DAX KEVIN REY S.

GO
PERIPHERAL NERVE INJURIES
Definition
• Any disorder involving either axon or myelin sheath of the peripheral nervous
system
• Injuries of the nerves supplying the upper and lower extremities
• Nerve injury – damage or severance of some or all of the conducting fibers within
a nerve as a result of trauma
• Neuropathy – umbrella term, disease, inflammation or damage to peripheral
nerves
Epidemiology
• Males > females it is thought because males are more adventurous than females
• Elderly
• During pregnancy
• Desk jobs
Etiology
• Traumatic – laceration, contusion, traction, compression, iatrogenic
• Non-traumatic
Pathophysiology
Most causes of neuropathy are divided into two types: segmental demyelination and
degeneration. These are based on whether the initial insult to the nerve is to the myelin or to the
axon. Localized nerve injuries are classified according to the nature of the injury and whether it
was produced by compression or trauma.
Demyelination - the myelin is degenerating
Degeneration - axon itself is degenerating
It can be primary demyelination or a primary axonal degeneration, both may be present but one
is primary.
1. Segmental Demyelination − Neuropathies initially produced by injury to the myelin
covering the nerve are often called Gombault demyelination or simply segmental
demyelination
• What happens in demyelination is degeneration of the myelin sheath that
covers the nerve
1. Axonal Degeneration − Nerve injury to the axon only secondarily affects the myelin
coating. Axonal degeneration is caused primarily by toxins such as alcohol,
vincristine, arsenic and thallium. Since the myelin coating of the nerve tends to
remain intact, its nerve conduction will be close to normal if the axon is still capable
of function. Therefore, additional clinical and electrodiagnostic techniques must be
used in evaluation.
• Primary axonal degeneration = Axon degenerates and the myelin sheath
may also demyelinate secondarily.
• Later on, the axon will continue to degenerate until it can no longer function
to transmit nervous signals, so it can also affect the muscles and the
sensory nerve endings.
1. Wallerian Degeneration
• Breakdown of axons and sometimes involves the myelin sheath
1. Breaking up of the axons
2. Degeneration of the nerve occurs if the axon is injured by the neurotmesis
or with axonotmesis. It takes place below the site of the lesion and
sometimes above it as far as the first Node of Ranvier
• Nodes of Ranvier are junctions between myelin sheath in which the
action potential will jump that makes the action potential conduct
faster as compared to axons without a myelin sheath that is
because of the Nodes of Ranvier
1. Degeneration is usually completed in 2 weeks and the electromyogram will
then show fibrillation potential
• Example there is neurotmesis or axonotmesis then wallerian
degeneration is possible, in which the axon and possibly the myelin
sheath will continue to degenerate in the site distal to the injury in 2
weeks and in EMG it will show fibrillation potentials as a sign of
denervation and because the peripheral nervous system has the
capacity to heal, the peripheral nerves as well as its myelin will also
attempt to heal → (letter d)
1. The fibrillary process of axon penetrates the fibrin and connective tissue in
scar and enters the distal end of nerve
• This healing may also go anomalous, anomalous healing = aberrant
regeneration
 • Aberrant regeneration is when nerve fibers will heal and will attach
to another or adjacent nerve fiber. It is an unwanted healing and it
can result in synkinesis which is movement of one muscle may also
result in the movement of another muscle which is unwanted.
1. In healing, rate of growth of axons: 4-5 mm a day in favorable conditions
2. Average: 3 mm/day after injury
3. 2 mm regeneration a day after suture
4. Tinel’s sign of a painful response on percussion of the nerve trunk distal to
the injury is useful to determine rate of growth
Type of Neuropathy
1. Demyelination – occurs when the myelin sheath is disrupted
2. Axonopathy – can be caused by toxic or metabolic derangements, trauma, compression,
traction or transection leading to conduction block or decreased NCV (nerve conduction velocity)
because it involves the axon
• In the diagram below, as seen in primary demyelination the axon is still intact,
however, the myelin sheath is degenerating. But it doesn't mean that in primary
demyelination, there is no axonal degeneration, there can be a secondary axonal
degeneration (2nd broken circle on the diagram labeled as primary demyelination).
• And in primary axonal degeneration, there can also be secondary demyelination
• In primary axonal degeneration, the axon is breaking down and the myelin sheath
is intact. There can still be secondary demyelination. That explains in multiple
sclerosis, it's not just the myelination in the disease, but later on during the disease
it also affects the axon.

