Tension-type headache as the unique pain experience of a patient with congenital insensitivity to pain.

Posted on October 5, 2009 by Maurice Preter MD
Pain. 2005 Oct;117(3):478-83.Click here to read Links
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Tension-type headache as the unique pain experience of a patient with congenital insensitivity to pain.

Danziger N, Willer JC.

Département de Neurophysiologie Clinique, Centre Hospitalo-Universitaire, Pitié-Salpêtrière, Paris, France. ndanziger@hotmail.com

Congenital insensitivity to pain (CIP) is a rare clinical syndrome characterized by dramatic impairment of pain perception since birth and is generally caused by a hereditary sensory and autonomic neuropathy (HSAN) with loss of the small-calibre, nociceptive nerve fibres. We report the case of a 32-year-old woman with CIP and a presumptive diagnosis of HSAN type V, who experienced physical pain for the first and unique time in her life shortly after the sudden loss of her brother. This patient had sustained innumerable painless injuries during childhood, including bone fractures and severe burns. The only pain she ever felt consisted in an intense headache, which took place in a context of strong emotional overload and anxiety, 3 weeks after her younger brother died suddenly in a car accident. The description of this inaugural episode of headache fulfilled the diagnostic criteria of episodic tension-type headache. This case strongly suggests that the transcription of the grief of bereavement into physical pain may sometimes occur independently of the peripheral mechanisms of nociception and despite the lack of previous pain experience. In the light of recent experimental data showing that the same neural mechanisms that regulate physical pain may also control the expression of separation distress and the feeling of social exclusion, this unique case helps to better understand why some patients may feel physically hurt after the loss of someone they love.

PMID: 16154693 [PubMed – indexed for MEDLINE]


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Socially isolated children 20 years later: risk of cardiovascular disease.

Posted on October 5, 2009 by Maurice Preter MD

Arch Pediatr Adolesc Med. 2006 Aug;160(8):805-11.Click here to read Cited in PMC, LinkOut

Socially isolated children 20 years later: risk of cardiovascular disease.

Caspi A, Harrington H, Moffitt TE, Milne BJ, Poulton R.

Author Affiliations: Department of Psychology, University of Wisconsin, Madison, USA. a.caspi@iop.kcl.ac.uk

OBJECTIVE: To test the hypothesis that children who occupy peripheral or isolated roles in their peer groups (isolated children) are at risk of poor adult health. DESIGN: Longitudinal study of an entire birth cohort. SETTING: Dunedin, New Zealand. PARTICIPANTS: A total of 1037 children who were followed up from birth to age 26 years. INTERVENTIONS: Measurement of social isolation in childhood, adolescence, and adulthood. MAIN OUTCOME MEASURES: When study members were 26 years old, we measured adult cardiovascular multifactorial risk status (overweight, elevated blood pressure, elevated total cholesterol level, low high-density lipoprotein level, elevated glycated hemoglobin concentration, and low maximum oxygen consumption). RESULTS: Socially isolated children were at significant risk of poor adult health compared with nonisolated children (risk ratio, 1.37; 95% confidence interval, 1.17-1.61). This association was independent of other well-established childhood risk factors for poor adult health (low childhood socioeconomic status, low childhood IQ, childhood overweight), was not accounted for by health-damaging behaviors (lack of exercise, smoking, alcohol misuse), and was not attributable to greater exposure to stressful life events. In addition, longitudinal findings showed that chronic social isolation across multiple developmental periods had a cumulative, dose-response relationship to poor adult health (risk ratio, 2.58; 95% confidence interval, 1.46-4.56). CONCLUSIONS: Longitudinal findings about children followed up to adulthood suggest that social isolation has persistent and cumulative detrimental effects on adult health. The findings underscore the usefulness of a life-course approach to health research, by focusing attention on the effect of the timing of psychosocial risk factors in relation to adult health.

PMID: 16894079 [PubMed – indexed for MEDLINE]

Posted in Health |

Family conflict in childhood: a predictor of later insomnia

Posted on October 5, 2009 by Maurice Preter MD

 Sleep. 2006 Aug 1;29(8):1063-7.Cited in PMC, LinkOut

Family conflict in childhood: a predictor of later insomnia.

Gregory AM, Caspi A, Moffitt TE, Poulton R.

