Introduction

Functional neurosurgery is a neurosurgical procedure done for improvement of symptoms by making small well-circumscribed lesions or through neuromodulation by brain, spinal cord, or nerve stimulation. It involves surgical management of central nervous system (CNS) disorders that do not have any gross anatomical abnormality, and it is quite different from nonfunctional neurosurgery. As compared to functional neurosurgery, nonfunctional neurosurgery typically involves surgical ablation of anatomically abnormal lesions. Providing symptomatic relief to patients with various CNS disorders and improving quality of life is the basic goal of functional neurosurgery, whereas, nonfunctional neurosurgery primarily focuses on removing the pathologic lesion with preservation of function of surrounding normal brain.

Originally, functional neurosurgery was performed mostly to alleviate symptoms of Parkinson disease (PD). Later on the indications were extended to treatment of chronic pain, spasticity, other movement disorders, epilepsy, and psychiatric disorders. Awake craniotomy is performed for both functional and nonfunctional neurosurgery, but the goals are different for both types of surgeries. In case of functional neurosurgery an awake state allows interaction with the patient facilitating maximum clinical improvement and alleviating unwanted side effects. However, an awake patient during nonfunctional neurosurgery allows removal of the pathological lesion while reducing damage to the adjacent vital areas.

Procedure

Currently, deep brain stimulation (DBS) is a commonly performed functional neurosurgical procedure. PD, essential tremors, dystonia, obsessive compulsive disorder, and refractory epilepsy are the conditions for which the US Food and Drug Administration has approved DBS as a treatment modality. In addition, DBS is increasingly used nowadays in the treatment of depression, Tourette syndrome, cluster headache, chronic pain, and multiple sclerosis.

The exact mechanism of modification of neuronal activity by DBS is inadequately known to us. Inhibition and/or activation of γ-aminobutyric acid (GABA)ergic cells and decrease in production of glutamate are few suggested effects of DBS. Moreover, the target sites for DBS are different for different disorders, and the stimulation of different sites have different effects as well. The effects of DBS are frequency dependent, with no therapeutic effect at <50 Hz and maximum relief of symptoms at >100 Hz. Different disease conditions and the therapeutic target areas for DBS are summarized in Table 28.1 .

Owing to the increased risk of intracranial hemorrhage, coagulopathy, recent use of antiplatelet medication, and uncontrolled hypertension are contraindications for DBS implantation. However, confused/extremely anxious patient, patients with communication difficulties, and procedure requiring abnormal/uncomfortable patient position are contraindications for awake craniotomy procedure.

The commonly used DBS hardware has four main components: multicontact intracranial quadripolar platinum iridium electrodes, a plastic ring and cap for fixation of the electrodes to the skull, a single- or dual-channel battery operated with externally implanted pulse generator (IPG), and an extension cables connecting the DBS electrode(s) to the IPG. The process of DBS starts with rigid head frame application under local anesthesia infiltration/scalp block and light sedation. Head frame application can be done in the operating room (OR), in the imaging facility, or in the preoperative preparatory area. Head frame application is followed by imaging studies [magnetic resonance imaging (MRI) or computed tomography (CT)] for accurate identification of target areas before insertion of the electrodes. However, frame application is not obligatory before imaging studies, as frameless navigation systems for DBS has also been described in the literature. After obtaining the requisite imaging the patient is taken to the OR and is placed either in the sitting or semisitting position followed by fixation of the head frame to the operating table ( Fig. 28.1 ). For electrode insertion a burr hole is created under local anesthesia infiltration/scalp block and moderate to heavy sedation.

Figure showing position of patient during functional neurosurgery.

To localize the target area for stimulation, several methods have been described. This step typically needs an awake and cooperative patient. Microelectrode recording (MER) is one of the method for precise localization of target area. In MERs, the electrode is gradually advanced in 0.5- to 1-mm increments along a trajectory toward the target nuclei while recording spontaneous neuronal discharges. The target area is identified via distinctive pattern of neuronal discharges. Brain navigation using the images (MRI/CT) obtained before is sometimes used to localize the target areas as well. Once precisely localized, the target area is stimulated to see the patient’s movements (macrostimulation) and to minimize the undesirable responses to stimulation. Following this step the electrode is secured and the wound is closed.

After the electrode is placed, the next step is electrode internalization and pulse generator insertion. This step can be performed on the same day, or it can be done on a different day. There is controversy regarding the appropriate timing for this step. A phenomenon called “microlesion” effect caused by edema around the freshly implanted electrode may also be one of the reasons to delay the aforementioned step. This effect may produce some degree of improvement of the patient’s symptoms without any stimulation, and this impedes the capability to check for stimulation-induced benefits. If this step performed on the same day, the head frame is removed and the patient is placed in supine position. This step involves tunneling the electrode(s) and connection of the extension cable through the scalp and subcutaneously on the side of the neck to an infraclavicular area where it is connected to the pulse generator. Intervals of intensely painful stimulations occur during the tunneling of the leads and creation of pocket for pulse generator implantation. So this step is done under general anesthesia. After the pulse generator is implanted a gap of few days is given before turning on the generator to allow healing of the implanted site.

Anesthetic Consideration

During DBS electrode insertion, anesthesiologists aim to provide adequate operating conditions and patient comfort as well as identify and manage perioperative complications. Anesthesiologists face many challenges during the perioperative management of patients who are scheduled for placement of a DBS device. Advanced age, associated comorbidities and psychiatric illness, and anesthetic drug interaction with ongoing medications are a few factors that need to be addressed while dealing with patients scheduled for DBS implantation. Nevertheless, anesthesiologists need to be familiar with effects of anesthetic agents on MERs, as signal alteration during testing may lead to inaccurate electrode placement.

