lucid interval and its importance in trauma and mental healthsreya paul
lucid interval importance in trauma patients and how to manage them in surgical knowledge.lucid interval in psychiatry and its importance. advanced trauma life support scoring, glasgow coma scale ,head injury management in surgery surgical management head trau a
Hydrocephalus comes from the Greek "hydro" meaning water and "cephalie", meaning brain. A watery fluid, known as cerebrospinal fluid or CSF, is produced constantly inside each of the four spaces or ventricles inside the brain: between 400 and 600mls is produced each day.
A short talk about two of the traumatic intracranial bleeds, namely extra and subdural hematomas. Directed to med students moving from basic into clinical teaching.
lucid interval and its importance in trauma and mental healthsreya paul
lucid interval importance in trauma patients and how to manage them in surgical knowledge.lucid interval in psychiatry and its importance. advanced trauma life support scoring, glasgow coma scale ,head injury management in surgery surgical management head trau a
Hydrocephalus comes from the Greek "hydro" meaning water and "cephalie", meaning brain. A watery fluid, known as cerebrospinal fluid or CSF, is produced constantly inside each of the four spaces or ventricles inside the brain: between 400 and 600mls is produced each day.
A short talk about two of the traumatic intracranial bleeds, namely extra and subdural hematomas. Directed to med students moving from basic into clinical teaching.
Ini merupakan contoh kertas kerja untuk membuat program di universiti..
TIPS utk lulus kertas kerja program:
-Penggunaan VOT berdasarkan pekeliling yg lengkap.
-Mempunyai Kemahiran Insaniah (KI)
-Tentatif prgram yg lengkap
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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.
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.
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Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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.
4. Traumatic brain injury (TBI) – leading cause of
death in children and young adults.
Peak age – 15 -24 yrs.
Secondary peak > 50 years of age.
Twice as often among males compared to
females.
Generally caused by motor vehicle accidents,
fall, assaults, violence and sports & recreation
5. Can be classified into primary and secondary
injuries.
By location – Intra or extra-axial.
By mechanism – penetrating/open or
blunt/closed.
By severity – minor, mild, moderate, or
severe using Glasgow Coma Scale score.
6. 1. SKULL RADIOGRAPH
Poor predictors.
Normal SXR does not exclude major
intracranial injuries.
7. 2. CT SCAN
Most important step in evaluation of head
trauma.
Modality of choice – fast, widely available,
and highly accurate in the detection of skull
fractures and intracranial hemorrhage.
Goal of imaging is to identify treatable
injuries to prevent secondary damage.
9. In a typicalTBI, CT images must be reviewed
using multiple windows and levels:
1) Brain window (W: 80, L: 40)
2) Intermediate window : to exaggerate contrast
between extra-axial blood and the adjacent skull
(W: 150, L: 75)
3) Bone window : to evaluate the osseous
structures (W: 2500, L: 500).
10.
11. 3. MRI
Recommended for patients with acuteTBI
when the neurologic findings are unexplained
by CT.
Valuable to show small/subtle extra-axial
blood collections, diffuse axonal injury,
brainstem injuries.
Higher sensitivity in the sub-acute and
chronic stages of head trauma.
12. A. PRIMARY HEAD INJURY
1. Scalp injury, skull vault, base of skull
fracture.
2. Primary haemorrhages:
a) Extra-axial – epidural, subdural,
subarachnoid, intraventricular
b) Intra-axial – diffuse axonal injury (DAI),
cortical contusions, intracerebral
haematoma, deep/ brainstem injury
13. 3. Primary vascular injuries:
a) Traumatic arterio–venous fistula (AVF)
b) Carotid-cavernous fistula (CCF)
c) Arterial pseudo-aneurysm
d) Arterial dissection/ laceration/ transaction/
occlusion
e) Dural sinus laceration/thrombosis/occlusion
f) Cortical vein rupture/thrombosis
4. Other : cranial nerve injury.
14. B. SECONDARY INJURY
a) Cerebral herniation
b) Traumatic ischemia, infarction
c) Diffuse cerebral swelling
d) Diffuse hypoxic injury
e) Secondary “delayed’’ hemorrhage
f) Secondary brain stem injury or haemorrhage
g) Others e.g. fatty embolism , infection
15. 1. SCALP INJURY, SKULL FRACTURE
SCALP INJURY
Soft-tissue lacerations
Subgaleal hematoma
most common manifestation
focal soft-tissue swelling beneath subcutaneous
tissue and above the temporalis muscle and skull.
Cephalohematoma
Residual foreign bodies
16.
17.
18. SKULLVAULT FRACTURE
Could be linear, depressed or diastatic
Depressed fracture usually associated with
intracranial injury
Diastatic fracture/ sutural diastasis
Seperation of cranial bones at suture site
Width of the suture > 3 mm (normal < 2 mm)
In adults, most common site is lambdoid suture
19. BASE OF SKULL FRACTURE
Should be sought when blood behind
tympanic membrane, otorrhoea, rinorrhoea,
echymosis surrounds the orbits without
direct orbital trauma, intracranial air, air
fluid level in PNS or mastoid air cells.
