Intracerebral hemorrhage/subdural hematoma

Intracerebral hemorrhage (ICH) occurs in approximately 1–5% of DBS cases (Figure 12.2).^{119–122,124,125,163,164} The incidence of ICH seems to be higher in DBS cases performed with microelectrode recording (MER) using multiple electrode passes^123,165 and in hypertensive patients, although controversy exists regarding this topic.⁵¹ Bleeding may occur several hours or even days after surgery. The risk of bleeding is usually less than 5% per lead implantation,^126,166 and around 0.6% of patients will suffer persistent neurological deficits, although the true rate is unclear because several papers have not reported the rate of ongoing neurological deficits.^166,167

Figure 12.2

Intracranial hemorrhage after DBS surgery. (a) CT scan showing an intraventricular hemorrhage following DBS lead implant into the right subthalamic nucleus. (b) CT scan showing a large right frontal hemorrhage along the lead tract following DBS lead implant into the subthalamic nucleus (STN). (c) CT scan showing a left STN DBS lead with bilateral panhemispheric subdural effusions, status post-bilateral posterior craniotomies and evacuation of extra-axial fluid.

Delayed deep cerebral venous bleeding/infarction

Cerebral venous thrombosis (CVT) or hemorrhage may occur when a thrombus forms in the large draining veins that enter the dura mater at the site of a burr hole or when a vein is injured or sacrificed during the DBS procedure. Symptoms include severe headache, seizures, change in mental status, and focal neurological deficit. The severity depends on how completely the thrombus occluded the venous territory, causing venous congestion, and on the compensation from collateral vessels.¹⁷⁰ Brain MRI venography will show the location of the thrombus in the vein and the dural sinus system.¹⁷¹ A large series of 728 patients reported that cortical/subcortical infarcts occurred in 0.4% of patients.¹²⁰

Seizure

The incidence of postoperative seizures after DBS surgery is approximately 0.4–3.1%.^{120,121,134,163} There are currently no data correlating seizure incidence with the number of microelectrode and/or DBS lead trajectories, although it is likely that greater brain instrumentation, especially if associated with hemorrhage, would place a patient at risk for seizures.

Sterile seroma

A seroma is a sterile accumulation of serum in a circumscribed location within the tissue. It is caused by an injury during the surgical procedure that may not fully and immediately subside. The remaining serous fluids result in a seroma, with the body usually absorbing the seroma gradually.

Pulmonary embolism

Pulmonary embolism (PE) occurs at an incidence of 0.4–4.9% after DBS surgery. The mortality rate of non-DBS related PE ranges from 8.6% to as high as 59.4%.¹²⁸ The risk of PE is increased in PD patients because of their immobility. PE should be suspected in patients who experience sudden onset of dyspnea, tachypnea, pleuritic chest pain, cough, and hemoptysis.

Pneumonia

Postoperative pneumonia is especially common in PD patients with pre-existing swallowing difficulties, which predispose them to aspiration. The incidence rate is approximately 0.6% in the 30 days following DBS surgery.¹²⁹

Postoperative confusion

Postoperative confusion is common following STN DBS surgery. The incidence in reports varies widely, from 1% to 36%.^{120,130–132,180} Many factors contribute to confusion, including penetration of the frontal lobe, transgression of the ventricular wall,¹⁸¹ long duration of surgery, withdrawal of dopaminergic medications, and pre-existing cognitive deficits. Postoperative confusion is usually transient.

Suboptimal DBS lead placement (Figure 12.3)

Suboptimal DBS lead placement is one of the most common causes of DBS failure.¹ Factors that may result in a misplaced lead include poor surgical technique, head movement or frame shift, misinterpretation of MER data, and brain shift.^125,136 The incidence varies from 1.2% to 12% of patients.^{120,121,125,133,136,163}

Figure 12.3

Suboptimal DBS lead location. Plain x-ray, AP (a) and lateral (b), showing suboptimal left DBS lead placement following STN DBS surgery. The best imaging technique to identify lead location is MRI, if available.

