Compressive Cervicothoracic Adhesive Arachnoiditis following Aneurysmal Subarachnoid Hemorrhage: A Case Report and Literature Review.
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ABSTRACT:
SUBMITTER: Rahmathulla G
PROVIDER: S-EPMC4110125 | biostudies-other | 2014 Aug
REPOSITORIES: biostudies-other
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Project description:Ruptured aneurysms of the lateral spinal artery (LSA) causing subarachnoid hemorrhage (SAH) are exceptionally rare. Unlike common aneurysms in the circle of Willis, LSA aneurysms present unique diagnostic and therapeutic challenges due to their complex anatomy. We reviewed the literature, examining case reports detailing LSA aneurysm occurrences, diagnoses, treatments, and complications, and our subsequent analysis highlights the clinical presentations, imaging findings, treatment methods, and anatomical features of the LSA. We identified 10 patients from 7 case reports of LSA aneurysm presenting with SAH, and combined with the present case, this comprised a total of 11 patients. An initial CT angiography identified LSA aneurysm in only 2 of 11 patients, while 5 cases were detected in transfemoral cerebral angiography. Seven patients had stenosis or occlusion of nearby arteries. Among the 10 patients treated, 7 underwent microsurgical clipping, and 3 had endovascular treatment; complications included PICA infarction and subdural hematoma. LSA aneurysms, though rare, should be considered in differential diagnoses of posterior fossa SAH. An accurate diagnosis often requires repeated imaging. It is proposed to individualize treatment strategies based on the unique anatomical structure and hemodynamic conditions of each patient, utilizing both endovascular and surgical approaches. Understanding the vascular anatomy and collateral pathways of the LSA is crucial for improving diagnostic accuracy and treatment outcomes.
| S-EPMC11355152 | biostudies-literature
Project description:Background Spinal intradural (subdural and subarachnoid) hematoma following percutaneous kyphoplasty is an extremely rare complication. In this report, we describe a case of subarachnoid hemorrhage with delayed paralysis after kyphoplasty and review the literature on similar cases to describe the complications of kyphoplasty and vertebroplasty (VP). Case Description An 80-year-old man underwent percutaneous kyphoplasty at a local hospital an osteoporotic vertebral fracture (OVF) at the T12 and L1 level. On the second day after kyphoplasty for T12 OVF, he developed paralysis of the lower limbs. At his initial visit to our clinic, he had a complete loss of sensation below T11 and complete paralysis of both lower extremities. Thoracolumbar magnetic resonance imaging revealed an intradural hematoma on the ventral side of the spinal cord, in the spinal canal from T5 to T12, compressing the spinal cord. Thoracolumbar computed tomography showed a fracture line in the medial cortex of the right pedicle at T12 and a tract from the spinal canal to the vertebral body. An emergency posterior decompression from T11 to L1 was performed. A small hole was found on the right side of the pedicle at T12, and tear of the nerve and subarachnoid hematoma were observed in the vicinity of the T11 nerve root. The subarachnoid hematomas were removed. Postoperatively, the neurological symptoms improved rapidly. Eventually, he was able to walk and was transferred for rehabilitation. Conclusions Percutaneous surgery through the pedicle might cause hematoma and bone cement leakage into the spinal canal. This can be a serious complication: hence prevention is important.
| S-EPMC9808104 | biostudies-literature
Project description:Study Design Case report. Objective Spinal subarachnoid hemorrhage (SSAH) makes up less than 1.5% of all the cases of subarachnoid hemorrhage. Most cases of spontaneous SSAH occur in association with coagulopathy, lumbar punctures, or minor trauma. Idiopathic SSAH is extremely rare with only 17 cases published. Idiopathic SSAH presents a diagnostic dilemma, and the appropriate investigations and treatment remain a matter of controversy. We report a case of idiopathic SSAH and a review of the literature regarding its clinical presentation, diagnosis, and treatment. Methods A 73-year-old woman presented to the emergency department after spontaneously developing severe right leg and lower back pain while bending over to vomit. After a review of the patient's history and examination, the magnetic resonance imaging (MRI) of the thoracolumbar spine revealed T1 hyperintensity and T2 hypointensity, a diffusion-restricted collection at the T11-T12 level, and a posterior collection from L3 to S1 producing a mild displacement of the thecal sac. Results The patient was taken for an L5 laminectomy. Intraoperatively, rust-colored, xanthochromic fluid was drained from the subarachnoid space, confirming SSAH. The thecal sac was decompressed. The cultures and Gram stains were negative. Computer tomography (CT) and CT angiography of the brain were normal. She recovered postoperatively with resolution of the pain and no further episodes of hemorrhage after 2 years of follow-up. Repeat thoracolumbar MRI, selective spinal angiogram, and six-vessel cerebral angiogram did not reveal pathology. Conclusion We suggest a clinical algorithm to aid in the diagnosis and management of such patients.
