Arachnoiditis, a complication of epidural blood patch for the treatment of low-pressure headache: A case report and systematic review.

OBJECTIVE: To report a case of arachnoiditis as a complication of epidural blood patch procedures and to systematically review the diagnostic workup, clinical outcomes, and treatment modalities reported in the literature. BACKGROUND: Epidural blood patching is an effective treatment for low-pressure headache secondary to spontaneous cerebrospinal fluid leak or iatrogenic post-dural puncture. Spontaneous intracranial hypotension is believed to be a rare headache disorder, but recently has been diagnosed at higher frequencies, making it an important differential diagnosis for intractable headaches. Arachnoiditis has surfaced as a rare complication of epidural blood patching. Symptom presentation does not always correlate with evidence of meningeal enhancement on imaging. Optimal methods for treatment remain largely unknown. METHODS: Databases Embase and PubMed were searched for all published studies on arachnoiditis post-epidural blood patch using a combination of the following medical subject headings and keywords: arachnoiditis, arachnoid inflammation, adverse event, and epidural blood patch. All original English-language articles that described arachnoid and/or meningeal inflammation in conjunction with epidural blood patch procedures were included for analysis. Title and abstract screening, data extraction, and risk of bias assessment were conducted independently and in duplicate by two reviewers. RESULTS: Seven other cases of arachnoiditis post-blood patch placement have been documented, most of which were diagnosed via magnetic resonance imaging. Six of these were a result of a spinal-epidural anesthesia for labor and delivery. Common symptoms reported were headache, back and radicular pain, paresthesia, and motor weakness. There are currently no proven consensus-based treatment recommendations available. While intravenous methylprednisolone followed by oral prednisone taper was found to be effective in the case presented, the benefit of other multi-modal therapies was unclear. CONCLUSIONS: Headache specialists who treat postural headache should be aware of arachnoiditis as a potentially severe complication of epidural blood patch. The case presented is the first of its kind to report arachnoiditis as a complication of high-volume blood patch for the treatment of spontaneous intracranial hypotension. More studies are required to determine suitable treatment options for post-epidural blood patch arachnoiditis.

[Arachnoiditis following spinal anesthesia-Case report and review of the literature]. / Arachnoiditis nach Spinalanästhesie ­ Fallbericht und Literaturübersicht.

A 61-year-old woman underwent a tension-free vaginal tape (TVT) operation due to stress incontinence. After technically difficult spinal anesthesia with two attempts the patient developed symptoms of nerve irritation, complained about neckache and headache and showed signs of agitation. The regimen was shifted to general anesthesia and surgery was performed. Because of postoperatively persistent headache and sensory disturbances an MRI scan of the lumbar spine was performed on the first postoperative day without pathological findings. The patient was able to leave the hospital after 1 week with significant relief of symptoms but 3 weeks later she developed neurocognitive impairment with memory deficits. A second MRI scan of the head now showed signs of disturbance of CSF circulation with hydrocephalus. Treatment was performed with drainage and ventriculoperitoneal shunt. Further evaluation showed a severe, multisegmental arachnoiditis and the patient developed a progressive paraparesis. The patient presented her case for assessment to a commission on medical malpractice 13 months after anesthesia. The commission detected no treatment errors. In connection to the case report a literature review of characteristics and etiologies of chronic adhesive arachnoiditis is given, which is a known but very rare complication of spinal anesthesia or similar procedures.

Subarachnoid neurocysticercosis: emerging concepts and treatment.

PURPOSE OF REVIEW: Subarachnoid neurocysticercosis (SUBNCC) is caused by a morphologically unique proliferative form of Taenia solium involving the subarachnoid spaces. Prolonged therapy based upon the pathophysiology of SUBNCC and long-term follow-up have shed light on the course of disease and led to highly improved outcomes. RECENT FINDINGS: SUBNCC has a prolonged incubation period of between 10 and 25 years characterized by cyst proliferation and growth and invasion of contiguous spaces leading to mass effect (Stage 1). With induction of the host-immune responses, cysts degenerate leading to a predominately inflammatory arachnoiditis (Stage 2) causing hydrocephalus, infarcts, and other inflammatory based neurological manifestations. Inactive disease (Stage 3) may occur naturally but mostly is a result of successful treatment, which generally requires prolonged intensive anthelminthic and antiinflammatory treatments. Cerebral spinal fluid cestode antigen or cestode DNA falling to nondetectable levels predicts effective treatment. Prolonged treatment with extended follow-up has resulted in moderate disability and no mortality. Repeated short intensive 8-14-day courses of treatment are also used, but long-term outcomes and safety using this strategy are not reported. SUMMARY: SUBNCC gives rise to a chronic arachnoiditis. Its unique ability to proliferate and induce inflammatory responses requires long-term anthelmintic and antiinflammatory medications.

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.

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.

Imaging Appearance of Advanced Chronic Adhesive Arachnoiditis: A Retrospective Review.

