Annals of General Psychiatry - Latest Comments

Anti-Depressants cause Sleep Apnea?

David Mills — 2009-11-27T00:00:00Z

Based on my own personal experience, I'm also wondering if there may be a linkage between anti-depressant use and sleep apnea. I've been on SSRI anti-depressants for about 7 years and have no other medical conditions. I was just diagnosed with sleep apnea with a significant "central" component.

I realize anti-depressants can also cause weight gain and increased weight can lead to "obstructive" sleep apnea. Whatever studies that would be designed to clarify a possible linkage between anti-depressants and sleep apnea would need to control for this possible affect.

Antidepressants cause sleep apnea

Tanya Vanasse — 2009-06-28T00:00:00Z

I have read this article and many others and I was hoping to get input on the following:

I don’t believe that Sleep Apnea and depression are related as a medical condition, but that the antidepressants we treat depression with cause the sleep apnea. I think we are giving depressive people sleep apnea by prescribing them medicine and then prescribing them BIPAP machines as well? I believe this to be the case and was wondering if the research community has seen evidence of this?

nova scotia drug rehab

Taylor bob — 2008-11-14T00:00:00Z

Everyone is addicted to something to some extent at some point in their life. The obvious addictions are substance addictions which include tobacco, alcohol and drugs.

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Taylor

nova scotia drug rehab

Alcohol abuse

Sam Sam — 2008-09-30T00:00:00Z

Alcohol abuse, as described in the DSM-IV, is a psychiatric diagnosis describing the use of alcoholic beverages despite negative consequences. It is differentiated from alcohol dependence by the lack of symptoms such as tolerance and withdrawal.

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Sam

Alcohol Addiction Treatment

Reasons for parents concern about Psychotropics

gurinder singh — 2007-12-23T00:00:00Z

Although Scientific facts differ from the parents's belief but results of this study are not surprising.Considering the fact that use of

antipsychotic treatment is associated with metabolic side effects that include various degrees of weight gain, dyslipidemia,

susceptibility to type 2 diabetes,it is natural for parents to consider psychotherapy as first choice of treatment.These adverse

effects associated with second-generation antipsychotics are also part of the metabolic syndrome, which has been associated with higher morbidity and mortality from cardiovascular disorders .Using presence of abdominal obesity and/or elevated fasting blood glucose may identify 100% of the patients with the metabolic syndrome. To change the belief of parents and patients we need to incorporate monitoring and dealing for metabloic effects protocols into our practice. Its the only way to ensure parents about safety in the use of Psychotrpic medication.

Schroder and O'Hara's Depression and Obstructive Sleep Apnea: An Informed Lay Perspective

Mary Bryan — 2007-08-19T00:00:00Z

Having received a diagnosis of mild to moderate Obstructive Sleep Apnea (OSA) only days ago (7/16/2007), I began an intensive search for journal articles and papers with three goals in mind:

1) to expand and deepen my own understanding of the condition;

2) to explore the relationship - if any - between

a) reduced oxygen saturation demonstrated via comprehensive sleep studies, and

b) clinical white matter changes observed on MRI (e.g., multiple lacunar infarcts, scattered tiny hemosiderin deposits, and other signs indicating subcortical stroke-related small vessel disease); and

3) to apply this information in the development of a research-based article or series of articles using language that is at once scientifically and medically accurate, and accessible to the informed lay reader, whether personally affected or concerned for a family member, loved one, or acquaintance. Schroder and O'Hara's review of the literature on Depression and Sleep Apnea both raised and answered questions that I had not yet begun to consider.

My own research and writing skills were honed decades ago when I was concentrating on academic work in psychology and educational administration. Despite repeated urging from professors and advisors to write for publication, I decided to focus my energies on then-current family and professional responsibilities, blissfully unaware of the changes that were already taking place in my own brain, and whose effects on my personal and professional competency would range from subtle to profound. I was in my early fifties, slightly overweight, but with blood pressure and all metabolic markers well within normal limits. My only health concerns were allergy-induced asthma and recurrent bronchitis and pneumonia during Upstate NY winter months.