Troubleshooting

1. Test stimulation amplitude thresholds that produce benefits and adverse effects for each electrode on the DBS lead and attempt programming at one month after surgery.

2. Evaluate the lead location using MRI (Figure 12.4), following the safety guidelines of the device manufacturer (a CT scan can be done if there are contraindications to an MRI) and determine the anatomical three-dimensional position of each electrode on the DBS lead.

3. Gather and review all data (clinical assessment, stimulation-related adverse effects, benefits derived from stimulation, and lead position) and decide whether there is an electrode that can be used to deliver stimulation and provide benefit.

If the benefit of device programming cannot be sustained for more than hours or a few days, or if stimulation-induced adverse effects occur at low stimulation thresholds, a suboptimally located lead should be suspected and replacement of the intracranial lead considered.¹¹⁶

Figure 12.4

A suboptimally placed DBS lead. (a) Brain MRI in the axial plane showing that the left DBS lead position is too deep beneath the pontomedullary junction. (b) Brain MRI in the sagittal plane demonstrating that the right DBS lead position is too shallow within the periventricular white matter of the centrum semiovale following STN DBS surgery. (c) Brain MRI in the axial plane revealing that the right DBS lead was placed too far medial after GPi DBS surgery.

Infection (Figure 12.5)

Infection is the most common device-related surgical complication. The incidence ranges from 3% to 10% in most series.^{120,121,124,126,134,163,164,182,183} In cases of high infection rates (12–15.1%),^124,184 the hospital infectious disease committee should be called in to investigate possible sources within the hospital and its employees. Most often, infection involves the neurostimulator in the pectoral region and not the DBS lead itself. In general, infected device components need to be removed and antibiotic treatment initiated. Treatment with antibiotics alone, without device removal, is not likely to be effective. If the infection involves the DBS lead itself, leaving it in place can potentially result in a severe intracranial infection, such as a subdural empyema or brain abscess.

Figure 12.5

DBS-related infection. (a) CT scan in the axial plane showing bilateral STN DBS lead implantation and a hypodensity in the right frontal area (vasogenic edema), which has resulted in a right-to-left subfalcine shift. (b) MRI scan in the axial plane showing fronto-parietal edema due to an infectious process.

Troubleshooting (Figure 12.6)

If the infection is superficial and mainly a localized skin infection of the surgical wound, it may be treated with intravenous or even oral antibiotics with adequate tissue penetration. A close clinical follow-up visit must be performed to evaluate the infection. If the infection does not improve with the antibiotics, the extension and neurostimulator should be removed. Repeat the culture and administer the appropriate antibiotics based on the findings of the culture (the antibiotic course should be for six to eight weeks). Implantation of new hardware can be performed once the infection has cleared.

Figure 12.6

Algorithm for troubleshooting deep brain stimulation infections.

If the infection is deep and involves purulence around the brain lead, it must be treated by immediate removal of the hardware. Perform culture studies and administer a sufficient course of antibiotics (usually at least six to eight weeks) prior to replacement of hardware. In severe cases of deep, purulent infection around the brain lead, it is often prudent to consult an infectious disease specialist.

Skin erosion

Skin erosion occurs mostly at the connector site that joins the DBS lead to the extension. It is usually a late-occurring complication, with an incidence of 0.6–6.5%.^{120,124,135,164} The original connector used in the past was bulkier, which may have contributed to this complication. Use of the newer connectors, combined with proper placement under the scalp and meticulous galea closure work, will decrease the risk of skin erosion.^126,136 Larger neurostimulators may also be more likely to cause skin erosions. Skin erosions may also occur because of extremely tight suturing over the device, or in those elderly patients with thin, frail skin.

