Neuromodulation: Technology at the Neural Interface Received: July 8, 2013

Revised: November 28, 2013

Accepted: December 12, 2013

(onlinelibrary.wiley.com) DOI: 10.1111/ner.12153

Differential Diagnosis of Psychiatric Symptoms After Deep Brain Stimulation for Movement Disorders Davin K. Quinn, MD*; Amanda Deligtisch, MD†; Caleb Rees, BA‡; Aaron Brodsky, MD*; Daniel Evans, MD*; Mohamad Khafaja, MD*; Christopher C. Abbott, MD* Objectives: The presence of a deep brain stimulator (DBS) in a patient with a movement disorder who develops psychiatric symptoms poses unique diagnostic and therapeutic challenges for the treating clinician. Few sources discuss approaches to diagnosing and treating these symptoms. Materials and Methods: The authors review the literature on psychiatric complications in DBS for movement disorders and propose a heuristic for categorizing symptoms according to their temporal relationship with the DBS implantation process. Results: Psychiatric symptoms after DBS can be categorized as preimplantation, intra-operative/perioperative, stimulation related, device malfunction, medication related, and chronic stimulation related/long term. Once determined, the specific etiology of a symptom guides the practitioner in treatment. Conclusions: A structured approach to psychiatric symptoms in DBS patients allows practitioners to effectively diagnose and treat them when they arise. Keywords: Deep brain stimulation, depression, movement disorders Conflict of Interest: The authors report no conflict of interest.

INTRODUCTION

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Address correspondence to: Davin Quinn, MD, UNM Department of Psychiatry, 2600 Marble Avenue NE, Albuquerque, NM 87131, USA. Email: dquinn@ salud.unm.edu * Department of Psychiatry, University of New Mexico Health Sciences Center, Albuquerque, NM, USA † Department of Neurology, University of New Mexico Health Sciences Center, Albuquerque, NM, USA ‡ School of Medicine, University of New Mexico, Albuquerque, NM, USA For more information on author guidelines, an explanation of our peer review process, and conflict of interest informed consent policies, please go to http:// www.wiley.com/bw/submit.asp?ref=1094-7159&site=1

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Deep brain stimulation (DBS) is the use of electric current passing through an implanted electrode in the brain to reversibly modulate neuronal activity and reduce symptoms of neurological disease. DBS has been Food and Drug Administration-approved for the treatment of Parkinson’s disease (PD), essential tremor (ET), and dystonia. Brain structures targeted by DBS in these movement disorders include the ventral intermediate nucleus of the thalamus (Vim) for ET, the globus pallidus interna (GPi) for dystonia and PD, and the subthalamic nucleus (STN) for PD. Despite its advantage of reversibility over traditional lesioning procedures, DBS carries significant risks and side effects, including postsurgical infection, intracerebral hemorrhage, seizures, cognitive impairment, psychosis, and mood disorders (1,2). The neuroanatomic targets of DBS for movement disorders also lie in close apposition to limbic and associative nuclei and tracts that may be affected by the DBS surgery, hardware, or stimulation (3). Complications necessitating urgent or emergent evaluation are not uncommon (4). The presence of a DBS in a patient who develops psychiatric symptoms poses unique diagnostic challenges for the treating practitioner, including limitations on diagnostic testing (5); the contributions of premorbid conditions, lesion effects, and stimulation effects (2); the decision to retain or remove the DBS (6); and the safety of psychiatric treatments such as medications and electroconvulsive therapy (ECT) (7). In 2006, the Movement Disorders Society put forth expert consensus guidelines regarding relevant preoperative, operative,

postoperative, and psychiatric issues in DBS for movement disorders (1,2,8–10). Other publications since that time have comprehensively reviewed psychiatric complications of DBS (11,12). However, these publications organized complications according to symptoms, which are nonspecific for etiology, whereas the stance of the practitioner evaluating a DBS patient is to elucidate the specific etiology of complications in order to guide treatment. In this review, the authors present a framework with which to categorize psychiatric symptoms in movement disorder DBS patients according to the temporal relationship of symptom onset to the multistage DBS process: 1) preimplantation; 2) intra-operative/perioperative; 3) stimulation parameter related (3 months) (see Table 1).

