Download MBBS (Bachelor of Medicine, Bachelor of Surgery) Neuroanaesthesia PPT 13 Dexmedetomidine In Neuroanesthesia Lecture Notes
OVERVIEW
? Introduction.
? Role of Dexmedetomidine in clinical neurosurgical anaesthesia ?
?Cerebral Vascular Disease.
?Intracranial Tumor Surgery.
?Traumatic Brain Injury (TBI).
?Spinal Cord Injury.
?Intraoperative Neurophysiology Monitoring.
?Sedation in Paediatric Patients With Neurosurgical Diseases.
?Benefits of Analgesia in Neurosurgery.
?The Neurocritical Care Unit.
?Awake Craniotomy.
?Epilepsy Surgeries Requiring Intraoperative Mapping.
?Stereotactic Neurosurgery/Deep Brain Stimulation.
? Summary
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INTRODUCTION
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? Dexmedetomidine is a highly selective 2-adrenergic receptor agonist acting on central
presynaptic 2-receptors primarily in the pontine locus ceruleus and peripheral postsynaptic 2-
receptors on vascular smooth muscle.
? The 2-adrenergic receptor agonist dexmedetomidine has sedative, anxiolytic, analgesic, and
sympatholytic effects.
? The potential advantages are:
?Neuroprotection
?Minimal impact on neuronal function including less interruption of neurophysiological
monitoring
?No increase in intracranial pressure (ICP).
?In healthy subjects receiving dexmedetomidine, cerebral metabolic rate of oxygen
consumption (CMRO2) is decreased with CMRO2-CBF coupling unchanged, indicating that
brain tissue oxygen delivery is little affected
?Stable hemodynamics
?Opioid and anesthesia sparing effects
?Minimal respiratory depression and maintenance of airway reflexes and patency during
awake procedures.
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ROLE OF DEXMEDETOMIDINE IN CLINICAL
NEUROSURGICAL ANAESTHESIA
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CEREBRAL VASCULAR DISEASE
? Carotid endarterectomy (CEA):
?Patients frequently have concomitant peripheral vascular disease and other related
comorbidities, and are prone to hemodynamic fluctuations caused by surgical stimulation or
perioperative medications.
?Intraoperative hypotension and the reduction in CBF caused by dexmedetomidine can
potentially risk inadequate oxygen delivery that may necessitate the use of intracarotid shunts
during awake CEA (although a prospective case series showed that dexmedetomidine as the
primary sedative did not increase the incidence of shunts as compared with historical controls.
?Hypotensive episodes in the post anesthesia care unit after CEA, however, are more frequent
with dexmedetomidine, and patients may require more hemodynamic interventions.
?There is no direct clinical evidence that dexmedetomidine exacerbates impaired dynamic
cerebral vascular autoregulation in carotid artery stenosis.
?Similarly, there is no human evidence that dexmedetomidine worsens or causes cerebral
ischemia, although high-dose dexmedetomidine was found to be associated with ischemic brain
injury exacerbation in animals.
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? Intracranial aneurysm/ SAH/ AVM/ ICH:
?The relationship between CBF and CMRO2 is preserved when using dexmedetomidine in patients
with unruptured intracranial aneurysms or arterial venous malformation.
?In a small retrospective study, sedation after unruptured cerebral aneurysm clipping with
dexmedetomidine infusion (0.4 to 0.9 g/kg/h) showed comparable blood pressure to propofol
(0.5 to 5.0mg/kg/h), but with a lower heart rate.
?Sixty-six percent of dexmedetomidine sedated patients, however, required additional propofol
boluses to prevent agitation while intubated.
?In a recent case series of 12 patients, coil embolization of intracranial aneurysms was performed
successfully under monitored anesthesia care (MAC) with dexmedetomidine without adverse
hemodynamic or respiratory events.
?Nevertheless, these case series are retrospective and underpowered, and prospective
randomized trials are needed to elucidate the effectiveness and safety of adding
dexmedetomidine during intracranial aneurysm surgery, which requires systemic and cerebral
hemodynamic stability.
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?Animal studies of SAH with cerebral vasospasm have found that dexmedetomidine attenuated
brain edema, reduced vasospasm, and ameliorated neurological deficits.