Institute of Psychiatry, King’s College London, United Kingdom. a.gregory@iop.kcl.ac.uk

STUDY OBJECTIVES: To examine the association between childhood exposure to family conflict and insomnia at 18 years of age. DESIGN: Longitudinal prospective data on an entire birth cohort were obtained. Parents completed the Conflict subscale of the Moos Family Environment Scale when the study members were 7, 9, 13, and 15 years of age. Insomnia was examined in a standardized interview when the participants were aged 18 years. SETTING: Participants were born in Dunedin, New Zealand, and were interviewed at this location. PATIENTS OR PARTICIPANTS: One thousand thirty-seven children born between April 1, 1972, and March 31, 1973, enrolled in the study (52% male). At age 18 years, 993 (97% of living cohort members) provided data. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: The mean level of family conflict at age 7 to 15 years predicted insomnia at 18 years after controlling for sex, socioeconomic status, sleep problems at 9 years, and self-reported health (odds ratio [95% confidence interval] = 1.42 [1.17-1.73], p < .001). There was a dose-response relationship, whereby the more assessments at which families scored in the top 25% for conflict, the greater the young person’s likelihood of developing insomnia at age 18 years. This association was present even after controlling for depression at 18 years. CONCLUSIONS: This study demonstrates a modest but robust longitudinal link between family conflict during childhood and insomnia experienced at 18 years of age. Future work needs to replicate this finding in different populations and to elucidate the mechanisms underlying this association.

PMID: 16944675 [PubMed – indexed for MEDLINE]

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Increased prevalence of white matter hyperintensities in patients with panic disorder.

Posted on October 5, 2009 by Maurice Preter MD
J Psychopharmacol. 2008 Nov 21. [Epub ahead of print]Click here to read Links

Increased prevalence of white matter hyperintensities in patients with panic disorder.

Bae S, Kim J, Hwang J, Lee Y, Lee H, Lee J, Lyoo I, Renshaw P, Yoon S.

Interdisciplinary Program in Brain Science and Department of Psychiatry, Seoul National University and Hospital, Seoul, South Korea.

AbstractThe aim of the current study is to compare the prevalence, severity and location of cerebral white matter hyperintensities (WMH) between patients with panic disorder (PD) and healthy control subjects. Patients with PD (n = 24) and matched healthy control subjects (n = 24) were scanned using a 3.0 Tesla whole-body magnetic resonance scanner. Axial T2-weighted and fluid-attenuated inversion recovery images were acquired and evaluated for the prevalence, severity and location of WMH using the modified composite scale of Fazekas and Coffey and coded separately for deep and periventricular WMH. Logistic regression analyses were used to assess the association between WMH and the diagnosis of PD. A greater severity of total WMH was associated with a diagnosis of PD in a dose-dependent pattern (odds ratio [OR] = 8.8, P = 0.005 for mild WMH; OR = 27.7, P = 0.007 for moderate to severe WMH). Deep WMH, where most group differences originated, were predominantly located in the frontal region of the brain (n = 16 in PD, n = 1 in control). The current report is the first study to report an increased prevalence of WMH in patients with PD.

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Increased risk of acute myocardial infarction for patients with panic disorder: a nationwide population-based study.

Posted on October 5, 2009 by Maurice Preter MD
Psychosom Med. 2009 Sep;71(7):798-804. Epub 2009 Jul 10.Click here to read Links

Increased risk of acute myocardial infarction for patients with panic disorder: a nationwide population-based study.

Chen YH, Tsai SY, Lee HC, Lin HC.

School of Public Health, Taipei Medical University, Taipei, Taiwan.

OBJECTIVE: To examine prospectively the relationship between a diagnosis of panic disorder and the risk of acute myocardial infarction within 1 year of follow-up. Panic disorder is associated prospectively with coronary artery disease, but the risk of acute myocardial infarction associated with panic disorder has not been specifically investigated. METHOD: This nationwide population-based study used data from the Taiwan National Health Insurance Research Database covering the years 2000 to 2005. A total of 9641 patients diagnosed with panic disorder in 2004 were included, together with 28,923 matched nonpanic disorder enrollees as a comparison cohort. Cox proportional hazard regressions were conducted to compute hazard ratios, after adjustment for comorbid medical disorders and sociodemographic characteristics. RESULTS: Results indicated that 4.77% of patients with panic disorder (approximately one in 21) experienced an acute myocardial infarction episode within a year, compared with 2.73% of patients in the comparison cohort. The adjusted hazard of acute myocardial infarction was significantly higher (1.75 times, 95% Confidence Interval = 1.55-1.97) for patients with panic disorder, relative to the comparison cohort. The association persisted in further analyses stratified by hypertension, coronary heart diseases, and age. CONCLUSION: Panic disorder was identified as an independent risk factor for subsequent acute myocardial infarction. Comprehensive multidisciplinary approaches are needed to optimize primary and secondary prevention of acute myocardial infarction among patients with panic disorder.

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