Carbamazepine in Bipolar Disorder With Pain

Rahman, Tahir; Campbell, Austin; O’Connell, Christopher R.; Nallapula, Kishan

doi:10.4088/pcc.14r01672

Cited by 3 publications

(1 citation statement)

References 34 publications

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“…It has been demonstrated that dysfunctions of glial mechanisms, including self-reinforcing interplay between dysfunctional energy homeostasis, inflammation, and astroglial signaling, play important roles in pathomechanisms of development of several neuropsychiatric disorders, including epilepsy, bipolar disorder, schizophrenia, and chronic pain [1,2,3,4]. Both preclinical and clinical studies have demonstrated astroglial abnormalities in central nervous system of patients with epilepsy and other neuropsychiatric disorders [1,5,6,7].…”

Section: Introductionmentioning

confidence: 99%

Carbamazepine Attenuates Astroglial L-Glutamate Release Induced by Pro-Inflammatory Cytokines via Chronically Activation of Adenosine A2A Receptor

Okada

Fukuyama

Shiroyama

et al. 2019

IJMS

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Carbamazepine (CBZ) binds adenosine receptors, but detailed effects of CBZ on astroglial transmission associated with adenosine receptor still need to be clarified. To clarify adenosinergic action of CBZ on astroglial transmission, primary cultured astrocytes were acutely or chronically treated with CBZ, proinflammatory cytokines (interferon γ (IFNγ) and tumor necrosis factor α (TNFα)), and adenosine A2A receptor (A2AR) agonist (CGS21680). IFNγ and TNFα increased basal, adenophostin-A (AdA)-evoked, and 2-amino-3-(3-hydroxy-5-methyl-isoxazol-4-yl)propanoic acid (AMPA)-evoked astroglial L-glutamate releases. In physiological condition, CGS21680 increased basal astroglial L-glutamate release but glutamate transporter inhibition prevented this CGS21680 action. CBZ did not affect basal release, whereas glutamate transporter inhibition generated CBZ-induced glutamate release. Furthermore, AdA-evoked and AMPA-evoked releases were inhibited by CBZ but were unaffected by CGS21680. Contrary to physiological condition, chronic administrations of IFNγ and TNFα enhanced basal, AdA-, and AMPA-evoked releases, whereas IFNγ and TNFα decreased and increased CGS21680-evoked releases via modulation A2AR expression. Both chronic administration of CGS21680 and CBZ suppressed astroglial L-glutamate release responses induced by chronic cytokine exposer. Especifically, chronic administration of CBZ and CGS21680 prevented the reduction and elevation of A2AR expression by respective IFNγ and TNFα. These findings suggest that A2AR agonistic effects of CBZ contribute to chronic prevention of pathomechanisms developments of several neuropsychiatric disorders associated with proinflammatory cytokines.

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Section: Introductionmentioning

confidence: 99%

Carbamazepine Attenuates Astroglial L-Glutamate Release Induced by Pro-Inflammatory Cytokines via Chronically Activation of Adenosine A2A Receptor

Okada

Fukuyama

Shiroyama

et al. 2019

IJMS

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Risk of psychiatric disorders following trigeminal neuralgia: a nationwide population-based retrospective cohort study

et al. 2015

J Headache Pain

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BackgroundTN is one of the most common causes of facial pain. A higher prevalence of psychiatric co-morbidities, especially depressive disorder, has been proven in patients with TN; however, a clear temporal-causal relationship between TN and specific psychiatric disorders has not been well established. We performed a nationwide population-based retrospective cohort study to explore the relationship between TN and the subsequent development of psychiatric disorders, including schizophrenia, bipolar disorder, depressive disorder, anxiety disorder, and sleep disorder.MethodsWe identified subjects who were newly diagnosed with TN between January 1, 2000 and December 31, 2010 in the Taiwan National Health Insurance Research Database. A comparison cohort was constructed for patients without TN who were matched according to age and sex. All TN and control patients were observed until diagnosed with psychiatric disorders, death, withdrawal from the National Health Institute system, or until December 31, 2010.ResultsThe TN cohort consisted of 3273 patients, and the comparison cohort consisted of 13,092 matched control patients without TN. The adjusted hazard ratio (aHR) of depressive disorder, anxiety disorder and sleep disorder in subjects with TN was higher than that of the controls during the follow-up [aHR: 2.85 (95 % confidence interval: 2.11–3.85), aHR: 2.98 (95 % confidence interval: 2.12–4.18) and aHR: 2.17 (95 % confidence interval: 1.48–3.19), respectively].ConclusionsTN might increase the risk of subsequent newly diagnosed depressive disorder, anxiety disorder, and sleep disorder, but not schizophrenia or bipolar disorder. Additional prospective studies are required to confirm these findings.

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Pain Psychiatry of Trigeminal Neuralgia

Kim

Schneider

2018

Effective Techniques for Managing Trigeminal Neuralgia

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In addition to the repeated episodes of paroxysmal, electrical facial pain classically associated with the disease, many patients with trigeminal neuralgia (TN) suffer from severe emotional distress. At present, there is no universally agreed pathophysiological explanation for the high incidence of depression and anxiety within this patient population. Despite the unclear understanding, the psychiatric comorbidities should be addressed as a part of comprehensive, multi-modal approach. Anticonvulsants or serotonin and norepineprhine reuptake inhibitors are viable pharmacological options that can supplement the currently used carbamazepine therapy. For medically refractory cases, surgical interventions are being suggested as effective alternatives in managing both the pain and the psychiatric complaints of TN. Examples include microvascular decompression, stereotactic radiosurgery, and repetitive transcranial magnetic stimulation. Continued research to understand TN should take into account the psychiatric burden in this population in order to promote a holistic treatment approach.

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Carbamazepine in Bipolar Disorder With Pain

Abstract: Carbamazepine was found to have strong preclinical data for the treatment of comorbid bipolar mood disorder and chronic pain disorders. While requiring more studies in this population, we propose that this treatment modality may benefit patients.

Cited by 3 publications

References 34 publications

Carbamazepine Attenuates Astroglial L-Glutamate Release Induced by Pro-Inflammatory Cytokines via Chronically Activation of Adenosine A2A Receptor

Carbamazepine Attenuates Astroglial L-Glutamate Release Induced by Pro-Inflammatory Cytokines via Chronically Activation of Adenosine A2A Receptor

Risk of psychiatric disorders following trigeminal neuralgia: a nationwide population-based retrospective cohort study

Pain Psychiatry of Trigeminal Neuralgia

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