Superficial Siderosis of the Brain as a Late Complication of Subarachnoid Haemorrhage

2003 ◽  
Vol 17 (1) ◽  
pp. 87-87 ◽  
Author(s):  
Konstantinos Spengos ◽  
Marios Panas ◽  
Sofia Sameli ◽  
Konstantinos Vemmos ◽  
Konstantinos Sfangos ◽  
...  
Keyword(s):  
Subarachnoid Haemorrhage ◽  
Late Complication ◽  
Superficial Siderosis ◽  
The Brain

Superficial siderosis of the brain following unexplained subarachnoid hemorrhage: MRI diagnosis and clinical significance

1992 ◽  
Vol 34 (5) ◽  
pp. 407-410 ◽  
Author(s):  
P. M. Bourgouin ◽  
D. Tampieri ◽  
D. Melancon ◽  
R. del Carpio ◽  
R. Ethier
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Clinical Significance ◽  
Superficial Siderosis ◽  
Mri Diagnosis ◽  
The Brain

scholarly journals Critical care of subarachnoid haemorrhage

2017 ◽  
Vol 04 (04) ◽  
pp. S49-S55
Author(s):  
Michael Souter
Keyword(s):  
Critical Care ◽  
Subarachnoid Haemorrhage ◽  
Neurological Outcome ◽  
Neurocritical Care ◽  
Comprehensive Evaluation ◽  
Haemorrhagic Stroke ◽  
Care Team ◽  
Evidence Based ◽  
New Treatment ◽  
The Brain

AbstractSubarachnoid haemorrhage (SAH) is a consistent presentation of haemorrhagic stroke of significance to clinicians in neurocritical care, inducing consequent effects on non-neurological systems, while at the same time, rendering the brain vulnerable to secondary physiological insult modifying neurological outcome, despite control of the original point of haemorrhage. Coordinated treatment depends on comprehensive evaluation of both cerebral and systemic physiology, identifying and treating impaired function. The presence of a dedicated neurocritical care team can benefit outcome. Protocols of care have evolved to meet evidence-based challenges, discarding potentially deleterious components of hypervolaemia and haemodilution, while maintaining pressure-guided perfusion. Treatment targets have also evolved with a shift in focus away from SAH-associated vasospasm, towards actual ischaemic outcome – illustrated by lack of effectiveness of pharmaceutical treatments of vasospasm. Clinicians must consequently review pathophysiological mechanisms of injury and devise new treatment opportunities.

scholarly journals Haemoglobin causes neuronal damage in vivo which is preventable by haptoglobin

2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Patrick Garland ◽  
Matthew J Morton ◽  
William Haskins ◽  
Ardalan Zolnourian ◽  
Andrew Durnford ◽  
...  
Keyword(s):  
Subarachnoid Haemorrhage ◽  
Prolonged Exposure ◽  
Neuronal Damage ◽  
Clinical Importance ◽  
Large Vessel ◽  
Therapeutic Window ◽  
Neurofilament Light Chain ◽  
Neurofilament Light ◽  
The Brain

Abstract After subarachnoid haemorrhage, prolonged exposure to toxic extracellular haemoglobin occurs in the brain. Here, we investigate the role of haemoglobin neurotoxicity in vivo and its prevention. In humans after subarachnoid haemorrhage, haemoglobin in cerebrospinal fluid was associated with neurofilament light chain, a marker of neuronal damage. Most haemoglobin was not complexed with haptoglobin, an endogenous haemoglobin scavenger present at very low concentration in the brain. Exogenously added haptoglobin bound most uncomplexed haemoglobin, in the first 2 weeks after human subarachnoid haemorrhage, indicating a wide therapeutic window. In mice, the behavioural, vascular, cellular and molecular changes seen after human subarachnoid haemorrhage were recapitulated by modelling a single aspect of subarachnoid haemorrhage: prolonged intrathecal exposure to haemoglobin. Haemoglobin-induced behavioural deficits and astrocytic, microglial and synaptic changes were attenuated by haptoglobin. Haptoglobin treatment did not attenuate large-vessel vasospasm, yet improved clinical outcome by restricting diffusion of haemoglobin into the parenchyma and reducing small-vessel vasospasm. In summary, haemoglobin toxicity is of clinical importance and preventable by haptoglobin, independent of large-vessel vasospasm.