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Table 1. Potential Etiologies of Neuropsychiatric Symptoms in DBS Patients. I. Preimplantation Preexisting psychiatric disorder Mood disorders Psychotic disorders Anxiety disorders Somatoform disorders Substance use disorders Preexisting neurologic disorder DBS-indicated conditions Essential tremor Dystonia Multiple sclerosis Tourette’s syndrome Parkinson’s disease Other dementias Parkinson’s-plus disorders Vascular dementia Alzheimer’s disease Lewy body dementia Frontotemporal dementia Normal pressure hydrocephalus Huntington’s disease Other basal ganglia disorders (Wilson’s disease, Fahr’s disease) Other neurologic comorbidities Cerebrovascular disease Epilepsy Cerebral atrophy Brain mass Leukoencephalopathy Ventricular enlargement Other preexisting medical conditions II. Intra-operative/perioperative Anticipatory anxiety Acute stress disorder Seizures Intracerebral hemorrhage Intracerebral hematoma Ischemia Edema Hydrocephalus Intracerebral abscess Cerebritis Multiple passes of electrodes Excess stimulation during placement Postoperative confusional state Microlesion effect Mania Apathy Psychosis Dementia III. Stimulation parameter related Excess amplitude (voltage) Current spread Insufficient current Ventral/medial contact Higher pulse width Monopolar setting IV. Device malfunction DBS off Lead migration Lead breakage Battery depletion Cable disconnection Short circuit Electromagnetic interference Patient manipulation V. Medication related Withdrawal of dopamine Dopamine dysregulation syndrome Other drug toxicities/withdrawal Anticholinergics Antidepressants Sedative hypnotics Antipsychotics Anticonvulsants Corticosteroids VI. Chronic stimulation/long term Exacerbation of preimplantation condition Psychological reaction to DBS Disappointment in response Change in role/adjustment reaction Progression of disease Chronic stimulation related

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DBS, deep brain stimulator.

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Preimplantation Psychiatric symptoms following DBS may be due to conditions that were present before the DBS implantation, including preexisting psychiatric disorders, comorbid medical conditions, and the disease treated by DBS itself (1). Movement disorders are highly associated with depression and other psychiatric symptoms: the prevalence of depressive symptoms in ET and dystonia can range from 25 to 50% (13,14) and in PD patients from 50 to 60% (15,16). In ET, dysfunction in the cerebellum, inferior olive, and thalamus is thought to underlie symptomatology (17), but it is not known whether this pathophysiology contributes to the higher rates of depression in ET patients. In dystonia, several lines of evidence point to a relationship between dysfunction in cortical–subcortical circuits and psychiatric symptoms, but this has not been explored in depth (18,19). In PD, a link between disease pathophysiology and psychiatric symptoms has been established. Lewy bodies accumulate in brain stem nuclei such as the dorsal raphe and locus coeruleus, causing cerebral monoaminergic dysregulation leading to symptoms such as depression, anxiety, and psychosis (20). The bradykinesia and apathy of PD and severe psychomotor retardation of depression may be difficult to differentiate (20,21). Therefore, a high level of suspicion must be maintained for the presence of preexisting psychiatric symptoms in PD patients referred for DBS. Somatoform disorders, masquerading as DBS-indicated movement disorders or as DBS complications, must be considered in the course of initial assessment or subsequent evaluation of complications (22). The standard practice is to treat active psychiatric symptoms until remission prior to implantation (2). The presence of depressive symptoms prior to implantation has been associated with a higher rate of major depression after DBS for PD in several trials (23,24), although this is not a consistent finding (25). The mortality associated with STN and GPi DBS for PD beyond implantation is almost entirely due to successful suicides (0.45%) (26), which explains why severe ongoing non-medication-related psychiatric symptoms in candidate patients are a contraindication to DBS (1). Despite careful preoperative screening, patients may have co-occurring disorders that are difficult to distinguish from the condition for which DBS is indicated and that carry significant risks of psychiatric symptoms themselves. These include neurodegenerative diseases such as vascular dementia, Alzheimer’s dementia, and Lewy body dementia (1). Co-occurring neurological conditions that can worsen psychiatric outcomes may be contraindications for DBS and include stroke or structural brain abnormality, epilepsy, cerebral atrophy, brain masses, white matter disease, and ventricular enlargement (1). Intra-Operative/Perioperative Psychiatric symptoms can occur at any time during surgical implantation of DBS in the target brain region or shortly after the procedure while the DBS is off. (For technical descriptions of the procedures involved, please see Rezai et al. and Machado et al. [8,9].) Anxiety, agitation, and psychosis have been reported in the operating room before any electrodes are passed into the brain because of the stress of being awake and alert for the stereotactic procedure (9,27). Acute intracerebral hemorrhage, hematoma, edema, hydrocephalus, venous air embolism, and cerebral ischemia from electrode placement have all been reported and, although often asymptomatic, may cause immediate change in mental and neurologic status (6,28–34). The number of microelectrode passes through the brain may increase the risk of intracranial hemorrhage (35).

