A Novel Technique Using Magnetic Resonance Imaging in the Supine and Prone Positions for Diagnosing Lumbar Adhesive Arachnoiditis: A Preliminary Study.

BACKGROUND: Lumbar adhesive arachnoiditis is a debilitating neuropathic condition and is difficult to diagnose owing to lack of definitive diagnostic criteria. By focusing on the intrathecal mobility of nerve roots, we assessed whether useful diagnostic criteria could be established using MRI. METHODS: Seventeen patients with a high risk for lumbar adhesive arachnoiditis and 18 no-risk patients with chronic low back pain and/or leg pain participated in this study. The patients underwent MRI in both the supine and prone positions. Eleven axial T2-weighted images between the L2 and L5/S levels were obtained, and the proportion of the low-intensity area in the dorsal half to the total low-intensity area in the dural sac was calculated for each axial view. RESULTS: At some lumbar levels, the low-intensity area in the dorsal half of the dural sac was relatively larger in patients with a high risk for lumbar adhesive arachnoiditis than in the no-risk patients. In the no-risk group, the proportion of the low-intensity area in the dorsal half in the supine position was significantly higher than that in the prone position at all lumbar levels. However, in the high-risk group, at some levels, the proportions were not significantly different in the dorsal half of the dural sac between the supine and prone positions. CONCLUSION: In patients with a known risk for lumbar adhesive arachnoiditis, nerve roots lose their potential to migrate in the dural sac in the gravitational force direction on MRI.

Arachnoiditis ossificans associated with syringomyelia: a case report.

The association of arachnoiditis ossificans with syringomyelia is a rare pathological entity. We present an unusual case who presented with progressive myelopathy caused by arachnoidits ossificans and syringomyelia. The pathophysiology and treatment strategy of this rare entity are still controversial.

Idiopathic opticochiasmatic arachnoiditis.

: A critical review of the literature indicates that idiopathic opticochiasmatic arachnoiditis, once considered an important consideration in patients with otherwise unexplained optic atrophy, is not a valid disease entity.

[Flexible endoscopy in surgical treatment of spinal adhesive arachnoiditis and arachnoid cysts].

Thecaloscopy is less invasive exploration of spinal subarachnoid space with ultra-thin flexible endoscope and endoscopic fenestration of scars and adhesions. Thecalopscopy was used in Russian neurosurgery at the first time. Since 2009 we operated 32 patients with following diagnosis: 17--spinal adhesive arachnoiditis (8--local forms, 9--diffuse forms), 12--spinal arachnoid cysts (7--posstraumatic cysts, 5--idiopathic cysts), 3--extramedullary tumors (thecaloscopic videoassistance and biopsy). In all cases we realized exploration of subarachnoid space and pathologic lesion with endoscopic perforation of cyst or dissection of adhesions using special instrumentation. Mean follow-up in our group was 11.4 months. Neurological improvement (mean 1.4 by modified Frankel scale, 1.8 by Ashworth spasticity scale) was seen in 87% of patients operated for spinal arachnopathies. Temporary neurological deterioration (mild disturbances of deep sensitivity) was seen in 9% of patients and managed successfully with conservative treatment. 1 (3.1%) patient was operated 3 times because of relapse of adhesions. There were no serious intraoperative complications (e.g., serious bleeding, dura perforation etc). Postoperative complications included 1 CSF leakage and 1 postoperative neuralgic pain. Mean term of hospitalization was 7.6 days. According to our data, we suppose that thecaloscopy is efficient and safe method, and should be widely used for spinal arachnopaties, adhesive arachnoiditis and arachnoid cysts. Taking into account that adhesive spinal arachnoiditis is systemic process and spinal arachnoid cysts can be extended as well, thecaloscopy may be regarded as the most radical and less-invasive way of surgical treatment existing currently in neurosurgery.

Severe adhesive arachnoiditis resulting in progressive paraplegia following obstetric spinal anaesthesia: a case report and review.

A 27-year-old woman developed severe adhesive arachnoiditis after an obstetric spinal anaesthetic with bupivacaine and fentanyl, complicated by back pain and headache. No other precipitating cause could be identified. She presented one week postpartum with communicating hydrocephalus and syringomyelia and underwent ventriculoperitoneal shunting and foramen magnum decompression. Two months later, she developed rapid, progressive paraplegia and sphincter dysfunction. Attempted treatments included exploratory laminectomy, external drainage of the syrinx and intravenous steroids, but these were unsuccessful and the patient remains significantly disabled 21 months later. We discuss the pathophysiology of adhesive arachnoiditis following central neuraxial anaesthesia and possible causative factors, including contamination of the injectate, intrathecal blood and local anaesthetic neurotoxicity, with reference to other published cases. In the absence of more conclusive data, practitioners of central neuraxial anaesthesia can only continue to ensure meticulous, aseptic, atraumatic technique and avoid all potential sources of contamination. It seems appropriate to discuss with patients the possibility of delayed, permanent neurological deficit while taking informed consent.

