1. The document discusses various spinal cord syndromes including complete cord transection syndrome, Brown-Sequard syndrome, central cord syndrome, posterior column syndrome, posterolateral cord syndrome, combined anterior horn cell-pyramidal tract syndrome, anterior horn cell syndrome, and anterior spinal artery occlusion syndrome.
2. It describes the key features of each syndrome such as the patterns of sensory and motor deficits and common causes.
3. Examples of features mentioned include flaccid paralysis, loss of all sensory modalities, and autonomic disturbances for complete cord transection syndrome and unilateral motor and sensory deficits for Brown-Sequard syndrome.
2. Objectives…
• Basic spinal cord Anatomy
• Types of spinal cord lesions
• Main spinal cord syndromes-Eight!
• Common clinical presentation
• Basic Neuroimaging-MRI/CT appearances
• Other spinal cord lesions
• Summary
3. Spinal cord Anatomy
31 pairs of spinal cord segments,45 cm
Ventral-motor & Dorsal-sensory functions
Combined –mixed spinal nerves
neuroforamina
Foramen magnum lower margin of L1
Vert. & SC segments –not nessasarily the
same( SC is shorter than the vert.)
Blood supp-1 ant.spinal artery& 2 post.spinal
arteries (vertebral)
Ant.2/3 & dorsal columns respectively.
4.
5.
6. Spinal cord lesions
• Intra medullary vs extramedullary lesions
• Complete vs incomplete lesions
7. Intramedullary Extramedullary
Root pain rare Root pain common
Corticospinal signs-late early
LMN signs- several
segments
localized
Dissociated sen.loss +/- BSS if lateral cord
compression
CSF changes-minimally
altered/NL
Early & marked
May have sacral sparing
8. • Incomplete:
– Sensory, motor or both functions are partially
present below the neurologic level of injury
– Some degree of recovery
• Complete:
– Absence of sensory and motor function below the
level of injury
– Loss of function to lowest sacral segment
– Minimal chance of functional motor recovery
12. • Results in
1. Spinal shock
2. Spastic paralysis(hypertonic,hyperfeflexic)
3. Loss of all sensory modalities bilaterally
4. Autonomic disturbances
• Spinal shock-
1. Complete loss of voluntary movements,
sensations below the level of lesion
2. Loss of all reflexes in isolated cord segments
13. 3.Duratin varies-1-6 weeks commonly
• Spastic paralysis
1. Follows the period of spinal shock
2. Initially positive Babinski sign ,later-increased
tone & deep tendon reflexes
3. Disuse muscle atrophy
• Loss of superficial reflexes(abdominal,
cremasteric) below the level
14. • Loss of all sensations bilaterally below the lesion
1. Loss of propioception, vibration,tactile
discrimination, pain,temp, light touch, viseral
sensibility
2. Complete lesion-no recovery
• Autonomic disturbances
1. Bowel/bladder dysfunction-urinary
retention/constipation
2. Initial retention due to loss of vol.control
3. Flaccid neuropathic bladder with overflow
incontinence with recovery……
15. • Spastic neuropathic bladder with autonomic
bladder
5.few-’’ mass reflex’’ bowel/bladder empty on a
segmental autonomic basis reflexly.
6. Vasomotor instability-Cutaneous BV below do
not respond to cold/hot stimuli
7.Anhydrosis-Honer’s syndrome may occur in some.
8.Sexual dysfunction
• Transection of SC above C5- not survive due to
involvement of phrenic nerve nuclei-res.paralysis
• Below C5-quadriplagic/between Cx & L-S
segments-paraplagic.
17. • Motor changes-
1. UMN signs below the hemisection on I/L side
2. LMN signs at the level on I/L side
• Sensory changes-
1. Pain/temp loss on C/L side –upper level of
sen. Loss is few segments below the
leasion.(?)
2. Vib. & propi, loss on I/L side
3. There may be band of sensory loss on the I/L
side at level of the leasion.
18. • Causes-
1. MS
2. Angioma
3. Glioma
4. Trauma
5. Myelitis
6. Post radiation myelopathy
20. • Expanding central canal in the SC –more in
Cervical cord,symetrical leasions
• STTsalways affected- fibers cross through
syrinx
• CSTs spares until syrinx very large
• DCs always spared
• nerve roots at sequential levels affected
• Clinical triod-
1. Loss of pain/temp. over neck, shoulders &
arms-’’cape distribution’’
2. Amyotrophy-weakness,atrophy ,areflexia of
hands/arms
21. • 3.UMNL in lower limbs
• Other features horner’s syndrome(syrinx
affecting sym. Nerves & C8/T1
• Charcot’s joints-long standing ,loss of pain
sensation
• Associated kypphoscoliosis.
• Syringobulbia syrinx in brain
stem/extention-facial dissociated sensory
loss,bulbar palsy,nystagmus & cebellar ataxia
25. • Due to Vit.B12 deficiency
• DCs symmetrically degenarate,loss of
vibration & propioception over feet,+ve
Rhomberg’s sign, Ataxic gait
• CSTs symetrical UMN signs in LLs(spastic
paraparesis),extensor planters, absent AJ,
possible brisk KJ
• STTs spared or involved as part of PN(less
common & mild)
• Others optic atrophy with centrocecal
scotomata,dementia,autoimmune
disease(pernicious anemia)
28. • typical form of MND, AD inheritance, mutation in
SOD1
• Mixed UMN & LMN degeneration with cerebral
motor pathways & brain stem nuclei
• Muscle wasting or weakness with preserved or
brisk reflexes, sphincter involvement is very late if
at all.
• Progressive bulbar involvement(20%) sialorrhoea,
dysarthria,dysphagia
• Cognition generally spared, 15% FTD
• Sensory-NOT affected, superficial reflexes-
preserved
• ANS-intact
30. • CAUSED BY SPINAL MUSCULAR ATROPHY.
• MOTOR
• weakness ,atrophy and fasciculations.
• Hypotonia, depressed reflexes.
• Muscles of trunk and extremities are affected.
• Sensory system is not affected.
32. • MOTOR-Flaccid and areflexic paraplegia
• SENSORY-
• Loss of pain and temperature.
• Preservation of position and vibration.
• AUTONOMIC-
• urinary incontinence.
• Spinal cord infarction usually occurs in T1 to
T4 segment. and L1
• Occurs due to syphilitic arteritis ,aortic
dissection, atherosclerosis of aorta, SLE &
AIDS,AVM
33. • Posterior spinal artery
occlusion/syndrome-
• Uncommon.
• Loss of proprioception and vibratory sense.
• Pain and temperature is preserved.
• Absence of motor deficit.