?However, clinical neuronal protection related to dexmedetomidine use in patients with SAH has
not been confirmed.
?Animal studies have implied that after focal cerebral infarction, dexmedetomidine infusion
improved microregional oxygen supply/consumption balance, thereby decreasing cortical
infarction size with more cell survival compared with saline. This neuronal protective effect of
dexmedetomidine was stronger when combined with propofol or lidocaine.
?However, this neuroprotective effect in cerebral ischemia was not mediated by central -
adrenoceptors and not related to the inhibition of presynaptic norepinephrine or glutamate
release, but rather by inhibiting the stress hormone and inflammatory response, as well as
through activation of a signaling pathway of cell growth, proliferation, and survival.
?In response to stroke, certain inflammatory mediators and stress hormones are activated, which
can be inhibited by dexmedetomidine based on preclinical studies.
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INTRACRANIAL TUMOR SURGERY
? Dexmedetomidine prevents sudden increases in ICP and brain swelling.
? As an anesthetic adjuvant results in less cardiovascular variability during operations and an early
emergence.
? In a prospective randomized controlled trial, infusing dexmedetomidine at 0.7 g/kg/h as an
adjunct to propofol-fentanyl anesthesia in this setting improved hemodynamic stability and
reduced fentanyl and antihypertensive agent consumption.
? A systematic review of 254 patients from 5 randomized controlled trials involving functional
endoscopic sinus surgery found that dexmedetomidine provided better surgical visibility than
saline control or sevoflurane alone as its hypotensive action and hemodynamic stability reduced
intraoperative bleeding, although the quality of the operative field was similar among
dexmedetomidine, esmolol, and remifentanil groups.
? In a recent randomized controlled trial, 4 commonly used anesthetic agents for neurosurgery with
different mechanisms of action (midazolam, propofol, fentanyl, and dexmedetomidine) were
titrated to an equivalent mild sedation in patients with supratentorial mass lesions before any
surgical intervention. Dexmedetomidine compared with the other agents resulted in a much
lower incidence of unmasked or exacerbated neurological deficits.
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? A recent animal study found 2-adrenoceptor expression in C6 glioma cells (a malignant glioma
cell line), so that dexmedetomidine may have an interaction with the tumor through regulating
multiple molecular signal pathways and directly activating 2-adrenoceptors in gliomas.
? This seems to indicate that the "response" of tumors to anesthetics is strongly associated with the
tumors' histologic properties.
? Therefore, to evaluate dexemedetomidine's effects on neurological outcome in brain tumor
patients, extensive disease-centered studies with carefully defined clinical phenotypes are
needed.
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TRAUMATIC BRAIN INJURY (TBI)
? Sedation in TBI may have therapeutic significance besides facilitating airway control.
? The purpose of sedation in TBI includes optimizing CMRO2 and CBF, reducing elevated ICP, and
preventing secondary brain injury.
? In a retrospective case series, in which 85 severe TBI patients in the intensive care unit (ICU)
received a median dose of dexmedetomidine of 0.49 g/kg/h for 32 hours (median infusion
period) to maintain "cooperative sedation," midazolam and propofol requirements nearly
disappeared indicating the effectiveness of dexmedetomidine as the sole agent for mild sedation
for TBI patients.
? Another prospective study observed 198 severe TBI patients who received dexmedetomidine
and/or propofol sedation. Dexmedetomidine was associated with longer "calm to light
sedation" targets compared with propofol alone in the first 7 days after infusion.
? Although dexmedetomidine was associated with a higher degree of hypotension compared with
propofol, there were no differences in adverse events between the groups.
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? A case report of an alcohol-dependent TBI patient showed that dexmedetomidine as a
continuous infusion (0.5 to 1.5 g/kg/h for 8 d) facilitated sedation and controlled agitation
when benzodiazepine treatment failed, without neurological or respiratory depression.
? Systemic hypotension or hypertension can be disastrous for TBI patients with impaired cerebral
autoregulation because it can decrease cerebral perfusion pressure, increase ICP, and lead to
poor clinical outcomes.
