The document discusses the anatomy of cerebral veins and its application in cerebral venous thrombosis (CVT). It begins with an overview of the anatomy of cerebral veins, including superficial cerebral veins that drain the cortical surfaces and deep cerebral veins that drain deep white and gray matter. It then discusses dural sinuses and veins that receive cerebral veins, such as the superior and inferior sagittal sinuses, straight sinus, transverse sinus, and cavernous sinus. The document then covers CVT epidemiology, risk factors, clinical presentations, diagnosis, and treatment, focusing on puerperal CVT specifically. Puerperal CVT is more common in India than Western countries and its incidence has decreased in recent decades due to improved obst
Cisterns of brain and its contents along with its classification and approach...Rajeev Bhandari
This presentation tell us about the basic of cistern , according to its classification both supra tentorial and infratentorial along with ventral and dorsal cistern. basically the cistern contains are well explained on this slide nerve , artery and vein. I hope it will help to rembember well about the contains of cistern and different location of cisterns.
Anatomy of the posterior cerebral circulation from the neuroradiology point of view. Anatomy of the vertebral artery. Anatomy of the basilar artery. Important for Neuroradiologists and Neurointerventionalists.
Before embarking on an approach, the surgeon should be familiar with both the ventricular anatomy and the options for optimally Accessing lesions in third ventricle is a surgical challenge because of its difficult corridor as well as deeper location, need of neural incision, preservation of vascular, thalamus and hypothalamus and likely risk of fornix injury.
Liliequist membrane may be understood as a projection formed by an arachnoid membrane extending from the dorsum sellae to the mammillary bodies coined after Liliequist (1956). It has surgical importance in Endoscopic third ventriculostomy and cisternostomy.
Cisterns of brain and its contents along with its classification and approach...Rajeev Bhandari
This presentation tell us about the basic of cistern , according to its classification both supra tentorial and infratentorial along with ventral and dorsal cistern. basically the cistern contains are well explained on this slide nerve , artery and vein. I hope it will help to rembember well about the contains of cistern and different location of cisterns.
Anatomy of the posterior cerebral circulation from the neuroradiology point of view. Anatomy of the vertebral artery. Anatomy of the basilar artery. Important for Neuroradiologists and Neurointerventionalists.
Before embarking on an approach, the surgeon should be familiar with both the ventricular anatomy and the options for optimally Accessing lesions in third ventricle is a surgical challenge because of its difficult corridor as well as deeper location, need of neural incision, preservation of vascular, thalamus and hypothalamus and likely risk of fornix injury.
Liliequist membrane may be understood as a projection formed by an arachnoid membrane extending from the dorsum sellae to the mammillary bodies coined after Liliequist (1956). It has surgical importance in Endoscopic third ventriculostomy and cisternostomy.
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
VENOUS DRAINAGE OF HEAD, FACE, NECK AND BRAINDrVishal2
THIS SEMINAR ON VENOUS DRAINAGE OF HEAD, FACE, NECK AND BRAIN ENCOMPASSES ALL THE POSSIBLE DETAILED EXPLANATION ALONG WITH DIAGRAMMATIC ILLUSTRATIONS OF THE SAME. APPLIED AND SURGICAL ANATOMY ALONG WITH RECENT MODALITIES HAS BEEN ADDED HEREIN..
USMLE CVS 006 007 Development of the heart anatomy .pdfAHMED ASHOUR
The development of the heart is a complex and highly regulated process that begins early in embryonic life.
Understanding the stages of heart development is crucial for recognizing
and addressing congenital heart defects that may occur during this intricate process.
The blood supply to the central nervous system (CNS), including the brain and spinal cord, is crucial for maintaining the metabolic needs of neural tissues.
Neurosurgical interventions related to the blood supply of the CNS are often aimed at addressing vascular abnormalities, preventing strokes, and managing conditions affecting blood vessels in the brain.
Cavernous Sinus Thrombosis.
Introduction:
RNA interference (RNAi) or Post-Transcriptional Gene Silencing (PTGS) is an important biological process for modulating eukaryotic gene expression.
It is highly conserved process of posttranscriptional gene silencing by which double stranded RNA (dsRNA) causes sequence-specific degradation of mRNA sequences.
dsRNA-induced gene silencing (RNAi) is reported in a wide range of eukaryotes ranging from worms, insects, mammals and plants.
This process mediates resistance to both endogenous parasitic and exogenous pathogenic nucleic acids, and regulates the expression of protein-coding genes.
What are small ncRNAs?
micro RNA (miRNA)
short interfering RNA (siRNA)
Properties of small non-coding RNA:
Involved in silencing mRNA transcripts.
Called “small” because they are usually only about 21-24 nucleotides long.
Synthesized by first cutting up longer precursor sequences (like the 61nt one that Lee discovered).
Silence an mRNA by base pairing with some sequence on the mRNA.
Discovery of siRNA?
The first small RNA:
In 1993 Rosalind Lee (Victor Ambros lab) was studying a non- coding gene in C. elegans, lin-4, that was involved in silencing of another gene, lin-14, at the appropriate time in the
development of the worm C. elegans.
Two small transcripts of lin-4 (22nt and 61nt) were found to be complementary to a sequence in the 3' UTR of lin-14.
Because lin-4 encoded no protein, she deduced that it must be these transcripts that are causing the silencing by RNA-RNA interactions.
Types of RNAi ( non coding RNA)
MiRNA
Length (23-25 nt)
Trans acting
Binds with target MRNA in mismatch
Translation inhibition
Si RNA
Length 21 nt.
Cis acting
Bind with target Mrna in perfect complementary sequence
Piwi-RNA
Length ; 25 to 36 nt.
Expressed in Germ Cells
Regulates trnasposomes activity
MECHANISM OF RNAI:
First the double-stranded RNA teams up with a protein complex named Dicer, which cuts the long RNA into short pieces.
Then another protein complex called RISC (RNA-induced silencing complex) discards one of the two RNA strands.
The RISC-docked, single-stranded RNA then pairs with the homologous mRNA and destroys it.
THE RISC COMPLEX:
RISC is large(>500kD) RNA multi- protein Binding complex which triggers MRNA degradation in response to MRNA
Unwinding of double stranded Si RNA by ATP independent Helicase
Active component of RISC is Ago proteins( ENDONUCLEASE) which cleave target MRNA.
