Time to implement a national referral pathway for suspected cauda equina syndrome: review and outcome of 250 referrals.

INTRODUCTION: Cauda equina syndrome (CES) is a condition with significant implications and medico-legal profile. The literature still lacks large primary studies to provide strong evidence for a robust management pathway. Statements from Neurosurgical and Spinal societies support early diagnosis and imaging but this has not resulted in any noticeable shift in referral pattern. We strongly feel the need for a nationally agreed, evidence-based referral pathway in practice. We present our large series and in-depth analysis of the referral pathway to provide strong evidence for more robust referrals and management. METHODS: We reviewed 250 referrals of suspected CES (sCES) to the regional neurosurgical unit, evaluating the importance of clinical findings and the imaging pathway. RESULTS: After clinico-radiological evaluation only 32 (13%) had confirmed CES requiring urgent surgery. There was no significant difference in terms of clinical presentation between these true cases of CES (tCES) and false cases (fCES). Imaging was therefore the key rate-limiting step. MRI was the most common investigation used. 73 patients presented without imaging out of hours (OOH). In this group, investigation was delayed to the next day in 60/73 (82%) patients while only 13 (18%) patients underwent OOH MRI. Only 2 (3%) were able to have this at their local hospital. CONCLUSIONS:  As with previous studies we conclude that signs/symptoms are insufficient to identify tCES. Taking into consideration the improved outcome with early diagnosis, the importance of early scanning in diagnosing tCES, and the poor availability of OOH MRI scanning outside of neurosurgical units, we recommend a national policy of 24/7 MRI availability for cases of sCES at all hospitals with MRI scanners. This would remove the 87% of patients not requiring urgent surgery from an unnecessary and distracting referral process.

Quantifying the clinical aspects of the cauda equina syndrome - The Cauda Scale (TCS).

AIM: To quantify the clinical findings in patients with potential cauda equina syndrome (CES). METHODS: Three domains were selected: bladder function (B), perianal sensation (S) and anal tone/squeeze (T). A quantified score was given to symptoms and signs in each domain. RESULTS: The lowest score in each domain and the lowest sum score (the most severe lesion) is 0. The best sum score is 9 (the normal patient). CONCLUSION: TCS can improve the clinical assessment and management of patients with possible CES and improve communication between the doctors who are called upon to assess and treat such patients.

Guidelines for cauda equina syndrome. Red flags and white flags. Systematic review and implications for triage.

INTRODUCTION: Patients with cauda equina syndrome (CES) are frequently referred late when neurological damage cannot be reversed. National Guidelines for emergency referral, imaging and treatment of CES contain symptoms and/or signs that are those of late often, irreversible CES. Referral at this stage may be too late for that patient. METHODS: Seven sources were reviewed. Advice re emergency referral/imaging/treatment were reviewed. Symptoms/signs were compared with a standard classification of CES. RESULTS: 37 recommendations: 12 (32%) were symptoms/signs of bilateral radiculopathy (treatment usually leads to favourable outcomes). Thirteen recommendations (35%) were described in an imprecise way (could be interpreted as early or late CES). Twelve sets of symptoms/signs (32%) were those of late, often irreversible CES where an unfavourable outcome would be expected. CONCLUSIONS: Thirty-two percent of the so-called "red flag" symptoms and signs of CES in seven sources were definitely those of late, irreversible CES. These could be seen as "white flags" [flags of defeat and surrender]. Thirty-five percent of the recommendations if interpreted pessimistically (e.g. absent perineal sensation or urinary incontinence) would also be white flags; potentially therefore two-thirds of the so-called "red flag" symptoms/signs of CES could be those of late irreversible CES. Only 32% of the symptoms/signs were true "red flags" i.e. they warn of further, avoidable damage ahead. Guidelines should be redrawn to emphasise referral of patients who are at risk of developing CES or who have early CES. It is illogical for these guidelines to emphasise the clinical features of severe, often untreatable, CES. Demand for emergency MRI will increase; MRI is part of triage and should be performed at the DGH.

