Magendie's foramen debridement and catheterisation for the treatment of syringomyelia due to diffuse craniocervical junction arachnoiditis. A case report and technical note.

A 36 year old woman was referred to our department for symptomatic lumbar spinal arachnoiditis following an epidural anaesthesia for childbirth. She did not had other known causative factor and she was free of any neurological symptoms before. She rapidly developed lower limbs impairment by compressing intradural lumbar collections and arachnoiditis requiring surgical decompression and subsequently internal cerebrospinal fluid shunting for acute hydrocephalus. Three years and the half later, she developed a severe tetraparesis due to a massive syrinx consecutive to the fourth ventricle outlets obstruction cause by the ongoing diffuse craniocervical junction arachnoiditis. Our aim was to treat all the problems in one step. An open fourth ventriculostomy of the Magendie's foramen with catheter insertion from the fourth ventricle down to the upper cervical subarachnoid space improve both the patient status and imagery.

CNS cryptococcosis presenting with cerebellar stroke and spinal arachnoiditis.

A 67-year-old man presented with a low-grade fever for 2 months, weakness of all four limbs for five days and altered sensorium for two days. He was recently diagnosed with AIDS and was treatment-naive. Investigations revealed a CD4 count of 27cells/mm3 MRI brain and spine exhibited bilateral cerebellar lesions with diffusion restriction, and severe arachnoiditis at the level of the lumbar spine. High suspicion of central nervous system tuberculosis in an endemic country like ours, led us to start antitubercular therapy and steroids. Repeated lumbar punctures resulted in a dry tap leading to a delay in diagnosis. Serum cryptococcal antigen detection came positive, following which antifungal treatment was initiated. Later a small amount of cerebrospinal fluid sample was obtained which confirmed the diagnosis of cryptococcosis. However, the patient worsened and succumbed to the illness. This case highlighted the rare presentation of cryptococcal cerebellar stroke and spinal arachnoiditis.

Spinal arachnoiditis leading to recurrent reversible myelopathy: A case report.

Context: A patient followed in the outpatient spinal cord injury support clinic at a VA Medical Center with a prior remote history of a gunshot wound to the back and multiple prior myelograms presented with a recurrent waxing and waning weakness of the left lower extremity and intermittent incontinence of bowel and bladder.Findings: During the evaluation, the patient experienced an immediate albeit temporary improvement in symptoms after a diagnostic lumbar puncture performed for CT myelogram. The symptoms of myelopathy reoccurred several weeks, but then the patient had a similar experience with rapid improvement in symptoms after an accidental fall down a flight of steps. Subsequently, the foot weakness and incontinence returned one week later. The patient ultimately developed permanent improvement in signs and symptoms after surgical intervention which included intradural lysis of adhesions, incision of the arachnoid membrane and resection of a cystic lesion.Clinical relevance: Patients who experience unexpected, albeit transient improvement in myelopathic symptoms who are known or suspected to have arachnoiditis should be evaluated for surgically remediable lesions. Remediation of these lesions can potentially improve long term outcome.

Transiting Nerve Rootlet Abnormalities on MRI after Lumbar Laminectomy: Associations with Persistent Postoperative Pain.

OBJECTIVE: To determine whether changes in the transiting nerve rootlet or its surroundings, as seen on MRI performed after lumbar hemilaminectomy, are associated with persistent postoperative pain (PPP), commonly known as the failed back surgery syndrome. MATERIALS AND METHODS: Seventy-three patients (mean age, 61 years; 43 males and 30 females) who underwent single-level partial hemilaminectomy of the lumbar spine without postoperative complications or other level spinal abnormalities between January 2010 and December 2018 were enrolled. Two musculoskeletal radiologists evaluated transiting nerve rootlet abnormalities (thickening, signal alteration, distinction, and displacement), epidural fibrosis, and intrathecal arachnoiditis on MRI obtained one year after the operations. A spine surgeon blinded to the radiologic findings evaluated each patient for PPP. Univariable and multivariable analyses were used to evaluate the association between the MRI findings and PPP. RESULTS: The presence of transiting nerve rootlet thickening, signal alteration, and ill-distinction was significantly different between the patients with PPP and those without, for both readers (p ≤ 0.020). Conversely, the presence of transiting nerve rootlet displacement, epidural fibrosis, and intrathecal arachnoiditis was not significantly different between the two groups (p ≥ 0.128). Among the above radiologic findings, transiting nerve rootlet thickening and signal alteration were the most significant findings in the multivariable analyses (p ≤ 0.009). CONCLUSION: On MRI, PPP was associated with transiting nerve rootlet abnormalities, including thickening, signal alterations, and ill-distinction, but was not associated with epidural fibrosis or intrathecal arachnoiditis. The most relevant findings were the nerve rootlet thickening and signal alteration.