DICER: endonuclease (RNase Family III)
Argonaute: Central Component of the RNA-Induced Silencing Complex (RISC)
One strand of the dsRNA produced by Dicer is retained in the RISC complex in association with Argonaute
ARGONAUTE PROTEIN :
1.PAZ(PIWI/Argonaute/ Zwille)- Recognition of target MRNA
2.PIWI (p-element induced wimpy Testis)- breaks Phosphodiester bond of mRNA.)RNAse H activity.
MiRNA:
The Double-stranded RNAs are naturally produced in eukaryotic cells during development, and they have a key role in regulating gene expression .
The increased availability of biomedical data, particularly in the public domain, offers the opportunity to better understand human health and to develop effective therapeutics for a wide range of unmet medical needs. However, data scientists remain stymied by the fact that data remain hard to find and to productively reuse because data and their metadata i) are wholly inaccessible, ii) are in non-standard or incompatible representations, iii) do not conform to community standards, and iv) have unclear or highly restricted terms and conditions that preclude legitimate reuse. These limitations require a rethink on data can be made machine and AI-ready - the key motivation behind the FAIR Guiding Principles. Concurrently, while recent efforts have explored the use of deep learning to fuse disparate data into predictive models for a wide range of biomedical applications, these models often fail even when the correct answer is already known, and fail to explain individual predictions in terms that data scientists can appreciate. These limitations suggest that new methods to produce practical artificial intelligence are still needed.
In this talk, I will discuss our work in (1) building an integrative knowledge infrastructure to prepare FAIR and "AI-ready" data and services along with (2) neurosymbolic AI methods to improve the quality of predictions and to generate plausible explanations. Attention is given to standards, platforms, and methods to wrangle knowledge into simple, but effective semantic and latent representations, and to make these available into standards-compliant and discoverable interfaces that can be used in model building, validation, and explanation. Our work, and those of others in the field, creates a baseline for building trustworthy and easy to deploy AI models in biomedicine.
Bio
Dr. Michel Dumontier is the Distinguished Professor of Data Science at Maastricht University, founder and executive director of the Institute of Data Science, and co-founder of the FAIR (Findable, Accessible, Interoperable and Reusable) data principles. His research explores socio-technological approaches for responsible discovery science, which includes collaborative multi-modal knowledge graphs, privacy-preserving distributed data mining, and AI methods for drug discovery and personalized medicine. His work is supported through the Dutch National Research Agenda, the Netherlands Organisation for Scientific Research, Horizon Europe, the European Open Science Cloud, the US National Institutes of Health, and a Marie-Curie Innovative Training Network. He is the editor-in-chief for the journal Data Science and is internationally recognized for his contributions in bioinformatics, biomedical informatics, and semantic technologies including ontologies and linked data.
Cancer cell metabolism: special Reference to Lactate PathwayAADYARAJPANDEY1
Normal Cell Metabolism:
Cellular respiration describes the series of steps that cells use to break down sugar and other chemicals to get the energy we need to function.
Energy is stored in the bonds of glucose and when glucose is broken down, much of that energy is released.
Cell utilize energy in the form of ATP.
The first step of respiration is called glycolysis. In a series of steps, glycolysis breaks glucose into two smaller molecules - a chemical called pyruvate. A small amount of ATP is formed during this process.
Most healthy cells continue the breakdown in a second process, called the Kreb's cycle. The Kreb's cycle allows cells to “burn” the pyruvates made in glycolysis to get more ATP.
The last step in the breakdown of glucose is called oxidative phosphorylation (Ox-Phos).
It takes place in specialized cell structures called mitochondria. This process produces a large amount of ATP. Importantly, cells need oxygen to complete oxidative phosphorylation.
If a cell completes only glycolysis, only 2 molecules of ATP are made per glucose. However, if the cell completes the entire respiration process (glycolysis - Kreb's - oxidative phosphorylation), about 36 molecules of ATP are created, giving it much more energy to use.
IN CANCER CELL:
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
introduction to WARBERG PHENOMENA:
WARBURG EFFECT Usually, cancer cells are highly glycolytic (glucose addiction) and take up more glucose than do normal cells from outside.
Otto Heinrich Warburg (; 8 October 1883 – 1 August 1970) In 1931 was awarded the Nobel Prize in Physiology for his "discovery of the nature and mode of action of the respiratory enzyme.
WARNBURG EFFECT : cancer cells under aerobic (well-oxygenated) conditions to metabolize glucose to lactate (aerobic glycolysis) is known as the Warburg effect. Warburg made the observation that tumor slices consume glucose and secrete lactate at a higher rate than normal tissues.
Slide 1: Title Slide
Extrachromosomal Inheritance
Slide 2: Introduction to Extrachromosomal Inheritance
Definition: Extrachromosomal inheritance refers to the transmission of genetic material that is not found within the nucleus.
Key Components: Involves genes located in mitochondria, chloroplasts, and plasmids.
Slide 3: Mitochondrial Inheritance
Mitochondria: Organelles responsible for energy production.
Mitochondrial DNA (mtDNA): Circular DNA molecule found in mitochondria.
Inheritance Pattern: Maternally inherited, meaning it is passed from mothers to all their offspring.
Diseases: Examples include Leber’s hereditary optic neuropathy (LHON) and mitochondrial myopathy.
Slide 4: Chloroplast Inheritance
Chloroplasts: Organelles responsible for photosynthesis in plants.
Chloroplast DNA (cpDNA): Circular DNA molecule found in chloroplasts.
Inheritance Pattern: Often maternally inherited in most plants, but can vary in some species.
Examples: Variegation in plants, where leaf color patterns are determined by chloroplast DNA.
Slide 5: Plasmid Inheritance
Plasmids: Small, circular DNA molecules found in bacteria and some eukaryotes.
Features: Can carry antibiotic resistance genes and can be transferred between cells through processes like conjugation.
Significance: Important in biotechnology for gene cloning and genetic engineering.
Slide 6: Mechanisms of Extrachromosomal Inheritance
Non-Mendelian Patterns: Do not follow Mendel’s laws of inheritance.
Cytoplasmic Segregation: During cell division, organelles like mitochondria and chloroplasts are randomly distributed to daughter cells.
Heteroplasmy: Presence of more than one type of organellar genome within a cell, leading to variation in expression.
Slide 7: Examples of Extrachromosomal Inheritance
Four O’clock Plant (Mirabilis jalapa): Shows variegated leaves due to different cpDNA in leaf cells.
Petite Mutants in Yeast: Result from mutations in mitochondrial DNA affecting respiration.