The opportunity to work at the same academic level in Florida arose in 1997, and my allergy and asthma symptoms subsided dramatically. Then, MRI following a 2001 automobile accident revealed the presence of small lacunar infarcts in the putamen and corona radiata. I was 61. Neuropsychological assessment in subsequent years demonstrated striking discrepancies (>2 SD's) between verbal and performance scores, and a diagnosis of major depression accompanied bilateral knee arthroscopies to remove and repair meniscal tissues torn in a serious fall and what seemed a never-ending cascade of physical, neurological, and psychological challenges. Problems with balance, vision, incontinence (both urinary and fecal), bradyphrenia, fluctuating blood pressure changes, short-term memory, and functional ADLs developed with varying levels of severity. And as physicians, neurologists, and psychologists considered - and then ruled out - possible explanations including NPH and Binschwanger's syndrome, my research kept pace, with corresponding growth in my understanding of the conditions and diseases that I didn't have.

Finally, in 2004, there was a consensus that the most likely cause for my complex symptomatology was MCI/Early AD with unrelated physical conditions. By this time, the efforts to perform my professional responsibilities were exhausting, and I was able to take advantage of an early retirement opportunity and return from eight years working in Florida to live closer to family members in Upstate New York. Circulatory complications from my arthroscopies led to my arrival in NYS with both legs Unna booted, and I also enrolled in a local NIH study on detecting early AD via newly-developed 3-T MR technologies. On six-month follow-up, the study director determined that my imaging data was inconsistent with early AD, and I was dismissed from the study because - as he expressed it - my situation was too complicated to continue in the study as a control. He did offer the opinion that my symptoms might be the result of pseudodementia, a term I first considered perjorative.

Fortunately, I was being seen for med management by a psychiatric senior resident whose supervisor was closely attuned to the mind-body continuum. In response to the stress of once again entering the Twilight Zone of not knowing what was happening to my mind/brain, we developed a therapeutic relationship that was warm, trusting, and mutually respectful. My persistent need to validate my experiences and understanding with research was met with patience, understanding, and encouragement to develop trust in my own judgement, and to resume writing - both for my own benefit, and possibly that of others.

In January of 2007, a serious and drawn-out respiratory infection and recurrent Fe-deficiency anemia led to a new series of tests - pulmonary, gastroenterology, and a sleep study. (I am currently scheduled for a C-PAP follow-up to the initial sleep study.) Then, in May, a serious assault resulted in hearing loss, and MRI was used to rule out permanent acoustic damage, also providing up-to-date images of my white matter changes for comparison to earlier baseline images.

It is far too soon to assess the degree to which Shroder and O'Hara's research will benefit my own situation, but I am planning to provide copies of their paper to my primary physician and pulmonologist, as well as the psychiatrist whose predecessor was so important to my understanding and acceptance of my condition. My high level of cognitive reserve will not offset my increasing WMCs forever, and I am resolved to make the most of my remaining productive time, both for myself and for others dealing with similarly confusing and frustrating challenges. MB

Judgement call

rich winkel — 2007-05-12T00:00:00Z

This article remarkable for its morally oblivious outlook.

According to the author, the nazi psychiatrists, who actually

showed hitler how mass murder could be carried out cheaply and

efficiently on an industrial scale, were merely guilty of

"allowing philosophical constructs to define clinical practice,

focusing exclusively on preventative medicine, allowing political

pressures to influence practice, blurring the roles of clinicians

and researchers, and falsely believing that good science and good

ethics always co-exist."

Apparently these crimes were errors of clinical and philosophical

judgement, not symptomatic of any kind of character shortcomings

or psychopathologies on the part of the psychiatrists.

That this explanation seems adequate to the author raises the

question of whether he may be suffering from the same affliction

as the objects of his study: a lack of what their victims

might have referred to as a "moral compass" and a need to simulate

a rough approximation of human empathy and insight by hacking them

out of some kind of behavioral rule book. The notion of a cold

blooded mass murderer evaluating philosophical constructs, political

pressures and clinical strategies in the course of pursuing his

chosen vocation is certainly not likely to satisfy those seeking

a deeper understanding of what the hell was wrong with these people.

The author's silence on the psychological motivations of the

perpetrators is especially deafening given that it's no secret that

schools of clinical psychology and psychiatry are magnets for

emotionally troubled people (Psychology Today, July/August 1997,

http://www.findarticles.com/p/articles/mi_m1175/is_n4_v30/ai_19571456)

among which are certainly both "classic" and "compensatory"

narcissists often found in the medical professions.

http://www.ptypes.com/narcissisticpd.html

http://www.ptypes.com/compensatory-narpd.html

Overlooking this fundamental insight puts vulnerable patients at needless risk.

That this article could be provided to a public audience with an

invitation to distribute freely is also symptomatic of an amazing

lack of foresight, not to mention insight, on the part of the

editors. The blind leading the wounded.

