Spinal Cord Lesion Localization

Spinal Cord Lesion Localization

Myelopathy – any disease of spinal cord

Intramedullary – in substance of spinal cord

Extramedullary – outside substance of spinal cord

What kind of symptoms are seen in patient with spinal cord diseases?

Weakness -- #1 symptom seen

upper motor neuron – lesion in precentral gyrus down to lateral corticospinal tracts
lower motor neuron – lesion in ventral horn cells, neuromuscular junction, or muscles
mixed upper+lower weakness

sensory disturbances

autonomic disturbances (sweating, sexual, bowel, etc)

UMN weakness	LMN weakness
No wasting	Wasting present
Tone increased	Tone decreased
Fasciculations absent	May be present
Muscle stretch reflexes exaggerated	Depressed or absent
Abdominal reflexes -absent (lower rib cage down to pelvis, stroke abdominal muscles with q-tip)	Usually preserved
Plantar reflex – extensor	Flexor

Anatomical Considerations of Spinal Cord Lesions

Somatotopic organization of fibers

dorsal columns (fasciculus gracilis and fasciculus cuneatus) Þ sacral, lumbar, thoracic, cervical: medial to lateral)

lateral spinothalamic tracts: opposite, Cervical, Thoracic, Lumbar, Sacral Þ medial to lateral)

Blood supply of spinal cord – lesion may not correspond to spinal cord level.

Categories of symptoms/signs

(1) Radicular Symptoms – symptoms due to lesions of nerve roots

Compression of dorsal (posterior) nerve root – most common symptom is PAIN reflected in specific dermatome!

Therefore, it is important know where the pain starts and where it goes.

Compression of ventral (anterior) nerve roots – localized weakness and atrophy of involved mucles takes place

Fasciculations may be present. Reflexes are diminished then abolished. Follows the myotome
example: C5 nerve root: ipsilateral brachioradialis reflex may be diminished or absent.

(2) Segmental Symptoms – symptoms due to lesions of dorsal/ventral horn cells.

Ventral: Give rise to segmental muscular weakness, atrophy, and loss of reflexes; indistinguishable from involvement of anterior nerve roots.
Dorsal: Rarely gives rise to pain of the character which occurs with dorsal nerve roots

(3) Motor symptoms and signs – paraparesis, monoparesis, tri/quadriparesis

depends on: level of lesion, degree of involvement – complete/incomplete, extent of lesion – single or multiple levels affected, whether lesion is intra- or extra-medullary

compression of spinal cord Þ spastic paralysis below lesion; however the level of weakness may not correspond to the level of the lesion and a lesion such as a progressive lesion of the cervical region may spare the upper extremities.

spastic paraparesis (lower limbs) most likely results from diaschesis (remote effect of compromised blood supply). There is indirect compression of the anterior spinal artery causing ischemia of lateral cortico-spinal tract. (Remember: as a lesion moves medially in the lateral cortico-spinal tract that leg fibers (sacral segments) affected 1^st)

two sets of arteries supplying a spinal cord (both come off vertebral artery):

Vertebral artery Þ posterior spinal artery (smaller) Þ posterior pial arteriolar plexus – supply only dorsal tracts.

Vertebral arteryÞ anterior spinal arteryÞ anterior median spinal artery Þ sulcal artery and circumferential artery – anterior pial arteriolar plexusÞ supplies the rest

(4) Sensory Changes

in large lesions with advanced compression the sensory level may correspond to the level of the lesion; in slow compression the sensory level may not be affected at all or the level may be much lower. (Again, remember that legs will be affected first, however, this will be in the lateral spinothalamic tract which is just medial to the lateral cortico-spinal tract.)

example: Loss of all sensory below T7 but still have sensation on butt – sacral sparing. Etiology: Intramedullary (growing medialÞ lateral) lesion; sacral segments are spared, cause in periphery of spino-thalamic tracts.

example: loss of pain and temperature feeling between C7-T3 or T4. Etiology: Syringomyelia – lesion in anterior white commisure.

example: loss of light touch on left side of body, loss of pain on right side of body. Etiology: Spinal cord hemisection on left side – Brown/Sequard syndrome. Remember that anterolateral system decussates at level of spinal cord and the DCML decussates up in the medulla.

(5) Reflex Changes

usually depressed at site of lesion and exaggerated below level of lesion.

acutely may be depressed for a few weeks, as a rule brisk, ankle clonus may be obtained, extensor plantars, superficial reflexes depressed

at site of lesion, reflexes may give paradoxical response (e.g., C7 lesionÞ triceps flex instead of extend forearm)

there are segments for reflexes – biceps (c5, c6), triceps (c7), ankle jerk (s1), knee (L3,L4), trunk (T7-T12)

examples: left side reflexes absent in triceps – lesion in C7, abdominal reflex is depressed and exaggerated knee jerk and ankle jerk – lesion in T10

(6) Autonomic Changes

decreased sweating below level of lesion

disturbances of urination, bowels, and sexual disturbances

parasympathetic Innervation of bladder (detrussor): S2-S4

sympathetic Innervation of bladder : T12-L2

innervation of pelvic floor, anus: S2-S4

somatic motor and sensory innervation of the pelvic floor: S2-S4

Sphincters: anal tone, bulbocavernosus reflex – can determine whether upper motor or lower motor lesion

ß anal tone, ß bulbocavernosus reflex – Lower Motor Lesion, could be due to lesion at conus medullaris.

bulbocavernosus reflex = squeeze tip of penis Þ flex anal sphincter

Bladder Dysfunction

Normal urination: as bladder fills there is little Ý in pressure, when urinate pressure Ý significantly

Lower motor neuron bladder disturbance Þ parasympathetic lesion

bladder is flaccid and capacity is increased, anal sphincter tone and bulbocavernosus reflex are decreased, no increase in pressure. Symptoms: hesitancy, overflow incontinence, difficulty passing urine, have to push hard, retention of urine (1000-1500 ml in bladder)

Upper motor neuron bladder disturbance (spastic bladder)

acute transection of spinal cord Þ shock stage (urinary retention and flaccidity of the bladder) Þ spastic contractions of bladder, constant incontinence = reflex neurogenic bladder

partial lesion of both corticospinal tracts (can be due to multiple sclerosis or slow compression of spinal cord from tumor) : pass urine frequently, urgency, can control sphincter for a short while. Can be treated with anti-cholinergic medication= uninhibited neurogenic bladder or detrussor hyper-reflexia.

with both types, the bladder capacity is diminished, anal sphincter and bulbocavernosus reflex is intact

Lesion between the conus medullaris and pontine bladder center Þ urge incontinence

Sphincter and detrussor are coordinated Þ lesion between pons and the cortical bladder center

Lesion of conus medullaris Þ overflow incontinence

Any lesion Þ voiding occurs when detrussor pressure (Pd) > sphincter pressure (Ps)