Academia.edu no longer supports Internet Explorer.
To browse Academia.edu and the wider internet faster and more securely, please take a few seconds to upgrade your browser.
2011, Progress in Neuro-Psychopharmacology and Biological Psychiatry
Panic patients have many functional deficiencies in the hypothalamic-pituitary-adrenal (HPA) axis. Previous studies have shown changed pituitary gland volume in some psychiatric disorders that have functional deficiencies in the HPA axis. However, to date no study has evaluated the pituitary gland volume in patients with panic disorder (PD). We investigated the pituitary gland volume in patients with PD (n = 27) and ageand sex-matched healthy controls (n = 27), using 1.5-T magnetic resonance imaging in this study. Analysis showed that patients with PD had significantly smaller pituitary volume compared to healthy subjects. Patients with agoraphobia especially had a significantly smaller pituitary volume than patients without agoraphobia. There was a significant relationship between the pituitary volume and both the severity of symptoms and the illness duration in the patient group. The results show that patients with PD have reduced pituitary volume, which may reflect the functional abnormalities seen in this disorder. These findings may help us better understand the pathology of PD.
Background: The hypothalamus is a brain structure involved in the neuroendocrine aspect of stress and anxiety. Evidence suggests that generalized anxiety disorder (GAD) and panic disorder (PD) might be accompanied by dysfunction of the hypothalamus-pituitary-adrenal axis (HPA), but so far structural alterations were not studied. We investigated hypothalamic volumes in patients with either GAD or PD and in healthy controls. Methods: Twelve GAD patients, 11 PD patients and 21 healthy controls underwent a 1.5T MRI scan. Hypothalamus volumes were manually traced by a rater blind to subjects' identity. General linear model for repeated measures (GLM-RM) was used to compare groups on hypothalamic volumes, controlling for total intracranial volume, age and sex. Results: The hypothalamus volume was significantly reduced (p¼ 0.04) in GAD patients, with significant reductions in both the left (p¼ 0.02) and right side (p ¼ 0.04). Patients with PD did not differ significantly (p¼ 0.73). Anxiety scores were inversely correlated with hypothalamic volumes.
Neuropsychopharmacology, 2006
Anxiety and depressive disorders are among the most common psychiatric disorders with a high number of hospital admissions and a lifetime prevalence of up to 25%. So far, the pathophysiological mechanisms for anxiety disorders remain to be found. Preclinical studies suggest that changes in hypothalamic-pituitary-adrenocortical (HPA) system function are causally related to the expression of anxietyrelated behavior. The findings on HPA system function in patients with anxiety disorders are, however, heterogeneous. Both hypo-and hyperresponsiveness of HPA response in various anxiety disorders under different experimental conditions were found. In order to characterize putative case/control differences in HPA system function, we performed a Dex-CRH test, a widely used test to pick up changes in HPA system regulation with high sensitivity, in 30 patients with panic disorder, 35 patients with major depressive episode and in 30 controls individually matched for ethnicity, age and gender. The results indicate a similar dysregulation of the HPA system response in the Dex-CRH test in both patient groups. This finding further underlines the hypothesis that both, depression and panic disorder, share impaired HPA system regulation, supporting the notion that the impairment is involved in the pathophysiology of these clinical conditions. However, differences in the suppression effects and psychopathological correlation patterns between depressed and panic patients suggest different biological mechanisms of HPA system dysregulation in both disorders.
International Journal of Psychiatry in Clinical Practice, 2020
Objective: It has been hypothesised that early-onset panic disorder (PD) may constitute a biologically distinct subtype of PD, but the few relevant data are inconclusive. We systematically explored for potential psychopathological and hormonal differences between early-onset (age at onset 27 years) versus lateonset PD, in consecutively-referred, medication-free, acutely-ill PD outpatients, moreover without comorbid mental disorders except agoraphobia (N ¼ 54; age ¼ 32.3 ± 7.5 years; early-onset ¼ 27; females ¼ 38). Methods: Hormones assessed (plasma levels) included adrenocorticotropic hormone (ACTH), cortisol and dehydroepiandrosterone sulphate (DHEAS). Psychopathological measures included panic attacks' number during last three weeks, the Agoraphobic Cognitions and the Body Sensations Questionnaires and the Hamilton Anxiety Rating Scale. Results: Early-onset PD patientscompared to their late-onset counterpartshad longer duration of the disease. The two onset-groups demonstrated similar panic and anxiety symptoms and similar ratios of smokers/never-smokers. However, early-onset patients demonstrated significantly greater ACTH and DHEAS levels and higher (marginally significant) cortisol levels than the late-onset patients. Moreover, in the early-onset patients only, significant positive correlations emerged between ACTH levels and the severity of both panic and anxiety symptomatology. Conclusions: These findings suggest that the two onset-groups demonstrate significant differences in the hypothalamic-pituitary-adrenal axis functioning, at least when acutely-ill. KEY POINTS Early-onset panic disorder (EOPD) may differ biologically from late-onset PD (LOPD). EOPD was correlated with greater adrenocorticotropic hormone (ACTH) plasma levels. EOPD was correlated with greater dehydroepiandrosterone sulphate plasma levels. In EOPD only, ACTH levels were positively correlated with panic and anxiety symptoms.
