Category Archives: Medicine

The Therapeutic Alliance: The Essential Ingredient for Psychotherapy

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umbrellas

 I am currently writing on the ‘therapeutic alliance’ – its relation to mindfulness, psychotherapy, understanding, and ‘being listened to…’   What follows is an interesting article that I came across that may interest some of you…

Excerpt:

Have you ever tried to change the way you do something? It could be anything — the way you hold your tennis racket, blow into a flute, meditate — you name it. If so, think about that experience. No matter how motivated you were to change, and no matter how much you knew that it would help your serve, musicality, or sense of inner peace, it can be difficult and scary to change even the smallest thing. In order to change, you have to give up your old way of doing something first and then try the new way. That means that for a while you’re in a free fall — you no longer have your old habit to rely on and you don’t yet have the new one.

The anxiety of trying to change something as complex and entrenched as how you relate to people close to you or manage stress takes the feeling to a whole new level. Yet, that’s just what you do when you enter psychotherapy. Just as you had to put yourself into the hand of your teachers and coaches, in therapy you need to gradually do just that with your therapist to help you through what can be a harrowing adventure. The foundation for therapy is called the therapeutic alliance (1, 2). When it’s there, you know that your therapist is there to help you, no matter how hard the going gets.

The therapeutic alliance might be the most important part of beginning a psychotherapy. In fact, many studies indicate that the therapeutic alliance is the best predictor of treatment outcome (3-5).

See entire article:

http://www.huffingtonpost.com/deborah-l-cabaniss-md/therapeutic-alliance_b_1554007.html

 

A mad world A diagnosis of mental illness is more common than ever – did psychiatrists create the problem, or just recognise it?

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Unfortunate Events

When a psychiatrist meets people at a party and reveals what he or she does for a living, two responses are typical. People either say, ‘I’d better be careful what I say around you,’ and then clam up, or they say, ‘I could talk to you for hours,’ and then launch into a litany of complaints and diagnostic questions, usually about one or another family member, in-law, co-worker, or other acquaintance. It seems that people are quick to acknowledge the ubiquity of those who might benefit from a psychiatrist’s attention, while expressing a deep reluctance ever to seek it out themselves…

…While a continuous view of mental illness probably reflects underlying reality, it inevitably results in grey areas where ‘caseness’ (whether someone does or does not have a mental disorder) must be decided based on judgment calls made by experienced clinicians. In psychiatry, those calls usually depend on whether a patient’s complaints are associated with significant distress or impaired functioning. Unlike medical disorders where morbidity is often determined by physical limitations or the threat of impending death, the distress and disruption of social functioning associated with mental illness can be fairly subjective. Even those on the softer, less severe end of the mental illness spectrum can experience considerable suffering and impairment. For example, someone with mild depression might not be on the verge of suicide, but could really be struggling with work due to anxiety and poor concentration. Many people might experience sub-clinical conditions that fall short of the threshold for a mental disorder, but still might benefit from intervention.

See link for interesting article on psychiatry…and bits about the importance of psychotherapeutic intervention…

http://aeon.co/magazine/being-human/have-psychiatrists-lost-perspective-on-mental-illness/

Medicinal

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Medicinal

“Medication Time! Medication Time!”

My music is a kind of poetical literature in instrumental form. In each piece, I attempt to tell a story.

This experimental, ambient piece tells the story of before, during, and after taking medication. In the past (a long ago past), I was highly against taking any kind of medication as part of treatment, as I considered medication a form of mind-control and I did not want anyone mucking about with my mind, despite the fact that, at that time, my mind was quite unfriendly towards me and regarded as monstrous. I explain this, to further illuminate the influence behind this particular piece and why I created it.