DBS lead or wire break (Figure 12.7)

Most lead or wire breaks occur between the extension cable and the DBS brain lead, which is usually located below the mastoid process.^{137,163,189–192} Head turning can mobilize the DBS lead connector and can break the system circuit. The incidence of lead or wire break has been reported in various series to range between 0.94% and 8.5%.^{120,163,190–192} There may be a difference in lead fracture rates in different disease targets,¹⁹⁰ although this is unclear.¹⁹³ In addition, in a large retrospective review involving 531 procedures, Servello et al. showed a statistically significant association with infectious complications in the Tourette syndrome subgroup, again suggesting possible differences between diseases or disease targets (although the etiology underpinning the differences is unknown).¹⁹⁴ If a difference exists, one potential explanation would be the increased involvement of violent head movements in ET, dystonia, or Tourette patients, although there could be inherent differences in the different targets. This could also skew reported rates of complications based on the composition of studies. Some patients may feel an “electric shock” sensation that is worsened by pressing on the area of the lead. Impulse control disorders such as trichotillomania¹⁹⁵ and twiddler syndrome have been reported to cause DBS lead or wire fractures.^196–199 In twiddler syndrome, the patient deliberately or subconsciously spins the neurostimulator in the chest region. When the patient spins the neurostimulator, the lead is shortened and an open circuit occurs, causing an electrical sensation in the patient’s body. Alternatively, this may also result in a lead fracture.

Figure 12.7

Example of a DBS lead fracture. Plain x-ray film series through the skull, neck, and chest of a “twiddler” patient demonstrating a DBS extension coursing through the neck and terminating in the left chest wall. (a) There is discontinuity in the wiring at the level of the left mastoid process. (b, c) The DBS lead and extension are coiled in the extracranial soft tissues; this is usually a result of ongoing manual manipulation of the neurostimulator.

Lead migration (Figure 12.8)

Lead migration is a rare event, occurring in 0.5% in a large series of 728 patients,¹²⁰ although some have reported rates higher than 4% (reviewed by Boviatsis et al.¹⁶³). Migration usually occurs when fixation of the lead to the skull is inadequate.^136,189 In dystonia, the lead may possibly shift downward due to head movement, dragging the extension cable and neurostimulator upward.²⁰² Another potential cause of lead migration is skull growth in children over time, and in this case the lead migrates dorsally.¹¹⁶

Figure 12.8

Lead migration in a patient with GPi DBS. Plain skull x-ray lateral (a) and AP (b) showing lead migration status post GPi DBS in a patient with generalized torsion dystonia who developed worsening of symptoms that were previously controlled by DBS. The left lead had moved 10.4 mm downward and the right lead had moved 4.7 mm upward.

Battery (neurostimulator) life and failure

Battery (neurostimulator) life is dependent on inherent battery voltage, stimulator parameters and usage, battery chemistry, impedance fluctuations, interpolation errors, usage patterns, and self-discharge. Estimators of battery life typically employ calculations based on initial battery capacity and current drain. The main contributor to current drain is therapeutic impedance.^204,205 In addition, battery life estimation varies by neurostimulator model and requires device-specific algorithms. Battery replacement algorithms should incorporate clinical status, as reduced symptom control can occur toward the end of battery service life.^204,205

Neurostimulator malfunction (Figure 12.9)

Most neurostimulator malfunctions have occurred with earlier neurostimulator models and are now uncommon. Patients complained of shocking sensations or intermittent stimulation around the neurostimulator site.¹³⁶

Figure 12.9

Assessment of neurostimulator malfunction.

Neurostimulator migration

Neurostimulator migration results mainly from a change in the subcutaneous position of the device and may be due to inadequate securing of the device during implantation or due to obesity of the patient.¹²⁰ Compulsive behavior (twiddler syndrome) may increase the risk of device migration and lead or extension fracture.¹⁹⁹

Pain/discomfort over the neurostimulator

Pain/discomfort over the neurostimulator is mostly found in thin patients whose lead-extension path has one tissue tunnel for both lead extensions (36%), rather than in those with a single tunnel for each lead extension (11%).¹³⁸

Troubleshooting

Test stimulation through each electrode on the DBS lead is frequently performed in a unipolar configuration, with a gradual escalation of stimulation amplitude applied; amplitude thresholds for the emergence of adverse effects should be explored and documented. If stimulation-related adverse effects occur outside the expected range (that is, at relatively low levels of stimulation) or not at all, imaging should be performed (preferably with a brain MRI following the safety precautions provided by the device manufacturer or with CT scan fused to the preoperative MRI). This procedure will usually help to verify if the DBS lead is in an acceptable position, and it can help in choosing the best electrode on the DBS lead for therapeutic stimulation. If the DBS lead is found to be in a suboptimal location, stereotactic surgical repositioning, possibly with physiological guidance, may be required.

