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First, Do No Harm: Imaging in Patients with Deep Brain Stimulators

By Hannah Checkeye


 

CASE PRESENTATION

Summary:

A 29-year-old female with a past medical history of Tourette's syndrome status post deep brain stimulator placement (2011), Ehlers-Danlos Syndrome, deep vein thrombosis during pregnancy, and migraines presents to the emergency department complaining of two weeks of headache and eye pain, nausea, vertigo, and photophobia, as well as an acute episode of right lower extremity weakness earlier in the day. The headache was partially improved with meclizine but was fully relieved by sleep. She reported that her symptoms felt unlike her usual migraines, which usually involve stabbing pain behind her temples and are associated with an aura and floaters. She denied fever, cough, shortness of breath, chest pain, abdominal pain, vomiting, diarrhea, dysuria, neck stiffness, speech difficulty, numbness/tingling, or rash.

 

Vital Signs at Triage:

BP 135/90, P 99, Temp 35.5°C, RR 18, SpO2 100% on RA

 

Pertinent Physical Exam:

GCS 15. NIHSS 1. Pupils dilated to 8 mm secondary to atropine drop use for ocular spasms. Mild esotropia present. Left eye in spasm and unable to fully assess. Unable to assess for nystagmus and EOMI as a result. No nuchal rigidity. No cranial nerve V, VII- XII deficits. Reflexes normal with exception of mute right planter response. Decreased sensation to fine touch below the right knee (85%) compared to the left. Coordination intact.

Strength

R

L

Arm abduction

5

5

Elbow flexion

5

5

Elbow extension

5

5

Wrist extension

5

5

Finger extension

5

5

Grip

5

5

Hip flexion

5

5

Knee flexion

4

5

Knee extension

4

5

Ankle dorsiflexion

4+

5

Ankle plantarflexion

5

5

 ED Course + Significant Findings after Admission:

WBC slightly elevated 11.55, CMP & LFTs wnl

Consulted neurology - recommended CT head, MRI brain, LP to rule out idiopathic intracranial hypertension (IIH). Interrogated DBS and was found to be functioning correctly.

  • CT head showed bilateral DBS leads placed in the ventral medial thalami, small area of hypodensity in the left basal ganglia possibly 2/2 artifact. No acute territorial infarction or intraparenchymal hemorrhage. No mass. No midline shift.  No acute hydrocephalus or extra-axial fluid collection.

  • Consulted ophthalmology, patient was noted to be at baseline vision without evidence of papilledema on exam

  • Admitted for further evaluation and coordination of MRI and LP

  • MRI head/brain with MR angiography and MR venogram performed, showed no acute infarction or intraparenchymal hemorrhage. No mass. No midline shift. Evidence of left frontal and right frontal deep brain stimulator with encephalomalacia along the bilateral tracts. Left parieto-occipital artifact. Small right chronic cerebellar infarct.

  • LP without fluoroscopy was performed with a small dose of fentanyl because patient was found to have a positive pregnancy test. Opening pressure was 27 but not high enough to confidently diagnosis her with IIH. LP was complicated by post LP headache which improved over a few days.

  • CMV negative, VZV negative, VDRL negative, EBC negative, HSV 1&2 negative, fungal culture no growth

  • Discharged with plan for close follow up with neurology, ophthalmology, and MFM.





Clinical Question: What unique complications should be considered when evaluating patients with deep brain stimulators?


BACKGROUND

Deep brain stimulation (DBS) is a procedure that involves the placement of electrodes into certain structures (such as the subthalamic nucleus, globus pallidus interna, ventral intermediate nucleus of the thalamus) within the brain. These electrodes are then connected to a pulse generator that is implanted in the chest wall. The pulse generator, like a pacemaker, is controlled by a computer that relays stimulation parameters such as amplitude and frequency. While the mechanism of its effects is still debated, it is approved for the treatment of essential tremors, Parkinson disease, dystonia, and treatment refractive obsessive-compulsive disease [5].

 

SUMMARY OF EVIDENCE

  • As a note, many of the studies referred to focused on patients with Parkinson’s disease, but findings are likely generalizable to most patients with movement-based disorders who undergo deep brain stimulator placement. For studies who looked generally at patients who had movement-based disorders, the findings were largely similar.

  • The most common complications of deep brain stimulation overall are infection and lead migrations, with less common complications including circuit-related impedance, cerebral bleeds, device failure, and device-related trauma [1, 3, 4, 8, 12].

  • Surgical complications after stimulator placement include infection (most common), cerebral bleeds (most common cause of morbidity and mortality), lead placement, cerebral edema, wound dehiscence, seizure, CSF leak, pneumocephalus and inadequate stimulation [1, 3, 4, 8, 12].

  • The most common device-related complication is migration of the leads, while other complications include battery failure, inadequate stimulation, impedance, and lead fracture [1, 3, 10, 12].

  • While it is rare, idiopathic intracranial hypertension may also be a complication of deep brain stimulation and may present atypically [6].

