Psychiatric comorbidity in different organic vertigo syndromes.

J Neurol. 2008 Mar 14 [Epub ahead of print]
Psychiatric comorbidity in different organic vertigo syndromes.
Eckhardt-Henn A, Best C, Bense S, Breuer P, Diener G, Tschan R, Dieterich M.
Dept. of Psychosomatic Medicine, Klinikum Stuttgart – Bürgerhospital, Tunzhoferstrasse 14–16, 70191, Stuttgart, Germany, A.Eckhardt@klinikum-stuttgart.de.
OBJECTIVE : A high degree of psychiatric disorders has repeatedly been described among patients with organic vertigo syndromes and attributed to vestibular dysfunction. Yet almost no investigations exist which differentiate between various organic vertigo syndromes with regard to psychiatric comorbidity. The following prospective, interdisciplinary study was carried out to explore whether patients with different organic vertigo syndromes exhibit different psychological comorbidities. METHODS : 68 patients with organic vertigo syndromes (benign paroxysmal positioning vertigo (BPPV) n = 20, vestibular neuritis (VN) n = 18,Menière’s disease (MD) n = 7, vestibular migraine (VM) n = 23) were compared with 30 healthy volunteers.All patients and control persons underwent structured neurological and neuro-otological testing. A structured diagnostic interview (-I) (SCID-I) and a battery of psychometric tests were used to evaluate comorbid psychiatric disorders. RESULTS : Patients with VM and MD showed significantly higher prevalence of psychiatric comorbidity (MD = 57%, VM = 65%) especially with anxiety and depressive disorders, than patients with VN (22%) and BPPV (15 %) compared to normal subjects (20 %). These elevated rates of comorbidities resulted in significantly elevated odds-ratios (OR) for the development of comorbid psychiatric disorders in general (for VM OR = 7.5, for MD OR = 5.3) and especially for anxiety disorders (for VM OR = 26.6, for MD OR = 38.7). CONCLUSION : As a consequence, a structured psychological and psychometric testing and an interdisciplinary therapy should be proceeded in cases with complex and prolonged vertigo courses, especially in patients with VM and MD. Possible reasons of these unexpected results in VM and MD are discussed.
PMID: 18338198 [PubMed – as supplied by publisher]
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Our results suggest normal HPA responses to stress and ACTH stimulation in patients with CPP but reduced adrenal reactivity in patients with FMS, name

Psychosomatic Medicine 70:65-72 (2008)
© 2008 American Psychosomatic Society
ORIGINAL ARTICLES
HPA Axis Reactivity and Lymphocyte Glucocorticoid Sensitivity in
Fibromyalgia Syndrome and Chronic Pelvic Pain
Katja Wingenfeld, PhD, Christine Heim, PhD, Iris Schmidt, PhD, Dieter
Wagner, PhD, Gunther Meinlschmidt, PhD and Dirk H. Hellhammer, PhD

From the Department of Psychobiology, University of Trier, Trier,
Germany (K.W., C.H., I.S., D.W., G.M., D.H.H.); Department of
Psychiatry and Psychotherapy Bethel, Bielefeld, Germany (K.W.);
Department of Psychiatry and Behavioral Sciences, Emory University
School of Medicine, Atlanta, GA (C.H.); and Institute of Psychology,
University of Basel, Switzerland (G.M.).

Address correspondence and reprint requests to Katja Wingenfeld, PhD,
Department of Psychiatry and Psychotherapy, Bethel, Remterweg 69–71,
33617 Bielefeld, Germany. E-mail: katja.wingenfeld@evkb.de

Objective: Chronic pelvic pain (CPP) and fibromyalgia syndrome (FMS)
have been associated with hypothalamic-pituitary-adrenal (HPA) axis
alterations, i.e., mild hypocortisolism and enhanced feedback
sensitivity. We tested the hypothesis of reduced cortisol release in
response to a psychosocial stressor and pharmacological stimulation.
Furthermore, glucocorticoid (GC) sensitivity was evaluated.

