Spinal cord lesions
Etiology Lesion location
Poliomyelitis Poliovirus, single stranded RNA virus Anterior horn ( LMN )
Spinal muscular atrophy / Genetic Anterior horn ( LMN )
webbing-Ho mann disease / Autosomal recessive SMN1 mutation
abby baby
Amyotrophic lateral sclerosis / Lou Idiopathic Corticospinal tract ( UMN )
Gehrig disease SOD1 mutation / zinc copper Anterior horn ( LMN )
superoxide dismutase de ciency Brain stem CN ( dysphasia )
ASA occlusion Stroke, anterior spinal artery Spinothalamic tract ( loss of pain and temp
Lesion occlusion below the lesion )
location
LMN Coticospinal tract ( UMN below the lesion )
( the lesion are below because it’s a tract so
we need connection with each part of spinal
cord
Anterior horn ( LMN damage ) level of the
lesion
Spinal cord
Tabes dorsalis Tertiary syphilis ( t pallidum ) Demyelination of posterior columns ( ataxia,
Romberg positive ) and dorsal root ( loss
re ex ankle and knee )
( because the pathway of the re ex info get
into dorsal root and then synapse in anterior
horn then leave spinal cord )
Syringomyelia Associated with kyphoscloiosis The symptoms depend on the size of cyst
( spinal curve ) lling central canal / spinal canal but lesion
Trauma: can happen after years happen only in the level of the syrinx
Congenital: associated to Chiari I Location of lesion usually C2-T9 ( e ect hand
malformation of cerebellum and back with normal legs )
Small size:
Spinothalamic tract damage because spinal
canal is the location of crossing = bilateral
loss of pain / temp in the level of the lesion
Big size cyst sym include:
Anterior horn ( LMN )
Lateral horn ( disturb SNS of face = Horner’s
syndrome )
Subacute combined degeneration B12 de ciency SCD
Demyelination of Spinocerebellar tracts
Lateral Corticospinal tracts ( UMN damage
usually of the lower extremities, Positive
Babinski )
Dorsal columns ( ataxia, positive Romberg )
Brown - sequard syndrome Trauma or tumor Half of the spinal cord
At the level of the lesion:
Ipsilateral loss of all sensation + LMN
Below the level of the lesion:
Ipsilateral UMN + ipsilateral proprio /
vibration loss + contralateral pain / temp loss
Lesion above T1:
Ipsilateral horn syndrome = constricted pupil
+ eyelid droop
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Etiology Lesion location
Cauda equine syndrome Compression cauda equina • Severe low back pain
Massive disk rupture • “Saddle anesthesia”
Trauma, tumor • Loss of anocutaneous re ex
• Bowel and bladder dysfunction
• Normal Babinski
Conus medullaris syndrome Same symptoms of cauda equina syndrome +
perinatal anesthesia bilateral, impotence
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Poliomyelitis Weeding- Ho man Amyotrophic lateral sclerosis / Lou
disease / spinal Gehrig ( baseball player died 2 years
muscular atrophy / after diagnosis ) disease
appy baby syndrome
Etiology Poliovirus, single stranded RNA Autosomal recessive Idiopathic neuron start to die
virus SMN1 mutation Linked to SOD1 mutation ( encodes
superoxide dismutase 1 )
Familial cases:
• Zinc copper superoxide dismutase
de ciency
• Increased free radical damage
Transmission Fecal-oral transmission - -
replication in lymphoid tissue of
oropharynx and small intestine
spread to CNS via bloodstream.
Destruction Anterior horns Congenital degeneration Combined UMN white matter lesion
location of anterior horns (corticospinal/corticobulbar) and LMN
(brainstem/spinal cord anterior horn lesion)
degeneration.
Symptoms Neuro symptoms 4-5 days later LMN lesion only No sensory symptoms, No sensory or
LMN lesion asymmetric symmetric weakness bowel/bladder de cits.
weakness Hypotonia
Flaccid paralysis Flaccid paralysis LMN signs:
Symptoms of viral meningitis Tongue fasciculations accid limb weakness
( headache, fever, neck sti ness ). fasciculations
Respiratory muscle involvement atrophy
leads to respiratory failure. bulbar palsy (dysarthria, dysphagia, tongue
atrophy).
Diagnosis
CSF shows: UMN signs:
WBCs (lymphocytic pleocytosis) spastic limb weakness
slight increase of protein (with no hyperre exia
change in CSF glucose). clonus
pseudobulbar palsy (dysarthria, dysphagia,
Poliovirus can be isolated from emotional lability).
stool or throat secretions.
Cranial nerves can be involved causing
Dysphagia most need feeding tube
Classical • Unvaccinated child Flabby baby and death in • Most common 40-60 years old
presentation • Febrile illness few months • Usually fatal 3-5 years
• Neuro symptoms 4-5 days later • Common cause of death:
• Weakness (legs>arms) • Fatal (most often from respiratory failure).
• Flaccid muscle tone aspiration pneumonia because they
can’t swallow due to muscle weakness =
they can’t clear seacreation from the
back of throat and end up aspirating it
Classic Presentation
• 50-year old patient
• Slowly progressive course
• Arm weakness
• Dysphagia to solids/liquids
• Some accid muscles
• Some spastic muscles
• No sensory symptoms
• Riluzole for treatment (↓glutamate
release neurons)
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