The management of radiculopathy, neurogenic claudication and cauda equina syndrome

NEUROSURGERY

The management of radiculopathy, neurogenic claudication and cauda equina syndrome

communicate with other roots to form plexi and thereon peripheral nerves. The root traverses four zones: (1) the central canal (intrathecal); (2) the lateral recess (within the root sleeve); (3) the foramen; and (4) the extraforaminal space (Figure 2). The nomenclature of the root is related to the spinal region. In the thoracic and lumbar spine the nerve is named by the pedicle underneath from which it exits; at the L4/5 segment the L4 nerve exits (underneath the L4 vertebra’s pedicle.) In the cervical spine there is an additional root that exits above the atlas that is confusingly named the C1 root. Therefore, all cervical nerve roots are named by the pedicle above which they exit; at the C5/6 segment the C6 nerve exits (above the C6 pedicle.) Furthermore, this nomenclature anomaly leads to the nerve exiting at the cervico-thoracic junction (C7/T1) being referred to as the C8 root.

Nick Carleton-Bland Martin Wilby

Abstract Radiculopathy is a commonly encountered symptom in neurosurgical practice. This article discusses the clinical presentation, anatomy, pathophysiology and treatment of radiculopathy, neurogenic claudication and cauda equina syndrome.

Pathology Radiculopathy is a multifactorial pathology involving both a mechanic compression and an inflammatory component leading to a ‘chemical neuroradicululitis’.1 Indeed in human and animal models, compression to nerve roots alone, with the absence of inflammatory mediators, causes only mild discomfort.2 A common source of both compression and inflammation and accounting for 90% of radiculopathy is nucleus pulposis herniation, a ‘slipped disc’. Most intervertebral disc prolapses are paracentral and cause inflammation and compression in zones 1 and 2. Irritation here can cause symptoms in the transiting root (e.g. a L4/5 disc prolapse irritating the L5 transiting root, manifesting as a foot drop and pain to the great toe.) Less common is foraminal and extra-foraminal compression in zones 3 and 4, which cause an exiting nerve issue (e.g. a far lateral disc at L3/4 compressing the exiting L3 nerve manifesting as quadriceps weakness and pain and paraesthesia to the knee). The acute inflammatory response leads to phagocytosis of the disc material. This often leads to resorption and resolution of the radiculopathy; however, in a significant minority there is a failure of disc resorption and a chronic, fibrotic reaction occurs. The failure of resorption leads to continuing compression and inflammatory cytokine production and thence continuing radiculopathy.

Keywords Acute foot drop; cauda equina syndrome; lumbar canal stenosis

Introduction Radiculopathy is a symptom generated by pathology affecting the most proximal part of the peripheral nerve system (PNS) e the nerve roots. Radiculopathy manifests in all modalities subsumed by the root, commonly pain, paraesthesia and motor weakness. In addition, some patients report joint proprioceptive alteration and skin perfusion changes (Table 1). Peripheral neuropathy is differentiated from radiculopathy by the distribution of the symptoms. Root symptoms are ‘referred’ to the limb in the corresponding dermatome and myotomal distribution (Figure 1). The nature of the pain is often described as an ‘electric shock’. It is severe, often associated with axial spinal pain, exacerbated by limb extension and is recalcitrant to opioid pharmacotherapy. Radiculopathy is a common condition with a 3% prevalence in the UK population. The disability radicular symptoms cause has significant impact to the patient’s quality of life, social and economic function.

Anatomy

Nerve fibre types

The nerve roots ‘radiate’ from the spinal cord, hence radiculopathy. The root comprises a condensation of both efferent ventral roots containing lower motor neurons and afferent dorsal first order sensory neurons. The root navigates a short distance from within the spinal canal to exit the spinal column and commonly then goes on to

Nerve fibre types Type A a b g d Type B

Nick Carleton-Bland BSc(Hons) MSc PGCert MBBS(Lond) MRCS(Eng) is a Consultant Neurosurgeon at the Walton Centre, Liverpool and Honorary Lecturer at the University of Liverpool, UK. Conflicts of interest: none declared.

FRCS(Neuro. Surg)

Type C (unmyelinated)

Martin Wilby MB BChir MA FRCS (SN) PhD is a Consultant Neurosurgeon at the Walton Centre, Liverpool, UK and Director of Research. Conflicts of interest: none declared.

