This document discusses various congenital spinal anomalies. It begins by classifying spinal dysraphisms into open and closed types. Open dysraphisms include myelomeningocele and myeloschisis which result from failed neural tube closure. Closed dysraphisms can involve subcutaneous masses like lipomas or no mass. Imaging findings and embryological basis are described for various anomalies like diastematomyelia, caudal agenesis, and segmental spinal dysplasia. The development of the spinal cord and vertebrae are also summarized.
Acute Transverse Myelitis
Blockage of the Spinal Cord’s Blood Supply
Cervical Spondylosis
Compression of the Spinal Cord
Hereditary Spastic Paraparesis
Subacute Combined Degeneration
Syrinx of the Spinal Cord and Brain Stem
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.
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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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
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.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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.
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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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
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
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.
4. SPINAL CORD DEVELOPMENT
1. GASTRULATION – 2nd or 3rd WEEK
Formation of the trilaminar disk
2. PRIMARY NEURULATION - 3-4 WEEKS
Notochord and overlying ectoderm interact to form the neural plate.
Neural plate folds and bends forming the neural tube – closes
zipperlike manner
3. SECONDARY NEURULATION – 5-6 WEEKS
Secondary neural tube formed by caudal cell mass- initially solid
followed by cavitation by process called retrogressive differentiation
forms conus medullaris and filum terminale.
9. TERMINOLOGY
Spina Bifida
•Synonym for spinal
dysraphism
•Defective fusion of the
posterior elements.
•Aperta = OSD
Occulta= CSD
Placode
Segment of flattened, non
neurulated embryonic
neural tissue.
Tethered Cord
Syndrome
• Not malformation
• Occur as part of
lipomyelomeningocele,
tight filum terminale,
diastematomyelia
• Limited spinal cord
movement leading due to
abnormal tissue
attachments.
• The clinical picture
involves :-
motor and sensory
dysfunction,
muscleatrophy, decreased or
hyperactive reflexes, urinary
inconti-nence, spastic gait.
10. OPEN SPINAL DYSRAPHISMS
•Exposure of covering neural tissue/meninges through midline defect
in the back
•99% are myelomeningoceles.
•Clinical picture includes sensorimotor deficits of the lower
extremities, bowel and bladder incontinence, hindbrain dysfunction,
intellectual and psychological disturbances.
•Because neurulation does not occur, the cutaneous ectoderm does
not detach from the neural ectoderm and remains in a lateral
position. This results in a mid-line skin defect.
•Role of MRI – presurgical evaluation and look for associated
anomalies – SURGICAL EMERGENCY
•MC LOCATION – Lumbosacral
11. MYELOCELE MYELOMENINGOCELE
Neural placode
protrudes above
the skin surface
Placode is
flush with
skin surface
There is no
expansion of
underlying
subarachnoi
d space.
HEMIMYELOCELE AND HEMIMYELOMENGICELE – associated with diastematomyelia
and one hemicord fails to neurulate.
14. CHIARI I
Sagittal T1 weighed image shows
tonsillar ectopia (arrow). Posterior
fossa is small.
Axial T1 weighed image showing
crowding of the foramen magnum
due to tonsils (T).
15. CHIARI
II
CHIARY II WITH HYDROMYELIA
Sagittal images very small
posterior cranial fossa and the
typical cascade of herniations
constituting the hallmark of
the Chiari-II malformation.
16. CHIARI III CHIARI IV
CHIARI II + CEPHALOCELE SEVERE
CEREBELLAR HYPOPLASIA
+MYELOMENINGOCELE
17. CLOSED SPINAL DYSRAPHISMS
WITH A SUBCUTANEOUS MASS
Lipoma with dorsal defects
Myelocystocele(Terminal or cervical)
Meningocele
18. LIPOMAS WITH DURAL DEFECT :
LIPOMYELOCELE
AND LIPOMYELOMENINGOCELE
THESE ABNORMALITIES RESULT FROM A DEFECT IN
PRIMARY NEURULATION WHEREBY MESENCHYMAL
TISSUE ENTERS THE NEURAL TUBE AND FORMS
LIPOMATOUS TISSUE.
19. C/F : subcutaneous fatty
mass above the gluteal
crease.