Basilar fracture cause compression or
entrapment of cranial nerves.
Fracture of optic canal cause loss of vision.
20. Sphenoidal fractures can cause disruption of
intra- cavernous internal carotid artery,
leading to pseudo- aneurysm or a carotid
cavernous fistula.
Petrous temporal bone fracture
Transverse or longitudinal (relative to long axis of
bone)
Longitudinal – direct temporal impact, 70%
Transverse – occiput or frontal impact
Can cause hearing loss from ossicular bone fracture/
dislocation, otorhinorrhoea from CSF leak, facial
nerve palsy, vascular injury, perilymphatic fistula
21.
22. 2. PRIMARY HEMORRHAGES
a) EXTRA-AXIAL HEMORRHAGES
EXTRA/EPIDURAL HEMATOMA (EDH)
Usually within first 24-48 H.
Occurs between the inner table of the skull and
the dura with a biconvex configuration.
Etiology – disruption of middle meningeal
artery, laceration of diploic veins or dural sinus.
23. May cross dural attachments but not sutures.
Usually associated with overlying skull fracture
and secondary intracranial mass effect/ injuries.
Can be acute, subacute and chronic.
Hypodense area within indicates active bleed.
Imaging criteria where EDH may be treated
conservatively:
(1) Diameter less than 1.5 cm
(2) Minimal mid line shift < 2 mm
(3) Neurologically intact without focal deficit.
24.
25.
26. SUBDURAL HEMATOMA (SDH)
Interposed between the dura and arachnoid.
Typically crescent shaped with concave
medial and convex lateral border.
May cross suture lines but not dural (falx or
tentorial) attachments.
Common sites: over the fronto-parietal
convexities, middle cranial fossa, para- falcial
area, inter- hemispheric fissure.
27. Acute SDH – homogenously hyperdense, up to
40% mixed hyper/ hypodense due to unclotted
blood - serum extruded during clot retraction.
Subacute SDH – isodense within a few days to a
few weeks, may be difficult to diagnose, wider
window helpful.
Chronic SDH – typically low attenuation, mixed
density in 5% due to recurrent haemorrhage,
enhancement in post contrast, calcification in
0.3 to 2.7% cases.
28.
29.
30.
31. SUBARACHNOID HAEMORRHAGE (SAH)
Can result from the disruption of small pial
vessels, extension into the subarachnoid
space by a contusion or hematoma or
diffusion of intraventricular hemorrhage.
Very common, but rarely causes mass effect.
Typically appears as linear or serpentine area
of hypendensity in the basal cisterns, the
sulci, the Sylvian fissure and inter-
hemispheric fissure.
32. Normal calcified or ossified falx may be
mistaken for parafalcine SAH in older
adolescents.
“Pseudo sub-arachnoid haemorrhage” is seen
in cases of severe diffuse cerebral oedema.
Posterior parafalcine or inter-hemispheric
SAH can mimic the “Empty delta sign’’ of
superior sagittal sinus thrombosis.
Rapidly cleared within 1 week.
33.
34.
35. INTRAVENTRICULAR HEMORRHAGE (IVH)
Can result from rotationally induced tearing
of subependymal veins along the surface of
the ventricles, by direct extension of a
parenchymal hematoma into the ventricular
system or from retrograde flow of SAH into
the ventricular system via the fourth
ventricular outflow foramina.
36. Shows high density intraventricular blood
with or without a fluid level.
Occasionally focal choroid plexus hematoma
noted.
At risk for developing both communicating
and non communicating hydrocephalus
secondary to obstruction and ependymitis
from the irritant effects of the blood.
37.
38. 2. PRIMARY HEMORRHAGES
b) INTRA-AXIAL HEMORRHAGES
DIFFUSEAXONAL INJURY (DAI)
Most common type of primary traumatic
injury.
Results from rotational acceleration and
deceleration forces that produce shearing
deformations of brain tissue.
39. Disruption of accompanying blood vessels
show numerous small hemorrhage foci.
Diffuse & bilateral.
Clinically, characterized by loss or severe
impairment of consciousness beginning at
the moment of direct impact.
In chronic stage can result in overwhelming
cognitive and psychiatric problems.
MRI more superior to CT to detect DAI.
40. CT findings:
Early imaging may be subtle or normal.
Foci of decreased density.
May show some degrees of cerebral swelling.
May show small focal hemorrhage or small
petechial haemorrhage particularly at the
gray-white junction and corpus callosum.
May show extensive injury.
41. Locations ( according to severity of trauma):
Peripheral lobar white matter at cortico-
medullary junction.
Common at the parasagital regions of frontal
lobe, periventricular regions of temporal lobe.
Internal & external capsules, corona radiata,
cerebral peduncles.
Corpus callosum.
Brain stem – posterolateral quadrants of mid
brain and upper pons.
42.
43.
44. CORTICAL CONTUSION
Common type, in 21% ofTBI patients.
Mechanism: linear acceleration-deceleration
forces /penetrating trauma /direct impaction.
Tissue necrosis, capillary disruption, petechial
hemorrhage followed by liquefaction and
oedema after 4 to 7 days.
