Isoflurane blunts electroencephalographic and thalamic-reticular formation responses to noxious stimulation in goats

Joseph F. Antognini, Earl Carstens

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

Background: Anesthetics, including isoflurane, depress the electroencephalogram (EEG). Little is known about the quantitative effects of isoflurane on EEG and subcortical electrical activity responses to noxious stimulation. The authors hypothesized that isoflurane would depress the results of EEG and subcortical response to noxious stimulation at concentrations less than those needed to suppress movement. Furthermore, determination of regional differences might aid in elucidation of sites of anesthetic action. Methods: Ten goats were anesthetized with isoflurane, and minimum alveolar concentration (MAC) was determined using a noxious mechanical stimulus. Depth electrodes were inserted into the midbrain reticular formation and thalamus. Needle electrodes placed in the skull periosteum measured bifrontal and bihemispheric EEG. The noxious stimulus was applied at each of four anesthetic concentrations: 0.6, 0.9, 1.1, and 1.4 MAC. Results: At an isoflurane concentration of 0.6 MAC, the noxious stimulus activated the midbrain reticular formation, thalamic, and bifrontal- hemispheric regions, as shown by decreased high-amplitude, low-frequency power. For all channels combined (mean ± SD), total (-33 ± 7%), delta (-47 ± 12%), theta (-23 ± 12%), and alpha (-21 ± 6%) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 0.9 MAC, total (- 35 ± 5%), delta (-42 ± 7%), theta (-35 ± 8%), and alpha (-23 ± 11%) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 1.1 MAC only one site, and at 1.4 MAC, no site, had decreased power after the noxious stimulus. Conclusions: Isoflurane blunted EEG and midbrain reticular formation-thalamus activation response to noxious stimulation at concentrations (1.1 MAC or greater) necessary to prevent movement that occurred after noxious stimulation. It is unknown whether this is a direct effect or an indirect effect via action in the spinal cord.

Original languageEnglish (US)
Pages (from-to)1770-1779
Number of pages10
JournalAnesthesiology
Volume91
Issue number6
StatePublished - 1999
Externally publishedYes

Fingerprint

Reticular Formation
Isoflurane
Goats
Electroencephalography
Anesthetics
Thalamus
Electrodes
Periosteum
Skull
Needles
Spinal Cord
Midbrain Reticular Formation

Keywords

  • Anesthetic mechanisms
  • Pain
  • Spinal cord

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Isoflurane blunts electroencephalographic and thalamic-reticular formation responses to noxious stimulation in goats. / Antognini, Joseph F.; Carstens, Earl.

In: Anesthesiology, Vol. 91, No. 6, 1999, p. 1770-1779.

Research output: Contribution to journalArticle

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title = "Isoflurane blunts electroencephalographic and thalamic-reticular formation responses to noxious stimulation in goats",
abstract = "Background: Anesthetics, including isoflurane, depress the electroencephalogram (EEG). Little is known about the quantitative effects of isoflurane on EEG and subcortical electrical activity responses to noxious stimulation. The authors hypothesized that isoflurane would depress the results of EEG and subcortical response to noxious stimulation at concentrations less than those needed to suppress movement. Furthermore, determination of regional differences might aid in elucidation of sites of anesthetic action. Methods: Ten goats were anesthetized with isoflurane, and minimum alveolar concentration (MAC) was determined using a noxious mechanical stimulus. Depth electrodes were inserted into the midbrain reticular formation and thalamus. Needle electrodes placed in the skull periosteum measured bifrontal and bihemispheric EEG. The noxious stimulus was applied at each of four anesthetic concentrations: 0.6, 0.9, 1.1, and 1.4 MAC. Results: At an isoflurane concentration of 0.6 MAC, the noxious stimulus activated the midbrain reticular formation, thalamic, and bifrontal- hemispheric regions, as shown by decreased high-amplitude, low-frequency power. For all channels combined (mean ± SD), total (-33 ± 7{\%}), delta (-47 ± 12{\%}), theta (-23 ± 12{\%}), and alpha (-21 ± 6{\%}) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 0.9 MAC, total (- 35 ± 5{\%}), delta (-42 ± 7{\%}), theta (-35 ± 8{\%}), and alpha (-23 ± 11{\%}) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 1.1 MAC only one site, and at 1.4 MAC, no site, had decreased power after the noxious stimulus. Conclusions: Isoflurane blunted EEG and midbrain reticular formation-thalamus activation response to noxious stimulation at concentrations (1.1 MAC or greater) necessary to prevent movement that occurred after noxious stimulation. It is unknown whether this is a direct effect or an indirect effect via action in the spinal cord.",
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T1 - Isoflurane blunts electroencephalographic and thalamic-reticular formation responses to noxious stimulation in goats

AU - Antognini, Joseph F.