Diff both based on
lipoma – placode
interface
Lipomyelocele :
placode-lipoma interface
within spinal canal.
Lipomyelomenigocele:
Outside the spinal canal
due to sub-arachnoid
space expansion.
20. Lipomyelomeningocele. Axial
schematic of lipomyelomeningocele shows
placode–lipoma interface (arrow) lies
outside of spinal canal due to expansion
of subarachnoid space.
Lipomyelomeningocele. Axial T1-weighted
MR image in
18-month-old boy shows
lipomyelomeningocele (arrow)
that is differentiated from lipomyelocele by
location of
placode–lipoma interface outside of spinal
21. TERMINAL MYELOCYSTOCELE
Herniation of large
terminal syrinx
(syringocele) into a
posterior meningocele
through a posterior spinal
defect is referred to as a
terminal .
The terminal syrinx and
meningocele components
do not usually
communicate with each
other.
MYELOCYSTOCELE(N
TERMINAL)
Dilated central canal
herniates through a
posterior spina bifida
defect.
covered with skin
MC -cervical or
cervicothoracic regions
24. MENINGOCELE
Herniation of a CSF-filled sac lined by
dura and arachnoid mater is referred
to as a meningocele. The spinal cord is
not located within a meningocele but
may be tethered to the neck of the
CSF-filled sac .
2 types…
Posterior meningoceles herniate
through a posterior spina bifida
(osseous defect of posterior spinal
elements) and are usually lumbar or
sacral in location but also can occur in
the occipital and cervical regions
Anterior meningoceles are usually
presacral in location but also can
occur elsewhere
26. CLOSED SPINAL DYSRAPHISMS
WITHOUT A SUBCUTANEOUS MASS
Simple dysraphic states
intradural lipoma,
filar lipoma,
tight filum terminale,
persistent terminal ventricle
dermal sinus.
Complex dysraphic states be
divided into two categories:
A) disorders of midline
notochordal integration,
dorsal enteric fistula,
neurenteric cyst, and
diastematomyelia,
B)disorders of notochordal
formation,
caudal agenesis and
segmental spinal dysgenesis
27. LIPOMA
2 Types : Intradural lipoma and Filar lipoma
Embryological defect : focal premature disjunction of epidermal from neural
ectoderm.
INTRADURAL LIPOMA
Lipoma within the dural sac
MC : Lumbosacral spine
a/w tethered-cord syndrome
FILAR LIPOMA
Fibrolipomatous thickening of the filum terminale is referred to as a filar
lipoma.
MR : T1 hyperintense signal + thickened filum terminale
28. Diagrammatic representations of
spinal lipomas. A: Intradural
lipoma.
The pia-arachnoid encloses
the spinal cord and the lipoma.
The lipoma lies predominantly
within a midline cleft in the
dorsal spinal cord but fungates
beneath the pia to bulge into the
dorsal subarachnoid space.
B: Lipomyelocele.
C: lipomyelomeningocele.
BOTH ANOMALIES OF
PRIMARY NEURULATION
29. INTRADURAL
LIPOMA
Sagittal T1-weighted (A) and sagittal T2-
weighted fat-saturated (B) MR images show
Large intradural lipoma (arrows), which is
hyperintense on T1-weighted image and
hypointense
on T2-weighted fat-saturated image. Lipoma
is
attached to conus medullaris, which is low
lying.
30. FILAR LIPOMA
Sagittal (A) and
axial (B) T1-
weighted MR
images I shows
filar lipoma
(arrows),
which has
characteristic T1
hyperintensity and
marked thickening
of filum terminale
31. SIMPLE DYSRAPHIC STATES
TIGHT FILUM TERMINALE
hypertrophy and shortening of the
filum terminale.
EMBRYOLOGY : incomplete
involution of the distal spinal cord
during embryogenesis.
This condition causes tethering of the
spinal cord and impaired ascent of the
conus medullaris.
The conus medullaris is low lying
relative to its normal position(above the L2–L3 disk level).
32. SAGITTAL T2-WEIGHTED
MR IMAGE IN 12-MONTH-
OLD BOY SHOWS
TIGHT FILUM
TERMINALE,
CHARACTERIZED BY
THICKENING AND
SHORTENING OF FILUM
TERMINALE (BLACK
ARROW) WITH LOW-
LYING CONUS
MEDULLARIS.