OBJECTIVE: Chronic adhesive arachnoiditis (CAA) is rare and has potentially devastating clinical consequences. The objective of this article is to review the clinical features of CAA and describe its appearance on imaging, to increase radiologists' awareness of this challenging diagnosis. MATERIALS AND METHODS: Twenty-nine cases of advanced CAA seen at our institution over 18 years (1995-2013) were retrospectively reviewed. Chart review was performed, with attention given to data on clinical presentation, suspected cause, and interventions performed. All patients underwent MRI, and seven patients also underwent CT myelography. Clinical and imaging features were evaluated and categorized. RESULTS: The 29 patients ranged in age from 23 to 96 years and included 11 women and 18 men. Suspected underlying causative factors included trauma (n = 10), prior surgery (n = 9), nontraumatic subarachnoid hemorrhage (n = 7), infection (n = 3), myelography with iophendylate used as contrast medium (n = 1), Guillain-Barré syndrome (n = 1), ankylosing spondylitis (n = 1), and unknown causes (n = 1). Imaging characteristics include loculated CSF collections (n = 23), nerve root clumping, enhancement, and displacement (n = 15), cord swelling with increased T2 signal (n = 12), arachnoid septations (n = 11), cord atrophy (n = 6), syrinx (n = 5), and intrathecal calcifications (n = 3). Ten patients underwent surgical procedures, and most had only brief clinical improvement. CONCLUSION: CAA is a rare cause of devastating neurologic symptoms and chronic pain. The imaging features of CAA range from subtle to severe. Advanced arachnoiditis can present with spinal cord swelling and syrinx formation, which can mimic other disease processes. Inclusion of advanced CAA in the differential diagnosis can prevent unnecessary interventions.

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.

Delayed spinal arachnoiditis with syringomyelia following aneurysmal subarachnoid haemorrhage: a case report with patient experience.

BACKGROUND AND IMPORTANCE: Syringomyelia, or the formation of fluid-filled cysts within the spinal cord, associated with delayed spinal arachnoiditis is an uncommon complication of aneurysmal subarachnoid haemorrhage. To date, about 18 cases have been reported in medical literature, with just two reported in patients under the age of 35 years. CLINICAL PRESENTATION: A 27-year-old female patient complained of sudden, severe headaches in the occipital region, nuchal rigidity, and drowsiness when she presented at our institution. A head computed tomography scan revealed intraventricular bleeding in the lateral and fourth ventricles with more extensive haemorrhaging in the frontal horns. A left posterior inferior cerebellar artery (PICA) aneurysm was confirmed via digital subtraction angiogram, and endovascular embolization was done. Two years later, the patient reported intense pain in the lower back along with symptoms suggestive of spinal cord compression. Spinal magnetic resonance imaging (MRI) showed spinal adhesions from C1 to L4, syringomyelia with some vasogenic oedema extending from T3 to T9 level, and a cyst in the lumbar region. Consequently, a right hemilaminectomy was performed along with microsurgical release of arachnoid adhesions and placement of a subdural drain. Radiological and symptomatic improvements were observed. Since then, the patient's clinical condition has remained stable during the past three years of follow-up visits. CONCLUSIONS: Literature on optimal treatment modalities and patient prognosis is scarce and debated. The time for symptom improvement depends on the level and extent of spinal cord involvement. Rehabilitation may be required for most patients, as complete symptomatic recovery may not be attainable.

Increasing back and radicular pain 2 years following intrathecal pump implantation with review of arachnoiditis.

BACKGROUND: Implanted intrathecal drug delivery pumps are now regularly used for the treatment of chronic benign and cancer-related pain that is refractory to conservative treatment methods. In most cases, the pumps are successful at reducing the intensity of pain and improving function and quality of life for pain patients. Limited studies have discussed the complications associated with intrathecal pump placement. SETTING: Academic tertiary care center. SUMMARY: We describe an unusual case of a patient who presented with progressive weakness and worsening lumbar and lower extremity pain following implantation of an intrathecal drug delivery system (IDDS). Work-up for the patient's symptoms includes a magnetic resonance imaging, which revealed lumbar arachnoiditis. Patient underwent a laminectomy and detethering of spinal cord and nerve roots below level of catheter insertion. There was transient improvement in her pain and weakness. Subsequent surgery for pump explantation revealed a retained Touhy introducer needle from her pump placement procedure. CONCLUSION: The entire IDDS was removed including the retained Touhy introducer needle. The patient later went on to receive a successful spinal cord stimulator trial and implantation with moderate relief of her chronic pain.

Arachnoid ossificans of thoracolumbosacral spine in the advanced ankylosing spondylitis: a case report.

Arachnoid ossificans is a rare type of chronic arachnoiditis characterised by the presence of calcification or ossification of the dura and arachnoid. There are a few reports of these findings in relation to various disease entities, but only one case has been reported in relation to ankylosing spondylitis. We describe a 76-year-old man of ankylosing spondylitis with arachnoiditis ossificans, who has suffered from low back pain and neuropathic leg pain.