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HEURISTICS FOR ASSESSMENT Infections of the skin over the electrode or implantable pulse generator do occur, and while encephalitis and meningitis have not been reported following DBS implantation, cases of cerebritis and intracerebral abscesses around the device and electrodes have necessitated removal of hardware (8,36,37). Seizures during or after electrode implantation are uncommon but have been reported in several institutional case series (6,31), and a recent meta-analysis found the rate of postoperative seizures to range from 0 to 13% (38). Up to 36% of DBS patients experience a confusional state following the surgery, which typically resolves spontaneously after several days (10). Factors associated with this confusion, particularly in STN DBS, include age, Parkinson’s diagnosis, effects of anesthesia or pain medications, implantation of bilateral vs. unilateral leads, and violation of the ventricular wall during implantation (39–42). Structural microlesions created by electrode placement are postulated to explain immediate benefit seen in patients’ Parkinson’s and tremor symptoms even before stimulation is applied (43). This “microlesion” hypothesis may also explain psychiatric symptoms occurring intra-operatively and in the first postoperative days, such as psychosis, mania, apathy, and acute dementia (31,44–50).

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Device Malfunction Psychiatric symptoms in a DBS patient should prompt examination of the DBS equipment and whether the circuitry is intact, the device is turned on, and the parameters are set to appropriate tolerable values. DBS device malfunction can result in rapid loss of stimulation, leading to onset or recurrence of severe motor and psychiatric symptoms (74–76). Malfunction may occur as a result of lead migration, lead fracture, equipment failure, short circuit, or battery depletion (27,29,77,78). Patient dislocation of the device from dystonic movements or obsessive manipulation should be explored if circumstances suggest this (79,80). Any environmental sources of electromagnetic interference such as cardiac pacemakers, implantable or external cardiac defibrillators, magnetic resonance imaging (MRI), and security checkpoints pose a potential risk of causing the DBS to change settings or turn off, according to the manufacturer’s online manual (10,81). Cases of adventitious current or heat at the electrode site induced by MRI, diathermy, and cardioversion leading to severe neurologic injury have been reported (5,82,83). If MRI is to be used for a DBS patient, only scanners that are equipped with 1.5 Tesla horizontal bores, transmit– receive head coils, average head-specific absorption rates below 0.1 watts/kg, and dB/dt gradients of 20 Tesla/sec or less are permitted according to manufacturer’s warnings (84,85). The manufacturer’s documentation recommends caution when performing ECT in patients with DBS because of similar concerns for the above; numerous case reports attest to the safety of ECT, both bilateral and unilateral, in patients with DBS, as long as attention is paid to ensuring proper indications for ECT are met, turning off DBS prior to each treatment, setting DBS voltage to zero, making sure ECT electrodes are not placed on DBS hardware, and obtaining pre- and post-ECT series brain scans (7).

