Sunday, November 16, 2008

Responses to panic induction procedures in subjects with multiple chemical sensitivity/idiopathic environmental intolerance: understanding the relationship with panic disorder.

Environ Health Perspect. 2002 Aug;110 Suppl 4:669-71.Related ArticlesCited ArticlesCompound (MeSH Keyword)Substance (MeSH Keyword)Free in PMCCited in PMCLinkOut
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Responses to panic induction procedures in subjects with multiple chemical sensitivity/idiopathic environmental intolerance: understanding the relationship with panic disorder.

Tarlo SMPoonai NBinkley KAntony MMSwinson RP.

Gage Occupational and Environmental Health Unit, University of Toronto, Toronto, Ontario, Canada. susan.tarlo@utoronto.ca

Idiopathic environmental intolerance (IEI), also known as multiple chemical sensitivity, is a clinical description for a cluster of symptoms of unknown etiology that have been attributed by patients to multiple environmental exposures when other medical explanations have been excluded. Because allergy has not been clearly demonstrated and current toxicological paradigms for exposure-symptom relationships do not readily accommodate IEI, psychogenic theories have been the focus of a number of investigations. A significantly higher lifetime prevalence of major depression, mood disorders, anxiety disorders, and somatization disorder has been reported among patients with environmental illness compared with that in controls. Symptoms often include anxiety, lightheadedness, impaired mentation, poor coordination, breathlessness (without wheezing), tremor, and abdominal discomfort. Responses to intravenous sodium lactate challenge or single-breath inhalation of 35% carbon dioxide versus a similar breath inhalation of clean air have shown a greater frequency of panic responses in subjects with IEI than in control subjects, although such responses did not occur in all subjects. Preliminary genetic findings suggest an increased frequency of a common genotype with panic disorder patients. The panic responses in a significant proportion of IEI patients opens a therapeutic window of opportunity. Patients in whom panic responses may at least be a contributing factor to their symptoms might be responsive to intervention with psychotherapy to enable their desensitization or deconditioning of responses to odors and other triggers, and/or may be helped by anxiolytic medications, relaxation training, and counseling for stress management.

Tuesday, November 11, 2008

Panic attacks in an individual with bilateral selective lesions of the amygdala.

Arch Neurol. 2006 Dec;63(12):1798-801. Related Articles, LinkOut
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Panic attacks in an individual with bilateral selective lesions of the amygdala.

Wiest G, Lehner-Baumgartner E, Baumgartner C.

Department of Neurology, Medical University of Vienna, Vienna, Austria. gerald.wiest@meduniwien.ac.at

OBJECTIVE: To describe the unique case of a patient with panic attacks and bilateral selective amygdala lesions due to Urbach-Wiethe disease. DESIGN: Case report. SETTING: Epilepsy Monitoring Unit, Medical University of Vienna. Patient A 38-year-old man with Urbach-Wiethe disease developed spontaneous panic attacks and depressive mood, which ceased after antidepressive treatment. INTERVENTIONS: Video electroencephalography monitoring, magnetic resonance imaging, and neuropsychological testing. RESULTS: Extended video electroencephalography monitoring excluded an epileptic etiology of the panic attacks. Results of cranial magnetic resonance imaging showed bilateral selective calcifications of the whole amygdaloid complex. Neuropsychological testing revealed selective memory impairment of autobiographic episodes with preserved memory for autobiographic facts. CONCLUSIONS: Our findings indicate that the occurrence of panic attacks does not critically depend on the integrity of the amygdala. Furthermore, the neuropsychological findings in our patient suggest that the amygdala represents an essential neural substrate for the processing of episodic autobiographic memories.

Publication Types:
  • Case Reports

PMID: 17172622 [PubMed - indexed for MEDLINE]

Monday, November 10, 2008

Treatment of nocturnal disturbances and excessive daytime sleepiness in Parkinson's disease.

Neurology. 2004 Oct 26;63(8 Suppl 3):S35-8. Related Articles, Substance (MeSH Keyword), LinkOut

Treatment of nocturnal disturbances and excessive daytime sleepiness in Parkinson's disease.

Barone P, Amboni M, Vitale C, Bonavita V.

Department of Neurological Sciences, University of Napoli Federico II, Via Pansini 5, 80131 Naples, Italy.

