This document discusses cerebral venous thrombosis, including the major dural sinuses and cortical veins that can be affected. CT and MRI are important imaging modalities for diagnosis. CT can detect thrombi directly and identify signs of venous infarction. MRI and MR venography can identify thrombi by their abnormal signal and absence of flow void, as well as demonstrate venous infarction and edema. Common etiologies of cerebral venous thrombosis include hypercoagulability states, infection, trauma, and low flow states. Clinical manifestations vary but can include increased intracranial pressure symptoms, stroke symptoms, and seizures.
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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.
Objectives of this presentation are
Introduction to ct
Cross sectional anatomy
Common important pathologies
This presentation is aimed to educate beginers to help in ct interpretetion.
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.
Objectives of this presentation are
Introduction to ct
Cross sectional anatomy
Common important pathologies
This presentation is aimed to educate beginers to help in ct interpretetion.
This presentation provides sufficient material for anyone who wants is interested in interventional radiology. Here we will discuss the available facilities, mechanisms and equipments.
In my opinion this presentation will prove a footstep in interventional radiology
Neuroimaging is the use of various techniques to either directly or indirectly image the structure, function of the nervous system.
Neuroimaging plays a pivotal role in the diagnosis of central nervous system (CNS) disorders.
Main modalities of neuroimaging techniques are CT scan and MRI.
Definition of stroke and cerebrovascular disorders and pathophysiology of cerebral infarct and CT imaging overview of acute-subacute and chronic infarcts and penumbra.
causes of cerebral edema , Radiological signs of acute infarct and hemorrhagic infarct and comparison of MRI and CT in the diagnosis of acute infarct
Role of diffusion weighted imaging (DWI) and diffusion perfusion mismatch
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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
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Learning Objectives
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Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
3. Major dural sinuses:
• Superior sagittal sinus, transverse, straight and
sigmoid sinuses.
Cortical veins:
• Vein of Labbe, which drains the temporal lobe.
• Vein of Trolard, which is the largest cortical vein that
drains into the superior sagittal sinus.
Deep veins:
• Internal cerebral and thalamostriate veins.
Cavernous sinus.
4.
5.
6.
7.
8.
9. CT scan of a 45-year-old woman with clinical suspicion of dural sinus thrombosis.
Lateral (A), anteroposterior (B), caudocranial (C), and oblique sagittal (D) MIP of
CTA data set after MMBE. The projections demonstrate normal appearance of the
superior sagittal sinus (arrowheads), the transverse sinuses (arrows), the deep
venous system, and the superficial cortical veins without any overlying bone
structures.
10. Indications For CT and MRI in
Acute stroke
Indications for CT in suspected stroke
• Early diagnosis if possible
• Differentiation between ishcemic and
heamorrhagic stroke
• Exclusion of stroke mimics-tumors
11. Indication for MRI
• If CT is normal and clinical suspicion high
• Assessment of diffusion and perfusion
mismatch
• Detection of stroke in posterior fossa
• Detection of underlying cause
• Assessment of intra and extracranial vessels
by MR angiography
• Exclusion of venous sinus thrombosis
12. Appearance of Blood on Scans
On CT
• Acute –Higher attenuation than underlying
brain
• Sub acute-Similar attenuation to brain
• Chronic-Lower attenuation than underlying
brain
15. WT FAT H2O MUSC LIG BONE
T1 B D I D D
T2 I B I D D
WW2--> water white on T2 weighted image
16. Venous sinus thrombosis
• < 2% of all strokes
• Accounts for up to 50% of strokes during
pregnancy and puerperium
• Important cause of stroke especially in
children and young adults
• It is a difficult diagnosis because of its
nonspecific clinical presentation and subtle
imaging findings
17. ETIOLOGY
• Spontaneous
Septic causes( especially in children)
• Sinusitis, Otitis, Mastoiditis, Sub/epidural
empyema
• Meningitis, encephalitis, Brain abscess, Face
and scalp cellulitis, septicemia
Trauma > Fracture through sinus wall,jugular vein
catheriziation
Low flow states > CHF, Dehydration ,Shock
Hypercoagulability states
18. Pathogenesis
• Dural sinus thrombosis leads to venous
congestion, venous infarction ,brain
edema and heamorrhage
20. Imaging
• CT brain , CTV
• MRI brain and MRV
• Cerebral angiography
Look for
• Direct signs of a thrombus
• Infarction in a non-arterial location, especially
if it is bilateral and hemorrhagic
• Cortical or peripheral lobar hemorrhage
• Cortical edema
21. • Dense Clot sign on NECT
• Cord sign
• Empty delta sign on CECT
• Replacement of flow void by abnormal
signal intensity on MRI
• MRV absence of flow
• Non filling of thrombosed veins on
Angiography
• Venous infarction, edema
27. ABSENCE OF NORMAL FLOW
VOID ON MR
Patent cerebral veins usually will
demonstrate low signal intensity due to flow
void.