Standards of care in cauda equina syndrome.

What constitutes cauda equina syndrome (CES), how it should be subclassified and how urgently to image and operate on patients with CES are all matters of debate. A structured review of the literature has led us to evaluate the science and to propose evidence-based guidelines for the management of CES. Our conclusions include this guidance: pain only; MRI negative - recommend: analgesia, ensure imaging complete (not just lumbar spine) adequate follow-up. Bilateral radiculopathy (CESS) with a large central disc prolapse - recommend: discuss with the patient and if for surgery, the next day (unless deteriorates to CESI in which case emergency surgery); CESI - recommend: the true emergency for surgery by day or night; a large central PLID with uncertainty as to whether CESI or CESR (e.g. catheterised prior to CESR) or where there is residual cauda equina nerve root function or early CESR - recommend: treat as an emergency by day or night. Where there has been prolonged CESR and/or no residual sacral nerve root function - recommend: treat on the following day's list.

Cauda equina syndrome. An emergency, some unexpected severe symptoms and conservative treatment.

An 83 years old physician, doing only office work and no exercise, presented with cauda equine, due to a large intervertebral disk hernia between L1-L2 vertebrae, after an unorthodox movement. He also had a facet syndrome, a muscular spasm in the gluteus, a small fracture in the periphery of the body of the L2 vertebra and pain in the L4-L5, due to a previous vertebral hernia five years ago. All L1-L5 left lateral area was painful. He felt an unbearable pain. He also had a degree of paralysis of the gastrointestinal (GI) and the genitourinary system. He could not take analgesics or anti-inflammatory drugs per os because of the paralysis of the GI system. His pain was relieved only by intramuscular injections of parecoximbe (a cyclooxigenase-2 inhibitor, COX-2). The disc hernia was treated without surgery. After 43 days in bed, he was able to start exercising in order to treat muscles' atrophy.

Neurological deterioration in cauda equina syndrome is probably progressive and continuous. Implications for clinical management.

Fifty-six human and animal studies of cauda equina syndrome (CES) were reviewed. The evidence from human studies was poor (level IV). Evidence from animal studies and limited evidence from human studies suggest that structural and functional neurological losses are a progressive, continuous process. The longer the cauda equina nerve roots are compressed the greater the harm and the poorer the extent of recovery. This should prompt diagnosis and surgery for all CES patients as soon as practicably possible.

Pudendal nerve stimulation for bowel dysfunction in complete cauda equina syndrome.

OBJECTIVE: Pudendal nerve stimulation (PNS) aims to maximize afferent or efferent stimulation from the sacral plexus. BACKGROUND: We hypothesized this may be a promising new treatment for patients with bowel dysfunction in complete cauda equina syndrome (CES). METHODS: Thirteen patients with complete CES [8 constipation predominant (group 1) and 5 incontinence predominant (group 2)] had a 3-week trial of PNS. Patients who showed a 50% or more improvement in symptoms during the trial phase proceeded to permanent neurostimulator implantation. RESULTS: Five (63%) of the 8 patients in group 1 showed a 50% or more improvement in bowel symptoms during the trial phase and were permanently implanted. The mean Cleveland Clinic constipation score, sense of incomplete evacuation (%), and straining during defecation (%) improved from 17 ± 3.2 to 10 ± 4.5, 94 ± 18% to 30 ± 35%, and 81 ± 23% to 44 ± 38%, respectively. All 5 patients in group 2 showed a 50% or more reduction in incontinent episodes during the trial phase. The mean St Mark's score, ability to defer defecation, and the number of incontinent episodes per week improved from 18 ± 1.0 to 3.8 ± 2.5, 2.2 ± 1.8 to 11 ± 5.5 minutes, and 9.4 ± 10.7 to 0.4 ± 0.5 episodes, respectively, per week. During a median follow-up of 12 (10-22) months of permanent implantation, one patient lost efficacy at 6 months due to lead migration and another required removal and reimplantation of the neurostimulator due to wound infection. CONCLUSIONS: PNS is an effective treatment in the short term for bowel dysfunction in some patients with complete CES.