Nocturnal disturbances are common in Parkinson's disease (PD) patients, with almost 70% of these patients reporting nocturnal disturbances. The etiology of sleep disturbances in patients with PD is still controversial. They might be dependent on dopaminergic drugs, on disease progression, or on a combination of these two factors. Nocturnal disturbances can be categorized in four groups: 1) PD-related motor symptoms, including nocturnal akinesia, early-morning dystonia, painful cramps, tremor, and difficulty turning in bed; 2) treatment-related nocturnal disturbances; 3) psychiatric symptoms, including hallucinations, vivid dreams, depression, dementia, insomnia, psychosis, and panic attacks; 4) other sleep disorders, including insomnia, REM behavioral disorder (RBD), restless legs syndrome (RLS), periodic leg movements (PLMS), and excessive daytime sleepiness (EDS). Specific treatment options are supplied for every group. A global evaluation of nocturnal disturbances would provide clinicians with a valuable tool to establish an optimal regimen that could positively influence all nocturnal disturbance categories and thus improve PD management on. However, it is important to consider that management of some nocturnal disturbances in a group may worsen nocturnal symptoms of another group or may increase EDS. PD-related symptoms can be treated with long-acting DA agonists to obtain continuous DA receptor stimulation during the night. Both treatment-related nocturnal disturbances and psychiatric symptoms may be related to drug treatment, and therefore, in both cases, drug reduction or discontinuance should be considered. Some sleep disorders, such as RLS and PLMS, may be controlled by DA agents, and others, such as insomnia and EDS, may be improved by reducing dopaminergic stimulation.

Publication Types:
  • Review

PMID: 15505142 [PubMed - indexed for MEDLINE]

Emptiness in agoraphobia patients.

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Emptiness in agoraphobia patients.

Milrod B.

Weill Cornell College of Medicine, USA. bmilrod@mail.med.cornell.edu

In light of new research findings about the efficacy of psychodynamic treatment for panic disorder and agoraphobia, it seems a prudent time to carefully address psychoanalytic thinking about the treatment of agoraphobia. The literature has highlighted oedipal contributions to its genesis and clinical unraveling in psychoanalysis. While those contributions are indeed central to the disorder, structural deficits in the self-representation often become a central focus of treatment once symptomatic remission has been achieved in psychoanalytic treatment. This aspect of the clinical presentation of agoraphobia has not yet been specifically addressed in the psychiatric literature. Some aspects of the phenomenon have been described by psychoanalysts. It is more difficult to treat this "emptiness" than the overt symptoms of agoraphobia, as described in DSM-IV. Nonetheless, this phenomenon may be one of the contributors to the chronicity of the disorder. Two clinical cases illustrate these points.

Publication Types:
PMID: 17915656 [PubMed - indexed for MEDLINE]

Can carotid body perfusion act as a respiratory controller?

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Can carotid body perfusion act as a respiratory controller?

Virkki A, Polo O, Gyllenberg M, Aittokallio T.

Biomathematics Research Group, Department of Mathematics, University of Turku, FIN-20014 Turku, Finland. arho.virkki@utu.fi

The carotid bodies contain chemoreceptor cells that respond to hypoxia and hypercapnia/acidosis of the arterial blood. Since the carotid bodies receive exceptionally high blood perfusion through branches of the external carotid artery, their impulse activity to the respiratory center is thought to be determined mainly by the arterial partial pressures of oxygen (O(2)) and carbon dioxide (CO(2)). However, this paradigm explains the observed increase in ventilation neither during mentally agitated states nor physical exercise. The objective of the work was to test whether physiologically feasible reductions in carotid body perfusion could explain such respiratory overdrive using a flow-sensitive mathematical model of the carotid body chemoreception. The model is based on the law of mass balance and on the description of the chemical reactions in the arterial blood and inside the receptor cells. The neural response to the arterial O(2) and CO(2) levels is assumed to be mediated via the controller's intracellular O(2) partial pressure and pH. The model predicts that the O(2) response is affected even by moderate changes in blood flow, whereas the CO(2) response is not altered until blood flow is severely limited. Reducing blood flow increases neural stimulus but decreases sensitivity to changes in the partial pressures of arterial O(2) and CO(2). An example is given in which relatively small changes in blood flow significantly modify the carotid body sensitivity to CO(2). These results suggest that limiting perfusion of the carotid bodies through vasoconstriction can offer a powerful mechanism to drive breathing beyond metabolic needs. This observation may provide important insight into the control of ventilation, e.g., during transition from wakefulness to sleep, before physical exercise or during panic attack.