Fig. 1The beginning of the music portrays what triggers the (almost daily) psychotic episode (the affected part of SchizoAffective Disorder) and a depiction of the resulting mood and state of mind/consciousness (which is why the music grows from dark to a kind of chasing feel, as if the mind were chased by the impending psychosis). The middle of the piece/story portrays taking the medications (I no longer hold the same beliefs I did when I was younger about medication, I can now see its use and I now comprehend much more about the beneficial chemical effects it can have on the brain, which has an effect on the body and state of mind) and how differently the mind is affected and the semblance of peace it brings afterward (which sort of explains the lyrics in the middle, “Little did I know. . .”). But the medication lasts only a while and is not impervious to further triggers (shown in the immediacy of the return to the psychosis). The end portrays the return to the psychosis. . . and time again for medication. Basically, this piece illustrates the endless daily loop of life for a mind schizo affected (the reason behind the ending looping back to the beginning, although not exactly, because not every episode is the same).

Untitled*Image Credits (all artwork used with permission through CC license)–
“biTteRNeSS bEfoRE bREakFASt” by Sippanont Samchai
“Fig.1″ by Vacon Sartirani
“Untitled” by Andres Yeah

What is Retrogenesis?

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Retrogenesis is a term that has been applied in recent years to dementia — Alzheimer’s disease in particular — to describe the progression by which a person loses skills.  A great deal of work on this concept has been done by Dr. Barry Reisberg and others over the last 30 years.

When a child grows and develops, from infancy onward, it passes through a series of well-documented landmarks or developmental milestones.  These have been studied in detail, and it is possible to determine how far along the child is in her development by observing and measuring certain behaviors, and comparing them to landmarks demonstrated by other children.  An example of an early landmark is the ability to hold her head up independently, and these progress through the ability to sit up, to eat solid food, to walk, to speak, to perform complicated mathematical operations, and so on through to adulthood.  It is possible for a person who is familiar with these landmarks to predict what stage a child will progress through next, and if she is developing at an expected rate.

Dr. Reisberg and others have been able to demonstrate that persons with certain forms of dementia, including Alzheimer’s disease, lose skills in the reverse order that they are developed by children.  For example, a person with dementia may lose the power of abstract thought, and later the ability to dress herself, followed by the ability to feed herself independently, and so on.  Certain behaviors exhibited by the individual have been shown to correlate with specific stages of dementia, so that it is possible to predict what skills she will have difficulty with next.  This applies not only to physical function, but also to thought processes.

There are occasions, however, in which a person with dementia will not show a pattern of regression that is totally in line with what would be expected. This can usually be credited to other disease processes that might be present in the individual.  For example, if she has severe rheumatoid arthritis, she might lose the ability to walk independently sooner than might be expected.

The similarities between the acquisition of skills in childhood and the deterioration of those same skills in a person with dementia is observable not only in their order, but also in the temporal sequence.  Most children take about 20 years to develop from infancy to young adulthood.  Likewise, the interval from the time a person shows the first clinical indications of Alzheimer’s to the time they become totally dependent on others usually spans about 20 years.

It is possible to relate behaviors observable in a person with dementia to a specific developmental stage exhibited by a child.  This allows health care professionals to conjecture, on the basis of observable (and measurable) behaviors, those which are not readily apparent with regards to linguistic and emotional factors.  For instance, if an individual displays grooming skills equivalent to those typically seen in a 3-year-old child, it might also be extrapolated that she would understand language at the same level.  As a result, a caregiver might do well to keep instructions simple, and refrain from using too many abstract concepts.

There are some important points to remember, however, when considering the process of retrogenesis.  For one thing, while the person with dementia may show a regression in physical/functional, cognitive, and linguistic skills, she will not show an actual physical regression.  Therefore, while it is quite common for a person with Alzheimer’s, who is at the end stage (and near death) to show a grasp reflex such as might be seen in an infant, it is important to remember that the individual is still a 6-foot-tall man who worked all his life as a farmer — and quite likely has a very firm grip.  It is equally as important to remember that these individuals need to be accorded the same respect that would ordinarily be given to any adult.  Even if she may have the linguistic skills of a 5-year-old, it would be wrong to “talk down” to her.