Neuropsychopharmacology, 1995
In this paper the authors examine the interrelationship of both the noradrenergic (NA) system and the hypothalamic-pituitary-adrenal (HPA) axis and its implications for panic disorder (PD). Seventeen PD patients and 16 healthy volunteers were challenged orally 12 weeks apart with the a2-agonist clonidine (13 healthy volunteers and 12 patients repeated the challenge). Between challenges, PD patients were treated with fluoxetine, with 10 of 12 improving at least moderately. Both during the acute phase of the illness and during the phase of pharmacological improvement, patients demonstrated a greater percentage of reductions of plasma 3-methoxy-4-hydroxyphenylglycol (MHPG) and plasma cortisol during clonidine challenge. We used correlational matrices to examine the relationship between the NA system, as reflected by plasma MHPG, and the HPA axis, as reflected by plasma cortisol measures. Healthy volunteers exhibited multiple significant "couplings" between either baseline or maximal decrease ("1max
Biological Psychiatry, 1991
Psychiatry and Clinical Neurosciences, 2009
Aims: Another structure in the obsessive–compulsive disorder (OCD) circuit may be the pituitary gland because of the fact that limbic–hypothalamic–pituitary–adrenal (LHPA) axis abnormality has been reported in patients with OCD. There has been only one prior study, however, concerning pituitary volumetry, in which the sample was a pediatric group. The purpose of the present study was therefore to investigate this in an adult OCD patient group using magnetic resonance imaging (MRI).Methods: Pituitary volume was measured in 23 OCD patients and the same number of healthy control subjects. Volumetric measurements were made on T1-weighted coronal MRI, with 2.40-mm-thick slices, at 1.5 T, and were done blindly.Results: A statistically significantly smaller pituitary volume was found in OCD patients compared to healthy controls (age and intracranial volume as covariates). With regard to gender and diagnosis, there was a significant difference in pituitary gland volume (F = 4.18, P < 0.05). In addition, post-hoc analysis indicated near-significant difference in men with OCD as compared with women with OCD (P = 0.07) and significant difference between control men and control women (F = 10.96, P < 0.001).Conclusions: Taking into consideration that the prior study found decreases in pituitary volume in pediatric patients with OCD as compared with healthy control subjects, future large MRI studies should investigate pituitary size longitudinally, with a careful characterization of hypothalamo-pituitary-adrenal (HPA) function in conjunction with anatomic MRI evaluation.