? Moderate to severe TBI patients may also suffer paroxysmal sympathetic hyperactivity (PSH) due
to elevated ICP, which presents with elevated heart rate, blood pressure, respiratory rate,
temperature, sweating, and posturing.
? A case report showed that 0.2 to 0.7 g/kg/h dexmedetomidine continuous infusion effectively
controlled this syndrome when routine medication therapy failed.
? Another retrospective study included 90 severe TBI patients who received dexmedetomidine or
propofol/midazolam sedation in the neuro ICU for consecutive days, and found that the
dexmedetomidine regimen group had a lower probability to be diagnosed with PSH.
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SPINAL CORD INJURY
? Recent animal studies have found that intravenous dexmedetomidine attenuated spinal ventral
neuronal degeneration and preserved neurological function and neuronal viability after
transient spinal cord ischemia or ischemia-reperfusion.
? These beneficial effects were associated with improved cell survival and antiapoptotic factors, as
well as with the attenuation of microglial activation, proinflammatory cytokine production,
decreased interleukin-6, tumor necrosis factor-alpha, and reduced neutrophil infiltration, all of
which indicate an anti-inflammatory effect.
? Clinically, there is no direct evidence of improved functional outcome by virtue of
dexmedetomidine's theoretical spinal cord protective or anti-inflammatory effects.
? In a single case of a focal inflammatory spinal cord disorder, namely transverse myelitis,
hemodynamic instability was reported as the major concern response. In that case,
dexmedetomidine sedation resulted in severe hypertension and bradycardia, which may have
been due to an exaggerated peripheral vasoconstrictor response due to the lack of spinal reflexes.
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? In terms of injury biomarkers, a prospective study found reduced levels of the stress hormone
cortisol and the inflammatory response marker interleukin-10 after intraoperative
dexmedetomidine infusion in cervical spine surgery.
? However, those stress response biomarkers and cytokine concentrations could not be correlated
with any postoperative functional recovery parameter.
? Although dexmedetomidine does not attenuate the injury in patients with cervical cord lesions,
its practical use lies perhaps in helping to prevent secondary injury by facilitating awake
fiberoptic intubation.
? A subsequent randomized controlled trial related to the performance of awake fiberoptic
intubation in simulated cervical injury patients found that adding dexmedetomidine sedation (1
g/kg bolus over 10min followed by 0.5 to 0.7 g/ kg/h) did not compromise hemodynamic
instability and resulted in better patient tolerance and satisfaction compared with the use of
midazolam alone.
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INTRAOPERATIVE NEUROPHYSIOLOGY MONITORING
? Intraoperative neurological injuries are usually detected as changes in the latencies or
amplitudes of evoked potentials (EPs).
? As such, intraoperative EP monitoring in spine surgeries should preferably be minimally affected
by the anesthetic regimen.
? Dexmedetomidine has been increasingly used to reduce the requirement of other anesthetics
that may impair EP signal acquisition, and its effects on EPs have been observed and investigated
thoroughly in spine surgery.
? SSEPs are generally well maintained under dexmedetomidine (0.2 to 0.7 g/kg/h) during spine
surgeries, with retention of the ability to monitor consistent and reproducible potentials.
? For motor evoked potentials (MEPs), most clinical studies found that clinically relevant doses of
dexmedetomidine also do not affect the signal, but patients receiving a higher loading dose (1
g/kg) or with a higher plasma concentration (0.8 ng/mL) do experience MEP amplitude
reduction or even signal loss.
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? Of note, all currently available evidence regarding the effects of dexmedetomidine on EPs stems
from spine surgeries.
? The impact of dexmedetomidine on EPs in the setting of different neuronal pathologic diseases
may vary, especially for those with impaired cerebrospinal tracts.
? As for intracranial surgeries, knowledge of how dexmedetomidine affects EP acquisition and the
latencies and amplitudes of MEPs and SSEPs for intracranial tumor or cerebrovascular pathologies
is lacking.
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SEDATION IN PEDIATRIC PATIENTS WITH NEUROSURGICAL DISEASES
? Sedation is usually required for imaging studies (eg,magnetic resonance imaging [MRI], computed
tomography [CT]) in pediatric patients.
