2. TOPIC
DESCRIBE THE ANATOMY OF THE SPINAL CORD
DESCRIBE THE BLOOD SUPPLY OF THE SPINAL CORD
WHAT ARE THE EFFECTS OF DISRUPTION OF EACH OF THE MAJOR
BLOOD SUPPLY
DESCRIBE THE PATHOPHYSIOLOGY OF HEMITRANSECTION OF THE
SPINAL CORD
3. PRESENTATION OUTLINE
HISTORIC BACKGROUND
EMBRYOLOGICAL DEVELOPMENT OF THE SPINAL CORD
GROSS ANATOMY OF THE SPINAL CORD
BLOOD SUPPLY OD THE SPINAL CORD
RECAP OF MAJOR BLOOD SUPPLY OF THE SPINAL CORD
EFFECT OF DISRUPTION OF EACH BLOOD SUPPLY
HEMITRANSECTION OF THE CORD
DEFINITION
EPIDEMIOLOGY
PATHOPHYSIOLOGY
MANAGEMENT
CURRENT RESEARCH
4. HISTORICAL BACKGROUND
3000-2500BCE Egypt Edwin Smith Papyrus
460-370BCE Greece Hippocrates
129-210 CE Rome Galen, spinal cord research
1881 USA James Garfield (US President)
1895 Germany Wilhelm Rontgen (X-Ray)
1913 USA Henry Ford (Automobile)
1995 USA Christopher Reeve
2008 Australia Mackay-Sim et All phase I/IIa trials of
autologous transplant olfactory ensheathing cells
Today: we need to invest more in spinal cord research as Africans
5. DEVELOPMENT OF THE SPINAL CORD
start at 3rd weed of fetal development
Neural Plate (ectoderm)
Neural Folds
Neural Tube
Cranial and caudal Neuropores
Cranial closes at Day 25 (20 somites stage),
Caudal 2 days later
8. MOLECULAR REGULATION
Sonic HedgeHog in Notochord represses expression of PAX3,
PAX7, MSX1 and MSX2
Bone Morphogenic Proteins expressed in non neuronal ectoderm
upregulate PAX3 and PAX7
11. GROSS ANATOMY. EXTERNAL
Cylindrical structure located in spinal canal of vertebral colum
Covered by meninges, PIA, ARACHNOID and DURA
Suspended by denticulate ligaments (sheaths of dura)
Ends as the conus medullaris (all the segmental nerve roots below
L1)
12. GROSS ANATOMY. EXTERNAL
Filum terminal (streak of pia matter)/ Cauda equine (lumbosacral
roots)
31 pairs of spinal nerves which each divide into ventral and
dorsal Primary rami
surface is marked by furrows
Deep VENTRAL MEDIAN FISSURE
DORSAL MEDIAN SULCUS
14. GROSS ANATOMY …INTERNAL
H shape in transverse section
Central canal lined by ependymal cells
Gray matter consists of
Dorsal horn
Ventral horn
Intermadiate ZONE
Lateral horn (preganglionic ØΣ neurons, thoracic and upper lumbar)
Gray matter has three main categories of neurons
Motor cells (α and ϒ motor neurons )
Cell bodies of tract cells
interneurons
15.
16. White matter consists of three FUNICULI
Dorsal funiculus ( Gracile and cuneate Fasciculi)
Lateral funicullus
Ventral funicullus
Dorsolateral tract of LISSAUER at apex of dorsal horn
axons decussate in the ventral white commissure
GROSS ANATOMY …INTERNAL..
17. NEURONAL ARCHITECTURE OF SPINAL CORD
10 layers of neurons (I to X): LAMINAE of REXED
Lamina II, the substantia gelatinosa (interneurons that can
modify pain)
Lamina VII
(nucleus dorsalis ( gives rise to dorsal spinocerebellar tract)
Intermediolateral cell colum(preganglionic sympathetic
neurons)
Lamina IX, motor neurone, supply skeletal muscles
Dictinctive colums of motor neurons
ACCESSORY NUCLEUS (C1-C5)
PHRENIC NUCLEUS (C3-C5)
NUCLEUS OF ONUF (S2 and S3)
18.