scholarly journals DHEA Attenuates Microglial Activation via Induction of JMJD3 in Experimental Subarachnoid Haemorrhage

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Tao Tao ◽  
Guang-Jie Liu ◽  
Xuan Shi ◽  
Yan Zhou ◽  
Yue Lu ◽  
...  
Keyword(s):  
Subarachnoid Haemorrhage ◽  
Microglial Activation ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Early Brain Injury ◽  
Protective Effects ◽  
In Vivo Models ◽  
The Brain

Abstract Background Microglia are resident immune cells in the central nervous system and central to the innate immune system. Excessive activation of microglia after subarachnoid haemorrhage (SAH) contributes greatly to early brain injury, which is responsible for poor outcomes. Dehydroepiandrosterone (DHEA), a steroid hormone enriched in the brain, has recently been found to regulate microglial activation. The purpose of this study was to address the role of DHEA in SAH. Methods We used in vivo models of endovascular perforation and in vitro models of haemoglobin exposure to illustrate the effects of DHEA on microglia in SAH. Results In experimental SAH mice, exogenous DHEA administration increased DHEA levels in the brain and modulated microglial activation. Ameliorated neuronal damage and improved neurological outcomes were also observed in the SAH mice pretreated with DHEA, suggesting neuronal protective effects of DHEA. In cultured microglia, DHEA elevated the mRNA and protein levels of Jumonji d3 (JMJD3, histone 3 demethylase) after haemoglobin exposure, downregulated the H3K27me3 level, and inhibited the transcription of proinflammatory genes. The devastating proinflammatory microglia-mediated effects on primary neurons were also attenuated by DHEA; however, specific inhibition of JMJD3 abolished the protective effects of DHEA. We next verified that DHEA-induced JMJD3 expression, at least in part, through the tropomyosin-related kinase A (TrkA)/Akt signalling pathway. Conclusions DHEA has a neuroprotective effect after SAH. Moreover, DHEA increases microglial JMJD3 expression to regulate proinflammatory/anti-inflammatory microglial activation after haemoglobin exposure, thereby suppressing inflammation.

High Incidence of Radiation Induced Cavernous Hemangioma (RICH) in Long Term Survivors Who Underwent BMT with Radiation Therapy During Childhood or Adolescence.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 4292-4292
Author(s):  
Takashi Koike ◽  
Noriharu Yanagimachi ◽  
Hiromasa Yabe ◽  
Miharu Yabe ◽  
Tsuyoshi Morimoto ◽  
...  
Keyword(s):  
Radiation Therapy ◽  
Cavernous Hemangioma ◽  
Late Complication ◽  
Weighted Image ◽  
Primary Disease ◽  
High Incidence ◽  
Radiation Induced ◽  
Long Term Survivors ◽  
The Brain