It is not known why this retrogenesis occurs with Alzheimer’s disease and other dementias.  It has been theorized that the myelin, or white matter covering the axonal processes that extend out from the nerve is injured.  This myelin is produced continually through the life of the individual.  It may be that the myelin which develops later deteriorates first, with the older myelin breaking down later on in the process.

Source:

http://www.encyclopedia.com/doc/1G2-3402200359.html

Antipsychotics and Brain Shrinkage

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Antipsychotics and Brain Shrinkage:

An Update

Joanna Moncrieff June 19, 2013

Evidence that antipsychotics cause brain shrinkage has been accumulating over the last few years, but the psychiatric research establishment is finding its own results difficult to swallow. A new paper by a group of American researchers once again tries to ‘blame the disease,’ a time-honoured tactic for diverting attention from the nasty and dangerous effects of some psychiatric treatments. In 2011, these researchers, led by the former editor of the American Journal of Psychiatry, Nancy Andreasen, reported follow-up data for their study of 211 patients diagnosed for the first time with an episode of ‘schizophrenia’. They found a strong correlation between the level of antipsychotic treatment someone had taken over the course of the follow-up period, and the amount of shrinkage of brain matter as measured by repeated MRI scans.

The group concluded that “antipsychotics have a subtle but measurable influence on brain tissue loss” (1). This study confirmed other evidence that antipsychotics shrink the brain. When MRI scans became available in the 1990s, they were able to detect subtle levels of brain volume reduction in people diagnosed with schizophrenia or psychosis. This lead to the idea that psychosis is a toxic brain state, and was used to justify the claim that early treatment with antipsychotics was necessary to prevent brain damage. People even started to refer to these drugs as having “neuroprotective” properties, and schizophrenia was increasingly described in neo-Kraeplinian terms as a neurodegenerative condition(2). The trouble with this interpretation was that all the people in these studies were taking antipsychotic drugs. Peter Breggin suggested that the smaller brains and larger brain cavities observed in people diagnosed with schizophrenia in these and older studies using the less sensitive CT scans, were a consequence of antipsychotic drugs(3), but no one took him seriously.

It was assumed that these findings revealed the brain abnormalities that were thought to constitute schizophrenia, and for a long time no one paid much attention to the effects of treatment. Where the effects of antipsychotics were explored, however, there were some indications that the drugs might have a negative impact on brain volume(4). In 2005, another American group, led by Jeffrey Lieberman who headed up the CATIE study, published the largest scanning study up to that point of people with a first episode of psychosis or schizophrenia(5). The study was funded by Eli Lilly, and consisted of a randomised comparison of Lilly’s drug olanzapine (Zyprexa) and the older drug haloperidol. Patients were scanned at the start of the study, 12 weeks and one year later and patients’ scans were compared with those of a control group of ‘healthy’ volunteers. At 12 weeks haloperidol-treated subjects showed a statistically significant reduction imageof the brain’s grey matter (the nerve cell bodies) compared with controls, and at one year both olanzapine- and haloperidol-treated subjects had lost more grey matter than controls. The comparative degree of shrinkage in the olanzapine group was smaller than that in the haloperidol group, and the authors declared the olanzapine-related change not to be statistically significant because, although the result reached the conventional level of statistical significance (p=0.03) they said they had done so many tests that the result might have occurred by chance. In both haloperidol and olanzapine treated patients,however, there was a consistent effect that was diffuse and visible in most parts of the brain hemispheres.

The idea that schizophrenia or psychosis represent degenerative brain diseases was so influential at this point, that the authors first explanation for these results was that olanzapine, but not haloperidol, can halt the underlying process of brain shrinkage caused by the mental condition. They did concede, however, that an alternative explanation might be that haloperidol causes brain shrinkage. They never admitted that olanzapine might do this. It seems as if Eli Lilly and its collaborators were so confident about their preferred explanation, that they set up a study to investigate the effects of olanzapine and haloperidol in macaque monkeys. This study proved beyond reasonable doubt that both antipsychotics cause brain shrinkage. After 18 months of treatment monkeys treated with olanzapine or haloperidol, at doses equivalent to those used in humans, had approximately 10% lighter brains than those treated with a placebo preparation.(6) Still psychiatrists went on behaving as if antipsychotics were essentially benign and arguing that they were necessary to prevent an underlying toxic brain disease (Jarskoget al 07 Annual review).

