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14 Articles in Volume 19, Issue #5
Agonism and Antagonism of the Muscles of the Shoulder Joint: An SEMG Approach
Analgesics of the Future: The Potential of IV Formulations for Post-Op Treatment of Pain
Blood Biomarkers Show Promise for Precision Pain Management
Can I Call Myself a “Pain Specialist?”
Cases in Urine Drug Monitoring Interpretation: How to Stay in Control (Part 2)
Fear-Avoidance and Chronic Pain: Helping Patients Stuck in the Mouse Trap
How to Avoid Patient Alienation When Discussing Stress
Managing Phantom Limb Pain with Medication
Nerve Blocks Lead to Improved Quality of Life
Sacroiliac Joint Dysfunction: New Methods in Evaluation and Management
SCS Therapy in a Patient with Advanced Bilateral Kienbocks
Thoracic Epidural Abscess with Cord Compression Following a High-Frequency SCS Trial
What is the evidence to support clonidine as an adjuvant analgesic?
What’s In A Name? In This Case, That Which We Call Addiction Is Not Dependence

SCS Therapy in a Patient with Advanced Bilateral Kienbocks

In this retrospective case report, the authors use neuromodulation to manage pain associated with advanced Keinbock disease and comorbid symptoms of CRPS.
Pages 50-53

Kienbock Disease is a rare disease of the wrist characterized by osteomalacia of the lunate. Common treatment for advanced stages of the disease is surgical. Some patients, however, may be refractory to surgical intervention and go on to develop complex regional pain syndrome (CRPS) symptoms. In this retrospective case presentation, the authors describe the use of spinal cord stimulation (SCS) to treat a patient with advanced-stage Kienbock Disease.

Case Presentation

A 63-year-old female presented to the pain clinic at Saint Elizabeth Medical Center with a history of Kienbock Disease affecting both of her wrists; the disease had been diagnosed 4 years prior. Under Lichtman Classification, she was categorized as Stage IIIb (see Table I for the detailed stages). Her condition has been complicated by symptoms of CRPS Type II of her left hand, wrist, and forearm; symptoms began after surgical carpectomy with fusion of her left wrist followed by multiple revisions. The patient presented with unbearable bilateral hand pain, presumed to be caused by Kienbock Disease in the right hand and both Kienbock Disease and superimposed CRPS in the left hand.

The patient reported constant, 10 out of 10 pain ratings in both hands which severely limited her functional ability. She was unable to use either hand and kept both extremities wrapped in multiple layers of gauze. In her left hand, pain was associated with allodynia and hyperalgesia over the affected areas along with local swelling, skin temperature and color changes, and restricted hair growth and nail changes.

The patient failed medical management with agents including Tylenol, NSAIDs (contraindicated due to gastric ulcer), cyclobenzaprine, tizanidine, pregabalin, and duloxetine. Gabapentin and oxycodone provided only mild pain relief. She underwent multiple sessions of physical and occupational therapy with minimal pain relief. She had used a transcutaneous electrical nerve stimulation (TENS) unit and participated in a home exercise regimen with minimal relief. In her desperation, she began to inquire about the possibility of hand transplantation surgery.

Due to a lack of response to the above therapies and to help with the CRPS in her left hand, the authors performed a two-lead cervical spinal cord stimulator trial with T2-T3 and T3-T4 lead entry points, with both lead tips advanced to the superior border of the C2 vertebral body and spanning from C2 to C6 vertebral levels. The patient reported excellent relief in bilateral upper extremities from hands to elbows immediately during and immediately after a 7-day trial period. She reported that the entire pain areas on both sides were completely covered within the distribution of the paresthesia-based stimulation. She further stated that the trial gave her more than 80% pain relief in both hands.

The patient also stated that, for the first time since she started having pain, she was able to shake people’s hands without wearing bandages, to touch her husband with her bare hands, and to interact with her dogs. She reported needing less gabapentin and opioids and was able to attend social events without feeling drowsy or experiencing pain. After the successful SCS trial, the authors proceeded with permanent placement of an SCS implant (see Figures 1 and 2). At her 1-month and 6-month follow-up, the patient reported continuous improvement of her pain with only minor hand pain and no limitations in any functional capacity.

Figure 1. Final position of the cervical spinal cord stimulator leads (anteroposterior view), as described by the literature, should cover the C2-C7 spine to provide analgesia to the upper extremity.

Figure 2. Final position of the cervical spinal cord stimulator leads (controlateral view), as described by the literature, should cover the C2-C7 spine to provide analgesia to the upper extremity.