CLASSIFICATION OF NERVE INJURIES

2 classifications:
1. Seddon's classification - 3 sub types
2. Sunderland's classification
Seddon’s Classification
• Neuropraxia
• Segmental demyelination, axon is intact as well as its protective coverings
• Action potential is slowed or blocked at point of demyelination; normal
above and below point of compression
• Muscle does not atrophy; temporary sensory symptoms
• Good example is ¨binhod¨ or numbness, especially when we sleep
in an improper position that can compress our nerves
• (-) Wallerian degeneration
• Cause: mild ischemia from nerve compression or traction
• Recovery is usually complete
Pacaldo 11-20
• Axonotmesis it is now the axon that is affected
• Loss of axonal continuity but connective tissue coverings remain
intact (peripheral nerves are covered by 3 layers, epineurium, perineurium
and endoneurium, these are the connective tissue coverings)
• (+) Wallerian degeneration distal to lesion
• Muscle fiber atrophy and sensory loss
• Cause: prolonged compression or stretch causing infarction and
necrosis (there will be no more blood supply to the axon that is why there
is axonal degeneration, but the protective coverings and the myelin remain
intact)
• Recovery is incomplete; surgical intervention may be required.
• Neurotmesis (most severe out of the 3)
• Complete severance of nerve fiber with disruption of connective tissue
covering (as well as possibly its myelin sheath, it’s the axon + connective
tissue covering + myelin sheath affected)
• (+) Wallerian degeneration distal to lesion
• Muscle fiber atrophy and sensory loss is highly possible
• Cause: gunshot or stab wounds, avulsion, rupture
• No recovery without surgery; recovery depends on surgical intervention
and correct regrowth of individual nerve fibers in endoneurial tubes.
• Poor prognosis

• In neuropraxia it's just the myelin sheath and there is segmental demyelination but
the axon is intact.
 • In axonotmesis, the axon is now affected but the protective coverings around the
axon is intact and the myelin is possible intact.

• Complete severance of the peripheral nerve or the axon. It affects the axon, the
protective coverings, as well as the myelin sheath.
Sunderland’s Classification (basically similar to Seddon’s classification but expanded
according to the layer of the protective coverings affected)
• Type 1 Injury (Neuropraxia)
• Focal conduction block; primarily motor function and proprioception
affected; some sensation and sympathetic function may be present. i
• Involves segmental demyelination or local myelin injury, primarily large
fibers.
• (-) Wallerian degeneration
• Recovery in weeks to months
• A good example is “binhod”
• Type 2 (Axonotmesis) loss of axonal continuity, there is degeneration of the axon
• Loss of nerve conduction at injury site and distally
• Disruption of axonal continuity with Wallerian degeneration
• But the protective coverings covering the axon are intact: Endoneurial
tubes, perineurium, and epineurium intact
• Damage start inside the axon
• Good prognosis; axonal regeneration required for recovery.
• Type 3 Injury (similar to axonotmesis or type 2 injury, but the difference is that
aside from the axon affected, the endoneurium is also damaged but the
perineurium and epineurium are preserved)
• Loss of nerve conduction at injury site and distally
• Loss of axonal continuity and endoneurial tubes
• Perineurium and epineurium preserved
• Disruption of endoneurial tubes, hemorrhage, and edema produce
scarring; poor prognosis; surgery may be required.
• Type 4 Injury (the same as type 3, the difference is that in type 3 the axon +
endoneurium affected, this time in type 4 it's now the axon + endoneurium +
perineurium affected.)
• Loss of nerve conduction at injury site and distally
• Loss of axonal continuity
• Only epineurium is intact
• Total disorganization of and guiding elements; intraneural scarring (caused
by the repair of the astrocytes around the axons, but with this repair it can
potentially lead to a neuroma formation) and axonal misdirection
• (+) neuroma formation (the peripheral nerve attempts to repair itself but in
the end there is scarring and that scarring can grow large forming a
neuroma which is a benign enlargement of the peripheral nerve)
• Poor prognosis, surgery necessary to correct it.
• Type 5 Injury (Neurotmesis)
• Loss of nerve conduction at injury site and distally
• Complete severance of entire nerve (this is equivalent to neurotmesis in
Seddon’s classification, which means that the axons, all the protective
coverings as well as the myelin sheath are all severed)
• Surgical modification of nerve ends required
• Prognosis guarded and dependant on nature of injury and local factors

