INTRODUCTION

In the United States, there are currently over two million amputees, with experts anticipating that number to double within the next 30 yr.1 With this expected increase, optimizing amputee care will become even more essential. Amputee research, including that on unusual conditions affecting this population, will be critical to achieving this goal. “Jumpy stump syndrome” is defined by dystonic, choreiform, and myoclonic movements of the amputated limb.2–4 These patients may also experience associated neuropathic pain, including phantom or residual limb pain.3 While there is a detailed body of research regarding amputee-related pain conditions, our understanding of this movement disorder is limited to a few individual case studies. It is believed that “jumpy stump syndrome” can begin shortly after initial amputation or years later. It has been conjectured that this movement disorder is caused by peripheral nerve damage associated with amputation and neuroma formation, but others have suggested that this may be a form of spinal myoclonus or conversion disorder associated with psychological or emotional trauma.2,5–8 In this paper, we will present a review of the current literature on etiology and treatment modalities for “jumpy stump syndrome”, as well as our own experience with this unusual problem and our unique treatment approach.

Etiology

Early reports of “jumpy stump syndrome” date back to the mid-1800s. Hancock’s first account described “convulsive movements” in the stump of an above-elbow amputee, and Mitchell documented “chorea of stumps” in civil war amputees.9,10 Numerous case reports have since detailed various presentations of stump movements while conjecturing possible etiologies.

Although Hancock suspected neuromas may influence involuntary movement, “jumpy stump syndrome” was traditionally thought to be a form of spinal reflex myoclonus.9,11–13 Steiner et al. later reported five cases of “jumping amputation stumps”, suggesting the phenomenon represented an “alternating reflex segmental myoclonus” in which afferent pathways reduced inhibitory spinal intraneuronal influence over motor neurons.11 Iacono et al. later hypothesized that involuntary movements in two post-amputation patients arose from neural generators intrinsic to the spinal cord.14 Mera et al. described a 76-year-old male with movements of his stump two months after above-knee amputation and theorized that this was caused by a loss of normal sensory input, resulting in the tonic inhibition of sensory neurons.15 Thus, the authors concluded that “autonomous neural activity within the spinal cord” led to the jumpy stump movements.15 Baruah diagnosed spinal myoclonus in a patient with a jumping thigh stump, also observing contraction of the buttocks, and ipsilateral lower abdomen movement.12 Similarly, Devetag Chalaupka et al. described a patient who developed involuntary jerks of the stump thirty days after an above-knee amputation. In this case, electrophysiologic findings showed that the limb movements were involuntary and myoclonic in nature and limited to the muscles innervated by L2-L4 spinal segments.13

Turner et al. reported on a patient who previously underwent a through-hip amputation of the left leg following a chronic methicillin-resistant Staphylococcus aureus (MRSA) infection to the knee.16 Two years prior to this, the patient also underwent a left shoulder replacement that was complicated by MRSA. The patient consistently described uncontrollable ‘jumping’ of all limbs beginning in the immediate post-amputation period. Over a month later, widespread and continuous myoclonic jerks of the stump were visible, seeming to trigger activity in the other limbs. At one point, the left arm (ipsilateral to the stump) briefly demonstrated similar myoclonus activity seen at the amputation site, raising the possibility of retrograde propagation of spinal myoclonus from the amputation site. However, it was only observed in the left arm, which had also been affected by prosthesis infection with MRSA but had not required amputation.16 Steiner et al. also mentioned the common theme of infection in their cases, thus chronic infection may possibly contribute to local afferent hyperexcitability.11

In 2009, Tyvaert et al. described the case of a 55-year-old male above the shoulder amputee who was diagnosed with myoclonus generated from the left latissimus dorsi and pectoralis major.17 EMG confirmed myoclonus, and the authors postulated that the patient’s injury originated from the spinal cord, while also resulting in brachial plexus damage, causing abnormal C5 dermatomal stimulation. They further considered neuromas as the potential cause of the patient’s myoclonus due to the sensation of pain which preceded jerking movements and ceased after anesthetic injection.17 Jancovik further supported that jumping stump is a form of segmental myoclonus but also postulated that stump dystonia could be the result of the reorganization of somatosensory and motor maps.18

