A proposed framework for cerebral venous congestion

2021 ◽  
pp. 197140092110292
Author(s):  
Anirudh Arun ◽  
Matthew R Amans ◽  
Nicholas Higgins ◽  
Waleed Brinjikji ◽  
Mithun Sattur ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Clinical Symptoms ◽  
Case Series ◽  
Venous Hypertension ◽  
Venous Congestion ◽  
Venous Stasis ◽  
Anatomical Location ◽  
Peripheral Vasculature ◽  
Developing Area ◽  
The Brain

Background While venous congestion in the peripheral vasculature has been described and accepted, intracranial venous congestion remains poorly understood. The characteristics, pathophysiology, and management of cerebral venous stasis, venous hypertension and venous congestion remain controversial, and a unifying conceptual schema is absent. The cerebral venous and lymphatic systems are part of a complex and dynamic interaction between the intracranial compartments, with interplay between the parenchyma, veins, arteries, cerebrospinal fluid, and recently characterized lymphatic-like systems in the brain. Each component contributes towards intracranial pressure, occupying space within the fixed calvarial volume. This article proposes a framework to consider conditions resulting in brain and neck venous congestion, and seeks to expedite further study of cerebral venous diagnoses, mechanisms, symptomatology, and treatments. Methods A multi-institution retrospective review was performed to identify unique patient cases, complemented with a published case series to assess a spectrum of disease states with components of venous congestion affecting the brain. These diseases were organized according to anatomical location and purported mechanisms. Outcomes of treatments were also analyzed. Illustrative cases were identified in the venous treatment databases of the authors. Conclusion This framework is the first clinically structured description of venous pathologies resulting in intracranial venous and cerebrospinal fluid hypertension. Our proposed system highlights unique clinical symptoms and features critical for appropriate diagnostic work-up and potential treatment. This novel schema allows clinicians effectively to approach cases of intracranial hypertension secondary to venous etiologies, and furthermore provides a framework by which researchers can better understand this developing area of cerebrovascular disease.

Regional parenchymal enhancement with mixed cavernous/venous malformations of the brain

1997 ◽  
Vol 86 (1) ◽  
pp. 154-158 ◽  
Author(s):  
Christopher H. Comey ◽  
Douglas Kondziolka ◽  
Howard Yonas
Keyword(s):  
Clinical Symptoms ◽  
Vascular Malformations ◽  
Venous Hypertension ◽  
Venous Malformations ◽  
True Nature ◽  
Cavernous Malformations ◽  
Content Type ◽  
Growth Factor Release ◽  
The Brain ◽  
Parenchymal Enhancement

✓ With improvements in imaging technology, the detection of both cavernous malformations and venous malformations has increased markedly in recent years. Although much has been learned about the association of cavernous and venous malformations, important questions regarding the true nature of such a relationship remain unanswered. It has been proposed that certain venous malformations produce local venous hypertension with resultant microhemorrhage, growth factor release, and creation of cavernous malformations. The authors report on two patients with cerebellopontine venous malformations associated with cavernous malformations. Both patients demonstrated persistent regional parenchymal enhancement associated with the vascular malformations. In addition, both patients had significant clinical symptoms referable to the region of affected brain. This previously undescribed finding may represent an imaging correlate to the complex interaction among venous malformations, venous hypertension, and cavernous malformations.

scholarly journals CLIPPERS Spectrum Disorder: A Rare Pediatric Neuroinflammatory Condition

2019 ◽  
Vol 6 ◽  
pp. 2329048X1983109 ◽  
Author(s):  
Tarishi Nemani ◽  
Anaita Udwadia-Hegde ◽  
Purva Keni Karnavat ◽  
Ritu Kashikar ◽  
Shridhar Epari
Keyword(s):  
Clinical Symptoms ◽  
Case Series ◽  
Brain Biopsy ◽  
Distinct Pattern ◽  
Spectrum Disorder ◽  
The Brain ◽  
Lymphocyte Infiltrate ◽  
Pediatric Onset ◽  
Steroid Sparing ◽  
Rule Out

CLIPPERS (chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids) is a recently described, rare neuroinflammatory disorder diagnosed by clinical symptoms involving the brain stem with a distinct pattern on neuroimaging and a perivascular T-lymphocyte infiltrate on brain biopsy. It is a condition usually described in adults in the fourth to fifth decade. We report a case of 13-year-old Indian boy who presented with recurrent episodes of ataxia and diplopia with onset at 7 years of age. He was investigated extensively to rule out infective, neoplastic, autoimmune, and demyelinating conditions over a span of 6 years. The diagnosis of CLIPPERS was entertained on the basis of clinico-radio-pathological correlation. Treatment with steroids and steroid-sparing agents, particularly methotrexate, seems to provide a promising outcome. With very few cases in literature so far, reporting of a larger case series with pediatric onset may expand it to CLIPPERS spectrum disorder.

scholarly journals High frequency of cerebrospinal fluid autoantibodies in COVID-19 patients with neurological symptoms