CLINICAL MANIFESTATIONS
• Sensory symptoms:
• Paresthesia
• Dysesthesia
• Hyperalgesia
• Hyperpathia
• Allodynia
• Absent sensation
• Flaccid muscle weakness (considering that this is a LMN lesion)
• Autonomic dysfunction
• Orthostatic intolerance
• Cardiac arrhythmias
• Flaccid bladder (if it involves the peripheral nerve supply of the bladder)
• Vomiting
• Constipation
 • Diarrhea
• Sweating abnormalities
• Pain associated with peripheral neuropathy (if this is a general neuropathy of
the body)
• Hyporeflexia and hypotonia
• (+) fasciculation (abnormal muscle movement as a result of denervation that can
be seen in the naked eye) and fibrillation (can only be seen in electromyographic
studies) potentials (signs of LMN lesions)
COMPLICATIONS
• Soft tissue or joint contractures secondary to immobility
• Muscle atrophy secondary to disuse
• Deep vein thrombosis
• Pressure sores secondary to disuse
• Deep vein thrombosis
• Pressure sores secondary to impaired sensation
• Heterotrophic ossification
• Reflex sympathetic dystrophy
• Aberrant regeneration and synkinesis
• Aberrant regeneration - when the nerve fibers heal in a different direction
and connect to an adjacent nerve fiber resulting to synkinesis
• Deformities
Neuropathies of the Upper Extremity
Brachial Plexus Injuries:
Erb-Duchenne Palsy
• C5-C6 affectation (upper plexus)
• Involves compression or tearing of the upper trunk of brachial plexus
• Cause: traction injury (birth); radiation
• If ibira ang baby there will be stretch; common in pedia
• Sensation and motor paralysis on innervation
• Loss of abduction and lateral rotation of shoulder, weak elbow flexion and
supination
• Axillary (ABD and ER) and musculocutaneous (ELB FLEX and SUP) nerve
are affected
• Axillary: deltoids & infraspinatus
• musculocutaneous: for weak elbow flexion & supination
• (+) Waiter’s tip / Porter’s tip / Policeman’s tip deformity
• Can cause ms imbalance for the pt
• SH ADD and IR and elbow EXT is stronger
• Therefore having this deformity below

Klumpke’s Palsy
• C8-T1 affectation (lower plexus)
• Cause: compression by a cervical rib or stretching of the arm overhead
• Sensation and motor paralysis along ulnar nerve distribution (C8-T1), paralysis of
intrinsic muscles of the hand (innervated by ulnar nerve)
• (+) Clawhand deformity
• Horner’s syndrome: ptosis, anhidrosis, miosis