Methods: Plasma total and salivary-free cortisol concentrations were
measured in response to a standardized social laboratory stressor, the
Trier Social Stress Test, and to adrenocorticotropin (ACTH)1–24
stimulation. In the Trier Social Stress Test, we additionally measured
ACTH. GC sensitivity was measured by dexamethasone inhibition of
lipopolysaccharide-induced interleukin-6 and tumor necrosis factor-
alpha production in whole blood.

Results: There were no HPA axis alterations in women with CPP (N = 18)
in these tests. Patients with FMS (N = 17) showed lower total cortisol
release in response to the social stressor and exogenous ACTH, but
normal free cortisol and ACTH levels compared with controls (N = 24).
GC sensitivity was similar in all groups.

Conclusions: Our results suggest normal HPA responses to stress and
ACTH stimulation in patients with CPP but reduced adrenal reactivity
in patients with FMS, namely in total cortisol release. Free cortisol
on the other hand was unaltered, possibly reflecting an adaptation to
reduced circulating total cortisol.

Key Words: chronic pelvic pain • fibromyalgia syndrome • hypothalamic-
pituitary-adrenal axis • cortisol • glucocorticoid sensitivity

Abbreviations: FMS = fibromyalgia syndrome; CPP = chronic pelvic pain;
HPA = hypothalamic-pituitary-adrenal; TSST = Trier Social Stress Test;
ACTH = adrenocorticotropin; GC = glucocorticoid; GR = glucocorticoid
receptor; BMI = body mass index; LPS = lipopolysaccharide; IL-6 =
interleukin-6; TNF-{alpha} = tumor necrosis factor-alpha.

Posted in Psychiatry/Neurology |

Effect of Social Support on Nocturnal Blood Pressure Dipping

Effect of Social Support on Nocturnal Blood Pressure Dipping
Carlos J. Rodriguez, MD, MPH, Matthew M. Burg, PhD, Joyce Meng, MD,
Thomas G. Pickering, MD, DPhil, Zhezhen Jin, PhD, Ralph L. Sacco, MD,
MS, Bernadette Boden-Albala, DrPH, Shunichi Homma, MD and Marco R. Di
Tullio, MD

From the Department of Medicine (C.J.R., M.M.B., J.M., T.G.P., S.H.,
M.R.D.T.), Columbia University, New York, New York; Department of
Neurology (R.L.S., B.B.-A.), Columbia University, New York, New York;
Department of Epidemiology (C.J.R., R.L.S.), Columbia University,
Mailman School of Public Health, New York, New York; Department of
Sociomedical Science (B.B.-A.), Columbia University, Mailman School of
Public Health, New York, New York; Department of Biostatistics (Z.J.),
Columbia University, Mailman School of Public Health, New York, New
York; Department of Neurology (R.L.S.), University of Miami, Miami,
Florida; and Section of Cardiovascular Medicine (M.W.B.), Yale
University, New Haven, Connecticut.

Address correspondence and reprint requests to Carlos J. Rodriguez,
Division of Cardiology, Columbia University, 622 W 168th street; PH
3-342, New York, NY 10032. E-mail: cjr10@columbia.edu

Objective: To determine if nocturnal blood pressure (BP) dipping among
non-Hispanic blacks is influenced by social support. Non-Hispanic
blacks have higher rates of cardiovascular morbidity and mortality
from hypertension and are more likely to have ambulatory blood
pressure (ABP) that remains high at night (nondipping).

Methods: A total of 68 non-Hispanic black normotensive and 13
untreated hypertensive participants (age 72 ± 10 years, 48% female)
free of clinical cardiovascular disease completed 24-hour ABP
monitoring and a questionnaire that included a modified version of the
CARDIA Study Social Support Scale (CSSS). Nondipping was defined as a
decrease of <10% in the ratio between average awake and average asleep
systolic BP. Analyses were adjusted for age, gender, and systolic BP.

Results: The prevalence of nondipping was 26.8% in subjects in the
highest CSSS tertile versus 41.1% in the lowest CSSS tertile (p = .
009). On adjusted analysis, CSSS was analyzed as a continuous variable
and remained independently and inversely associated with nondipping
(odds ratio 0.27, 95% Confidence Interval 0.08–0.94, p = .04).