Abstract Abstract 4292 INTRODUCTION Radiation induced cavernous hemangioma (RICH) is a late complication of cerebral radiation therapy. An increased number of long term surviving blood and marrow transplantation (BMT) recipients have recovered from their primary disease but are at risk of RICH. METHODS We investigated 66 patients who underwent BMT during childhood or adolescence. We evaluated RICH numbers, size, location and their annual changes. Furthermore we developed scoring system of RICH in order to classify severity. MRI of the brain was performed annually for 5 to 27 years after BMT, including gradient-echo sequence (T2* weighted image). RICH SCORE 1-4 is designated as mild, 5-9 as moderate and 10 or more as severe. RESULTS Twenty-five patients (37.9%) was diagnosed RICH. The age at the time of the diagnosis was 11-40 years old (median 27 years old). The age at the time of BMT was 1-22 years old (median 9 years old). The period from BMT to diagnosis was 10-24 years (median 16 years). All cases received TBI as conditioning of BMT and/or cranial radiation (CR) prior to BMT as treatment of primary disease. RICH was found in 25/48 (52%) who received TBI and/or CR, and was not found in any of 18 patients without radiation therapy to the brain. Total dose to the brain was 10-36 Gy. Clinical manifestations were present only in four cases. RICH SCORE ranged 1-18 points (median 4 points). Small RICHs tended to be recognized only by T2* weighted image, but not by routine imaging methods. Classification of the severity was mild in 13 patients, moderate in 8 patients and severe in 4 patients. Severity was correlated with higher radiation dose and/or with younger ages at transplantation. RICH SCORE increased yearly in 7 of 25 patients. One case developed giant RICH more than 40mm as shown in the attached image. CONCLUSION High incidence of RICH was found in long term survivors who underwent BMT with radiation therapy. Since all of those patients did not show RICH before BMT and all positive patients had a history of radiation therapy to the brain, the cause of RICH in those patients was considered to be radiation. Careful and long term evaluation with MRI including T2* weighted image is necessary in BMT recipients who received radiation therapy prior and/or during BMT. Disclosures: Ando: Alexion: Research Funding.

Effect of dietary β carotene on cerebral aneurysm and subarachnoid haemorrhage in the brain apo E−/− mice

2011 ◽  
Vol 32 (3) ◽  
pp. 343-355 ◽  
Author(s):  
K. Gopal ◽  
P. Nagarajan ◽  
T. Avinash Raj ◽  
P. Jahan ◽  
H. S. Ganapathy ◽  
...  
Keyword(s):  
Subarachnoid Haemorrhage ◽  
Cerebral Aneurysm ◽  
Apo E ◽  
The Brain ◽  
Β Carotene

scholarly journals Hemosiderosis of Central Nervous System: a case report of a rare and underdiagnosed disease

2021 ◽  
Vol 10 (11) ◽  
pp. e270101119579
Author(s):  
Cássio Marques Perlin ◽  
Lanusa Alquino Colombo ◽  
Anderson Dillmann Groto ◽  
Bruno Gleizer da Silva Rigon
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Superficial Siderosis ◽  
Medical Clinic ◽  
Resonance Imaging ◽  
System A ◽  
Magnetic Resonance Imaging Mri ◽  
Brain And Spinal Cord ◽  
The Brain

Superficial Siderosis (SS) of Central Nervous System is a rare disease characterized by the deposit of hemosiderin in the brain and spinal cord. Clinically, it is characterized by progressive sensorineural ataxia and deafness associated with injury of superior motor neuron. The diagnosis is made by magnetic resonance imaging (MRI) of the encephalon and spinal cord. The objective of the study is to report the case of a patient with characteristic elements of the syndrome, accompanied in a private medical clinic.

scholarly journals Hemispherectomy for Seizures Revisited

1983 ◽  
Vol 10 (2) ◽  
pp. 71-78 ◽  
Author(s):  
Theodore Rasmussen
Keyword(s):  
Postoperative Complication ◽  
Late Complication ◽  
Therapeutic Effectiveness ◽  
Neurologic Deterioration ◽  
Highly Effective ◽  
Occipital Pole ◽  
Refractory Seizures ◽  
The Cost ◽  
The Brain

SUMMARY:The serious, late complication of superficial cerebral hemosiderosis, which appears after several years in 1/4–1/3 of patients who have undergone hemispherectomy, has resulted in recent years in a considerable reluctance to carry out this operation despite the fact it has proved to be highly effective in patients with medically refractory seizures associated with hemiplegia. Preservation of a small portion of the hemisphere, usually the frontal or occipital pole, has proved to be effective in preventing this late complication, but at the cost of a significant reduction in the effectiveness of the operation in reducing the patients’ seizure tendency. Preserving the frontal and occipital poles but disconnecting them from the rest of the brain, resulting in a functional complete but anatomical subtotal hemispherectomy, retains the therapeutic effectiveness of a complete hemispherectomy while still protecting adequately against the serious late postoperative complication of superficial cerebral hemosiderosis and its associated neurologic deterioration, hydrocephalus and sometimes death.

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