RCVS is usually a benign cerebral vascular dysregulation induced clinico-radiological syndrome presents typically with recurrent thunderclap headache with or without ischemic/hemorrhagic stroke or cerebral edema with vasoconstriction. Various risk factors are responsible for this syndrome.
I am a Neurosurgeon with advanced training in Interventional vascular Neurosurgery(FINR) from Zurich, Switzerland, and FMINS-Fellowship in minimally invasive and Endoscopic Neurosurgery from Germany.
I am presently working in Columbia asia hospitals, Bangalore.
My areas of interest are Vascular Neurosurgery, Stroke specialist, interventional neuroradiology.
RCVS is usually a benign cerebral vascular dysregulation induced clinico-radiological syndrome presents typically with recurrent thunderclap headache with or without ischemic/hemorrhagic stroke or cerebral edema with vasoconstriction. Various risk factors are responsible for this syndrome.
I am a Neurosurgeon with advanced training in Interventional vascular Neurosurgery(FINR) from Zurich, Switzerland, and FMINS-Fellowship in minimally invasive and Endoscopic Neurosurgery from Germany.
I am presently working in Columbia asia hospitals, Bangalore.
My areas of interest are Vascular Neurosurgery, Stroke specialist, interventional neuroradiology.
Parkinsonism is a clinical syndrome and, typically, when the condition
appears to be idiopathic and responsive to levodopa therapy, is referred
to as Parkinson’s disease1
• The four cardinal features of the parkinsonian syndrome are:2
– Bradykinesia
– Muscular rigidity
– Resting tremor
– Postural instability (and gait impairment)
• These features are not always observed in every patient, at any given
time
To make a diagnosis of PD, the physician must distinguish between
different forms of parkinsonism:1
– Parkinson’s disease
– Secondary parkinsonism
– Parkinsonism as part of another neurodegenerative disorder (e.g., multiple
system atrophy, progressive supranuclear palsy, corticobasal degeneration, or
Lewy body dementia)
SCALES COMMONLY USED IN
PARKINSON’S DISEASE
RESEARCH
SCALES COMMONLY USED IN
PARKINSON’S DISEASE
RESEARCH
Progressive multifocal leukoencephalopathy (PML) is a disease of the white matter of the brain, caused by a virus infection that targets cells that make myelin--the material that insulates nerve cells (neurons). Polyomavirus JC (often called JC virus) is carried by a majority of people and is harmless except among those with lowered immune defenses. The disease is rare and occurs in patients undergoing chronic corticosteroid or immunosuppressive therapy for organ transplant, or individuals with cancer (such as Hodgkin’s disease or lymphoma). Individuals with autoimmune conditions such as multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus -- some of whom are treated with biological therapies that allow JC virus reactivation -- are at risk for PML as well. PML is most common among individuals with HIV-1 infection / acquired immune deficiency syndrome (AIDS). Currently, the best available therapy is reversal of the immune-deficient state, since there are no effective drugs that block virus infection without toxicity. Reversal may be achieved by using plasma exchange to accelerate the removal of the therapeutic agents that put patients at risk for PML. In the case of HIV-associated PML, immediately beginning anti-retroviral therapy will benefit most individuals. Several new drugs that laboratory tests found effective against infection are being used in PML patients with special permission of the U.S. Food and Drug Administration. Hexadecyloxypropyl-Cidofovir (CMX001) is currently being studied as a treatment option for JVC because of its ability to suppress JVC by inhibiting viral DNA replication.
In general, PML has a mortality rate of 30-50 percent in the first few months following diagnosis but depends on the severity of the underlying disease and treatment received. Those who survive PML can be left with severe neurological disabilities.
Sequencing in management of Multiple sclerosisAmr Hassan
Sequencing of DMTs for individual multiple sclerosis patients should be designed in such a way to maximize disease control and minimize risk based on the mechanism of action, pharmacokinetic and pharmacodynamic properties of each therapy. This includes the DMT patients are being switched from to those they are being switched to. The reversibility of immune system effects should be a key consideration for DMT sequence selection. This feature varies across DMTs and should factor more prominently in decision making as newer treatments become available for the prevention of disability accumulation in patients with progressive MS. In this short review, we discuss the landscape of existing therapies with an eye to the future when planning for optimal DMT sequencing. While no cure exists for MS, efforts are being directed toward research in neuroregeneration with the hope for positive outcomes.
A neuromuscular disorder that leads to weakness of skeletal muscles.
Symptoms
Causes
Prevention
Complications
Common tests & procedures
Neurological examination:
Repetitive nerve stimulation test:
Antibody test:
Pulmonary function tests (PFTs): To check any breathing difficulty.
