Neuropathies and Spinal Cord Lesions Flashcards
(84 cards)
What are the cervical myotomes?
C5 - shoulder abduction and adduction, elbow flexion C6 - elbow flexion and wrist extension C7 - elbow extension, wrist flexion C8 - wrist flexion, finger flexion T1 - finger abduction
What myotomes are the biceps and brachioradialis reflexes?
C5 and C6
What myotome is the triceps reflex?
C7
What are the lumbosacral myotomes?
L2 - hip flexion and adduction
L3 - hyp adduction and knee extension
L4 - knee extension, foot inversion and dorsiflexion
L5 - hip extension and abduction, knee flexion, great toe dorsiflexion
S1 - knee flexion, foot plantarflexion and eversion
What are the myotomes for the lower limb reflexes?
Knee - L3/4
Great toe - L5
Ankle - S1
What is the common cause of spinal cord disease in 16-30 yo.?
Likely trauma of C4/5 or C5/6
What is the common cause of spinal cord disease in 30-50 yo.?
Likely disc disease of C5/6 or L4/5 or L5/S1
What is the common cause of spinal cord disease in 40+ yo.?
Likely malignancy
What are the potential causes of spinal cord problems?
Trauma Iatrogenic Osteoporosis Corticosteroid use Osteomalacia Osteomyelitis Tumour infiltration Disc herniation Infection
How do spinal cord problems present?
Back pain Numbness and paraesthesia Weakness and paralysis Bladder and bowel dysfunction Hyper-reflexia Spinal shock Neurogenic shock
What happens in spinal shock?
Loss of reflexes, tone and motor function
What happens in neurogenic shock?
Following cervical or high thoracic injury
Bradycardia, hypotension, warm dry extremities, peripheral vasodilation, venous pooling, priapism, low cardiac output
When should a CT C Spine <1hr be considered?
GCS < 13 Intubated >65yo High impact injury Focal neurological deficit Paraesthesia of UL or LL
How is Spinal cord compression managed?
Immobilise C spine - collar and backboard
Intubate if above C5
Decompressive surgery
Supportive management - VTE prophylaxis, maintain vitals, nutrition, catheter, laxatives, pressure sore prevention
If malignancy - palliative
Abscess - IV Vancomycin, metronidazole and cefotaxime + surgery
What are the ascending tracts?
Take sensory information from the body to the brain
Dorsal columns - posterior spinal cord - fine touch, vibration, proprioception
Decussate at the medulla
Spinothalamic tracts - anterior part of spinal cord - pain and temperature
Decussate immediately, ascend contralaterally
What are the descending tracts?
Motor information from UMNs to muscles
Pyramidal - conscious control, extrapyramidal - unconscious, reflexive
Pyramidal - corticospinal tract and corticobulbar tract
Extrapyramidal - reticulospinal, vestibulospinal, rubrospinal and tectospinal
All originate in the brainstem, carry motor fibres for unconscious responsive movements.
What is the corticospinal tract?
Communicates with primary motor cortex, premotor cortex, supplementary motor cortex
Converges in internal capsule, then divides into lateral and anterior tracts
Lateral decussates in medulla, anterior ipsilateral
What is the corticobulbar tracts?
From primary motor cortex and terminate in the brainstem at the motor nuclei
Then synapse onto cranial nerve motor nuclei - LMNs to supply the head and neck
What are the signs of UMN lesions?
Hypertonia Spastic Fasciculations absent Minimal atrophy Exaggerated reflexes/clonus Babinski's sign present
What are the signs of LMN lesions?
Hypotonia Flaccid Fasciculations present Marked atrophy Diminished reflexes Absent Babinski's
What is the pathophysiology behind the difference in UMN and LMN damage?
Impaired ability for motor neurones to regulate descending signals, so gives disordered spinal reflexes.
Corticospinal tract can help in conscious inhibition - if sever UMNs, there is loss of inhibitory tone of muscles
No LMN inhibition leads to LMN activation and constant contraction of muscles, sensory info not received so body thinks we are not compensating. No UMN to inhibit LMN anymore - lots of firing.
Initial flaccid paralysis then hypertonia, hypereflexia.
If LMNs damaged or lost, nothing to tell muscles to contract, so hypotonia and flaccid paralysis.
How do UMN and LMN lesions differ in the face?
Upper half of the face receives bilateral cortical supply, so UMN damage forehead is spared
Lower half receives contralateral cortical supply
What is decerebrate and decorticate posturing?
Decerebrate posturing - upper limb extension, a lesion below the red nucleus prevents the red nucleus from activating upper limb flexors
Decorticate posturing - upper limb flexion - a lesion above the red nucleus prevents inhibition of the red nucleus so there is flexion of the upper limb
What is the red nucleus?
In the rostral midbrain involved in motor coordination
Pale pink due to iron - Hb and ferritin