Progressive quadriparesis and inflammation: A common disease, a rare presentation.

A previously healthy, 10-years-old girl presented with progressively worsening pain and weakness of the limbs for the past 2 weeks. It initially started with low-grade fever lasting for 4 days followed by severe pain over bilateral lower and upper limbs. Gradually she became bed-ridden. On examination, she had severe neck rigidity, generalized tenderness all over the body, generalized hyperalgesia, hyporeflexia, bilateral extensor plantar response and toe-walking. An initial clinical diagnosis of Landry-Guillain Barry syndrome was considered. Nerve conduction study showed generalized, demyelinating polyneuropathy. She was administered IVIG and was evaluated for other causes of arachnoiditis. MRI brain and spine showed enhancement and clumping of nerve roots in the conus and cauda equina. CECT chest showed necrotic mediastinal lymphnodes. A final diagnosis of disseminated tuberculosis with tuberculous arachnoiditis was considered and she was administered ATT, pulse methylprednisolone followed by maintenance oral corticosteroids. Currently, after 5 months of therapy, she has recovered clinically.

Prolonged inflammation leads to ongoing damage after spinal cord injury.

The pathogenesis of spinal cord injury (SCI) remains poorly understood and treatment remains limited. Emerging evidence indicates that post-SCI inflammation is severe but the role of reactive astrogliosis not well understood given its implication in ongoing inflammation as damaging or neuroprotective. We have completed an extensive systematic study with MRI, histopathology, proteomics and ELISA analyses designed to further define the severe protracted and damaging inflammation after SCI in a rat model. We have identified 3 distinct phases of SCI: acute (first 2 days), inflammatory (starting day 3) and resolution (>3 months) in 16 weeks follow up. Actively phagocytizing, CD68+/CD163- macrophages infiltrate myelin-rich necrotic areas converting them into cavities of injury (COI) when deep in the spinal cord. Alternatively, superficial SCI areas are infiltrated by granulomatous tissue, or arachnoiditis where glial cells are obliterated. In the COI, CD68+/CD163- macrophage numbers reach a maximum in the first 4 weeks and then decline. Myelin phagocytosis is present at 16 weeks indicating ongoing inflammatory damage. The COI and arachnoiditis are defined by a wall of progressively hypertrophied astrocytes. MR imaging indicates persistent spinal cord edema that is linked to the severity of inflammation. Microhemorrhages in the spinal cord around the lesion are eliminated, presumably by reactive astrocytes within the first week post-injury. Acutely increased levels of TNF-alpha, IL-1beta, IFN-gamma and other pro-inflammatory cytokines, chemokines and proteases decrease and anti-inflammatory cytokines increase in later phases. In this study we elucidated a number of fundamental mechanisms in pathogenesis of SCI and have demonstrated a close association between progressive astrogliosis and reduction in the severity of inflammation.

A rare cause of progressive neuropathy: Arachnoiditis ossificans.

Arachnoiditis ossificans (AO) is a rare type of chronic arachnoiditis characterized by the presence of calcification or ossification of the spinal arachnoid which is usually associated with progressive neurological deficits. It is usually followed by prior history of trauma, surgery, infection, or myelography. Magnetic resonance imaging and computed tomography are the characteristics that are helpful in the diagnosis of most cases. Prognosis and treatment depends on the site and clinical presentation of the patients. We present a case of a young female who presented with a long-standing history of neurological symptoms and a intradural lesion mimicking a tumor.

