A case of pituitary apoplexy masquerading as subarachnoid hemorrhage.
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ABSTRACT:
SUBMITTER: Choudhury M
PROVIDER: S-EPMC4771846 | biostudies-other | 2016 Mar
REPOSITORIES: biostudies-other
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Project description:BackgroundDense exudate during the calcification of cerebral cysticercosis in basal subarachnoid space was easy to be misdiagnosed as subarachnoid hemorrhage (SAH); clinical evaluation and MRI can help differentiate SAH from pseudo-SAH.Case presentationA case of ventricular expansion accompanied by high-density shadows in cisterna circinata cerebri was taken to the hospital for treatment due to sudden faint. This patient was diagnosed as subarachnoid hemorrhage according to computed tomography (CT) in another hospital. We believe that the high density in cisterna circinata cerebri was misdiagnosed as subarachnoid hemorrhage (SAH) 1 year ago. The main etiology of SAH is aneurysm; non-aneurysmal SAH associated with cerebral cysticercosis is extremely rare. Only 5 patients have been reported.ConclusionThis case indicated that although the specificity of CT for SAH is very high, the physicians should be aware of rare false positive findings, called pseudo-SAH.
| S-EPMC8411545 | biostudies-literature
Project description:BackgroundPituitary dysfunction (PD) is a common complication after aneurysmal subarachnoid hemorrhage (aSAH). The prevalence of PD varies widely at a global level and no recent meta-analysis is available. Therefore, the aim of our systematic review and meta-analysis was to summarize the updated estimates of worldwide prevalence of PD after aSAH.MethodsScopus, Embase, Web of Science, and PubMed databases were used to comprehensively search the appropriate literature and a random-effects meta-analysis on the results of the available studies was performed. The heterogeneity in the prevalence estimates was evaluated by subgroup analysis in terms of types of PD, and acute and chronic phases of aSAH. The onset of PD within 6 months after aSAH was considered as acute, while that after 6 months was considered as chronic.ResultsTwenty-seven studies with 1848 patients were included in this analysis. The pooled prevalence of PD in the acute phase was 49.6% (95% CI, 32.4-66.8%), and 30.4% (95% CI, 21.4-39.4%) in the chronic phase. Among the hormonal deficiencies, growth hormone dysfunction was the most prevalent in the acute phase, being 36.0% (95% CI, 21.0-51.0%), while hypoadrenalism was the most prevalent in the chronic phase, being 21.0% (95% CI, 12.0-29.0%). Among the six World Health Organization regions, the South-East Asia Region has the highest prevalence of PD in the acute phase (81.0%, 95%CI, 77.0-86.0%, P < 0.001), while the European Region had the highest prevalence of PD in the chronic phase (33.0%, 95%CI, 24.0-43.0%, P < 0.001). Moreover, single pituitary hormonal dysfunction occurred more frequently than the multiple one, regardless of acute or chronic phase.ConclusionsAlmost half (49.6%) of the included patients with aSAH developed PD complication in the acute phase, while 30.4% of the patients developed them in the chronic phase. Although prevalence varies globally, the high healthcare burden, morbidity and mortality require greater awareness among clinicians.
