PNS (week 11)

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57 Terms

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PNS

­Spinal and peripheral nerves  of the trunk and extremities

­Sensory receptors within the organs of the body

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Proprioceptors

­ – static and dynamic position changes

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Photoreceptors

­ – vision

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Thermoreceptors

­ – detect heat and cold

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Mechanoreceptors

­ – touch, muscle length, audio and vestibular function

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Nocireceptors

­ – pain

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­Cutaneous receptors

– in the skin monitor immediate environment for pain, pressure, touch, vibration

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Exteroreceptors

­ – monitor surroundings and perceive pain and tactile stimulation

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 Specialized receptors

­Muscle spindle – monitor muscle

  • length and proprioception

­Golgi tendon organs – monitor

  • muscle tension and joint position

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 Spinal nerves exit from

the spinal cord

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Referred pain

– nerve roots supply the internal organs, muscle, and skin so if there is pain in an internal organ, you will feel it in your skin because it has the same nerve root

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 Two major networks of peripheral nerves

­Brachial plexus – consists of nerves that supply the UEs

­Lumbar and sacral plexus – consists of nerves that supply the LEs

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Response to injury of the PNS

•PNS damage caused by: heredity, trauma, infections, toxins, metabolism

•Myelin

•Either fibers will demyelinate or will regenerate

•Usually longest nerve fibers are affected first

•Usually distal to proximal

•Often sensory problems are noticed first and called paresthesias (burning, tingling, prickling)

•Impaired proprioception and tactile

•Most common motor symptom is distal muscle weakness and abnormal tone (hypotonicity or flaccidity)

•In a myopathy, weakness tends to be proximal

•In a neuropathy, motor symptoms tend to first occur distally

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Wallerian degeneration

 Occurs after axonal injury in both PNS and CNS.

 Occurs when a nerve fiber is cut or crushed and part of the axon becomes separated from the neuron's cell body causing degeneration distal to the injury

 Usually begins within 24–36 hours of an injury.

 After injury, the axon degenerates and is followed by the myelin sheath breaking down and infiltration by macrophages.

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Neuropraxia

­temporary damage to nerve caused by pressure on the axon

­May cause temporary paralysis of muscles supplied by the damaged nerve 

­No muscle atrophy occurs

­Patients will fully recover, usually lasts 6-8 weeks

­Most common cause is external pressure on the nerve from a direct blow (football injury)

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Axonotmesis

­prolonged pressure on nerve with muscle atrophy

­Neural sheath is intact so the axon may or may not grow back

­If it does not grow back, then permanent paralysis or muscle atrophy occurs

­Axons grow very slowly ~1mm per day

­Crush injury or contusion

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Neurotmesis

­axon and axon sheath are damaged

­Most serious

­Surgery may be able to suture the nerve back together

­Partial recovery is possible but not complete recovery

­Most commonly caused by trauma especially MVA and lacerations and stretch injuries from dislocations

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Pns lesions

­Peripheral nerve lesions: usually involve compression or external trauma to the nerve axon

­Compression is caused by chronic inflammation, tumor, or any other growth that compresses a nerve

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radiculopathy

 Occurs when there is compression of a nerve as it exits the intervertebral foramina of the vertebra.

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Pns testing : Testing for the neurological system:

­Dermatomes

­Deep tendon reflexes (DTRs)

­Electrodiagnostic testing: electromyography and nerve conduction studies

­Manual muscle testing (MMT)

­Myotomes 

­Neural tension testing/nerve stretching

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Phalen’s wrist flexion tests for the Median Nerve

Flexing both wrists then press the backs of the hands together to increase flexion

+ if tingling and/or paresthesia in dermatome of the median nerve in hand over thumb, index and middle fingers, and lateral palm (30-60 sec)

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Tinel’s sign

•Detects irritation of a nerve by compression

•Involves tapping lightly over the nerve

+ if tingling or “pins and needles” in the dermatome of the nerve

Caused by hypersensitivity of the nerve due to injury and inflame

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Thoracic Outlet test

Common tests: Allen test, Adson’s maneuver, and provocative elevation test

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Symptoms: Thoracic Outlet

edema of UE, neck and shoulder pain, pallor of UE, weakness and atrophy of hand muscles, tingling of hand and forearm, poor circulation to forearm and hand