Translational Psychiatry, 2024
This systematic review addresses the complex nature of Panic Disorder (PD), characterized by recurrent episodes of acute fear, with a focus on updating and consolidating knowledge regarding neurochemical, genetic, and epigenetic factors associated with PD. Utilizing the PRISMA methodology, 33 original peer-reviewed studies were identified, comprising 6 studies related to human neurochemicals, 10 related to human genetic or epigenetic alterations, and 17 animal studies. The review reveals patterns of altered expression in various biological systems, including neurotransmission, the Hypothalamic-Pituitary-Adrenal (HPA) axis, neuroplasticity, and genetic and epigenetic factors leading to neuroanatomical modifications. Noteworthy findings include lower receptor binding of GABAA and serotonin neurotransmitters in the amygdala. The involvement of orexin (ORX) neurons in the dorsomedial/perifornical region in triggering panic reactions is highlighted, with systemic ORX-1 receptor antagonists blocking panic responses. Elevated Interleukin 6 and leptin levels in PD patients suggest potential connections between stress-induced inflammatory changes and PD. Brain-derived neurotrophic factor (BDNF) and tyrosine receptor kinase B (TrkB) signaling are implicated in panic-like responses, particularly in the dorsal periaqueductal gray (dPAG), where BDNF's panicolytic-like effects operate through GABAA-dependent mechanisms. GABAergic neurons' inhibitory influence on dorsomedial and posterior hypothalamus nuclei is identified, potentially reducing the excitability of neurons involved in panic-like responses. The dorsomedial hypothalamus (DMH) is highlighted as a specific hypothalamic nucleus relevant to the genesis and maintenance of panic disorder. Altered brain lactate and glutamate concentrations, along with identified genetic polymorphisms linked to PD, further contribute to the intricate neurochemical landscape associated with the disorder. The review underscores the potential impact of neurochemical, genetic, and epigenetic factors on the development and expression of PD. The comprehensive insights provided by this systematic review contribute to advancing our understanding of the multifaceted nature of Panic Disorder and pave the way for targeted therapeutic strategies.
2000
Objectives: Animal model studies may allow greater elucidation of the cerebral circuits involved in the genesis of panic disorder (PD), but these stu- dies have not yet been fully analyzed. Methods: The authors review recent literature on the neurobiology and neuroanatomy of PD. Results: In this update, the authors present a revision of data that demonstrates the existence of a
Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999), 2018
The beneficial effects of psychopharmacological and cognitive behavioral therapy (CBT) on the brain are not well understood. In a previous study, we found smaller pituitary volumes in patients with obsessive-compulsive disorder (OCD). The purpose of this study was to examine the effect of CBT on pituitary gland volume. A total of 81 patients with various anxiety disorders and the same number of healthy controls underwent magnetic resonance imaging, and their pituitary gland volumes were compared at baseline. Pituitary gland volumes were also measured before and after CBT in the patient group. OCD patients had smaller pituitary gland volumes at baseline than healthy controls (0.54±0.29 cm3 for OCD patients vs. 0.82±0.30 cm3 for healthy controls; p < 0.001). We found no significant changes in OCD patient pituitary gland volume after the 16-week treatment period, with mean pre- and post-treatment values of 0.54±0.29 cm3 and 0.56±0.32 cm3, respectively (p > 0.05). Our results indi...
Progress in Neuro-Psychopharmacology and Biological Psychiatry, 2010
To date, no study has examined the pituitary volumes in patients with hypochondriasis. In the present study, we evaluated pituitary volumes in patients with hypochondriasis and healthy controls. Twenty individuals with hypochondriasis (ten males, ten females), aged 20 to 48 years, and healthy controls were included into the study. The pituitary volumes were obtained. Volumetric measurements were made with T1-weighted coronal MRI images, with 2.4-mm-thick slices, at 1.5 T, and were done blindly. Volumetric measurements did not demonstrate group differences in the brain measurements, i.e., whole brain volume, white, and gray matter volumes (P > 0.05). We found significantly smaller pituitary volumes of the whole group of hypochondriac patients compared to healthy controls (age and ICV as covariates). To conclude, the results from the current investigation suggest that hypochondriac patients had smaller pituitary volumes compared with healthy controls. This could be the keystone to a better understanding of the neurobiological basis of hypochondriasis.
Pharmacopsychiatry, 1997
m Nocturnal urinary cortisol. norepinephrine, epinephrine, testosterone, and melatonin secretion patterns were studied in male patients with DSM IVIICD-10 panic disorder (n= 16) over two series of 5 consecutive nlghts each. Nighttime urinary excretion of cortisol, norepinephrine, and epinephrine was significantly elevated in drug-free patients compared to normal individuals ( n = 13). Measurements were repeated after 4 weeks, and the same differences were found again. There were high correlations between the first and the second series of measurements. Testosterone and melatonin levels did not differ between panic patients and controls. Pemglia et al.: Psychoimmunoendocrine aspects of panic disorder. Neuropsychobiology 26 (1992) 12-22 Braune. S., M. Albu, M. Frohler. 1: Hohn. G. Scheibe: Psychophysiological and biochemical changes in patients with panic attacks in a defined situational arousal. Eur. Arch. Psychiatry Clin. Neurosci. 244 (1994) 86-92 Cameron, 0. G., M. R Lee, G. C Curtis, D. S. McCann: Endocrine and physiological changes during "spontaneous" panic attacks. Psychoneuroendocrinology 12 (1987) 321 -331 Cameron, 0. G . R M. Nesse: Systemic hormonal and physiological abnormalities in anxiety disorders. Psychoneuroendocrinology 13 (1988) 287-307 Cameron. 0. G.. C. B. Smith, P. j. Hollingsworth, R M. Nesse. G. C. Curtis: Platelet alpha 2-adrenergic receptor binding and plasma catecholamines. Before and during imipramine treatment in patients with panic anxiety. Arch. Gen. Psychiatry 41 (1984) 1144-1148 Cameron, 0. G., C B. Smith, M. A. Lee, PI. Hollingsworth, E. M. Hill, G.
