W09 - GROWTH, INJURY, REPAIR X2 Flashcards
ANTERIOR and DORSAL roots
MOTOR NERVE FIBRES = ANTERIOR/VENTRAL
SENSORY NERVE FIBRES. POSTERIOR/DORSAL
Motor efferent unit
Found in ANTERIOR HORN CELL (grey matter)
Sensory unit
Cell bodies in POSTERIOR ROOT GANGLIA outside the SCord
Structural makeup of the nerve
AXONS (endoneurium) > FASCICLES (perineurium) > NERVE (epineurium)
Fiber types
Aa (largest) = muscle stretch and tension
Aß = touch pressure vibration proprio
Aγ = efferent motor
Aδ = sharp pain, light touch, temp
B = symp pre-gang motor
C = dull aching burning pain and temp
Axonotmesis
The axons and their myelin sheath are damaged in this kind of injury, but the endoneurium, perineurium and epineurium remain intact.
*followed by WALLERIAN DEGENERATION
neurotmesis
complete transection of a peripheral nerve
*no recovery unlessrepaired by SUTURING or GRAFTING
* miswiring risk during regeneration
= poor prognosis
Neurapraxia
Blockage of conduction = slight loss
*reversible
Classic Conditions of Compression
CARPAL TUNNEL SYNDROME = median nerve at wrist
SCIATICA = spinal root by IV disc
MORTON’S NEUROMA = DIGITAL NERVE IN 2ND OR 3RD WEB SPACE OF FOREFOOT)
Direct nerve injury
Blow laceration = resection
Indirect nerve injury
Avulsion, traction
Closed and Open Neve Injuries
CLOSED
- nerve injuries in continuity (epineurium preservation)
- recovery or sx after 3mos
- nil recovery = electromygraphy
•typical stretching of nerve
OPEN
- nerve division = neurotmetic injuries
- early sx
- wallerian degeneration
Clinical features of Nerve Injury
-DYSAETHESIAE
- PARESIS
+paralysis
+ dry skin (nil stim of sweat glands) - Diminished/absent reflexes
Healing of Nerve Injury
Axonal death distally > then to site
Proximal axon budding
- pain to return first
- Tinel’s sign = tap over site of nerve and paraesthesia will be felt as far distally as regeneration has progressed
Rule of 3
Immediate surgery within 3 days for clean and sharp injuries
Early surgery within 3 weeks for blunt/contusion injuries
Delayed surgery, performed 3 months after injury, for closed injuries.
UMN Lesion Findings
⇩strength
⇧tone, deep tendon reflexes
+Babinski’s sign, Cnus
LMN Lesion Findings
⇩strenght, tone, reflexes
nil Clonus, Babinski’s Sign
+ATROPHY
Cortical V Cancellous (Trabecular) Bone
CORTICAL = lamellae, concentric, outer layer
* resists BENDING, TORSION
CANCELLOUS = metaphysis, sute of physis
* resists COMPRESSION
Stages of Bone Fracture
(1) INFLAMMATION: immediate
* mediators are released = attract repair cells
* angiogen.
> NSAIDs can reduce ability to repair
Loss of haematoma as aprt of Hx reduce biological drive to repair
Replacing platelet concentrates to promote repair drive
(2) SOFT CALLUS, collagen matrix being laid down
* end-point = fragments united by cartilage/fibrous tissue
> Demineral. Bone Matrix can replace cartilage
Replace bone to skip this step via bone graft
(3) HARD CALLUS = convt to woven bone
limit movement, endochrondral bone form.
(4) BONE REMODELLING = conv to lamellar bone, medullary canal reconstituted
Significance of Autogenous Cancellous Bone Graft
GOLD STANDARD OF BONE GRAFT
Allograft Bone
Allograft bone (bone banks) osteoconductive but not osteoinductive *mechanism of substitution rather than synthesis
Delayed Union
failure to heal in expected time d/t disruption to repair
- distraction, instability
- infection
- steorids
- smoking
- warfarin, NSAID, ciproflox.
(non-union where bone fails to heal)
Ligament v Tendon
Ligaments = ⇩%collagen, ⇧proteoglycans and water, less organised collagen fibres, rounder fibroblasts
Collagen fibre (type 1)
Damage to Ligaments
When forces exceed strength ligament,