Publication Types:
PMID: 17936799 [PubMed - indexed for MEDLINE]

Orthostatic panic attacks among Vietnamese refugees.

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Orthostatic panic attacks among Vietnamese refugees.

Hinton DE, Hinton L, Tran M, Nguyen M, Nguyen L, Hsia C, Pollack MH.

Harvard Medical School, Massachusetts General Hospital, Department of Psychiatry, Boston 02114, USA. devon_hinton@hms.harvard.edu

Viewed historically and cross-culturally, orthostatic-induced dizziness, i.e., dizziness caused by standing up from a sitting or a lying position, forms a key aspect of many syndromes: irritable heart (American Civil War), effort syndrome (World War I and World War II), chronic fatigue syndrome (contemporary USA), Gulf War syndrome (contemporary USA), and orthostatic dysregulation (contemporary Japan). Among Vietnamese refugees attending a psychiatric clinic, this study documents a high rate of orthostatic panic (OP), as well as certain processes seemingly generating these panic attacks, viz., flashbacks and culturally specific catastrophic cognitions. Case examples are used to demonstrate OP's phenomenology and relevance to clinical care. To illustrate the mechanisms producing OP, we adduce the multiplex model of panic generation. Culturally appropriate care of Vietnamese refugees should include assessment and treatment of OP.

Publication Types:
PMID: 18089637 [PubMed - indexed for MEDLINE]

Childhood trauma, trauma in adulthood, and psychiatric diagnoses: results from a community sample.

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Childhood trauma, trauma in adulthood, and psychiatric diagnoses: results from a community sample.

Zlotnick C, Johnson J, Kohn R, Vicente B, Rioseco P, Saldivia S.

Department of Psychiatry and Human Behavior, Warren Alpert Medical School of Brown University, Providence, RI 02912, USA. czlotnick@butler.org

This study compared the prevalence rates of various psychiatric disorders in persons with first onset of a potentially traumatic event (PTE) in childhood, persons with first onset of a PTE in adulthood, and those with no history of a PTE in a representative sample of Chileans. The Diagnostic of Statistical Manual of Mental Disorders, Revised Third Edition (DSM-III-R), posttraumatic stress disorder, and antisocial personality disorder modules from the Diagnostic Interview Schedule and modules for a range of DSM-III-R diagnoses from the Composite International Diagnostic Interview were administered to 2390 Chileans. The study found that exposure to a lifetime PTE was associated with a higher probability of psychiatric morbidity than no PTE exposure. A PTE with childhood onset relative to adult onset was related to lifetime panic disorder, independent of the number of lifetime and demographic differences between the 2 groups. Childhood interpersonal trauma compared with interpersonal trauma in adulthood was significantly associated with lifetime panic disorder, agoraphobia, and posttraumatic stress disorder. Our findings suggest that specific disorders are linked to interpersonal trauma and PTEs that occur in childhood rather than later in life.

PMID: 18243889 [PubMed - indexed for MEDLINE]

Effects of experimental panic on neuroimmunological functioning.

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Effects of experimental panic on neuroimmunological functioning.

van Duinen MA, Schruers KR, Kenis GR, Wauters A, Delanghe J, Griez EJ, Maes MH.

School of Mental Health and Neurosciences, Maastricht University, The Netherlands. marlies.vanduinen@pn.unimaas.nl

OBJECTIVE: Psychoimmunological research in panic disorder (PD) so far focussed on single time point evaluation in resting conditions. No robust evidence for changes in the immune system was found using this method. However, PD is characterized by the occurrence of unexpected panic attacks (PAs). The current research focuses on cytokine and acute phase protein (APP) levels and mitogen-induced cytokine secretion following 35% CO(2) inhalation-induced panic. METHODS: Eighteen PD patients and 18 matched healthy control subjects underwent both a placebo and a 35% CO(2) inhalation on separate days. Blood samples for cytokine and APP determination were taken before and after the inhalation. In addition to serum determination, whole blood samples were cultured and stimulated with mitogens for assessment of the functional capacity of the immune system. RESULTS: The 35% CO(2) inhalation induced significantly higher levels of anxiety in PD patients as compared to the control subjects, but no differences in immune parameters were found, either in basal conditions or after experimental panic induction. CONCLUSION: In our sample we do not find any changes in serum levels or functional capacity of several immunological parameters in the experimentally provoked PAs. Similar results have been found in social phobia, whereas in other affective disorders such as depression and posttraumatic stress disorder, immune changes are evident. Changes seem to coincide with alterations in hypothalamic-pituitary-adrenal (HPA) axis function. Therefore, the bidirectional communication pathway between the immune system and the HPA axis might play a role in some affective disorders, but it does not specifically seem to be involved in the etiology of PD.