Intrapleural migration of a spinal catheter in a patient with arachnoiditis and extensive epidural scarring after tethered cord release: a case report and review of literature.

OBJECTIVE: The objective of this study was to report a case of new onset refractory pain from intrapleural migration of a spinal catheter five months after the implantation of an intrathecal drug delivery system (IDDS). MATERIALS AND METHODS: A 57-year-old man had intractable pain because of multiple intradural spinal explorations for tethered cord release. His pain was effectively treated with intrathecal morphine via an IDDS. Five months after the implantation, the patient developed return of the original pain more than two weeks after intrapleural migration of the intrathecal catheter. RESULTS: The migration was documented by computed tomography, and repositioning of the catheter rendered the patient comfortable. The gradual onset of pain may have been due to decreasing delivery of drug to the cerebrospinal fluid as the catheter tip migrated further away from the dura. To our knowledge, this complication has not been reported in the literature. CONCLUSION: Physicians and nursing staff that place and manage an IDDS should be aware of this complication.

[Fulminant adhesive arachnoiditis]. / Zlepne zapalenie pajeczynówki o piorunujacym przebiegu.

Adhesive arachnoiditis is a rare disease with insidious course. It causes damage of the spinal cord and nerve roots. The causes of adhesive arachnoiditis include earlier traumatic injury of the spinal cord, surgery, intrathecal administration of therapeutic substances (e.g. anaesthetics, chemotherapy) or contrast media, bleeding, and inflammation. It can also be idiopathic or iatrogenic. We present the case of a 42-year-old patient with fulminant adhesive arachnoiditis which was provoked by spinal surgery and caused severe neurological disability with profound, progressive, flaccid paraparesis and bladder dysfunction. The electromyography (EMG) showed serious damage of nerves of both lower limbs at the level of motor roots L2-S2 and damage of the motor neuron at the level of Th11-Th12 on the right side. Magnetic resonance imaging of the lumbosacral and thoracic part of the spinal cord demonstrated cystic liquid spaces in the lumen of the dural sac in the bottom part of the cervical spine and at the Th2-Th10 level, modelling the lateral and anterior surface of the cord. Because of the vast lesions, surgery could not be performed. Conservative treatment and rehabilitation brought only a small clinical improvement.

The leptomeninges as a critical organ for normal CNS development and function: First patient and public involved systematic review of arachnoiditis (chronic meningitis).

BACKGROUND & IMPORTANCE: This patient and public-involved systematic review originally focused on arachnoiditis, a supposedly rare "iatrogenic chronic meningitis" causing permanent neurologic damage and intractable pain. We sought to prove disease existence, causation, symptoms, and inform future directions. After 63 terms for the same pathology were found, the study was renamed Diseases of the Leptomeninges (DLMs). We present results that nullify traditional clinical thinking about DLMs, answer study questions, and create a unified path forward. METHODS: The prospective PRISMA protocol is published at Arcsology.org. We used four platforms, 10 sources, extraction software, and critical review with ≥2 researchers at each phase. All human sources to 12/6/2020 were eligible for qualitative synthesis utilizing R. Weekly updates since cutoff strengthen conclusions. RESULTS: Included were 887/14286 sources containing 12721 DLMs patients. Pathology involves the subarachnoid space (SAS) and pia. DLMs occurred in all countries as a contributor to the top 10 causes of disability-adjusted life years lost, with communicable diseases (CDs) predominating. In the USA, the ratio of CDs to iatrogenic causes is 2.4:1, contradicting arachnoiditis literature. Spinal fusion surgery comprised 54.7% of the iatrogenic category, with rhBMP-2 resulting in 2.4x more DLMs than no use (p<0.0001). Spinal injections and neuraxial anesthesia procedures cause 1.1%, and 0.2% permanent DLMs, respectively. Syringomyelia, hydrocephalus, and arachnoid cysts are complications caused by blocked CSF flow. CNS neuron death occurs due to insufficient arterial supply from compromised vasculature and nerves traversing the SAS. Contrast MRI is currently the diagnostic test of choice. Lack of radiologist recognition is problematic. DISCUSSION & CONCLUSION: DLMs are common. The LM clinically functions as an organ with critical CNS-sustaining roles involving the SAS-pia structure, enclosed cells, lymphatics, and biologic pathways. Cases involve all specialties. Causes are numerous, symptoms predictable, and outcomes dependent on time to treatment and extent of residual SAS damage. An international disease classification and possible treatment trials are proposed.

