Стимуляция спинного мозга в лечении запущенной формы болезни Паркинсона

In 1817 James Parkinson described the major clinical features of this chronic, progressive disease and he was first to open the surgical or lesional concept of treatment of PD when reported contralateral cessation of tremor following cerebrovascular accident in a patient. In the past one hundred years attempts to lesioning of motor cortex and then subcortical stractures were made [1-3]. Development of stereotactic techniques [4] for placing of subcortical lesions relieved tremor in high percentage of treated patients, decrease operative mortality and morbidity. The introduction of deep brain stimulation (DBS) 20 years ago [5] has brought the treatment of PD on the new level by allowing control of major symptoms associated with advanced PD like tremor, rigidity, dyskinesias. DBS is ef- fective, reversible technique with low morbidity in comparison to traditional neuroablative techniques. However, adverse effects of this treatment option include falls, depression, motor dysfunction, head- aches, pain, speech disorder and deaths reported after DBS [6]. To this date there are no reports in literature about the effects of SCS on the symptoms related to advance PD.

Methods

A 75-year-old male patient with a ten-year history of PD presented with intractable dyskinesias in upper extremities and also moderate dystonia and bradykinesia in lower extremities. He was treated in the past by experienced neurologist specialized in movement disorders. All necessary adjustments were made in the dosing, timing and frequency of medications to reduce levodopa related dyskinesias. Upon presentation to our clinic the patient was taken madopar (levodopa 100 mg-beserazide 25 mg) one capsule three times per day and piribedil 50 mg one tablet three times daily. The patient was also involved in the physical and occupational therapy for rehabilitation purpose. His past medical history was unremarkable with the exception of well controlled hypertension and the patient was very active prior to the time when late stage of PD brought intractable dyskinesias. He encountered extreme difficulty to execute activities of daily living and was not able to drive an automobile. He was offered DBS by neurosurgeon but declined neurosurgical intervention because of concerns about potential complications and sought alternative treatment options for his intractable arm dyskinesias. In our clinic he was offered SCS trial with placement of percutaneous cervical epidural leads and the patient chose to proceed with this less invasive option. No psychological evaluation was performed prior to SCS procedure. This study was approved by IRB to characterize the safety and efficacy of SCS for control of symptoms related to Parkinson disease.

Two 8-electrode standard Octad Leads (Medtronic Inc., Minneapolis, MN) was placed in the epidural space percutaneously through the T3-T4 intervertebral space with final electrodes positioned between C3, C4, C5 and C6 (Fig. 1). The procedure was done with C-arm guidance in an ambulatory surgical center with use local anesthesia only. Both leads were connected to a temporary extension cord and to an external stimulator. During intraoperative testing different stimulation parameters were used with the purpose to achieve control of the dyskinesias in the upper extremities. When parameter settings of amplitude 1,5 volts, pulse width 350 microseconds, and frequency 50 Hz the patient felt parenthesis in both arms but at the same time dyskinesias got worse. All ranges of pulse width and frequency on the level of sensory threshold led to exaggerated dyskinesia. The extent of dyskinesias was becoming worse by increasing amplitude above the sensory threshold level. The amplification of dyskinesias at sensory threshold was minimal with pulse width 210 microseconds and frequency 50 Hz and they were completely aborted at these parameters when we brought the amplitude down to sub-threshold level 0,5 volts. During the two day SCS trial the patients experienced complete disappearance of dyskinesia in upper extremities and dystonia in both arms and legs. Post-stimulation effect lasted for 90 seconds after turning stimulation off. Stimulator parameters programmed for amplitude 0,5 volts, pulse width 210 microseconds, and frequency 20 Hz. The temporary leads were removed after two days of continuous stimulation.

Two weeks later the patient underwent implantation with permanent leads and Restore Ultra rechargeable generator (Medtronic Inc., Minneapolis, MN). Preoperatively we discussed with the patient the options for location of the implanted generator and he chose the left supragluteal area. Each of the two permanent leads were anchored to fibroaponeurotic tissue in the wound created in the upper lumbar area (Fig. 2) with 2-0 nonabsorbable suture of braided polyester (Ethibond) and Titan Anchors (Medtronic Inc., Minneapolis, MN). The leads were tunneled to the left supragluteal area where the subcutaneous pocket was created for the generator. Leads were then connected to a Restore Ultra rechargeable generator (Fig. 3). The procedures were performed in an ambulatory surgery center with intravenous sedation and local anesthesia administered by the surgeon. The post-operative course was uneventful. The initiation of spinal cord stimulation after implantation started right after the surgery in recovery unit.