Surgical treatment of a thoracic ventral intradural arachnoid cyst associated with syringomyelia: case report.

The pathogenesis of thoracic ventral intradural spinal arachnoid cyst (ISAC) is unknown due to its extremely low incidence. In addition, its surgical treatment is complicated because of the ventral location, large craniocaudal extension, and frequent coexistence of syringomyelia. The optimal surgical strategy for thoracic ventral ISAC remains unclear and continues to be a matter of debate. In this report, the authors describe an extremely rare case presenting with a compressive thoracic ventral ISAC associated with syringomyelia that was successfully treated with a simple cyst-pleural shunt. The patient's medical history revealed bacterial spinal meningitis along with an extensive spinal epidural abscess, suggesting the incidence of extensive adhesive arachnoiditis (AA) to be a plausible cause for this pathology. Thoracic ventral ISAC reportedly occurs secondary to AA and is commonly associated with syringomyelia. Placement of a cyst-pleural shunt is an effective, safe, and uncomplicated surgical strategy, which can provide sufficient cyst drainage regardless of the coexistence of AA, and thus should be considered as primary surgical treatment. Syrinx drainage could be reserved for a later attempt in case the cyst-pleural shunt fails to reduce the extent of syringomyelia.

Spinal adhesive arachnoiditis following the rupture of an Adamkiewicz aneurysm: Literature review and a case illustration.

BACKGROUND: The rupture of an isolated spinal aneurysm is an exceptional occurrence. It might be responsible for a spinal subarachnoid haemorrhage (SSAH) that in rare cases can be complicated by arachnoiditis. Among the former the adhesive type is the most severe leading to the formation of a cyst and/or a syrinx. PATIENTS AND METHODS: The literature review was performed via a PubMed search using the following keywords. Adhesive arachnoiditis; spinal subarachnoid haemorrhage; spinal arachnoiditis; spinal arachnoid cyst; arachnoid cyst .Thesearch yielded 24 articles. Given the fact that only a few studies had been reported on the subject, we decided to include all studies regarding adhesive arachnoiditis after SAH leading to a descriptive literature review. Furthermore, a case illustration of a 57 year old man harbouring this type of rare pathology is described. RESULTS: Twenty-four case reports were found regarding spinal adhesive arachnoiditis (SAA) following SSAH. Posterior cerebral circulation bleeding (66.7%) most often occurred followed by spinal (9.1%) and anterior cerebral circulation (9.1%) respectively. The mean time between the haemorrhage and the SAA onset was 10 months. A higher predominance of symptomatic thoracic SAA was found. Including the present case, 80% of patients had a laminectomy, 72% had a micro adhesiolysis, and 56% a shunt placement. Cervical and upper thoracic involvement appeared to have a better outcome. CONCLUSION: Although most authors suggested surgical treatment, the long-term outcome remains unclear. Early stage diagnosis and management of this rare and disabling pathology may lead to a better outcome. Larger co-operative studies remain essential to obtain a better understanding of such a rare and complex disease.

Corrosion of Harrington rod in idiopathic scoliosis: long-term effects.