Medication Related Medications taken concomitantly with DBS may themselves cause psychiatric symptoms. The typical regimens of medications utilized in ET, dystonia, and PD can cause substantial side effects such as physiologic withdrawal, psychosis, dopamine dysregulation syndrome, addiction, depression, mania, anxiety, delirium, and serotonin syndrome (20,86,87). DBS patients with psychiatric symptoms may be prescribed with antidepressants, anxiolytics, antipsychotics, and mood stabilizers, all of which may cause iatrogenic harm through toxicity or withdrawal mechanisms (88). The addition of STN DBS for PD to a dopaminergic regimen can precipitate symptoms of dopamine excess (65). On the other hand, rapid reduction of dopaminergic medications following STN DBS to avoid toxicity can precipitate a dopamine withdrawal syndrome, depression, anxiety, catatonia, neuroleptic malignant syndrome, or Parkinsonism-hyperpyrexia syndrome in susceptible patients (75,89–91). STN DBS is often accompanied by a poststimulation reduction in levodopa doses, which potentially accounts for the

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Stimulation Parameter Related Following successful DBS lead and generator implantation (typically after one week to allow microlesion effects to subside), the patient’s stimulator is turned on and programmed for maximum benefit with minimum side effects (10). The DBS clinician serially activates contact points spaced along the electrode and documents clinical effects of each combination across a range of voltages with pulse width and frequency held constant (typically 60 msec and 130 Hz) (10). At any point in treatment with DBS, a patient may have their parameters adjusted, such as when efficacy declines or side effects manifest. Stimulation titration or adjustment, including intra-operatively, may cause transient psychiatric symptoms as electrical current spreads into non-motor subregions of the target structure or into neighboring structures with limbic and associative connections and functions (3). In the thalamus, stimulation at the Vim may spread to the mediodorsal or ventral anterior nuclei, although their relative remoteness from Vim suggests this is unlikely, and psychiatric complications of Vim DBS are considered rare (3,51,52). In the GPi, anteromedial subregions involved in limbic and associative circuits lie adjacent to posteroventral somatomotor subregions (3). In the STN, posterolateral somatomotor regions lie close to ventromedial associative and dorsomedial limbic regions (3,9,51). As stimulation amplitude (voltage) is increased, the risk of side effects from current spread to these areas and other limbic areas and fiber tracts increases (3,53). These side effects of stimulation are time locked with the “on” state and span the entire gamut of psychiatric symptoms, including acute depression and suicidality, anxiety, panic and fear, psychosis, mania, executive dysfunction, hypersexuality, aggression, impulsivity, pseudobulbar affect, pathological gambling and impulse dyscontrol, and mirthful laughter (46,54–66). Electrical parameters of the stimulation may also determine side effects. In STN DBS, higher voltages, monopolarity, and stimulation through ventral and medial contacts on the electrodes may be more likely to cause mood symptoms (67–70). In the COMPARE trial, both STN and GPi DBS patients experienced more negative affects with ventral stimulation (67). Increasing the pulse width of the current may have variable effects on cognition, depending on the indication and target region (71,72) Stimulation parameter-related effects generally remit quickly (“washout”) when parameters are adjusted or when the DBS is

turned off (2) and may respond to appropriate pharmacologic therapies (73). Insidious symptoms that are not clearly time locked to stimulation may also develop during this period and persist despite cessation of stimulation (see section on “Chronic Stimulation Related/Long Term”). Abrupt stimulation termination should be performed only in an appropriately monitored setting, as sudden return of the movement disorder symptoms can be expected, sometimes constituting a medical emergency such as status dystonicus or Parkinsonian akinetic crisis (74,75).

QUINN ET AL. association of STN DBS with higher rates of depression compared with GPi DBS in several large head-to-head trials in PD (2). However, depression following STN DBS and levodopa reduction may not respond to increased dopaminergic medication, suggesting that dopamine withdrawal is not the only mechanism accounting for depression in STN DBS (92,93).