Slide 8: Importance of Extrachromosomal Inheritance
Evolution: Provides insight into the evolution of eukaryotic cells.
Medicine: Understanding mitochondrial inheritance helps in diagnosing and treating mitochondrial diseases.
Agriculture: Chloroplast inheritance can be used in plant breeding and genetic modification.
Slide 9: Recent Research and Advances
Gene Editing: Techniques like CRISPR-Cas9 are being used to edit mitochondrial and chloroplast DNA.
Therapies: Development of mitochondrial replacement therapy (MRT) for preventing mitochondrial diseases.
Slide 10: Conclusion
Summary: Extrachromosomal inheritance involves the transmission of genetic material outside the nucleus and plays a crucial role in genetics, medicine, and biotechnology.
Future Directions: Continued research and technological advancements hold promise for new treatments and applications.
Slide 11: Questions and Discussion
Invite Audience: Open the floor for any questions or further discussion on the topic.
Observation of Io’s Resurfacing via Plume Deposition Using Ground-based Adapt...Sérgio Sacani
Since volcanic activity was first discovered on Io from Voyager images in 1979, changes
on Io’s surface have been monitored from both spacecraft and ground-based telescopes.
Here, we present the highest spatial resolution images of Io ever obtained from a groundbased telescope. These images, acquired by the SHARK-VIS instrument on the Large
Binocular Telescope, show evidence of a major resurfacing event on Io’s trailing hemisphere. When compared to the most recent spacecraft images, the SHARK-VIS images
show that a plume deposit from a powerful eruption at Pillan Patera has covered part
of the long-lived Pele plume deposit. Although this type of resurfacing event may be common on Io, few have been detected due to the rarity of spacecraft visits and the previously low spatial resolution available from Earth-based telescopes. The SHARK-VIS instrument ushers in a new era of high resolution imaging of Io’s surface using adaptive
optics at visible wavelengths.
THE IMPORTANCE OF MARTIAN ATMOSPHERE SAMPLE RETURN.Sérgio Sacani
The return of a sample of near-surface atmosphere from Mars would facilitate answers to several first-order science questions surrounding the formation and evolution of the planet. One of the important aspects of terrestrial planet formation in general is the role that primary atmospheres played in influencing the chemistry and structure of the planets and their antecedents. Studies of the martian atmosphere can be used to investigate the role of a primary atmosphere in its history. Atmosphere samples would also inform our understanding of the near-surface chemistry of the planet, and ultimately the prospects for life. High-precision isotopic analyses of constituent gases are needed to address these questions, requiring that the analyses are made on returned samples rather than in situ.
(May 29th, 2024) Advancements in Intravital Microscopy- Insights for Preclini...Scintica Instrumentation
Intravital microscopy (IVM) is a powerful tool utilized to study cellular behavior over time and space in vivo. Much of our understanding of cell biology has been accomplished using various in vitro and ex vivo methods; however, these studies do not necessarily reflect the natural dynamics of biological processes. Unlike traditional cell culture or fixed tissue imaging, IVM allows for the ultra-fast high-resolution imaging of cellular processes over time and space and were studied in its natural environment. Real-time visualization of biological processes in the context of an intact organism helps maintain physiological relevance and provide insights into the progression of disease, response to treatments or developmental processes.
In this webinar we give an overview of advanced applications of the IVM system in preclinical research. IVIM technology is a provider of all-in-one intravital microscopy systems and solutions optimized for in vivo imaging of live animal models at sub-micron resolution. The system’s unique features and user-friendly software enables researchers to probe fast dynamic biological processes such as immune cell tracking, cell-cell interaction as well as vascularization and tumor metastasis with exceptional detail. This webinar will also give an overview of IVM being utilized in drug development, offering a view into the intricate interaction between drugs/nanoparticles and tissues in vivo and allows for the evaluation of therapeutic intervention in a variety of tissues and organs. This interdisciplinary collaboration continues to drive the advancements of novel therapeutic strategies.
Professional air quality monitoring systems provide immediate, on-site data for analysis, compliance, and decision-making.
Monitor common gases, weather parameters, particulates.
A brief information about the SCOP protein database used in bioinformatics.
The Structural Classification of Proteins (SCOP) database is a comprehensive and authoritative resource for the structural and evolutionary relationships of proteins. It provides a detailed and curated classification of protein structures, grouping them into families, superfamilies, and folds based on their structural and sequence similarities.
1. ANATOMY OF CEREBRAL VEINS AND ITS APPLICATION IN
CLINICAL MEDICINE-CEREBRAL VENOUS THROMBOSIS
PRESENTER – DR AMAR PATIL
PG MEDICINE
2. PREVIEW
Anatomy of Cerebral Veins and Sinuses.
Epidemiology of Cerebral Vein and Sinus Thrombosis.
(Puerperal and nonpuerperal)
Risk Factors of Cerebral Vein and Sinus Thrombosis.
Clinical Presentations of Cerebral Vein and Sinus Thrombosis.
Radiological Diagnosis of Cerebral Venous Thrombosis.
Treatment of Cerebral Venous and Sinus Thrombosis.
Interventional Neuroradiology in the Treatment of Cerebral Venous
Thrombosis.
Complications of Cerebral Vein and Sinus Thrombosis.
Long-Term Prognosis of Cerebral Vein and Sinus Thrombosis.
3. ANATOMY OF CEREBRAL VEINS
The cerebral veins are divided into
The superficial and
Deep groups.
The superficial group drains the cortical surfaces.
The deep group drains the deep white and gray matter and collects into
channels that course through the walls of the ventricles and basal cisterns
to drain into the internal cerebral, basal, and great veins.
4. SUPERFICIAL OR
EXTERNAL CEREBRAL VEINS
Drain the surface (cortex) of cerebral hemisphere:
3 groups:
Superior cerebral veins
Middle cerebral veins
Inferior cerebral veins.
5. Superior cerebral veins
8 to 12 in number
Drain- Superolateral and
Medial surface
Ascends upwards ->
Arachnoidmater ->Subdural space-
> Superior saggital sinus.
Middle cerebral veins
Four in number : 2 on each side
Superficial middle cerebral vein
Deep middle cerebral vein.
6. Superficial middle cerebral vein :
Lies superficially in lateral sulcus.
Anteriorly, drains into cavernous
sinus.
Posteriorly, communicates with
Superior sagittal sinus through
superior anastomotic vein (of
Troland).