Conclusions: Social support may be an important predictor of BP
dipping at night. These findings suggest that social support may have
positive health affects through physiologic (autonomic) pathways.

Key Words: ambulatory blood pressure monitoring • social support •
African-Americans • hypertension

Abbreviations: BP = blood pressure; ABP = ambulatory blood pressure;
NOMASS = Northern Manhattan Stroke Study; CSSS = CARDIA Social Support
Scale; BMI = body mass index; OR = odds ratio; SD = standard deviation.

Posted in Psychiatry/Neurology |

Hypoxic changes in the central nervous system of noise-exposed mice.

Acta Otolaryngol Suppl. 2007 Oct;(558):73-7.
Related Articles, Links

Hypoxic changes in the central nervous system of noise-exposed
mice.

Kim YJ, Kang HH, Ahn JH, Chung JW.

Department of Otolaryngology, Pundang Jaesang Hospital, DaeJin
Medical Center, Seongnam City, Kyunggi Do, Korea.

CONCLUSION: After a noise-induced transient threshold shift,
hypoxia occurred in the central nervous system, especially in the
auditory cortex, the hippocampus, and the inferior colliculus.
OBJECTIVES: Noise-induced inner ear hypoxia was shown by measurement
of an increase in hypoxia-inducible factor-1 alpha, which is
expressed? in the nucleus under hypoxic conditions. This study uses
pimonidazole to localize site-specific hypoxic changes occurring in
the mouse central auditory pathway during noise-induced auditory
threshold shift. METHOD: BALB/c hybrid mice with normal hearing were
exposed to 122 dB SPL white noise for 3 h. Immediately after exposure
to the noise, and 7 d after noise exposure, the brains of mice were
collected. Brains were cryosectioned into slices 15 microm thick and
examined by immunofluorescence after staining with pimonidazole HCl.
RESULTS: After 3 h of exposure to 120 dB SPL noise, the hearing
thresholds of mice decreased to 51.1+/-8.6 dB SPL (n =14), but hearing
recovered in 7 d. After noise exposure, pimonidazole signal increased
in the auditory cortex, the hippocampus, and the inferior colliculus.
The pimonidazole signal remained elevated after 7 d. In control mice,
pimonidazole did not stain any brain region.

Publication Types:

* Research Support, Non-U.S. Gov’t

PMID: 17882574 [PubMed – indexed for MEDLINE]

Posted in Psychiatry/Neurology |

Proenkephalin expression and enkephalin release are widely observed in non-neuronal tissues.

Proenkephalin expression and enkephalin release are widely observed in non-neuronal tissues.

Denning GM, Ackermann LW, Barna TJ, Armstrong JG, Stoll LL, Weintraub NL, Dickson EW.

Department of Emergency Medicine, University of Iowa Hospitals and Clinics, 200 Hawkins Drive, C-43 GH, Iowa City, IA 52242-1009, United States.

Enkephalins are opioid peptides that are found at high levels in the brain and endocrine tissues. Studies have shown that enkephalins play an important role in behavior, pain, cardiac function, cellular growth, immunity, and ischemic tolerance. Our global hypothesis is that enkephalins are released from non-neuronal tissues in response to brief ischemia or exercise, and that this release contributes to cardioprotection. To identify tissues that could serve as potential sources of enkephalins, we used real-time PCR, Western blot analysis, ELISA, immunofluorescence microscopy, and ex vivo models of enkephalin release. We found widespread expression of preproenkephalin (pPENK) mRNA and production of the enkephalin precursor protein proenkephalin (PENK) in rat and mouse tissues, as well as in tissues and cells from humans and pigs. Immunofluorescence microscopy with anti-enkephalin antisera demonstrated immunoreactivity in rat tissues, including heart and skeletal muscle myocytes, intestinal and kidney epithelium, and intestinal smooth muscle cells. Finally, isolated tissue studies showed that heart, skeletal muscle, and intestine released enkephalins ex vivo. Together our studies indicate that multiple non-neuronal tissues produce PENK and release enkephalins. These data support the hypothesis that non-neuronal tissues could play a role in both local and systemic enkephalin-mediated effects.

PMID: 18082911 [PubMed – as supplied by publisher]

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