Differentiation of neonatal dorsal root ganglion-derived neural stem cells into oligodendrocytes after intrathecal transplantation into a cauda equina lesion model.

Cauda equina syndrome (CES) is characterized by varying patterns of low back pain, sciatica, lower extremity sensorimotor loss, and bowel and bladder dysfunction. The prognosis for complete recovery of CES is dependent on not only the time before surgical intervention with decompression but also the severity of the nerve damage. Delayed or severe nerve compression impairs the capability of nerve regeneration. Transplantation of neural stem cells (NSCs) may facilitate axon regeneration and functional recovery in a spectrum of neurological disorders. Our study shows that the NSCs derived from early postnatal dorsal root ganglion (DRG) are able to proliferate to form neurospheres and differentiate into O4(+) oligodendrocytes but not glial fibrillary acidic protein (GFAP(+)) astrocytes or ßIII-tubulin(+) neurons in vitro. After intrathecal transplantation into the lumbar spinal canal stenosis animal model, most of the GFP-expressing NSCs were induced to differentiate into oligodendrocytes in vivo. Although the recovery of sensorimotor function was not significantly improved in rats with transplantation therapy, our results implied that subarachnoid microinjection of NSCs may promote axon regeneration of DRG neurons in the cauda equina model after nerve injury.

Hip pain and cauda equina syndrome.

Acute cauda equina syndrome secondary to a spinal epidural abscess as a result of a psoas abscess is very uncommon. We report the case of a 64-year old with a 6-day history of left hip pain, which progressively worsened until she presented to the emergency department with systemic infective symptoms and classical acute cauda equina syndrome. A good clinical outcome was achieved by urgent posterior decompression, followed by CT-guided drainage of the psoas abscess and appropriate antibiotic treatment.

Assessing and managing patients with cauda equina syndrome.

Cauda equina syndrome is a surgical emergency that requires prompt assessment and swift surgical intervention. Compression of the cauda equina can result in loss of power and sensation to the lower limbs, back pain and loss of bladder and bowel function. Research regarding timing of surgery and surgical outcome continues to be debated. Nurses have an important role in recognising symptoms of cauda equina syndrome and supporting the patient and effectively managing care based on individual healthcare needs.

[Neurological involvement in brucellosis; clinical classification, treatment and results]. / Brusellozda sinir sistemi tutulumu; klinik siniflama, tedavi ve sonuçlar.

The aim of this retrospective study was to describe and to categorize different clinical pictures of patients with neurobrucellosis in our clinic, and present demographical and laboratory data about the patients. Hospital records of 430 patients with brucellosis between 2003 and 2009, were retrospectively reviewed. Out of 430 patients, 19 (4.4%) had neurobrucellosis. These patients were classified into four groups: Meningitis group (n= 14, 13 cases of subacute/chronic meningitis, one case of acute meningitis), encephalomyelitis group (n= 3, one case of meningoencephalomyelitis, one case of cerebellar abscess and one case of transverse myelitis), polyradicular group (n= 1, Miller-Fisher Syndrome), and others (n= 1, one case of intradural abscess). Ten patients (52.6%) were female, and the mean age of the patients was 48.8 years. About 47.4% of the patients had fever, 26% of the patients had neck stiffness and 5% of the patients were in an unconscious state. Out of 19 patients, 18 underwent lumbar puncture and they had positive brucella antibody test in cerebrospinal fluid (CSF) by standard tube agglutination method. Brucella spp. Were grown in four patient's blood culture and one patient's CSF culture. There were cranial nerve involvement in five cases, the most frequent being the sixth cranial nerve. Out of 19 patients, three recovered with sequela (paraparesis, hearing loss, dementia and sphincter disfunction) and 16 patients recovered completely. Although neurobrucellosis is most frequently presented as subacute/chronic meningitis, it may be associated with different clinical pictures. The classical triad of meningitis (fever, neck stiffness, unconsciousness) is rarely seen in brucellosis-related meningitis. Brucellosis should be kept in mind in patients with unexplained neurological findings particularly in areas where brucellosis is endemic. In addition, a current classification of neurobrucellosis, related to involved location of nervous system, clinical picture and pathogenesis, is needed.