Andreasen’s 2011 paper was widely publicised however, and it started to be increasingly acknowledged that antipsychotics can cause brain shrinkage. Almost as soon as the cat was out of the bag, however, attention was diverted back to the idea that the real problem is the mental condition. Later in 2011 Andreasen’s group published a paper that reasserted the idea that schizophrenia is responsible for brain shrinkage, in which there is barely a mention of the effects of antipsychotics that were revealed in the group’s earlier paper(7). In this second paper, what the authors did was to assume that any brain shrinkage that could not be accounted for by the method of analysis used to explore the effects of antipsychotic treatment must be attributable to the underlying disease. The way they had analysed drug treatment in the first paper only looked for a linear association between antipsychotic exposure and changes in brain volume, however. A linear analysis only detects an association that is smooth and consistent- in other words an association in which brain volume shrinks by a consistent amount with each increment in antipsychotic exposure.

The total effect of drug treatment may not follow this pattern however. It seems from other evidence that there is a threshold effect whereby being on any amount of an antipsychotic has the greatest relative effect, with a levelling out of the impact as duration of exposure reaches a certain level.(8) In any case, without a comparison group which has not been medicated, a virtual impossibility in this day and age, it is simply not possible to conclude that the whole effect is not drug-induced. The latest paper by this research group replicates the findings on antipsychotic-induced brain shrinkage, but also claims that brain volume reduction is related to relapse of the psychotic disorder(9). Relapse was defined retrospectively by the research team for the purposes of this particular analysis, however, and not at the time the study data were collected. Moreover, the definition used does not refer to any significant change in functioning, but only to a deterioration in the severity of symptoms. But the group’s previous analysis of severity of symptoms, using data collected at the time, found that severity had only a weak association with brain volume changes, and moreover that symptom severity was correlated with antipsychotic exposure.(1)

The most recent analysis ignores the probable association between antipsychotic treatment intensity and relapse, but it seems likely that people undergoing periods of ‘relapse,’ or more accurately deterioration of symptoms, would be treated with higher doses of antipsychotics. If this is so, and the two variables ‘relapse’ and ‘treatment intensity’ are correlated with each other, then the analysis is questionable since the statistical methods used assume that the variables are independent of each other. So Andreasen’s group have found strong evidence of an antipsychotic-induced effect, which they have replicated in two analyses now. The predictive value of the severity of symptoms, on the other hand (which is essentially what relapse appears to define) is weak in the initial analysis, and in neither analysis was it clearly differentiated from drug-induced effects. These researchers seem determined to prove that ‘schizophrenia’ causes brain shrinkage, although their data simply cannot establish this, as none of their subjects seem to have gone without drug treatment for any significant length of time. So even though their recent analysis once again confirms the damaging effects of antipsychotics, they conclude that the results demonstrate the need to make sure patients take, and do not stop, their antipsychotic medication.

The only concession made to the antipsychotic-induced changes revealed is the suggestion that low doses of antipsychotics should be used where possible. Yet other prominent psychiatric researchers have now abandoned the idea that schizophrenia is a progressive, neurodegenerative condition, and do not consider that Andreasen’s study provides evidence of this.(10) Bizarrely, Nancy Andreasen is a co-author of a recently published meta-analysis which combines results of 30 studies of brain volume over time, which clearly confirms the association between antipsychotic treatment and brain shrinkage (specifically the grey matter) and finds no relationship with severity of symptoms or duration of the underlying condition.(11) What should antipsychotic users and their families and carers make of this research?

