2026 年 13 巻 p. 323-327
Deep brain stimulation lead fracture may necessitate intracranial lead replacement. If deep brain stimulation was clinically effective before the fracture, reimplantation along the original trajectory to the same target is preferable; however, detailed technical descriptions remain limited. We present a 70-year-old woman with Parkinson disease who underwent subthalamic nucleus-deep brain stimulation. Two months after surgery, partial impedance abnormalities were detected on the left lead. At 12 months, all contacts demonstrated abnormal impedance, accompanied by worsening motor symptoms. Fourteen months after the initial surgery, we attempted to place a new lead by manually advancing it through the scar tissue that had formed along the original lead tract. Stereotactic reimplantation using a Leksell frame was prepared as a contingency if this scar-guided approach proved unsuccessful. After reopening the prior incision, the original lead was removed without resistance, and the cortical entry point was clearly identified. The preinserted stylet was removed from a new deep brain stimulation lead, which was then gently advanced through the original entry point along the pre-existing tract without reinsertion of the stylet. The lead progressed smoothly, and C-arm fluoroscopy confirmed that the tip corresponded to the prior position. Intraoperative test stimulation improved symptoms without adverse effects. Postoperative computed tomography confirmed that the reimplanted lead was positioned in an almost identical location to the prior lead. Stimulation was resumed with clinical benefit, and lead function remained normal at 6 months. Scar-guided reinsertion may represent a practical alternative; however, stereotactic backup should remain readily available, as adequate tract formation cannot be reliably predicted preoperatively.
Deep brain stimulation (DBS) is an established and effective treatment for movement disorders such as Parkinson disease, essential tremor, and dystonia. In DBS therapy, cranial surgery is typically performed once, and subsequent management generally requires only periodic replacement of the implantable pulse generator (IPG) in the chest. However, replacement of the intracranial lead may occasionally be necessary because of infection, inadequate therapeutic effect (e.g., lead migration or suboptimal target), or lead fracture.1) In cases of infection at the burr hole (lead entry) site, standard management generally involves removal of the intracranial lead, antibiotic therapy, and subsequent stereotactic reimplantation along a new trajectory. Similarly, when DBS efficacy is insufficient, stereotactic revision commonly redirects the electrode toward a revised target through a new trajectory.1,2) By contrast, in cases of lead fracture following satisfactory therapeutic benefit, reimplantation along the identical trajectory to the same target is conceptually optimal. However, reports describing practical techniques for such reimplantation remain limited.3) Here, we report a case in which we successfully reimplanted an electrode to the same target along the pre-existing trajectory by utilizing the scar tissue that had formed around the original lead.
This case report was prepared after informed consent was obtained from the patient. A 70-year-old woman developed Parkinson disease at 55 years of age. Because of wearing-off and dyskinesia, bilateral subthalamic nucleus (STN)-DBS was planned at 69 years of age.
Initial DBS surgeryThe initial procedure was performed under local anesthesia using the Leksell Model G stereotactic frame (Elekta AB, Stockholm, Sweden). Magnetic resonance imaging (MRI) and computed tomography (CT) were fused for targeting, and a DBS lead (Medtronic model B33005; Medtronic Inc., Minneapolis, MN, USA) was implanted targeting the left STN. On the right side, the STN could not be identified by microelectrode recording, and an electrode was not implanted. On the same day as lead implantation, additional skin incisions were made in the right parietal region and infraclavicular area under general anesthesia. A subcutaneous pocket was created in the right chest, and the IPG (Percept RC; Medtronic Inc., Minneapolis, MN, USA) was implanted. Postoperatively, left STN stimulation improved motor symptoms.
Two months later, electrode implantation into the right STN was performed. Preoperative testing demonstrated impedance abnormalities in the left lead (all contacts except 1a and 2a showed >5,000 Ω). Skull radiography did not reveal an obvious abnormality. To determine whether the problem was located at the extension lead or within the intracranial lead, the junction was intentionally disconnected intraoperatively, and impedance testing was repeated directly on the intracranial lead. The same abnormal pattern was reproduced, indicating that the abnormality originated in the intracranial lead rather than at the junction or in more distal hardware. As stimulation through the remaining 2 contacts still provided adequate clinical benefit, we did not replace the left lead at that stage and instead, selected close follow-up to avoid the added invasiveness of intracranial revision.
Thereafter, follow-up continued; however, 12 months after the initial left-sided surgery, impedance abnormalities were detected in all contacts of the left lead, and motor symptoms deteriorated (Table 1). Although skull radiography did not localize the site of lead damage, reimplantation of the left intracranial lead was considered necessary.