May be hemorrhagic or non-hemorrhagic.
45. Coup: Direct impact to stationary brain. Injury
at the site of impaction.
Counter coup: Impact of moving brain on
stationary clavarium opposite to the site of
the coup and produced injury.
Focal lesion primarily involving superficial
gray matter, with relative sparing of the
underlying white matter.
46. Location – orbitofrontal and temporal lobes
most frequently involved.
Beneath an acute subdural hematoma or a
depressed skull fracture.
Associated with a better prognosis than DAI,
unless accompanied by brainstem injury or
significant mass effect.
47. CT findings:
Initially may be subtle or absent.
Early findings –characteristic “salt and pepper”
pattern of focal /multiple poorly defined mixed
areas of hypodensity and hyperdensity
(petechial hemorrhage).
Diffuse oedema and mass effect in immediate
post-traumatic period, then gradually diminish
over time.
Some degree of contrast enhancement.
Isodense to brain after 2 – 3 weeks.
48.
49.
50.
51. INTRACEREBRAL HEMATOMA
Frequently associated with other primary
extra- and intra-axial injuries.
May be delayed with 48 hours (lucid) interval.
Due to shear-induced hemorrhage from
rupture of small intraparenchymal vessels.
Differentiated from hemorrhagic contusion
by sharply marginated margin, perifocal
hypodensity and mass effect.
52. Mostly located in the frontotemporal white
matter, other site basal ganglia
Acute hematoma (< 3 days):
CT: Homogenous high density lesion (50 -70
HU) with irregular well-defined margins.
Usually surrounded by low attenuation area
(oedema, contusion) with mass effect.
53. Subcute Hematoma (3 – 14 Days):
NCCT: Gradual decrease in density from
periphery inward and becomes isodense to
brain parenchyma.
CECT: Peripheral rim enhancement at inner
border of perilesional lucency.
54. Chronic Hematoma (> 14 Days):
CT: Gradual decreased attenuation/
hypodensity.
Later – lucent hematoma (cephalomalacia
due to proteolysis and phagocytosis &
surrounding atrophy) with adjacent sulcal
enlargement and ventricular dilation with
ring blush ( DDX : tumor )
57. Most often injured artery is the internal
carotid artery (ICA) especially at sites of
fixation – in the carotid canal at the base of
the petrous bone, and at its exit from the
cavernous sinus beneath the anterior clinoid
process.
Conventional angiograms is the gold
standard for confirmation and delineation of
the vascular injuries.
MRA, CTA serve as important screening tools.
58. CCF:
Results from full-thickness arterial injury.
Leads to communication between the
cavernous portion of ICA and the surrounding
venous plexus.
Resulting in venous engorgement of the
cavernous sinus and its draining branches:
the ipsilateral superior ophthalmic vein and
inferior petrosal sinus.
61. DIFFUSE CEREBRAL SWELLING
Due to an increase in cerebral blood volume
(hyperemia), vasogenic edema, or increase in
tissue fluid (cerebral or cytotoxic edema).
CT – effacement of the cerebral sulci and
cisterns and compression of the ventricles.
In cerebral edema, the gray–white matter
differentiation is lost.
In cerebral hyperemia, the gray–white matter
differentiation is preserved.
62.
63.
64. BRAIN HERNIATION
Occurs secondary to mass effect produced by
other causes.
Subfalcine herniation: most common form, the
cingulate gyrus displaced across midline under
the falx cerebri.
Uncal herniation: the medial temporal lobe is
displaced over the free margin of tentorium.
Important clue - effacement of ambient and
lateral suprasellar cisterns.
65. Transtentorial herniation – downward or
upward herniation in cerebellum/cerebrum.
Translar ( trans sphenoidal ) herniation –
downward or upward herniation.
Tonsilar herniation.
Miscellaneous - trans dural / trans cranial
herniation.
66.
67. ISCHAEMIA OR INFARCTION
Occurs as a result of increased intracranial
pressure or mass effect on cerebral
vasculature by herniation or hematoma.
ACA infarction – secondary to subfalcine
herniation which displaces the ACA to the
contralateral side, trapping the
callosomarginal branches of theACA.
68. Uncal herniation can cause ischaemia in the
posterior cerebral artery territory.
Tonsillar herniation can cause ischemia in the
posterior inferior cerebellar artery territory.
69.
70. Encephalomalacia and atrophy.
Pneumocephalus, pneumatocele formation.
CSF leaks and fistula.
Acquired encephalocoele or leptomeningeal
cyst.
Cranial nerve injuries.
Diabetes incipidus.
Hydrocephalus.
Subdural hygroma.
Post traumatic abscess.
71.
72. The goal of imaging in the management of
head trauma is to identify treatable injuries to
prevent secondary damage.
CT continues to be the modality of choice in
the evaluation of acute head injury.
CT is preferred in the acute setting because it
is accurate, fast, widely available and can
easily accommodate life-support and
monitoring equipment.
73. MRI is indicated for patients with acuteTBI
when the neurologic findings are unexplained
by CT.
MRI is also the modality of choice for
subacute or chronic injury.