| S-EPMC10116717 | biostudies-literature
Project description:Introduction and importance Subarachnoid hemorrhage (SAH) is mostly associated with head trauma. Non-traumatic subarachnoid hemorrhage is mostly due to vascular abnormalities: either hemorrhage from ruptured aneurysm or bleeding from arteriovenous malformation. Aneurysmal hemorrhage is the biggest cause in non-traumatic cases. Warfarin is associated with cerebral intraparenchymal hemorrhage, but it is rarely associated with SAH. Case presentation Here, we report the case of a 45-year-old male patient who was admitted to the neurology ward of our hospital due to acute ischemic stroke. The patient was treated with a vitamin K antagonist (warfarin). However, on the third day, his condition deteriorated (his GCS regressed from 11/15 to 5/15). His pupils were anisocoric. Brain CT showed extensive subarachnoid hemorrhage without intraparenchymal involvement. Cerebral magnetic resonance angiography ruled out aneurysmal rupture. The patient was intubated and transferred to the intensive care unit. Due to his poor condition, neurosurgical intervention could not be done. The patient was managed conservatively, but the patient passed away 4 days later in the intensive care unit. Clinical discussion Non-traumatic SAH is mostly caused by aneurysmal rupture. Warfarin increases the risk of intracranial hemorrhage and mostly causes intraparenchymal hemorrhage. Isolated warfarin-related SAH without parenchymal involvement is a rare event. Here we present a young male patient with an isolated warfarin-induced SAH. Conclusion Warfarin is rarely associated with isolated subarachnoid hemorrhage. This case highlights a young male patient with spontaneous SAH after warfarin therapy for acute ischemic stroke. Aneurysmal rupture and trauma should be excluded before a diagnosis of warfarin-induced SAH is made. Highlights • Non-traumatic subarachnoid hemorrhage (SAH) is mostly caused by aneurysmal rupture.• Warfarin increases the risk of intracranial hemorrhage and mostly causes intraparenchymal hemorrhage. Isolated warfarin-related SAH without parenchymal involvement is a rare event.• Here we present a young male patient with isolated SAH due to warfarin treatment for acute ischemic stroke.
| S-EPMC9793204 | 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: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:The diagnosis of cerebral vasospasm after Subarachnoid-Hemorrhage is currently very difficult, additional tools such as blood biomarkers are necessary. We tested the ability of gene expression profiles of blood cells to predict vasospasm. 32 patients suffering subarachnoid-hemorrhage were included in this prospective monocentre study. They were grouped according to have a complicated cerebral vasospasm (Vasospasm) or not (Control) and Paired according to age (+/- 10 years), sex, Fisher grade (+/- 1), location, smoking (at least 3 first parameters). Gene expression profiles of blood cells were determined using 25,000~gene microarray. Blood sample: 2.5 mL harvested in PAXgene® Blood RNA tubes (PreAnalytix) RNA extraction: PAXgene® Blood RNA kit (Qiagen). We used a Universel Reference RNA (Stratagene). RNA amplification and labelling: kit Amino Allyl MessageAmp II (Ambion). We hybridized 4 microarrays per patient using pangenomic microarrays from the "Réseau National des Génopôles" (Illkirch, France). 2 slides were hybridized with reference RNA labelled Cy3 and patient RNA labelled Cy5, and 2 slides were hybridized with reference RNA labelled Cy5 and patient RNA labelled Cy3. Hybridation : Agilent protocol with few modifications : 750 ng of each labelled RNA were hubriddized at 60°C during 17 hours in an Aglient hybridization oven. After washings, Slides were scanned with a GenePix 4000B scanner (Molecular Devices). Image intensity data were extracted with GenePix Pro 6.0 analysis software. Quantification of Cy3 and Cy5 and selection of good spots were performed using the MAIA software (Novikov E and Barillot E. Software package for automatic microarray image analysis (MAIA). The ACUITY software was then used to normalize log ratios Cy3/Cy5 with Lowess non linear normalization, to filter out genes not present in at least 3 slides out of 4, to evaluate the reproducibility of the 4 microarrays of each patient (hierarchical clustering, Self Organizing Maps). Statistical analyses to insure reproducibility was performed using Excel (correlation coefficients, ANOVA). Only slides that passed all reprocubility tests were validated.
2014-05-08 | E-GEOD-37924 | biostudies-arrayexpress
Project description:The diagnosis of cerebral vasospasm after Subarachnoid-Hemorrhage is currently very difficult, additional tools such as blood biomarkers are necessary. We tested the ability of gene expression profiles of blood cells to predict vasospasm.
2014-05-08 | GSE37924 | GEO
Project description: Not available
| S-EPMC10657139 | biostudies-literature
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