Elavarasi et al. detailed a case of a right above elbow amputee presenting with spasmodic contractions stemming from structural central nervous system pathology.19 The patient presented with right facial spasms in conjunction with right lower choreiform movements. This led researchers to conduct an MRI of the patient’s brain which revealed “lacunar infarcts in the left anterolateral thalamus and left frontal subcortical white matter.”19 Additionally, there are two cases which describe tardive dyskinesia as the origin of “jumpy stump syndrome”.20,21 In 1985, Jankovic et al. treated a 58-year-old woman with left above the elbow amputation suffering from dystonic movements caused by tardive dyskinesia from the consumption of metoclopramide, an antiemetic.20 A more recent report described a 66-year-old male below knee amputee with involuntary stump movements caused by tardive dyskinesia following Haloperidol use, a first-generation antipsychotic.21

The idea that “jumpy stump syndrome” may result from peripheral nerve damage was initially published by Kulisevsky et al. in 1992.22 The authors described two above-knee amputation patients with “jumpy stump syndrome”, neither of which had accompanying neuropathic pain or phantom limb syndrome, and postulated that this movement disorder may represent an abnormal presentation of peripheral nerve injury.22 Later, Alusi et al. considered peripheral, central, and psychogenic origins when presenting three patients who developed “clonic” movements in their lower limb stumps within two months of amputation.23 The authors noted that peripheral triggers were present in all patients, along with phantom limb sensations and/or pain. They concluded that the phenomenon may be centrally mediated but peripherally triggered and that pre-amputation psychogenic factors seemed to play a role.23

Three case reports further support the notion that “jumpy stump syndrome” has a potential psychogenic origin. One report details a 42-year-old male with left below knee amputation stemming from a nonorganic, psychogenic origin.6 He suffered from 18-20 involuntary stump movements daily that developed years after initial amputation. His psychiatric evaluation revealed that his condition caused severe pain, work truancy, and high levels of anxiety and depression, all leading to suicidal thoughts. On observation, the patient showed signs of extreme discomfort and profuse sweating. Physical examination of the stump resulted in sudden, rhythmic convulsions of the amputated limb as well as powerful contractions of the hamstrings and quadriceps which occurred when the patient was excited, but ceased upon distraction.6 Davis et al. described a below the knee amputee whose leg tremors varied and at times ceased during mental distraction.7 This patient was also depressed with suicidal ideation.7 Parashar presented a 14-year-old male above the knee amputee who developed involuntary jerky stump movements two years after amputation.8 The patient showed symptoms of anxiety and depression associated with his severe stump pain and jerky movements of his stump. However, he experienced little to no “jumpy stump” or associated pain while doing things he enjoyed such as playing video games. Further, after two months of psychological intervention, the patient reported complete improvements in symptoms.8

More recent evidence has further credited peripheral nervous system pathology as the etiology of “jumpy stump syndrome”. One report described a 66-year-old male who underwent hemipelvectomy and developed involuntary pelvic stump movements without pain or phantom sensations just days after surgery.4 Because no abnormalities were found on his brain CT or spinal cord MRI and no cortical discharge was measured on electroencephalography or somatosensory evoked potentials (SSEPs), the authors assumed movements were caused by peripheral myoclonus.4

In four cases, neuromas were thought to be the cause of abnormal stump movements. Buntragulpoontawe et al. described a 38-year-old male with bilateral transfemoral amputation presenting with painful, involuntary movements of both residual limbs.24 MRI confirmed the presence of multiple neuromas of the sciatic and femoral nerves. The patient’s pain and spasms were successfully treated by injecting the sciatic neuromas with phenol.24 Both Buntragulpoontawe et al. and Tyvaert et al. reported that palpating the neuromas provoked painful involuntary movement in their respective patients.17,24 However, this was not the case for the 57-year-old male below-knee amputee patient presented by Briand et al., who experienced repetitive muscle contractions in his stump.25 Sonography of the stump revealed neuromas of the right common peroneal and tibial nerves, which the authors hypothesized was the genesis for abnormal stump movements.25 Most recently, Giray et al. suggested that the jumping stump of 57-year-old male trans-radial amputee, was caused by neuroma formation. Ultrasound identified a hypoechoic mass in the left ulnar nerve, which was confirmed to be a neuroma, and involuntary movements ceased following surgical excision of the neuroma.5

Despite the variety of reports that are listed, none agree on a definitive etiology of “jumpy stump syndrome”. This suggests that the etiology for this movement disorder is multifactorial or possibly different in each patient. Given this conclusion and our current knowledge, you must consider psychiatric, central nervous system, and peripheral nervous system factors when evaluating a patient with symptoms of this affliction. After examining these possible causes, a differential diagnosis should be formed to address them in order of likelihood.

