Spinal Cord: Cauda Equina, Cervical Spine Injuries, Brown Sequard, Anterior/Post/Central, B12/VitE deficiency, ALS, MS Flashcards
Cauda equina
-presentation
-pathophysiology, most common causes
-investigations, management
Low back pain
Bilateral sciatica => shooting pains down both legs
Saddle anaesthesia, reduced sensation when wiping
Low anal tone
Urinary/bowel incontinence, reduced awareness of filling
LMN signs
Compression of LS nerve under L2
-L4-5, L5/S1, disc prolapse
Tumour, trauma, infection, hematoma
Urgent MRI to exclude CES
-Bloods - underlying infection, inflammation, malignancy
-LP - infection of tumour in vertebral canal
Surgical decompression
+dexmeth if tumour related
Epidemiology of spinal trauma
More common in men
Age peaks in 20s
Majority are cervical
Vertebral anatomy
-no of CTLS vertebrae
-SC end
C1-7
T1-12
L1-5
S1-4
Nerve roots go above the vertebrae until C8
Then go under
SC ends between L1-2 in adults, L3 in children
CS tract
-functions
-decussation
-location in cord
-consequences of injury
Motor
BS/medulla
Posterolateral to dorsal horn
Ipsilateral motor loss
ST tract
-functions
-decussation
-location in cord
-consequences of injury
Pain, temperature
On entry into cord
Anterolateral to ventral horn
Contralateral pain, temperature loss
Dorsal columns
-functions
-decussation
-location in cord
-consequences of injury
Vibration, proprioception
BS/medulla
Posterior
Ipsilateral loss of vibration, proprioception
Describe the presentation of primary spinal cord injuries
Central cord - CST damaged
-can walk into the pub, cannot pick up a drink (bilateral upper M, S loss)
-hyperextension injury
Anterior cord - ST, CST damage
-loss of ipsilateral CS below lesion
-loss of contralateral ST below injury
-dorsal preserved
-flexion/vascular injury
Brown Sequard - hemisection damage
-ipsilateral CS, dorsal loss
-contralateral ST loss
-penetrating trauma
Types of spinal cord injury and their properties
-primary
-secondary
Primary - immediate effect
-compression, penetrating trauma => SC looks normal immediately after
-unavoidable damage
Secondary - minutes => hours
-ischemia, hypoxia, inflammation
-progressive neuro deterioration
-preventable
Neurogenic shock vs spinal shock
-pathophysiology
-BP, HR
-Motor effects
Neurogenic - disruption of ANS pathway => loss of SNS, vasomotor tone
-systemic low BP, HR, => resp insufficiency
-warm, flushed skin
Spinal - temporary unresponsive peripheral neurons
-flaccid paralysis
-no reflexes, sensory, motor function
Possible cervical spine fractures
C1 - Jefferson fracture
Axial loading into lateral masses
C2 - Odontoid process fracture
-common in elderly, low impact injury => neck pain, severe head/SC instability
Hangman fracture
-cervical hyperextension => pars interarticularis fracture
Possible thoracic spine injuries
-most common causes
-location of fracture
-mechanism of injury
Most common cause
-osteoporosis
-trauma
Location
-Anterior column = ALL - central body
-Middle column = central body - PLL
-Posterior column = PLL - SL, LL
Wedge - compression of anterior vertebral body
-Burst - compression from above
-Dislocation - part of spinal column breaks away
-Seatbelt - forceful flexion
Subacute combined degeneration of the spinal cord
-cause
-tract affected and presentation
Cause
-VitB12, E deficiency
CS - bilateral spastic
ST - bilateral pain, temp loss
Dorsal - bilateral fine, vibration loss
MS
-epidemiology, risk factors
-types
-presentation
-pathophysiology
Women 20-40s
Low VitD, smoking, early life obesity
Relapsing remitting - most common
-1-2 month attack
Primary progressive - progressive deterioration from onset
Secondary progressive - RR => deteriorate
Motor, sensory, cerebellar symptoms that relapse and remit
-asymmetrical
-Urthoffs, Lhermitte
-optic neuritis, trigeminal neuralgia
-autonomic - urinary incontinence, sexual dysfunction
-DANISH
Pathophysiology - chronic cell mediated AI => demyelination of CNS
MS
-investigations, diagnosis
-management
Diagnosis made on
- 2+ relapses AND 2+ lesions OR
- 1 lesion + evidence of past relapse
MRI - high signal T2 lesion on brain and spine
-periventricular plaque
-Dawson’s fingers - hyper intense lesions perpendicular to corpus callosum
CSF - oligoclonal bands in CSF and not in serum
-increased intrathecal IgG synthesis
Management - lifestyle
-exercise
-reduce smoking
-healthy diet
Relapse - dev of new symptoms/worsening of existing symptoms for 24hrs+ in absence of other causes after a stable period of 1 month min
METHYLPRED
-mild - PO
-severe - IV
Maintenance - DMARDS
Cognition - OT, neuropsych assessment
Emotional lability, pain - amitryptiline
Mobility, fatigue - exercise program
Spasticity - baclofen/gabapentin
ALS
-presentation
Spectrum of UMN, LMN involvement => gradual loss of motor function which will eventually affect swallowing, breathing
UMN
-spasticity, hyperreflexia, Babinski, weakness
LMN
-atrophy, fasciculations (hyperexcitability of compensating motor neurones), areflexia, weakness
Thenar, 1st dorsal web, Tibialis ant, tongue atrophy
-initially asymmetrical
-speech slurring, clumsy hands, trips
-labile emotions, weight loss