With Transverse sinus via inferior
anastomotic vein of Labbe.
Deep Middle Cerebral Vein
Lies deep in lateral sulcus.Joins
anterior cerebral vein to form the
basal vein.
7. INFERIOR CEREBRAL VEINS
Drains :
Inferior surface,
Lower parts of medial
and superolateral
surfaces.
8. BASAL VEIN OF ROSENTHAL
Basal vein of Rosenthal:
Formed at base of brain
By union of three veins:
(1) Anterior cerebral
vein:Accompanies anterior
cerebral artery. Drains
medial surface.
(2) Deep middle cerebral vein
(3) Striate vein
Basal vein terminate into Great
cerebral vein of Galen
9. GREAT CEREBRAL VEIN OF GALEN
Length 2cm
Union of 2 internal
cerebral vein
Receives two basal
veins.
Two internal cerebral
veins joins to form->
Great cerebral vein of
Galen-> Straight sinus.
10. DURAL SINUSES AND VEINS
The dural sinuses receive cerebral veins from the superficial and deep parts.
These are: (1) superior and inferior sagittal
(2) straight
(3) transverse
(4) tentorial
(5) cavernous
(6) superior petrosal.
11. SUPERIOR AND INFERIOR SAGITTAL SINUSES
Superior sagittal sinus
superiorly attached to the
falx cerebri ends with crista
galli. In about 60% of cases,
superior sagittal sinus ends
by becoming the right
transverse sinus.
At the termination of the
superior sagittal sinus is a
dilatation, known as
confluence of the sinuses. It
is also known as torcula
herophili.
12. The superior sagittal sinus also communicates with veins in the scalp through
emissary veins that pass through the parietal foramina. The cortical veins may
pass directly to the superior sagittal sinus, or they may join the meningeal
sinuses, which empty into the superior sagittal sinus.
Inferior sagittal sinus occupies the posterior two thirds of the free inferior
edge of the falx cerebri. It ends by joining the great cerebral vein to form
straight sinus.
13. STRAIGHT SINUS
This venous sinus is formed by
the union of the inferior sagittal
sinus with the great cerebral
vein.
It is attached to the tentorium
cerebelli. It may drain into
either the transverse sinus or,
most commonly, the left
transverse sinus.
14. TRANSVERSE SINUSES
These venous sinuses pass laterally
from the confluence of the sinuses in
the attached border of the tentorium
cerebelli.
The right transverse sinus, which is
usually larger, receives the majority of
the drainage from the superior sagittal
sinus. Receive blood from superficial
parts of the brain.
Left transverse sinus, left sigmoid sinus
and left internal jugular vein contain
blood mainly from the deep parts of
the brain drained by the internal
cerebral, basal and great veins.
15. TENTORIAL SINUSES
These sinuses divide into the medial and lateral groups.
The medial group drains into transverse sinuses and
The lateral group drains into both straight and transverse sinuses.
16. CAVERNOUS SINUSES
These large sinuses are about 2
cm long and 1 cm wide. They are
located on each side of sella
turcica and the body of the
sphenoid bone.
There are many trabeculae that
contain blood channels.
Each cavernous sinus receives
blood from the superior and
inferior ophthalmic veins, the
superficial middle cerebral vein in
the lateral fissure of the cerebral
hemispheres.
17. Many important structures pass
through the sinus –
Internal carotid artery
Abducent nerve (vi)
Structures present in the lateral
wall of the sinus include
Occulomotor nerve(iii)
Trochlear nerve (iv)
Opthalmic nerve (v 1)
Maxillary nerve (v 2)
18. PETROSAL SINUSES
These venous sinuses are small
channels that drain the
cavernous sinuses.
They run from the posterior
ends of the cavernous sinuses to
the transverse sinuses. Both of
petrosal sinuses lie in the
attached margins of the
tentorium cerebelli.
20. CEREBRAL VENOUS THROMBOSIS(CVT )
Epidemiology
Puerperal CVT and non-puerperal CVT
Etiology and risk factors.
Clinical features
management
21. DIFFERENCE BETWEEN ARTERIAL AND VENOUS STROKE
Arterial stroke
Mechanism- Vascular damage,
involves pertaining to the site of
involvement.
Pathology- at the site of endothelial
injury, usually occlude the blood flow.
Clinical presentation- acute or
insidious onset(usually hours), deficit
will be maximum at onset in embolic
stroke.
Venous stroke
Mechanism –venous stasis, decreased
fibrinolytic activity.
Pathology – at the area of stasis,
invariably occlude the blood flow, can
cause venous thromboembolism.
Clinical presentation – slowly
progressive(generally days), less severe,
associated with headache, seizures or
LOC.
22. CVT- INTRODUCTION
Cerebral venous thrombosis(CVT) is the presence of
acute thrombosis (a blood clot) in the dural venous sinuses, which
drain blood from the brain.
It involves the thrombosis of the cortical veins and the draining
venous sinuses, either alone or in combination.
Cerebral venous thrombosis is an uncommon cause of stroke with
extremely varied clinical presentations, predisposing factors, imaging
findings, and outcomes.
The first description of CVT, appearing in the French literature in
1825, was by Ribes, in a 45-year old man who died after a 6-month
history of severe headache, epilepsy, and delirium.
23. Venous infarctions in the course of venous thrombosis (involving sinuses,
deep and superficial veins) are much rarer than ischemic strokes of arterial
etiology (2.7 per million in general population) and constitute about 0.5–1%
of causes of all strokes.
They most often occur in young patients, more frequently in women (about
75% of patients) .
24. WHEN TO SUSPECT CVT?
Gradual onset.
History of cranial nerve palsies, diplopia, tinnitus.
Headache –throbbing type or band like or thunder clap also associated with
vomiting.(without any neurological signs difficult to diagnose)
History of seizures.
Patient in altered sensorium or in coma.
History of cancer, recent head injury, recurrent venous thrombosis,
autoimmune diseases such as systemic lupus erythematous, puerperium
and/or pregnancy and the use of oral contraceptives should all raise the
attention of the physician for a possible CVT.
26. PUERPERAL CVT
Puerperium and pregnancy, as predisposing factors for CVT, are well
known. Most of the pregnancy-related CVT occurs in the third trimester or
puerperium.
During pregnancy and for 6-8 weeks after birth, women are at increased
risk of developing venous thromboembolic (VTE) events.