Paresthesia

Paresthesia is defined as an abnormal sensation of the skin, such as numbness, tingling, pricking, or burning. As stimulation level is increased, transient paresthesia may occur, usually disappearing within a few seconds. At higher levels of stimulation, up to 10% of patients will experience persistent paresthesia.¹³⁹ This effect is due to electrical current from the active electrode(s) stimulating the ventralis caudalis (Vc) nucleus of the thalamus or alternatively the lemniscal fibers.²⁰⁶

Muscle contraction

Muscle contraction occurs when stimulation spreads into the internal capsule.²⁰⁷ The contracting muscles usually correspond to the region of the capsular homunculus.

Dysarthria

Approximately 5–25% of patients will experience stimulation-induced dysarthria with bilateral Vim DBS.^140–142 Dysarthria may be caused by stimulation current spread to the internal capsule/corticobulbar fibers, and this may commonly occur with Vim because the Vim is anatomically close to internal capsule.^208,209

Patients with dysarthria following Vim DBS should be examined in two conditions: “on” stimulation and “off” stimulation. Dysarthria due to stimulation will get worse when stimulation is “on.” This can sometimes be treated by decreasing the stimulation parameters or by changing the configuration of electrodes, especially to a bipolar montage. If the DBS lead was placed too lateral, the stimulation will influence corticobulbar fibers and cause dysarthria at a level of stimulation that is insufficient to control tremor. This problem can sometimes be managed by repositioning the DBS lead, although many patients opt to accept the presence of some dysarthria in exchange for tremor control (and can use their patient programmer to adjust stimulation levels to optimize either tremor control or clarity of speech, depending on their circumstances). Dysarthria can also occur with other DBS targets.

Postural instability/ataxia (Figure 12.11)

Postural instability and other problems with balance have been reported following Vim DBS, with an incidence of approximately 3–7%.¹⁴⁴ These problems seem to be associated with bilateral stimulation.²¹⁰ The symptoms may reverse in some cases with stimulation parameter changes,^{140–143,145,209} usually reductions in amplitude or pulse width, or switching to bipolar configuration. These issues may also emerge with other targets and diseases.

Figure 12.11

Vim DBS: stimulation-induced effects. Cn, caudate nucleus; GPe, globus pallidus externus; GPi, globus pallidus internus; IC, internal capsule; Md, nucleus mediodorsal thalamus; Pu, putamen; R, red nucleus; SNc, substantia nigra pars compacta; SNpr, substantia nigra pars reticulata; STN, subthalamic nucleus; Va, nucleus ventral anterior thalamus; Vc, nucleus ventrocaudal thalamus; Vim, nucleus ventral intermediate thalamus; VP, visual pathway/optic tract; Vop, nucleus ventral oral posterior thalamus; VSt, ventral striatum; Zi, zona incerta.

Dyskinesia/hemiballismus

Stimulation-induced dyskinesia with STN DBS appears to be a sign of a well-located DBS lead. Dyskinesia may occur minutes to hours after stimulation is initiated or increased, requiring that the clinician programmer be patient while evaluating the subject and, if possible, observe them after some time has passed. Controlling dyskinesia is best accomplished by balancing stimulation parameters and dopaminergic medication.¹⁴⁴ Often, reduction of medications is the most effective treatment. However, there are cases of “brittle” dyskinesia after STN DBS and in these cases a GPi DBS could be a possible rescue strategy if aggressive programming and medication changes cannot alleviate the issue.^211,212

