Spinal Cord Disorders Flashcards
Clinical signs for UMN:
- weakness
- atrophy
- atrophy v weakness
- fasciculations
- muscle tone
- muscle stretch reflexes
- clonus (=most brisk reflex)
- pathological reflexes (Babinski sign)
- more diffuse
- slight, general (often from disuse)
- severe weakness occurs with relatively little atrophy
- -never seen
- ^increased (except in spinal shock)
- ^increased (except in spinal shock)
- +/-can be present
- +present (except in spinal shock)
Clinical signs for LMN:
- weakness
- atrophy
- atrophy v weakness
- fasciculations
- muscle tone
- muscle stretch reflexes
- clonus (=most brisk reflex)
- pathological reflexes (Babinski sign)
- more focal
- focal, severe
- some strength may be preserved despite severe atrophy
- +/-can be present
- -decreased
- -decreased
- never present
- absent
Ex: GSW to R. arm, weakness in hand/forearm confined to a few muscles, over time develop severe atrophy–yet strength seems greater than would be expected
LMN signs
- found in a limb that has muscles innervated by anterior horn cells affected at the level of the SC lesion (different places: anterior horn cells, spinal root, plexus, or peripheral nerve)
- Ex: a bilateral SC lesion at the C5 level would injure the anterior horn cells or ventral motor roots there, producing LMN signs in the biceps brachii and deltoid muscle, but NOT in muscles innervated by other anterior horn cells at other levels
Note: paralyzed muscle, no reflex possible
UMN signs
- found in a limb when a SC lesion involves the CST rostral to the anterior horn cells (i.e. spinal cord, brain stem, motor cortex) that innervate the muscles of that limb
- IPSILATERAL to a CST lesion in the SC (cervical or thoracic level PRE-decussation)
- –or–
- CONTRALATERAL CST involvement in the brain (or brain stem); must know where it decussates(!)
Notes: no more voluntary action, just a good reflex
A. What is radicular (root) pain?
B. What causes it?
A. lightning, stabbing, shooting pain in the dermatomal distribution of a dorsal root
B. from inflammation or extra-medullary compression (eg herniated disc) of a dorsal root
- f/m a dull, local pain may occur from the extramedullary lesion itself
- f/m shingles from Herpes zoster
{-an intramedullay SC lesion may produce diffuse pain (or none at all)}
Tx: analgesics, anti-inflamm (oral or epidural corticosteroids) or nerve block procedures releive radicular pain in addition to surgical removal of causative lesions
What are the sensory signs and symptoms in spinal cord lesions?
- clinical sensory deficit corresponds to the SC level (not vertebral)
- during development, the vertebral column becomes longer than the SC
- **a metastatic tumor in the L1 vertebrae would expand and compress the SC at its L5, S1, or S2 levels
- SC lsion in the STT on one side creates pain and temp deficit in the contralateral body
Sensory signs in SC lesions-STT and DCT
STT lesion:
- contralateral deficit
-
suspended pattern of deficit with sacral sparing in intramedullary lesion (in SC)
- a lesion within or near the ctr of the SC will disrupt the decussating spinothalamic fibers; usually syrinx/sphingomyelia
- deficit up to a dermatomal level in extramedullary lesion (outside SC; ie vertebrae, typically compressing it, may occur with a tumor or herniated disc)
-
EXTRAmed=sacral involvement, INTRAmed=sacral sparing (**except later on in the disease)
- ***this can happen anywhere in the spincal cord (med=SC)
DCT lesion:
- ipsilateral deficit
SC syndromes: transection or transverse myelopathy
- as humans develop and grow, the bony vertebral column lengthens, but the SC does NOT
- LMN signs and level of sensory loss localize the spinal level of the lesion
- UMN signs develop in limb muscles innervated by anterior horn cells below the level of the lesion
- an acute, severe, traumatic lesion may present with [acute] spinal shock (eventually nml finding will manifest)
- etiology
- trauma
- inflammation (viral, MS, autoimmune)
- compression (tumor, spinal stenosis)
- ischemia
A. Define syringomyelia
B. CP
C. Etiology
A. cavity (syrinx) in the central gray matter which may expand; “classic” intramedullay lesion
B.
- usually occurs in the cervical or thoracic SC
- initial suspended (vestlike) spinothalamic sensory loss with sacral sparing
- interrupting decussating STT in the SC
- area of sensory impairment would approximate the area covered by wearing a cape/shawl
- position sense, vibration spared (b/c posterior or dorsal columns are generally spared)
- cavity may thn disrupt anterior horn cells (LMN signs), or may cause paraparesis [partial paralysis of the lower limbs] if CST is involved
C. etiology=abnml CSF flow or pressure with congenital (Chiari [back of the head, where brain and SC connect]) malformations: tumors –or– residual of trauma
Acute SC syndromes: occlusion of the anterior spinal artery
- sudden HYPERreflexic, spastic paraparesis, loss of pain and temp below the lesion level (lower thoracic or upper lumbar)
- paraplegia with UMN signs in the lower limbs
- thoracic level of sensory loss (without sacral sparing) to pain and temp
- preserved vibration and position sense (intact dorsal columns)
- etiology: stherosclerotic aortic disease or dissection –or– aortic surgery
Subacute combined degeneration of SC (posterolateral syndrome/sclerosis)
- lesions in posterior and lateral columns, usually thoracic level
- post and lat=COMBINED
-
loss of vibration and position sense in the lower limbs, but pain and temp preserved
- causes unsteadiness and falling if the pt stands or walks in the dark
- UMN signs (CST lesion) in lower limbs-spastic paraparesis
- Etiology:
- usually vit B12 deficiency
- copper deficiency
- HIV
- Histo (myelin stain): nml myelin-dark, demyelinated-pale
What are the major SC syndromes
- transection or transverse myelopathy
- syringomyelia
- occlusion of the anterior spinal artery
- subacute combined degeneration of SC (posterolateral syndrome)
-
ALS-sensory pathways NOT affected, get fasciculations
- diffuse weakness with UMN and LMN signs
- sacral sparing
- may initially just be thought to be a simple spinal cord lesion
- Tabes dorsalis
- Spinal cord hemisection (Brown-Sequard syndrome)
Tabes dorsal-is
- lightning pains from initial lumbosacral dorsal root lesions
- subsequent dorsal column degeneration leads to loss of vibration, position sense, then all sensory modalities
- areflexic
- preserved strength
- etiology: neurosyphilis
- **Charcot joints: severe, traumatic injury and deformation of ankle joints due to loss of sensation from tabes dorsalis
SPINAL CORD hemisection (Brown-Sequard syndrome)
-
controlateral spinothalamic deficit to pain and temperature sensation
- b/c: spinothalamic sensory fibers decussate within the SPINAL CORD-early then continue their aascending pathway
-
ipsilateral weakness (CST), ipsilateral dorsal column deficit of vibration and position sense
- fibers ascend up the same side of SC then decussate later in the MEDULLA-late
- CST: ipsi, UMN signs
- anterior horn cells: contra, LMN signs
- etiology:
- tumor (extramedullary)
- trauma
- herniated disc (with degenerative dz of the bony spine)
Examples of UMN lesions
- Cerebrovascular accident
- stroke! most common
- Intracranial tumour
- Cervical spine injury
