Failed Back Surgery Syndrome

FBSS, sometimes called postlaminectomy pain syndrome, is chronic pain that occurs after spinal surgery and is estimated to occur in about 40% of these patients ( ). The cause of this syndrome can be multifactorial. Somatic contributing factors include (persistent) pressure on the spinal nerve by residual or recurrent disc herniation or epidural fibrosis and/or traumatization of a nerve root. Psychological factors may also play an important role ( ) .

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  History : FBSS patients complain about persistent low-back pain, but can also have persistent leg pain in the projection territory of the affected nerve root.

  
  
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  Neurological exam : Neurological examination can be normal, but changes can be found in strength, sensibility, and reflexes in the distribution of the affected nerve root (see Fig. 49.2 and Table 49.2 ).

  
  
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  Diagnostic testing : Electromyography can be helpful, but is usually not necessary. Magnetic resonance imaging (MRI) can show either a compressive lesion such as epidural fibrosis and disc herniation or no actual lesion at all.

  
  
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  Spinal cord stimulation : Conventional SCS is recommended for the use in patients with pronounced leg pain and insufficient pain relief with conservative treatment, and is superior to reoperation ( ). In 2005 North et al. published a randomized controlled trial (RCT) in 50 patients with FBSS. Conventional SCS proved to be more effective than reoperation. Furthermore, a success rate of almost 50% (>50% pain relief) in the conventional SCS-treated FBSS patient group as compared to a success rate of about 10% in the nonSCS group was reported in another multicenter RCT ( ).

  
  

  Remarkably, conventional SCS is presently underutilized and only used in 2.4% of the cases of FBSS, and a longer delay to implantation has been shown to result in higher healthcare resource utilization ( ). For more information about SCS for FBSS and low-back pain we refer readers to Chapter 50 .

Postherpetic Neuralgia

A herpes zoster infection is a viral infection of the dorsal root ganglion. PHN is pain related to or following resolution of an acute herpes zoster infection, usually recognized by a typical dermatomal rash. There is no clear distinction between herpetic pain and postherpetic pain, but usually pain persisting for 3 months after resolution of the rash is considered PHN pain. PHN occurs more often in the elderly and is more often refractory to medical management ( ).

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  History : PHN is characterized by neuropathic pain in the distribution area of the affected nerve root (in the area of the herpes zoster rash). This pain is often intractable and can be long-lasting.

  
  
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  Neurological exam : Neurological examination can be normal, although changes can be found in sensibility in the distribution of the nerve root ( Fig. 49.2 and Table 49.2 ).

  
  
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  Diagnostic testing: Not necessary.

  
  
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  Neuromodulation: There are only a few positive case series of neuromodulation for refractory PHN and conventional SCS ( ). In a prospective case study of 28 patients with PHN, 82% of the patients achieved pain relief after conventional SCS ( ). In conclusion, the evidence for conventional SCS in PHN is very weak and treatment should only be done in a research setting.

Plexopathy (Traumatic)

Traumatic plexus lesions can arise after surgery but also from severe trauma. Based on the anatomy of the plexus, lesions can be subdivided in preganglionic (root avulsions), postganglionic, and combined lesions. Preganglionic lesions can lead to excruciating pain (or deafferentiation pain) ( ). It is thought that root avulsions lead to specific peripheral and central changes that differ from other peripheral neuropathies ( ).

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  History/neurological exam : Symptoms of a plexus lesion include weakness, loss of tendon reflexes, altered sensation, and frequently pain. The combination of miosis, ptosis, and anhydrosis (Horner sign) may point to avulsion of the C8 and T1 root.

  
  
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  Diagnostic testing : Electromyogram and nerve conduction studies (NCSs) can be of value, not only for diagnosis and in differentiating plexopathy from radiculopathy, but also in estimating the severity and degree of recovery. After a trauma, computed tomography–myelography is considered first-choice imaging when root avulsion is suspected ( ). MRI techniques can be used to demonstrate swelling and inflammation of the plexus.