  • Eye movement abnormalities after deep brain stimulator placement may include monocular eye deviation, conjugate eye movements, and eyelid apraxia [4].

  • MRI is a difficult to obtain imaging study for patients with deep brain stimulators. Risks include heating of the electrode tips, inducing currents, mechanical force, and dysfunction of the pulse generator [2,11]. DBS vendors have created specific guidelines for MRI acquisition based on each brand and model. Few adverse events have been noted when following these guidelines, but more recent studies have also shown the MRI can sometimes be reasonably obtained outside of these guidelines. In 2020, Boutet et al. released a framework with which providers can follow to guide these decisions and is included in the image below [2].

  • CT imaging can be safely obtained in patients with deep brain stimulators and images often have little to no artifact [11].

  • Deep brain stimulators are known to cause a lot of issues regarding EKQ acquisition and researchers have sought to find ways to minimize this. Studies have found that bipolar stimulation mode results in less EKG artifact, and that turning off bipolar stimulation mode may result in more artifact due to lack of suppression of movements. Furthermore, monopolar stimulation has been shown to result in greater EKG artifact [7, 9].



RECOMMENDATIONS

  1. For patients with deep brain stimulators presenting with neurological symptoms, make sure to include infection (regardless of time since placement), intracranial hemorrhages, and lead migrations high on your differential, and if suspected, place a timely consult to neurosurgery.

  2. MRI is a safe imaging modality when DBS specific guidelines are followed, and there may be some instances where it is reasonable outside of these guidelines.

  3. CT imaging is a safe and effective form of imaging for patients with deep brain stimulators.

  4. Studies have found that bipolar stimulation mode results in less EKG artifact than monopolar, and if possible and safe in the clinical scenario, should be used while obtaining an EKG.

REFERENCES

  1. Bennett J, MacGuire J, Novakovic E, et al. Characterizing Complications of Deep Brain Stimulation Devices for the Treatment of Parkinsonian Symptoms Without Tremor: A Federal MAUDE Database Analysis [published correction appears in Cureus. 2021 Aug 17;13(8):c46. doi: 10.7759/cureus.c46]. Cureus. 2021;13(6):e15539. Published 2021 Jun 9. doi:10.7759/cureus.15539

  2. Boutet A, Chow CT, Narang K, et al. Improving Safety of MRI in Patients with Deep Brain Stimulation Devices. Radiology. 2020;296(2):250-262. doi:10.1148/radiol.2020192291

  3. Boviatsis EJ, Stavrinou LC, Themistocleous M, Kouyialis AT, Sakas DE. Surgical and hardware complications of deep brain stimulation. A seven-year experience and review of the literature. Acta Neurochir (Wien). 2010;152(12):2053-2062. doi:10.1007/s00701-010-0749-8

  4. Deuschl G, Herzog J, Kleiner-Fisman G, et al. Deep brain stimulation: postoperative issues. Mov Disord. 2006;21 Suppl 14:S219-S237. doi:10.1002/mds.20957

  5. Fariba KA, Gupta V. Deep Brain Stimulation. [Updated 2023 Jul 24]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557847/

  6. Finet P, Delavallée M, Raftopoulos C. Idiopathic intracranial hypertension following deep brain stimulation for Parkinson's disease. Acta Neurochir (Wien). 2015;157(3):443-447. doi:10.1007/s00701-015-2354-3

  7. Frysinger RC, Quigg M, Elias WJ. Bipolar deep brain stimulation permits routine EKG, EEG, and polysomnography. Neurology. 2006;66(2):268-270. doi:10.1212/01.wnl.0000194272.79084.7e

  8. Jung IH, Chang KW, Park SH, Chang WS, Jung HH, Chang JW. Complications After Deep Brain Stimulation: A 21-Year Experience in 426 Patients. Front Aging Neurosci. 2022;14:819730. Published 2022 Apr 7. doi:10.3389/fnagi.2022.819730

  9. Mruk M, Stroop R, Boergel J, et al. Neurostimulator-induced ECG artefacts: A systematic analysis. Clin Neurol Neurosurg. 2021;203:106557. doi:10.1016/j.clineuro.2021.106557

  10. Pahwa R, Wilkinson SB, Overman J, Lyons KE. Bilateral subthalamic stimulation in patients with Parkinson disease: long-term follow up. J Neurosurg. 2003;99(1):71-77. doi:10.3171/jns.2003.99.1.0071

  11. Saleh C, Dooms G, Berthold C, Hertel F. Post-operative imaging in deep brain stimulation: A controversial issue. Neuroradiol J. 2016;29(4):244-249. doi:10.1177/1971400916639960

  12. Seijo FJ, Alvarez-Vega MA, Gutierrez JC, Fdez-Glez F, Lozano B. Complications in subthalamic nucleus stimulation surgery for treatment of Parkinson's disease. Review of 272 procedures. Acta Neurochir (Wien). 2007;149(9):867-876. doi:10.1007/s00701-007-1267-1

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