AU - Carstens, Earl

PY - 1999

Y1 - 1999

N2 - Background: Anesthetics, including isoflurane, depress the electroencephalogram (EEG). Little is known about the quantitative effects of isoflurane on EEG and subcortical electrical activity responses to noxious stimulation. The authors hypothesized that isoflurane would depress the results of EEG and subcortical response to noxious stimulation at concentrations less than those needed to suppress movement. Furthermore, determination of regional differences might aid in elucidation of sites of anesthetic action. Methods: Ten goats were anesthetized with isoflurane, and minimum alveolar concentration (MAC) was determined using a noxious mechanical stimulus. Depth electrodes were inserted into the midbrain reticular formation and thalamus. Needle electrodes placed in the skull periosteum measured bifrontal and bihemispheric EEG. The noxious stimulus was applied at each of four anesthetic concentrations: 0.6, 0.9, 1.1, and 1.4 MAC. Results: At an isoflurane concentration of 0.6 MAC, the noxious stimulus activated the midbrain reticular formation, thalamic, and bifrontal- hemispheric regions, as shown by decreased high-amplitude, low-frequency power. For all channels combined (mean ± SD), total (-33 ± 7%), delta (-47 ± 12%), theta (-23 ± 12%), and alpha (-21 ± 6%) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 0.9 MAC, total (- 35 ± 5%), delta (-42 ± 7%), theta (-35 ± 8%), and alpha (-23 ± 11%) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 1.1 MAC only one site, and at 1.4 MAC, no site, had decreased power after the noxious stimulus. Conclusions: Isoflurane blunted EEG and midbrain reticular formation-thalamus activation response to noxious stimulation at concentrations (1.1 MAC or greater) necessary to prevent movement that occurred after noxious stimulation. It is unknown whether this is a direct effect or an indirect effect via action in the spinal cord.

AB - Background: Anesthetics, including isoflurane, depress the electroencephalogram (EEG). Little is known about the quantitative effects of isoflurane on EEG and subcortical electrical activity responses to noxious stimulation. The authors hypothesized that isoflurane would depress the results of EEG and subcortical response to noxious stimulation at concentrations less than those needed to suppress movement. Furthermore, determination of regional differences might aid in elucidation of sites of anesthetic action. Methods: Ten goats were anesthetized with isoflurane, and minimum alveolar concentration (MAC) was determined using a noxious mechanical stimulus. Depth electrodes were inserted into the midbrain reticular formation and thalamus. Needle electrodes placed in the skull periosteum measured bifrontal and bihemispheric EEG. The noxious stimulus was applied at each of four anesthetic concentrations: 0.6, 0.9, 1.1, and 1.4 MAC. Results: At an isoflurane concentration of 0.6 MAC, the noxious stimulus activated the midbrain reticular formation, thalamic, and bifrontal- hemispheric regions, as shown by decreased high-amplitude, low-frequency power. For all channels combined (mean ± SD), total (-33 ± 7%), delta (-47 ± 12%), theta (-23 ± 12%), and alpha (-21 ± 6%) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 0.9 MAC, total (- 35 ± 5%), delta (-42 ± 7%), theta (-35 ± 8%), and alpha (-23 ± 11%) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 1.1 MAC only one site, and at 1.4 MAC, no site, had decreased power after the noxious stimulus. Conclusions: Isoflurane blunted EEG and midbrain reticular formation-thalamus activation response to noxious stimulation at concentrations (1.1 MAC or greater) necessary to prevent movement that occurred after noxious stimulation. It is unknown whether this is a direct effect or an indirect effect via action in the spinal cord.

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KW - Spinal cord

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