2020 ◽  
Author(s):  
Christiana Franke ◽  
Caroline Ferse ◽  
Jakob Kreye ◽  
S Momsen Reincke ◽  
Elisa Sanchez-Sendin ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
High Frequency ◽  
Clinical Symptoms ◽  
Epileptic Seizures ◽  
Neurological Symptoms ◽  
Neurofilament Light Chain ◽  
Neurofilament Light ◽  
Intensive Care Patients ◽  
Neuronal Autoantibodies ◽  
The Brain

AbstractCOVID-19 intensive care patients occasionally develop neurological symptoms. The absence of SARS-CoV-2 in most cerebrospinal fluid (CSF) samples suggests the involvement of further mechanisms including autoimmunity. We therefore determined whether anti-neuronal or anti-glial autoantibodies are present in eleven consecutive severely ill COVID-19 patients presenting with unexplained neurological symptoms. These included myoclonus, cranial nerve involvement, oculomotor disturbance, delirium, dystonia and epileptic seizures. Most patients showed signs of CSF inflammation and increased levels of neurofilament light chain. All patients had anti-neuronal autoantibodies in serum or CSF when assessing a large panel of autoantibodies against intracellular and surface antigens relevant for central nervous system diseases using cell-based assays and indirect immunofluorescence on murine brain sections. Antigens included proteins well-established in clinical routine, such as Yo or NMDA receptor, but also a variety of specific undetermined epitopes on brain sections. These included vessel endothelium, astrocytic proteins and neuropil of basal ganglia, hippocampus or olfactory bulb. The high frequency of autoantibodies targeting the brain in the absence of other explanations suggests a causal relationship to clinical symptoms, in particular to hyperexcitability (myoclonus, seizures). While several underlying autoantigens still await identification in future studies, presence of autoantibodies may explain some aspects of multi-organ disease in COVID-19 and can guide immunotherapy in selected cases.

Fibrinolytic Activity of Cerebro-Spinal Fluid and the Development of Artificial Cerebral Haematomas in Dogs

1969 ◽  
Vol 21 (02) ◽  
pp. 294-303 ◽  
Author(s):  
H Mihara ◽  
T Fujii ◽  
S Okamoto
Keyword(s):  
Cerebrospinal Fluid ◽  
Carboxylic Acid ◽  
Fibrinolytic Activity ◽  
Clinical Implications ◽  
Trans Form ◽  
Plate Method ◽  
Blood Samples ◽  
Fibrin Plate ◽  
The Brain

SummaryBlood was injected into the brains of dogs to produce artificial haematomas, and paraffin injected to produce intracerebral paraffin masses. Cerebrospinal fluid (CSF) and peripheral blood samples were withdrawn at regular intervals and their fibrinolytic activities estimated by the fibrin plate method. Trans-form aminomethylcyclohexane-carboxylic acid (t-AMCHA) was administered to some individuals. Genera] relationships were found between changes in CSF fibrinolytic activity, area of tissue damage and survival time. t-AMCHA was clearly beneficial to those animals given a programme of administration. Tissue activator was extracted from the brain tissue after death or sacrifice for haematoma examination. The possible role of tissue activator in relation to haematoma development, and clinical implications of the results, are discussed.

Chapter 10: Diagnosis

2019 ◽  
Author(s):  
Gerhard Dobler
Keyword(s):  
Cerebrospinal Fluid ◽  
Viral Encephalitis ◽  
Clinical Symptoms ◽  
Serological Tests ◽  
Specific Antibodies ◽  
Cross Reactions ◽  
Neuro Imaging ◽  
Tbev Infection

• TBE appears with non-characteristic clinical symptoms, which cannot be distinguished from oth-er forms of viral encephalitis or other diseases. • Cerebrospinal fluid and neuro-imaging may give some evidence of TBE, but ultimately cannot confirm the diagnosis. • Thus, proving the diagnosis “TBE” necessarily requires confirmation of TBEV-infection by detec-tion of the virus or by demonstration of specific antibodies from serum and/or cerebrospinal fluid. • During the phase of clinic symptoms from the CNS, the TBEV can only rarely be detected in the cerebrospinal fluid of patients. • Most routinely used serological tests for diagnosing TBE (ELISA, HI, IFA) show cross reactions resulting from either Infection with other flaviviruses or with other flavivirus vaccines.

Chapter 10: Diagnosis

2020 ◽  
Keyword(s):  
Cerebrospinal Fluid ◽  
Viral Encephalitis ◽  
Clinical Symptoms ◽  
Serological Tests ◽  
Specific Antibodies ◽  
Cross Reactions ◽  
Neuro Imaging ◽  
Tbev Infection

TBE appears with non-characteristic clinical symptoms, which cannot be distinguished from other forms of viral encephalitis or other diseases. Cerebrospinal fluid and neuro-imaging may give some evidence of TBE, but ultimately cannot confirm the diagnosis. Thus, proving the diagnosis “TBE” necessarily requires confirmation of TBEV-infection by detection of the virus or by demonstration of specific antibodies from serum and/or cerebrospinal fluid. During the phase of clinic symptoms from the CNS, the TBEV can only rarely be detected in the cerebrospinal fluid of patients. Most routinely used serological tests for diagnosing TBE (ELISA, HI, IFA) show cross reactions resulting from either infection with other flaviviruses or with other flavivirus vaccines.