PMID: 18291246 [PubMed - indexed for MEDLINE]

Panic disorder in patients with chronic heart failure.

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Panic disorder in patients with chronic heart failure.

Müller-Tasch T, Frankenstein L, Holzapfel N, Schellberg D, Löwe B, Nelles M, Zugck C, Katus H, Rauch B, Haass M, Jünger J, Remppis A, Herzog W.

Department of Psychosomatic and General Internal Medicine, University of Heidelberg, Heidelberg, Germany. Thomas.Mueller-Tasch@med.uni-heidelberg.de

OBJECTIVE: Our objective was to assess the prevalence of panic disorder, its influence on quality of life (QoL), and the presence of further anxiety and depressive comorbid disorders in outpatients with chronic heart failure (CHF). METHODS: In a cross-sectional study, anxiety and depressive disorders were diagnosed according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition diagnostic criteria in patients with CHF who were aged > or =18 years and had New York Heart Association (NYHA) Functional Classes I-IV, using the Patient Health Questionnaire. Health-related QoL was evaluated using the Short-Form 36 Health Survey (SF-36). RESULTS: Of the 258 participating patients, 24 (9.3%) fulfilled diagnostic criteria for panic disorder. Seven of these (29.2%) were diagnosed with comorbid anxiety disorders, 11 (47.3%) were diagnosed with comorbid depressive disorder, and 5 (20.8%) were diagnosed with other anxiety disorders and any depressive disorder. Female gender [odds ratio (OR)=3.1; 95% confidence interval (95% CI)=1.2-7.8; P=.02] and a lower level of education (OR=0.3; 95% CI=0.1-0.9; P=.04) were associated with the presence of panic disorder. In patients with panic disorder, QoL was significantly more restricted on all subscales of the SF-36 as compared to those without panic disorder, even when age, gender, and NYHA functional class were controlled for (P=.05 to <.01). CONCLUSION: Approximately 1 of 10 patients with CHF suffers from panic disorder, many of whom also have additional anxiety or depressive comorbid disorders. Female gender and a low level of education are positively associated with the presence of panic disorder. QoL is severely limited by the presence of panic disorder. Diagnosis of mental disorders and treatment offers for affected patients should be available in patient care.

Publication Types:
PMID: 18291245 [PubMed - indexed for MEDLINE]

Alexithymia and cognitive dysfunctions in patients with panic disorder.

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Alexithymia and cognitive dysfunctions in patients with panic disorder.

Galderisi S, Mancuso F, Mucci A, Garramone S, Zamboli R, Maj M.

Department of Psychiatry, University of Naples SUN, Naples, Italy. sgalderi@tin.it

BACKGROUND: In patients with panic disorder (PD), the difficulty to identify and manage emotional experience might contribute to the enduring vulnerability to panic attacks. Such a difficulty might reflect a dysfunction of fronto-temporo-limbic circuits. The present study was designed to test the hypothesis that drug-free patients with PD, as compared with healthy subjects (HS), show a higher prevalence of alexithymia, greater difficulty in emotional stimuli processing and poorer performance on neuropsychological tests exploring the activity of fronto-temporo-limbic circuits. METHODS: Alexithymia, general cognitive abilities, focused and sustained attention, working memory, secondary memory, incidental learning, susceptibility to interference from both cognitive and emotional stimuli, and ability to recognize facial emotional expressions were assessed in 32 drug-free patients with PD and 32 HS. RESULTS: Alexithymia was more frequent in patients with PD than in HS. Patients with PD, as compared to HS, had lower verbal cognitive abilities and more difficulty to inhibit interference from nonverbal stimuli and from panic-related words; they performed better than HS on the test assessing spatial incidental learning. Anxiety, panic symptomatology and verbal cognitive abilities (VIQ) were associated with alexithymia. CONCLUSIONS: Findings are compatible with a dysfunction of frontolimbic circuits, in particular orbitofrontal and cingulate cortices. A reduction in verbal cognitive abilities was also observed, which might suggest reduced abstraction and symbolization in these patients. Copyright (c) 2008 S. Karger AG, Basel.