PURPOSE: Metal implants have been used to treat adolescent idiopathic scoliosis since the 1960s. Only recently, however, it has the issue of metal-bone breakdown secondary to metal corrosion in situ come to light, raising concerns of possible long-term complications from the resulting metallosis and inflammation of spinal tissues. We present a case of a patient with neurological deficit, pain, and disability with Harrington rod in place for over 30 years, to bring attention to the issue of bio-corrosion of metal implants and its effect on human tissue. We call attention to the need for protocols to better diagnose and treat these patients. METHODS: We provide a complete review of the history and clinical manifestations as well as serum metal, X-ray, and CT/myelogram test results. RESULTS: A 52-year-old female with spinal fusion and Harrington rod presents with pain, lymphedema, disability, and neurological deficits including thoracic outlet syndrome, hyperreflexia, peripheral muscle weakness and atrophy, hypertonicity, Raynaud's phenomenon, and balance and gait abnormalities. Serum chromium levels were elevated (26.73 nmol). X-rays showed no evidence of rod breakdown. Serial X-rays can demonstrate subtle corrosive changes but were not available. Adhesive arachnoiditis was diagnosed via CT/myelogram. CONCLUSION: We hypothesize that bio-corrosion is present in this case and that it is associated with intraspinal metallosis. Trauma secondary to a motor vehicle accident, as well as arachnoiditis, and their possible effects on this case are outlined. Challenges in proper diagnosis and management are discussed.

Central Nervous System Tuberculosis.

Central nervous system tuberculosis (CNS-TB) takes three clinical forms: meningitis (TBM), intracranial tuberculoma, and spinal arachnoiditis. TBM predominates in the western world and presents as a subacute to chronic meningitis syndrome with a prodrome of malaise, fever, and headache progressing to altered mentation and focal neurologic signs, followed by stupor, coma, and death within five to eight weeks of onset. The CSF formula typically shows a lymphocytic pleocytosis, and low glucose and high protein concentrations. Diagnosis rests on serial samples of CSF for smear and culture, combined with CSF PCR. Brain CT and MRI aid in diagnosis, assessment for complications, and monitoring of the clinical course. In a patient with compatible clinical features, the combination of meningeal enhancement and any degree of hydrocephalus is strongly suggestive of TBM. Vasculitis leading to infarcts in the basal ganglia occurs commonly and is a major determinant of morbidity and mortality. Treatment is most effective when started in the early stages of disease, and should be initiated promptly on the basis of strong clinical suspicion without waiting for laboratory confirmation. The initial 4 drug regimen (isoniazid, rifampin, pyrazinamide, ethambutol) covers the possibility of infection with a resistant strain, maximizes antimicrobial impact, and reduces the likelihood of emerging resistance on therapy. Adjunctive corticosteroid therapy has been shown to reduce morbidity and mortality in all but late stage disease.

Adhesive arachnoiditis in mixed connective tissue disease: a rare neurological manifestation.

The overall incidence of neurological manifestations is relatively low among patients with mixed connective tissue disease (MCTD). We recently encountered a case of autoimmune adhesive arachnoiditis in a young woman with 7 years history of MCTD who presented with severe back pain and myeloradiculopathic symptoms of lower limbs. To the best of our knowledge, adhesive arachnoiditis in an MCTD patient has never been previously reported. We report here this rare case, with the clinical picture and supportive ancillary data, including serology, cerebral spinal fluid analysis, electrophysiological evaluation and spinal neuroimaging, that is, MRI and CT (CT scan) of thoracic and lumbar spine. Her neurological deficit improved after augmenting her immunosuppressant therapy. Our case suggests that adhesive arachnoiditis can contribute to significant neurological deficits in MCTD and therefore requires ongoing surveillance.

Una evolución inusual en un paciente con amigdalitis aguda / An unusual outcome in a patient with acute tonsillitis

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Encasement of the Cauda Equina After Early Childhood Meningitis: Case Report and Review of the Literature.

BACKGROUND: Arachnopathy following meningitis has been described in the setting of chronic spinal arachnoiditis and more recently as shunt-related progressive myelopathy due to meningeal thickening. CASE DESCRIPTION: We describe an atypical case of a patient who presented with chronic arachnopathy 5 decades after an episode of meningitis. We also review the literature concerning arachnopathies occurring in the context of early childhood meningitis. Although our case bore clinical and radiologic similarities to chronic spinal arachnoiditis and shunt-related progressive myelopathy, time to symptom onset, intraoperative findings, pathophysiology, and surgical outcome set it apart from both conditions. CONCLUSIONS: It is challenging but worthwhile to recognize this separate entity because, in contrast to both shunt-related progressive myelopathy due to meningeal thickening and adhesive arachnoiditis, surgery involving microsurgical dissection of the thick arachnoid encasement of the cauda equina may be curative in medically refractory cases.