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Chronic Stimulation Related/Long Term (More Than Three Months Postimplant) While many prospective trials of Vim for ET, GPi for dystonia, and GPi and STN DBS for PD have reported mild overall improvements in mood and cognition following chronic stimulation, questions remain regarding whether DBS, and STN DBS in particular, can cause long-term psychiatric symptoms (93–95). In both GPi and STN DBS for PD, symptoms unresponsive to parameter changes may emerge during or after the stimulation phase, including depression, mania, emotional lability, aggression, impulsivity, psychosis, and anxiety (11,92). Apathy and anger have also been found to variably increase in STN DBS patients after surgery (28,67,93,96). Emotional lability, detected in an early series of DBS for PD (97), was prevalent in 84% of STN patients and 72% of GPi in a recent large prospective trial (98). Several trials have documented increased rates of depression in STN DBS patients compared with GPi patients (67,99), but this not a consistent finding across studies (98).The risk of suicide after DBS has attracted significant attention. A 2008 retrospective study found an elevated risk of suicide after DBS for PD (0.45%), which was associated with postoperative depression (26). In contrast, a recent large clinical trial found no increased risk of suicide for DBS patients compared with medically treated PD patients and no significant differences in suicide risk between GPi and STN DBS (100). A recent longitudinal study of GPi DBS for dystonia documented one suicide among 40 patients treated, indicating a potential risk in that population as well (101). The relative risk of depression and suicide after DBS for various conditions and targets continues to be a controversial topic. Vim DBS for ET is not thought to cause significant long-term mood symptoms, suggesting that choice of target region may alter the risk of chronic psychiatric complications (as explained in section on “Stimulation Parameter Related”), but very few studies have assessed this specifically (52). Findings of cognitive sequelae after DBS vary between the different targets studied. A mild decline in verbal fluency has been found in ET patients one year after Vim DBS, particularly with bilateral lead placement (52,94,102). GPi DBS for dystonia is not thought to be associated with cognitive impairment (103). In PD, however, STN and to a lesser extent GPi DBS are associated with decreased verbal fluency (104–107); STN DBS may also be associated with mild decrements in attention, processing speed, and executive function when compared with nonsurgical controls (108–110). If the electrode trajectory passes through the caudate nucleus when targeting STN or resides outside the usual target zone, word fluency at six months post-DBS is more likely to be impaired (111). When cognitive impairment develops greater than one year after implantation, it is generally attributed to a presurgical vulnerability or to the progressive course of an underlying neurodegenerative disease (2). In one study, the rate of conversion to dementia after DBS for PD was the same as that in a medically treated PD population (112), and conversion to dementia following DBS for PD was associated with presurgical hippocampal volume (113). Whether chronic stimulation can cause psychiatric symptoms independent of factors already mentioned has not yet been www.neuromodulationjournal.com

adequately answered. In addition to levodopa reduction contributing to mood changes, neurobiological interactions may exist between presurgical vulnerabilities and DBS stimulation leading to an affective “unmasking” phenomenon, or neuroplastic changes occurring downstream from targets in limbic pathways (2,3). Psychosocial theories have also been advanced to explain rates of depression after DBS, in which patient expectations are not realized despite clinical improvement, or when patient’s social situations, roles, or coping mechanisms become more difficult to manage (97,114). Tolerance to DBS can lead to lower quality of life; Vim DBS in particular seems to be associated with significant rates of loss of efficacy (115). While STN DBS effect in PD appears robust over long periods (116), given time, the motor and cognitive symptoms eventually dominate the clinical picture following DBS for PD (107).