Publication Types:
PMID: 18332616 [PubMed - indexed for MEDLINE]

Elevated brain lactate responses to neural activation in panic disorder: a dynamic 1H-MRS study.

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Elevated brain lactate responses to neural activation in panic disorder: a dynamic 1H-MRS study.

Maddock RJ, Buonocore MH, Copeland LE, Richards AL.

[1] 1Department of Psychiatry, University of California Davis Medical Center, Sacramento, CA, USA [2] 3Imaging Research Center, University of California Davis Medical Center, Sacramento, CA, USA.

Converging evidence suggests that patients with panic disorder have a metabolic disturbance that may influence the regulation of arousal systems and confer vulnerability to 'spontaneous' panic attacks. The consistent finding of elevated brain lactate responses to various metabolic challenges in panic disorder appears to support this model, although the mechanism of this effect is not understood. Several mechanisms have been proposed to account for elevated brain lactate responses in panic disorder, including (1) brain hypoxia due to excessive cerebral vasoconstriction, and (2) a metabolic disturbance affecting lactate metabolism. Recent studies have shown that neural activation (for example, sensory stimulation) causes local lactate accumulation in the presence of increased oxygen availability. The current study used proton magnetic resonance spectroscopic measures of visual cortex lactate changes during visual stimulation in 15 untreated patients with panic disorder and 15 matched volunteers to critically test these two proposed mechanisms of elevated brain lactate responses in panic disorder. Visual cortex lactate/N-acetylaspartate increased during visual stimulation in both groups. The increase was significantly greater in the panic patients than in the comparison group. There were no group differences in end-tidal pCO(2). The finding that visual stimulation leads to significantly greater visual cortex lactate responses in panic patients is not predicted by the hypoxia model. These results suggest that a metabolic disturbance affecting the production or clearance of lactate is the cause of the elevated brain lactate responses consistently observed in panic disorder and provide further support for metabolic models of vulnerability to this illness.Molecular Psychiatry advance online publication, 8 January 2008; doi:10.1038/sj.mp.4002137.

PMID: 18180759 [PubMed - as supplied by publisher]

[Foreign accent syndrome in a case of dissociative (conversion) disorder]

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[Foreign accent syndrome in a case of dissociative (conversion) disorder]

[Article in Japanese]

Tsuruga K, Kobayashi T, Hirai N, Kato S.

Department of Psychiatry, Jichi Medical University.

Psychiatric symptoms are often manifested in verbal expression. Generally, the contents of such expression are pathological. The formal abnormalities of speech are also observed in various mental disorders, as far as quantitative abnormalities are concerned. However, disturbance of intonation, namely disprosody, is more commonly observed in organic disorders of the brain. When the accent of words and the intonation of sentences changes from that of a native speaker, the speech sounds like the broken language of untrained foreigners. Such foreign accent syndrome is usually an issue of neuropsychology. In this paper, the authors report a case of foreign accent syndrome without organic brain syndrome. The patient was a 44-year-old woman, who developed panic disorder about year after her father's death. Then she developed aphonia. After aphonia was resolved, she began to speak haltingly as if a Chinese woman was trying to speak Japanese. Organic brain diseases were subsequently excluded. She had complicated familial conflicts, including a divorce from a violent and faithless husband, interpersonal difficulties with her husband's parents, and her pubertal daughter. We diagnosed her with dissociative (conversion) disorder of ICD-10. Our patient is clinically interesting, because case reports of dysprosody are unusual and often involve organic brain diseases. We suppose that foreign accent syndrome in our patient is a variant of aphonia, and the patient unconsciously assigned the symptom two ambivalent rolls: to snow that she cannot speak well, and to express her meaning. In addition, she had a Chinese-speaking aunt-in-law who was her ideal role model. We surmise that her symptom signifies identification with her aunt-in-law.

Publication Types:
PMID: 18416192 [PubMed - indexed for MEDLINE]

The effects of acute exercise on CO(2) challenge reactivity.

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The effects of acute exercise on CO(2) challenge reactivity.

Smits JA, Meuret AE, Zvolensky MJ, Rosenfield D, Seidel A.

Department of Psychology, Southern Methodist University, Dedman College, P.O. Box 750442, Dallas, TX 75275, United States.

