Total UE nerve compression

MOI of brachial plexus injury at birth

• Shoulder dystocia or traction injury during delivery
• Can occur with or without a fracture

Erb’s palsy

• most common

• arm extension, IR and adduction

• muscles for waiter’s tip

• decreases sensation in C5-6 dermatome

Total/Global Brachial Plexus Birth Injury

• might require surgery

• C5-T1 involvement

• 10-20% of injuries

• Complete UE involvement with paralysis and decreased or absent sensation

Klumpke’s Palsy

• Much lower incidence from this mechanism of injury
• Wrist and hand intrinsics – clawed hand deformity
• Normal shoulder function
• Decreased sensation in
• C8-T1 dermatome

predictors of brachial plexus birth injury

• Shoulder dystocia
• Prolonged labor or fetal distress

prognosis of brachial plexus birth injury

• Majority have spontaneous resolution with conservative therapy (PT or OT)
• Surgery
• If nerve root avulsion is present
• Non-reassuring serial assessments over 3 months
• Total/Global brachial plexus injuries

surgical progression for brachial plexus birth injury

• Nerve surgery/microsurgery, ideally by 6 months of age
• Later tendon transfer as a follow-up if unsuccessful
• Potential for osteotomies – older child with glenohumeral dysplasia as a result of BPBI

PT intervention for brachial plexus nerve injury

• Neonatal period – PROM multiple times per day
• Infancy – Promote AROM and motor development
• Toddler and beyond- strengthening, ongoing PROM, compensation vs. recovery

Charcot-Marie-Tooth (CMT)

• Hereditary motor and sensory neuropathy

CMT type 1

• Demyelinating neuropathy
• “NCS results show slower nerve conduction velocities (<38 m/s) with relatively uniform findings across tested nerves.”

CMT type 2

• Axonal neuropathy
• “NCS results show faster conduction velocities (>38 m/s), significantly reduced amplitudes, and variable findings between nerves.”

diagnosis of CMT

• Most frequently in adolescence and teen years
• Can have onset of symptoms as toddler or later in 3rd or 4th decade
• Earlier diagnosis with genetic testing and understanding of carrier status

LE symptoms of CMT

• Distal weakness with high foot arches
• Decreased sensation
• Loss of balance/increase in falls
• Muscle atrophy and weakness can progress more proximally in the legs, ankles and feet.
• Toe curling (hammertoes)

UE symptoms of CMT

• Distal weakness with intrinsic weakness
• Decreased sensation
• Loss of manual dexterity and strength balance/increase in falls

progression of CMT

• Onset age is variable
• Bracing can be used to decreased deformity or increase function (ex. Foot drop)
• Concerns for neuropathic pain with progression
• MSK vs. neuropathic pain differential

interventions for CMT

• ankle foot orthosis

• exercise program

• orthopedic and podiatric referrals

• adaptive equipment and/or hand splints

ankle foot orthosis

• Dorsiflexor weakness
• Ankle instability and impaired balance
• Poor push-off
• Fatigue

exercise program for CMT

• Endurance
• Strengthening
• Balance

nutritional deficiencies

• Presenting symptoms for this category are most likely paresthesia, tingling or pain
• May not be isolated peripheral neuropathy (ex. seizure or other neurological symptoms)
• Myeloneuropathy can also occur with UMN and LMN symptoms

• B6: infants, could be seen as seizure, most treatable

Neurofibromatosis

• Genetic condition resulting in benign nerve tumors

• NF1 (most common): affects skin

• NF2: affects auditory nerves

• Schwannomatosis: one part of the body and asymptomatic in some

Guillain-Barre Syndrome

• Autoimmune response that progresses rapidly
• Paresthesias in hands and feet that can progress to weakness and paralysis
• Rare with evolving understanding of etiology, but 60-70% had infection in prior 1-2 months

Vincristine Neuropathy

• Vincristine is a chemotherapeutic agent, discontinued when VIPN is identified
• Acute or long-term effects
• Early detection
• Intervention may include serial casting or bracing for foot drop