Flow voids are best seen on T2-weighted
and FLAIR images.
A thrombus will manifest as absence of flow
void.
28.
29.
30. VENOUS INFARCTION
Due to the high venous pressure hemorrhage
is seen more frequently in venous infarction
compared to arterial infarction.
Often bilateral and in the midline in an atypical
location or in a non-arterial distribution.
38. Transverse MIP image of a Phase-Contrast angiography.
The right transverse sinus and jugular vein have no signal due to
thrombosis.
39. Acute thrombus in a 35-year-old woman with a severe headache
for 5 days. Axial T2W MR image (a) and axial T1W MR image (b) show a thrombus in
the left sigmoid sinus (arrows). The signal in the thrombus, compared with that in
the normal brain parenchyma, is hypointense in a and iso- to hyperintense in b. (c)
Frontal MIP image from coronal TOF MR venography shows a lack of flow in the
distal portion of the left transverse sinus and the sigmoid sinus (arrows).
41. PITFALLS IN CT
Arachnoid granulations produce well-
defined focal filling defects within the dural
venous sinuses and measure 2–9 mm in
diameter. They are isoattenuating (one-
third) or hypoattenuating (two-thirds)
relative to brain parenchyma
Arachnoid granulations
49. Transverse sinus flow gap. (a) Coronal image from TOF MR venography
shows an apparent interruption of flow in the medial part of the left transverse sinus
(arrows).
(b) Oblique MIP image from contrast-enhanced MR venography shows enhancement
indicative of normal flow in the medial part of the left transverse sinus (arrow).
The MR-techniques that are used for the diagnosis of cerebral venous thrombosis are: Time-of-flight (TOF), phase-contrast angiography (PCA) and contrast-enhanced MR-venography:
Time-of-Flight angiography is based on the phenomenon of flow-related enhancement of spins entering into an imaging slice.As a result of being unsaturated, these spins give more signal that surrounding saturated spins.
Phase-contrast angiography uses the principle that spins in blood that is moving in the same direction as a magnetic field gradient develop a phase shift that is proportional to the velocity of the spins. This information can be used to determine the velocity of the spins. This image can be subtracted from the image, that is acquired without the velocity encoding gradients, to obtain an angiogram.
Contrast-enhanced MR-venography uses the T1-shortening of Gadolinium.It is similar to contrast-enhanced CT-venography.
When you use MIP-projections, always look at the source images.
T2
T1
TOF MR venography
An intrasinus thrombus in the subacute stage may have markedly increased signal intensity on MR images that may be misinterpreted as evidence of flow on TOF MR venograms
T1-shortening shine-through in a patient with thrombosis of the superior sagittal sinus and transverse sinuses. Lateral MIP image from coronal TOF MR venography shows an area of thrombosis
with a signal of intermediate intensity (arrows) resembling that of normal sinus flow but less intense than that in patent cortical veins (arrowheads).
Contrast enhanced MR-venography is the most reliable MR technique.
CT-venography is even more reliable, because it is easy and less sensitive to pitfalls
TOF MR venography, contrast-enhanced MR venography, and CT venography are the most useful techniques for diagnosis of this condition.
Knowledge of normal venous variations and potential pitfalls related to image interpretation
are important for achieving an accurate diagnosis.
Dense clot sign
Dense cord sign
empty delta sign
Flair - flow void
Thrombosis of the left transverse sinus in a 42-year-old woman.
(a, b) Axial unenhanced CT images show left cerebellar and temporal hematoma with increased attenuation in the left transverse sinus (cord sign) (* in a).
(c) On a 3D MIP image from CT venography, the left transverse sinus is not visible.
Signal
Normal MR sequences
1.T2
2.T1
3.Flair
4.DWI(diffusion weighted image)
5.ADC (Apparent diffusion coefficient)
6. GE (Gradient echo sequences)
7.T1 post contrast
8.MRV
9.3D MRV
10.MRA
11.T2
12.T1