Pregnancy induces several Prothrombotic changes in the coagulation
system that persists at least during early puerperium. Hypercoagulability
worsens after delivery as a result of anemia, volume depletion,
dehydration and trauma.
27. Physiological changes during pregnancy include increase in red cell mass
and plasma volume with dilutional anemia.
The plasma levels of protein S decline progressively during pregnancy
while protein C levels remain unchanged.
There is also increase in D-dimer levels in late pregnancy due to
increased thrombin generation and fibrinolysis. Coagulation factors may
be elevated during postpartum state up to 12 weeks.
These changes during pregnancy and postpartum period confer a higher
risk of venous thrombosis.
28. EPIDEMIOLOGY
What is the Magnitude of the Problem in India?
It has been thought that the incidence of puerperal CVT may be more in
India compared to the western countries. This was probably due to the
reporting of many large series of puerperal CVT from India in the 70's and
80's.
Vascular diseases are the most common disorders of the brain. They mainly
affect older population, but in 25% of cases they also occur in patients
younger than 55 years old.
29. EPIDEMIOLOGY
In the largest hospital-based prospective cohort study from India (Nizam's
Institute Venous Stroke Registry [NIVSR]) by Narayan et al., 428 consecutive
patients with CVT were enrolled over a period of 8 years from a tertiary care
hospital from South India, the mean age of the patients in this study was
31.3 years.
Most of the earlier case series from India reported a higher proportion of
women suffering from CVT than men.
In 1957, Padmavati et al., for the first time from India, reported 15 cases of
CVT in puerperium in an epidemiological study evaluating the causes of
hemiplegia in 44 women. It was at that time recognized as a diagnosis which
was mostly made at autopsy and considered lethal.
30. EPIDEMIOLOGY
In a study by Nagaraja et al., A large hospital-based case series of 317 patients
with CVT recruited over a period of 8 years during the 80's had only 15 male
patients.
This gender bias was usually attributed to gender-specific risk factors like the
usage of oral contraceptives (OCPs) and the influence of other factors such as
pregnancy, puerperium, and hormone replacement therapy.
In contrast to this, the recent case series from India do not show this trend of
female dominance.
31. EPIDEMIOLOGY
In the study of 428 patients of CVT recruited from a tertiary care hospital of
Hyderabad, Narayan et al., had a larger proportion of males than
females.(M=53.7% F= 46.3%)
Showing a similar trend, a large prospective study by Pai N et al., which
recruited 612 consecutive patients of CVT from various hospitals of Mumbai
had a male to female ratio of 3:2.
The plausible reason for this change in gender trends over the last two
decades could be the improvement in obstetric care.
32. INCIDENCE OF PUERPERAL CVT
In the recent years with improving health-care system, there is a reduction in
the pregnancy-related CVT. The occurrence of pregnancy-related venous
thrombosis has been reported to be 9.8% to 17% of all the CVT.
The prevalence of CVT in Indian population is about 4.5/1000 obstetric
admissions.
CVT is more common in primigravidae.
In 1984, Srinivasan, reported 135 cases of stroke in women, of whom only 6
had an arterial stroke, and the rest had a CVT.
33. In the recent times, a change in this trend has been noted. The NIVSR cohort
study and the study by Pai et al., have reported only 9.8% and 8% patients in
the postpartum or pregnant state, respectively.
CVT was found to be 12 times more common in India than in Western
countries. An angiographically proven study reported that 50% of the total
cases of stroke in young women were related to pregnancy and puerperium,
95% of which were due to CVT.
34. RISK FACTORS
Increasing maternal age, increased duration of hospital stay, cesarean
delivery, instrument-assisted delivery, hypertension, infections, and
excessive vomiting in pregnancy increase the risk of developing CVT.
Cultural practices such as water deprivation, unhygienic home deliveries,
anemia, and malnutrition have been proposed to promote pregnancy-
related CVT in India.
Nagaraja et al., (2007) stated that the pregnancy and puerperium increase
the risk of thrombotic events, and these risks are likely to be increased in
women who are carriers of thrombophilic gene polymorphisms.
35. CLINICAL PRESENTATION-PUERPERAL CVT
In contrast to the arterial stroke, which can be easily diagnosed clinically in a
majority of the cases, CVT has no single pattern of presentation, and it may be
difficult to diagnose it on clinical grounds alone.
Clinical findings in CVT fall into two major categories: Those related to
increased intracranial pressure due to impaired venous drainage; and, those
related to focal brain injury from venous ischemia/infarction or hemorrhage.
36. CLINICAL PRESENTATIONS IN VARIOUS INDIAN STUDIES.
Symptoms(%) Nagaraja D
al(n=76)
Srinivasan K
et al(n=135)
Narayana et
al(n=428)
Pai et
al(n=628)
Headache 72 78 88.3 61.9
Fever 22 15 5.4 -
Seizuers 68 64 39.9 31.2
Altered
sensorium
93.4 43 14.5 -
Focal deficits 65.4 47.4 27.3 47.7
Papilloedema 27 15.5 63.4 62.4
37. NON PUERPERAL CVT
Epidemiology and incidence
Etiology
Risk factors
Clinical presentation
Management .
38. EPIDEMIOLOGY
CVST is a disease with potentially serious consequences and usually
affecting young to middle-aged people. Strokes in the young account for
nearly 30% of all cases of stroke in India and cerebral venous thrombosis
(CVT) accounts for 10-20% of these cases.
Banerjee et al., in an autopsy series in late 1980's found that CVT
accounted for almost 10% of all strokes in India.
In a hospital-based study from South India in the 1980's, 15% of strokes
were in individuals <40 years of age and CVT accounted for 15-20% of
these cases.
39. INCIDENCE
CVST represents 0.5%-1% of all strokes.
various study revealed significant number of patients affected by CVST in
2nd and 3rddecade of life, predominantly affecting female population,
approximately one third.
Most common sinus affected in male is sigmoid and transverse sinus
thrombosis. Sagittal sinus is most commonly affected in female population.
40. CAUSES OF CVT
Infective Causes Non Infective Causes
Local – Intracranial infections like
abscess, subdural empyema and
meningitis.
Local – Head injury, Post
Neurosurgery, Tumours like
cholesteatoma, meningioma)
Regional infection – Otitis,
Sinusitis, Orbital cellulitis.