Longitudinal Clinical Course, UPDRS Scores, Left Stimulation Settings, and Lead Status
| Time point | UPDRS score | Left stimulation settings* | Impedance findings | Medication | Clinical findings | ||||
|---|---|---|---|---|---|---|---|---|---|
| Part I | Part II | Part III(DBS ON, Med ON/OFF) | Part III(DBS OFF, Med ON/OFF) | Part IV | |||||
| *Record active contact, amplitude/current, pulse width, and frequency. — indicates not available or not assessed. DBS: deep brain stimulation; Med: medication; STN: subthalamic nucleus; UPDRS: Unified Parkinson’s Disease Rating Scale |
|||||||||
| Preoperative | 1 | 3 | — | 9/34 | 8 | — | — | Levodopa/carbidopa 400 mg Ropinirole 12 mg Rasagiline 1 mg Amantadine 50 mg | Wearing-off and dyskinesia |
| Postoperative (1 month) | 3 | 3 | 2/8 | 5/15 | 7 | C+2-, 1.3 mA, 60 us, 125 Hz | Within normal range | Levodopa/carbidopa 300 mg Ropinirole 8 mg Rasagiline 1 mg Amantadine 50 mg | Motor symptoms improved after left STN stimulation |
| Postoperative(2 months; before right STN implantation) | — | — | — | — | — | C+2-, 1.5 mA, 60 us, 125 Hz | Abnormally high impedance (>5,000 Ω) at all contacts except 1a and 2a | Levodopa/carbidopa 300 mg Ropinirole 8 mg Rasagiline 1 mg Amantadine 50 mg | No obvious abnormality on skull radiography; benefit maintained; left lead not replaced |
| Postoperative(6 months) | 3 | 4 | 1/3 | 9/10 | 4 | C+1a/2a-, 1.9 mA, 60 us, 130 Hz | Abnormally high impedance (>5,000 Ω) at all contacts except 1a and 2a | Levodopa/carbidopa 300 mg Ropinirole 4 mg Rasagiline 1 mg Amantadine 50 mg | Motor improvement was maintained |
| Postoperative(1 year) | 0 | 4 | 4/22 | 7/27 | 8 | Stimulation off | Abnormally high impedance (>5,000 Ω) at all contacts | Levodopa/carbidopa 300 mg Ropinirole 4 mg Rasagiline 1 mg Amantadine 50 mg Opicapone 25 mg | Motor symptoms worsened |
| Post-revision(1 month; 15 months after initial surgery) | 0 | 0 | 4/9 | 17/26 | 8 | C+2-, 1.4 mA, 60 us, 130 Hz | Within normal range | Levodopa/carbidopa 300 mg Ropinirole 4 mg Rasagiline 1 mg Amantadine 50 mg Opicapone 25 mg | Motor symptoms improved |
| Post-revision(6 months; 20 months after initial surgery) | — | — | — | — | — | C+2-, 1.2 mA, 60 us, 130 Hz | Within normal range | Levodopa/carbidopa 300 mg Ropinirole 4 mg Rasagiline 1 mg Amantadine 50 mg | Lead function remained normal; symptoms were well controlled |
Reimplantation along the existing lead trajectory was selected as the primary strategy. As 14 months had passed since the left-sided surgery, we anticipated scar tissue around the lead tract and planned to advance a new lead through the scar tissue along the original tract. As a contingency in the event of unsuccessful scar-guided insertion, stereotactic reimplantation along a new trajectory using a Leksell frame was prepared.
Under sedation, the Leksell frame was applied. A CT scan was obtained, fused with the preoperative MRI, and stereotactic planning was performed for an alternative trajectory. Using C-arm fluoroscopy, the tip of the existing lead was marked on the lateral view. The prior left frontal incision was reopened, and the tissue surrounding the lead was dissected carefully. The lead was removed without resistance, and the intracranial entry point was clearly visualized. The explanted left intracranial lead was inspected visually, and no grossly visible break or other apparent external damage was identified. A new DBS lead (Medtronic model B33005) was then prepared. After removal of the preinserted stylet, the new lead was advanced slowly through the original entry point along the prior trajectory. The lead advanced smoothly without resistance, and C-arm fluoroscopy confirmed that the lead tip coincided with the original position. Intraoperative test stimulation improved motor symptoms without evident adverse effects. The lead was anchored with a burr-hole cap. Subsequently, under general anesthesia, the intracranial lead was connected to the subclavicular IPG via the extension lead. Impedance measurements across all contacts were within the normal range.
No postoperative complications occurred. Postoperative CT confirmed that the newly implanted intracranial lead was positioned in an almost identical location to the prior lead (Figure 1). Left-sided stimulation was resumed, resulting in improvement in motor symptoms. Subsequent manufacturer analysis of the explanted lead demonstrated conductor damage, although the exact site of failure was not specified in the available report. At 6 months after reimplantation, lead function remained normal, and symptoms were well controlled.
Comparison of lead positions before and after reimplantation.
Fused images of preoperative MRI and CT with postoperative CT after reimplantation, generated using the Medtronic Stealth Station S8 navigation system. The white electrode represents the newly reimplanted lead, while the black electrode indicates the original lead position. The upper row shows wide-field views demonstrating the entire trajectory; the lower row shows magnified views at the electrode tip level. The left column shows probe view; the center and right columns show trajectory view. The reimplanted lead follows the same trajectory as the original lead, although the reimplanted lead is positioned 0.5 mm deeper than the original lead.