Neuropsychobiology, 1992
Stress-responsive neurohormonal systems are involved in major depression (MD) and panic disorder (PD). The immune system, which is closely connected with ncuronal and hormonal systems, has been studied in MD: a systemic immune activation has been recently reported. To determine whether similar changes in the immune function are present also in PD, we studied leukocyte enumeration by flow cytometry in conjunction with monoclonal antibody staining, in 18 PD, 23 MD in drug-free conditions and 20 controls. We found a significantly higher percentage of HLADR+(p<0.001) and of CD19 cells (p<O-OI) in P D and MD and a lower percentage of CD3 (p<O.O5) in PD. Urinary free cortisol levels were higher in M D compared to PD. A pattern of lymphocyte subpopulation distribution compatible with an activation of the immune system was found in M D and PD. This activation was present also with high glucocorticoid levels, suggesting a possible defect of glucocorticoid receptors.
Alpha Psychiatry, 2025
Background: This review updates our understanding of the neuroanatomical and neurocircuitry factors involved in panic disorder (PD). Many aspects remain undetermined. Methods: Clinical studies and a randomized controlled trial were identified via PubMed database and included in this review. Results: The search, following PRISMA guidelines, identified 13 human studies and 3 animal studies. Nine human studies compared brain activity and connectivity between regions in PD patients. Neural activity in the amygdala was highlighted in six studies. The hippocampus had higher activation in PD patients compared to those with social phobia, but generally showed less activity compared to healthy controls. The parahippocampal gyrus and thalamus exhibited greater activation in PD patients than healthy controls. Activity in the prefrontal cortices was also noted, particularly the ventromedial prefrontal cortex (vmPFC), ventrolateral prefrontal cortex (vlPFC), dorsomedial prefrontal cortex (dmPFC), and dorsolateral prefrontal cortex (dlPFC). Other regions involved included the dorsal midbrain, left brainstem (showing hyperactivation), S1, and right caudate, which showed increased activity in PD patients. The left intraparietal sulcus (IPS) exhibited hypoactivation in response to predictable cues compared to unpredictable or neutral cues within the default mode network (DMN). Three animal studies suggested that electrical and chemical activation of the dorsal periaqueductal gray (dPAG) in rats elicited fight-or-flight behaviors, providing a model for panic attacks. Conclusions: Neuroimaging studies suggest several key regions involved in PD pathophysiology, including the brainstem, amygdala, hippocampus, parahippocampal gyrus, thalamus, insula, and prefrontal and cingulate cortices. Hypersensitivity in the brainstem and amygdala plays a role in activating the fear network. Further prospective studies are needed to identify the neuroanatomical sites involved in PD and fear circuitry.
Depression and …, 2007
Dysregulation of the hypothalamicpituitaryadrenal (HPA) axis may play a role in panic disorder. HPA studies in patients with panic disorder, however, have produced inconsistent results. Seeking to understand the inconsistencies, we reexamined endocrine data from ...
Clinical Neuropharmacology, 1992
Stress-responsive neurohormonal systems are involved in major depression (MD) and panic disorder (PD). The immune system, which is closely connected with ncuronal and hormonal systems, has been studied in MD: a systemic immune activation has been recently reported. To determine whether similar changes in the immune function are present also in PD, we studied leukocyte enumeration by flow cytometry in conjunction with monoclonal antibody staining, in 18 PD, 23 MD in drug-free conditions and 20 controls. We found a significantly higher percentage of HLADR+(p<0.001) and of CD19 cells (p<O-OI) in P D and MD and a lower percentage of CD3 (p<O.O5) in PD. Urinary free cortisol levels were higher in M D compared to PD. A pattern of lymphocyte subpopulation distribution compatible with an activation of the immune system was found in M D and PD. This activation was present also with high glucocorticoid levels, suggesting a possible defect of glucocorticoid receptors.