CASE PRESENTATION

A 28-year-old male patient presented to an outside institution after he developed complex regional pain syndrome and painful flexion contracture of the extremity following arthroscopic repair of a medial meniscus tear. A left L3 sympathetic block was attempted but failed to reduce his pain, leaving the option of undergoing a left above knee amputation (AKA). Six years following the AKA, the patient experienced worsening posterior thigh and stump pain and underwent two subsequent revisions. The first revision resected an exostosis of the distal femur and the subsequent revision addressed fluid collection in the stump perceived to be the cause of pain. The patient’s pain persisted, and 6 mo following the last revision he developed severe stump spasms with uncontrollable movements (Figure 1). The spasms were painful and nearly continuous during activity. He denied phantom pain throughout this time.

FIGURE 1: Video demonstrating jumping stump (26 wk prior to TMR) (Supplement Figure S1, Supplemental Digital Content 1, https://links.lww.com/COP/A81).

At this time, the patient presented to our clinic for evaluation. A recent MRI prior to his visit displayed findings suggestive of a stump neuroma of the distal sciatic nerve measuring 1.1 cm in diameter. Additionally, while the patient stated that he was bothered by his symptoms, he denied any significant depressive episodes and was of good mood and affect. As previous intervention had not solved the patients pain issues, and it did not appear to be psychiatric in origin, it was decided to work through diagnostic and therapeutic measures to clarify the differential diagnosis. While the neuroma could have potentially been contributing to the patients’ pain, it was still unclear as to whether the pain had a peripheral or central etiology. Therefore, there was relatively limited harm in treating the neuroma non-surgically prior to discussing resection. The patient attempted taking pramipexole (Mirapex), baclofen (Gablofen), and carbidopa/levodopa (Sinemet) for 2-3 wk periods each, all of which did not relieve any symptoms. The patient was then referred to neurology where a nerve block of the left fascia iliaca was performed to achieve neurolysis of the sartorius. However, this procedure was unsuccessful, signifying the pain was not centralized. At this point in time with the failure of non-operative treatment and severe pain persistence, surgical intervention was entertained to address the perceived peripheral etiology. However, evaluation of the current literature showed that there was no standardized treatment. Due to his persistent symptoms, the failure of above treatments, and lack of consensus, we decided to perform a femoral nerve decompression and sciatic nerve targeted muscle reinnervation (TMR). TMR, while initially designed to treat acute and chronic residual phantom pain, has seen success in helping amputee populations with distal and centralized pain and was identified as a potential solution to address the symptomatology in this case. This procedure was chosen to achieve the goal of reducing pain and minimizing choreiform movements.

A longitudinal incision was made over the posterior thigh and the posterior compartment of the leg was dissected. A 1-cm neuroma on the sciatic nerve was identified at the distal nerve stump and was resected. Then, three acceptable distal targets were then found to create the TMR, one of which penetrated the adductor compartment, one in the vastus lateralis, and one in the hamstring. The adductor, hamstring, and vastus lateralis motor nerves were anastomosed using a centro-central approach to the divided sciatic nerve and wrapped with an Axogen nerve protector. The posterior compartment was then closed using standard sutures. The patient was then flipped supine and an anterior longitudinal incision was created over the anterior thigh and the anterior compartment was dissected. Intraoperatively, fasciculations and spasms and muscle was noted as light touch of the femoral nerve caused the thigh to jump (Figure 2). A tortuous, fatty mass which appeared to have adhesions to deep fascia was then visualized and carefully dissected out. The lateral femoral cutaneous nerve and femoral nerve as it exited the inguinal ligament were then identified and decompressed (Figure 3). Adhesions surrounding the femoral nerve were carefully dissected and the nerve and its branches were found to have no further areas of compression. The wound was then irrigated and closed with interrupted sutures.