Evaluation of tenoxicam on prevention of arachnoiditis in rat laminectomy model.

Post laminectomy arachnoiditis has been shown by experiments with rats and post operative radiological imaging in humans. The purpose of this experimental study was to determine the efficacy of tenoxicam in preventing arachnoiditis in rats. Twenty-four Wistar rats were divided into two groups, and L3 laminectomy was performed. In the tenoxicam group, 0.5 mg/kg tenoxicam was applied intraperitoneally. Normal saline was applied intraperitoneally in the control group. Later, the rats were killed at weeks 3 and 6, and the laminectomy sites were evaluated pathologically for arachnoiditis. The results showed that 6 weeks after surgery, the tenoxicam group showed lowest arachnoiditis grades. However, statistically significant difference was not found in arachnoiditis between the control group and the tenoxicam group. Based on these findings it is concluded that application of the tenoxicam after lumbar laminectomy did not effectively reduce arachnoiditis. Performing the most effective surgical technique without damage around tissue in a small surgical wound and having meticulous hemostasis in surgery seem to be the key for preventing arachnoiditis effectively.

Arachnoiditis Ossificans of the Lumbar Spine: A Rare Cause of Progressive Cauda Equina Syndrome.

Arachnoiditis ossificans of the spine is a rare entity defined as an ossification of the leptomeninges resulting in neurologic decline. We describe the case of a 42-year-old woman, without any obvious predisposing factor, who presented with a progressive cauda equina syndrome. The imaging findings on magnetic resonance imaging were confusing by showing an atypical intraspinal lesion extending from L1 to S1. The computed tomography scan was more specific by showing suggestive images of a huge arachnoiditis ossificans of the lumbar spine. The patient underwent a large lumbar laminectomy with an incomplete resection of the ossified arachnoid. The histologic study confirmed the bony nature of the lesion. This illustrative case highlights the importance of helical computed tomography scan with multiplanar reconstruction for the diagnosis of arachnoiditis ossificans.

Neurocysticercosis causing sudden death.

Neurocysticercosis causes significant morbidity due to neurologic manifestations including seizures. Sudden unexpected death in epilepsy (SUDEP) is responsible for mortality associated with seizure disorders. This case highlights death from neurocysticercosis and possible SUDEP in a nonendemic country.

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 new approach for observing cerebral cisterns and ventricles via a percutaneous lumbosacral route by using fine, flexible fiberscopes.

OBJECT: To establish a new method for the diagnosis of central nervous system diseases, the authors visualized the cerebral cisterns and ventricles via a percutaneous lumbosacral route by using newly developed fine, flexible fiberscopes. METHODS: Fine, flexible fiberscopes, 0.9 and 1.4 mm in diameter, were introduced up to the cerebral cisterns and ventricles through a percutaneous lumbosacral route in awake patients with chronic headache and/or neck pain or those undergoing spinal surgery and in whom MR imaging did not disclose any particular abnormalities in the brain. A lumbosacral subarachnoid puncture was made with a modified method of a continuous epidural block. RESULTS: In 25 of 31 patients tested, the cerebellomedullary and/or pontine/interpeduncular cisterns were easily and safely reached, and the brainstem structures were visualized. Advancement of the fiberscope beyond the spinal level was abandoned in 6 patients with adhesive spinal arachnoiditis, because the fiberscopes encountered resistance seemingly caused by arachnoid adhesions. Further advancement of the fiberscopes up to the fourth and third ventricles was successfully achieved in 2 patients. A number of arachnoid filaments were found in the cerebellomedullary cistern in 4 patients: 2 with chronic spinal arachnoiditis, 1 with a spinal arachnoid cyst, and 1 with posttraumatic pain syndrome. None of the patients reported pain or any major complication except a postspinal headache and light fever, which were encountered in 4 and 1 patient, respectively. CONCLUSIONS: The approach to the supraspinal structures via the lumbosacral route by using a fine, flexible fiberscope may provide a new, minimally invasive, and safe way to observe the cerebral cisterns and/or brainstem regions.

Cervicothoracic postarachnoiditic hydrosyringomyelia secondary to pedicular hook dislocation: case report.