HEURISTIC FOR DIFFERENTIAL DIAGNOSIS AND TREATMENT Based on the available information regarding psychiatric complications in DBS, it is possible to make the following recommendations (see Fig. 1 for algorithm): 1. Practitioners should inquire about a history of symptoms prior to implantation, not only from the patient but also from collateral information sources such as family, long-term treaters, medical records, and the team that implanted the DBS. Preimplantation conditions that are exacerbated after DBS should be treated according to standards of care for psychiatric illnesses. 2. Symptoms that occur during or shortly after implantation surgery must be thoroughly assessed for possible intracerebral lesions, infections, seizures, and microlesion effects with appropriate clinical examination, imaging, or electrophysiological tests. Care must be taken not to expose DBS patients to electromagnetic fields that may cause iatrogenic harm, such as in standard MRI machines. 3. Symptoms occurring within three months after DBS implantation or shortly after parameter change may be stimulation related, and parameter adjustment or a trial of DBS off with an adequate“washout”period (up to several weeks) may resolve the symptoms. Current spread to adjacent limbic and associative structures given their proximity to somatomotor targets is especially noteworthy in GPi and STN DBS. Practitioners should keep in mind the risks of return of severe motor symptoms with DBS off. Symptoms that do not respond well to changes in parameters may be treated as primary psychiatric symptoms. 4. Any new symptom should prompt examination of the DBS equipment and whether the circuitry is intact, the device is turned on, and the parameters are set to appropriate tolerable values. Hardware malfunctions require rapid troubleshooting and repair of the device, and may necessitate device removal or replacement. 5. Comprehensive vetting of medication regimens in symptomatic DBS patients must occur, including analysis of recent dosing changes, initiation or cessation of drugs, and drug–drug interactions via p450 and other pharmacokinetic mechanisms. The status of dopaminergic medications and their role in ongoing symptoms should receive particular attention. Medicationrelated symptoms may respond to appropriate adjustments in doses to ameliorate toxicity or withdrawal. 6. When psychiatric symptoms occur greater than three months after DBS implantation, practitioners should consider whether

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HEURISTICS FOR ASSESSMENT When did the psychiatric symptom begin?

Preimplantation

Obtain collateral history/prior records, rule out prior conditions

Intra-operative or perioperative setting (before stimulation)

Rule out anxiety, seizure, bleed, ischemia, infection

During stimulation titration (< 3 months postop)

Assess stimulation settings (contacts, voltage, pulsewidth)

Treat as underlying/ comorbid condition

Consider post-op confusion, microlesion effect

Check for medication changes/effects

If intractable, consider trial DBS off

If intractable, weigh DBS removal

Check for hardware malfunction

Chronic outpatient setting (> 3 months postop)

Check for pre-DBS condition

Consider psychologic reaction

> 3mo postop, long-term DBS effect (STN and GPi)

Figure 1. Flowchart for assessment of psychiatric symptoms after deep brain stimulation for movement disorders. DBS, deep brain stimulator; GPi, globus pallidus interna; STN, subthalamic nucleus.

the symptom is due to exacerbation or progression of a preexisting condition, or a psychological reaction to the patient’s postDBS condition, and elicit appropriate confirmatory history. Chronic stimulation leading to psychiatric symptoms is a reasonable hypothesis if other etiologies are ruled out, especially in light of potential differences between the common DBS targets and their proximity to limbic areas (Vim < GPi < STN). Long-term symptoms may also be treated as primary disorders with standard interventions, but in the event of severe symptoms that do not respond to usual therapies, with evidence implicating the DBS, the risks and benefits of removal of the DBS should be weighed with the patient.

elucidate etiologies of these symptoms and thoughtfully select effective interventions for their patients.

Authorship Statement Drs. Quinn, Deligtisch, and Abbott and Mr. Rees contributed substantially to the conception, design, acquisition of data, and interpretation of data. Drs. Quinn, Brodsky, Khafaja, and Evans assisted with drafting and critically revising of the article for important intellectual content. Dr. Abbott gave final approval to the version to be published. Dr. Abbott receives grant support from UNM CTSC 1KL2 RR 31976-1 and the Dana Foundation Program in Brain and Immuno-Imaging.

