Functional Neurosurgery

Jaimie M. Henderson MD¹

Paul R. Gigante MD¹

Lawrence M. Shuer MD¹

Richard A. Jaffe MD, PhD²

¹SURGEONS

²ANESTHESIOLOGIST

FUNCTIONAL NEUROSURGERY—INTRODUCTION: THE SURGICAL TREATMENT OF PAIN, MOVEMENT DISORDERS, AND EPILEPSY

INTRODUCTION

Jaimie M. Henderson MD

Functional neurosurgery differs from most surgical subspecialties in that it aims to alter the function of the nervous system, rather than addressing anatomical abnormalities. The most common treatment areas include chronic pain, epilepsy, and movement disorders. Each of these disease states has a distinctive anesthetic requirement dictated by the specific pathophysiology and subsequent intraoperative objectives. Procedures may be performed under local anesthesia, conscious sedation, or GA and can be divided into ablative (destructive) or augmentative (nondestructive) techniques. Ablative techniques are less frequently performed because of their unpredictable duration of effect and irreversible nature of the lesion. Neuroaugmentation (electrical stimulation or continuous local drug administration) tends to produce more lasting benefits and, more importantly, can be changed to meet fluctuations in the patient’s symptoms.

One of the keys to successful functional neurosurgical therapies is target identification. Many targets can be identified anatomically on appropriate radiographic studies, whereas others may be difficult to visualize even with special techniques. However, even areas that can be targeted anatomically may vary in terms of their physiological function. Thus, it is important to incorporate physiological testing in many functional neurosurgical procedures. Most physiological confirmation techniques require that the patient be awake and cooperative during testing. Thus, the need for physiological identification often dictates a specific anesthetic technique.

Figure 1.2-1. Topographical anatomy of the ventrolateral thalamus. GPe = external segment of globus pallidus; GPi = internal segment of globus pallidus; SNc = substantia nigra pars compacta; SNr = substantia nigra pars reticulata; STN = subthalamic nucleus.

STEREOTACTIC PROCEDURES: DEEP BRAIN STIMULATION, PALLIDOTOMY, AND THALAMOTOMY

SURGICAL CONSIDERATIONS

Description: Many procedures are currently performed with frame-based stereotactic techniques, with intracranial access achieved via a burr hole or twist drill. There is a growing trend to use “frameless” stereotactic approaches, with two major systems currently in use. Real-time frameless localization can be achieved by replacing the stereotactic frame with rigidly attached skull markers (“fiducials”) that provide a fixed reference. Another innovative alternative is to produce a custom-made fixed trajectory guide using rapid prototyping techniques. Both of these approaches have been used successfully and appear to be equivalent in accuracy to a stereotactic frame.

Two approaches to identification of the functional target are used following initial stereotactic CT or MRI radiographic localization; both require patient cooperation. In one approach, the target is confirmed by assessing symptomatic resolution during high-frequency macrostimulation and by identifying surrounding structures using their characteristic stimulation-evoked responses. In the other approach, before stimulation testing, single-neuron recordings are performed to localize the appropriate target through somatotopic kinesthetic and/or somatosensory responses. In an awake patient, appropriate stimulation is delivered to the skin or by passive and active movement of the joints. This technique utilizes specialized high-impedance microelectrodes and amplifiers susceptible to interference from monitoring equipment, which may necessitate manual measurements of BP and clinical assessment of oxygenation. Anesthesia or sedation can modify neuronal activity significantly and, thus, interfere with functional mapping. For example, propofol has been shown to inhibit globus pallidus and subthalamic neurons for several minutes beyond its behavioral effects. In addition, many of these agents have been shown to change evoked potential (EP) responses, raising the possibility that they could alter stimulation thresholds for either the internal capsule or optic tract.

Thermal ablation for pallidotomy or thalamotomy typically is performed with a radiofrequency (RF) lesion generator operating at 500 kHz, which may interfere with some types of monitoring equipment; however, the ablation process only lasts 12-30 sec.