Disorders of the Cauda Equina.

PURPOSE OF REVIEW: Cauda equina dysfunction (often referred to as cauda equina syndrome) is caused by a diverse group of disorders that affect the lumbosacral nerve roots. It is important to recognize dysfunction of the cauda equina quickly to minimize diagnostic delay and lasting neurologic symptoms. This article describes cauda equina anatomy and the clinical features, differential diagnosis, and management of cauda equina disorders. RECENT FINDINGS: The diagnosis of disorders of the cauda equina continues to be a challenge. If a compressive etiology is seen, urgent neurosurgical intervention is recommended. However, many people with clinical features of cauda equina dysfunction will have negative diagnostic studies. If the MRI is negative, it is important to understand the diagnostic evaluation and differential diagnosis so that less common etiologies are not missed. SUMMARY: Cauda equina dysfunction most often occurs due to lumbosacral disk herniation. Nondiskogenic causes include vascular, infectious, inflammatory, traumatic, and neoplastic etiologies. Urgent evaluation and surgical intervention are recommended in most cases of compressive cauda equina syndrome. Other types of treatment may also be indicated depending on the etiology.

Guillain-Barre syndrome: a clinical study in King Chulalongkorn Memorial Hospital.

BACKGROUND: Guillain-Barre Syndrome (GBS) is an acute,fatal, but treatable polyradiculopathy. Clinical data concerning this entity is scarce in Thailand The purpose of the present study was to describe clinical profiles and management of GBS as well as to determine prognostic factors in GBS. MATERIAL AND METHOD: Clinical data of GBS in King Chulalongkorn Memorial Hospital during 2002-2007 were searched by using in-patients hospital database. Asbury and Cornblath's criteria were applied for the diagnosis of GBS. Clinical data, electrophysiological data, management, and clinical prognostic factors were collected and analyzed by SPSS version 16. RESULTS: Fifty-five patients with GBS were recruited, 26 wire male and 29 were female. Mean age was 43 +/- 17 years. History of antecedent infection included: respiratory tract 29%, gastrointestinal tract 7%, ear 2%, and non-specific infection 14%. Initial presentations were limb weakness 87%, limb numbness 78%, bulbar weakness 31%, and facial weakness 18%. Electrodiagnostic study revealed demyelinating process in 54% and axonopathy in 46%. Twenty-nine patients received intravenous immunoglobulin while 13 patients underwent plasmapheresis. Clinical outcomes were satisfactory in most of the patients and only two patients died from sepsis and pneumonia. On discharge, the status of the patients were Hughes grade 1-4 in 73%, 14%, 5%, and 4% respectively. Bulbar paresis as the presenting symptom was the only clinical prognostic factor that significantly determined airway compromised and subsequently respiratory failure. CONCLUSION: Clinical features of GBS in the present series were characterized by generalized muscle weakness with mild numbness in combination with facial and bulbar paresis in nearly half of patients. Respiratory failure was encountered in 9% of cases. Clinical outcomes were satisfactory in most of the patients with or without specific treatment. The most significant predictor for adverse clinical course was the bulbar paresis as a presenting symptom and patients who presented with less disability score had a better recovery.

Factors affecting neurological outcome in traumatic conus medullaris and cauda equina injuries.