Paresthesia

Paresthesia usually occurs as a result of current spread to the medial lemniscus, which passes ventroposteriorly to the STN. In most instances, these paresthesias are transient, disappearing rapidly. Persistent paresthesia may indicate that the DBS lead is located too deep, posterior, and medial. Adjusting the stimulation parameters or electrode configuration usually resolves this problem.¹⁴⁴

Muscle contraction

Muscle contraction in STN DBS may be due to current spread into the internal capsule.^144,207 The muscles that contract correspond to the region of the capsular homunculus.²⁰⁸

Dysarthria/dysphonia/hypophonia

The prevalence of impaired speech after STN DBS ranges from 4% to 17%,^{130,146–148} and this impairment typically occurs after bilateral STN DBS. Most studies assume that speech impairment is due to current spread to internal capsule and corticobulbar fibers,^208,209,213 but it may be also be related to the progression of PD.

Gait impairment/postural instability

Gait impairment and postural instability are often refractory to DBS treatment and may actually worsen post-DBS. Patients with Parkinson’s disease who have improvements in gait impairment and postural instability with levodopa treatment are more likely to have benefit, but this is unpredictable. Patients who did have improvement in axial symptoms with DBS tend not to have sustained benefits.²¹⁷ It remains unknown whether these symptoms are amenable to targeting of other structures, such as the PPN.

Abnormal eye movements/diplopia

Double vision (diplopia) is usually due to stimulation of supranuclear oculomotor fibers below or medial to the STN, resulting in disconjugate eye movement. Patients may experience dizziness when viewing images displaced horizontally, vertically, or diagonally.

Apraxia of eyelid opening

Apraxia of eyelid opening (ALO) is a condition where patients who have otherwise normal eyelids have difficulty opening the eyelids and experience involuntary closure of the eyes. It most commonly occurs following STN stimulation in patients who obtain good motor symptom improvement with the DBS.^208,219 This adverse event is relatively infrequent, occurring with an incidence of approximately 5%.^134,164 The mechanism of ALO is not well understood, and it can occur with low energy parameters. Adjustment of the stimulation parameters may or may not be of benefit.

Neuropsychiatric complications (Figure 12.14)

Neuropsychiatric complications vary greatly in their manifestations. These complications have been increasingly documented following DBS treatment. Some of the more common neuropsychiatric conditions that have been observed following DBS surgery and/or with DBS treatment are transient confusion, anxiety, apathy, hypomania, emotional instability, depression, suicidal tendencies, psychosis/hallucination, and compulsive or impulsive behavior.²²⁰ A psychiatric referral may be needed to assist in evaluation and treatment of the patient.^221–223

Figure 12.14

Management of neuropsychiatric complications.

Anxiety or emotional reactivity is the most common nonmotor symptom in PD. It occurs in 75% of patients pre- and postoperatively.^152,154 Anxiety frequently occurs in patients who suffer from depression, panic attacks, and phobia. A trial of a benzodiazepine, cognitive behavioral therapy (CBT), and exposure therapy could be useful, depending on the individual situation. There are also now counseling and online programs that can be useful to address anxiety.

Transient confusion has been reported to occur in 1–36% of patients in the immediate postoperative phase.^{130–132,224} Because it usually improves with time, no immediate treatment is needed.

Apathy also occurs, with a reported approximate incidence of 4–25% after STN DBS therapy.^130,225 It is sometimes precipitated by depression associated with the reduction of dopaminergic medication that may occur when motor symptoms are improved by DBS; increasing the dose of levodopa or a dopamine agonist may therefore help to alleviate the apathy. The patient should be assessed for depression or mood disorder and given antidepressants if needed. Depression itself occurs in 1.5–25% of patients following STN DBS treatment.^{130,131,151,157} It can be caused by many factors, such as the natural history of PD itself, dopaminergic medication withdrawal, current spread to the medial limbic system, and psychosocial factors such as unrealistic patient expectations and poor family support. This manifestation can be managed by treating the underlying cause of the depression by adjusting levodopa or dopaminergic medication, giving antidepressant medications, modifying the stimulation parameters, and by consulting with a psychiatrist.²²⁰

Hypomania occurs in 4–15% of patients post-DBS surgery.^131,151 Treating postoperative hypomania can be performed by adjusting the dose of levodopa and by administering a trial of antidepressants and mood stabilizers. A cholinesterase inhibitor may be given if cognitive impairment is present, and CBT may also be beneficial. In some cases, changing the active stimulation electrode used for treatment has improved the situation.