A variety of movement disorders are amenable to surgical treatment. They can be divided into akinetic (e.g., Parkinson’s) and hyperkinetic (e.g., dystonias, tremor, spasticity) syndromes. Idiopathic Parkinson’s disease (PD) is best treated with either deep brain stimulation (DBS) or RF ablation targeted to a functional subcomponent of either the subthalamic nucleus or globus pallidus interna (Fig. 1.2-2). Tremor syndromes are treated by targeting the ventral intermedius thalamic nucleus (thalamotomy or stimulation), whereas dystonias are treated by stimulation of the globus pallidus interna. Spasticity is not treated stereotactically, but through the administration of intrathecal baclofen (GABA-like synaptic inhibition) in the lumbar cistern via an internalized pump system. Abrupt loss of intrathecal infusion of baclofen, however, can quickly lead to a serious withdrawal syndrome with dysautonomia, circulatory collapse, and death within hours. Spasticity refractory to intrathecal baclofen may be amenable to selective dorsal root rhizotomy performed through an open laminectomy.

For DBS, mapping and implantation of the intracranial stimulating electrode is performed under local anesthesia to permit monitoring of behavioral and physiologic responses. A 2-3 cm linear incision (burr-hole access) or stab wound (twist-drill access) generally is placed near the coronal suture and 10-50 mm from the midline in the frontal bone. This can be accomplished under propofol sedation for patient comfort. Subsequently, minimal or no sedation is used, as patient cooperation is necessary during the functional mapping component of the case. If single-neuron recordings are used, propofol should be discontinued at least 20 min in advance of mapping because it can produce prolonged suppression of target neuronal activity. If analgesia is needed, use a low-dose (0.01-0.05 mcg/kg/min) remifentanil infusion. Local anesthetics should not contain epinephrine. Avoid central-acting β-blockers (e.g., propranolol), which suppress tremor activity in target neurons. Sedation with meperidine in patients taking selegiline is contraindicated. No dopaminergic antagonist (e.g., metoclopramide, droperidol) should be given to Parkinsonian patients or patients with dopamine-responsive dystonia. To enhance single-cell responses, withhold medications prescribed for target symptoms for 8-24 h. In some cases (e.g., Parkinson’s disease), this may result in a rebound HTN requiring active treatment; however, patients will resume their medications postop (often in the postanesthesia recovery area), and the HTN will resolve. The implantable pulse generator (IPG) may be placed in an infraclavicular subcutaneous pocket during a separate surgical procedure or at the time of the intracranial electrode implantation. Implantation of the IPG and subcutaneous tunneling of the electrode lead can be done under MAC, but is best tolerated under GETA. To facilitate intubation, the calvarial wound is closed
temporarily, and the stereotactic localizing apparatus is removed. Closure consists of a single, interrupted suture for stab wounds or two-layer suture/staple closure for a burr hole. IPG pockets are closed in two layers. The subcutaneous layer is closed with absorbable sutures, and the skin is closed with staples or sutures.

Figure 1.2-2. Anatomical locations for therapeutic lesions (thalamotomy and pallidotomy) for the surgical treatment of Parkinson’s disease. Inset shows the plane of the coronal section through the diencephalon, identifying the lesions. (Reproduced with permission from Mason LJ, Cojocaru TT, Cole DJ: Surgical intervention and anesthetic management of the patient with Parkinson’s disease. In: Jaffe RA, Giffard RG, eds. International Anesthesiology Clinics: Topics in Neuroanesthesia. Little, Brown, Boston: 1996; 4(34):141.)

Usual preop diagnosis: Medically intractable idiopathic PD with disabling L-dopa-induced dyskinesia, bradykinesia, or rigidity; severe fluctuations in medication responses; dystonia musculorum deformans; post-CVA dystonia; occasionally, torticollis; tremor; movement disorders