• can be caused by leukemia

• might lose significant ROM in ankle

traumatic injury

Mechanism also described in adults
• Transection
• Crush injury
• Compression

Distal symmetric polyneuropathy

• Typically subclinical in children
• Up to 3% in children with T1D < 18y
• Consider risk of T1D and earlier onset T2D

Thoracic outlet

Group of pathologies thatcompress/restrict brachial plexus and subclavian vessels that produce variant symptoms

Hyperabduction test

Raise arm above the head in frontal planei can monitor radial pulse

Elevated arm stress test

- shoulder 90/90 - repeated grasp for one minute

Subclavicular compression

• Will not feel good

Provocative tests

• AdSon's test

• Costoclavicular maneuver

• Hyper abduction test

• Elevated arm stress

• Upper limb tension test

Scalene triangle

Between anterior and middle scalene

• brachial plexus and subclavian artery

Who is most likely to get surgery

Vascular TOS

TOS classification

Vascular and neuralgic

True neurologic

Will have diminished strength, sensation, and reflexes

Compression

• Posture

• Trauma often early repetitive stress injury

• - ulnar side of arm -

• fewer associated problems

Tension

• History of trauma and fibrosis

• Associated problems in shoulder_e-spine,myofasical

• Longstanding symptoms and irritability is high

What profile do people typically have?

Both compression and tension

Double crush syndrome

Nerve is irritated at more than one location

Cervical spine

• ROM resting,

• Spurling’s ,

• facet palpation,

• anterior and posterior glides

What happens to a nerve that is e tethered and stress is put on it?

The strain is increased

Peripheral nerve injuries in shoulder

• Spinal accessory (x1) -

• long thoracic

• Suprascapular

• - axillary

• - scm/ut -

• serratus anterior

• Supra/infraspinatus

• Deltoid

Moi of TOS

• Trauma, repetitive motion overhead, postural with

Trauma

Seatbelt, compresses or stretches nerve roots at later stage fibrosis may form causing symptoms

Repetitive motion

Repeated motions overhead or repeated pressure on shoulders

Posture

• Forward head posture unloads plexus

• Shortened SCM, Levator scapulae, pecs

• Lengthened middle and lower trap

Symptoms of TOS

• Sensory before motor

• Low plexus more common

• Vascular involvement

Upper plexus

Middle and upper trunk, radial side, irritated by scalenes

Low plexus

Medial side, irritated by 1st rib

Treatment stages

1. Protect and rest

2. Address impairments

3. Maintenance

How to avoid downward stress on shoulder girdle

• Shower straps/bags

• Weight in hand

• Strapless bra

• Breast reduction surgery

• Supporting arm w/ walking and driving

Treatment in phase 2

• Nerve mobility

• Adjacent tissue mobility

• Postural issues

Treatment for adhesions

gliders

What should a patient with trauma or traction injury do early

Nerve glides to avoid neurological adhesions

Gliders or sliders

Create tension on one end and release tension at the other end

More excursion and lower strain

Tensioners

Create tension at both ends of the nerve

Passive interventions

• Medications

• Splinting

• Manual therapy

• Thermal modalities

• Taping

Central mechanism interventions

• Aerobic exercise

• Laterality training

• Graded motor imagery

Near dynamic

• Reduction of intraneural edema

• Temporang hypoalgesia

• Local and distant anti-inflammatory effect

• Peripheral nerve regeneration

• Endogenous opioid release

Maintenance

- brace for posture

• diaphragmatic breathing

• Education and active coping → management

• Aerobic exercise

TOS Surgery

Scalenotomy

First rib resection

For those who exhausted conservative

what are the layers of nerves

• epineuriim

• perineruium

• endoneruium

epineruium

combination of CT and fat that is the outer layer of the nerve and surrounds the entire nerve and fasciculi. It acts like a cushion to protects against compression. IT doesn’t allow for solutions to diffuse

how does mechanical trauma affect the structure of epineurium?

if it a straight run, there is less cushion. However, if there is more twists and turns, than there is more

perineurium

it is a multilayered CT that has a diffusion barrier to protect agaisnt infection, resists tension and maintain intrafascicular fluid pressure. it’s integrity is important to determine nerve health.