19. Dorsal root branches into two divisions
Lateral: group C (unmyelinated) and group A
(myelinated) axons
enter the tract of Lissauer and divide into asc and
desc branches
synapse with tract cells of SPINOTHALAMIC FIBRES
Medial: large caliber myelinated fibers, enter the
spinal cord medial to dorsal horn and ascend in
posterior funicullus
concerned with other sensory modalities except
pain and temperature
NEURONAL ARCHITECTURE OF SPINAL CORD…
DORSAL HORN
20.
21. Lamina IX
Two types of motor neurons
ALPHA. Numerous, supply extrafusal fibers of
striated muscles
each alpha neuron receives at least 20.000
synaptic contacts
GAMMA. Smaller, less numerous, supply
intrafusal fibers of neuromuscular spindles
interneurons: RENSHAW CELLS receives excitatory
input but form inhibitory synaptic junctions on
motor neurones
NEURONAL ARCHITECTURE OF SPINAL CORD
VENTRAL HORN
24. DORSAL FUNICULUS
IPSILATERAL
Discriminative touch, vibration, joint position sense
Gracilis fasciculus medially (lower limb)
Cuneatus fasciculus laterally(upper limb)
Both end in medulla (gracilis and cuneatus nuclei)
25. LATERAL FUNICULUS
LATERAL CORTICOSPINAL TRACT
From cortex of frontal lobe, medullary pyramid, DECUSSATE and
enter lateral funiculus
From frontal cortex: terminate in intermediate gray matter and
ventral horn
From parietal cortex: terminate in dorsal horn
26. LF- DORSAL SPINOCEREBELLAR TRACT
Present only above level L3
Axons arise from Clarke’s colum
Terminate ipsilaterally in the cerebellar cortex
27. LF- SPINOTHALAMIC TRACT
Cells of origins are in laminae IV and V-VI
Consist of axons of neurons located in gray matter of opposite ½
of cord
Tactile, thermal and painful stimuli
29. VENTRAL FUNICULUS
Contains only descending tracts
Ventral corticospinal (decussate at segmental levels) skilled
volitional movements
Vestibulospinal tract: uncrossed arises from vestibular nucleus of
Deiters in the medulla
Reticulospinal tracts: control ordinary activities that do not require
conscious effort
Descending bundle of the lateral horn are ipsilateral excitatory
axons to the preganlionic sympathetic neurons
31. SEGMENTAL ARTERIES
ANT RADICULAR POST RADICULAR
12 ant radicular contribute to pia plexus 14 post radicular
join the join the
ANT SPINAL A POST SPINAL A
sulcal branches Largest radicular a
In upper lumbar region
(ADAMKIEWICZ)
Supply small plexuses present in pia supply
Ventral gray horns VASORORONA remainder of dorsal gray horns
Part of dorsal gray horns supply white matter beneath pia dorsal funiculi of white matter
Ventral and lat white funiculi
32.
33. Live operative picture of radicular artery
Note the small size in relation to the spinal nerve
36. SEGMENTAL SPINAL ARTERIES COMPROMISE
Hypotension
Aortic aneurysm
Aortic dissection
Devascularisation surgery (idiopathic)
COMPROMISE OF ANT AND POST SPINAL ARTERIES
37. ANTERIOR SPINAL ARTERY
ANTERIOR CORD SYNDROME
Bilateral disruption of the corticospinal tract, causing motor
deficits,
Bilateral disruption of the spinothalamic tract, causing sensory
deficits in the form of pain/temperature sense loss.
42. HEMITRANSECTION OF THE SPINAL
CORD
Brown-Séquard syndrome is an incomplete spinal cord lesion
characterized by a clinical picture reflecting hemisection injury of
the spinal cord, often in the cervical cord region
Patints suffer from ipsilateral upper motor neuron paralysis and
loss of proprioception, as well as contralateral loss of pain and
temperature sensation. A zone of partial preservation or
segmental ipsilateral lower motor neuron weakness and
analgesia may be noted.
Loss of ipsilateral autonomic function can result in Horner
syndrome
43. PATHOPHYSIOLOGY
Brown-Séquard syndrome results from damage to or loss of
ascending and descending spinal cord tracts on 1 side of the
spinal cord.
Scattered petechial hemorrhages develop in the gray matter
and enlarge and coalesce by 1 hour postinjury.
Subsequent development of hemorrhagic necrosis occurs within
24-36 hours.
White matter shows petechial hemorrhage at 3-4 hours.