Parsonage-Turner Syndrome
• “Brachial plexus neuritis”
• Idiopathic rapid onset of pain in the shoulder and arm, followed by progressive
weakness and atrophy of muscles supplied by the brachial plexus
• Causes: autoimmune, may be due to viral infection, vaccinations, exposure to
environmental factors
Thoracic Outlet Syndrome
• Compression of nerves and blood vessels in the thoracic outlet
• Due to scalene muscle entrapment or hypertrophy, costoclavicular syndrome, or
coracoid process entrapment, or enlarged first rib
• Manifestations:
• Sharp, stabbing pain along ulnar distribution of the hand and arm
• Affects lower trunk of brachial plexus
• Pain along the side of the neck
• Weakness of intrinsic muscles of the hand
• Tingling and sensory symptoms along the ulnar distribution
• Hand discoloration - blood vessels are compressed
 • Special tests: Military brace, Roos test, adsons maneuver, halsteads
maneuver
Branch Involvement
Dorsal Scapular Nerve Injury
• C5 nerve root
• Rhomboids and levator scapulae weakness
• Weakness of scapular retraction
• (+) posterior winging/tipping of scapula
Long Thoracic Nerve Injury
• C5-C7 nerve root
• Common cause: radical mastectomy - removal of entire breast usually due to
breast cancer
• Serratus anterior weakness - responsible for reinforcement of strength of anterior
scapula
• Weakness of shoulder flexion and abduction, difficulty reaching overhead
• (+) medial winging/open book paralysis - medial side tips backward
Suprascapular Nerve Injury
• C5-C6 nerve root
• Common cause: forceful scapular and shoulder abduction - rare injury
• Supraspinatus and infraspinatus weakness
• Weakness of shoulder abduction and external rotation
• Motor only - No sensory loss, no loss of DTR
Musculocutaneous Nerve Injury
• C5-C6 nerve root
• Common cause: trauma to upper arm
• Weakness of coracobrachialis, biceps, and brachialis
• Weakness of elbow flexion and forearm supination
• Loss of biceps reflex
• Noticeable atrophy of elbow flexors
Axillary Nerve Injury
❑Common cause: anterior shoulder dislocation and fracture of surgical neck of humerus
❑ Deltoids and teres minor weakness, innervated by axillary nerve
❑ Weakness of shoulder abduction beyond 90 degrees
• Responsibility of deltoid is SH abd beyond 0-90
• Supraspinatus 0-90 only
❑ Sensory loss along lateral shoulder

-deltoid atrophy
Radial Nerve Entrapment Syndromes
-can be damaged at several levels
1. At the level of the axilla (highest level)
❑ Crutch palsy – due to fracture or dislocation of upper level of humerus, or compression of
axillary nerves and vessels due to prolonged use of crutches
-collection of nerves and vessels that passes the axilla is affected
❑ All muscles of the radial nerve are paralyzed
-if at this highest level is affected
❑ (+) wrist drop
2. At the level of the spiral groove
❑ “Honeymoon palsy” or “Saturday night palsy”
❑ Most frequent site of radial nerve injury
❑ All muscles of the radial nerve are paralyzed except triceps (spared)
-spared because the branch that innervates the triceps is before the level of the spiral groove
-can still extend elbow
❑ Can also be due to posterior dislocation of elbow or fracture of midshaft of humerus
❑ (+) wrist drop
-because it paralyzes the wrist extensors there will still be a wrist drop
3. At the elbow level
❑ “Posterior interosseous nerve syndrome”, “supinator syndrome”, “Arcade of Frohse syndrome”,
or “radial tunnel syndrome”
❑ Spared muscles: triceps brachii, anconeus, ECRL, brachioradialis
❑ Wrist drop absent due to spared ECRL
4. At the wrist level
❑ “Cheralgia Paresthetica” or “Wartenberg’s disease”
❑ Superficial branch of radial nerve affected
❑ Pure sensory symptoms
❑ Common cause: tight watch/wrist band
Manifestations of Radial Nerve Entrapment
❑ Triceps usually spared
-unless the highest level of axilla is affected
❑ Loss of ability to extend MCP joint, wrist, and thumb (wrist drop)
-unable to extend wrist
❑ Mild weakness of supination
❑ Weak thumb abduction
❑ Weak grip