CONCLUSION

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Quinn D.K., Deligtisch A., Rees C., Brodsky A., Evans D., Khafaja M., Abbott C.C. 2014. Differential Diagnosis of Psychiatric Symptoms After Deep Brain Stimulation for Movement Disorders. Neuromodulation 2014; 17: 629–636

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DBS is a fast-growing treatment that is increasingly used in ET, dystonia, and PD to ameliorate symptoms. As such, practitioners must become familiar with the potential risks and side effects of DBS as they will be increasingly called upon to treat patients with DBS devices who manifest psychiatric symptoms. By utilizing a differential diagnostic heuristic, clinicians can more comprehensively

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COMMENTS As deep brain stimulators become more prevalent in the general population, awareness of their psychiatric sequelae becomes increasingly important both to the specialist—neurosurgeon, psychiatrist or neurologist—and general physician, family practitioner or emergency medicine doctor. The authors present a thorough review of psychiatric problems related to DBS for movement disorders and intuitive heuristic for categorizing them. Underlying neuroanatomy of relevance is also explained in their educational review. The importance cannot be overemphasized of motoric corticostriatal loops lying in parallel, adjacent, segregated circuits with limbic and cognitive loops all altered by the same types of neuromodulatory monoamine neurotransmitters. Thus psychiatric and psychological problems occurring both in relation to

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64. Okun MS, Raju DV, Walter BL et al. Pseudobulbar crying induced by stimulation in the region of the subthalamic nucleus. J Neurol Neurosurg Psychiatry 2004;75:921– 923. 65. Lim SY, O’Sullivan SS, Kotschet K et al. Dopamine dysregulation syndrome, impulse control disorders and punding after deep brain stimulation surgery for Parkinson’s disease. J Clin Neurosci 2009;16:1148–1152. 66. Krack P, Kumar R, Ardouin C et al. Mirthful laughter induced by subthalamic nucleus stimulation. Mov Disord 2001;16:867–875. 67. Okun MS, Fernandez HH, Wu SS et al. Cognition and mood in Parkinson’s disease in subthalamic nucleus versus globus pallidus interna deep brain stimulation: the COMPARE trial. Ann Neurol 2009;65:586–595. 68. Raucher-Chéné D, Charrel CL, de Maindreville AD, Limosin F. Manic episode with psychotic symptoms in a patient with Parkinson’s disease treated by subthalamic nucleus stimulation: improvement on switching the target. J Neurol Sci 2008;273:116–117. 69. 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Schilbach L, Weiss PH, Kuhn J, Timmermann L, Klosterkötter J, Huff W. Pharmacological treatment of deep brain stimulation-induced hypomania leads to clinical remission while preserving motor benefits. Neurocase 2012;18:152–159. 74. Apetauerova D, Schirmer CM, Shils JL, Zani J, Arle JE. Successfully bilateral deep brain stimulation of the globus pallidus internus for persistent status dystonicus and generalized chorea. J Neurosurg 2010;113:634–638. 75. Kim JH, Kwon TH, Koh SB, Park JY. Parkinsonism-hyperpyrexia syndrome after deep brain stimulation surgery: case report. Neurosurgery 2010;66:E1029. 76. Mahgoub NA, Kotbi N. Acute depression and suicide attempt following lowering the frequency of deep brain stimulation. J Neuropsychiatry Clin Neurosci 2009;21:468. 77. Piacentini S, Romito L, Franzini A, Granato A, Broggi G, Albanese A. Mood disorder following DBS of the left amygdaloid region in a dystonia patient with a dislodged electrode. Mov Disord 2008;23:147–150. 78. 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QUINN ET AL. DBS and the disorders it treats should always be considered clinically and mechanistically when evaluating a patient with DBS. DBS should always be undertaken with a multi-disciplinary team including a psychologist and/or psychiatrist conducting pre-operative evaluations of patients considered for DBS. These principles apply especially in DBS for non-movement disorders such as pain, OCD, depression or Tourette’s syndrome, but are pertinent to consider in movement disorders including Parkinson’s disease. Erlick Pereira, MD Oxford, United Kingdom

*** This article provides a bird’s eye overview of the many neuropsychiatric challenges that may be encountered even in the context of“successful” DBS. As such, it is a helpful guide to those looking for a recent review on the subject. Michael Pourfar, MD New York City, NY, USA

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Differential diagnosis of psychiatric symptoms after deep brain stimulation for movement disorders.

The presence of a deep brain stimulator (DBS) in a patient with a movement disorder who develops psychiatric symptoms poses unique diagnostic and ther...
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