peripheral nerve injuries Flashcards
transient ischaemia
=’mini stroke’. where the blood supply to your brain is temporarily disrupted
15 mins numbness and tingling
30 mins Loss of pain sensibility
45 mins Muscle weakness
aetiology–> brief blood clot blockage in brain. could also be a blockage in artery to heart
clinical presentation–> Weakness, numbness or paralysis in the face, arm or leg, typically on one side of the body, Slurred or garbled speech or difficulty understanding others, Blindness in one or both eyes or double vision, Vertigo or loss of balance or coordination
findings–> pysical exams and tests- vision, eye movements, speech and language, strength, reflexes, and sensory system. Carotid ultrasonography- narrowing or clotting in the carotid arteries, Computerized tomography (CT) or computerized tomography angiography (CTA) scanning- evaluate blood vessels in the neck and head. MRI- evaluate the arteries in the neck and brain. Echocardiography- difficult to find blood clots. Arteriography- gives a view of arteries in the brain not normally seen in X-ray imaging
pathophysiology–> Thecommon issue is the transient interruption of arterial blood flow to an area of the brain supplied by that particular artery.
management–> medications (anti-platelet drugs, Anticoagulants). surgery- carotid endarterectomy. Angioplasty- stenting
neuropraxia
=injury to peripheral nerves. demyelination
Reversible physiological nerve conduction block. Spontaneous recovery after a few days or weeks
aetiology–> bone fractures, dislocation, Tears and injuries to ligaments and tendons, after surgery, giving birth, dental work. May be due to mechanical compression which causes segmental demyelination
clinical presentation–> burning, numbness, stinging, weakness
types–> axillary neuropraxia, brachial plexus neuropraxia, radial nerve neuropraxia, Sural nerve neuropraxia
findings–> nerve conduction tests. MRI to rule out other conditions
pathophysiology–>the conduction of nerve impulses is blocked in the injured area. Motor and sensory conduction are partially or entirely lost
management–> splints and limb supports, physical rehabilitation, avoidance of the aggravating activity, and neuropathic pain medications (analgesics, antidepressants, anticonvulsants, corticosteroids, anesthetics)
Axonotemesis
=More severe form of nerve injury seen in closed fractures, dislocations, obstetric palsies, HNPs. emyelination and axon block
Loss of conduction but nerve is in continuity and neural tubes are intact. Axonal regeneration starts within hours of nerve damage via neurotrophic factors. distal end will undergo wallerian degeneration
aetiology–> penetrating injuries (crash), pulling forces and injection of toxic substances
clinical presentation–>burning, numbness, loss of feeling, tingling
pathophysiology–> stretching can result in patchy ischemia with decreased vasa nervorum flow. As stretching progresses, necrosis, intraneural connective tissue destruction, and hemorrhage are likely. Disruption of trophic factor transportation, increased intracellular calcium, and degradation of cytoskeletal elements proceeds. The Schwann cell phenotype switches to a phagocytic state with the recruitment of macrophages. Once myelin is cleared by phagocytosis, Schwann cells encompass the endoneurium to create the nerve conduit known as bands ofBüngner
management–> surgery- primary repair, secondary repair, (internal or external) neurolysis, nerve graft, and nerve transfer (repair types). physical therapy
nerves
Brain and spinal cord=CNS
Section of spinal cord:
Dorsal side of spinal cord (back)
Ventral side of spinal cord (front)
Dorsal roots and ventral roots—>clusters of neurons that connect to form a spinal nerve
A nerve is not one neuron but many all packaged together
Spinal nerves are part of peripheral nervous system
Surrounding the nerves are sheaths(epineurium)
Lots of neurons=fasicle—> surrounded by another sheath (perineurium)
In each fasicle there are neurons—> can be unmyelinated or myelinated with Schwaan cells
Around these myelinated neurons there’s another sheath called endoneurium
Typical motor neuron:
Dendrites, soma, axon, schwaan cells (myelinated), terminal bulbs
Nerve injuries-
CNS:
Most CNS fibers do not regenerate
1-clean up is slow
2- oligodendrocytes inhibit regeneration
3- environment is not optimal
PNS:
Can regenerate
1-clean up of damaged parts of cell faster
2-schwaan cells assist in regeneration process
3- time is of the essence
If cell body (soma) is damaged the cell cannot regenerate
If axon or terminal is damaged then it can regenerate (1mm/day)
neurotmesis
=nerve severence
demyelination and axon loss plus one of the following: damage of a-endoneurium—> fair growth. b- perineurium —> poor growth. c- epineurium—> no growth
aetiology–> serious injury with forceful impact and, in a lot of instances, a laceration that cuts through the nerve
clinical presentation–> pain, uncomfortable sensations, complete loss of sensory and motor function of the affected nerve
findings–> EMG- will show no motor unit action potentials (MUAPs) under voluntary control, but fibrillations are not present. MRI- assess peripheral nerve injury. It can display the morphologic changes of nerves and provide quantitative indexes to monitor nerve degeneration and regeneration dynamically. ultrasound- Differentiation of neurapraxia or axonotmesis from neurotmesis is done byobserving nerve continuity and the demonstration of proximal and distal nerve stumps
pathophysiology–> transection of a nerve and is the worst degree of peripheral nerve injury. In neurotmesis, the entire nerve, including the endoneurium, perineurium, and epineurium, is completely severed. Neurotmesis leads to the rupture of the axon, myelin sheath, and connective tissues
management–> repair- allow reinnervation of the target organs by guiding regenerating sensory, motor, and autonomic axons into the environment of the distal nerve with minimal loss of fibers at the suture line. For optimal nerve regeneration, nerve stumps must be precisely aligned without tension and repaired atraumatically with minimal tissue damage and a minimal number of sutures
double crush phenomenon
=proposed that if a nerve is
impaired at one location it
makes that patient more
susceptible to other
entrapments along the same
neuraxis
wallarian degeneration
results when a nerve
fiber is cut or crushed,
in which the part of
the axon separated
from the neuron’s cell
body degenerates
distal to the injury
brachial plexus injury
aetiology–> traction and stabbing. Not commonly injured by clavicular fractures
clinical features–> depends on severity and location. less severe- burning sensation radiating down one arm, numbness and weakness in arm. should only be brief but may last a few days. more severe- weakness/ inability to use certain muscles in hand, arm or shoulder, complete lack of movement and feeling in arm, hand and shoulder, severe pain
findings–> EMG- valuates the electrical activity of the muscles when they contract and when they’re at rest. nerve conduction studies- measure the speed of conduction in the nerve when a small current passes through the nerve. MRI- show the extent of the damage caused by a brachial plexus injury and can help assess the status of arteries that are important for the limb or for its reconstruction. CT scan–> detailed picture of the spinal cord and nerve roots
pathophysiology–>Injuries that occur proximal to the dorsal root ganglion are appropriately termed “preganglionic,” while injuries distal to the dorsal root ganglion are termed “postganglionic.”