The present study examined the effects of acute exercise on anxiogenic responding to 65% O(2)/35% CO(2) challenge. Participants (N=92) were 51 female and 41 male volunteers ranging in age from 17 to 24 (M=19.43, SD=1.31). Participants had no history of panic attacks and were randomized to moderate treadmill exercise (i.e., 70% of HR(max)) or quiet rest prior to taking a single vital capacity inhalation of 35% CO(2)/65% O(2). Gender and measures of negative affectivity and anxiety sensitivity were included in the design as control variables. Results indicated participants who exercised prior to challenge showed significantly reduced reactivity compared to their counterparts who rested prior to challenge. Importantly, the effect sizes for the advantage of exercise over rest remained in the medium to large range (i.e., partial eta(2)>.07) after controlling for the effects of gender, anxiety sensitivity, and negative affectivity. These findings are the first to demonstrate that the anti-panic effects of exercise are unique from, and cannot be better explained by, established risk factors of CO(2) challenge reactivity.

PMID: 18603261 [PubMed - as supplied by publisher]

"Anxietas tibiarum". Depression and anxiety disorders in patients with restless legs syndrome.

J Neurol. 2005 Jan;252(1):67-71. Related Articles, Cited in PMC, LinkOut

"Anxietas tibiarum". Depression and anxiety disorders in patients with restless legs syndrome.

Winkelmann J, Prager M, Lieb R, Pfister H, Spiegel B, Wittchen HU, Holsboer F, Trenkwalder C, Ströhle A.

Max Planck Institute of Psychiatry, Munich, Germany.

BACKGROUND: Symptoms of anxiety and depression in patients with restless legs syndrome (RLS) have been observed. However, it is unclear whether rates of threshold depression and anxiety disorders according to DSM-IV criteria in such patients are also elevated. METHODS: 238 RLS patients were assessed with a standardized diagnostic interview (Munich-Composite International Diagnostic Interview for DSM-IV) validated for subjects aged 18-65 years. Rates of anxiety and depressive disorders were compared between 130 RLS patients within this age range and 2265 community respondents from a nationally representative sample with somatic morbidity of other types. RESULTS: RLS patients revealed an increased risk of having 12-month anxiety and depressive disorders with particularly strong associations with panic disorder (OR=4.7; 95% CI=2.1-10.1), generalized anxiety disorder (OR=3.5; 95% CI= 1.7-7.1), and major depression (OR=2.6; 95% CI=1.5-4.4). In addition, lifetime rates of panic disorder and most depressive disorders as well as comorbid depression and anxiety disorders were considerably increased among RLS patients compared with controls. CONCLUSIONS: The results suggest that RLS patients are at increased risk of having specific anxiety and depressive disorders. Causal attributions of patients suggest that a considerable proportion of the excess morbidity for depression and panic disorder might be due to RLS symptomatology.

Publication Types:
  • Comparative Study
  • Research Support, Non-U.S. Gov't

PMID: 15654556 [PubMed - indexed for MEDLINE]

Panic disorder respiratory subtype: a comparison between responses to hyperventilation and CO2 challenge tests.

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Panic disorder respiratory subtype: a comparison between responses to hyperventilation and CO2 challenge tests.

Freire RC, Lopes FL, Valença AM, Nascimento I, Veras AB, Mezzasalma MA, de-Melo-Neto VL, Zin WA, Nardi AE.

Laboratory of Panic & Respiration, Institute of Psychiatry, Federal University of Rio de Janeiro, Rua Visconde de Pirajá, 407/702, 22410-003, Rio de Janeiro, Brazil. rafaelcrfreire@terra.com.br

In this study 117 panic disorder patients were divided into a respiratory subtype group and a non-respiratory subtype group. The respiratory subtype patients were observed to be more sensitive to the 35% CO(2) inhalation challenge test and the hyperventilation test than the non-respiratory subtype patients.

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PMID: 17964660 [PubMed - indexed for MEDLINE]

Hot flashes and panic attacks: a comparison of symptomatology, neurobiology, treatment, and a role for cognition.

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Hot flashes and panic attacks: a comparison of symptomatology, neurobiology, treatment, and a role for cognition.

Hanisch LJ, Hantsoo L, Freeman EW, Sullivan GM, Coyne JC.

Department of Psychiatry, University of Pennsylvania, USA. hanisch@mail.med.upenn.edu

Despite decades of research, the causal mechanisms of hot flashes are not adequately understood, and a biopsychosocial perspective on hot flashes remains underdeveloped. This article explores overlooked parallels between hot flashes and panic attacks within 5 areas: course and symptomatology, physiological indicators, neurocircuitry and biochemical mechanisms, pharmacotherapy, and psychological treatment, noting both similarities and important differences between the 2 events. An integrative conceptual model is presented that identifies key ways in which psychological factors may influence the experience of hot flashes, with clinical implications and areas of future research. This model yields readily testable hypotheses and may provide a template for exploring the role of cognition in the frequency and severity of hot flashes and, in turn, a basis for the development of nonpharmacological treatments. (c) 2008 APA, all rights reserved.