The purpose of this review was to describe the relevant factors that influence neurological outcomes in patients who sustain traumatic conus medullaris injuries (CMIs) and cauda equina injuries (CEIs). Despite the propensity for spinal trauma to affect the thoracolumbar spine, few studies have adequately characterized the outcomes of CMIs and CEIs. Typically the level of neural axis injury is inferred from the spinal level of injury or the presenting neurological picture because no study from the spinal literature has specifically evaluated the location of the conus medullaris with respect to the level of greatest canal compromise. Furthermore, the conus medullaris is known to have a small but important variable location based on the spinal level. Patients with a CMI will typically present with variable lowerextremity weakness, absent lower-limb reflexes, and saddle anesthesia. The development of a mixed upper motor neuron and lower motor neuron syndrome may occur in patients with CMIs, whereas a CEI is a pure lower motor neuron injury. Many treatment options exist and should be individualized. Posterior decompression and stabilization offers at least equivalent neurological outcomes as nonoperative or anterior approaches and has the additional benefits of surgeon familiarity, shorter hospital stays, earlier rehabilitation, and ease of nursing care. Overall, CEIs and CMIs have similar outcomes, which include ambulatory motor function and a variable persistence of bowel, bladder, and potentially sexual dysfunctions.

[Use of rechargeable stimulators in 2 cases of cauda equina syndrome]. / Utilización de sistemas de estimulación recargables. A propósito de dos casos de síndrome de cola de caballo.

The first of the 2 cases of cauda equina syndrome we report occurred following phenolization of sacral roots after a series of operations for Hirsprung disease. The second occurred after trauma from a bullet that hit the spine. Fecal and urinary incontinence and neuropathic pain in the lower extremities were present in both cases. After various treatments failed, both patients were given dual spinal stimulation for integrated treatment of both incontinence and neuropathic pain. We applied a novel approach, connecting both stimulators to a single rechargeable generator, reducing medium- and long-term costs. Fewer generator replacements (every 2-3 years with the standard approach) and fewer generator implantations (2 each time with the usual system) are required when rechargeable generators are used. Patient quality of life is thus improved. The overall cost of the implants is reduced from their second year of use.

Impact of MR Neurography in Patients with Chronic Cauda Equina Syndrome Presenting as Chronic Pelvic Pain and Dysfunction.

BACKGROUND AND PURPOSE: Chronic cauda equina syndrome, defined as persistent damage of the cauda equina nerve roots within the spinal canal can be a challenging diagnosis with varied presentations. MR neurography imaging is more commonly being used to evaluate the lumbosacral spine of patients suspected of having subacute or chronic cauda equina syndrome. Our aim was to evaluate the impact of lumbosacral plexus MR neurography in the diagnostic thinking and therapeutic management of patients presenting with chronic pelvic pain and dysfunction and suspected chronic cauda equina syndrome. MATERIALS AND METHODS: Consecutive MR neurography lumbosacral plexus examinations at our institution were reviewed retrospectively. Relevant data collected included the following: patient demographics, clinical history, pertinent physical examination findings, preimaging diagnostic impression, prior MR imaging lumbar spine findings, MR neurography findings, postimaging diagnosis, and postimaging treatment plan. The impact of imaging on the preimaging clinical diagnosis and therapeutic management was evaluated. RESULTS: Of 185 studies of patients who presented with chronic pelvic pain and/or dysfunction, 23 with clinically suspected chronic cauda equina syndrome and imaging findings were included in the study (2 subjects were lost to follow-up). The mean ages were 53 ± 12 years and 53 ± 16 years for men and women, respectively. The common etiologies included arachnoiditis (n = 8), tethered cord (n = 2), and simple/Tarlov cysts (n = 3). Eighteen of 23 (78%) subjects had a change in diagnosis resulting from MR neurography findings, and 5/23 (22%) had no change. Seventeen of 21 (81%) subjects had a change in management, and 4/21 (19%) had no change. CONCLUSIONS: MR neurography impacts the diagnosis and therapeutic management of patients with suspected chronic cauda equina syndrome.

Cauda equina syndrome.