▪ SUMMARY OF PROCEDURE

Position	Supine
Incision	Linear (burr holes); stab-wound (twist drill)
Unique considerations	Minimal/no sedation. BP ↑ in patients who have their antihypertensive medications withheld. Manual vital sign monitoring if electronic monitors interfere with single-cell recordings. Be aware that BP cuff or iv’s may produce sensations that distract the patient during awake stimulation testing for sensory side effects.
Antibiotics + other meds	Ceftriaxone or cefazolin 1 g
Surgical time	3-5 h
EBL	25-150 mL
Postop care	Continue antibiotics at surgeon’s discretion, Parkinson’s medications. BP may ↓. Maintain MAP <90 mm Hg to prevent postop bleeding. PACU
Mortality	<0.5%
Morbidity	Overall: 8-27% Infection: < 10% Hardware failure: Rare Intracranial hemorrhage: 3.3-6% Cognitive disturbances
Pain score	2-3

ANESTHETIC CONSIDERATIONS

Parkinson’s disease (PD) is the most common movement disorder, affecting ˜1% of the population > 60 yr. It is caused by the loss of dopaminergic neurons in the substantia nigra → ↓ dopamine (dopamine/acetylcholine imbalance) in basal ganglia → movement disorder. Medical treatment is directed primarily to restoring dopamine levels by increasing the availability of the dopamine precursor (L-dopa), inhibiting liver dopa decarboxylase (carbidopa, usually given in combination with L-dopa as Sinemet), by releasing endogenous dopamine (amantadine [Symmetrel]) and by blocking MAO-B (selegiline [Eldepryl]). Medical treatment also may include dopamine agonists (pergolide [Permax]; bromocriptine [Parlodel]), and acetylcholine antagonists (amantadine [Symmetrel], benztropine [Cogentin]) to correct the dopamine/acetylcholine imbalance. Patients presenting for surgery usually have failed medical therapy. They will have been taken off their antiparkinsonian medications 8-24 h before surgery. This will maximize their symptoms to help assess treatment effects intraop; thus, preop assessment on the day of surgery will be difficult.

PREOPERATIVE

Respiratory	Autonomic dysfunction → esophageal dysfunction →↑ risk of aspiration. Patients typically have ↓ vital capacity 2° rigidity, dyskinesia →↓ respiratory function, and ↓ cough. Laryngospasm and respiratory failure may occur following withdrawal of antiparkinsonian medications. Tests: CXR; consider ABG; PFTs may be difficult to obtain.
Cardiovascular	Autonomic dysfunction → orthostatic hypotension. Dopamine replacement therapy → cardiac dysrhythmias, ↓ BP, and hypovolemia. In patients taking selegiline (MAOI): avoid meperidine →↑↑ BP, rigidity, agitation; sympathomimetics → exaggerated ↑ BP.
Neurological	The primary Sx of Parkinson’s disease include rigidity, tremor, bradykinesia, muscle weakness. Secondary symptoms include dementia, depression, and speech difficulty. Patients may alternate between a state of immobility and one of exaggerated tremor (which may interfere with intraop monitoring). PD medications are sedating—modafinil may be used to improve daytime function.
Renal	Urinary retention is common.
Gastrointestinal	Autonomic dysfunction → gastroparesis, ↑ incidence of reflux. Poor nutrition. Pharyngeal muscle dysfunction → dysphagia.
Laboratory	As indicated from H&P.
Premedication	None. These patients may have received small doses of fentanyl and/or midazolam to facilitate placement of the stereotactic frame. For frameless procedures, fiducial markers or mounting screws will have been placed before surgery.

INTRAOPERATIVE

Anesthetic technique: MAC, with minimal sedation limited to surgical opening and closing, as patient cooperation and typical neuronal activity are essential for the success of the procedure.