? Separation, confinement, and an unfamiliar environment create agitation and anxiety for
children, and in situations in which general anesthesia may not be preferred, effective sedation
with minimal respiratory depression is highly beneficial.
? A previous review extensively summarized early clinical studies of using dexmedetomidine as the
primary or rescue sedative during MRI or CT examination in pediatric populations.
? In this review, dexmedetomidine was superior to midazolam but inferior to propofol in
providing effective sedation, and this may be because propofol led to fewer procedure
interruptions and better parental satisfaction according to a comparison study of 1- to 7-year old
children undergoing MRI with propofol or dexmedetomidine sedation.
? Furthermore, the recovery time was slower in the dexmedetomidine cohort compared with
those who received propofol.
? However, the dosage of dexmedetomidine ranged widely, from 0.3 to 2 g/kg bolus over 10 to
15 minutes followed by 0.5 to 1.5 g/kg/h infusion rate, and there was no optimal dosage
identified.
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? For outpatient EEG monitoring in children, intravenously administered dexmedetomidine
provides effective sedation without agitation, hemodynamic fluctuation, or respiratory
depression, and was superior to midazolam in terms of minimum "drug effect" on the quality of
acquired EEG.
? Sedation for intracranial radiotherapy for a 21-month old child was reported to be safely
achieved with dexmedetomidine sedation, providing a smooth sedation "induction" and fairly
rapid recovery with airway protection.
? Perioperative infusion of dexmedetomidine at 0.2 g/kg/h as an adjunct sedative reduced
sevoflurane-related emergence delirium in children aged 1 to 10 years.
? Clinical research defining the optimal dosing strategy and duration of dexmedetomidine infusion
for sedation in pediatric TBI is lacking.
? Notably, dexmedetomidine was reported to be associated with significant bradycardia during
therapeutic hypothermia when combined with remifentanil for sedation in children with TBI.
? Despite the few animal studies there is a lack of clinical evidence regarding the potential
neuronal protective or toxic effects of dexmedetomidine in developing human brains following
neurological injury, or how dexmedetomidine affects CBF, CMRO2, and ICP in children.
? Further translational studies and clinical evidence are needed.
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BENEFITS OF ANALGESIA IN NEUROSURGERY
? Postoperative pain following craniotomy or spinal surgery may be significant and can lead to
postoperative agitation and hypertension, which should be properly managed to minimize
potential intracerebral haemorrhage and/or vasogenic edema.
? Opioids are effective in controlling pain but may cause respiratory depression.
? Dexmedetomidine can maintain airway reflexes and patency in spontaneously breathing
patients while providing analgesic effects.
? A previous meta-analysis included eight small sample size randomized controlled trials and found
that dexmedetomidine reduced intraoperative opioid consumption during intracranial
procedures, although the administration time and dose were variable among the included studies.
? Subsequent randomized controlled trials demonstrated that infusion of dexmedetomidine
between 0.2 and 0.7 g/kg/h during and after the operation reduced postoperative pain after
craniotomy and spine surgeries.
? It should be noted that Dexmedetomidine analgesic effect was not as potent as that of
remifentanil, and those receiving dexmedetomidine had longer emergence times.
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? To avoid such delayed emergence, a particular study made use of a 0.4 or 0.8 g/kg bolus of
dexmedetomidine for 10 minutes 1 h before the end of supratentorial craniotomy, with its
secondary outcome showing less postsurgical pain compared with control during emergence and
after transport to the ICU.
? The analgesic efficacy of dexmedetomidine has also been shown in studies in spine surgery,
mainly lumbar laminectomy, discectomy, or posterior lumbar interbody fusion. For spinal
tumor surgery, no retrospective or prospective study of dexmedetomidine's analgesic efficacy
was identified.
? Compared with oral clonidine premedication, dexmedetomidine possesses a noninferior opioid
and anesthetic-sparing effect, and equal postoperative recovery time, hemodynamic stability, and
blood loss during spine surgery.
? A randomized controlled trial study found that intraoperative dexmedetomidine infusion at 0.5
g/kg/h compared with saline improved the quality of recovery and reduced fatigue in the early
postoperative period after major spine surgery, when continuously infusing 0.2 g/kg/h for
another 24 hours postoperatively.
