Anterior cingulate cortex volume reduction in patients with panic disorder

Asami, Takeshi; Hayano, Fumi; Nakamura, Motoaki; Yamasue, Hidenori; Uehara, Kumi; Otsuka, Tatsui; Roppongi, Tomohide; Nihashi, Namiko; Inoue, Tomio; Hirayasu, Yoshio

doi:10.1111/j.1440-1819.2008.01800.x

Cited by 101 publications

(77 citation statements)

References 44 publications

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“…Neuroimaging studies report that chronic pain and psychiatric conditions are associated with structural and functional reorganisation of cortical structures (Asami et al, 2008;Burgmer et al, 2009;Flor et al, 2001;Hayes et al, 2012;Karl et al, 2001;Pleger et al, 2006), especially the primary somatosensory cortex (S1) in chronic pain conditions using functional magnetic resonance imaging (Vartiainen et al, 2009;Wrigley et al, 2009). Preclinical animal studies have also demonstrated that MS (maternal separation) rats exposed to WAS (water-avoidance stress) displayed an increased in activation of the S1, suggesting that stress in the adult MS rat results in enhanced sensory input to visceral noxious stimulation (Mendes-Gomes et al, 2011).…”

Section: Cortexmentioning

confidence: 99%

Genotype-dependent responsivity to inflammatory pain: A role for TRPV1 in the periaqueductal grey

Madasu

Okine

Olango

et al. 2016

Pharmacological Research

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Section: Cortexmentioning

confidence: 99%

Genotype-dependent responsivity to inflammatory pain: A role for TRPV1 in the periaqueductal grey

Madasu

Okine

Olango

et al. 2016

Pharmacological Research

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“…Changsheng Li proposed that social defeat stress induces the transition from acute to chronic plantar incision pain (29). Different spinal and supraspinal regions can be influenced by stress; thus, alterations to neurotransmitters within these regions play an important role in stress-pain interactions (36). For example, multiple studies have shown that the cortical structures (37), amygdala (38), periaqueductal grey (39), rostral ventromedial Medulla (28) and spinal cord dorsal horn mediate the process of stress-induced hyperalgesia.…”

Section: Figure 4 Effect Of Dexmedetomidine On the Gr Protein Expresmentioning

confidence: 99%

Dexmedetomidine Alleviates Presurgical Anxiety-Induced Persistent Postsurgical Pain via Decreasing the Expression of Glucocorticoid Receptor

Li¹,

Zhang²,

Yin³

et al. 2018

J Anesth Perioper Med

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Background: Preoperative anxiety can worsen postsurgical pain. Glucocorticoids play an important role in psychological anxiety and pain, but the effect of glucocorticoid receptor (GR) on persurgical anxiety-induced persistent postsurgical pain remains unknown. Methods: Adult male Sprague Dawley rats were randomly divided into 10 groups: control group, SPS group, incision group, 'SPS-plus-incision' group, saline group, metyrapone group, Dexmedetomidine group 1 (10 μg/kg), Dexmedetomidine group 2 (20 μg/kg), Dexmedetomidine group 3 (40 μg/kg) and Dexmedetomidine + Corticosterone group. Single-prolonged stress (SPS) was used to induce anxiety behaviors. Intraperitoneal injection of saline and dexmedetomidine was performed at 24 h after SPS and 0.5 h before incision. Intraperitoneal injection of metyrapone (25 mg/kg) was performed at 1h before SPS. Paw withdrawal mechanical threshold (PWMT) was tested at 24 h before SPS and on 1, 4, 7, 14, 21, and 28 days after incision. Corticosterone levels were determined using ELISA. The expression of GR was determined using Western blot. Results: The 'SPS-plus-incision' group decreased PWMT compared with control group and incision group from 1 to 28 days (P<0.05). SPS combined with incision increased plasma corticosterone levels compared with control group (P<0.05). A timedependent increase in GR was also observed in 'SPS-plus-incision' group (P<0.05). Metyrapone significantly blunted the SPS-induced persistent postsurgical pain (P< 0.05). Intraperitoneal administration of dexmedetomidine inhibits SPS-induced persistent pain compared with group saline (P<0.05). The expression of GR decreased after the intraperitoneal administration of dexmedetomidine (P<0.05). Pretreatment with corticosterone blocked this effect. Conclusions: Glucocorticoids contributed to presurgical anxiety-induced persistent postsurgical pain. Dexmedetomidine that decreased the expression of GR alleviated anxiety-induced persistent pain. These results indicated that dexmedetomidine may be an effective agent for preventing presurgical anxiety-induced persistent postoperative pain.