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.

Spinal arachnoiditis and cyst formation with subarachnoid haemorrhage.

We present the case of a 58-year-old lady with p-ANCA vasculitis who suffered a WFNS grade 1 subarachnoid haemorrhage (Fisher grade 1) secondary to a ruptured left posterior inferior cerebellar artery aneurysm and then developed a rare complication of radiologically progressive spinal arachnoiditis despite maintained clinical response to definitive treatment measures.

[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.

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.

[Complications of spinal anesthesia and how to avoid them]. / Spinalanästhesie - Typische Komplikationen und wie man sie vermeiden kann.

Spinal anesthesia is a safe procedure. The knowledge of complications may support efforts to minimize risks, speed up the recognition process and lead to adequate timely therapeutic approaches. Pain during insertion of the needle can be a warning signal for potential conus damage. Hypotension caused by spinal anesthesia should be treated by appropriate vasoactive drugs. Timely recognized cardiac arrest situations are usually well treatable. The incidence of postdural puncture headache should be less than 2% of cases. In case of a high degree of suffering the best currently available treatment is the epidural blood patch. Further complications like intracranial bleeding, infection, cauda equina syndrome or spinal hematoma need immediate differential diagnosis and therapeutic approaches. The residual risk for permanent harm can be estimated to be around 0,02 per thousand.

Syringomyelia as a delayed complication of lumbar-sacral adhesive arachnoiditis in Pott's disease.

Syringomyelia is the development of a fluid-filled cyst (syrinx) within the spinal cord and is an extremely rare chronic manifestation of tuberculosis. The syrinx so formed may expand over time, causing compression or destruction of spinal tracts and surrounding nerve roots. Development of syringomyelia in a patient of Pott's disease is particularly infrequent. We report this rare case of a 31-year-old man with syringomyelia as a prolonged complication of Pott's disease.

Polyclonal lymphocytic infiltrate with arachnoiditis resulting from intrathecal stem cell transplantation.

Stem cell treatment outside of studied and approved medical indications can have unforeseen adverse consequences. Here, we present a 74-year-old male that underwent such therapy. The patient presented to our institution with progressive lower extremity weakness and urinary incontinence. He had previously undergone intrathecal stem cell therapy in Moscow, Russia for weakness and fatigue. Magnetic resonance imaging of his thoracic and lumbar spine showed marked enlargement of the cauda equina nerve roots and abnormal mass-like soft tissue involving the thoracolumbar thecal sac. Surgical biopsy of the intrathecal soft tissue showed polyclonal lymphocytic and glial cell proliferation. The patient's symptoms did not improve with medical treatment or radiation, and he is currently under observation after multidisciplinary evaluation. Our patient's experience illustrates one of the potential risks of "stem cell tourism" and exemplifies the imaging and histopathologic features of this rare entity. We also compare our patient's treatment with other similar examples of stem cell treatments in our institution and others. These have had a wide spectrum of results. In some instances, intrathecal stem cells have caused abnormal imaging findings without any associated patient symptoms. In extreme examples, however, stem cell treatments have resulted in central nervous system neoplasms. Our patient's lesion is quite unique, with only one similar lesion having been previously published.

Abnormalities in spinal cord ultrastructure in a rat model of post-traumatic syringomyelia.

BACKGROUND: Syringomyelia is a serious complication of spinal cord trauma, occurring in approximately 28% of spinal cord injuries. Treatment options are limited and often produce unsatisfactory results. Post-traumatic syringomyelia (PTS) is presumably related to abnormalities of cerebrospinal fluid (CSF) and interstitial fluid hydrodynamics, but the exact mechanisms are unknown. METHODS: Transmission electron microscopy (TEM) was used to investigate in detail the interfaces between fluid and tissue in the spinal cords of healthy Sprague-Dawley rats (n = 3) and in a rat model of PTS (n = 3). PTS was induced by computer-controlled impact (75 kDyn) to the spinal cord between C6 and C8, followed by a subarachnoid injection of kaolin to produce focal arachnoiditis. Control animals received a laminectomy only to C6 and C7 vertebrae. Animals were sacrificed 12 weeks post-surgery, and spinal cords were prepared for TEM. Ultra-thin spinal cord sections at the level of the injury were counterstained for structural anatomy. RESULTS: Spinal cords from animals with PTS displayed several abnormalities including enlarged perivascular spaces, extracellular edema, cell death and loss of tissue integrity. Additionally, alterations to endothelial tight junctions and an abundance of pinocytotic vesicles, in tissue adjacent to syrinx, suggested perturbations to blood-spinal cord barrier (BSCB) function. CONCLUSIONS: These findings support the hypothesis that perivascular spaces are important pathways for CSF flow into and out of the spinal cord, but also suggest that fluid may enter the cord through vesicular transport and an altered BSCB.