ASSFN Clinical Case: Bilateral STN DBS Implant for Parkinson s Disease

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Transcription:

ASSFN Clinical Case: Bilateral STN DBS Implant for Parkinson s Disease

Parkinson s Disease Cardinal Signs: Resting tremor Rigidity Bradykinesia Postural instability Other Symptoms Dystonia Dysphagia Autonomic dysfunction Kyphosis Depression Dementia Masked facies Micrographia

PD Diagnosis Medical history and physical examination Primary means of diagnosis Medication response 2 month challenge of levodopa or dopamine agonist Imaging MRI (may rule out other diagnoses) Dopamine transporter SPECT (DaT scan) Loss of dopamine neurons in PD as well as in atypical Parkinson-like diseases May distinguish between PD and essential tremor

Parkinson s Pathology Loss of pigmented dopaminergic neurons in the substantia nigra pars compacta (SNpc) Lewy bodies and neurites

Anti-PD Medications Carbidopa/levodopa Levodopa crosses the BBB Carbidopa acts as a peripheral decarboxylase inhibitor Entacapone Catechol-o-methyltransferase (COMT) inhibitor Reduces peripheral metabolism of levodopa Monoamine oxidase inhibitors Selegiline Rasagiline Other dopamine agonists Ropinirole Pramipexole Anticholinergic agents Trihexyphenidyl Benztropine Second-line for tremor only

Indication for Surgical Management Response to medication worsens with PD progression Medication wears off before next dose Motor fluctuations between on and off time Dyskinesias Abnormal involuntary movements Side effect of dopamine agonists and levodopa Dystonia Rigid posturing Early morning and during off periods

Rationale for Surgical Management SNpc dopaminergic degeneration causes improper functioning of direct and indirect pathways Modulation of overactive STN or GPi activity to overcome thalamic inhibition and allow for motor functioning

DBS Advantages Reversible Non-destructive Stimulation titration Maximize therapeutic effects Minimize side effects Bilateral implantation Superior efficacy compared to best medical management* Disadvantages Surgical risks Infection Finite battery life Disease progression may lessen DBS effect in the long term for some patients *Folle= et al 2010, Deuschl et al 2006, Weaver et al 2009, Williams et al 2010.

Case PresentaIon 59 year old right- handed female CC: Referred for advanced Parkinson s disease Symptoms Began in 1996 with RLE tremor, diagnosed in 2000. Takes stalevo 3x a day, wears off between doses During off periods, unable to perform ADLs Tremor persists during on periods Some balance difficulty has fallen twice Important rigidity and bradikynesia Clawing of toes in the right foot Irregular jerking torso movements (dyskinesia) Sleepiness (medicaion side effect) PMH: Cholecystectomy, urinary urgency

Management Referred for surgical consideraion EvaluaIon by muli- disciplinary team including movement disorder specialist, neuropsychiatry, and neurosurgery Documented response to levodopa challenge

PreoperaIve 3T MRI scan 1-2 days before surgery AnI- PD medicaions stopped the night before surgery Frame placed the morning of surgery Head CT obtained in frame MRI and CT merged Surgical target coordinates calculated and trajectory reviewed

TargeIng Surgical target planning using a planning staion.

IntraoperaIve PaIent s head secured in semi- reclined posiion Frame is assembled Fluoroscopy prepared A`er prepping and draping, burrhole is made using stereotacic coordinates Microelectrode is lowered with electrophysiologic recording and simulaion

IntraoperaIve Surgical target confirmed using coordinates, paient response to microsimulaion, and lack of side effects to microsimulaion Microelectrode removed and DBS lead placed Fluoroscopic confirmaion of target locaion Lead connected and test simulaion performed Lead secured using locking skull cap Incision closed with lead coiled under scalp

IntraoperaIve Fluoroscopy Fiducials a=ached to Leksell frame allow for precise targeing of DBS lead.

PostoperaIve Course Confirmatory head CT obtained Frame removed PaIents usually discharged POD 1-2 Extension and IPG placed during second surgery within 1-2 weeks SImulaIon begins within several weeks and opimal parameters are gradually derived with tesing

PostoperaIve CT PostoperaIve CT in frame demonstraing lead posiion.

PostoperaIve CT Scout imaging demonstraing leads (no frame).

References 1. Williams A, Gill S, Varma T, Jenkinson C, Quinn N. Deep brain simulaion plus best medical therapy versus best medical therapy alone for advanced Parkinson's disease (PD SURG trial): a randomised, open- label trial. Lancet Neurol. 2010;9(6):581-91. 2. Weaver FM, Folle= K, Stern M, Hur K, Harris C, Marks WJ, et al. Bilateral deep brain simulaion vs best medical therapy for paients with advanced Parkinson disease: a randomized controlled trial. JAMA. 2009;301(1):63-73. 3. Folle= KA, Weaver FM, Stern M, Hur K. Pallidal versus subthalamic deep- brain simulaion for Parkinson's disease. N Engl J Med. 2010; 362:2077-91. 4. Deuschl G, Schade- Brionger C, Krack P. A randomized trial of deep- brain simulaion for Parkinson's disease. N Engl J Med. 2006; 355:896-908.

Authors Jennifer J. Cheng, MD MS 1 William S. Anderson, MD PhD 1 1 The Johns Hopkins Hospital, Department of Neurosurgery, Meyer Bldg, Room 8-181, 600 N. Wolfe Street, BalImore 21287