Induction	Low-dose remifentanil (0.01-0.05 mcg/kg/min), propofol (25-75 mcg/kg/min), or dexmedetomidine (0.1-0.4 mcg/kg/h) may be used for sedation during burr-hole placement. If propofol or dex is used, it should be discontinued 20-30 min before electrophysiologic recording or mapping. In the event of an airway emergency in framed procedures, a means of releasing the patient from the stereotactic frame must be readily available.
Maintenance	BP control is important to decrease the risk of intracranial hemorrhage during passage of the recording and stimulating electrodes. If not otherwise contraindicated, MAP should be kept 10-20% below normal for that patient. This usually can be accomplished without an arterial line by using an infusion of NTG and/or esmolol titrated to effect, or by using small doses of atenolol (0.5-1 mg increments iv). Esmolol and atenolol are preferred over other parenteral β-blockers because CNS penetration is limited → minimal effect on central tremor.
Emergence	Postop BP control can be continued by using atenolol or labetalol titrated to effect at the end of the procedure. The patient is usually transported to the PACU, then to the neurology ward for postop monitoring. Antiparkinsonian medication should be given in the PACU and may result in a further reduction in BP.
Blood and fluid requirements	Minimal blood loss IV: 18-20 ga ×1 NS/LR @ 1-2 mL/kg/h	For unilateral procedures, iv should be placed in the ipsilateral arm (relative to side of surgery).
Monitoring	Standard monitors (see p. B-1)	Exaggerated tremors and/or neurologic testing in these patients may interfere with monitoring. It may be helpful to place the BP cuff on a leg (less tremor). For unilateral procedures, monitors should not be placed on the contralateral arm and leg, which must be kept free for testing.
Positioning	[check mark] and pad pressure points [check mark] stereotactic frame clearance	Patient comfort may be improved by placing pillows under the knees to relieve lower back strain. A massage therapist can greatly improve patient comfort during the procedure.
Complications	Intracerebral hemorrhage Loss of airway in stereotactic frame	Dx: ↓ mental status and hemiparesis. CT scan usually required to confirm Dx. Emergency craniotomy may be necessary. Rx: may require rapid removal of the stereotactic frame.

POSTOPERATIVE

Complications

Intracranial hemorrhage

Motor deficit

Visual field deficit

Aphasia

Intracranial hemorrhage may require emergency craniotomy. The surgeon should be notified immediately if any new deficits are noted.

Tests

None

Unless otherwise indicated.

Pain management

Usually not necessary

Suggested Readings

1. Balachandran R, Mitchell JE, Dawant BM, Fitzpatrick JM: Accuracy evaluation of microtargeting platforms for deep-brain stimulation using virtual targets. Biomedical Engineering. IEEE Transact 2009; 56(1):37-44.

2. Benabid AL, Torres N: New targets for DBS. Parkinsonism Relat Disord 2012; 18(Supp 1):S21-3.

3. Deuschl G, Schade-Brittinger C, Krack P, et al: A randomized trial of deep-brain stimulation for Parkinson’s disease. N Engl J Med 2006; 355(9):896-908.

4. Fasano A, Daniele A, Albanese A: Treatment of motor and non-motor features of Parkinson’s disease with deep brain stimulation. Lancet Neurol 2012; 11(5):429-42.

5. Heit G, Murphy G, Jaffe R, Golby A, Silverberg GS: The effects of propofol on human globus pallidus neurons. Stereotact Funct Neurosurg 1997; 67(1-2):74.

6. Holloway KL, Gaede S, Starr PA, Rosenow JM, Ramakrishnan V, Henderson JM: Frameless stereotaxy using bone fiducial markers for deep brain stimulation. J Neurosurg 2005; 103:404-13.

7. Joint C, Nandi D, Parkin S, Gregory R, Aziz T: Hardware-related problems of deep brain stimulation. Move Disord 2002; 17(Suppl 3):S175-80.

8. Krack P, Fraiz V, Mendes A, et al: Postoperative management of subthalamic nucleus stimulation for Parkinson’s disease. Mov Disord 2002; 17(Suppl 3):S188-97.

9. MacIver MB, Hill BC, Henderson JM, Bronte-Stewart JM, Jaffe RA, Brock-Utne JG: Human subthalamic neuron spiking exhibits subtle response to sedatives. Anesthesiology 2011; 115:254-64.

10. Moro E, Lang AE: Criteria for deep-brain stimulation in Parkinson’s disease: review and analysis. Expert Rev Neurother 2006; 6(11):1695-705.

11. Pereira EA, Green AL, Nandi D, Aziz TZ: Deep brain stimulation: indications and evidence. Expert Rev Med Devices 2007; 4(5):591-603.

12. Rozet I: Anesthesia for functional neurosurgery: the role of dexmedetomidine. Curr Opin Anaesthesiol 2008; 21(5):537-43.