Ulnar Nerve Entrapment Syndromes

1. At the elbow level (highest level)
❑ Cause: fracture of lateral epicondyle secondary to excess cubitus valgus
❑ All muscles of the ulnar nerve affected
❑ Symptoms most likely appear during elbow flexion
❑ Cubital tunnel syndrome – acute
❑ Tardy ulnar palsy – chronic
❑ (+) Clawhand deformity
❑ (+) guttering between the metacarpals of the dorsal hand
2. At the level of the wrist (Tunnel of Guyon)
❑ “Biker’s palsy” or “Handle bar palsy”
❑ Compression of the ulnar nerve by the pisohamate ligament
❑ Pure sensory loss at little finger and medial half of ring finger
Manifestations of Ulnar Nerve Entrapment
❑ Clawhand – unopposed action of the EDC in the 4th and 5th digit
❑ MCP hyperextended, DIP and PIP flexed
❑ Inability to abduct and adduct fingers due to paralysis of palmar and dorsal interossei
❑ Inability to flex DIP joints due to paralysis of medial half of FDP
❑ Weak thumb opposition (d/t affectation of adductor pollicis)
❑ Loss of opposition and abduction of little finger
❑ Resisted palmar flexion of the wrist results in deviation of the wrist to the radial side due to
paralysis of FCU
❑ Passive Benediction sign – inability to fully open the hand
❑ Loss of sensation on the medial 1 and ½ finger

Median Nerve Entrapment Syndromes

1. At the elbow level (highest level)
❑ “Supracondylar process syndrome”
❑ Compression of the median nerve at the elbow due to hypertrophy of ligament of Struther
❑ All muscles affected starting at the pronator teres and down
❑ Weakness of grip, wrist and hand flexion, and pronation
2. Pronator Teres Syndrome
❑ Compression of the median nerve by the pronator teres
❑ All muscles affected except pronator teres (spared)
-branch of median nerve that innervates the pronator teres is before the level of injury (so PT is
spared)
❑ Weakness of grip, wrist and hand flexion
3. Anterior Interosseous Nerve Syndrome
❑ Superficial branch of the median nerve
❑ Weakness of FPL, 1st and 2nd FDP, and pronator quadratus
❑ Gantzer’s muscle – anomalous accessory long head of the FPL may compress the anterior
interosseous nerve
❑ (+) Kiloh-Nevin sign, (-) OK sign
-tend to do pulp to pulp approximation instead of tip to tip
4. Carpal Tunnel Syndrome (wrist level)
-starts as sensory sx then progresses which can affect the muscles and can potentially cause
atrophy in the thenar eminence muscle which results in ape hand deformity
❑ Compression of median nerve beneath flexor retinaculum
❑ Weakness of APB, FPB, opponens pollicis, lateral ½ of lumbricals in later stages
❑ Paresthesias and tingling along the lateral hand and fingers
Manifestations of Median Nerve Entrapment
❑ Loss of sensation on the lateral 3 and ½ fingers particularly on the tips of the index and middle
fingers
❑ Loss of thumb opposition
❑ Loss of ability to make a fist
❑ Difficulty in prehension, gripping and fine motor activities
❑ Weakness of wrist and hand flexion, pronation
❑ (+) Ape hand/Simian crease deformity
-because of atrophy in the thenar eminence of the hand
-occurs in later stages
❑ Active Benediction sign – inability to make a fist
-because of median nerve entrapment
Note: Passive benediction - ulnar nerve
Active benediction - median nerve

Neuropathies of the Lower Extremity

Obturator Nerve Entrapment
• Common causes: pelvic or hip surgery, pregnancy, fractures
• Often rare, this nerve is responsible for the innervation of the hip adductor muscles.
• Sensory loss on the medial thigh, but not significant
• Weakness of hip adductors
• Difficulty in crossing legs (this is due to the weakness of the hip adductors)
Femoral Nerve Entrapment

• Causes: anterior hip dislocation, femoral fracture, during child delivery

• Weakness of hip flexors and knee extensors (specifically the quadriceps femoris
muscle, hence the loss of the knee jerk reflex)
• Knee jerk reflex is lost
• Loss of sensation in the anterior thigh, pain on medial aspect of the knee and leg
 • (+) forward lurching during gait (A.K.A. Quadriceps Gait = compensatory motion
when there is a weakness of the quadriceps muscle.)
Lateral Femoral Cutaneous Nerve Entrapment

