Nerve injury and repair Flashcards
prognosis of recovery
2 factors
- violence of the injury - mechanism of injury
- interval between injury and repair
- age (most important)
- comorbidities (DM and renal disease)
urgent repair is best for the outcome of a nerve injury
no repair of nerves immediately when
- general bad condition of the patient
- bad skills of the operating team
- bad equipment
- viability or state of the nerve trunks
- risk for local or systemic sepsis
- condition of the nerve is earlier restored with a musculotendinous transfer
motor unit
multiple muscle fibers may be innervated by a single axon (100-2000)
innervation ratio = muscle fibers / axons
receptors in skin
adaptation rapid speed slow
small Meissner (touch) Merkel (pressure)
(shallow)
large Pacinian (vibration) Ruffini (streching)
(deep)
also in the dermis - Nociceptors and Thermoreceptors
pain describtion
dysesthesia:
when touching is painful
hyperalgesia:
when threshold to pain appears lowered
hyperpathia:
when treshold or pain is elevated, but once reached, the painful stimulus is excessively felt
lightining pain:
sudden severe shooting pain
causalgia:
spontaneous burning sensation in the distribution of the injured nere
types of nerve fibers
large fibers myelinated:
motor, light touch, 2-PD, vibration sense
small fibers are not myelinated:
joint position perceptioin (proprioception), temperature perception, pain perception
Type Type caliber NLG e.g.
(Erlanger/ (Loyd/ mikrometer m/s
Gasser) Hunt)
A-alpha I 15 100 EF: muscles
AF: tendon/
muscle spindle
A-beta II 8 60 AF: touch
A-gamma 5 30 EF: muscle sp
A-delta III 3 20 AF: temp pain
B III 3 10 preganlionic
vegetative fib
C IV 1 1 postganglionic
veg EF, visceral pain
pathophysiology of nerve injury
seddon classification
conduction block - neuroproxia
lesion in continuity - axonotmesis
complete division - neurotmesis
sunderland classification
expanded for axonotmesis - which part is transected (II - IV - endoneurium, perineurium and epineurium is intact)
sunderland’s classification directly correlates with the histologic findings
- injured nerve undergo morphological changes decribed by August Waller - called Wallerian degeneration of the nerve
- begins 24 to 48h after the injury - distinctive loss of fascicular elements are lossed with a microscope
- process (degradation of axoplasm and axolemma) is fascilitated by a calcium influx accompanied by proteases at the time of the injury
- Myelin is phagocytosed
- distal Schwann cell’s de-differentiate into Büngner’s bands that align along the basal lamina - scaffold for regeneration
- bands span the gap between the injured nerve ends to help organize the reperative response and outgrowth of the healthy end
- this response is further mediated by a host of inflammatory cytokines which recruit macrophages to the site of the injury
- common neutrophic factors include nerve growth factor (neurotropin 3-5, epidermal growth factors, insulin-like growth factors I and II, glial-derived neurotropic factor and brain-derived neurotropic factors) - advancement of the growing cone
- neurotropism describes the ability of the regenerating growth cone to preferentially select its correct destination (motor Schwann cell tubes for motor fascicles and sensory tubes for sensory fascicles)
- axon sprouding for regeneration - maybe multiple sprouding
- collateral sprouds outside the basal lamina
- terminal sprouds inside the basal lamina
- a growth core occur with green staining for growing axons (Filopodia and Lamellopodia)
Wallerian degeneration needs about 2-3 weeks to occur in EMG
- Sunderland I and II
recover without surgical intervention
- Sunderland III
variable spontaneous recovery
- Sunderlang IV and V
needs surgery
clinic evaluation
sensory evaluation:
2-PD is standard
Monofilament testing is good for recovery observation and in comparison to the not injured side
Electrodiagnostic testing:
nerve conduction studies - NCS
electromyography - EMG
usually tested 3 weeks after injury, can distinguish between
- neuropraxia
- nerve and axon transection
- neuropathy secondary to systemic illness or compression
latency time: from stimulus to recording site
- measures fastest fibers
- slowing: demyelination or neuropathy
- amplitude: number of units detected (comparison to other side)
- amplitude decreased: decreased numbers conducting fibers
EMG
- low or high amplitudes
- insertional activity, fibrilliations, increased spontaneous activity as a sign for axonal injury
- detectable: 1 week to 1 year post-injury
- cave: Demyelination with intact axons does nto usually result in findings
- regeneration: long duration, small amplitudes, polyphasic motor unit potentials
- acute degeneration
- fibrilliation potentials and positive sharp waves (positive waves in EMG goes down!!!)
