Explore the vast range of titles available.

Cauda equina syndrome (CES) is a rare condition with a disproportionately high medico-legal profile. It occurs most frequently following a large central lumbar disc herniation, prolapse or sequestration. Review of the literature indicates that around 50–70% of patients have urinary retention (CES-R) on presentation with 30–50% having an incomplete syndrome (CES-I). The latter group, especially if the history is less than a few days, usually requires emergency MRI to confirm the diagnosis followed by prompt decompression by a suitably experienced surgeon. Every effort should be made to avoid CES-I with its more favourable prognosis becoming CES-R while under medical supervision either before or after admission to hospital. The degree of urgency of early surgery in CES-R is still not in clear focus but it cannot be doubted that earliest decompression removes the mechanical and perhaps chemical factors which are the causes of progressive neurological damage. A full explanation and consent procedure prior to surgery is essential in order to reduce the likelihood of misunderstanding and litigation in the event of a persistent neurological deficit.

Background Primary Human herpesvirus-7 (HHV-7) infection usually occurs during childhood and causes several clinical manifestations: mainly exanthem subitum ( roseola infantum ), followed by a lifelong latent state with possible reactivation in case of immunodeficiency. Nevertheless, some considerably different approaches exist regarding the natural history of HHV-7 and the possible consequences of HHV-7 infection in immunocompetent adults. In particular, little is known about its pathogenic role in central nervous system (CNS) disease in nonimmunosuppressed adults. Specifically, in case of encephalitis, it is important to distinguish between infectious encephalitis and postinfectious encephalomyelitis for the management of patients Case presentation We describe here a case of encephalitis associated to human herpesvirus-7 with associated polymyeloradiculopathy in an immunocompetent patient which may contribute to the delineation of the approach to a patient profile with a similar clinical presentation and evolution to those presented in the literature. Conclusions This case may alert clinicians to consider this specific etiology in the differential diagnosis of encephalopathy in patients with suspected infectious encephalitis who do not respond to acyclovir or in patients who develop acute polymyeloradiculopathy, considering that HHV-7 may be a pathological factor and that a timely diagnosis is crucial for the early administration of specific treatment.

Background The long-term use of an oral corticosteroid suppresses immunity. Here, we describe a case involving a patient with weakness in the bilateral lower extremities due to cytomegalovirus (CMV) lumbosacral polyradiculitis. Case presentation A 64-year-old man visited a university hospital for symmetric motor weakness in both lower extremities (Medical Research Council grade: 2). Symptoms started 1 month before and gradually aggravated. The patient had been taking oral prednisolone for 10 years in order to control pain in multiple joints due to seronegative rheumatoid arthritis. He also had neuropathic pain on the entire right lower extremity and voiding difficulty. Gadolinium-enhanced magnetic resonance imaging revealed enhancement along the entire lumbosacral nerve roots. In the cerebrospinal fluid analysis (CSF), elevated white blood cell (WBC) count (19 cells/μL) and protein level (142.5 mg/dL) were observed. CMV detection by polymerase chain reaction (PCR) was positive. We diagnosed the patient as having lumbosacral polyradiculitis due to CMV. Ganciclovir (250 mg twice daily) was administered intravenously. Two months after initiating Ganciclovir, in the CSF analysis, CM detection by PCR was negative, and no WBC was found. Conclusion We reported a patient who had symmetric motor weakness in the bilateral lower extremities induced by CMV lumbosacral polyradiculitis. Its occurrence seems to be related to immunosuppresion due to the long-term use of an oral corticosteroid. When a patient who is taking an oral corticosteroid shows motor weakness in the bilateral lower extremities, CMV lumbosacral polyradiculitis is one of the possible disorders to be differentiated.

Suspected cauda equina syndrome is a common presentation in emergency departments, but most patients (≥70%) have no cauda equina compression on imaging. As neurologists become more involved with ‘front door’ neurology, referral rates of patients with these symptoms are increasing. A small proportion of patients without structural pathology have other neurological causes: we discuss the differential diagnosis and how to recognise these. New data on the clinical features of patients with ‘scan-negative’ cauda equina syndrome suggest that the symptoms are usually triggered by acute pain (with or without root impingement) causing changes in brain–bladder feedback in vulnerable individuals, exacerbated by medication and anxiety, and commonly presenting with features of functional neurological disorder.

A man in his mid-20s presented with a 5-month history of bilateral lower limb weakness and wasting along with bladder symptoms and erectile dysfunction. Additionally, he had binocular diplopia and progressive drooping of both eyelids. His clinical presentation was suggestive of bilateral third cranial nerve involvement with lumbosacral polyradiculopathy. Initial treatment with steroids for suspected idiopathic lumbosacral polyradiculopathy syndrome proved ineffective, as his symptoms progressively worsened without other systemic manifestations. We diagnosed a rare and treatable neurological condition, primary neurolymphomatosis, presenting as lumbosacral polyradiculopathy with bilateral third cranial nerve involvement. A definitive diagnosis was established only after nerve root biopsy, highlighting the crucial role of biopsy in confirming the diagnosis. Our case underscores the importance of early consideration for an invasive nerve root biopsy, enabling prompt treatment and an improved prognosis.