CT scan: To rule out a presence of tumor in thymus.
Magnetic resonance imaging (MRI): MRI of the chest is performed to rule out a presence of tumor in thymus.
Edrophonium (Tensilon) test:
Medication
Procedures
Nutrition
Prediction of outcome of Multiple sclerosisAmr Hassan
Prediction of outcome of Multiple sclerosis
An understanding of the natural history of multiple sclerosis(MS) in a patient is important to begin proper treatment at the correct time, especially when there is a high risk for poor prognosis. Factors that predict unfavorable prognosis are a primary or secondary progressive course, older age at disease onset, short interval between first and second attacks, initial cerebellar or pyramidal symptoms, a large number of functional systems involved at onset, moderate to severe disability within the first 2 years, and the presence of typical plaques or greater lesion volume shown by magnetic resonance imaging results during the first 5 years. However, there are no established laboratory tests able to predict long-term prognosis.
Lifestyle modification in epilepsy
Lifestyle Modifications
Lifestyle modifications can include:
Adequate sleep: Fatigue is one of the most common seizure triggers, and disrupted sleep can make the brain more vulnerable to misfiring.
Avoiding drugs and alcohol: These can be triggers for seizures in patients with epilepsy. Even one or two drinks can provoke seizures.
Minimizing emotional stress: Although there is not definitive proof that stress causes seizures, those who maintain healthy stress levels have reported that they believe it reduces their risk.
Frequency of exercise: In addition to a range of health benefits, regular exercise can help reduce risk of seizure. However, you should consult your physician before starting a new exercise routine, as some exercise can, rarely, cause seizures.
Childhood demyelinating syndromes
In the past decade, the number of studies related to demyelinating diseases in children has exponentially increased. Demyelinating disease in children may be monophasic or chronic. Typical monophasic disorders in children are acute disseminated encephalomyelitis and clinically isolated syndromes, including optic neuritis and transverse myelitis. However, some cases of acute disseminated encephalomyelitis or clinically isolated syndrome progress to become chronic disorders, including multiple sclerosis and neuromyelitis optica. This review summarizes the current knowledge on monophasic and chronic demyelinating disorders in children, focusing on an approach to diagnosis and management.
Diabetic polyneuropathy
Diabetic polyneuropathy (DPN) is defined as peripheral nerve dysfunction. There are three main alterations involved in the pathologic changes of DPN: inflammation, oxidative stress, and mitochondrial dysfunction.
Excessive daytime sleepiness
The most common causes of excessive daytime sleepiness are sleep deprivation, obstructive sleep apnea, and sedating medications. Other potential causes of excessive daytime sleepiness include certain medical and psychiatric conditions and sleep disorders, such as narcolepsy.
Vagal Nerve stimulation
Vagus nerve stimulation (VNS) is a medical treatment that involves delivering electrical impulses to the vagus nerve. It is used as an add-on treatment for certain types of intractable epilepsy and treatment-resistant depression. Frequent side effects include coughing and shortness of breath. Serious side effects may include trouble talking and cardiac arrest.
Dystonia
Dystonia is a movement disorder in which your muscles contract involuntarily, causing repetitive or twisting movements.
The condition can affect one part of your body (focal dystonia), two or more adjacent parts (segmental dystonia) or all parts of your body (general dystonia). The muscle spasms can range from mild to severe. They may be painful, and they can interfere with your performance of day-to-day tasks.
Dystonia: Causes, Types, Symptoms, and Treatments
Trigeminal neuralgia is sudden, severe facial pain. It's often described as a sharp shooting pain or like having an electric shock in the jaw, teeth or gums.
Trigeminal neuralgia
Contents
Overview
Symptoms
Causes
Diagnosis
Treatment
Nootropics and smart drugs are natural or synthetic substances that can be taken to improve mental performance in healthy people.
They have gained popularity in today’s highly competitive society and are most often used to boost memory, focus, creativity, intelligence and motivation.
Here’s a look at the ]best nootropics and how they enhance performance.
Nystagmus is a condition of involuntary (or voluntary, in some cases)eye movement, acquired in infancy or later in life, that in extremely rare cases may result in reduced or limited vision. Due to the involuntary movement of the eye, it has been called "dancing eyes"Contents
1 Causes
1.1 Early-onset nystagmus
1.2 Acquired nystagmus
1.3 Other causes
2 Diagnosis
2.1 Pathologic nystagmus
2.2 Physiological nystagmus
3 Treatment
4 Epidemiology
Basics of Neuroradiology
Neuroradiology is an essential tool in management of patients with neurological and neurosurgical disorders. The aim of this presentation will be to acquaint the reader to understand how images are formed on a computed tomography (CT) and magnetic resonance imaging (MRI) along with a review of the relevant neuroanatomy. This understanding will be helpful to the reader in interpretation of images and diagnosis of various neurological disorders.