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Modality

Conduction speed

Diameter

Motor, proprioception Pressure Muscle spindle Pain/temperature Autonomic (preganglionic) Pain Autonomic (Post-ganglionic)

80e120 m/s

13e20 mm

0.5e2 m/s

0.1e1.5 mm

Table 1

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Please cite this article in press as: Carleton-Bland N, Wilby M, The management of radiculopathy, neurogenic claudication and cauda equina syndrome, Surgery (2018), https://doi.org/10.1016/j.mpsur.2018.09.006

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Myotomal distribution of root symptoms Trigeminal nerve branches C2

T2

C3

T3

C4

T4

C5 C6 C7

T5 T6 T7

C8

T8 T9 T10 T11 T12 T1

S2–S4 L1

Level

Myotome

L3 L4

C6

Wrist extension

C7

Elbow extension

L5

C8

Finger extension

T1

Finger abduction

L3

Knee extension

L5

Great toe extension

L2

S1

Figure 1

 screen for upper motor neuron pathology  examine for important time-critical deficits (acute painful foot drop and CES)  fitness for surgery. Clinical examination should include root tension manoeuvres (Lasegue and Braggard’s) and neurological testing-tone; power; reflexes and sensation. Tone and reflexes should be normal or reduced. If hyperreflexia and hypertonia are found, assessment must be made of the cervicothorcaic spine. Motor and sensory deficits often help corroborate the history and aid localization. Perianal sensory loss is a statistically significant predictor of cauda equina compression.4

Assessment The goals of the patient’s history are to:  assess if the symptoms are likely neurological in origin  to localize the level of the lesion  consider the nature of the lesion  screen for emergency conditions (see Box 1)  screen for anaesthetic risk factors. In the history it is mandatory to enquire about perianal sensation and urogenital symptoms. The specific urinary dysfunction of neurological aetiology is insensate urinary incontinence, i.e. the patient has no desire to void, is in retention and has overflow leakage. This so called ‘autonomic dysfunction’ is vital to recognize and act upon in a time critical manner (see Cauda Equina syndrome below). Goals of clinical examination:  confirm localization as suggested by history SURGERY --:-

Imaging The core radiological assessment is a sagittal and paired axial T2 MRI imaging performed within 6 months of onset of

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Nerve root anatomy Dura

L4 pedicle ‘Exiting’ L4 root and dural sleeve ‘Transiting’ L5 root

L4/5 disc L5 pedicle

‘Exiting’L5 root and dural sleeve Zone

1

2 3

4

Figure 2

symptoms and assessment. In this sequence CSF appears as white hyperintensity, in stark contrast to the isointense neural structures and the dark discs (Figure 3). The CSF surrounding the neural structures is used as a proxy for compression; absence of CSF represents neural compression. Patients with older implantable ferromagnetic devices such as pacemakers will require a CT myelogram. Goals of imaging:  confirm the clinical localization and the nature of the compression  screen for other levels of potential concern  allow review of bone marrow suggestive of bony benign and malignant pathology  assess for conus and lower spinal cord  review the root through all four zones.

Red flags that suggest cauda equina syndrome include3 C

C

C

C

C

Severe or progressive bilateral neurological deficit of the legs, such as major motor weakness with knee extension, ankle eversion, or foot dorsiflexion Recent-onset urinary retention (caused by bladder distension because the sensation of fullness is lost) and/or urinary incontinence (caused by loss of sensation when passing urine) Recent-onset faecal incontinence (due to loss of sensation of rectal fullness) Perianal or perineal sensory loss (saddle anaesthesia or paraesthesia) Unexpected laxity of the anal sphincter

Box 1

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Figure 3

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Treatments

Controversies The natural history of radiculopathy has been characterized by a number of observational studies. The outcome is that 75% of patients at three months and 95% of patients at one year will have recovered with conservative management.6,7 Surgical interventions such as injection therapy or surgery are known to be effective and provide faster pain relief with associated improvement in patient experience. However, there is associated risk with operation including the potential for nerve damage and paralysis. Therefore, the timing of the intervention is controversial, as many patients will improve without intervention. Therefore, most UK surgeons offer the patient surgery or injection therapy after 3e6 months of failed conservative management. Another controversy is the choice of intervention as both root injection and microdiscectomy have good efficacy; this is question is currently the subject of a randomized controlled trial.8

The majority (90%) of patients with radiculopathy are treated non-surgically.1 Antineuropathics such as pregabalin, gabapentin and amitriptyline are effective and are first-line treatment in radiculopathy without motor symptoms as per NICE guidelines. The mechanism of action of the GABAergics works at the root and spinal cord level reduce ascending pain fibre neuronal discharge. The tricyclics function by reducing reuptake of 5-HT and NA thus augmenting the paraaqueductal grey descending inhibition system.