OBGY – Pregnancy, Post Partum,
OCP’s
General – Bacterial sepsis,
Typhoid, TB, Mycoplasma
pneumonia, hepatitis virus B and
C
Any surgery
Severe dehydration of any cause
Inherited Thrombophilia – Anti-
thrombin C deficiency, Protein
41. CAUSES OF CVT
Non infective causes - contd
Acquired coagulation disorders –
Nephrotic syndrome, APLA,
Homocystinemia
Inflammatory diseases like SLE,
Behcet’s disease
Medications – IV or intrathecal
Drugs
Oral contraceptives
Hormone replacement therapy
Androgens.
42. CAUSES OF CVT
Blood disorders
Leukaemia
Anemia
Myeloproliferative disorders
Polycythemia
Sickle-cell trait
Thrombotic thrombocytopenic purpura
Heparin-induced thrombocytopenia
Coagulopathies
Protein S, protein C deficiency
Antithrombin III deficiency
Factor V Leiden deficiency.
Antiphospholipid antibodies
44. POLYCYTHEMIA AND THROMBOSIS
PV is a myeloproliferative disorder manifested by overproduction of erythrocytes,
granulocytes, and megakaryocytes.
The incidence of thrombosis and bleeding in PV was reported to be 12-39% and 1.7-
20%, respectively.
In PV, arterial, venous or microcirculatory thrombosis may occur. The frequency of
venous events is less than for arterial ones
5. Elliott MA, Tefferi A. Thrombosis and haemorrhage in polycythaemia vera and essential thrombocythaemia. Br J
Haematol. 2005;128:275–290
45. ANEMIA AND CVT
Several mechanisms have been proposed to explain the association between
IDA and thrombosis, as iron is an important regulator of thrombopoiesis: low
iron levels disinhibit megakaryocyte activity , which provokes secondary
thrombocytosis, thus leading to a hypercoagulable state.
In addition, microcytosis alters red cells deformability, which increases
viscosity and possibly the risk of venous thrombosis.
Finally, anemic hypoxia secondary to iron deficiency may occur as the
oxygen-carrying capacity of erythrocytes decreases, especially in situations
where the metabolic demands are increased.
All these conditions lead to a turbulent blood flow, causing platelets to come
more frequently in contact with the endothelial lining.
46. ANEMIA AND CVT
In a study by Anand Viswanathan et al.,in 121 prospectively recruited
patients with noninfectious causes of CVT and 120 healthy age- and sex-
matched controls.
Severe anemia (hemoglobin <9 g/dL) was more common in patients with
CVT than in controls (14 vs. 2 patients; P=0.005).
Most patients with severe anemia were female (n=15; 94%).
48. CLINICAL PRESENTATIONS OF CEREBRAL VEIN AND SINUS THROMBOSIS.
The presenting features of CVT usually depend on the sinuses involved,
speed of occlusion, involvement of the cortical veins and the presence of
collaterals.
Symptoms of CVT have been grouped under three major clinical
syndromes-
1- Isolated intracranial hypertension syndrome( headache with or without
vomiting ,papilledema ,and visual problems )
2- Focal syndrome (focal deficits or seizures or both)
3- Encephalopathy ( multifocal signs ,mental status changes ,stupor or
coma )
49. ISOLATED INTRACRANIAL HYPERTENSION SYNDROME
Headache is the most common and least specific of all symptoms of CVT . It
is usually the first symptom in CVT .
Headache is gradual in onset , increase over a period of days to weeks ,
severe in intensity sometimes throbbing type.
Bilateral diffuse associated with vomiting.
In some patients it may be severe thunderclap type of headache mimicing
subarachnoid haemorrhage .
In patients with raised ICP it is severe, diffuse ,generalized pain which
worsens on valsalva manouver and recumbence. Visual obscurations may
occur coinciding with these bouts .
It may resemble migrane with aura .
50. Patients affected by cerebral venous thrombosis
can present with threatened vision, visual
obscuration, visual loss and constriction of the
visual field.
Papilledema on fundoscopy can be initially
evidenced as optic disc swelling, elevating and
blurring.
Furthermore, papilledema is commonly
associated with other signs of intracranial
hypertension such as headache, vomiting and
bradycardia.
In the absence of treatment, papilledema is
known to lead to optic atrophy.
51. FOCAL SYNDROME (FOCAL DEFICITS OR SEIZURES OR BOTH)
Seizures the next commonest symptom occur in about 40 to 70% of
patients with sinus thrombosis.
They may be focal but more commonly generalized.
Life threatening status epilepticus or clusters may be seen in 20% patients.
Neurological signs develop in 50% of patients with sinus thrombosis and
include monoparesis, or hemiparesis.
Focal neurological deficits such as paresis, dysphasia, visual-spatial
disorders, and homonymous hemianopia are common symptoms in 15% of
patients affected by cerebral venous thrombosis and they can be observed
in up to 50% during the course of the disease.
52. FOCAL SYNDROME
Cranial nerve palsies are reported in 12% of all cases of cerebral venous
thrombosis.
The cranial nerves that have been described to be involved are III, IV, V, VI,
VII, VIII, IX, X and XI, and the involvement can be multiple or single.
In patients with lateral sinus thrombosis, diplopia due to VI nerve palsy
and signs of V nerve irritation with temporal and retro-orbital pain, it has
also long been known as the Gradenigo syndrome, suggesting
involvement of the nerves at the petrous apex.
53. FOCAL SYNDROME
In rare cases, cranial nerve palsies can be the only sign of cerebral venous
thrombosis, especially when there is the involvement of the
transverse/sigmoid sinus (VI, VII and VIII cranial nerves) .
The unilateral or bilateral VI cranial nerve involvement can also be due to
the intracranial hypertension itself.
The involvement of the III, IV, V and VI cranial nerves can be due to the
thrombosis of the anterior cavernous sinus.
An involvement of the IX, X and XI cranial nerves is possible when the
location of the thrombosis is in the posterior cavernous sinus or the
internal jugular vein, or the deep venous system or the cerebellar veins.
54. CAVERNOUS SINUS SYNDROME
Cavernous sinus thrombosis is rare and represents about 0.5–2% of all
cerebral venous thrombosis it can have infective etiology especially in
younger patients, and has characteristic clinical features.
Cavernous sinus thrombosis, often secondary to infection from orbital
cellulitis (frequently Staphylococcus aureus), a cutaneous source on the face,
or sinusitis (especially with mucormycosis in diabetic patients), is the most
frequent cause;.
other etiologies include aneurysm of the carotid artery, a carotid-cavernous
fistula (orbital bruit may be present), meningioma, nasopharyngeal carcinoma
and other tumors.