treatment of nerve injuries
acute:
with sharp penetrating injuries
6-12 weeks:
traction and crushing injuries (serial exams and NCS/EMG)
- primary: 1-3 weeks
- secondary: all others
cave: published data does not always clear benefits from directly repair
reasons for secondary repair
- delay for self clearence and maybe spontaneous recovery
- timing of repair is related to the ability to find the extend irrecoverably damaged nerve tissue
orietation in epineural repair:
- blood vessels in the nerve
- fascicles
- repair <72hours of injury - stimulation of distal motor vibers wil produce muscle contraction (muscle endplates go down over 6-7 days)
- stains: acetylcholine esteras - motor neuron, carbonic anhydrase - sensory axons
autografting:
- gold standard for large defects - results are not gold (10cm or greater)
- greater defects may need a vascularized nerve (15cm or greater)
- grafts: sural nerve (most common), medial / lateral cutaneous antebrachii, PIN
allograft:
- processed, acellular - act as scaffold
- Schwann Cells grow in, but isograft better because of an endoneurinal architecture
- outcome near normal 2PD with most digital nerves with gaps <3cm or less, cave of other conditions!!!
- non-processed allograft requires immunosuppression
conduits:
- 15mm gaps in digital nerves
- always less than 3cm
- > than 3cm autograft from the leg
remark:
- nerve tubes degrade by plasmins and proteases
- gap size not greater than 3cm
- the longer the tube is, the more “hourglassing” occurs which is bad for contact of the sprouding nerve and regeneration
nerve specific generalizations
Radial > median > ulnar
C5/6 > C8/TH1
upper trunk > lower trunk
tibial > peroneal
1 Coaptation > 2 coaptations
2 Coaptations > 1 coaptations with tension
specific problems of degeneration and regeneration
long time: loss of Schwann cells and trophic support over time
sensory:
loss of sensitivity, hyperesthesias from neuroma
loss of ability to reinnervate about 5 years
motor:
atrophy - loss af ability to reinnervate about 1,5-2 years
specific problems of reinnervation
- end organ degeneration - no function
- incorrect receptor maybe innervated - changing of brain mapping is necessary
- receptor in wrong location - changing of brain mapping
- axon continutiy can not maintain the effector - sensory nerve to a muscle or vice versa - effector not supported
nerve transfers
used for defects that can be reinnervated faster with transfer than with graft or direct repair because of the long distance of nerve growth
for each coaptation is a loss of 10-15% of neurons - good surgical technique is acquired not to use grafts
indications:
recipient:
still viable
time of surgery (3-6 month)
EMG characteristics
intact neuromuscular junction
less muscle degeneration (3-12 month)
fibrilliation and sharp waves (reinnervation possible)
donor:
healthy
robust (axon count minimum 30% of the recipient)
expandable nerve
if possible synergistic - better for relearning of the brain
most common transfers:
- spinal accessory nerve to supraclavicular nerve (to musculocutaneus or axillary nerve is possible)
- Leechavengvong (Somsak) - nerve to long head of triceps to the anterior branch of the axillary nerve
- oberlin (single or double) ulnar - muculocutaneus nerve (motor branch of biceps maybe in combination of the median nerve to the motor branch of the brachialis)
- AIN to distal ulnar motor (end to end) best recovery for the intrinsic muscles
upcoming transfers:
- supinator to PIN
- median to radial (FCR branch to PIN, FDS branch 1 to ECRB)
- brachialis to AIN
- ADM to APB
- “supercharge” - AIN/PQ to ulnar motor reversed end to side
- sensory transfers (intercostal)
radial nerve palsy
often limited by gap length
nerve transfer great for the right patient at the right time
(in comparison tendon transfer is the most common treatment - 5:1, high reliable, time-intensive, no independent finger extension)