13. Tierney TS, Sankar T, Lozano AM: Deep brain stimulation emerging indications. Prog Brain Res 2011; 194:83-95.

SURGICAL ANALGESICS: SPINAL CORD STIMULATION, INTRATHECAL PUMPS, AND CORTICAL STIMULATION

SURGICAL CONSIDERATIONS

Description: Chronic pain arises from a variety of etiologies. It can involve both neuropathic and nociceptive processes and occur in a variety of anatomical distributions (e.g., radicular versus a hemibody pattern). Therapeutic interventions are dictated by the pathophysiology of the pain, its qualitative nature, etiology, and the patient’s prognosis. Many common procedures for chronic pain are directed at the spinal cord and may consist of epidural or intrathecal medications or electrical stimulation.

For chronic spinal cord stimulation (e.g., postlaminectomy syndrome) an epidural electrode is implanted either percutaneously or via an open laminectomy. Percutaneous electrodes are easier to implant and have less associated surgical pain. The surgical electrode (implanted via laminectomy) confers greater mechanical stability in the epidural space. In addition, given its larger contact size, it can generate higher current densities with less drain on the implanted system. For percutaneous electrodes, a small skin incision is made two to three vertebral levels caudal to the target region of the spinal cord. For “surgical paddle” electrodes, the skin incision is made one to two levels caudal to the target zone of the spinal cord, and a laminectomy is performed to provide access to the epidural space. Incisions are closed in the standard fashion.

Most percutaneous electrode placements and some paddle electrode placements are done awake so that intraoperative test stimulation can be performed. The procedures are done in the prone or lateral position with consequent implications for airway management in the sedated patient. Localization of the electrodes is accomplished initially based on radiographic criteria; however, these localizations are only approximate, and it is recommended that the electrode placement be confirmed by intraop stimulation. The patient needs to be sufficiently alert to communicate the quality, distribution, and intensity of the stimulation-induced paresthesias. Surgical paddle placement requires a variable extent of muscle dissection and laminectomy, which may be done under general anesthesia or with epidural anesthesia for patient comfort. If done under general anesthesia, response to paddle test stimulation may be measured by manual palpation of musculature stimulated at higher test voltage, and/or using intraoperative electrophysiologic monitoring. To assess efficacy, the electrode may be externalized and percutaneous stimulation used for assessment. If there is ≥ 50% reduction in pain, the patient may return to the OR for internalization of the implantable pulse generator (IPG). Postop, these patients can have an exacerbation of pain, particularly if neuropathic in nature. They may require iv lidocaine or ketamine infusions to return them to their preop baseline, even with a functioning and appropriately located stimulating electrode.

For pain of central origin (e.g., poststroke, multiple sclerosis, and trigeminal nerve pathology), surgical procedures are often directed at the thalamus and cortex. Thalamic interventions include stereotactic insertion of stimulating electrodes into sensory thalamus. Thalamic DBS requires awake mapping of the somatotopic representation of the affected body part through either microelectrode mapping or stimulation-induced paresthesias. For medically intractable neuropathic pain syndromes, epidural motor cortex stimulation has shown mixed results. Functional mapping of the motor cortex for epidural stimulation can be done with anatomical and physiological mapping under GA via a craniotomy, with the anesthetic tailored to minimize interference with EP recording. The incision consists of a 5-10 cm linear or 5 × 10 cm trapezoidal incision placed over and paralleling the motor cortex.

Identification of the appropriate location on the motor strip can be done initially with epidural mapping using SSEPs elicited from the part of the body where the pain originates. In cases of denervation syndromes, SSEP may not be present, and the minimum intensity point for epidural stimulation-induced movements is used. In rare cases, the surgeon may elect to perform the surgery awake to facilitate mapping. To assess efficacy, the electrode may be externalized and percutaneous stimulation assessed for overall therapeutic efficacy. If there is ≥ 50% reduction in pain, the patient will return to the OR for internalization of the IPG. Closure consists of calvarial reconstruction with externalization of leads. The craniotomy incision is closed in the standard fashion. If a percutaneous trial is done, the IPG implant requires a second GETA with reopening of wounds.