CT: computed tomography; MRI: magnetic resonance imaging
Lead fracture is a common hardware-related complication of DBS. Recent studies have reported an incidence of 5.2%-8.4% per patient and 2.8%-5.1% per electrode.4-6) Fractures most frequently occur approximately 9-13 mm from the lead-extension connection,4) and proposed contributing factors include repetitive mechanical stress related to neck motion, trauma, athletic activity, and Twiddler syndrome.4,5) Diagnosis of lead fracture relies on clinical symptoms, particularly sudden deterioration of previously stable benefit, together with impedance abnormalities and radiographic findings. When such symptom worsening raises suspicion of lead fracture or other hardware failure, device interrogation should first be performed to identify the abnormality and determine whether any contacts remain usable. If one or more contacts remain usable, temporary reprogramming can be attempted. If symptoms remain inadequately controlled, plain radiographs of the skull, neck, and chest should be obtained to evaluate for fracture, disconnection, twisting, or migration. When the damaged site is identified, the affected component should be replaced accordingly. If radiographs do not localize the site of failure, the extension lead should be disconnected from the intracranial lead, and impedance of the intracranial lead should be measured directly to determine whether the abnormality lies in the extracranial or intracranial component. Extracranial abnormalities warrant replacement of the extension lead and, if necessary, the IPG, whereas intracranial abnormalities warrant replacement of the intracranial lead.4,5)
In our case, impedance abnormalities were initially limited to several contacts, and because 2 contacts remained usable, lead replacement was deferred at that stage. During follow-up, however, the abnormality progressed to involve all contacts and was accompanied by worsening motor symptoms. Although plain radiographs failed to localize the site of failure, direct impedance testing of the intracranial lead after disconnection from the extension lead indicated that the intracranial lead was the most likely source of failure, which was later confirmed by the manufacturer's analysis.
In patients who experienced robust therapeutic benefit before lead fracture, the preferred approach is reimplantation along the identical trajectory to the same target. However, there are few reports regarding specific reimplantation methods in such cases.3) It has been reported that a fibrous sheath with a thickness of 5-25 μm is frequently formed around the intracranial lead.7) Stereotactic reinsertion along the original trajectory may interact with this sheath, potentially causing deviation from the intended trajectory. Moreover, the original tract may not remain perfectly straight.8) Therefore, stereotactic reinsertion may not necessarily reproduce the original tract and may require planning of a new entry point and trajectory, thereby increasing invasiveness and, in some cases, necessitating an additional burr hole.
Conversely, the sheath itself can serve as a guide for reinsertion. Malinova et al.3) described a method in which the fractured lead was removed and a new lead was manually advanced through the residual fibrous sheath along the original tract without the use of a stereotactic frame. They reported a success rate of 71% (10 of 14 leads); failed cases subsequently underwent stereotactic surgery in a separate procedure. Our approach is conceptually aligned with their technique but differs in 2 respects: a Leksell frame was applied as a contingency for immediate conversion to stereotactic placement if the scar-guided reinsertion failed, and lead placement was performed under local anesthesia with intraoperative test stimulation to support functional verification of lead position. As in the report by Malinova et al.,3) the stylet was removed prior to insertion, and C-arm fluoroscopy was used for intraoperative confirmation.We do not suggest that this scar-guided approach should be recommended for all cases of lead fracture; however, we consider it a reasonable option in selected patients in whom the previous lead had provided clear therapeutic benefit.
Currently, there is no method to confirm the presence or extent of peri-lead scar tissue preoperatively. DiLorenzo et al.7) systematically reviewed pathological findings around DBS leads and found a fibrous sheath in 39 of 49 cases, with 10 cases showing no sheath. Notably, all 28 cases implanted for ≥12 months had a sheath, whereas among those implanted for <12 months, 11 cases had a sheath and 10 did not.7) In the series by Malinova et al.,3) the 2 failures of scar-guided reimplantation occurred at 3 and 11 months after the initial implantation. Collectively, these findings suggest that a sufficiently developed scar tissue may not always be present within 12 months. In this case, 14 months had passed since the initial implantation, and scar-guided reinsertion was feasible. However, given the limited data available, adequate scar formation cannot be guaranteed even beyond 12 months, highlighting the importance of a predefined contingency strategy.
ConclusionsIn DBS lead fracture requiring intracranial lead replacement, reimplantation along the same trajectory may be achievable by using the peri-lead fibrous tract. Because tract formation cannot be predicted reliably before surgery, a contingency plan should be established, including the option to convert to Leksell frame-based stereotactic placement if scar-guided reimplantation is unsuccessful.
Author Miki Fujimura is one of the Editorial Board members of the Journal. This author was not involved in the peer-review or decision-making process for this paper.
All authors have no conflict of interest.