URGENT X-RAY DIAGNOSTICS OF INTRACRANIAL PYOINFLAMMATORY OTORHINOSINUSOGENIC COMPLICATIONS.

An analysis of the results of X-ray CT and MR-imaging was made in 46 patients aged from 13 to 78 years old. The patients were admitted to multifield hospitals in Kursk at the period from 2005 to 2015. The research included the nasal cavity, paranasal sinuses, mastoid and pyramid of the temporal bones and the brain. The study could be repeated with bolus contrast medium infusion. The condition of the patients was evaluated in dynamics at intervals of 5-7 days and these data was associated with clinical picture. The authors presents a complex of symptoms and an algorithm of differentiated X-ray diagnostics of diseases of the ENT organs and the main nosological forms of pyoinflammatory diseases of arachnoid membrane and substances of the brain.

Arachnoiditis ossificans after spinal surgery.

This article presents an unusual case of arachnoiditis ossificans after spinal surgery. A case of arachnoiditis ossificans secondary to lumbar fixation and decompression surgery for the treatment of multilevel lumbar fractures is reported and the relevant literature is reviewed. A 29-year-old man who previously underwent posterior pedicle screw fixation and fusion for multiple lumbar spine fractures reported lower back stiffness and discomfort 23 months postoperatively. A laminectomy was performed at L2 and at L3-L4. At L2, bone fragments from the burst fracture had injured the dural sac and some nerve roots. A posterolateral fusion was performed using allogeneic bone. Postoperatively, there were no signs of fever, infection, or systemic inflammatory responses. Arachnoiditis ossificans of the thecal sac from L1-L5 was diagnosed by magnetic resonance imaging and computed tomography at the 2-year follow-up. His postoperative neurological status progressively improved and he regained motor and sensory functions. Because of neurological improvements, fixation hardware was removed without further decompression. The authors report a case of arachnoiditis ossificans secondary to lumbar fixation and decompression surgery, which involved a large region. Arachnoiditis ossificans is a relatively rare disorder with unclear etiologies and limited treatment options. Spinal surgical intervention of arachnoiditis ossificans should be carefully considered because it may lead to poor outcomes and multiple revision surgeries.

Spinal arachnoid cyst associated with arachnoiditis following subarachnoid haemorrhage in adult patients: A case report and literature review.

OBJECTIVE: Arachnoiditis is an inflammatory process resulting with the fibrosis of arachnoid mater. It can vary in severity from mild thickenings to catastrophic adhesions that ruins subarachnoid space. As a result, arachnoid cysts can be formed. Arachnoid cyst induced by symptomatic spinal arachnoiditis is a rare complication of subarachnoid haemorrhages. In this article, we aimed to present a case of spinal arachnoid cyst formation following subarachnoid haemorrhage and examine similar cases in the literature. CASE REPORT: Forty-six years old, previously healthy female patient has been treated medically for headaches due to perimesencephalic subarachnoid bleeding. Approximately two and a half months later, she started to have severe headaches and diplopia. We detected hydrocephalus and performed ventriculoperitoneal shunt surgery. Two months later, she started to have complaints of weakness in her lower extremities. On neurological examination, she had paraparesis and on spinal magnetic resonance imaging she had an arachnoid cyst lengthening from C7 to T2 and compressing the spinal cord posteriorly. We performed partial laminectomy, drainage of arachnoid cyst and replacement of cystopleural T tube shunt. On follow-up, her lower extremity strength has ameliorated. She was taken into a physical therapy and rehabilitation programme. Three months later she was able to walk with a crutch. CONCLUSION: Subarachnoiditis and associated arachnoid cyst can cause severe morbidity. This rare situation (which especially occurs following subarachnoid haemorrhage of posterior fossa) should be known and physicians should keep in mind that it requires urgent surgical procedure.