Problem Encountered in Patients Undergoing Deep Brain Stimulation

Candidates for functional neurosurgery have different primary disease conditions, and each disease condition has its associated problems ( Table 28.2 ). Patients undergoing functional neurosurgery for different disorders are usually on multiple pharmacological agents and these medications have their own groups of problems ( Table 28.3 ).

Table 28.2

Table Summarizing Different Diseases and Associated Problems

Disease	Problems Associated
Parkinson disease	Behavioral and psychiatric abnormalities (dementia, depression, anxiety, hallucinations, psychosis, daytime somnolence), autonomic dysfunction (orthostatic hypotension), cardiac arrhythmias, hypertension, respiratory system abnormality (restrictive/obstructive lung disease, involuntary movements of glottis and supraglottis structures causing upper airway obstruction, laryngospasm, respiratory arrest, aspiration pneumonitis), acute exacerbation of the symptoms or the development of neuroleptic malignant syndrome following interruption of pharmacological therapy
Alzheimer disease	Depression, hallucinations, delusions, anxiety, aggression, agitation Patient with advanced disease state are sensitive to central nervous system depressant effects of anesthetic agents. Delayed emergence and higher risk for postoperative delirium
Multiple sclerosis–associated tremor	Features of associated multiple sclerosis in the form of visual problems (due to optic neuritis, decreased visual acuity, diplopia, or nystagmus), cranial nerve dysfunction weakness, paresthesia, ataxia, spasticity, and contracture (leading to difficult surgical positioning), autonomic dysfunction (leading to exaggerated hypotension after general or regional anesthesia), respiratory insufficiency, exaggerated sensitivity to hyperthermia (elevation of body temperature leading to deterioration of neurological function), perioperative corticosteroid supplementation may be needed in patients receiving steroids, risk of succinylcholine induced hyperkalaemia
Essential tremor	Cardiovascular complications related to pharmacological therapy (i.e., β-blockers)
Dystonia	Hemodynamic instability, laryngospasm, poor nutritional status, communication problem, growth retardation
Epilepsy	Developmental delay, seizures, drug interaction with anesthetic agents

 

Table 28.3

Table Summarizing Different Pharmacological Agents and Associated Problems

Disease	Pharmacological Agents	Problems Associated With Use
Parkinson disease	Levodopa	Nausea and vomiting, orthostatic hypotension, cardiac arrhythmias (especially in patients with preexisting cardiac conduction disturbances) hallucination, confusion, drug-induced dyskinesia, neuroleptic malignant syndrome (if discontinued suddenly)
	Dopamine receptor agonist (bromocriptine, pergolide ropinirole, pramipexole)	Orthostatic hypotension, hallucination, confusion, nausea, fatigue, “sleep attacks” (with ropinirole, pramipexole use), rare reports of pulmonary and reteroperitoneal fibrosis (with bromocriptine use)
	Dopamine receptor agonist (apomorphine)	Nausea and vomiting, QT prolongation, hallucinations, dyskinesia, behavioral disturbances
	Selective MAO-B inhibitors (selegiline)	Anxiety, insomnia, abnormal glucose tolerance, nausea, dyspepsia, dizziness, dyskinesia
	Catechol-O-methyl transferase inhibitors (tolcapone, entacapone)	Nausea, orthostatic hypotension, confusion, hallucinations, hepatotoxicity (with tolcapone use)
	Antiviral agents (amantadine)	Dizziness, lethargy, anticholinergic effects, sleep disturbance, nausea, and vomiting
	Muscarinic receptor antagonists (trihexyphenidyl, benztropine mesylate, diphenhydramine hydrochloride)	Sedation confusion, constipation, urinary retention, visual disturbances
Alzheimer disease	Tacrine, donepezil, rivastigmine, galantamine	Abdominal cramping, anorexia, nausea, vomiting, diarrhea, hepatotoxicity (with tacrine use)
	Memantine	Headache or dizziness
Depression	Tricyclic antidepressants (imipramine desipramine, clomipramine, amitriptyline, nortriptyline)	Orthostatic hypotension, cardiac arrhythmias, palpitation, tachycardia urinary retention, dry mouth, visual disturbance, sedation, weight gain
	Selective serotonin reuptake inhibitors (citalopram, fluoxetine sertraline, paroxetine)	Headache, agitation, insomnia, nausea, vomiting Serotonin syndrome
	MAO inhibitors (clorgyline, moclobemide, selegiline, phenelzine, tranylcypromine, and isocarboxazid)	Agitation, hallucinations, hyperreflexia, fever, convulsions, postural hypotension
MS	Corticosteroid	Fluid retention, weight gain, gastric disturbances, fragile skin, osteoporosis, emotional lability
	Interferon	Flulike symptoms, increased spasticity. dermal injection site reactions, anaphylactic shock, insomnia, headache, and depression
	Mitoxantrone	Cardiomyopathy, reduced left ventricular ejection fraction, and irreversible congestive heart failure
	Cyclophosphamide	Congestive heart failure and hemorrhagic myocarditis, pericarditis, and necrosis
	Azathioprine, methotrexate	Bone marrow suppression
Essential tremor	Primidone	Dizziness, drowsiness, excitation, tiredness, headache, loss of appetite, nausea, or vomiting
	Propranolol	Cardiac arrhythmia, accentuation of myocardial insufficiency, worsening of obstructive lung disease, fatigue

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