• “Meralgia Paresthetica”
• Causes: compression of nerve as it passes through the inguinal ligament (due to
tight pants or tight garments)
• Tingling and numbness along the lateral aspect of the thigh (pure sensory
only) (lateral aspect of the thigh is where the lateral femoral cutaneous nerve
innervates and is located at this region)
Superior Gluteal Nerve Entrapment
 • Cause: compression by spasm of the piriformis muscle (so when the piriformis
muscle is spastic, it does not only compress the sciatic nerve, but as well as the
superior gluteal nerve - This affects the gluteus medius and gluteus minimus
muscles
• Claudication-type buttock pain, weakness of abduction, tenderness to palpation
• Weakness of gluteus medius and gluteus minimus muscles
• (+) Trendelenburg gait with unilateral affectation; (+) waddling gait (also known as
the “Chorus Girl Sign” or Chorus Girl Swing Gait” so “muki-ay si patient
ani”) with bilateral affectation
• If it is bilateral affectation, the gait would be waddling gait, but if it is unilateral
affectation only, then the patient has trendelenburg gait wherein there is pelvic
drop. There is a weakness of the opposite gluteus medius (the one na nakatukod
sa ground ang weak) during the swing phase. So if naka swing phase imo left leg,
then naa pelvic drop, ang weakness ana is the right gluteus medius.
• There is a pelvic drop because the opposite gluteus medius cannot act as a “type
1” lever during the mid swing of the opposite leg. Thus, it cannot stabilize enough
to prevent pelvic drop.
• Gluteus Medius acts as a Type 1 lever during midswing and midstance of the gait.
• Compensation: Trunk bending to the affected side
Inferior Gluteal Nerve Entrapment
 • Cause: compression of piriformis muscle (along with the sciatic nerve & superior
gluteal nerve)
• Produces low back and buttock pain
• Weakness of gluteus maximus muscle
• (+) backward lurching during gait (prominent sign that there is an inferior gluteal
nerve entrapment)
• This is opposite to your femoral nerve injury, since femoral nerve injury, there is
a FORWARD LURCHING during gait.
• Compensation: Leaning the trunk backwards during gait.
Sciatic Nerve Entrapment

•
L4-S3 nerve root
•
“Fat wallet syndrome”, “Injection palsy”, or “Piriformis syndrome (when there is a
spasm or hyperactivity of the piriformis, this can possibly impinge the sciatic nerve
and may produce sciatica symptoms)”
• Pain on passive medial rotation on an extended hip (Freiberg sign)
• Pain and weakness on abduction and lateral rotation of hip (sign of Pace and
Nagel)
• Causes high steppage gait and there is sensory alteration in the entire foot except
the instep and medial malleolus (because this is innervated by the saphenous
branch of the femoral nerve), along with muscle atrophy
• Entrapment of distal sciatic nerve - hamstring spared
• Manifestations:
• Loss of knee flexion (due to loss of innervation to the hamstrings)
• (+) steppage gait
• Inability to run; exhibits foot drop (because your common peroneal nerve
also arises from your sciatic nerve)
• Loss of Achilles tendon reflex
• Inability to stand on toes or heels
• Loss of sensation on the lateral side of the leg and foot
• Diminished sensation on the posterior aspect of the leg and plantar surface
of the foot
Common Peroneal Nerve Entrapment

• Rises from the sciatic nerve or one of the branches of sciatic nerve
• “Cross leg palsy”, “Cast palsy” or “Bedridden palsy”
• Entrapment of the common peroneal nerve at the fibular head
• Muscles innervated by superficial and deep peroneal nerve affected
 •
Cause: habitual sitting in a crossed-leg position, prolonged squatting, improper
application of elastic bandage and plaster casts
• Inability to dorsiflex and evert the foot, (+) foot drop on swing and (+) foot slap on
stance
• The difference between foot drop and foot slap, is that the foot drop is seen during
the swing phase of the gait, while on the other hand, foot slap is seen during the
stance phase of the gait especially during heel strike, the foot will slap on the
ground which the name of the gait is “steppage gait”.
Deep Peroneal Nerve Entrapment

• Also a branch of the common peroneal nerve.