The mainstay of surgical treatment of trigeminal neuralgia is microvascular decompression of the trigeminal nerve in the prepontine cistern (see p. 44). In patients who are poor surgical candidates, treatment is accomplished with ablative procedures aimed at the gasserian ganglia, using chemolytic, mechanical, or RF techniques. Patients who fail gasserian ganglion interventions or have atypical facial pain may be candidates for thalamic DBS or motor cortex stimulation. Stereotactic radiosurgical techniques are increasingly utilized as an ablative treatment for trigeminal neuralgia, particularly in the elderly (> 65 yr old) population or in other surgically averse candidates. Radiosurgery employs highly focused beams of radiation to partially ablate the intracisternal portion of the trigeminal nerve while sparing surrounding structures (brain stem and other cranial nerves). The downside to radiosurgery is that the effects and consequent pain relief may take weeks to months to manifest, as opposed to other surgical and ablative treatments whose effects are immediate.

For pain unresponsive to spinal cord stimulation or because of unacceptable side effects of parental medications, continuous intrathecal administration of analgesics can be accomplished with an implantable medication delivery system. An incision is made over the L3-L4, L4-L5, or L5-S1 spinous process and a second incision is placed in the RLQ of the abdomen. An intrathecal catheter is then placed and anchored to the lumbodorsal fascia. A tunneling tool is used to bring the catheter from the lumbar spinal region to the abdomen. This tunneling procedure is rarely tolerated without GETA or deep sedation. A reservoir or continuous-delivery pump is then placed in the abdomen and attached to the catheter. Both incisions are closed in two layers.

Intrathecal narcotics (typically morphine) can produce satisfactory results because therapeutic drug concentrations can be achieved at the level of spinal opiate receptors without influencing higher CNS opiate systems. This therapeutic intervention can be assessed through a percutaneous catheter trial. Patients who experience ≥ 50% reduction in pain are candidates for a totally implanted pump system. These are low-morbidity procedures (5-10%) with infections and hardware failures constituting the greatest problems. Abrupt cessation of medications—through either patient noncompliance with refill schedules (10-12 wk) or hardware failure—however, can lead to a serious withdrawal syndrome.

Usual preop diagnosis: Chronic pain

▪ SUMMARY OF PROCEDURE

Position	Prone/lateral
Incision	2-3 levels above target area (spinal cord stimulation) + laminectomy; L3, 4, 5 (intrathecal pump) + 2nd incision RLQ of abdomen.
Unique considerations	Patient communication important; therefore, avoid oversedation. Copious use of local anesthetics (avoid overdosing).
Antibiotics	Cefazolin 1 g
Surgical time	1.5-3 h
EBL	25 mL
Postop care	May have ↑ pain during recovery period
Mortality	< 0.5%
Morbidity	Overall: 5-10% Infection Hardware failure Withdrawal Sx
Pain score	3-8

ANESTHETIC CONSIDERATIONS

PREOPERATIVE

Patients with chronic pain often present unique challenges to the anesthesiologist and surgeon. They may be intolerant of any additional pain (e.g., iv placement, positioning on the OR table, postop pain) and seemingly immune to typical doses of systemic analgesics while remaining vulnerable to respiratory depression. In most cases, patients should continue their usual pain medications and co-analgesics until ˜2 h before surgery. Typically any transdermal fentanyl patch should be left in place unless its location will be subject to intraoperative heating, compression, or other manipulation. A detailed h/o of patient pain, effective (and ineffective) pain management techniques and drugs, and the current medication regime (including the use of both over and under the counter drugs and herbals) is essential.

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Tags: Anesthesiologist's Manual of Surgical Procedures

May 23, 2016 | Posted by drzezo in ANESTHESIA | Comments Off

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Respiratory	Chronic pain → ↓ physical activity → ↓ respiratory reserve.
Cardiovascular	Ventricular dysrhythmias have been associated with methadone at doses > 200 mg/day. Chronic pain → ↓ physical activity → ↓ cardiovascular reserve.
Neurological	A careful neurologic assessment is essential to detect preexisting deficits.
Psychological

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