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Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
4. Introduction
• The presence of a blood clot in the dural venous
sinuses draining blood from the brain.
• Cerebral venous sinus thrombosis is
much less common than arterial thrombosis.
• Estimated incidence is estimated to be between 2
and 5 per million per year
.
Cerebral Venous Sinus Thrombosis
5. Cerebral Venous Sinus Thrombosis
• Introduction.
• Populations at Risk.
• Risk factors & Etiology
• Anatomy .
• Investigations
• Clinical features & Specific Diagnostic Landmarks.
• Treatment.
6. Cerebral Venous Sinus Thrombosis
• Introduction.
• Populations at Risk.
• Risk factors & Etiology
• Anatomy .
• Investigations
• Clinical features & Specific Diagnostic Landmarks.
• Treatment.
11. Cerebral Venous Sinus Thrombosis
• Introduction.
• Populations at Risk.
• Risk factors & Etiology
• Anatomy .
• Investigations
• Clinical features & Specific Diagnostic Landmarks.
• Treatment.
12. Clinical Picture
Saposnik, G., Barinagarrementeria, F., Brown Jr, R. D., Bushnell, C. D., Cucchiara, B., Cushman, M., ... & Tsai, F. Y. (2011). Diagnosis and management of cerebral venous thrombosis: a statement
for healthcare professionals from the American Heart Association/American Stroke Association. Stroke, 42(4), 1158-1192
Eur J Neurol. 2017 Oct;24(10):1203-1213. doi: 10.1111/ene.13381. Epub 2017 Aug 20..
17. DD
Saposnik, G., Barinagarrementeria, F., Brown Jr, R. D., Bushnell, C. D., Cucchiara, B., Cushman, M., ... & Tsai, F. Y. (2011). Diagnosis and management of cerebral venous thrombosis: a statement
for healthcare professionals from the American Heart Association/American Stroke Association. Stroke, 42(4), 1158-1192
Eur J Neurol. 2017 Oct;24(10):1203-1213. doi: 10.1111/ene.13381. Epub 2017 Aug 20..
18. Specific Diagnostic Landmarks: Cavernous Sinus
Causes of exophthalmoses and congestion of orbit
:-
1. Orbital tumors.
2. Meningioma.
3. Sphenoid Tumors.
Slow
onset
4. AV Fistula → D.D. by
- orbital bruit
- Pulsating Exophthalmoses
- Decrease Exophth. On Carotid a. is occluded by digital pressure.
19. Cerebral Venous Sinus Thrombosis
• Introduction.
• Populations at Risk.
• Risk factors & Etiology
• Anatomy .
• Investigations
• Clinical features & Specific Diagnostic Landmarks.
• Treatment.
20. • D-dimer level greater than 500 μg/L.
• Thrombophilia testing:
Protein C
Protein S
Antithrombin III
Antiphospholipid antibodies (lupus anticoagulant and
anticardiolipin antibodies); Genetic testing for factor V Leiden
and prothrombin G20210A mutations.
Labs
24. CTV versus MRV?
CTV can be used as An alternative to MRV
N.B. MRI has the advantage of showing the
thrombus itself and being more sensitive in
detecting parenchymal lesions
33. -Can be useful in patients with
inconclusive CTV or MRV in whom a
clinical suspicion for CVT remains high
-Surgical thrombectomy
Catheter Cerebral Angiography
Saposnik, G., Barinagarrementeria, F., Brown Jr, R. D., Bushnell, C. D., Cucchiara, B., Cushman, M., ... & Tsai, F. Y. (2011). Diagnosis and management of cerebral venous thrombosis: a statement
for healthcare professionals from the American Heart Association/American Stroke Association. Stroke, 42(4), 1158-1192
Eur J Neurol. 2017 Oct;24(10):1203-1213. doi: 10.1111/ene.13381. Epub 2017 Aug 20..
34. Cerebral Venous Sinus Thrombosis
• Introduction.
• Populations at Risk.
• Risk factors & Etiology
• Anatomy .
• Investigations
• Clinical features & Specific Diagnostic Landmarks.
• Treatment.