| S-EPMC4577320 | biostudies-other
Project description:Aneurysmal subarachnoid hemorrhage is a neurologic emergency that requires immediate patient stabilization and prompt diagnosis and treatment. Early measures should focus on principles of advanced cardiovascular life support. The aneurysm should be evaluated and treated in a comprehensive stroke center by a multidisciplinary team capable of endovascular and, operative approaches. Once the aneurysm is secured, the patient is best managed by a dedicated neurocritical care service to prevent and manage complications, including a syndrome of delayed neurologic decline. The goal of such specialized care is to prevent secondary injury, reduce length of stay, and improve outcomes for survivors of the disease.
| S-EPMC8147706 | biostudies-literature
Project description:Aneurysmal subarachnoid hemorrhage (SAH) is a worldwide health burden with high fatality and permanent disability rates. The overall prognosis depends on the volume of the initial bleed, rebleeding, and degree of delayed cerebral ischemia (DCI). Cardiac manifestations and neurogenic pulmonary edema indicate the severity of SAH. The International Subarachnoid Aneurysm Trial (ISAT) reported a favorable neurological outcome with the endovascular coiling procedure compared with surgical clipping at the end of 1 year. The ISAT trial recruits were primarily neurologically good grade patients with smaller anterior circulation aneurysms, and therefore the results cannot be reliably extrapolated to larger aneurysms, posterior circulation aneurysms, patients presenting with complex aneurysm morphology, and poor neurological grades. The role of hypothermia is not proven to be neuroprotective according to a large randomized controlled trial, Intraoperative Hypothermia for Aneurysms Surgery Trial (IHAST II), which recruited patients with good neurological grades. Patients in this trial were subjected to slow cooling and inadequate cooling time and were rewarmed rapidly. This methodology would have reduced the beneficial effects of hypothermia. Adenosine is found to be beneficial for transient induced hypotension in 2 retrospective analyses, without increasing the risk for cardiac and neurological morbidity. The neurological benefit of pharmacological neuroprotection and neuromonitoring is not proven in patients undergoing clipping of aneurysms. DCI is an important cause of morbidity and mortality following SAH, and the pathophysiology is likely multifactorial and not yet understood. At present, oral nimodipine has an established role in the management of DCI, along with maintenance of euvolemia and induced hypertension. Following SAH, hypernatremia, although less common than hyponatremia, is a predictor of poor neurological outcome.
| S-EPMC4463029 | biostudies-other
Project description:Background?Despite widespread utilization of chiropractic treatment for various ailments, there is a paucity of documentation regarding intracerebral hemorrhage related to chiropractic trauma. Stroke has been reported from cervical manipulation, although with a suggested low incidence. Activator treatment, an instrument that produces a high-velocity, low-amplitude impact to the spine, is considered especially safe. There are no prior reports of intracerebral hemorrhage resulting from a chiropractic activator treatment. Case Description?A 75-year-old woman was admitted to the hospital with a history of headaches, visual difficulties on the right, and speech disturbance of relatively acute onset. CT scan showed a brain hemorrhage in an unusual location. Extensive evaluation was undertaken because this was thought to be a spontaneous event. No cause was found on imaging. Subsequent history revealed a chiropractic activator treatment applied directly to the junction of the back of her head and the upper cervical spine immediately prior to the onset of symptoms. Her clinical course is described. Conclusions?This appears to be the first report linking traumatic intracerebral hemorrhage with a chiropractic activator treatment. The use of this modality in an elderly population, with widespread utilization of anticoagulants and platelet inhibitors, is of potential concern.
| S-EPMC5167612 | biostudies-other
Project description:Microscopic polyangiitis (MPA) is a systemic small-vessel vasculitis associated with anti-neutrophil cytoplasmic antibody (ANCA) and predominantly causes kidney and pulmonary injuries. Subarachnoid hemorrhage, a life-threatening manifestation of the central nervous system (CNS), rarely occurs in patients with ANCA-associated vasculitis (AAV). We report the case of a young man with spontaneous SAH recurrence and active nephritis. The patient was treated with a glucocorticoid pulse and intravenous cyclophosphamide (CTX) in combination with decreasing cerebral perfusion pressure and analgesic therapy. All the patients' symptoms except the proteinuria resolved. We reviewed the clinical characteristics of 34 previously reported cases of SAH with AAV, comprising six cases of MPA, eight cases of granulomatosis with polyangiitis (GPA), and 19 cases of eosinophilic granulomatosis with polyangiitis (EGPA), and one case of unclassified AAV. All the cases showed features of active vasculitis. Concomitant nephritis and peripheral neuropathy were found in the MPA and EGPA cases with SAH, respectively. Renal and pulmonary manifestations were predominant in the patients with GPA and SAH. Ten patients had aneurysmal abnormalities, and six patients had cardiac abnormalities. Thirty-one patients were treated with glucocorticoids, and 18 patients received concurrent immunosuppressants. Patients with SAH had a mortality rate of 38.2%. The presence of cerebrovascular events or cardiac involvement in patients with AAV and SAH is associated with increased mortality of 64.3%. Our study indicates that SAH should be cautioned as a disease occurring in patients with AAV. Early diagnosis with aggressive immunosuppressive therapy can help improve the prognosis of patients with SAH.
