Anesthesia and analgesia
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Anesthesia and analgesia · Jun 2004
Case ReportsIntracranial hypotension caused by cervical cerebrospinal fluid leak: treatment with epidural blood patch.
This report describes treatment with cervical epidural blood patch of low cerebrospinal fluid (CSF) pressure headache resulting from spontaneous CSF leak via a tear in a cervical dural cuff. The leak was diagnosed by a dynamic computed tomography (CT)-myelography study followed by gadolinium enhanced magnetic resonance imaging(MRI)-scan. The epidural needle was inserted with the aid of image intensifier and CT-scan to guide the needle to the precise site of the CSF leak. Blood mixed with gadolinium was injected, and subsequent MRI scanning provided the first description of spread of blood after cervical epidural blood patch. ⋯ Low cerebrospinal fluid (CSF) pressure may cause severe posturally-related headache. In the patient, a vertebral disc protrusion in the neck seems to have contributed to a CSF leak. An injection of blood into the epidural space at the precise site of the CSF leak was followed by complete and lasting resolution of the headache.
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Anesthesia and analgesia · Jun 2004
Comparative StudyIsoflurane reduces glutamatergic transmission in neurons in the spinal cord superficial dorsal horn: evidence for a presynaptic site of an analgesic action.
The minimum alveolar concentration (MAC) of a volatile anesthetic defines anesthetic potency in terms of a suppressed motor response to a noxious stimulus. Therefore, the MAC of an anesthetic might in part reflect depression of motor neuron excitability. In the present study we evaluated the effect of isoflurane (ISO) on neurons in the substantia gelatinosa driven synaptically by putative nociceptive inputs in an in vitro spinal cord preparation of the rat. Whole-cell patch-clamp recordings were performed in neurons with their soma in the substantia gelatinosa of transverse rat spinal cord slices. We investigated the effect of ISO on excitatory postsynaptic currents (EPSC) evoked by dorsal root stimulation (eEPSC), spontaneous (sEPSC), and miniature (mEPSC) EPSC. ISO reversibly reduced the amplitude of eEPSC to 39% +/- 22% versus control. ISO decreased the frequency of sEPSC and mEPSC to 39% +/- 26% and 63% +/- 7%. Neither the amplitudes nor the kinetics of mEPSC and sEPSC were altered by ISO. We conclude that ISO depresses glutamatergic synaptic transmission of putative nociceptive primary-afferent inputs, presumably by reducing the release of the excitatory transmitter. This effect may contribute to an antinociceptive action of volatile anesthetics at the spinal cord level. ⋯ The present electrophysiological in vitro experiments provide evidence that the volatile anesthetic isoflurane reduces excitatory transmitter release at the first site of synaptic integration of nociceptive inputs, the spinal cord superficial dorsal horn. This effect may contribute to the anesthetic action of volatile anesthetics at the spinal cord level.
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Anesthesia and analgesia · Jun 2004
Case ReportsDiagnosis of intracranial arterial stenosis using transcranial Doppler flowmetry.
In this case report we describe the use of transcranial Doppler flowmetry during induction of anesthesia in a patient with a large pituitary tumor. In this patient, both IV anesthesia induction and onset hyperventilation were followed by severe decreases of flow velocity in the middle cerebral artery of the affected side. Transcranial Doppler detected critical blood flow reduction in response to anesthesia induction and onset of hyperventilation in a brain tumor patient.
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Anesthesia and analgesia · Jun 2004
Comparative StudyThe effects of local pentoxifylline and propentofylline treatment on formalin-induced pain and tumor necrosis factor-alpha messenger RNA levels in the inflamed tissue of the rat paw.
We sought to determine whether local administration of pentoxifylline (PTF) or propentofylline (PPTF), which hinders cytokine production, influences pain threshold and formalin-induced pain behavior in rats or the level of tumor necrosis factor-alpha (TNF-alpha) messenger RNA (mRNA) concentrations in the inflamed paw tissue. PTF (0.5, 1, or 2 mg) and PPTF (1 or 2 mg) injected intraplantarly (i.pl.) had no significant effect on pain threshold. Injection of 0.1 mL of a 12% formalin solution subcutaneously into the dorsal surface of the left hindpaw induced pain behavior (47.6 +/- 4.6 incidents per 5 min), and PTF injected at doses of 1 and 2 mg/100 microL i.pl. before (but not after) formalin was effective in antagonizing (33.6 +/- 2.5 and 23.6 +/- 3.4 incidents per 5 min, respectively) formalin-induced pain behavior. A similar antagonistic effect was observed after PPTF treatment at a dose of 2 mg/100 microL; however, in contrast to PTF, at a later time point (85-90 min) after the formalin challenge, this effect was independent of the scheme of PPTF administration, before or after formalin. The effect of PTF on formalin-induced pain behavior did not parallel paw volume as measured by plethysmometer; however, PTF per se significantly increased the paw volume. Formalin injection significantly increased the TNF-alpha mRNA level in the inflamed tissue of the rat hind paw (150%). PTF administered before, but not after, formalin significantly antagonized (by approximately 40%) the observed increase in the level of TNF-alpha mRNA. Our study demonstrates and provides biochemical evidence that preemptive inhibition of proinflammatory cytokine synthesis by the use of PTF and PPTF, phosphodiesterase, and glial activation inhibitors is useful in antagonizing hyperalgesia in formalin-induced pain. Moreover, local administration of PTF may be a valuable approach to the treatment of inflammatory pain. ⋯ This study demonstrates and provides biochemical evidence that preemptive inhibition of proinflammatory cytokine synthesis by local administration of pentoxifylline and propentofylline is useful in antagonizing hyperalgesia in formalin-induced pain. Moreover, local administration of pentoxifylline could be regarded as a valid approach to the treatment of inflammatory pain.