? The effectiveness of dexmedetomidine as an analgesic was demonstrated both when given as an
intravenous infusion and as an epidural injection.
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? Neither for craniotomy nor for spinal surgery has a standard dexmedetomidine administration
strategy been established with regards to dose, time of initiation, duration, and combination with
other drugs.
? Moreover, the intensity of pain varies with different craniotomy approaches, for example,
supratentorial craniotomies are associated with less pain than infratentorial procedures.
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THE NEUROCRITICAL CARE UNIT
? It is exceptionally important in the neurosurgical population to control agitation and provide
analgesia, so as to improve tolerance to mechanical ventilation and accelerate time to extubation
in order to maintain intracranial homeostasis and enable early neurological assessment.
? A recent well-designed randomized controlled trial compared the infusion of dexmedetomidine
for <7 days with saline in a propofol-based sedation regimen in the general ICU (including only a
few neurosurgical patients) in patients with agitated delirium and requiring mechanical
ventilation. This study found that dexmedetomidine facilitated early extubation and was
associated with more ventilator-free hours.
? Another randomized control trial enrolled 150 craniotomy patients who were not extubated
when admitted to the neuro ICU, where dexmedetomidine infusion at 0.6 g/kg/h was initiated 2
hours after craniotomy and up until 30 minutes after extubation, or for a maximum 24 hours.
Patients who received dexmedetomidine demonstrated a decreased incidence of agitation
compared with the saline group.
? Most studies do demonstrate a significant reduction of opioid requirement when using
dexmedetomidine, and this analgesic effect may be an important reason for less agitation and
better ventilator tolerance neurocritical care patients receiving continuous sedation.
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? A retrospective propensity-matched cohort data analysis of 342 patients from 2 medical centers
showed that dexmedetomidine and propofol were associated with an equal prevalence of
hypotension (defined as MAP <60 mmHg, 23% vs. 26%) and bradycardia (defined as heart rate
<50 beats/min, 8.6% vs. 5.5%).
? However, other studies frequently demonstrate that dexmedetomidine is more commonly
associated with bradycardia, which requires close attention, especially with higher doses and
longer durations of infusion, as are used when weaning off other sedatives in the neurocritical
care unit.
? A prospective study found that dexmedetomidine improved cognitive function in neuro ICU for
patients without forebrain injury compared with propofol, which reduced cognitive function. This
was attributed to the better antiagitation and analgesic effects of dexmedetomidine
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AWAKE CRANIOTOMY
? Awake craniotomy is performed in patients with intracranial lesions in or near eloquent brain
areas requiring cortical mapping and intraoperative neurofunctional testing to maximize
resection while reducing risk of disability.
? Two different anesthesia management regimens are advocated:
?The "asleep-awake-asleep" technique in which endotracheal intubation or laryngeal mask airway
placement is performed for the asleep portions of the procedure, and
?The "awake-awake-awake" technique in which mild sedation without invasive airway
manipulation is used during the pre-mapping and post-mapping phases.
? Local anesthetic infiltration to the incision site and/or a scalp block is generally used with both
approaches.
? Special anesthesia considerations during the "awake" portion of any such procedure include the
need for cooperative sedation and sufficient analgesia without respiratory depression, as well
as the need for minimal interference with neurofunctional testing or cortical mapping.
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? Solely propofol-based sedation with an unprotected airway in "asleep-awake-asleep"
craniotomy, compared with general anesthesia, carries the concerns of a higher incidence of
respiratory depression in obese patients, arterial haemoglobin desaturation, a higher level of
PaCO2, hypertension, hypotension, and tachycardia.
? Dexmedetomidine reported as a useful adjuvant during "awake" state sedation, or even as an
effective rescue sedative when a propofol-remifentanil regimen results in oversedation,
respiratory depression, or discomfort.
? Other case reports have demonstrated that planned endotracheal intubation or laryngeal mask
airway placement was able to be avoided outright with the use of dexmedetomidine.
? In high-risk patients with airway compromise and severe comorbidities, continuous infusion of
dexmedetomidine (0.5 to 1.0 g/kg loading dose followed by 0.2 to 0.7 g/kg/h infusion) as the
primary sedative combined with scalp nerve block and small doses of opioid was reported to
facilitate prolonged and complex "awake" procedures without any airway manipulation required.