Prevalence of suicide attempts after DBS varies from 0.5% to 2.9%.^{46,153,154,220} Depression, hypomania/mania, and psychotic symptoms should be evaluated, and patients exhibiting the behaviors and symptoms of these neuropsychiatric conditions in most cases should be admitted to the hospital and also referred to a psychiatrist for proper outpatient management.

Psychosis (11%) and transient hallucination (16%) have been reported in association with DBS.⁵⁴ The physician should consider admitting the patient to adjust dopaminergic medication and possibly also changing stimulation settings. An atypical antipsychotic may be given to treat psychosis. Most clinicians use clozapine or quetiapine, which tend to not worsen PD motor symptoms.

Impulsive–compulsive disorder (ICD, e.g., pathological gambling, hypersexuality, binge eating, compulsive shopping, and hoarding) may be present or be precipitated by DBS.^226,227 There may also be an underlying dopamine dysregulation that can be unmasked or worsened by DBS. It is important that patients be monitored pre- and postoperatively for the possibility of emergence of ICD and dopamine dysregulation syndrome (DDS). These cases can be managed by decreasing or discontinuing dopaminergic medication (particularly dopamine agonists), adjusting DBS parameters, treating with atypical antipsychotics, and also using drugs such as valproic acid or naltrexone.^211,228

Cardiovascular reflexes

Based on the pathophysiological circuitry model of basal ganglia function in PD, there is an increased excitatory output from the STN that may possibly result in an increased inhibitory output from the thalamus.²²⁹ This is hypothesized to reduce the compensatory tachycardic response to postural changes required to prevent symptomatic orthostasis,²³⁰ and the effects of DBS have been implicated in autonomic function.

An observation by Sauleau et al.,²³¹ who directly monitored patients for intraoperative autonomic changes following STN DBS for PD, revealed that 88% of patients had tachycardia within seconds after stimulation, followed by a hypertensive interval after approximately 1 minute. This effect was temporary, and the autonomic system returned to normal a few minutes following discontinuation of DBS.¹⁵⁵ Some studies suggest that tachycardia may persist for six months after DBS treatment with high-frequency stimulation²³² and disappear after one year.¹⁵⁵ The long-term clinical significance of transient tachycardia and hypertension is still unknown.

Bladder function

Nonmotor symptoms are highly prevalent in advanced PD patients, with the most common in large studies being nocturia, urinary urgency, and constipation. Although there is a large amount of data on the motor benefits of DBS in Parkinson disease, there are very few data on the effects of DBS on these nonmotor symptoms. Most studies have employed a questionnaire to assess nonmotor symptoms pre-DBS and post-DBS.^233,234 There have been conflicting reports on the effects of DBS on urinary function. Early studies have shown some benefits in urinary symptoms that were measurable by urodynamic studies with STN DBS.²³⁵ In a study by Winge et al., patients who underwent DBS showed improvements in symptoms of nocturia without changes in bladder emptying.²³⁶ Subsequent questionnaire-based studies reported no difference in urinary symptoms after DBS.^233,234 There have been isolated case reports of urinary retention following STN DBS in those with previously normal bladder function.²³⁷ Taken together, the data are very limited, although some patients may report a benefit in urinary symptoms and a minority may experience worsening.

Sialorrhea

Increasing sialorrhea as an adverse effect of STN DBS has been reported.^152,238 This issue may also be complicated by the coexistence of worsening in cognitive function, which may contribute to a reduced control of secretions. Increased drooling has been reported in patients who underwent STN DBS.²³⁹ It is unclear whether this is an effect of DBS or if there are other factors, such as natural progression of disease or modification of medication regimen, that may influence outcome.