55. CAVERNOUS SINUS SYNDROME
Often, the onset in the anterior cavernous sinus
thrombosis is abrupt with headache, ocular pain,
chemosis, proptosis, ocular nerve palsy (III, IV, VI and
the ophthalmic division of V) and fever in the case of
infective etiology.
In some cases, ocular nerve palsy can be the
exclusive symptom. Posterior cavernous sinus
thrombosis, spreading to the inferior petrosal sinus,
may cause palsies of cranial nerves VI, IX, X and XI
without proptosis.
56. ENCEPHALOPATHY
A generalized encephalopathic illness without localizing signs or recognizable
features of raised intracranial pressure is another pattern of presentation.
A depressed level of consciousness is the most constant finding, varying from
drowsiness to deep coma.
Disturbances of consciousness and cognitive dysfunctions such as delirium
,apathy , frontal lobe syndrome ,multifocal deficits can be present .
57. MANAGEMENT OF CVT
Laboratory Studies
Current guidelines from AHA/ASA recommend routine blood studies
consisting of
Complete blood picture
Prothrombin time
Activated partial thromboplastin time
Other investigations –
D-dimer testing ( elevated levels support the diagnosis of CVT however
normal levels do not exclude the diagnosis ).
Values of D-dimer levels >500 ng/mL may be significant.
58. Testing for protein C, protein S, and Antithrombin deficiency is generally
indicated 2 to 4 weeks after completion of anticoagulation.
ESR,ANA-systemic lupus erythematosus, Wegener granulomatosis, and
temporal arteritis.
59. RADIOLOGICAL
The imaging findings in CVT can be generally divided into indirect and
direct signs of CVT .
The findings include ‘direct signs’, i.e. primarily caused by the thrombosis of
veins and sinuses and ‘indirect signs’ when they are secondary to the
effects of thrombosis.
60. DIRECT SIGNS OF CVT ON CT SCAN
The cord/dense sign.
In 2–25% of patients, the
fresh thrombus can be
visualized as a subtle focus of
hyperdensity within the
occluded sinus on plain CT.
This is best seen within the
large straight and superior
sagittal sinuses.
61. The dense delta (filled
triangle) sign.
This is seen on plain CT, as
a dense triangle (from
hyperdense thrombus)
within the superior sagittal
sinus.
It is seen in up to 60% of
patients.
62. The empty delta (empty triangle) sign.
This is seen on CT after contrast
administration, as a bright triangle
surrounding a central hypodense
core.
It represents contrast enhancement of
the dilated collaterals surrounding
the clot. It is seen in 25–52% of
patients with sagittal, straight, and
lateral sinus thrombosis.
63. INDIRECT SIGNS OF CVT ON CT SCAN
Indirect signs are more frequent. Venous stasis and hyperaemia caused by
occlusion of the sinuses.
Irregular hyperdense or mixed density lesions suggestive of haemorrhagic
infarctions which are either small or large, single or multiple.
Diffuse edema of the brain may be seen.
64. MAGNETIC RESONANCE IMAGING
At a very early acute stage (day 1–3), there is an absence of flow void and the
thrombi appear isointense on T1- and hypointense on T2-weighted images.
At the subacute stage (day 4–21), the thrombus becomes hyperintense,
initially on T1- (day 4–9) then on T2-weighted images (day 10–15).
At the chronic stage (21–35 days), the MRI pattern is more variable. The
thrombosed sinus can either remain totally or partially occluded or can
recanalize.
65. Gadolinium-enhanced MRI showing decreased flow in
the left transverse sinus (a), and a corresponding ‘empty
delta sign’ (b).
68. MANAGEMENT
The main issues in CVT is the progression of thrombosis with resultant
cerebral edema, raised intra-cranial hypertension, central or uncal herniation
and death.
If the vital parameters are maintained during acute phase, alternative channels
open up and re-canalization of sinuses occur naturally.
So the main stay of treatment evolves round decreasing cerebral edema and
ICH and prevention of progression of thrombosis.
69. PUERPERAL CVT- TREATMENT
In a study by Nagaraja et al., prospectively randomized 57 women with
puerperal CVT from South India into a treatment group and a placebo group.
Twenty-nine patients received IV unfractionated heparin (UFH), 5000 IU every
6 h, and then dose-adjusted to reach aPTT of 1.5 times the initial value, and
28 subjects were in the control group.
Two patients in the control group died, and one had a residual paresis at 6
months. In the heparin group, all patients recovered.
70. In an open-label trial by Nagaraja et al., On 150 patients with CVT, 73 received
low-dose heparin (2500 thrice daily) and 77 did not receive heparin.
There was a reduction of death (8 vs. 18; P < 0.001) and increase in complete
recovery (34 vs. 14; P < 0.001) in the group which received heparin compared
to that which did not receive heparin.
71. TREATMENT STRATEGIES
For women with CVT during pregnancy, LMWH in full anticoagulant doses
should be continued throughout pregnancy, and LMWH or vitamin K
antagonist with a target INR of 2.0 to 3.0 should be continued for at least 6
weeks postpartum (for a total minimum duration of therapy of 6 months)
It is to advise women with a history of CVT that future pregnancy is not
contraindicated.
72. TREATMENT
Heparin : indicated During the acute stage.
Dosage : IV Bolus of 3,000–5,000 IU, then 1,000–1,500, IU (average 1,200IU)
per hour.
Aim: until aPTT is doubled.
Until clinical condition is stable (continuous stabilization of symptoms or
complete remission usually within 10–14 days.)
73. TREATMENT
LMWH : During the acute stage
Dosage : antifactor Xa U/kg per 24 h.
Duration : Until clinical condition is stable (continuous stabilization of
symptoms or complete remission usually within 10–14 days)
74. ORAL ANTICOAGULANT
Warfarin : Subacute stage
Days 1 and 2,10 mg/day
- 3rd day, according to INR values
Aim : Target INR 2.0–3.0
Duration (1) Povoked CVT - 3-6 months
(associated with transient risk factor)
(2) Unprovoked CVT - 6-12 months
(3) recurrent/ CVT with severe THROMBOPHILIA / VTE after
CVT- indefinite anticoagulation
75. AED
Phenytoin : Prophylactic in patients at risk for seizures, and in all patients
after the first seizure.
Aim : Avoidance of seizure in acute phase and to prevent status epilepticus.
