromes are Alzheimer’s disease (AD), Friedrich’s ataxia, Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and spinal muscle atrophy. These are serious illnesses which tend to be life-threatening. (But the category excludes neoplasms, hemorrhage, and trauma as well as multiple sclerosis, which is a breakdown of the myelin sheath over the nerves. Also excluded are pathologies involving neural death of known cause (hypoxia, poison, infections)). Advancing age is the main risk factor for neurodegeneration. Symptomatic relief is possible, but it is generally considered incurable.

In terms  of symptoms, some will manifest predominantly cognitively (e.g., dementias) and others with motor aberrations (Friedrich’s ataxia, PD, Huntington’s disease). Common features in the pathogenesis of this group include oxidative stress, mitochondrial dysfunction, excitotoxicity, disrupted axonal transport, and neuroinflammation with microglial activation.  The constant production of reactive oxygen species in neurons leads to nuclear DNA oxidation, and if the damaged DNA is not adequately repaired, it can lead to dysfunction and apoptosis. Such damage has been observed in AD, PD, ALS, and vascular dementia. Evidence from neurotoxicology shows that such poisoning involves mitochondrial dysfunction similar to that seen in PD and Huntington’s.

Excitotoxicity from the excess of the important transmitter glutamine as also been implicated in the development of AD and ALS. Furthermore, the association between inflammation and neurodegeneration has been empirically established since the 1980s. Microglial activation is a secondary factor intensifying an inflammatory cascade which has been deduced from autopsy findings in patients with PD. Neuroinflammation from abnormal protein production is seen in AD. Finally, in ALS, decrease in a substance mediating anterograde axonal transport causes toxicity at synapses and general disruption of transmission.

The common property of the diseases in this class is specific neuronal loss. In PD, for example, it is a loss of dopaminergic neurons in the substantia nigra and other areas of the brain, resulting in reduced levels of dopamine and metenkephalin and striatal acetylcholine hyperactivity. In ALS, there is destruction of upper and lower motor neurons with progressive weakness and spasticity. Uncontrollable laughter and crying occurs, and death is usually caused by failure of the respiratory muscles. In AD, cortical and limbic degeneration occurs as a result of senile plaques, beta-amyloid deposits, and neurofibrillary tangles. Although most cases have late onset and unclear etiology, a minority of cases are familial, some of which have early onset (< 60 years) and can be traced to abnormalities on 5 different chromosomes.

The treatment for neurodegeneration leaves a great deal to be desired, but levodopa and support drugs like selegiline are widely used for PD. Riluzole, a glutamine inhibitor, is said to “modestly” extend survival in ALS, but 50% of patients are dead within 3 years of onset. For AD, some limited improvement of symptoms is seen with cholinesterase inhibitors (e.g., rivastigmine) and memantine, an NMDA-receptor antagonist which may increase independence in the patient for awhile. Drugs that should be avoided for all diseases in this category are those causing orthostatic hypotension and anticholinergic effects (such as the tricyclic antidepressant, amitryptaline); those causing extrapyramidal symptoms (e.g., high-potency antipsychotics); and those causing paradoxical agitation reactions, such as benzodiazepines. More research should go into not only finding more effective medication and other treatments, but also developing more effective interventions for improving the quality of life for these patients, most of whom will steadily deteriorate on their way to the end.

Wm. Doe, Ph.D. – July 2016


O.Hardiman & C.P. Doherty, Eds. (2011). Neurodegenerative Disorders: A Clinical Guide.     London: Springer.

S. Przedborski et al (2003). Neurodeneration: What is it and where are we? J. Clin. Invest., 111 (1).

D.W. Dickson & R.O. Weller, Eds. (2011). Neurodegeneration: The Molecular Pathology of Dementia and Movement Disorders. Oxford: Wiley-Blackwell.

Merck Manual, 19th Ed. (2011). Whitehouse Station, N.J.: Merck, Sharp, & Dohme.


No doubt we have all, at some time, experienced palpitations, that is, a subjective sense of abnormal heart activity: fluttering, racing, skipping; and this may or may not signify the presence of disease. The mechanism responsible for palpitations, per se, is unknown. By contrast, arrhythmia (e.g., fibrillation, flutter, tachycardia, bradycardia) is the objective abnormality of signal conduction, the most common of which are premature atrial and ventricular contractions. Both are usually harmless, but other arrhythmias are not; some can even be fatal.

The heart has its own electrical conduction system. The signal which will lead to a heartbeat starts at the top of the organ, in a group of cells called the sinoatrial (SA) node. This so-called pacemaker sends out an electrical signal which causes the upper chamber (atria) to contract. A lower node, the atrioventricular (AV node) then sends a signal to the ventricles, which then contract. The SA node then sends another, repeating the cycle. One cycle is one heartbeat. The passage of ions across the cardiac cell membrane, notes the Merck Manual, “is regulated through specific ion channels that cause cyclical depolarization and repolarization of the cell called an action potential
.” This involves influx of sodium, then its inactivation, followed by an influx of potassium and then its egress. Calcium and chloride ions are also involved. In other words, the action potential is the signal that triggers contractions. Basically, it is the same sort of process which occurs in the central nervous system, a sort of electrochemical impulse.

Atrial flutter, as the name suggest, is a less chaotic phenomenon than atrial fibrillation. The flutter arises from a short circuit, typically in the right atrium, and is more amenable to treatment. When the regulatory sinus node fails to work properly as a  pacemaker, a condition called sick sinus syndrome results: heartbeats are too slow, pauses too long, or there may be stops. The result can be shortness of breath, lightheadedness, fatigue, and blackouts. Treatment can be complex, involving both medication and an artificial pacemaker implant.