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Project description:Interleukin 6 (IL-6) is a prominent proinflammatory cytokine. Neuroinflammation in general, and IL-6 signaling in particular, appear to play a major role in the pathobiology and pathophysiology of aneurysm formation and aneurysmal subarachnoid hemorrhage (SAH). Most importantly, elevated IL-6 CSF (rather than serum) levels appear to correlate with delayed cerebral ischemia (DCI, "vasospasm") and secondary ("vasospastic") infarctions. IL-6 CSF levels may also reflect other forms of injury to the brain following SAH, i.e., early brain damage and septic complications of SAH and aneurysm treatment. This would explain why many researchers have found an association between IL-6 levels and patient outcomes. These findings clearly suggest CSF IL-6 as a candidate biomarker in SAH patients. However, at this point, discrepant findings in variable study settings, as well as timing and other issues, e.g., defining proper clinical endpoints (i.e., secondary clinical deterioration vs. angiographic vasospasm vs. secondary vasospastic infarct) do not allow for its routine use. It is also tempting to speculate about potential therapeutic measures targeting elevated IL-6 CSF levels and neuroinflammation in SAH patients. Corticosteroids and anti-platelet drugs are indeed used in many SAH cases (not necessarily with the intention to interfere with detrimental inflammatory signaling), however, no convincing benefit has been demonstrated yet. The lack of a robust clinical perspective against the background of a relatively large body of data linking IL-6 and neuroinflammation with the pathophysiology of SAH is somewhat disappointing. One underlying reason might be that most relevant studies only report correlative data. The specific molecular pathways behind elevated IL-6 levels in SAH patients and their various interactions still remain to be delineated. We are optimistic that future research in this field will result in a better understanding of the role of neuroinflammation in the pathophysiology of SAH, which in turn, will translate into the identification of suitable biomarkers and even potential therapeutic targets.
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Project description:Bullous pemphigoid (BP) is a rare, life-threatening autoimmune blistering disease with pruritus and tension blisters/bullous as the main clinical manifestations. Glucocorticosteroids are the main therapeutic agents for it, but their efficacy is poor in some patients. Tofacitinib, a small molecule agent that inhibits JAK1/3, has shown incredible efficacy in a wide range of autoimmune diseases and maybe a new valuable treatment option for refractory BP. To report a case of refractory BP successfully treated with tofacitinib, then explore the underlying mechanism behind the treatment, and finally review similarities to other cases reported in the literature. Case report and literature review of published cases of successful BP treatment with JAK inhibitors. The case report describes a 73-year-old male with refractory BP that was successfully managed with the combination therapy of tofacitinib and low-dose glucocorticoids for 28 weeks. Immunohistochemistry and RNA sequencing were performed to analyze the underlying mechanism of tofacitinib therapy. A systematic literature search was conducted to identify other cases of treatment with JAK inhibitors. Throughout the 28-week treatment period, the patient experienced clinical, autoantibody and histologic resolution. Immunohistochemical analysis showed tofacitinib significantly decreased the pSTAT3 and pSTAT6 levels in the skin lesions of this patient. RNA sequencing and immunohistochemical testing of lesion samples from other BP patients identified activation of the JAK-STAT signaling pathway. Literature review revealed 17 previously reported cases of BP treated with four kinds of JAK inhibitors successfully, including tofacitinib (10), baricitinib (1), upadacitinib (3) and abrocitinib (3). Our findings support the potential of tofacitinib as a safe and effective treatment option for BP. Larger studies are underway to better understand this efficacy and safety.
2024-11-13 | GSE278926 | GEO
Project description:Introduction:Subarachnoid Hemorrhage (SAH) is caused by an aneurysmatic origin in 80% of cases. In the adult population, the risk of shunt dysfunction is about 16% in the first year, with proximal mechanical obstruction being the most frequent cause. Case report:An 81-year-old man with a history of shunt system placement presented among clinical data of shunt dysfunction. The brain Computed Tomography (CT) showed dilation of the ventricular system, with no other associated injury. The cause of the dysfunction was a SAH determined by a lumbar puncture (LP) study. We performed an angiography reporting 3 aneurysms. Discussion:The risk of shunt dysfunction at one year is 40% and at two years, the risk ups to 53% with obstruction of the system and infection being the two principal causes. The usefulness of a lumbar puncture for late detection of SAH lies in the red cells in the Cerebrospinal Fluid (CSF). When the CT is negative and the clinical suspicion remains, the lumbar puncture (LP) continues with higher sensitivity despite is over 12 hours of the onset clinic symptoms. Conclusion:This case encourages to follow a rigorous protocol study for patients with multiple shunt dysfunction and chronic hydrocephalus. Also, this case invites to consider a hidden SAH secondary to a vascular pathology as a differential diagnosis for a multiple shunt dysfunction.
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