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PMID: 18298271 [PubMed - indexed for MEDLINE]

Separation anxiety disorder in childhood as a risk factor for future mental illness.

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Separation anxiety disorder in childhood as a risk factor for future mental illness.

Lewinsohn PM, Holm-Denoma JM, Small JW, Seeley JR, Joiner TE Jr.

Oregon Research Institute, Eugene, OR 97403, USA. pete@ori.org

OBJECTIVE: To ascertain the extent to which childhood separation anxiety disorder (SAD) confers risk for the development of psychopathology during young adulthood (ages 19-30). METHOD: A subset of the participants of the Oregon Adolescent Depression Project (n = 816) was used. Subjects provided retrospective reports of lifetime mental illness (including SAD) and concurrent reports of current mental illness at age 16 and were then followed prospectively until age 30. Diagnostic assessments were conducted twice during adolescence and again at ages 24 and 30. Based on diagnosis during childhood/adolescence, the subjects were partitioned into four orthogonal groups: SAD (n = 42), other anxiety disorders (n = 88), a heterogeneous psychiatric disorders control group (n = 389), and a not mentally ill control group (n = 297). Adjusting for demographic variables that were significantly associated with group status and for comorbid disorders prior to age 19, the results were analyzed with hierarchical multiple logistic regression. RESULTS: SAD was a strong (78.6%) risk factor for the development of mental disorders during young adulthood. The major vulnerabilities were for panic disorder and depression. CONCLUSIONS: Because SAD creates a major vulnerability for mental disorders during young adulthood, clinicians should be sensitive to the presence of SAD, and children and adolescents with SAD should be treated. Future research should evaluate whether successful treatment of SAD and/or the provision of a preventive intervention during childhood/adolescence reduce the risk for future psychopathology.

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PMID: 18356763 [PubMed - indexed for MEDLINE]

High risk studies and developmental antecedents of anxiety disorders.

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High risk studies and developmental antecedents of anxiety disorders.

Hirshfeld-Becker DR, Micco JA, Simoes NA, Henin A.

MGH Clinical and Research Program in Pediatric Psychopharmacology, 185 Alewife Brook Parkway, Suite 2000, Cambridge, MA 02138, USA. dhirshfeld@partners.org

The past two decades have witnessed significant growth in our understanding of the developmental antecedents of anxiety disorders. In this article, we review studies of offspring at risk for anxiety disorders, longitudinal studies of the course of anxiety disorders in clinical, epidemiologic, and at-risk samples, studies of hypothesized temperamental risk factors for anxiety, and give a brief overview of the literature on environmental risk factors. Clear developmental antecedents to anxiety disorders identified include (1) childhood anxiety disorders [in particular, separation anxiety and overanxious disorder/general anxiety disorder (GAD)], (2) behavioral inhibition which predicts later social phobia, (3) anxiety sensitivity which predicts later panic disorder, and (4) negative affectivity, which predicts a spectrum of psychopathology including anxiety disorders. Further prospective studies are needed to examine the roles of environmental factors such as parenting practices, peer influences, stressful life events, and perinatal stressors. Future studies could benefit from (1) beginning earlier in development and following individuals into adulthood, (2) assessing the overlap between multiple temperamental constructs, (3) greater use of observational measures of temperament and of parent-child and peer interactions, (4) greater attention to parental psychopathology which may confound associations noted, (5) exploration of other features of anxiety disorders (neurofunctional correlates, cognitive features, other aspects of emotional regulation) as potential precursors, and (6) intervention studies exploring whether modifying developmental antecedents can alter the course of anxiety disorders. Copyright 2008 Wiley-Liss, Inc.

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PMID: 18409200 [PubMed - indexed for MEDLINE]

Characteristics of fatigue in panic disorder patients.

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Characteristics of fatigue in panic disorder patients.

Kaiya H, Sugaya N, Iwasa R, Tochigi M.

Outpatient Clinic for Anxiety Disorders, Akasaka Mental Clinic, Tokyo, Japan.