Obviously it sounds frightening and worrying, but the first thing to stress is that the reductions in brain volume that are detected in these MRI studies are small, and it is not certain that changes of this sort have any functional implications. We do not yet know whether these changes are reversible or not. Of course the value of antipsychotics has been much debated on this site and elsewhere, and their utility almost certainly depends on the particular circumstances of each individual user, so it is impossible to issue any blanket advice. If people are worried, they need to discuss the pros and cons of continuing to take antipsychotic treatment with their prescriber, bearing in mind the difficulties that are associated with coming off these drugs.(12)

People should not stop drug treatment suddenly, especially if they have been taking it for a long time. People need to know about this research because it indicates that antipsychotics are not the innocuous substances that they have frequently been portrayed as. We still have no conclusive evidence that the disorders labeled as schizophrenia or psychosis are associated with any underlying abnormalities of the brain, but we do have strong evidence that the drugs we use to treat these conditions cause brain changes. This does not mean that taking antipsychotics is not sometimes useful and worthwhile, despite these effects, but it does mean we have to be very cautious indeed about using them.

Reference List (1) Ho BC, Andreasen NC, Ziebell S, Pierson R, Magnotta V. Long-term Antipsychotic Treatment and Brain Volumes: A Longitudinal Study of First-Episode Schizophrenia. Arch Gen Psychiatry 2011 Feb;68

(2):128-37. (2) Lieberman JA. Is schizophrenia a neurodegenerative disorder? A clinical and neurobiological perspective. Biol Psychiatry 1999 Sep 15;46(6):729-39. (3) Breggin PR. Toxic Psychiatry. London: Fontana; 1993(4) Moncrieff J, Leo J. A systematic review of the effects of antipsychotic drugs on brain volume. Psychol Med 2010 Jan 20;1-14. (5) Lieberman JA, Tollefson GD, Charles C, Zipursky R, Sharma T, Kahn RS, et al. Antipsychotic drug effects on brain morphology in first-episode psychosis. Arch Gen Psychiatry 2005 Apr;62(4):361-70. (6) Dorph-Petersen KA, Pierri JN, Perel JM, Sun Z, Sampson AR, Lewis DA. The influence of chronic exposure to antipsychotic medications on brain size before and after tissue fixation: a comparison of haloperidol and olanzapine in macaque monkeys. Neuropsychopharmacology 2005 Sep;30(9):1649-61. (7) Andreasen NC, Nopoulos P, Magnotta V, Pierson R, Ziebell S, Ho BC. Progressive brain change in schizophrenia: a prospective longitudinal study of first-episode schizophrenia. Biol Psychiatry 2011 Oct 1;70(7):672-9. (8) Molina V, Sanz J, Benito C, Palomo T. Direct association between orbitofrontal atrophy and the response of psychotic symptoms to olanzapine in schizophrenia. Int Clin Psychopharmacol 2004 Jul;19(4):221-8. (9) Andreasen NC, Liu D, Ziebell S, Vora A, Ho BC. Relapse duration, treatment intensity, and brain tissue loss in schizophrenia: a prospective longitudinal MRI study. Am J Psychiatry 2013 Jun 1;170(6):609-15. (10) Zipursky RB, Reilly TJ, Murray RM. The Myth of Schizophrenia as a Progressive Brain Disease. Schizophr Bull 2012 Dec 7. (11) Fusar-Poli P, Smieskova R, Kempton MJ, Ho BC, Andreasen NC, Borgwardt S. Progressive brain changes in schizophrenia related to antipsychotic treatment? A meta-analysis of longitudinal mri studies. Neurosci Biobehav Rev 2013 Jun 13. (12) Moncrieff J. Why is it so difficult to stop psychiatric drug treatment? It may be nothing to do with the original problem. Med Hypotheses 2006;67(3):517-23. This entry was posted in Antipsychotics, Blogs, Featured Blogs, Foreign Correspondents, Psychiatric Drugs by Joanna Moncrieff. Bookmark the permalink.