FIGURE 2: Intraoperative video demonstrating spasms with stimulation of the femoral nerve (Supplement Figure S2, Supplemental Digital Content 2, https://links.lww.com/COP/A82).FIGURE 3:

Intra-operative photographs of the TMR procedure.

One week post-operatively, the patient noted that the stump was still moving slightly but it was much improved overall (Figure 4). The sartorius displayed continued spastic movements and decreased sensation to the stump from the femoral nerve was noted. The patient continued taking methocarbamol and diazepam. At 3 wk post-operatively, the patient’s visual analogue pain score (VAS) decreased to 2/10 (compared to 6/10 pre-operatively), but he continued to have spastic movements of the sartorius and lateral hip flexors, triggered by prolonged sitting.

FIGURE 4: Stump spams 6 days post-op from TMR (Supplement Figure S4, Supplemental Digital Content 3, https://links.lww.com/COP/A83).

Seven weeks post-operatively the patient returned to clinic with continued spastic movements of the stump. Management therapies were discussed, including injection of Botox or isopropyl alcohol as these have been shown to treat chronic pain conditions as well as spasticity.26 Due to the pain being refractory to other methods, and the patient desiring long lasting relief from pain, the patient’s left sartorius muscle was injected with 30 mL of 70% isopropyl.26 The muscle stopped spasming almost immediately after the injection. Two weeks following the injection, the patient noted he still experienced a “tiny wiggle” of the muscle but overall, he felt that his symptoms were almost entirely resolved.

Three months after the injection (5 mo post-TMR), the patient reported that his symptoms were stable. At this time, physical activity with lateral movement triggered some involuntary ‘wiggling’ of the muscles, however he reported no problems with normal daily office work. His symptoms were stable at 6 mo (8 mo post-op from TMR), and he stated that the pain was 90% improved and spasms were 80% improved.

RESULTS/DISCUSSION

Currently, there is no standardized treatment algorithm for “jumpy stump syndrome”.4 Multiple interventions including psychological therapy, oral medications, injections, surgical neuroma excision, and spontaneous recovery have been described, with varying efficacy, to reduce or treat the symptoms associated with this diagnosis. However, we believe TMR should be considered when a patient experiencing “jumpy stump syndrome” is believed to have pain that is peripheral in nature.

For cases of “jumpy stump syndrome” that are thought to be psychogenic in origin, acceptance and commitment therapy (ACT), physiotherapy, psychotherapy, and cognitive behavioral therapy (CBT) may be effective treatment approaches. Parashar reported a case of a 14-year-old boy, initially treated with physiotherapy and psychotherapy which resulted in symptomatic improvement after 2 wk. He then participated in ACT and after 2 mo, reported cessation of jerky movements, and 100% improvement in pain.8

Oral pharmacological treatments such as antimyoclonic, anticonvulsant, antiparkinson, and clobazam drugs have shown promise in decreasing jumpy stump symptoms, but more studies are needed to fully validate their effects.4,19 Benzodiazepines have also been used to treat jumpy stump with varying efficacy.13,16,25 Devetag Chalaupka et al. reported complete improvement of symptoms in an above-knee amputee patient using 0.5 mg TID of clonazepam and 3 yr later, the patient stopped using clonazepam with no return of symptoms.13 Another report found that benzodiazepines attenuated movements in a patient that developed uncontrollable “jumping” of all limbs after through-hip amputation.16 Initially, oral diazepam successfully controlled the patient’s symptoms; however, uncontrollable limb movements returned after debridement and closure of the amputation skin flap. The patient then received a dose of temazepam which calmed symptoms within six hours, followed by oral clonazepam, which allowed the patient to remain asymptomatic with no visible myoclonus 5 days later.16 Conversely, one report of a below-knee amputee patient showed no response to treatment with clonazepam, starting at 0.75 mg/day and increasing to 1.5 mg/day.27 Baclofen, a skeletal muscle relaxant used for treating spasms, has shown potential in reducing jumpy stump symptoms. A case study of 2 amputees showed that treatment with 20-40 mg of Baclofen per day successfully eliminated the occurrence of involuntary spasms.14 In another patient with involuntary leg spasms three years following above-knee amputation, pramipexole (a dopamine agonist used for Parkinson’s disease and restless leg syndrome) was also effective in reducing the number of jumpy stump episodes.28,29 One year later, the patient reported daily consumption of 0.27 mg, with improved sleep quality and only 4 jumping stump episodes per month compared to 40 at baseline. When pramipexole was discontinued, episodes increased to 50, but fell again upon resuming the 0.27 mg pramipexole.29 In addition to treating neuropathic pain, gabapentin may help attenuate involuntary stump movements. Mera et al. described a 76-year-old male above-knee amputee experiencing continuous involuntary stump movements.15 The patient was initially treated with Baclofen; however, this was discontinued as he developed a confused state and stump spasms persisted. Gabapentin (300 mg) was then prescribed, and all spasms ceased within 24 hr. When gabapentin was discontinued, involuntary spasms returned, but once resumed, spasms improved with complete cessation at 6 mo.15