It was suggested that fatigue is one of characteristics of panic disorder. Fatigue was assessed in 360 patients with panic disorder using the Japanese version of the Multidimensional Fatigue Inventory (MFI-J). The scores for general fatigue and reduced activity were significantly higher in the patients than in the controls. These tendencies were also observed in men when the subject group was differentiated according to sex, but not in women. In contrast, the trend for higher score for physical fatigue was observed only in the female patients. Thus, the present study suggests that the characteristics of fatigue vary with sex in panic disorder.

PMID: 18412848 [PubMed - indexed for MEDLINE]

Measurement of panic-like responses following intravenous infusion of sodium lactate in panic-prone rats.

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Measurement of panic-like responses following intravenous infusion of sodium lactate in panic-prone rats.

Sajdyk TJ, Keim SR, Thielen SR, Fitz SD, Shekhar A.

Indiana University Medical Center, Indianapolis, Indiana, USA.

This unit describes a putative animal model for panic disorder. The basic premise is that pharmacological disruption of critical brain regions implicated in the circuitry of anxiety will lead to a condition similar to that of the human disorder. A clinically relevant test, the sodium lactate challenge, is utilized to assess parallels between the human condition and this rat model.

PMID: 18428590 [PubMed - indexed for MEDLINE]

A panic attack-like unusual stress reaction.

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A panic attack-like unusual stress reaction.

Schenberg LC, Dos Reis AM, Ferreira Póvoa RM, Tufik S, Silva SR.

Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, ES, Brazil.

Ever since the seminal studies of Hans Selye, activation of hypothalamus-pituitary-adrenal (HPA) axis is emblematic of stress. Consequently, the lack of HPA axis responses following the undisputable psychological stress of a panic attack stands out as one of the most intriguing findings of contemporary psychiatry. On the other hand, the defensive behaviors and aversive emotions produced by stimulation of the dorsal periaqueductal gray matter (DPAG) have been proposed as a model of panic attacks. Therefore, we examined whether the plasma levels of 'stress hormones' corticotropin and prolactin show any change following the DPAG-evoked freezing and flight behaviors of the rat. Rats bearing an electrode into the DPAG and an intra-atrial catheter were stimulated at 9:00 a.m., 18-24 h after the catheter implantation. Blood samples were withdrawn just before 1-min stimulation of DPAG, immediately after (5 or 15 min) and throughout 3 to 27 h following stimulation. In another experiment, samples were withdrawn either before or following a prolonged stimulation (5 min) of the DPAG with flight threshold intensity. Hormones were measured by either chemiluminescent or double-antibody immunoassays. Hormone plasma levels following freezing and flight behaviors were compared to those of resting or restraint-stressed rats. Data show that stress hormones remain unaltered following the DPAG-evoked defensive behaviors. Not even the 5-min stimulation of DPAG with the flight threshold intensity changed corticotropin plasma levels significantly. As far as we known, this is the first demonstration of the lack of stress hormone responses following the intense emotional arousal and physical exertion of a fear-like behavior in rats. Data add new evidence of DPAG involvement in spontaneous panic attacks.

PMID: 18423636 [PubMed - as supplied by publisher]

The effectiveness of anticonvulsants in psychiatric disorders.

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The effectiveness of anticonvulsants in psychiatric disorders.

Grunze HC.

University of Newcastle School of Neurology, Neurobiology and Psychiatry, Leazes Wing, Royal Victoria Infirmary, Queen Victoria Rd., Newcastle upon Tyne NE14LP, United Kingdom. heinz.grunze@ncl.ac.uk

Anticonvulsant drugs are widely used in psychiatric indications. These include mainly alcohol and benzodiazepine withdrawal syndromes, panic and anxiety disorders, dementia, schizophrenia, affective disorders, bipolar affective disorders in particular, and, to some extent, personality disorders. A further area in which neurology and psychiatry overlap is pain conditions, in which some anticonvulsants, and also typical psychiatric medications such as antidepressants, are helpful. From the beginning of their psychiatric use, anticonvulsants have also been used to ameliorate specific symptoms of psychiatric disorders independently of their causality and underlying illness, eg, aggression, and, more recently, cognitive impairment, as seen in affective disorders and schizophrenia. With new anticonvulsants currently under development, it is likely that their use in psychiatry will further increase, and that psychiatrists need to learn about their differential efficacy and safety profiles to the same extent as do neurologists.

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PMID: 18472486 [PubMed - indexed for MEDLINE]