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Thoracic Outlet

Caused by compression of nerves and blood vessels as they pass between the clavicle and 1st rib before they enter the arm

May be caused by tight anterior scalenes or pectoralis minor muscle, presence of cervical rib, or a reduced space between the 1st rib and the clavicle

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Allen Test

•Pt sits in a chair

•Shoulder is abducted to 90 degrees and examiner performs horizontal extension and lateral rotation of the arm with elbow flexed

+ of radial pulse disappears when the patient’s head is rotated to the opposite side of the arm being tested

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Neuropathy, peripheral neuropathy, and polyneuropathy Etiology

•The cause is unknown in 30% of people with this, 30% is caused by diabetes, Guillain-Barre’, alcoholism, autoimmune disease, environmental toxins, Lyme disease, etc

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Neuropathy, peripheral neuropathy, and polyneuropathy prognosis

•May be mild or debilitating

•Sensory loss in the distal extremities can lead to skin breakdown and amputation

•If severe peripheral neuropathy, may be unable to gait without assistive devices

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Neuropathy, peripheral neuropathy, and polyneuropathy S/S

­Atrophy in distal muscle with possible fasciculations and muscle cramping

­Altered or loss of sensation – “glove or stocking” distributuion

­Loss of vibratory, touch, pressure, temperature, kinesthetic awareness

­Numbness of skin

­Inability to do fine motor tasks

­Decreased balance, coordination and gait

­Loss of weight-bearing function leads to bone degeneration

­Hypotension or orthostatic hypotension

­Progression of weakness in muscles of face and torso lead to swallowing and eating problems

­Intestinal problems if nerves to internal organs are involved

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Neuropathy, peripheral neuropathy, and polyneuropathy medical

­Depends on the cause of neuropathy

­Team approach to treatment

­If diabetic, control BS, good nutrition, and vitamins

­Stop drinking alcohol and smoking

­Take care of feet – inspection, orthotic shoes

­Treat open wounds ASAP

­Medications: analgesics, antidepressants, antiepileptic medications like gabapentin

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Neuropathy, peripheral neuropathy, and polyneuropathy PT

­Patient education on foot and skin care, positioning

­Orthotic recommendations like for AFO for foot drop

­Gait training

­Balance and coordination exercises

­Strengthening

­Stretching

­Endurance ex

­HEP

­Aerobic activities

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Carpal Tunnel Syndrome (CTS)

 Most common entrapment neuropathy

 Compression of the median nerve within the carpal tunnel at the wrist

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Carpal Tunnel Syndrome (CTS) Etiology

usually occupational activities where repetitive movement are needed but also could be from any cause that decreases the space in the carpal tunnel like RA, infections, CHF, pregnancy, and tumors

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CTS S/S

 Hallmark sign: nocturnal pain – awakens by painful numbness in hand; distal pain in forearm or wrist and radiating to thumb, index and middle fingers

 If progresses, will have thenar weakness and atrophy resulting in loss of grip strength, inability to pinch and sensory loss causing clumsy hand

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CTS medical

 almost 50% of cases are bilateral;

­Phalen’s test, Tinel’s test, nerve conduction study

­splint with wrist in neutral and thumb slightly abducted

­ injection of methylprednisolone proximal to the tunnel has resulted in relief of 77% of the patients

­surgical release if failed traditional conservative treatment for 2-3 months

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CTS PT

 patient education – take a 5 minute break once an hour if typing continuously

­modification of work space

­after surgery, nerve and tendon gliding tech to decrease scarring and adhesions

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Sciatica

 Radiculopathy occurring most often between 40-60 yrs old

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Sciatica etiology

originates in the low back and travels through the buttock and down the large sciatic nerve in the back of the leg; caused by compression on the sciatic nerve from herniated disc (most common), bone spur, spinal stenosis, tight piriformis muscle

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Sciatica S/S

radiating constant pain in one or both legs and buttocks; possibly tingling, numbness or weakness; coughing, sneezing or prolonged sitting can worsen symptoms

 Pain that is worse when sitting

 Leg pain that is often described as burning, tingling or searing (vs. a dull ache)

 Weakness, numbness or difficulty moving the leg or foot

 A sharp pain that may make it difficult to stand up or to walk

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sciatica medical

­Selective epidural injection has short-term relief of pain

like NSAIDS; if it progresses, could have significant leg

weakness and bowel/bladder problems-may need surgery;