33. SIMPLE DYSRAPHIC STATES
TERMINAL VENTRICLE
Persistence of a small, ependymal
lined cavity within the conus
medullaris is referred to as a
persistent terminal ventricle .
It appears to represent the point of union
between primary and secondary neural tube.
Key imaging features include
lack of contrast enhancement, which differentiate
this entity from other cystic lesions
of the conus medullaris.
34. SAGITTAL T2-WEIGHTED
(A) AND SAGITTAL T1-
WEIGHTED CONTRAST-
ENHANCED (B) MR
IMAGES IN
12-MONTH-OLD BOY
SHOW
PERSISTENT TERMINAL
VENTRICLE
AS CYSTIC STRUCTURE
(ARROWS) AT INFERIOR
ASPECT OF
CONUS MEDULLARIS,
WHICH DOES NOT
ENHANCE.
35. SIMPLE DYSRAPHIC STATES
DERMAL SINUS
Epithelial lined fistula that
connects neural tissue or
meninges to the skin surface.
If the superficial ectoderm
fails to separate from the
neural ectoderm at one point.
MC : Lumbo sacral region
C/F : midline dimple , hairy
naevus , hyperpigmented
patch /capillary hemangioma
Infectious complication if not
surgically treated
36.
37. COMPLEX DYSRAPHIC STATES
DISORDERS OF MIDLINE
NOTOCHORDAL
INTEGRATION
Dorsal enteric fistula,
Neurenteric cyst
Diastematomyelia,
Caudal agenesis
Segmental spinal
dysgenesis.
DISORDERS OF
NOTOCHORDAL
FORMATION
38. DISORDERS OF MIDLINE NOTOCHORDAL
INTEGRATION
DORSAL ENTERIC FISTULA
Abnormal connection between the skin
surface and bowel.
NEURENTERIC CYSTS
Localized form of dorsal enteric fistula
Mucin-secreting epithelium (~GI tract )
lined cyst
MC : cervico-thoracic spine anterior to
spinal cord
39. SAGITTAL T2-
WEIGHTED (A)
AND AXIAL T1-
WEIGHTED
(B)MR IMAGES
SHOW
BILOBED
NEURENTERIC
CYST (ARROWS)
EXTENDING
FROM CENTRAL
CANAL INTO
POSTERIOR
MEDIASTINUM.
40. DISORDERS OF MIDLINE
NOTOCHORDAL INTEGRATION
DIASTEMATOMYELIA
Separation of the spinal cord into two hemicords.
The two hemicords are usually symmetric, although the
length of separation is variable.
Type 1 : Dual Dural-Arachnoid Tubes (Pang Type I) :
the two hemicords are located within individual dural
sacs separated by an osseous or cartilaginous septum
Type 2 : Single Dural-Arachnoid Tube (Pang Type II) :
Single dural tube containing two hemicords, sometimes
with an intervening fibrous septum
C/F : Hairy tuft , scoliosis , tethered cord syndrome.
41. posterior view of the patient reveals
the large patch of
long, silky hairs
overlying diastematomyelia and a
small sacral dimple.
Embryogenesis of split notochord syndrome
42. Sagittal T2-weighted
MR (A), axial T2-
weighted MR (B), and
axial CT with bone
algorithm (C) images
in 6-year-old boy
show
Two dural tubes
separated by
osseous bridge
(arrows), which is
characteristic for
type 1
diastematomyelia .
43. TYPE 2 DIASTEMATOMYELIA
Coronal T1- -weighted
(A),
weighted (A), and axial
T2-weighted (B)
MR images show
Splitting of distal cord
into two hemicords
(white arrows) within
single dural tube,
which
is characteristic for
type 2.
Incidental : filum
44. DISORDERS OF NOTOCHORDAL
FORMATION
CAUDAL AGENESIS
Total or partial agenesis of the spinal column
A/w anal imperforation, genital anomalies,
renal dysplasia or aplasia, pulmonary
hypoplasia, or limb abnormalities.