37. -Weight-based LMWH FAVORED OVER
adjusted-dose UFH
-UFH: teratogenic
-Followed by vitamin K antagonists,
-Regardless of the presence of ICH
Initial Anticoagulation
Saposnik, G., Barinagarrementeria, F., Brown Jr, R. D., Bushnell, C. D., Cucchiara, B., Cushman, M., ... & Tsai, F. Y. (2011). Diagnosis and management of cerebral venous thrombosis: a statement
for healthcare professionals from the American Heart Association/American Stroke Association. Stroke, 42(4), 1158-1192
Eur J Neurol. 2017 Oct;24(10):1203-1213. doi: 10.1111/ene.13381. Epub 2017 Aug 20..
38. -Low-molecular-weight heparin preferred
(does not cross the placenta)
-If no improvement:
-Fibrinolytic drug tissue plasminogen activator
(tPA), strep-tokinase (SK) or urokinase (UK), in
the dural sinus via a microcatheter
Initial Anticoagulation
Saposnik, G., Barinagarrementeria, F., Brown Jr, R. D., Bushnell, C. D., Cucchiara, B., Cushman, M., ... & Tsai, F. Y. (2011). Diagnosis and management of cerebral venous thrombosis: a statement
for healthcare professionals from the American Heart Association/American Stroke Association. Stroke, 42(4), 1158-1192
Eur J Neurol. 2017 Oct;24(10):1203-1213. doi: 10.1111/ene.13381. Epub 2017 Aug 20..
39. -Acetazolamide.
-Brain dehydrating measures
-No evidence to use steroids except if
suspected underlying
autoimmune/inflammatory process
Increased Tension?
Saposnik, G., Barinagarrementeria, F., Brown Jr, R. D., Bushnell, C. D., Cucchiara, B., Cushman, M., ... & Tsai, F. Y. (2011). Diagnosis and management of cerebral venous thrombosis: a statement
for healthcare professionals from the American Heart Association/American Stroke Association. Stroke, 42(4), 1158-1192
Eur J Neurol. 2017 Oct;24(10):1203-1213. doi: 10.1111/ene.13381. Epub 2017 Aug 20..
40. -Lumbar puncture, optic nerve
decompression, or shunts
Progressive Visual Loss?
Saposnik, G., Barinagarrementeria, F., Brown Jr, R. D., Bushnell, C. D., Cucchiara, B., Cushman, M., ... & Tsai, F. Y. (2011). Diagnosis and management of cerebral venous thrombosis: a statement
for healthcare professionals from the American Heart Association/American Stroke Association. Stroke, 42(4), 1158-1192
Eur J Neurol. 2017 Oct;24(10):1203-1213. doi: 10.1111/ene.13381. Epub 2017 Aug 20..
41. -Diagnostic: may be used if high clinical
suspicion despite negative CTV/ MRV
-Therapeutic:
May be considered if:
-Deterioration occurs despite intensive
anticoagulation treatment
-If severe hemorrhage?
Endovascular Maneuvers
Saposnik, G., Barinagarrementeria, F., Brown Jr, R. D., Bushnell, C. D., Cucchiara, B., Cushman, M., ... & Tsai, F. Y. (2011). Diagnosis and management of cerebral venous thrombosis: a statement
for healthcare professionals from the American Heart Association/American Stroke Association. Stroke, 42(4), 1158-1192
Eur J Neurol. 2017 Oct;24(10):1203-1213. doi: 10.1111/ene.13381. Epub 2017 Aug 20..
42. -Resistant to anti-coagulation therapy,
-Have worsening of symptoms,
-Not at risk for impending herniation
Endovascular Thrombolysis & Thrombectomy
Saposnik, G., Barinagarrementeria, F., Brown Jr, R. D., Bushnell, C. D., Cucchiara, B., Cushman, M., ... & Tsai, F. Y. (2011). Diagnosis and management of cerebral venous thrombosis: a statement
for healthcare professionals from the American Heart Association/American Stroke Association. Stroke, 42(4), 1158-1192
Eur J Neurol. 2017 Oct;24(10):1203-1213. doi: 10.1111/ene.13381. Epub 2017 Aug 20..
43. -Neurological
deterioration due to
severe mass effect
-Intracranial hemorrhage
causing intractable
intracranial hypertension,
Decompressive Hemicraniectomy
Saposnik, G., Barinagarrementeria, F., Brown Jr, R. D., Bushnell, C. D., Cucchiara, B., Cushman, M., ... & Tsai, F. Y. (2011). Diagnosis and management of cerebral venous thrombosis: a statement
for healthcare professionals from the American Heart Association/American Stroke Association. Stroke, 42(4), 1158-1192
Eur J Neurol. 2017 Oct;24(10):1203-1213. doi: 10.1111/ene.13381. Epub 2017 Aug 20..