? Dexmedetomidine was well-tolerated in obstructive sleep apnea patients who needed
continuous positive airway pressure during awake craniotomy.
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? A recent prospective, randomized study compared dexmedetomidine to propofol-remifentanil
based conscious sedation in awake craniotomy for supratentorial tumor resection, in which the
incidence of respiratory depression or airway obstruction was 20% with propofol-remifentanil
sedation versus zero in the dexmedetomidine group.
? Nevertheless, both strategies achieved the same efficacy of sedation and ability to provide
adequate conditions for intraoperative mapping.
? To avoid neurofunctional testing failure, dexmedetomidine is usually discontinued or reduced to
0.1 to 0.2 g/kg/h 10 to 20 minutes before mapping/testing and then resumed afterward.
? There is no evidence that the intraoperative conditions for testing provided by any sedative,
including dexmedetomidine or propofol, can be linked to better or worse postoperative
neurological outcomes.
? In a particular case, dexmedetomidine was successfully used for awake craniotomy in a pregnant
patient with oligoastrocytoma without notable maternal or fetal adverse effects, its success being
attributed to its central sedative and analgesic effects.
? However, the safety of using dexmedetomidine in the obstetric population is still unclear.
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EPILEPSY SURGERIES REQUIRING INTRAOPERATIVE MAPPING
? Localization of seizure foci and monitoring of brain function in epilepsy surgeries are crucial, and
these are usually achieved by use of the electroencephalogram (EEG) and/or
electrocorticography (ECoG).
? As these monitoring modalities are readily affected by most anesthetic agents, understanding the
benefits and drawbacks of dexmedetomidine and its interaction with EEG/ECoG monitoring in the
epilepsy population is important.
? For example, a reduced seizure threshold caused by dexmedetomidine might result in a false-
positive leading to an "over-aggressive" resection, while abolished epileptiform discharges may
cause a false-negative and result in surgical resection being aborted.
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? As dexmedetomidine has the property of reducing central noradrenergic transmission, early
studies proposed proconvulsant effects of dexmedetomidine and seizure threshold reduction.
? Conversely, in other animal models, dexmedetomidine increased seizure threshold.
? This inconsistency may stem from seizure architectures involving different neurotransmitter
pathways that may be modulated by dexmedetomidine to generate proconvulsant or
anticonvulsant effects.
? The interaction between dexmedetomidine and different central nerve system excitatory agents
implies disparate impacts on EEG interpretation.
? Although ECoG and EEG are well preserved as a whole and no major adverse clinical effects have
been described following dexmedetomidine, there have been cases exhibiting increased seizure
foci activity thereby challenging the suggestion that dexmedetomidine has anticonvulsant effects
in humans.
? While it remains unclear why the effects of dexmedetomidine on epileptiform activity are
variable, drug combinations, individual phenotypes, and preexisting neurological deficits may all
be contributing factors.
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? Small case series describe clinical experience with dexmedetomidine in adult patients undergoing
resection of epileptogenic foci, and report satisfactory operating conditions without a reduction
in epileptiform activity, the ability to obtain ECoG information, or the ability to perform cortical
mapping.
? In general, a "low dose" is recommended, whereby administration can be started with a bolus
of 0.3 to 0.5 g/kg over 10 minutes followed by an infusion of 0.2 to 0.5 g/kg/h, remembering
that individual infusion rates vary.
? It is important to note, however, that patients with seizure disorders taking P450 enzyme?
inducing anticonvulsant medications (eg, phenytoin and carbamazepine) have an increased
plasma clearance of dexmedetomidine, indicating that higher doses might be necessary to
maintain the desired sedation level.
? While dexmedetomidine has been successfully used as an adjuvant during epilepsy surgeries,
future randomized controlled trials will be necessary to determine its proconvulsant or
anticonvulsant effects, especially in terms of dosing, drug combination, and interaction with
specific seizure characteristics in both the adult and pediatric populations.
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STEREOTACTIC NEUROSURGERY/DEEP BRAIN STIMULATION
? Stereotactic neurosurgeries such as deep brain stimulator (DBS) placement are treatments for
patients with neurological movement disorders, for example, Parkinson disease (PD), Tourette
Syndrome, or Obsessive-Compulsive Disorder.