Dosage : 500-1000mg IV over 4-6hrs after first seizure.
- For prophylaxis 300mg tid orally
Prolonged treatment with AED for 1 year may be advised for patients with
early seizures and hemorrhagic lesions on admission brain scan, whereas in
patients without these risk factors AED therapy may be tapered off
gradually after the acute stage.
76. ANTI OEDEMA
Mannitol 20% : Critical rise of ICP, threatened herniation
Aim : Reduction of ICP
Dosage : 125ml IV over 15-20min. 4-6 times/day,
Duration : Usually for 48-72 hours.
77. Subsctance Indication Aim Doasge Duration
Acetaminoph
en
Mild headache Necessary pain relief 200-1000mg tid On demand
Tramadol Severe
headache
Necessary pain relief 50-100 mg tid
orally
On demand
79. THROMBOLYTIC THERAPY
Infusion of a thrombolytic agent into the dural venous sinus utilizing
microcatheter technique.
Limited to specialized centers ,should be considered for patients with
significant deficit.
Leads to breaks up the thrombus.
Particulate debris is directed into an effluent lumen for collection into
a disposable bag.
80. Alteplase
1 mg/cm infused via venous sinus catheter throughout clot, then 1-2 mg/hr.
Urokinase
250,000 U/hr instilled directly or via venous sinus catheter; additional doses
50,000 U; total dose 1,000,000 U over 2 hr.
Streptokinase
Loading dose: 1000-3000 IU/kg; followed by infusion of 1000-1500 IU/kg/h;
CVT, administered by direct infusion via catheter.
81. DECOMPRESSIVE HEMICRANIECTOMY
In patients with neurological deterioration due to severe mass effect or
intracranial haemorrhage causing intractable intracranial hypertension,
decompressive hemicraniectomy may be considered.
In a recent retrospective study by Srinivas D et al., in 2012 among 34 patients
(the largest series currently) who underwent decompressive craniectomy, 26
(76.4%) achieved a favorable outcome.
82. COMPLICATIONS
1 EARLY
2 LATE
1)EARLY
a) SEIZURES- 37% cases
RECOMMENDATIONS
Early initiation of AED in patients with CVT and single seizure with
parenchymal leisons for definite period is recommended to
prevent furthur seizure.
CVT with seizures without parenchymal lesion AED initiation is
probably recommended.
Patients without seizures routine use of AED is not recommended.
83. b) HYDROCEPHALUS
Communicating/ Obstructive
If obstructive- ventriculostomy/ VP shunt
c) INTRACRANIAL HYPERTENSION
Seen in about 40% of patients with CVT.
Treatment includes – Anticoagulation.
- Lumbar Puncture.
- Decompressive craniotomy.
84. LATE COMPLICATIONS
HEADACHE- observed in 50% patients coming for follow up.
Persistent or severe headache- rule out recurrence or intracranial HTN.
In patients with a history of CVT who complain of new, persisting, or severe
headache, evaluation for CVT recurrence and intracranial hypertension should
be considered.
VISUAL LOSS.
SEIZURES.
DURAL ARTERIOVENOUS FISTULA.
85. PROGNOSIS
CVT is associated with a good outcome (complete recovery or minor
residual symptoms or signs) in close to 80 % of patients.
Nevertheless, approximately 5% of patients die in the acute phase of the
disorder, and longer-term mortality is nearly 10%.
The main cause of acute death with CVT is neurologic, most often from
brain herniation.
Causes of death in acute phase may be because of Transtentorial
Herniation, Diffuse brain edema, Status epilepticus, Medical complications,
Pulmonary embolism.
Cause of death in later phase is generally due to underlying cause like
cancer.
86. RECANALIZATION
The recanalization rates of CVT at 3 months and 1 year of follow-up are
approximately 80% to 85%,respectively.
The highest rates of recanalization are observed in deep cerebral veins and
cavernous sinus thrombosis and the lowest rates in lateral sinus thrombosis.
A follow-up CTV or MRV at 3 to 6 months after diagnosis is done to assess for
recanalization of the occluded cortical vein/sinuses in stable patients.
88. REFERENCES
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long-term outcome of 428 patients of cerebral sinus venous thrombosis: Insights from Nizam′s Institute
Venous Stroke Registry, Hyderabad (India). Neurol India 2012;60:154-9.
Nagaraja D, Taly AB. Cerebral venous thrombosis. J Assoc Physicians India 1987;35:876.
Pai N, Ghosh K, Shetty S. Hereditary thrombophilia in cerebral venous thrombosis: A study from India. Blood
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Nagaraja D, Rao BS, Rao BSS, Taly AB, Subhash MN. Randomized controlled trial of heparin in puerperal
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Editor's Notes
The cavernous sinus communicates through the superior petrosal sinus with the junction of the transverse and sigmoid sinuses and through the inferior petrosal sinus with the sigmoid sinus.
Activated PC is the antithrombotic protein that normally cleaves and inactivates coagulation factors Va and VIIIa. In 1993, Dahlback et al. [18] described a new cause of familial thrombophilia characterized by a poor anticoagulant response to APC (APC-R) that was later related to a mutation in the blood coagulation FV gene
In all the four studies headache was the most common presenting complaint unless the patient is in post ictal confusion or in encephalopathy.followed by seizuers, altered senso..focal deficits..papilloedema and fever.
Headache is due to- inc..ICT..local irritation by thrombus
Deficits is coz…infarct/ haemorrhage
Pregnancy induces several prothrombotic changes in the coagulation system that persists at least during early puerperium. Hypercoagulability worsens after delivery as a result of volume depletion and trauma.
Drugs..Thalidomide..sildenafil…tamoxifen…ivig..lithium..ecstasy.
Nephrotic synd…hypercoagulability.. increased urinary loss of antithrombin
III, altered levels and/or activity of proteins C and S, hyperfibrinogenemia
Elderly…Gi malignancy
Polycythemia causes stasis of blood that result in hyperviscosity leading to the development of thrombosis.
Gradiengo- diplopia-6N..periorbital pain-5N
Over a few days, retinal
essudates, splinter hemorrhages and infarcts can be observed. Papilledema frequency
ranges from 45 to 86% in all cerebral venous thrombosis cases [2, 7] but
this finding is less common in acute cases. The presence of papilledema, associated with altered consciousness, age older than 33, intracerebral hemorrhage and an involvement of the straight sinus can be predictors of poor outcome [8].