By preventing the release of acetylcholine, injection of botulin toxin into the affected muscle has shown efficacy in some cases of “jumpy stump syndrome”.30 Botulin toxin has a 10-14 wk effect, and can decrease the release of substance P, resulting in a reduction of residual limb pain.30 There are multiple forms of botulin toxin, but only type A and type B are utilized in medical treatment. Compared to type B, type A botulin toxin is thought to have a lower affinity for nerve endings.30 Briand et al. described a below-knee amputee patient who failed to attain satisfactory symptom relief with pharmacological methods (acetylsalicylic acid, clonazepam, diclofenac, diltiazem, hydromorphone contin, perindopril, pantoprazole, and fluticasone/salmeterol combination puffer).25 A lidocaine and dexamethasone block of the sciatic nerve only temporarily improved myoclonus symptoms. Six injections of botulinum toxin type A were then given over a two-year period, until the ideal muscle group was identified. Once the correct group was injected, the patient’s self-reported satisfaction rate tripled with reduction of myoclonus and increased prosthetic wear time.25 Dave et al. described a case of a transtibial amputee who developed myoclonic discharges in their tibialis anterior and gastrocnemius.31 Botulin toxin type A (100 U) was diluted with saline (2 mL of 0.9%), and 75 U were injected into the tibialis anterior and 25 U into the gastrocnemius. At one month follow up, the patient reported a 70% decrease in spasming.31 Tyvaert et al. reported that injection of 30 U botulin toxin type A resulted in the cessation of myoclonic activity one week post-injection which lasted 14 wk in a patient with a shoulder disarticulation amputation.17 Rombauts et al. also reported that botulin toxin type A resulted in a temporary decrease in symptom severity for a 52-year-old male transtibial amputee who failed various pharmacological treatments.32 Unfortunately, due to costs and the patient’s fear of injections, the procedure was not repeated.32 Kern et al. detailed the effects of botulin toxin type B injections into muscular trigger points of four patients with dosages of 2500 IU or 5000 IU (two with upper limb amputation and two with lower limb amputation).30 Two patients reported that the injections themselves were painful, but all reported significant decreases in overall stump pain.30 These reports show that both Botulin Toxin A and B may have clinical utility in reducing pain and spasms associated with “jumpy stump syndrome”. Phenol injections have been used as a method to control spastic muscles by impeding signals to overstimulated nerves.33,34 One case report detailed the use of phenol injections for “jumpy stump syndrome”.24 A 38-year-old man with bilateral transfemoral amputations experienced painful “jumpy stump syndrome” for about 1 yr post-operatively.24 With limited response to oral pharmacological medications, phenol injections were attempted due to their “strong and lasting effects,” and ability to provide instant relief. MRI and ultrasound confirmed neuromas on the sciatic and femoral nerves, but the provider decided against injecting the femoral neuroma due to its proximity to important vascular structures.24 The sciatic neuroma was injected, and the patient reported an immediate 80% decrease in symptom severity that lasted just over 3 mo post-injection. The patient’s symptoms returned 6 mo later, but with less severity, and were controlled with oral methods.24 Neuromuscular blockade through injection of alcohol, phenol, or botulinum toxin has additionally shown to diminish the tone of overactive muscles.32,33 Alcohol or phenol can be injected directly onto the motor nerve, which leads to the breakdown of axons and proteins, reducing muscle tonicity and limiting stump spasms.32 Koh and Leng demonstrated that focal intramuscular block with alcohol is effective in controlling spasticity, both in the upper and lower extremities.35 In our case, injection of isopropyl alcohol into the patient’s sartorius almost entirely terminated the residual muscle spasms. This effect continued to be seen at 6 mo and allowed the patient to return to work with less discomfort. Given these results, isopropyl alcohol injection in addition to TMR may be effective treatment modalities to reduce the distressing symptoms of “jumpy stump syndrome”.