Intervention Peri-root steroid injection is an effective treatment. This intervention does not remove compression of the disc but reduces the production of inflammatory mediators. The procedure is usually performed as a day case. The patient is position prone on an x-ray table and the needle is introduced percutanously from a paramedial entry point to the foramen. Often the patient will have an exacerbation of symptoms when the needle abuts the root. Contrast is instilled to confirm the needle within the root sleeve and then a steroid and local anaesthetic is injected. Efficacy rates are high, with 66% of patients with good relief at a year. Surgery is an effective and very commonly performed treatment. Between 80% and 90% of patients treated with microdiscectomy have relief of the radicular pain in the immediate postoperative period, often motor and sensory symptoms respond less reliably and less immediately. The principle of the operation is to remove the compressive disc extrusion, but in addition, decompression of the lateral recess and foramen are achieved with osteo-ligamentous resection. The procedure is performed under general anaesthetics and can be as a day case. The patient is placed prone and x-ray is used to localize the level. A midline incision of the skin and lumbar fascia is performed and then the multifidus muscle is stripped from the spinous process to expose the lamina. A small laminotomy allows for fenestration of the ligamentum flavum. Beneath this layer is the thecal sac medially and exiting root laterally, often the root obscured by the overhanging facet joint. Medial facetectomy allows lateral recess and proximal foraminal decompression of the nerve root. The root is medialised to allow access to the disc. The disc annulus is incised and the fragment is removed. The Pan-European SPINE TANGO registry shows the incidence of common complications:  infection 3%  recurrent disc prolapse 5%  inadvertent durotomy (‘CSF leak’) 7%  continuing radicular symptoms 10%. Material but rare complications that are mandatory to discuss with the patient include:  1% nerve injury resulting in urogenital, motor or sensory deficits  1:4000 of iliac vessel injury during discectomy  very rare risk of visual deficit from prone positioning. Wrong-level surgery is not a risk of surgery, it is a ‘never event’ that intraoperative x-ray level checks should abolish. Despite this, in 2017 in the UK wrong-level or wrong-side spine surgery occurred 13 times.5

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Specific conditions Cauda equina syndrome Cauda equina syndrome (CESR) is a defined as a triad of symptoms including:  bilateral lower limb radicular pain  perianal sensory loss  insensate urinary retention and subsequent incontinence. Often the first symptom is the radiculopathy, followed later by the addition of perianal sensory loss and then finally the triad completed by episodes of incontinence. A patient progressing through these symptoms is termed a cauda equina in evolution (CESE). A clinical picture with the absence of the urinary dysfunction is termed impending cauda equina syndrome (CESI9). CESI, CESE and CESR represent a neurosurgical emergency and when seen mandates an urgent MRI scan (Figure 3). If there is radiological evidence of compression to the cauda equina that correlate with the clinical findings then surgical decompression should occur within 24e48 hours. Delays in recognition, investigation or treatment can leave the patient with devastating urogenital dysfunction that is a source of distress and morbidity for the patient and a source of great cost to the NHS; between 2010 and 15 CES claims have cost the NHS £25m in compensation and legal fees.10 Acute foot drop Ankle dorsiflexion is vital to locomotion. It is an action generated by tibialis anterior, extensor halluces longus and extensor digitorum longus. The supply to these muscles is mostly L5, with a less contribution from L4. The peripheral nerve that delivers the L5 outflow is the common peroneal nerve. An acute painful foot drop suggests compression and is a potential surgical treatment maybe indicated. Painless foot drop is likely a ‘medical’ aetiology such as diabetes. A favourite question for examiners is how one can differentiate between a foot drop of L5 root aetiology and a foot drop from a common peroneal nerve aetiology:  The L5 root aetiology will present with a weakness associated with back pain, gluteal weakness, radicular pain and paraesthesia in a dermatomal distribution, and relative preservation of the broadly innervated peroneus muscle group (L4-S1) leading to normal foot eversion.

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decompression can improve the claudicant symptoms greatly; however, caution must be exercised as this patient group has potentially multiple co-morbidity and anaesthetic input is vital to fully assess the risks of surgery.