BACKGROUND: Pedicular hook dislocation is a rare complication of spinal instrumentation. We report on the first case of hydrosyringomyelia secondary to intracanalar hook displacement after scoliosis surgery. CASE DESCRIPTION: A 15-year-old girl presented to our institution with a 7-month history of persistent neck and occipital pain as well as numbness of the lower extremities and previous dorsolumbar instrumentation with dorsal pedicular hooks and lumbar screws. Magnetic resonance imaging showed intramedullary cystic cavity from C5 to T7, isointense to cerebrospinal fluid (CSF) on T1- and T2-weighted images. Computed tomographic scan showed intracanalar displacement of the left hook. On admission, the patient presented with mild weakness of the lower extremities, hypalgesia below the level of T4, and urinary disturbance. The patient underwent surgical hook removal, T4 laminectomy, and midline dural opening: the arachnoid membrane was found to be thick and adhered to the dura and dorsolateral spinal cord. The arachnoid scarring was dissected, and the cord was untethered. A small posterior-median myelotomy was performed, and a syringosubarachnoid catheter was placed into the subarachnoid space to restore CSF flow. CONCLUSIONS: Late intracanalar displacement of spinal devices is an event that may complicate spinal instrumentation for scoliosis. This case highlights the importance of correct spinal device positioning and that of careful follow-up after instrumentation to detect complications early. We also discuss the pathogenetic pathway of the postarachnoiditic syringomyelia in this case.

Arachnoiditis ossificans.

Arachnoiditis ossificans is a rare type of chronic arachnoiditis characterised by the presence of calcification or ossification of the spinal arachnoid. There are a few reports of this condition in Japanese and western populations but no case has been reported in a Chinese population before. We describe a 35-year-old woman with typical findings of arachnoiditis ossificans. A brief review of the literature is also presented.

Spinal Arachnoiditis Ossificans: Report of Quadruple-Triggered Case.

BACKGROUND: Arachnoiditis ossificans (AO) is a rare condition often associated with previous spine surgery. Here we describe a unique case of a patient affected by ankylosing spondylitis (AS), presenting with progressive neurologic deterioration due to AO. We also review the literature on evaluation and management of patients suffering from AO. CASE DESCRIPTION: The 65-year-old patient had a history of previous spinal trauma and related thoracolumbar surgery. Magnetic resonance imaging revealed multiloculated intradural/extramedullary cysts on the posterior surface of the spinal cord at Th9-L1, with clustered nerve roots. Computed tomography, with 3-dimensional reconstruction, demonstrated a likely ossification of both the dura and arachnoid from Th9 to S1. Microsurgical debridement of scar tissue from previous surgery, drilling of posterior ossified plaques at Th11-Th12-L1, and marsupialization and drainage of arachnoid cysts at Th11-Th12 were performed. CONCLUSIONS: We submit that AS, spinal trauma, epidural hematoma, and related surgery may be synergistic and independent factors in the etiopathogenesis of AO. This should be considered in patients with AS and/or a history of spinal surgery who present neurologic worsening.

Upper cervical myelopathy due to arachnoiditis and spinal cord tethering from adjacent C-2 osteomyelitis. Case report and review of the literature.

Myelopathy caused by a spinal cord infection is typically related to an adjacent compressive lesion such as an epidural abscess. The authors report a case of progressive high cervical myelopathy from spinal cord tethering caused by arachnoiditis related to an adjacent C-2 osteomyelitis. This 70-year-old woman initially presented with a methicillin-sensitive Staphylococcus aureus osteomyelitis involving the C-2 odontoid process. She was treated with appropriate antibiotic therapy but, over the course of 4 weeks, she developed progressive quadriparesis. A magnetic resonance image revealed near-complete resolution of the C-2 osteomyelitis, but new ventral tethering of the cord was observed at the level of the odontoid tip. She subsequently underwent open surgical decompression and cord detethering. Postoperatively she experienced improvement in her symptoms and deficits, which continued to improve 1 year after her surgery. To the authors' knowledge, this is the first reported case of progressive upper cervical myelopathy due to arachnoiditis and cord tethering from an adjacent methicillin-sensitive S. aureus C-2 osteomyelitis.

Arachnoiditis ossificans with progressive syringomyelia and spinal arachnoid cyst.

We present a 30-year-old man with progressive spastic paraparesis. Spinal imaging revealed extensive calcification of the thoracic cord and cauda equina arachnoid, an intradural extramedullary cyst and evidence of rapidly progressing syringomyelia. Radiological diagnosis was arachnoiditis ossificans and an attempt at surgical decompression was made because of progressive neurologic deterioration. Due to tenacious adhesion of the calcified plaques to the cord and roots, only cyst drainage was achieved; the patient had no clinical improvement. A literature review revealed only two other cases reported in the literature with co-existence of arachnoiditis ossificans and syringomyelia. In none of the previous cases was there an intradural extramedullary arachnoid cyst, nor did the syrinx progress in such a rapid fashion. An attempt is made to explain possible pathophysiological mechanisms leading to this unusual pathology.

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.