management–> physical therapy. surgery- Neurolysis, Nerve graft, Nerve transfer, Muscle transfer. pain medications
Obstetric Brachial Plexopathy
=injury to the brachial plexus that occurs during birth usually as a result of a stretching injury from a difficult vaginal delivery
2 patterns:
1.erbs palsy (difficult birth/ baby position)
2.Klumpkes palsy (difficult birth- neuropraxia or scarring)
erbs palsy
aetiology–> Difficult birth – baby position
paralysis can be partial or complete; the damage to each nerve can range from bruising to tearing
most commonly involved root is C5 (akaErb’s point: the union of C5 & C6 roots)
most commonly involved nerves are thesuprascapular nerve,musculocutaneous nerve, and theaxillary nerve
clinical presentation–> Loss of sensation in the arm and paralysis and atrophy of the deltoid, biceps, and brachialis muscles
stunted growth in the affected arm
impaired muscular, nervous and circulatory development.
management–> Neonatal / pediatric neurosurgery
Nerve transplants, Sub Scapularis releases and Latissimus Dorsi Tendon Transfers.
Physical therapy focusing on the regaining of affected muscles
klumpkes palsy
=Lower plexus lesion C8-T1
clinical presentation–> usually arm presentation with subsequent traction/abduction from trunk
findings–> Physical exam -deficit of all of the small muscles of the hand (ulnar and median nerves)
“claw hand”
frequently associated with a preganglion injury and Horner’s Syndrome
long thoracic nerve injury
originates from the C5–C7 roots and descends in the axilla, posterior to the brachial plexus, to innervate the serratus anterior muscle
aetiology–> shoulder and neck injuries. could occur during surgery
clinical presentation–> shoulder pain, winged scapula, reduced overhead activity
pathophysiology–> axonotemesis
management–> surgery- Scapulothoracic fusion (fusion of the medial border of the scapula to the underlying 3 to 5 ribs)
spinal accessory nerve injury
located in the lateral aspect of the anterior horn of the spinal cord. innervates both the trapezius and the sternocleidomastoid muscles
aetiology–> superficial nerve so easily damaged. trauma or surgery
clinical presentation–> pain, asymmetry in shoulder, weak abduction
pathophysiology–> Axonal injury is typically followed by Wallerian degeneration. one of the small branches of the accessory nerve innervating the upper trapezius muscle may be damaged if it is not identified clearly during a neck dissection surgery. Stretchon theaccessory nerveimpairsintraneural microvascular flow,causing ischemia andsubsequently axonal rupture and degeneration.
management–>physical therapy
suprascapular nerve injury
It arises from the upper portion of the brachial plexus. Its motor innervation is to the supraspinatus and infraspinatus muscles
aetiology–> Injured in clavicular or scapular fractures
clinical presentation–> Benign etiology /pain syndrome possible. Shoulder weakness (Abd/ext rot). May masquerade as rot cuff disease or cervical spondylosis
pathophysiology–> repetitive overhead activity, rotator cuff pathology, and compression of the nerve at either the suprascapular or the spinoglenoid notch secondary to space-occupying lesions
management–> rehabilitation programs, nonsteroidal anti-inflammatory drugs, and lifestyle modification. physical therapy to strengthen surrounding muscles
axillary nerve injury
originates from the brachial plexus at the level of the axilla (armpit) and carries nerve fibers from C5 and C6
aetiology–> dislocation of shoulder
clinical presentation–> shoulder/ arm weakness, shoulder/ arm wasting (deltoid), tingling, numbness, abduction maintained by supraspinatus, retropulsion impossible (going posteriorly)
pathophysiology–> Propagated tension due to overstretching of the axillary nerve over the humeral head during shoulder dislocations may cause elongation of the free portion of the axillary nerve and the increased tension may even result in axillary nerve avulsions from the posterior cord of brachial plexus
management–> anti inflammatory medicines, surgery to release