Psychoneuroendocrinology, 1988
Among the studies of systemic hormonal and physiological abnormalities associated with anxiety disorders, the most consistent and extensive findings suggest (a) peripheral adrenergic hyperactivity (including increases in norepinephrine but not epinephrine) and functional dysregulation, (b) increased incidence of mitral valve prolapse in panic patients, and (c) normal suppressibility of the hypothalamic-pituitary-adrenal cortical endocrine system with dexamethasone in panic patients. Other less-certain findings include (a) increased circulating concentrations of plasma ACTH and/or cortisol, and prolactin, in panic patients, (b) increased platelet monoamine oxidase activity in generalized anxiety and/or panic patients, (c) decreased gonadal axis activity in some anxious individuals, (d) decreased nighttime melatonin plasma concentrations in panic patients, and (e) peripheral a2 and B-adrenoreceptor down-regulation, with normal semtonin binding parameters. These findings, taken together, provide tentative support for dysfunction in adrenergic and GABAergic central nervous system mechanisms in people with anxiety disorders. Abnormal anxiety and normal stress both show evidence of adrenergic hyperactivity; however, there appear to be differences in hormonal pmtiles, especially the apparent lack of increase of epinephrine during panic attacks, as well as differences in the reactivity of the system, and in the "trigger" mechanisms which determine when the response occurs.
Anais da Academia Brasileira de Ciências, 2005
A bibliographic search has been performed in MEDLINE using cortisol and panic as key-words, occurring in the title and/or in the abstract. Human studies were selected, with no time limit. The following publications were excluded: reviewarticles, case reports, panic attacks in disorders other than panic disorder, and studies on changes that occurred in-between panic attacks. The results showed that real-life panic attacks as well as those induced by selective panicogenic agents such as lactate and carbon dioxide do not activate the hypothalamicpituitary- adrenal (HPA) axis. Agonists of the colecystokinin receptor B, such as the colecystokinin-4 peptide and pentagastrin, increase stress hormones regardless of the occurrence of a panic attack and thus, seem to activate the HPA axis directly. The benzodiazepine antagonist flumazenil does not increase stress hormones, but this agent does not reliably induce panic attacks. Pharmacological agents that increased anxiety in both normal subje...
Progress in Neuro-Psychopharmacology and Biological Psychiatry, 2009
Objective: Obsessive-compulsive symptoms are induced or aggravated by stress, and the pituitary is a key component of the hypothalamic-pituitary-adrenal axis. We examined pituitary volume in drug-naïve and medicated male patients with obsessive-compulsive disorder (OCD). Methods: Volumetric magnetic resonance imaging studies were conducted on 62 male control subjects, medicated male patients (N = 50) and drug-naïve male patients (N = 12) with OCD. Results: Pituitary volume was significantly smaller in drug-naïve patients with OCD (464.97 ± 55.82 mm 3 ) compared to medicated patients (577.84 ± 129.11 mm 3 , P = 0.004) and control subjects (543.04 ± 113.70 mm 3 , P = 0.027), and no difference between control subjects and medicated patients (P = 0.174).
Journal of Neural Transmission, 2000
Background. Research on basal HPA axis activity in patients with panic disorder showed inconsistent results.
Journal of Neuropsychiatry and Clinical Neurosciences, 1989
Thirty consecutive lactate-sensitive panic disorder patients were studied with magnetic resonance imaging (MRI) to investigate the relationship between temporal lobe abnormalities and panic disorder. Neuroanatomical abnormalities, most involving the right temporal lobe, were found in 43% of patients, compared with 10% of the control subjects. Patients with temporal lobe abnormalities were significantly younger at the onset of panic disorder and had more panic attacks compared with patients with normal MRI scans (p<.05). These results suggest that panic disorder could be secondary to temporal lobe dysfunctions and that panic disorder patients with abnormal MRIs could have a worse prognosis than those with normal MRIs and would require long-term pharmacological treatment.
Loading Preview
Sorry, preview is currently unavailable. You can download the paper by clicking the button above.