Psychiatric agents and implications for perioperative analgesia

Catalani, Blas; Hamilton, Craig S.; Herron, Edwin W.; Urman, Richard D.; Fox, Charles J.; Kaye, Alan D.

doi:10.1016/j.bpa.2014.05.001

Cited by 18 publications

(24 citation statements)

References 63 publications

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“…Previous studies provided evidence showing that pain insensitivity in SCZ was independent of antipsychotic effects: (1) pain insensitivity in SCZ patients was reported before the introduction of antipsychotics (Hall & Stride, ; Marchand et al, ); (2) pain sensitivity was similarly reduced in both antipsychotic‐free and medicated patients (Potvin et al, ; Stubbs, Vancampfort, et al, ); (3) diminished pain sensitivity was observed in first‐degree relatives of SCZ patients (Hooley & Delgado, ). Nevertheless, these studies are rare and the antipsychotic effects on sensory perception are frequently addressed by pharmacologist (Catalani et al, ; Schreiber, Getslev, Backer, Weizman, & Pick, ). Thus, further studies on unmedicated patients are needed.…”

Section: Discussionmentioning

confidence: 99%

“…(2) pain sensitivity was similarly reduced in both antipsychotic-free and medicated patients (Potvin et al, 2008;; (3) diminished pain sensitivity was observed in firstdegree relatives of SCZ patients (Hooley & Delgado, 2001). Nevertheless, these studies are rare and the antipsychotic effects on sensory perception are frequently addressed by pharmacologist (Catalani et al, 2014;Schreiber, Getslev, Backer, Weizman, & Pick, 1999). Thus, further studies on unmedicated patients are needed.…”

Section: Limitations and Future Directionsmentioning

confidence: 99%

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A modality‐specific dysfunction of pain processing in schizophrenia

Zhou

Liang

et al. 2019

Human Brain Mapping

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Clinical observations showed that schizophrenia (SCZ) patients reported little or no pain under various conditions that are commonly associated with intense painful sensations, leading to a higher risk of morbidity and mortality. However, this phenomenon has received little attention and its underlying neural mechanisms remain unclear. Here, we conducted two experiments combining psychophysics, electroencephalography (EEG), and functional magnetic resonance imaging (fMRI) techniques to investigate neural mechanisms of pain insensitivity in SCZ patients. Specifically, we adopted a stimulus–response paradigm with brief stimuli of different sensory modalities (i.e., nociceptive, non‐nociceptive somatosensory, and auditory) to test whether pain insensitivity in SCZ patients is supra‐modal or modality‐specific, and used EEG and fMRI techniques to clarify its neural mechanisms. We observed that perceived intensities to nociceptive stimuli were significantly smaller in SCZ patients than healthy controls, whereas perceived intensities to non‐nociceptive somatosensory and auditory stimuli were not significantly different. The behavioral results were confirmed by stimulus‐evoked brain responses sampled by EEG and fMRI techniques, thus verifying the modality‐specific nature of the modulation of nociceptive information processing in SCZ patients. Additionally, significant group differences were observed in the spectral power of alpha oscillations in prestimulus EEG and the seed‐based functional connectivity in resting‐state fMRI (seeds: the thalamus and periaqueductal gray that are key nodes in ascending and descending pain pathways respectively), suggesting a possible contribution of cortical–subcortical dysfunction to the phenomenon. Overall, our study provides insight into the neural mechanisms of pain insensitivity in SCZ and highlights a need for systematic assessments of their pain‐related diseases.

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Section: Discussionmentioning

confidence: 99%

Section: Limitations and Future Directionsmentioning

confidence: 99%

A modality‐specific dysfunction of pain processing in schizophrenia

Zhou

Liang

et al. 2019

Human Brain Mapping

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“…This antiplatelet effect enhances this effect caused by nonsteroidal anti-inflammatory drugs (NSAIDs) and increases bleeding risk in patients taking warfarin and other nonvitamin K antagonist oral anticoagulants (NOACs). 1,6,[9][10][11][12] Serotonin is released by platelets and plays a role in their aggregation and clot formation. There may be less serotonin available for uptake by platelets with concomitant SSRI and SNRI use ( Figure 2).…”

Section: Bleeding and Antidepressantsmentioning

confidence: 99%

“…There may be less serotonin available for uptake by platelets with concomitant SSRI and SNRI use ( Figure 2). 9,11,13 Additionally, serotonin reuptake inhibition may also cause a decrease in serotonin receptor density on the platelet surface. 13 Patients taking SSRIs have a three-fold increased risk of a serious upper gastrointestinal (GI) bleeds.…”

Section: Bleeding and Antidepressantsmentioning

confidence: 99%

“…21 Agents capable of increasing serotonin levels and precipitating serotonin syndrome include antidepressants (SSRIs, SNRIs, TCAs, MAOIs) alone or in combination with other proserotonergic medications such as phenylpiperidine opioids (particularly meperidine, but potentially fentanyl and its derivatives) tramadol, dextromethorphan, ondansetron, metoclopramide, methylene blue, erythromycin, metronidazole, the antimigraine medications ''triptans,'' selegiline, the second generation (atypical) antipsychotics (eg, aripiprazole, clozapine, olanzapine, quetiapine, risperidone) St. John's wort, and 3,4-methylenedioxy-methamphetamine (MDMA or ecstasy). 1,3,9,12,[14][15][16]20,[22][23][24] It should be noted that serotonin antagonists, such as the 5-HT 3 antagonist antiemetics, may inhibit binding of serotonin to this subset of receptors thus increasing availability of serotonin to other serotonin receptors. In this way, serotonin syndrome may be precipitated.…”

Section: Serotonin Syndromementioning

confidence: 99%

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Anesthetic Considerations for Patients on Antidepressant Therapy – Part II

Saraghi

Golden

Hersh

2018

Anesthesia Progress

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Millions of patients take antidepressant medications in the United States for the treatment of depression or anxiety disorders. Some antidepressants are prescribed off-label to treat problems such as chronic pain, low energy, and menstrual symptoms. Antidepressants are a broad and expansive group of medications, but the more common drug classes include tricyclic antidepressants, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and monoamine oxidase inhibitors. A miscellaneous or "atypical" category covers other agents. Some herbal supplements that claim to have antidepressant activity will also be discussed. Part I of this series reviewed antidepressant pharmacology, adverse effects, and drug interactions with adrenergic agonists. In part II, drug-drug interactions with sedation and general anesthetics, bleeding effects, and serotonin syndrome will be discussed.

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Pharmacology of Psychiatric and Neurologic Drugs

Robbins

2024

Contemporary Dental Pharmacology

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Psychiatric agents and implications for perioperative analgesia

Cited by 18 publications

References 63 publications

A modality‐specific dysfunction of pain processing in schizophrenia

A modality‐specific dysfunction of pain processing in schizophrenia

Anesthetic Considerations for Patients on Antidepressant Therapy – Part II

Pharmacology of Psychiatric and Neurologic Drugs

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