2 Types
Type 1 : high position of conus + abrupt
termination of conus medullaris(D11/12)+
neuro deficit
Type II : low position(L1) + tethering of conus
medullaris
45. Sagittal T2-weighted (A) and
sagittal T1-
weighted (B) MR images in show
Type 1 caudal agenesis. Conus
medullaris is high in position and
wedge shaped (arrow) due to
abrupt termination.
INCIDENTAL -Distal cord syrinx
(arrowhead).
46. CAUDAL REGRESSION
SYNDROME
Partial agenesis of the thoracolumbosacral
spine
Imperforate anus
Malformed genitalia
Bilateral renal dysplasia or aplasia
Pulmonary hypoplasia
Extreme external rotation and fusion of the
lower
extremities (sirenomelia)
Sacral agenesis arises early in gestation,
probably
before the 10th week of gestation
47. DISORDERS OF NOTOCHORDAL
FORMATION
SEGMENTAL SPINAL DYSGENESIS
Segmental agenesis or dysgenesis of the
thoracic or lumbar spine + segmental
abnormality of the spinal cord/nerve roots +
congenital paraparesis / paraplegia, +
congenital lower limb deformities.
Three-dimensional CT reconstruction image (A) in
4-year-old girl and schematic illustration (B) show
multiple segmentation anomalies in lumbar spine
(superior to
inferior beginning at level of arrow): partial
sagittal partition,
butterfly vertebra, hemivertebra, tripedicular
vertebra,
and widely separated butterfly vertebra.
48. DEVEOPMENT OF VERTEBRAL
COLUMN
Formed form the sclerotome of somites
Sclerotome converts to loose mesenchyme (4TH WEEK)
It surrounds the notochord – forming the CENTRUM.
Extend to either side of neural tube and
surrounds it – forming the NEURAL ARCH.
Lateral extension from centrum- form transverse process
Notochord disappears in the region of vertebral
body.
In the region of the vertebral discs , it expands
and forms nucleus pulposus.
49. STAGE OF CHONDRIFICATION
6th week
2 centers of chondrification in each
Centrum appear
Fuse together at the end of embryonic period
(8th week) form cartilaginous centrum.
STAGES OF OSSIFICATION
Comprises of 2 stages:
1. primary ossification center
2. secondary ossification center
Primary ossification center at the end of 8th
week.
3 ossification centers are present by the end
of embryonic period
one in the centrum
one for each neural arch
The arches articulate with the centrum at
cartilaginous neurocentral joints.
Bony halves of the vertebral arch fuse together during
the first 3 to 5 years
50. Secondary ossification center
Time of development: after puberty
the 5 secondary ossification center appears at,
1. tip of spinous process
2. tip of each transverse process
3. superior rim of the vertebral body
4. inferior rim of the vertebral body
FATE OF NOTOCHORD
Cranial part: merged with basilar part of occipital bone
& posterior part of body of sphenoid
Notochord located in the vertebra undergo
degeneration and disappear
The ones located in between undergo mucoid
degeneration to form nucleus pulposus
52. ASOMIA(agenesis)
• Complete absence of body
of vertebra
• Posterior elements present
• FAILURE OF
OSSIFICATION CENTERES
TO APPEAR
HEMIVERTEBRA
U/L Wedge Or Lateral Vertebrae :
lack of ossification of one half of body.
Scoliosis results
Dorsal Or Ventral Hemivertebrae:
failure of ventral /dorsal half to ossify.
Kyphosis results
(A) Left hemivertebra
involving T11
(B) Dorsal
hemivertebra
involving L1
53. BUTTERFLY
VERTEBRA
Failure of fusion of
lateral halves of the body
Due to persistent
notochordal tissue
May be a/w spinabifida
and anterior
meningocele
CORONAL
CLEFT
Failure of fusion of
anterior and
posterior
ossification centres
Seperated by a
cartilage
plate
54. BLOCK VERTEBRA
(A) Block vertebra with
congenital fusion of C4 and
C5
Note the presence of a “waist”
at the site of fusion (arrow).
(B) Acquired vertebral body
fusion
of C5 and C6
Failure of segmentation
most often in
midthoracic or
thoracolumbar regions
and may involve 2-8
levels.