Troubleshooting

Most practitioners use anticholinergics and/or botulinum toxin in a case-by-case manner to treat this issue. Some practitioners use atropine drops under the tongue (Figure 12.15).

Figure 12.15

Algorithm for management of sialorrhea post-DBS.

Dysphagia

Dysphagia has been reported in 4–8% of patients after STN DBS.^148,156,158 It remains unclear whether this results directly from the DBS or if this change reflects disease progression and involvement of non-dopaminergic pathways. Troche et al. have performed a systematic review of all experimental studies of swallowing post-DBS and identified nine pertinent studies.²⁴⁰ All of these studies were only performed in those with STN DBS, and all were either bilateral or pooled bilateral and unilateral cases. There was no convincing evidence that swallowing was affected, but some measures of pharyngeal swallowing were noted to be worse. In a more recent series, a retrospective analysis of 33 patients who had unilateral DBS in either STN or GPi suggested that those having STN DBS performed worse on swallowing outcomes, although this study had limitations.²⁴¹ Taken together, there exists a paucity of studies addressing this question, and follow-up will require carefully designed studies to control for target, approach (unilateral versus bilateral), and outcome measures. In the experience of many clinicians, there are patients who report changes in swallowing after DBS. In many cases, however, the spread of DBS current to corticospinal and corticobulbar fibers beyond the intended target may be responsible for worsening of swallowing.

Hypersexuality

The prevalence of hypersexuality in PD is estimated at 2.4%.¹⁵⁹ Most studies^{160,242–244}report that men treated with STN DBS have an increased frequency, increased satisfaction, and decreased avoidance of sexual activity, especially those younger than 60 years of age. There were no significant changes observed in sexual functioning for women post-DBS, although this population has been less studied. The mechanism for excessive sexual arousal after DBS is currently unknown.

Weight gain

Weight gain is common after DBS at the STN or GPi targets. It occurs at an incidence of 6–100% after STN DBS^130,148,160and 26–96% after GPi DBS.⁵⁸ There have been no reports regarding weight gain after Vim DBS, but this phenomenon has been less studied. Most patients will have a weight gain of approximately 9.3–9.7 kg and an increase in body mass index by 4.7 kg/m² one year post STN DBS treatment.^248,249

There are several explanations for weight gain following STN DBS including: (1) changes in dopaminergic medications that may increase the drive for food intake or contribute to an ICD underlying the issue and leading to binge eating; (2) decreased energy expenditure may occur due to less motor fluctuation and dyskinesia; (3) normalization of energy metabolism following STN implantation may favor body weight gain (men gained mass, while women gained fat);²⁵⁰ (4) spread of electrical current into nonmotor regions, such as the hypothalamus, can induce changes in eating behavior; (5) other factors, such as changes in living style and physical activities, may be involved.

Muscle contraction

Muscle contraction with GPi DBS generally results from current spread into the internal capsule.²⁰⁷ The internal capsule is located posteriorly and medially to the GPi. Clinicians need to be very careful to distinguish between tonic muscle contraction and dystonia related to the underlying movement disorder, which can be challenging.

Dysarthria/hypophonia

Dysarthria/hypophonia with GPi DBS may possibly occur less frequently than in STN DBS (particularly if unilateral GPi is used), although it has been reported.^131,161 Speech and swallowing examinations conducted both on and off stimulation may aid in the diagnosis.

Visual phenomena

During intraoperative microelectrode recording, identification of the optic tract is used to help determine the ventral border of GPi.²⁵¹ If the DBS lead is implanted near the optic tract and electrical current spreads to the optic tract region, the patient may report seeing sparkles of light (phosphenes). Homonymous quadrantanopsia can occur after GPi DBS from a lesion of the optic tract, but this is rare in DBS (unless a stroke or hemorrhage has occurred) and is more commonly encountered in patients undergoing the ablative procedure of pallidotomy.²⁵²

Status dystonicus

There have been isolated case reports of status dystonicus, or dystonic storm, associated with sudden DBS failure or associated with changes in stimulation parameters.¹⁶² This phenomenon has been reported with pallidal stimulation, but presumably sudden cessation of STN DBS could also produce this issue.