ECT and determination of laterality of motor control (cerebral dominance)

iraj derakhshan — 2005-07-02T00:00:00Z

Dear Editor:

I read Dragocic's and colleagues atricle with interest [1]. They advocated use of fTCD in determining cerebral dominance in lieu of other techniques (tabulated in their table 1). What the respected authors did not address is the anatomy sustaining cerebral dominance codified as behavioral handedness; i.e. the laterality of the controlling moiety of a bilaterally distributed neuronal ensemble devoted to movements. The two moities are connected via an excitatory synapse by fibers traversing the callosum (anteriorly). This anatomy has been delineated conclusively elsewhere [2-5]. Thus, in neural right handers the directionality of callosal transfer is from left to right hemisphere. It is in the opposite direction in neural left handers. The laterality of motor control is dichotomous in nature. It has been shown that the relationship between neural (described above) to the behavioral handedness is statistical only. The two match in no more than 80 percent of occasions.

Thus, rather than using the methods described by the authors in table 1, the best way for determining a subject's laterality is to ascertain the reaction time of the subject by old-fashioned push-button technique as they respond to an stimulus. The side with the shorter response time is located opposite to the dominant hemisphere. Elsewhere, I have tabulated various implications of the above anatomy in humans (www.mimickingman.com). Thank you. I.Derakhshan, md, cbe; Neurologist

References:

1. Dragovic M, Allet L, Janca A.

Electroconvulsive therapy and determination of cerebral dominance. Ann Gen Hosp Psychiatry. 2004; 12;3:14. (electronic edition)

2. Derakhshan I. Laterality of motor control revisited: directionality of callosal traffic and

its rehabilitative implications. Top Stroke Rehabil. 2005;12:76-82.

3. Derakhshan I. Handedness and macular vision: laterality of motor control underpins both.

Neurol Res. 2004 ;26:331-337.

4.Derakhshan I, Franz EA, Rowse A. An exchange on Franz, Rowse, and Ballantine (2002). Handedness, neural versus behavioral: is there a measureable callosal difference? J Mot Behav. 2003;35:409-414.

5.Derakhshan I. Callosum and movement control: case reports. Neurol Res. 2003;25:538-542.

A possible error in calculating alpha coefficient

Jesus Sanz — 2005-05-14T00:00:00Z

Cronbach’s alphas for the Greek version of the State-Trat Anxiety Inventory (STAI), Form Y, were surprisingly low (0.19 for the State subscale and 0.39 for the Trait subscale) and not consistent with alpha coefficients reported in literature. Previous studies have found high alpha coefficients around 0.80s- 0.90s for both subscales and for a variety of samples: psychiatric patients, university students, adults from the general population, and so on (see, for example, Abdel-Khalek, A. M., 1989, Personality and Individual Differences, 10:277-285; Gauthier, J., 1993, Canadian Journal of Behavioural Science, 25:559-578; Iwata, N., 2000, Journal of Clinical Psychology, 56:793-806; Stanley, M. A., et al., 2001, Behaviour Research and Therapy, 39: 221-235). Furthermore, test-retest correlations for the Greek version of the STAI were so high as 0.96 and 0.98 (for State and Trait, respectively), whereas alphas were so low as 0.19 and 0.39. Although test-retest reliability and internal consistency reliability are not just the same, both indices are reliability estimates and, therefore, such high discrepancies do not make sense. Given that both subscales of the STAI are comprised of direct (or anxiety-present) items (e.g., I feel nervous) and inverse (or anxiety-absent) items (e.g., I am happy), a failure to reverse the inverse items prior to calculate the alpha coefficients may explain the very low alphas reported in this study. I would suggest authors to review the calculation of Cronbach’s alphas and check if the inverse items of the State and Trait subscales of the STAI were properly reversed prior to calculate alpha.

In response to requests about a clinical version for the STRS checklist

H. Stefan Bracha — 2005-03-31T00:00:00Z

We were delighted to receive a large number of emails commenting on our STRS checklist. Several colleagues have asked if a briefer clinical version is available. Below is a link to a modest tentatively weighted clinical version, which was just published. It is available open access, full-text, on-line at

http://www.currentpsychiatry.com/

A research-based weighing of the STRS is currently being developed, but the above tentatively weighted version may serve in the interm for disaster aftermath screening.

H. Stefan Bracha, MD

Research Psychiatrist

VA National Center for PTSD Honolulu