Giray et al. detailed the clinical course of a trans-radial amputee patient experiencing involuntary movements of his stump.5 The patient failed pharmacological treatments (gabapentin, pregabalin, duloxetine, tramadol, and hydrochloride), steroid injections, and local anesthesia. Given the ineffectiveness of these treatments, the patient opted for neuroma excision of the ulnar nerve, which resulted in the cessation of involuntary limb movements and decreased pain.5

Although most patients described in the literature have required some intervention to manage jumpy stump symptoms, Kulisevsky et al. presented a case study of patient who recovered spontaneously.22 The patient suffered from involuntary movements of the amputated limb, beginning 3 days after an above-knee amputation. The patient was given no medications or treatments outside of insulin. Yet, 3 mo later, she had full control of her limb, with no involuntary jerking. At one year follow up, the patient reported no return of jumpy stump symptoms.22 This case underscores the need to consider spontaneous recovery in patients with jumpy stump.

After amputation, nerves attempt to regenerate towards a muscle group and intrinsically try to reinnervate their target. If the targeted muscle group is damaged or lost (such as nerves attempting to regenerate towards the lost extremity), it can lead to neuroma formation. Previously, every strategy to deaden the end of a painful nerve involved hiding the nerve by burying it in muscle or bone.9 This knowledge led to the creation of TMR which was first performed in 2002.36 The goal of TMR is to redirect these severed nerves to a new muscle target, which should prevent the formation of neuromas and decrease the associated pain. Dumanian et al. described TMR as excising the neuroma and dividing the motor nerve of a nearby muscle, creating a denervated muscle segment.36 The severed nerve (from which the neuroma was removed) is then coapted to the motor nerve of the nearby muscle, creating a mixed nerve that reinnervates the muscle.36 TMR can lead to better control and overall function of prosthetics in amputees.36 In addition, TMR has been shown to significantly decrease neuroma-related residual limb pain and phantom limb pain. A review of five articles by McNamara et all, included 149 cases of patients who underwent TMR.37 The results showed that only 27% of patients developed neuromas following primary TMR. In addition, 90% of patients suffering from neuroma pain who underwent secondary TMR reported no pain following their procedure.37 Therefore, if neuromas are indeed a cause of “jumpy stump syndrome”, TMR may be a valuable tool to treat and even prevent this condition.

We acknowledge that follow-up past a year postoperatively and further patient data would better describe our findings. Additional studies can expand upon the data collected and provide evidence to support this manuscript.

CONCLUSIONS

“Jumpy stump syndrome” is an unusual consequence following amputation but can cause large amounts of distress in the afflicted patient. However, as can be surmised from the literature review, there are few reports describing its etiology and there is not a consensus in treatment. Our patient’s condition was not responsive to initial non-operative treatment which included oral pharmacological medications and a sympathetic block. Due to his unrelenting pain and limb movements, TMR was performed followed by isopropyl injection. Although TMR alone did not completely eliminate our patient’s jumping stump, it did reduce some involuntary spasming of the limb, and the patient reported a reduction in neuroma-related pain.

During surgery, the nerve and muscle were still hyperactive while the patient was under anesthesia before the neuroma was excised. This finding further indicates that his condition was likely not psychological, but peripheral in origin. Given the outcome, we believe TMR has the possibility of being utilized as a useful surgical treatment method to help reduce and prevent the worsening of the debilitating effects of “jumpy stump syndrome” in amputees when initial treatment fails. In this patient population, we believe TMR could be used in conjunction with other treatment methods such as oral drugs and isopropyl injections to ensure the most effective patient outcomes.

ACKNOWLEDGMENTS

Not applicable.

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