Approaches to Managing Keinbock Disease

Kienbock Disease is a disorder of the wrist involving osteomalacia of the lunate first described by Peste in 1843 and further described radiographically by Robert Kienböck in 1910.1 The rare disorder has a statistically unknown prevalence, however, incidental findings in retrospective studies cite an incidence of 7 in 100,000 patients.1,2 The disease occurs with breakdown and avascular necrosis of the lunate bone that leads to fragmentation and collapse of the lunate. This breakdown has classically been attributed to arterial disruption most commonly associated with trauma, but the disease may also occur after events that produce venous hypertension with elevated interosseous pressure. Severity of the disease and prognosis have been divided into a four-stage Lichtman classification system based on the degree of degeneration of the lunate and surrounding structures (see Table I).3

However, there is a lack of consensus among surgeons on the optimal treatment strategy, ranging from conservative management to complex surgery. In 2017, Lichtman, et al, put forth an algorithm for treatment ranging from immobilization of the wrist, to proximal row carpectomy and lunate replacement, to scaphocapitate fusion, and finally to salvage therapy with wrist fusion.4 It has been suggested that patients who are diagnosed and treated earlier in the course of the disease may have better outcomes than those patients who have prolonged delays in intervention.

In general, individuals with Kienbock Disease should not expect to return to normal wrist function, even after treatment. However, treatment may offer the greatest opportunity for long-term preservation of function and pain relief.5,6

Kienböck's disease is a condition where the blood supply to one of the small bones in the wrist, the lunate, is interrupted. (Source: 123RF)

Approaches to Managing CRPS

Complex regional pain syndrome is a chronic pain syndrome that most often affects one limb and usually after an injury, trauma to a peripheral nerve, or surgical intervention. It is a multifactorial disorder with clinical features of neurogenic inflammation, nociceptive sensitization, vasomotor dysfunction, and maladaptive neuroplasticity that leads to significantly increased activation of centralized pain processing.7 This wind-up of the central nervous system appears to be a key neurologic process involved in the induction and maintenance of the syndrome. CRPS occurs in two types, with similar signs and symptoms, but different causes. CRPS Type 1 commonly occurs after an illness or injury that did not directly damage the nerves in the affected limb. CRPS Type 2 tends to follow a distinct nerve injury.8

Like Kienbock Disease, there are a limited number of treatment modalities for improving symptoms of CRPS. Physical therapy is considered the gold standard in conjunction with combination therapy including anti-epileptics, antidepressants, lidocaine, ketamine, and opioids—all of which tend to provide positive outcomes with limited success (eg, mild short-term improvement of pain with significant, often long-term medication side effects).

Additionally, sympathetic interventional procedures have shown to be successful in some patients with CRPS. However, the use of SCS as part of a neuromodulation approach has shown to be very promising with Level I evidence of benefit.9

Using neuromodulation, spinal cord stimulator electrodes are placed at specific levels in the cervical spine. The use of electric signaling at those levels modulates the transmission of the incoming pain stimuli in association with the wide dynamic range neurons at that level of the dorsal horn and dorsal columns. The primary mechanism of action of SCS involves “overriding” this incoming stimulus with increased inhibition of the peripheral myelinated C fibers that are responsible for the transmission from sites of chronic pain.

Other proposed mechanisms of action include inhibition of wide dynamic range (WDR) neurons, the “gate-keepers” in the dorsal horn during pain transmission, activation of GABAergic inhibitory interneurons in the dorsal horn, activation of supraspinal mechanisms such as stimulation-induced suppression of central excitability, and stimulation-induced inhibition of the sympathetic nerves. Other mechanisms may include inhibition of the descending serotonergic neurons and locus coeruleus neurons, suppression of the neuroimmune response system influences, and antidromic vasodilation.10,11

Return to Patient Case

The patient described herein presented to our pain management clinic after seeing no improvement in her symptoms several years after undergoing a carpectomy and several revisions to her treatment regimen. She subsequently developed signs of hand muscle atrophy with allodynia and hyperalgesia to her non-dominant hand and skin color changes indicative of what one may find in cases of neuropathic pain and CRPS.

The patient failed conservative treatments and multiple interventional injections. Gabapentinoids did not provide pain relief. She did not tolerate tricyclic antidepressants (TCAs) nor serotonin and norepinephrine reuptake inhibitors (SNRIs) due to side effects. Several oral opioids were trialed with limited pain relief. The authors attempted stellate ganglion blocks with limited pain relief as well.

When the authors implanted a spinal cord stimulator in an attempt to improve the patient’s CRPS-like symptoms, however, the patient finally began to have persistent improvement of both her neuropathic and non-neuropathic pain. This finding suggests that there may be a significant component of the pain pathway from Kienbock Disease that may be centrally mediated or centrally amplified, or that there is a neuropathic component to the disease not involving CRPS. This possibility may be supported by the common knowledge that chronic pain is highly complex, involving an integrated network of regions and mechanisms throughout the body. Peripheral neurons and receptors, central spinal neurons, interneurons, and receptors, as well as supraspinal components of the brainstem, midbrain, subcortical structures, and cerebral cortex all likely play a role.

Further, due to brain plasticity, nociceptive input is not required for the perception of pain.12 However, further research in a larger patient population is needed to investigate this hypothesis.


The use of spinal cord stimulation as a salvage therapy may be beneficial or even indicated in patients who have failed conservative and surgical management and who have developed chronic neuropathic pain in the progression of Kienbock Disease who lack signs and symptoms of CRPS.

Last updated on: August 2, 2019
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