• “Anterior compartment syndrome”
• Cause: increased pressure in the anterior compartment of the leg where the
vascular supply to muscles is compromised; fracture of fibular head
• Loss of dorsiflexion, (+) foot drop or foot slap
• Loss of sensation over the space between the big toe and 2nd toe
• The gait of the patient will manifest a (+) steppage gait in which the foot will slap
on the ground during initial contact.
Superficial Peroneal Nerve Entrapment
• Also a branch of the common peroneal nerve.
• It is rare for this to be injured or entrapped.
• Cause: lateral or inversion sprain of the ankle
• Loss of foot eversion and loss of ankle stability (lateral stability of the ankle is lost)
Tibial Nerve Entrapment
a. At the level of the popliteal fossa (Baker’s cyst)
❑ Cause: posterior dislocation of the knee
❑ Inability to walk on toes, loss of plantarflexion, absent push-off
b. Tarsal Tunnel syndrome
❑ Formed by the medial malleolus, calcaneus, talus, and deltoid ligament of the foot
❑ Cause: trauma, inflammation, valgus deformity and chronic inversion
❑ Paresthesias on the plantar surface of the foot

• Inability to plantarflex the foot; continually dorsiflexes the foot during gait; aka as
CALCANEAL gait
• In pt.’s with deep peroneal nerve entrapment, they are unable to dorsiflex the foot
which causes the steppage gait/ foot drop/ foot slap
Medial Plantar Nerve Entrapment
-medial plantar nerve is a branch of tibial nerve
❑ “Jogger’s foot”
❑ Cause: entrapment at longitudinal arch (plantar calcaneonavicular ligament)
❑ Burning pain at heel
❑ Altered sensation in the sole of the foot behind the hallux
❑ Weakness of intrinsic muscles of the foot
Cranial Nerve Compression Syndromes
*cranial nerves are also considered your peripheral nerves
Olfactory Neuropathy
❑ Causes: hydrocephalus, increased intracranial pressure, skull fractures, cranial tumors,
infection
❑ Decreased or absent sense of smell (anosmia)
Optic Neuropathy
❑ Causes: skull fractures, increased pressure, tumors, infection, multiple sclerosis
❑ Visual field deficits in one eye, monocular blindness; anopia
Oculomotor, Trochlear, & Abducens Neuropathy
❑ Causes: basal skull fractures, increased pressure, brainstem tumors, vascular compromise
❑ Impaired or absent eye movements
Trigeminal Neuralgia
❑ Causes: tumor, multiple sclerosis, vascular compromise
❑ Pain on one side of the face along the distribution of the trigeminal nerve (usually V2 and V3);
commonly in the maxillary and mandibular divisions
❑ Weakness of muscles of mastication
❑ Altered tongue sensation; responsible for the general sensation of the tongue
❑ Loss of corneal reflex; unable to blink
Glossopharyngeal Neuropathy
❑ Compression of CN 9 at the brainstem, can also occur with throat or neck cancer
❑ Brief excruciating pain at the base of the tongue and radiates to the ear and neck
Vagus Neuropathy
❑ Causes: tumor, infection, trauma
❑ Hoarse voice, dysphagia, loss of gag reflex, abnormal body mechanisms (altered blood
pressure, heart rate, decreased production of gastric acid), peptic ulcer, nausea or vomiting,
abdominal bloating
❑ Deviation of uvula away from side of lesion (contralateral)
Spinal Accessory Neuropathy
❑ Common cause: radical neck dissection
❑ Trapezius muscle weakness
❑ Weakness of shoulder abduction, difficulty reaching overhead
❑ (+) lateral winging/sliding door paralysis
Hypoglossal Neuropathy
❑ Causes: brainstem tumors, vascular compromise, compression due to swelling
❑ Paralysis of the tongue, wasting/atrophy of one side of tongue ipsilateral to the lesion, deviation
of tongue ipsilateral to the lesion
Bell’s Palsy
Non-Traumatic Syndromes
1. Metabolic
❑ Diabetes mellitus – most common cause of polyneuropathy
❑ Sensory > motor; distal > proximal
❑ Glove and stocking distribution of numbness and tingling
❑ Cranial nerves 3 and 6 most affected
1. Toxic
❑ Lead neuropathy – most commonly affects radial nerve, (+) bilateral wrist drop