? The subthalamic nucleus, globus pallidus interna, and ventralis intermedius nucleus of the
thalamus are the 3 common target areas.
? The anesthetic considerations include an awake and cooperative patient, stable hemodynamics,
maintenance of ventilation, airway reflexes and patency due to limited airway access because of
a head frame, as well as minimizing anesthetic interference with microelectrode recordings
(MER) and macrostimulation.
? Propofol is commonly used as the sole sedative during DBS placement under MAC, and these
cases may include scalp blocks and/or local anesthesia with a background infusion of short acting
sedatives and narcotics (eg, remifentanil) during the procedure.
? Propofol can decrease subthalamic nucleus activity and interfere with MER, although this
interference can be terminated rapidly by stopping its administration.
? This suppression is mediated by GABA inhibitory pathways in the subthalamic nucleus and
globus pallidus that contain abundant GABAergic innervations.
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? To avoid this, dexmedetomidine has been suggested as an alternative sedative agent.
? It has been reported that dexmedetomidine (1.5 g/kg bolus over 20 min followed by 0.2 to 0.5
g/kg/h infusion) effectively controlled propofol-induced dyskinesia during bilateral subthalamic
nucleus DBS placement without adverse effect on MER.
? Dexmedetomidine has been shown to possess other advantages in DBS surgeries ?
?Easily arousable sedation
?Good patient cooperation
?No respiratory depression
?Anxiolytic
?Inhibit agitation and stress in prolonged surgery.
?Maintenance of hemodynamic stability.
? A 3-year retrospective study compared DBS surgeries performed with 0.3 to 0.8 g/kg/h
dexmedetomidine infusion titrating to Observer Assessment of Alertness and Sedation scale 4
versus patients without sedation, and found that dexmedetomidine not only protected
electrophysiological mapping but also provided better hemodynamic stability.
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? Lower infusion rates of dexmedetomidine are recommended for DBS surgery.
? High-dose ( >0.8 g/kg/h) infusion should be avoided for several reasons ?
?Oversedation (bispectral index< 80) may abolish MER by suppressing neuronal firing,
decreasing background electrical activity and spike amplitudes, and thus delaying the
commencement of MER or causing failure to guide electrode placement.
?Risk of respiratory suppression, especially in patients with obstructive sleep apnea.
?Clinically significant bradycardia.
? Anxiety and failure to cooperate are more frequent in pediatric awake stereotactic
neurosurgeries, thus hampering the procedure and increasing the risk of intracerebral bleeding.
? A combination of dexmedetomidine and propofol infusion in pediatric DBS placement provided a
safe, efficacious, and well-tolerated sedation with minimal respiratory depression.
? The combination of three non-GABAergic agents (dexmedetomidine, ketamine, and opioids) in
pediatric DBS surgery might be an optional anesthesia strategy to preserve MERs
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SUMMARY
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? The prevailing thought is that dexmedetomidine may be associated with ?
?Less cerebral hemodynamic perturbation,
?Minimal neurophysiological monitoring interference,
?Greater ability to achieve cooperative sedation without respiratory compromise in awake
procedures, and
?Acceptable pain control (alone or in combination with more potent analgesics).
? Low-range to mid-range infusion doses of dexmedetomidine seem to exert the above benefits in
perioperative neurosurgical care based on some current clinical evidence, although very notably
there is yet no standard dexmedetomidine administration strategy for these indications.
? Dexmedetomidine may result in severe bradycardia and hypotension and hence, should be used
very cautiously in patients.
? It is not a potent analgesic in its own right, but rather should be considered as an adjunct to a
"true" analgesic, such as an opioid. remain.
? It is unclear whether it is proconvulsant or anticonvulsant, or how it affects EPs in different
cerebral pathologies, and there is a lack of clinical evidence regarding neuronal protection or
toxicity following neuronal injury in both children and adults.
? Further disease-based translational studies are required to understand both short-term and long-
term neurological and neurocognitive outcomes after dexmedetomidine administration.
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THANK YOU
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This post was last modified on 07 April 2022