Single or double-level compression of the lumbosacral nerve roots located in the dural sac results in a polyradicular symptomatology clinically diagnosed as cauda equina syndrome. The cauda equina nerve roots provide the sensory and motor innervation of most of the lower extremities, the pelvic floor and the sphincters. Therefore, in a fully developed cauda equina syndrome, multiple signs of sensory disorders may appear. These disorders include low-back pain, saddle anesthesia, bilateral sciatica, then motor weakness of the lower extremities or chronic paraplegia and, bladder dysfunction. Multiple etiologies can cause the cauda equina syndrome. Among them, non-neoplastic compressive etiologies such as herniated lumbosacral discs and spinal stenosis and spinal neoplasms play a significant role in the development of the cauda equina syndrome. Non-compressive etiologies of the cauda equina syndrome include ischemic insults, inflammatory conditions, spinal arachnoiditis and other infectious etiologies. The use of canine, porcine and rat models mimicking the cauda equina syndrome enabled discovery of the effects of the compression on nerve root neural and vascular anatomy, the impairment of impulse propagation and the changes of the neurotransmitters in the spinal cord after compression of cauda equina. The involvement of intrinsic spinal cord neurons in the compression-induced cauda equina syndrome includes anterograde, retrograde and transneuronal degeneration in the lumbosacral segments. Prominent changes of NADPH diaphorase exhibiting, Fos-like immunoreactive and heat shock protein HSP72 were detected in the lumbosacral segments in a short-and long-lasting compression of the cauda equina in the dog. Developments in the diagnosis and treatment of patients with back pain, sciatica and with a herniated lumbar disc are mentioned, including many treatment options available.

Ultrastructural changes of compressed lumbar ventral nerve roots following decompression.

OBJECTIVE: To study whether there will be a permanent lumbar nerve root scarring or degeneration secondary to continuous compression followed by decompression on the nerve roots, which can account for postlaminectomy leg weakness or back pain. METHODS: The study was performed at the Department of Anatomy, Faculty of Medicine, King Abdul-Aziz University, Jeddah, Kingdom of Saudi Arabia during 2003-2005. Twenty-six adult male New Zealand rabbits were used in the present study. The ventral roots of the left fourth lumbar nerve were clamped for 2 weeks then decompression was allowed by removal of the clips. The left ventral roots of the fourth lumbar nerve were excised for electron microscopic study. RESULTS: One week after nerve root decompression, the ventral root peripheral to the site of compression showed signs of Wallerian degeneration together with signs of regeneration. Schwann cells and myelinated nerve fibers showed severe degenerative changes. Two weeks after decompression, the endoneurium of the ventral root showed extensive edema with an increase in the regenerating myelinated and unmyelinated nerve fibers, and fibroblasts proliferation. Three weeks after decompression, the endoneurium showed an increase in the regenerating myelinated and unmyelinated nerve fibers with diminution of the endoneurial edema, and number of macrophages and an increase in collagen fibrils. Five and 6 weeks after decompression, the endoneurium showed marked diminution of the edema, macrophages, mast cells and fibroblasts. The endoneurium was filled of myelinated and unmyelinated nerve fibers and collagen fibrils. CONCLUSION: Decompression of the compressed roots of a spinal nerve is followed by regeneration of the nerve fibers and nerve recovery without endoneurial scarring.

Development of a toolkit for early identification of cauda equina syndrome.

Aim To develop a simple cauda equina syndrome (CES) toolkit to facilitate the subjective examination of low back pain patients potentially at risk of CES. To undertake preliminary validation of the content of the toolkit. BACKGROUND: CES is a rare condition which can be very challenging to identify in a generalist medical setting. METHOD: A three phase iterative design with two stake holder groups; extended scope practitioners experienced in managing CES patients and CES sufferers. Toolkit development Synthesis of existing CES literature with CES patient data generated from in depth interviews. Toolkit validation Content validation of the draft toolkit with CES patients. Toolkit validation Content validation of the draft toolkit with extended scope physiotherapists. Findings A three arm toolkit has been developed for use with patients considered by the clinician as at risk of developing CES (eg, worsening low back pain with symptoms/signs of progressive sensory-motor deficit in the lower limbs); patient expertise, clinical expertise, research and pathways. Uniquely, the toolkit drew upon the lived experiences of patients suffering from CES to inform the content.