❑ Other causes include arsenic, gold, mercury, manganese, copper
1. Nutritional
❑ Vitamin B deficiency prone to neuropathy
1. Hereditary
❑ Charcot-Marie-Tooth disease – most common, leads to pes cavus and inverted
champagne bottle deformity
1. Post-infection
❑ Leprosy – most commonly affects ulnar nerve (UE) and common peroneal nerve (LE)
❑ Poliomyelitis – affects CN 9 and 10
1. Idiopathic
❑ Guillain-Barre syndrome, Bell’s palsy, Parsonage-Turner
1. Radiation
Diagnosis
 • Nerve Conduction Testing
• Electromyography
PT Assessment
1. Subjective examination
1. Onset: sudden or gradual
2. Progression: rapid or slow
3. Sensory or motor involvement or both
4. Distal or proximal involvement
5. Symmetrical or asymmetrical
6. Focal or generalized
7. Pain or autonomic involvement
8. Any associated diseases
1. Physical examination
1. Sensory assessment
2. Motor assessment – MMT
3. Reflex integrity – DTR
4. Flexibility – ROM, joint play
5. Special tests
6. Girth measurement
• For potential atrophy
1. Postural assessment
2. Gait assessment
3. Functional analysis
PT Management
1. Immobilization and splinting
• Beneficial if the injury comes with an acute injury to the bone, ligament, or
other tissues
1. Heating modalities
2. Electrical agents – TENS, ES
• TENS to modulate pain, ES for muscle reeducation
1. Peripheral nerve mobilization
2. Postural correction
3. ROM exercises, stretching exercises
4. Gentle multiple-angle isometrics
5. Strengthening exercises
6. Endurance exercises
7. Scar tissue mobilization
8. Orthosis
Management Guidelines
Acute Phase
• Immediately after injury or after surgery (eg. following decompression and
release or following repair of a lacerated nerve)
1. Immobilization – time dictated by the surgeon to protect the nerve, minimize
inflammation, and minimize tension at the injured/repaired site
• Prevent healing limb from being reinjured and to prevent patient from
experience excruciating pain
1. Movement – amount and intensity dictated by type of injury and surgical repair;
begin ROM to minimize joint and connective tissue contracture and adhesions
2. Splinting or bracing – necessary to prevent deformities and undue stress on
healing nerve tissue
❑ Cock-up splint – for CTS to position the thumb in opposition
❑ Radial nerve splint – prevent wrist drop
❑ Plantarflexion (Deep peroneal nerve) splint – prevent foot drop
1. Patient education – patient must learn to protect the extremity to avoid re-injury
due to loss of sensation
Recovery Phase
• Begins with signs of reinnervation (volitional muscle contraction and
hypersensitivity)
• As nerve begins to regenerate, there is an accompanying hypersensitivity
1. Motor retraining
• muscle hold in the shortened position
❑ When signs of volitional contraction occur, position the muscle in shortened position
and then hold
❑ ES to reinforce active effort
❑ When muscle demonstrate control of some range, begin gravity-eliminated, active-
assistive ROM
❑ Continue to protect the weak muscles with a splint or brace
 1. Desensitization
• using multiple textures for sensory stimulation
• During nerve recovery, it tends to be accompanied with hypersensitivity
❑ As nerve regenerate, there is increased sensitivity in the area that had previously
been without sensation
❑ Use multiple types of textures or contact for sensory stimulation: cotton, rough
material, sandpaper of various grades, Velcro
❑ Manipulate or place the extremity in the least irritating texture for 10 mins.
❑ Progress to more irritating but tolerable stimulus
❑ Slow vibration (30 cps), rapid vibration (256 cps)
1. Discriminative sensory re-education
• identification of objects with, then without, visual cues
Management Guidelines
Chronic Phase
- Reinnervation potential peaked with minimal or no signs of neurological recovery
1. Emphasize training for compensatory function when full neurological recovery does not
occur
2. Continue to wear supportive splint or brace
3. Preventive care must continue indefinitely