Myelinated fibers and long tracts show extensive structural
damage
45. PRESENTATION
Clinical history often reflects the etiology of Brown-Séquard
syndrome. Onset of symptoms may be acute or gradually
progressive. Complaints are related to hemiparesis or
hemiparalysis and sensory changes, paresthesias, or dysesthesias
in the contralateral limb(s). Isolated weakness or sensory changes
may be reported
46. PHYSICAL EXAMINATION
Pure Brown-Séquard syndrome (rarely seen in clinical practice) is associated
with the following:
Interruption of the lateral corticospinal tracts - Ipsilateral spastic paralysis
below the level of the lesion and Babinski sign ipsilateral to the lesion
(abnormal reflexes and Babinski sign may not be present in acute injury)
Interruption of posterior white column - Ipsilateral loss of tactile
discrimination, as well as vibratory and position sensation, below the level of
the lesion
Interruption of lateral spinothalamic tracts - Contralateral loss of pain and
temperature sensation; this usually occurs 2-3 segments below the level of
the lesion
Use ASIA impairment scale to assess degree of motor and sensory deficit
48. WORK UP
The diagnosis is made on the basis of history and physical
examination.
Laboratory work is not necessary to evaluate for the condition but
may be helpful in following the patient's clinical course.
Laboratory studies may also be useful in nontraumatic etiologies,
such as infectious or neoplastic causes. Purified protein derivative
and sputum for acid-fast bacilli should be ordered if tuberculosis is
suggested as an etiology.
If the cause of the SCI was traumatic, do a full traunma workup.
Recognize that hypotension may be the result of something other
than neurogenic shock. If, for example, the spinal injury was caused
by trauma, hypotension may result from hemorrhagic causes.
49. WORKUP
IMAGING
Xrays
CT
Magnetic resonance imaging (MRI) is very useful in determining the
exact structures that have been damaged in Brown-Séquard
syndrome, as well as in identifying nontraumatic etiologies of the
disorder. No contrast is necessary for acute injury, but if an intradural
etiology is suspected, a gadolinium or phase-contrast cine MRI scan
may be helpfu
50. TREATMENT
Physical therapy intervention starts in the acute care phase
of treatment. Therapy goals include the following:
Maintaining strength in neurologically intact muscles
Maintaining range of motion in joints
Preventing skin breakdown by proper positioning and weight
shifting
Improving respiratory function by positioning and breathing
exercises
Achieving early mobilization to increase tolerance of the upright
position
Providing emotional and educational support for the patient and
his/her family
51. TREATMENT …
Occupational therapy
SPINAL REDUCTION, STABILIZATION AND DECOMPRESSION
Consultation with MDT (multidisciplinary team)
52. MEDICAL MANAGEMENT
dependent on the etiology and acuity of onset.
Acute treatment of traumatic SCI involves immediate dosing of
methyl prednisolone.
Acute immobility that is unrelated to a bleed requires
anticoagulation therapy, if not contraindicated.
Gastrointestinal protection is strongly recommended.
Other medications are used to manage symptoms and
complications as needed, including antibiotics, antispasmodics, pain
medications, and laxatives.
53. MEDICAL MANAGEMENT …
Corticosteroids
Multiple studies have demonstrated improved outcomes for
patients with traumatic SCIs who were given high-dose steroids
early in the clinical course. (Although study by Pollard and Apple
did not find these results in incomplete cervical SCIs. )
These drugs have anti-inflammatory properties and cause profound
and varied metabolic effects. Corticosteroids modify the body's
immune response to diverse stimuli
54. REFERENCES
Cliinical anatomy (2014) venous drainage of the spina and spinal cord
Clinical anatomy (2015) blood supply of the human spinal cors
Barr’s , the human nervous system, 10th Ed
McCarron MO, Flynn PA, Pang KA, et al. Traumatic Brown-Séquard-plus
syndrome. Arch Neurol. Sep 2001;58(9):1470-2
Pollard ME, Apple DF. Factors associated with improved neurologic
outcomes in patients with incomplete tetraplegia. Spine. Jan 1
2003;28(1):33-9
Spinal Cord Injury Information Network. Facts and Figures at a Glance.
2013
Parmar H, Park P, Brahma B, et al. Imaging of idiopathic spinal cord
herniation. Radiographics. Mar-Apr 2008;28(2):511-8