45. Saposnik, G., Barinagarrementeria, F., Brown Jr, R. D., Bushnell, C. D., Cucchiara, B., Cushman, M., ... & Tsai, F. Y. (2011). Diagnosis and management of cerebral venous thrombosis: a statement
for healthcare professionals from the American Heart Association/American Stroke Association. Stroke, 42(4), 1158-1192
Eur J Neurol. 2017 Oct;24(10):1203-1213. doi: 10.1111/ene.13381. Epub 2017 Aug 20..
Decompressive Hemicraniectomy
46. -Suspected bacterial infection
+/-surgical drainage of purulent
collections of infectious
IV Antibiotics?
Saposnik, G., Barinagarrementeria, F., Brown Jr, R. D., Bushnell, C. D., Cucchiara, B., Cushman, M., ... & Tsai, F. Y. (2011). Diagnosis and management of cerebral venous thrombosis: a statement
for healthcare professionals from the American Heart Association/American Stroke Association. Stroke, 42(4), 1158-1192
Eur J Neurol. 2017 Oct;24(10):1203-1213. doi: 10.1111/ene.13381. Epub 2017 Aug 20..
47. -(CVT+single seizure) : early initiation of
antiepileptic drugs for a defined duration
is probably recommended to prevent
further seizures
-CVT+ no seizures: prophylactyic
antiepileptic use is not recommended
Antiepileptics
Saposnik, G., Barinagarrementeria, F., Brown Jr, R. D., Bushnell, C. D., Cucchiara, B., Cushman, M., ... & Tsai, F. Y. (2011). Diagnosis and management of cerebral venous thrombosis: a statement
for healthcare professionals from the American Heart Association/American Stroke Association. Stroke, 42(4), 1158-1192
Eur J Neurol. 2017 Oct;24(10):1203-1213. doi: 10.1111/ene.13381. Epub 2017 Aug 20..
48. • Provoked CVT (associated with a transient risk factor): 3 to 6
months, INR (2 – 3)
• Unprovoked CVT, 6 to 12 months
• Venous thromboembolism after CVT: for life
• First CVT (provoked or unprovoked) with severe
thrombophilia: for life
• Recurrent CVST: for life
Secondary Prevention
Saposnik, G., Barinagarrementeria, F., Brown Jr, R. D., Bushnell, C. D., Cucchiara, B., Cushman, M., ... & Tsai, F. Y. (2011). Diagnosis and management of cerebral venous thrombosis: a
statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke, 42(4), 1158-1192
Eur J Neurol. 2017 Oct;24(10):1203-1213. doi: 10.1111/ene.13381. Epub 2017 Aug 20..
49. Algorithm for the management of cerebral venous
thrombosis.
Saposnik, G., Barinagarrementeria, F., Brown Jr, R. D., Bushnell, C. D., Cucchiara, B., Cushman, M., ... & Tsai, F. Y. (2011). Diagnosis and management of cerebral venous thrombosis: a
statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke, 42(4), 1158-1192
Eur J Neurol. 2017 Oct;24(10):1203-1213. doi: 10.1111/ene.13381. Epub 2017 Aug 20..
50. • Cerebral venous thrombosis is a cerebrovascular disease of the
young, primarily of women.
• Headache is the most common symptom of cerebral venous
thrombosis.
• The most common clinical syndromes in cerebral venous
thrombosis include (1) intracranial hypertension, (2) focal
neurologic deficits (eg, motor weakness, sensory deficit,
aphasia), (3) encephalopathy, and (4) seizure disorder.
• MRI/magnetic resonance venography is the recommended
imaging for the diagnosis of cerebral venous thrombosis.
Specific sequences (eg, T2* susceptibility-weighted imaging) are
useful to assist in the diagnosis of isolated cortical venous
thrombosis.
Key points
51. • Transient risk factors for cerebral venous thrombosis include
pregnancy/puerperium, CNS or ear/sinus/mouth/face infections,
exposure to drugs (eg, oral contraceptives, steroids, cancer
treatments), head trauma, or procedures (eg, lumbar puncture,
jugular catheter placement).
• Chronic triggers of cerebral venous thrombosis include
hereditary or acquired thrombophilias that are established
causes of venous thromboembolism.
• Anticoagulation is the main treatment for the acute management
of cerebral venous thrombosis.
• All available guidelines recommend anticoagulation therapy for
the acute management of cerebral venous thrombosis.
Key points