Conclusion Spine surgery for relief of radiculopathy makes a clinically and statistically significant improvement in health-related quality of life. The cost per quality adjusted life year is half that of a hip replacement surgery or even coronary stenting, and so represent a cost-effective intervention.11 Injection therapy may prove to be equally effective to surgery for isolated radiculopathy management, but for CES, acute foot drop and neurogenic claudication surgical decompression remains the standard. A REFERENCES 1 Vad VB, Bhat AL, Lutz GE, Cammisa F. Transforaminal epidural steroid injections in lumbosacral radiculopathy: a prospective randomized study. Spine 2002; 27: 11e6. 2 Kulisch SD, Ulstrom CL, Michael CJ. The tissue origin of low-back pain and sciatica: a report of pain response to tissue stimulation during operations on the lumbar spine using local anesthesia. Orthop Clin N Am 1991; 22: 181e7. 3 Red flag signs e National Institute for Health and Care Excellence. Accessed at URL: https://cks.nice.org.uk/sciatica-lumbarradiculopathy#!diagnosissub:1. 4 Balasubramanian K, Kalsi P, Greenough C, Seetharam M. Reliability of clinical assessment in diagnosing cauda equina syndrome. BJNS 2010; V24. 5 NHS improvement never events. Accessed at URL: https:// improvement.nhs.uk/resources/never-events-data/. 6 Peul WC, van Houwelingen HC, van den Hout WB, et al. Surgery versus prolonged conservative treatment for sciatica. N Engl J Med 2007; 356: 2245e56. 7 Weinstein JN, Tosteson TD, Lurie JD, et al. Surgical vs nonoperative treatment for lumbar disk herniation: the Spine Patient Outcomes Research Trial (SPORT): a randomized trial. JAMA 2006 Nov 22; 296: 2441e50. 8 Wilby M, NERVES Study Group. Multi-centre randomised control trial comparing the clinical and cost effectiveness of transforaminal epidural steroid injection to surgical microdisectomy for the treatment of chronic radicular pain secondary to prolapsed intervertebral disc herniation: NErve Root Block VErsus Surgery (NERVES): trial protocol. In: National Institute for Health Research Evaluation, Trials and Studies (NETS) Project Portfolio. NIHR NETS, 2015. 9 Srikandarajah N, Boissaud-Cooke MA, Clark S, Wilby MJ. Does early surgical decompression in cauda equina syndrome improve bladder outcome? Spine 2015 Apr 15; 40: 580e3. 10 http://www.nhsla.com/Safety/Documents/DYK_Cauda_Equina_ Syndrome_Web.pdf. 11 Rasanen P, Ohman J, Sintonen H, et al. Cost-utility analysis of routine neurosurgical spinal surgery. J Neurosurg Spine 2006; 5: 204e9.

Figure 4

 The common peroneal nerve aetiology will have no gluteal weakness, no back pain, pain and paraesthesia limited to the first webspace and impaired foot eversion. Many neurosurgeons are moving to early decompression of a MRC grade <3/5 in a patient with <48 hours history and an appropriate sided disc prolapse. After this window functional stimulation and foot drop splints have similar efficacy and overall many root aetiology foot drops slowly improve. Lumbar canal stenosis Neurogenic claudication is placing an increasing burden on spinal services due to improvements in longevity and increased patient expectation. Clinical presentation:  older patients  classically pain/numbness/pins and needles down one or both legs when they walk or stand (worse with spine extended)  flexion improves symptoms ‘shopping trolley sign’  often vague symptoms (legs feel dead, start dragging legs)  symptoms usually alleviated with rest, but slowly and often incompletely  significant limitation to walking distance  neurological/autonomic signs uncommon  major differential diagnosis is vascular claudication. The compressive pathology is often asymptomatic and insidiously progresses to lead to significant neural compression before symptoms. The compression is mainly from facet joint hypertrophy and liagmentum flavum degeneration posteriorly, with some contribution from disc degeneration anteriorly to narrow the neural canal and lateral recess (Figure 4). The compression is likely symptomatic when walking due to relative ischaemia of the roots. Due to the intermittent nature and likely ischaemia basis for the pain, antineuropathics are unhelpful. Due to the non-inflammatory nature of the pathology, steroid injections have been shown not to be an efficacious treatment. Posterior

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Crown Copyright Ó 2018 Published by Elsevier Ltd. All rights reserved.

Please cite this article in press as: Carleton-Bland N, Wilby M, The management of radiculopathy, neurogenic claudication and cauda equina syndrome, Surgery (2018), https://doi.org/10.1016/j.mpsur.2018.09.006