endoneurium

inner layer of CT that surrounds indivdiual nerve cells. The outer layer is tight-packed collagen and the inner layer is reticular fibers to form endoneurial tubes.

difference between peripheral nerves and nerve roots

nerve roots do not have all the protective layers peripheral nerves do, thus they are more susceptible to injury and medication.

how are peripheral nerves supplied blood

they have extrinsic nutrient vessels that loop into and out the nerves. depending on the location, traction can squeeze the vessel

endoneurial vessels

longitudinal vessels that form the blood-nerve barrier, thus preventing protein leakage. it is sensitve to pressure and maintains a specific envorinment

pressure gradients in a nerve

Nutrient artery pressure > Fasicular cap presurre > intrafasciular pressure > epinueral venous pressure

how does external compression influence pressure?

it increases the pressure in EVP thus creating back pressure and increased pressure in IP. this ultimately increases the leakiness of endoneural vessels and can cause deoxygenated blood to maintain in the vessel. It will also occlude vessels in perineurium. It interferes with conduction, with even shorts periods of time causing lasting occlusion. It will even cause inflammation and more swelling in the endoneurium and demylination

how does traction impact nerves

if above the elastic limit, before permanat damage, the nereve can retun to normal. however, traction is very rate dependent meaning going to fast can create permanet damage. Traction will create reduced diamteres of the nerves and so on.

how do nerves protect against traction

waviness of CT, the connective tissue, and increased fasciular pressure and strength

friction

combo of traction and compression that can create mechanical irritation. it would lead to inflammation → fibrosis → adhesions → increased mechanical and metabolic stress

peripheral nerve injury

• neuropraxia - full recovery

• axonotmesis - periunum in tact

• neurotmesis - loss of axon

why don’t patients present as textbook?

because there are many areas other than the nerve that are impacted like peripheral tissue, dorsal root ganglion changes, dorsal horn changes, and cortical changes

inflammatory response to peripheral nerve injury

a casacade occurs form breakdwon of BNB, to ingestion of myelin and neurpathic pain

neuropathic pain

lesion of somatosensory system that leads to symptoms, could be allodynia or hyperalgesia

how can neurons be stimulated?

• synaptic transmission

• electrical stimulation

• magnetic stimulation

orthodromic conduction

normal conduction pattern

antidromic conduction

reverse of normal conduction pattern

F-wave

late response that is a compound AP ecoked by supramaximal antidromic stimulation of a motor nerve or mixed nerve

what would latency or absence of F wave indicate?

demylination

synaptic transmission

AP travels down axon to motor terminal. neurotransmitter is released into synaptic cleft. neurotransmitter binds to receptor in postsynaptic muscle and the response is elicited. neurotransmitter is than removed

neurotransmitter removal

• diffusion

• reuptake

• enzymatic destruction

• desensitization

synaptic fatigue

occurs if the presynaptic vessels release more neurotransmitters than reuptake them

receptor antagonist

inhibit neurotransmitter receptors

receptor agonist

mimic naturally occuring neurotransmitters

what is the cause for many neurological and psychiatric disorders?

defective neurotransmission

synaptic integration

process that multiple synaptic potentials combine within one postsynaptic neuron

neurotransmitter

chemical substance released by neuron that helps send signals to other neurons. can be excitatory or inhibitory. each neuron can only produce one type

criteria for neurotransmitter

• created by neuron

• present in presynaptic terminal to complete one defined action

• mimics action of the transmitter

• has a specific mechanism for removal

what happens with too many neurotransmitters?

hyperstimulation, increased synthesis, or defects in receptor binding, or degradation/removal

what happens if there are too few neurotransmitters?

decreased synthesis, defects in removal or receptor binding

acetylcholine

control muscle and neurons in the brain for memory

dopamine

feelings of pleasure

GABA

inhibitory neurotransmitter

norepinephrine

neurotransmitter and hormone. fight ot flight response, regulates normal brain processes

serotonin

mood, appetite, sensory oerception, pain pathways

how does PT interact with neurotransmitters?

modulates synaptic transmission processes

peripheral nerve injury

a LMN injury with a variety of causes and severity

three main processes of peripheral nerve injury

1. Wallerian degeneration
2. Axonal degeneration
3. Demyelination