Disease progression

Worsening of symptoms may occur over time, even when the patient has been deriving benefit from DBS for years. This may simply signify progression of the disease and may not necessarily be indicative of device failure. In essential tremor, there may be loss of benefit with long-term DBS, often attributed to tolerance; however, this is more likely to reflect disease progression and efforts should be made to rule out suboptimal lead placement.²⁵³

Poor DBS candidate/lack of evaluation by an interdisciplinary team

Ideally, an interdisciplinary team should be involved in selecting patients for treatment with DBS.^116,254,255

This team typically consists of a movement disorder-trained neurologist and neurosurgeon, a nurse and/or nurse practitioner, a physician assistant, a psychiatrist, a neuropsychologist, an occupational therapist, a nutritionist, a speech pathologist, a social worker, a financial counselor, and a home care case manager. Each team member independently assesses the patient, and the team then meets to review and discuss findings in a team setting. In the meeting, the interdisciplinary team will determine whether patients are suitable for treatment with DBS, develop a risk–benefit profile, and discuss the safest operative approaches (staged versus simultaneous lead insertion, DBS target, etc.). As discussed in detail in Chapter 2, a variety of criteria are considered in determining patient candidacy for treatment with DBS. For those with PD, patients need to have a clear diagnosis of idiopathic PD (preferably diagnosed by a movement disorder specialist²⁵⁶). They should not have atypical parkinsonian features. Patients should demonstrate a clear (even if only brief) response to dopaminergic medication, with improvement in the UPDRS motor score of at least 30% between the off- and on-medication states.²⁵⁷ There should be absence of active psychiatric illness and little or no cognitive impairment. Other considerations, such as age, general health, and patient expectations, should also be reviewed (Table 12.5).

Table 12.5 Favorable or unfavorable characteristics for DBS candidates.¹¹⁶

Diagnosis	Ideal characteristics for DBS	Potentially unfavorable characteristics for DBS
Parkinson’s disease	Significant “on/off” fluctuations, despite best medical treatment Dyskinesia Disabling tremor PD symptoms are clearly medication-responsive (e.g., significant improvement in the UPDRS motor scores in the “on” state compared to the “off” state) Non-fixed dystonia	Difficult to control hallucinations Moderate to severe cognitive problems Presence of multiple “primitive” reflexes Incontinence of bowel and bladder Gait and balance impairment that are not responsive to dopaminergic treatment Active, untreated psychiatric issues Underlying severe psychiatric diagnosis Structural abnormality on brain imaging (beyond mild atrophy, mild white matter hyperintensities, or calcifications) Underlying severe medical comorbidity
Dystonia	Diagnosis of primary generalized dystonia Cervical dystonia Tardive dystonia syndromes Dystonia is mobile (i.e., not fixed)	Presence of contractures Moderate to severe cognitive problems Presence of significant bony deformities Secondary etiologies/other dystonias (except tardive dystonia) Presence of multiple primitive reflexes Incontinence of bowel and bladder Active, untreated psychiatric issues Underlying severe psychiatric diagnosis Structural abnormality on brain imaging Underlying severe medical comorbidity Able to adequately control symptoms with pharmacological treatment
Essential tremor	Disabling postural/action tremor Medication refractory	Moderate to severe cognitive problems Presence of severe limb ataxia along with the essential tremor Presence of severe gait ataxia Presence of multiple primitive reflexes Incontinence of bowel and bladder Active, untreated psychiatric issues Underlying severe psychiatric diagnosis Structural abnormality on brain imaging Underlying severe medical comorbidity Still able to adequately control symptoms with pharmacological treatment

Notes: DBS, deep brain stimulation; PD, Parkinson’s disease; UPDRS, Unified Parkinson’s Disease Rating Scale.

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