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“…The biological approach to panic disorder and agoraphobia bases its theoretical claims on four major groups of empirical findings: (1) Studies indicating that patients with panic disorder and agoraphobia suffer from structural brain abnormalities, such as in the temporal lobe, the basal ganglia, the cingulate, and the brainstem (Asami et al, 2008;Barlow, 2004;Ham et al, 2007;Han et al, 2008;Lee et al, 2006;Stein, 2008); (2) Studies showing that genetics play a significant role in the etiology of panic disorder and agoraphobia (Chantarujikapong et al, 2001;Hettema, Neale, & Kendler, 2001;Kendler et al, 1999;Kendler et al, 2001;Nocon et al, 2008;Stein, 2008); (3) Findings obtained using the paradigm of the biological challenge, whereby panic attacks can be experimentally induced in panic disorder patients using a variety of chemical substances (e.g., sodium lactate infusion and CO 2 inhalation; see Abrams, Schruers, Cosci, & Sawtell, 2008;Barlow, 2004); (4) Research demonstrating that drug therapy is an effective intervention in the treatment of these disorders (Furukawa, Watanabe, & Churchill, 2006;Mavissakalian & Ryan, 1998;Westenberg, 1996).…”

Section: Biological Approach To Panic Disorder and Agoraphobiamentioning

confidence: 99%

Fear and Phobia: A Critical Review and the Rational-Choice Theory of Neurosis

Rofé¹,

Rofé²

2015

IJPS

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This article reviews the empirical status of theories of fear and phobia. Psychoanalysis received little support, as findings tend to refute its basic assumption that phobia results from repressed material. Although conditioning has its weaknesses, it appears to be the strongest explanation of simple phobia. Findings raise question as to whether interoceptive conditioning can account for the development of panic disorder and agoraphobia, as these disorders develop in the absence of environmental conditioning events. A significant body of research supports Clark's claim that catastrophic misinterpretation of bodily sensations are involved in both the development and treatment of panic disorder and agoraphobia. However, the causal relationship between the two remains unclear. Likewise, while biological factors certainly increase the vulnerability to developing fear and phobia, findings have not yet confirmed that these behaviors are controlled by biological mechanisms. A new theory, the Rational-Choice Theory of Neurosis (Rofé, 2010;Y. Rofé & Rofé, 2013), which preserves the psychoanalytic claim that bizarre phobias need to be explained within a theory that accounts for neuroses by one set of theoretical concepts, was used to resolve the theoretical confusion in this field.

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Anterior cingulate cortex volume reduction in patients with panic disorder

Abstract: Both manual ROI tracing and optimized VBM suggest a subregion-specific pattern of ACC volume deficit in panic disorder. In addition to functional abnormalities, these results suggest that structural abnormalities of the ACC contribute to the pathophysiology of panic disorder.

Cited by 101 publications

References 44 publications

Genotype-dependent responsivity to inflammatory pain: A role for TRPV1 in the periaqueductal grey

Genotype-dependent responsivity to inflammatory pain: A role for TRPV1 in the periaqueductal grey

Dexmedetomidine Alleviates Presurgical Anxiety-Induced Persistent Postsurgical Pain via Decreasing the Expression of Glucocorticoid Receptor

Fear and Phobia: A Critical Review and the Rational-Choice Theory of Neurosis

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