Vasopressin enhances the clearance of β-endorphin immunoreactivity from rat cerebrospinal fluid

1990 ◽  
Vol 122 (2) ◽  
pp. 191-200 ◽  
Author(s):  
C. G. J. Sweep ◽  
Margreet D. Boomkamp ◽  
István Barna ◽  
A. Willeke Logtenberg ◽  
Victor M. Wiegant
Keyword(s):  
Cerebrospinal Fluid ◽  
Receptor Antagonist ◽  
Short Duration ◽  
Lateral Ventricle ◽  
Underlying Mechanism ◽  
Terminal Phase ◽  
Intracerebroventricular Injection ◽  
Intracerebroventricular Administration ◽  
Biphasic Pattern ◽  
The Brain

Abstract The effect of intracerebroventricular (lateral ventricle) administration of arginine8-vasopressin (AVP) on the concentration of β-endorphin immunoreactivity in the cerebrospinal fluid obtained from the cisterna magna was studied in rats. A decrease was observed 5 min following injection of 0.9 fmol AVP. No statistically significant changes were found 5 min after intracerebroventricular treatment of rats with 0.09 or 9 fmol. The decrease induced by 0.9 fmol AVP was of short duration and was found 5 min after treatment but not 10 and 20 min. Desglycinamide9-AVP (0.97 fmol), [pGlu4, Cyt6]-AVP-(4–9) (1.44 fmol), Nα-acetyl-AVP (0.88 fmol), lysine8-vasopressin (0.94 fmol) and oxytocin (1 fmol) when intracerebroventricularly injected did not affect the levels of β-endorphin immunoreactivity in the cerebrospinal fluid 5 min later. This suggests that the intact AVP-(1–9) molecule is required for this effect. Intracerebroventricular pretreatment of rats with the vasopressin V1-receptor antagonist d(CH2)5Tyr(Me)AVP (8.63 fmol) completely blocked the effect of AVP (0.9 fmol). In order to investigate further the underlying mechanism, the effect of AVP on the disappearance from the cerebrospinal fluid of exogenously applied β-endorphin was determined. Following intracerebroventricular injection of 1.46 pmol camel β-endorphin-(1–31), the β-endorphin immunoreactivity levels in the cisternal cerebrospinal fluid increased rapidly, and reached peak values at 10 min. The disappearance of β-endorphin immunoreactivity from the cerebrospinal fluid then followed a biphasic pattern with calculated half-lifes of 28 and 131 min for the initial and the terminal phase, respectively. Treatment of rats with AVP (0.9 fmol; icv) during either phase (10, 30, 55 min following intracerebroventricular administration of 1.46 pmol β-endorphin-(1–31)) significantly enhanced the disappearance of β-endorphin immunoreactivity from the cerebrospinal fluid. The data suggest that vasopressin plays a role in the regulation of β-endorphin levels in the cerebrospinal fluid by modulating clearance mechanisms via V1-receptors in the brain.

scholarly journals Treatment and therapeutic strategies for pituitary apoplexy in pregnancy: a case series

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Yuya Kato ◽  
Yoshikazu Ogawa ◽  
Teiji Tominaga
Keyword(s):  
Pituitary Apoplexy ◽  
Clinical Symptoms ◽  
Case Series ◽  
Optimal Timing ◽  
Presenting Symptoms ◽  
Pathological Evaluation ◽  
Mother And Child ◽  
Life Threatening ◽  
In Pregnancy

Abstract Background Pregnancy is a known risk factor for pituitary apoplexy, which is life threatening for both mother and child. However, very few clinical interventions have been proposed for managing pituitary apoplexy in pregnancy. Case presentation We describe the management of three cases of pituitary apoplexy during pregnancy and review available literature. Presenting symptoms in our case series were headache and/or visual disturbances, and the etiology in all cases was hemorrhage. Conservative therapy was followed until 34 weeks of gestation, after which babies were delivered by cesarean section with prophylactic bolus hydrocortisone supplementation. Tumor removal was only electively performed after delivery using the transsphenoidal approach. All three patients and their babies had a good clinical course, and postoperative pathological evaluation revealed that all tumors were functional and that they secreted prolactin. Conclusions Although the mechanism of pituitary apoplexy occurrence remains unknown, the most important treatment strategy for pituitary apoplexy in pregnancy remains adequate hydrocortisone supplementation and frequent hormonal investigation. Radiological follow-up should be performed only if clinical symptoms deteriorate, and optimal timing for surgical resection should be discussed by a multidisciplinary team that includes obstetricians and neonatologists.

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