Medications like anti-inflammatories(naproxen, ibuprofen), muscle relaxers(flexeril), pain killers(narcotics)

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sciatica PT

­Single knee to chest

­Diagonal knee to chest

­Posture education and correction

­Strengthening and stretching

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Bell’s Palsy

 Affects the facial nerve on one side of the face

 Most often affects pts between 15-45 yo

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Bell’s Palsy etiology

 latent herpes virus, acoustic neuromas (rare and would have a slow onset); increase risk of people with DM or during pregnancy

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Bell’s Palsy S/S

 rapid unilateral facial paralysis often over night, drooping of the corner of the mouth, nasolabial fold flattening

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Bell’s Palsy medical

 : high dose corticosteroids asap; possible antiviral medications like acyclovir with corticosteroids has been shown to have 100% recovery if given within 3 days of onset

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Bell’s Palsy PT

e-stim, facial exercises

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Thoracic Outlet Syndrome

 Entrapment syndrome caused by pressure from structures in the thoracic outlet of the brachial plexus between the interscalenes triangle and inferior border of the axilla

 Vascular symptoms can occur also due to pressure on the subclavian artery

Can be divided into 3 groups: neurogenic(compression on brachial plexus), vascular (compression of subclavian artery and/or vein), disputed (nonspecific TOS with chronic pain and symptoms of brachial plexus involvement

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Thoracic Outlet Syndrome etiology

posture changes, trauma to shoulder girdle, body composition, congenital factors

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Thoracic Outlet Syndrome S/S

•paresthesias and pain in arm especially at night, tingling, paresis, weakness and atrophy

•If upper nerve plexus (C5-7), pain in neck; possibly radiation to face or ear, scapula and anterior chest

•If lower nerve plexus (C7-T1), pain and numbness in post neck and shoulder, medial arm and forearm, radiation into ulnarly innervated digits of the hand (half of the ring finger and all of the pinky)

•Vascular symptoms – coldness, edema in hand or arm, Raynaud’s phenomenon, fatigue in hand and arm, distention of superficial veins in hand

•Overhead and lifting activity with movement of head will produce symptoms of upper plexus

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Thoracic Outlet Syndrome medical

Adson’s maneuver and Allen’s test

•Conservative treatment with PT; if no results, surgery

•Surgical results:  70% have good or excellent results with supraclavicular or trans-axillary resection of the 1st rib

•Complications: pneumothorax, nerve compression, transient winging of the scapula

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Thoracic Outlet Syndrome PT

•postural and breathing exercises, stretching of scalenes and other tight muscles, strengthening of the shoulder girdle especially trapezius, levator scapulae, and rhomboids

•Avoid overhead exercises

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Diabetic Neuropathy

 It is a demonstrable disorder with diabetes mellitus without other causes of peripheral neuropathy. Common complication of DM and is progressive. Usually distally, symmetric pattern and called diabetic polyneuropathy.

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Diabetic Neuropathy etiology

caused by chronic metabolic disturbances that affect nerve cells and Schwann cells in diabetes; chronic hyperglycemia leads to abnormalities in micro-circulation that create capillary changes and local ischemia that affects the nerves

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Diabetic Neuropathy S/S

 Hallmark of acute sensory neuropathy is rapid onset of severe burning pain, deep aching pain, sudden sharp electrical type sensation, hypersensitivity of the feet and often worse at night

­Diabetic polyneuropathy is the most common type of diabetic neuropathy and 50% of the patients have this

­Small fiber involvement – leads to burning pain and paresthesias, more profound at night in feet and LEs(stocking pattern)

­Large fiber involvement – results in painless paresthesia with impaired vibration, proprioception, touch, and pressure along with loss of ankle DTRs

­Numbness 

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Diabetic Neuropathy prognosis

 slowly progressive disorder

­Since it’s a metabolic disorder, other systems are often affected like vascular

­More than 50% of non-traumatic amputations in the US are on diabetic patients

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Diabetic Neuropathy medical

 control hyperglycemia

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Diabetic Neuropathy PT

modalities to control pain, patient education to check feet and get appropriate wound care if needed, assistive device for gait, orthotics if needed