1The syndrome can progress to paraplegia with rectal and urinary incontinence and represents a surgical emergency.1 Sixty percent of patients are male with a mean age of 42 years, and 82% have a history of chronic low-back pain. In two-thirds of patients, the syndrome is associated with trauma or injury.2 However, cauda equina syndrome should be considered in patients whose chronic back pain has rapidly escalated regardless of a history of trauma or injury (Figure 1).1 4 Urinary symptoms (largely S2-mediated) can include altered urethral sensation, loss of desire to void, poor stream, feeling of retention and straining to void. Perineal symptoms (S2-S4) may or may not include numbness or pain.5 Although incontinence is an obvious symptom, urinary retention with or without overflow in the bladder rendered flaccid from sacral roots paresis is not; therefore, the patient at risk should be asked about this point. 2. Ahn UM, Ahn NU, Buchowski JM, et al. [Cauda] equina syndrome secondary to lumbar disc herniation: a meta-analysis of surgical outcomes. Spine 2000;25:1515-22.

More than 30% of U.S. adults report having experienced low back pain within the preceding three months. Although most low back pain is nonspecific and self-limiting, a subset of patients develop chronic low back pain, defined as persistent symptoms for longer than three months. Low back pain is categorized as nonspecific low back pain without radiculopathy, low back pain with radicular symptoms, or secondary low back pain with a spinal cause. Imaging should be reserved for patients with red flags for cauda equina syndrome, recent trauma, risk of infection, or when warranted before treatment (e.g., surgical, interventional). Prompt recognition of cauda equina syndrome is critical. Patient education should be combined with evidence-guided pharmacologic therapy. Goals of therapy include reducing the severity of pain symptoms, pain interference, and disability, as well as maximizing activity. Validated tools such as the Oswestry Disability Index can help assess symptom severity and functional change in patients with chronic low back pain. Epidural steroid injections do not improve pain or disability in patients with spinal stenosis. Spinal manipulation therapy produces small benefits for up to six months. Because long-term data are lacking for spinal surgery, patient education about realistic outcome expectations is essential.

Background DuraSeal ™ (Coviden, Waltham, MA, USA), a hydrogel sealant, is primarily used as an adjunct to a dural repair. Its use has also been described to seal off an annulotomy after a transforaminal lumbar interbody fusion when recombinant human bone morphogenetic protein-2 (rhBMP-2) is used. This aids in the reduction of postoperative radiculitis caused by rhBMP-2. However, as a result of its hydrophilic properties, DuraSeal ™ has the potential to swell, which could lead to compression of the thecal sac. Case Description We report a 57-year-old woman who developed cauda equina after a transforaminal lumbar 47 interbody fusion (TLIF) procedure in which the expansion of the DuraSeal ™ was believed to be the causative factor. The patient developed urinary retention, bowel incontinence, and paresthesias in the saddle region on postoperative Day 3. She underwent emergent exploration and decompression of the thecal sac. The gel-like DuraSeal™ material was causing significant compression of the thecal sac. Literature Review Multiple reports have documented that DuraSeal ™ , used as an adjunct to dural repair, can swell leading to compression of the spinal cord and/or neural elements. Our case demonstrates the use of DuraSeal ™ both over a site of a dural repair and over an annulotomy site, through which a TLIF was performed, is associated with the risk of developing postoperative cauda equina syndrome as a result of swelling of the DuraSeal ™ . Clinical Relevance Those using DuraSeal™ to seal off the annulotomy after a TLIF procedure performed with rhBMP-2 should use the product with an understanding of the potential postoperative swelling of the product and resulting neurologic sequela, particularly if DuraSeal ™ is used concomitantly at the site of dural repair.

Neurological manifestations of a primary Epstein-Barr virus (EBV) infection are rare. We describe a case with acute transverse myelitis and another case with a combination of polyradiculitis and anterior horn syndrome as manifestations of a primary EBV infection.The first case is a 50-year-old immunocompetent male diagnosed with acute transverse myelitis, 2 weeks after he was clinically diagnosed with infectious mononucleosis. The second case is an 18-year-old immunocompetent male diagnosed with a combination of polyradiculitis and anterior horn syndrome while he had infectious mononucleosis. The first patient was treated with methylprednisolone. After 1 year, he was able to stop performing clean intermittent self-catheterisation. The second patient completely recovered within 6 weeks without treatment.Primary EBV infection should be considered in immunocompetent patients presenting with acute transverse myelitis and a combination of polyradiculitis and anterior horn syndrome. Antiviral treatment and steroids are controversial, and the prognosis of neurological sequelae is largely unknown.