  
  
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  Neuromodulation : It is not clear whether conventional SCS is a suitable treatment for patients with plexopathy and intractable neuropathic pain. No well-conducted study has been done yet, and only case series are published ( ). Conventional SCS should probably only be considered when all conservative treatments have failed in plexopathy patients with intractable neuropathic pain.

Painful Diabetic Polyneuropathy

Diabetes mellitus (DM) is a major health problem worldwide; currently more than 400 million people live with it ( ). Diabetic neuropathy is a common complication of DM (50%), and the most common form of neuropathy in developed countries. The prevalence of PDP in the DM population is estimated at 15%–30% ( ). Neuropathic pain can be the first symptom of DM, and is caused by damage to the unmyelinated C-fibers and thinly myelinated Aδ-fibers. PDP patients can also experience muscle weakness, sensory loss, and autonomic dysfunction.

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  History: PDP patients usually (more than 80%) have a symmetrical length-dependent neuropathy and complain of pain in the extremities. Normally the pain starts distally, and usually the feet are more affected than the hands.

  
  
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  Neurological exam: Neurological examination often shows diminished proprioception and reduced vibration, pinprick and temperature sensation in the affected distribution area (symmetrical and length dependent), decreased or absent tendon reflexes (distal more than proximal), and muscle weakness, first in foot elevators. When predominantly small nerve fibers are affected, vibration sensation, tendon reflexes, and strength are normal.

  
  
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  Diagnostic testing: NCSs usually show abnormalities, though the diagnosis can be made based on clinical findings. A normal outcome of an NCS does not exclude diabetic neuropathy. Small-fiber neuropathy should be considered, and additional tests are recommended. Skin biopsy with quantification of intraepidermal nerve fiber endings and quantitative sensory testing are suggested to confirm this diagnosis ( ).

  
  
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  Neuromodulation: Until 2010 only observational studies were done. Pain relief of more than 50% was observed in 63% of patients across four observational studies (25 patients) at the end of 1 year of conventional SCS. These early observational studies were promising, but insufficient to make positive recommendations for daily practice ( ). In 2014 two multicenter RCTs showed that conventional SCS for PDP may be successful in about 50% of patients after 6 months ( ). In the study by de Vos et al., 37 of 40 patients had successful trials of stimulation (93%). In 60% (25 patients) the intervention group reported more than 50% pain reduction at 6 months, whereas in the control group (20 patients treated with best conventional practice) only 5% (1 patient) reported pain reduction of more than 50%. Treatment success in a trial by Slangen et al. was 77% (17 of 22 conventional SCS patients); 41% reported more than 50% pain relief during daytime, compared to none in the best medical treatment (BMT) group. During nighttime, 36% (eight patients) in the treated group versus 7% (one patient) in the BMT group reported greater than 50% pain relief. Both trials were well conducted and, besides the use of different conventional SCS devices, they appear to be comparable. Also, the secondary outcomes were generally positive. In the trial by Slangen et al. no significant effect of the treatment on patient quality of life was demonstrated, but it may be that this trial was too small to detect this ( ). In a follow-up study, quality of life was maintained after 24 months ( ). Thus patients with PDP may benefit from conventional SCS of the dorsal columns.

Complex Regional Pain Syndrome

Complex regional pain syndrome (CRPS) often occurs after trauma or surgery, but can also occur spontaneously. The affected area is often larger than the site of the original injury. CRPS can be subdivided into two types: CRPS type 1, which is the most common (no documented presence of nerve damage), and CRPS type 2 (with documented presence of nerve damage) ( ). The estimated incidence is 26 per 100,000 person years ( ).

The pathophysiology is complex and still under research, as multiple mechanisms may be involved, such as central and peripheral sensitization, altered sympathetic nervous system function, local changes in catecholamines, inflammatory responses, and involvement of genetic and psychological factors ( ). CRPS is a diagnosis based on history and careful physical examination, and is usually a diagnosis of exclusion. For diagnosing CRPS-1, the Budapest criteria (with a diagnostic sensitivity of 0.99 and specificity of 0.68) are recommended ( ).