A couple of other arrhythmias worth mentioning are Wolff-Parkinson-White syndrome and Brugada syndrome. The former is caused by an extra electrical pathway between the atria and ventricles, which bypasses the AV node, leading to short circuits and rapid heartbeats. Brugada syndrome, though not usually life-threatening, can manifest with syncope and sudden death. Involving a disturbance of nerve impulses down a bundle of fibers, basically an electric block, it is part of a group of disorders known an ion channelopathies, arrhythmogenic pathologies caused by genetic mutations adversely affecting ionic channel proteins which control cell membrane transit of sodium, potassium, and calcium. Often the cardiac arrest occurs during sleep or rest. Sudden death in young, apparently healthy people can be explained by such electrical abnormalities. Ventricular fibrillation is a life-threatening electrical storm, in which the heart is quivering in total chaos from ectopic foci. Ablation may be able to burn out these dangerous, abnormal centers of signal emittance. (Trivia: there is actually a Sudden Arrhythmia Death Syndrome Foundation.)

When people hear the term “heart attack”, they may picture a clot which breaks loose, blocking blood flow to the organ, causing a portion of it to die. However, as noted, sudden death may also occur from cardiac arrest resulting from an electrical disturbance that disrupts pumping action, causing blood to stop flowing to the rest of the body. Who is at highest risk for this arrhythmic death? Invasive tests can tell us a lot about reduced left ventricular function, but, as one cardiologist writes, “They typically have relatively high-negative predictive value, but a weakness is their rather low-positive predictive value.” Thus, there remains some uncertainty about risk and prognosis, which arguably reflects the uncertainty inherent in medicine and in the human condition itself.

~ Wm. Doe, Ph.D. – July 2016


D.H. Bennett (2006). Cardiac Arrhythmias: Practical Notes on Interpretation and Treatment. (7th Ed.) London: Hodder Arnold.

V. Furster et al, eds. (2008). Hurst’s The Heart (12th Ed.). New York: McGraw-Hill Medical.

R.S.Porter, ed. (2011). Merck Manual of Diagnosis and Therapy. (19th Ed.) Whitehouse Station, N.J.: Merck, Sharp, & Dohme.




It was recently reported in the British Medical Journal (now called BMJ) that medical errors are the third leading cause of death in the United States, after heart disease and cancer. (COPD and suicide were 4th and 5th). The annual number of error-related fatalities was said to exceed a quarter million, much higher than the top of the range stated in the classic 1999 study by the Institute of Medicine (IOM) called “To Err Is Human”. Martin Makary, the lead author and a pancreatic surgeon at Johns Hopkins, noted that the research was published in the BMJ after it was rejected by two American medical journals (JAMA and the New England Journal of Medicine), for reasons which are unclear. The IOM study is considered by some to have been groundbreaking for showing that, rather than preventable errors being rare or isolated, up to 98,000 occur yearly in the U.S. (4% of all deaths) and that, in general, they are not of an individual nature so much as a systemic one.

Dr. Makary and co-author, research fellow, Michael Daniel stated, “We calculated a mean rate of death from medical error of 251,454 a year using the studies reported since the 1999 IOM report and extrapolating to the total number of U.S. hospital admissions in 2013.” The two key points made in the controversial article (other than the claim that the errors are the third leading cause of deaths) are that (1) death certificates, upon which national vital statistics are based, “have no facility for acknowledging medical error”; and (2) “the system for measuring national vital statistics should be revised to facilitate better understanding of deaths due to medical care.” In listing strategies to reduce deaths, Makary emphasized systemic responsibilities: “Institute safety triggers to alert staff; facilitate a culture of speaking up/culture of safety; make remedies available; support clinician need; engineer hard stops for prevention.” Among several more specific suggestions, he includes adding an extra field on the death certificate asking whether a preventable complication contributed to the death, citing survey research showing high physician response to this issue, although the idea has been criticized as unrealistic because of the highly litigious atmosphere surrounding malpractice in the country.

Several criticisms of the BMJ paper by physicians I have seen seem self-serving, rambling, and actually somewhat incoherent, but a lengthy and better-written response comes from the science blogger who goes by “Orac” (pseudonym of a surgeon working in an American cancer center). First off, Orac argues that estimates of medical error depend on how it is defined, about which there is considerable disagreement. There are many ambiguous situations resulting in death of the patient which could be equally validly interpreted as not due to medical error as such. “Not every adverse event is preventable or due to medical error.” He then claims that the study is “nothing new” since it merely pools data of previous studies. Makary and David are also charged with misleading extrapolations of local data to the national level and compounding this by using numbers from a large study of Medicare recipients, which skewed the results due to sicker patients and a higher rate of adverse events “even if the care they received was completely free from error.”

Experts will continue to argue about the methodology involved in determining the true extent of fatal medical errors, but what stands out for me in all this is the matter of the culture of secrecy and silence in medicine that Makary and Daniel emphasize. Physicians need to speak up more, to make such errors more visible, and to foster, as the IOM study from 1999 urged, a culture of safety. In addition, they need to reach a consensus on what constitutes a medical error in the first place, if that is possible.

~ Wm. Doe, Ph.D., June 2016


M. Makary & M. Daniel (2016). Medical error: the third leading cause of death in the U.S. BMJ, 353 (2139).

Orac’s Respectful Insolence blog post –

D.C. Classen et al. (2011). ‘Global Trigger Tool’ shows that adverse events in hospitals may be ten times greater than previously mentioned. Health Affairs, 30(4), 581-589.

L.T. Kohn et al., Eds.(1999). To Err is Human: Building a Safer Health System. Washington, DC: National Academy Press.