Reduced Levels of Creatine in the Right Medial Temporal Lobe Region of Panic Disorder Patients Detected with 1H Magnetic Resonance Spectroscopy

Massana, Guillem; Gastó, Cristòbal; Junqué, Carme; Mercader, J.M.; Gómez, Beatriz; Massana, Joan; Torres, Xavier; Salamero, Manel

doi:10.1006/nimg.2002.1083

Cited by 40 publications

(18 citation statements)

References 19 publications

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“…The same group reported reduced levels of creatine and phosphocreatine in the right medial temporal lobe (including the amygdala and part of the hippocampus) in panic disorder. This was interpreted as potentially representing a hypermetabolic state in the right medial temporal region (Massana et al, 2002), which would be consistent with the findings of Sakai et al (2005). Finally, with respect to relevant neurotransmission findings, SPECT and PET studies have reported decreased GABA-benzodiazepine receptor binding in the medial temporal lobes (Kaschka et al, 1995;Malizia et al, 1998) and decreased 5-HT1 A receptor binding in the amygdala in panic disorder (Nash et al, 2008).…”

Section: Panic Disordermentioning

confidence: 69%

The Neurocircuitry of Fear, Stress, and Anxiety Disorders

Shin

Liberzon

2009

Neuropsychopharmacol

1,748

927

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Anxiety disorders are a significant problem in the community, and recent neuroimaging research has focused on determining the brain circuits that underlie them. Research on the neurocircuitry of anxiety disorders has its roots in the study of fear circuits in animal models and the study of brain responses to emotional stimuli in healthy humans. We review this research, as well as neuroimaging studies of anxiety disorders. In general, these studies have reported relatively heightened amygdala activation in response to disorder-relevant stimuli in post-traumatic stress disorder, social phobia, and specific phobia. Activation in the insular cortex appears to be heightened in many of the anxiety disorders. Unlike other anxiety disorders, post-traumatic stress disorder is associated with diminished responsivity in the rostral anterior cingulate cortex and adjacent ventral medial prefrontal cortex. Additional research will be needed to (1) clarify the exact role of each component of the fear circuitry in the anxiety disorders, (2) determine whether functional abnormalities identified in the anxiety disorders represent acquired signs of the disorders or vulnerability factors that increase the risk of developing them, (3) link the findings of functional neuroimaging studies with those of neurochemistry studies, and (4) use functional neuroimaging to predict treatment response and assess treatment-related changes in brain function.

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Section: Panic Disordermentioning

confidence: 69%

The Neurocircuitry of Fear, Stress, and Anxiety Disorders

Shin

Liberzon

2009

Neuropsychopharmacol

1,748

927

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“…In contrast, no changes of prefrontal cortical GABA, Glx, Cho, and NAA were observed in unmedicated, non-depressed patients with PD by Hasler et al (2009). Reduced tCr, NAA and Cho were found in the right medial temporal lobe of unmedicated PD patients (Massana et al, 2002). Yet another study reported reduced NAA/Cr and unchanged Cr and Cho/Cr in the left hippocampus in medicated PD patients (Trzesniak et al, 2010).…”

Section: Introductionmentioning

confidence: 87%

Decreased GABA levels in anterior cingulate cortex/medial prefrontal cortex in panic disorder

Long

Medlock

Džemidžić

et al. 2013

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Changes of various brain metabolites including γ-aminobutyric acid (GABA), measured by 1H-magnetic resonance spectroscopy (MRS), have been reported in panic disorder (PD). Deficits in GABA have been implicated in the pathophysiology of PD. Furthermore, it has been suggested that cortical metabolite changes in PD are familial. Eleven PD patients, including five with and six without a PD family history, and eight age- and gender-matched healthy controls without a family history of psychopathology were recruited. Each subject underwent MRS exams and behavioral assessments (resting visual analog anxiety level and the Panic Disorder Severity Scale). GABA was detected with a MEGA-PRESS J-editing sequence and fitted to minimize mac-romolecule contaminations. A significant decrease in GABA, expressed as the ratio of GABA over total creatine (GABA/tCr), was detected in the anterior cingulate cortex (ACC)/medial prefrontal cortex (mPFC) in PD patients (p<0.05), which tends to be pronounced in patients with a PD family history. No other patient/control differences in metabolites were noted in the ACC/mPFC or occipital cortex (OCC). Overall, our results indicate that deficits in GABA levels in PD patients vary by brain regions and possibly by family history status.

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“…Additionally, there was no relationship between total creatine and self-reported worry or intelligence. In a study of panic disorder, patients that were actively experiencing panic attacks exhibited reduced levels of total creatine in the right amygdalohippocampal region (Massana et al, 2002). Another study of panic disorder detected asymmetry of phosphocreatine levels in patients only, with the right frontal lobe having higher concentrations than the left (Shiori et al, 1996).…”

Section: Linking Creatine With Cognition and Emotionmentioning

confidence: 99%

Creatine metabolism and psychiatric disorders: Does creatine supplementation have therapeutic value?

Allen

2012

Neuroscience & Biobehavioral Reviews

155

135

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Athletes, body builders, and military personnel use dietary creatine as an ergogenic aid to boost physical performance in sports involving short bursts of high-intensity muscle activity. Lesser known is the essential role creatine, a natural regulator of energy homeostasis, plays in brain function and development. Creatine supplementation has shown promise as a safe, effective, and tolerable adjunct to medication for the treatment of brain-related disorders linked with dysfunctional energy metabolism, such as Huntington’s Disease and Parkinson’s Disease. Impairments in creatine metabolism have also been implicated in the pathogenesis of psychiatric disorders, leaving clinicians, researchers and patients alike wondering if dietary creatine has therapeutic value for treating mental illness. The present review summarizes the neurobiology of the creatine-phosphocreatine circuit and its relation to psychological stress, schizophrenia, mood and anxiety disorders. While present knowledge of the role of creatine in cognitive and emotional processing is in its infancy, further research on this endogenous metabolite has the potential to advance our understanding of the biological bases of psychopathology and improve current therapeutic strategies.

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Reduced Levels of Creatine in the Right Medial Temporal Lobe Region of Panic Disorder Patients Detected with 1H Magnetic Resonance Spectroscopy

Cited by 40 publications

References 19 publications

The Neurocircuitry of Fear, Stress, and Anxiety Disorders

The Neurocircuitry of Fear, Stress, and Anxiety Disorders

Decreased GABA levels in anterior cingulate cortex/medial prefrontal cortex in panic disorder

Creatine metabolism and psychiatric disorders: Does creatine supplementation have therapeutic value?

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