Budapest criteria:

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  Continuing pain which is disproportionate to any inciting event.

  
  
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  Must report at least one symptom in three of the four following categories:

  
  
  
  
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    sensory: reports of hyperesthesia and/or allodynia

    
    
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    vasomotor: reports of temperature asymmetry and/or skin color changes and/or skin color asymmetry

    
    
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    sudomotor/edema: reports of edema and/or sweating changes and/or sweating asymmetry

    
    
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    motor/trophic: reports of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nails, skin).

  
  
  
  
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  Must display at least one sign at time of evaluation in two or more of the following categories:

  
  
  
  
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    sensory: evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or deep somatic pressure and/or joint movement)

    
    
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    vasomotor: evidence of temperature asymmetry and/or skin color changes and/or asymmetry

    
    
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    sudomotor/edema: evidence of edema and/or sweating changes and/or sweating asymmetry

    
    
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    motor/trophic: evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nails, skin).

  
  
  
  
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  There is no other diagnosis that better explains the signs and symptoms.

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  History and neurological exam: Symptoms of CRPS may consist of pain (hyperalgesia, mechanical allodynia); other changes in sensibility, such as hypoalgesia and mechanical hypesthesia; autonomic dysfunction changes in pilomotor, sudomotor, and vasomotor reflex; and trophic changes and motor dysfunction such as dystonia.

  
  
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  Diagnostic testing: Specific additional tests for CRPS are not available. Other diagnoses, such as peripheral vascular disease or rheumatic disease, may be confused with CRPS. Additional testing may be required to rule out these diagnoses. In diagnosing CRPS-2, additional NCSs may be helpful.

  
  
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  Neuromodulation: There is limited evidence for the efficacy of conventional SCS for CRPS-1 patients, but it may be considered in those patients who do not respond to conservative medical management. In 2004 Kemler et al. demonstrated a 2-year positive effect of conventional SCS on pain relief in CRPS-1 patients in an RCT ( ). In this study, 54 CRPS-1 patients who had failed multiple treatment modalities, including surgical sympathectomy, were randomized to receive either conventional SCS and physical therapy or physical therapy alone. The intention-to-treat analyses showed pain reduction after 6 months in the implantation group, and the positive effects remained 2 years after implantation. CRPS-1 patients with cervical leads had similar pain reduction when compared with patients with lumbar leads ( ). After 5 years the SCS-implanted group’s results were still superior when compared to the control group (physical therapy alone) and the nonimplanted group (patients failing SCS testing), but the differences were smaller. Interestingly, 95% of the SCS group were willing to undergo this treatment again ( ). Conventional SCS provided effective long-term pain relief in 63% of CRPS-1 patients ( ). Furthermore, the authors of this study reported pain relief of at least 50% after test stimulation, which was associated with a better long-term outcome in these patients.

  
  

  In conclusion, there is limited evidence for efficacy of conventional SCS in CRPS-1, but it can be used as a last-resort treatment ( ). For more information about neuromodulation and CRPS we refer readers to Chapter 48 .

Phantom Limb Pain

Phantom pain is pain in a body part that is amputated and no longer exists, not to be confused with stump pain and phantom sensations. Again, as with CRPS, both peripheral and central mechanisms play a role in the development of phantom limb pain. Approximately 60%–80% of postamputation patients develop phantom pain.

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  History: Patients describe intermittent pain in the limb that is amputated. The pain attacks can last for seconds to hours.

  
  
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  Neurologic exam/diagnostic test: Exclude other causes such as radiculopathy, neuroma, and infection.

  
  
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  Neuromodulation: Because only case reports are available, current evidence is insufficient to recommend conventional SCS for phantom limb pain. Thus SCS should only be considered in treatment of phantom limb pain in a research setting ( ). Other forms of neuromodulation for phantom limb pain are being researched, and include high-frequency PNS for phantom limb pain ( ), dorsal root ganglion stimulation ( ), and peripheral nerve neuromodulation ( ).