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Clinical Medicine III > Peripheral Nervous System Disorders I > Flashcards

Peripheral Nervous System Disorders I Flashcards

1
Q

General overview of PNS disorders

A
  • PNS severs to link CNS to muscles, motor, and sensory end organs
  • Weakness & sensory loss are hallmarks of PNS lesions
  • Both somatic & autonomic NS can be affected by PNS pathology
  • ANS symptoms can occur in the same nerve distribution: lack of normal skin wrinkling, cessation of sweating, need to monitor cardiac irregularities & circulatory problems
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2
Q

How many pairs of spinal nerves and how many pairs of cranial nerves

A
  • 31 pairs of spinal nerves
  • 12 pairs of cranial nerves
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3
Q

Where are the cell bodies of ANS neurons located

A
  • Located in spinal cord, brainstem, & ganglia outside of CNS
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4
Q

Peripheral nerves are covered by __________, and are an extension of ___________

A
  • Protective sheaths
  • Meninges
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5
Q

What do the Epi-, peri-, and endo- aneurism cover

A
  • Cover the whole nerve, nerve fascicle, & single nerve axon, respectively
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6
Q

Describe the epineurium

A
  • Outermost layer
  • Extension of dura
  • Provides tensile strength through longest part of nerve
  • Can continue to encapsulate nerve endings (Meisner’s corpuscles)
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7
Q

Where are the cell bodies of peripheral motor and sensory neurons located

A
  • Motor: starts at the lower motor neurons in the spinal cord
  • Sensory: dorsal root ganglion
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8
Q

Describe the perineurium

A
  • Extension of arachnoid
  • Can encapsulate other nerve endings (Pacinian corpuscles, muscle spindles, Golgi tendon organs)
  • Can remain open ended: can allow toxins/viruses to gain access to NS
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9
Q

Describe the endoneurium

A
  • Surrounds individual nerve axons along with its myelin sheath
  • Provides continuity to direct regrowth of axons after injury
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10
Q

Describe myelin in the PNS

A
  • Phospholipid membrane b/w axolemma & endoneurium formed by Schwann cells in PNS
  • Myelin sickness determines conduction properties
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11
Q

What properties do different thickness of myelin nerves carry in the pNS

A
  • Very thick: very fast, proprioception (muscle spindle & GTOs), alpha (to skeletal muscle fibers)
  • Thick: fast, touch & pressure, Gamma (to muscle spindle)
  • Thin: slow, touch & temperature, to ANS ganglia
  • None: very slow, pain, from ANS ganglia to smooth muscle
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12
Q

Muscle fibers associated with the different fiber types

A
  • Alpha: 80-120 m/s, extrafusal muscle fibers
  • Beta: 33-75 m/s, intrafusal with collaterals to extrafusal
  • γ: 4-24 m/s, intrafusal muscle fibers
  • All are myelinated
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13
Q

Slide 8 chart(know the order but don’t need to know the speeds/#’s)

A
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14
Q

Describe the vascular supply of the peripheral nerves

A
  • Rich vascular supply makes them resistant to ischemia
  • Each peripheral nerve receives an artery that penetrates the epineurium
  • Branches of artery extend into perineurium as arterioles
  • Branches from arterioles enter endoneurium as capillaries
  • Vessel are coiled when limb is in shortened position becomes uncoiled during movement so vasculature is not stretched/damaged during movements
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15
Q

Describe the classification of peripheral nerve injuries (PNI)

A
  • Can be injured due to trauma, inherited disorders, environmental toxins, metabolic/nutritional disorders, infections
  • Trauma can cause compression, ischemia, stretching, may affect myelin, axons, motor units
  • Type & severity of injury determines response to trauma
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16
Q

What are the 3 categories of severity of peripheral nerve injuries (PNI)

A
  • Neuropraxia: temporary, no structural damage
  • Axonotmesis: axons are severed but the sheaths are still intact
  • Neurotmesis: whole nerve is severed including the sheaths
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17
Q

Describe neuropraxia

A
  • Results in temporary weakness and/or sensory loss
  • Segmental demyelination
  • Axons remain intact
  • Typically a result of blunt injury, compression, ischemia or disease
  • Slows/block local conduction at the site of injury, conduction above and below is normal
  • No atrophy of muscles
  • Recovery happens through re-myelination. Demyelination triggers molecular signals to remaining Schwann cells to start dividing mitotically, new Schwann cells move to injured site to form myelin
  • Typically, rapid full recovery of function (6-8 wks)
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18
Q

Describe axonotmesis

A
  • When axon gets damaged/disconnected, but outer coverings (endo-, peri- or epineurium) remain intact
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19
Q

Describe neurotmesis

A
  • When axon along with all its coverings (endo-, peri- and/or epineurium) are severed
20
Q

What does axonotmesis and neurotmesis have in common

A
  • Both typically happen due to physical injury (crush, stretch, laceration), disease or prolonged compression that produce area of infarction and necrosis
21
Q

Slide 13 chart

A
22
Q

Describe the effects on neurons following axonal damage

A
  • Damage to axon has cascading effects up & down the connection
  • Wallerian degeneration begins, completed in a few wks, myeline fragments, macrophages remove debris
  • Cell body undergoes chromatolysis (cell body swells & nucleus moves to the side)
  • If cell body remains viable, regeneration begins, it grows axon again with sprouting of growth cone
23
Q

Describe axonal regeneration in PNS and CNS

A
  • Difference between peripheral and central nervous system
  • Peripheral nerves can regenerate, but central nerves cannot
24
Q

Describe axonal regeneration following a PNS injury

A
  • After PN injury, Peri-/endo-neural sheath reforms rapidly, schwann cells produce neurotrophic factors and promote axonal growth
25
Q

Describe axonal regeneration following a CNS injury

A
  • After CN injury, distal segment of axon degenerates, reactive macrophages and astrocytes form glial scar that inhibit axon re-growth
26
Q

Describe axonal regeneration using growth cone

A
  • Finger-like projections (filopodia) extending from growth cones, sample environment for chemical cues (like neurotrophic factors) to guide regeneration
  • In the absence of endoneurial sheath, fibers get misguided or form neuromas
27
Q

What does the recovery of peripheral nerve s depend on

A
  • Depends on severity of injury
28
Q

What is chronic versus acute carpal tunnel syndrome (median nerve palsy) associated with

A
  • Compression of median nerve
  • Chronic: associated with performance of repetitive tasks by hand
  • Acute: rarer & directly associated with fractures, dislocation, & vascular disorders; may require urgent surgical intervention
29
Q

Etiology of carpal tunnel syndrome

A
  • Carpal tunnel is cylindrical and inelastic, none of the sides (bony or ligamentous) yields to expansion
  • Compression happens due to increased pressure inside the tunnel, due to accumulation of fluids or swelling of the structures
  • Pressure might increase 2 to 3 times with wrist flexion or extension
30
Q

Incidence of carpal tunnel syndrome

A
  • 2.8 per 1000
  • 1-27 lost work days
  • About 70% of all CTS cases occur in women, might be due to smaller tunnel
31
Q

Risk factors associated with carpal tunnel syndrome

A
  • Neuropathic conditions caused by DM, alcoholism, toxic exposure
  • Arthritic conditions
  • Metabolic conditions: pregnancy, hypothyroidism, obesity
  • Smoking
  • Structural anomalies in wrist, length/width of lumbricals, extra tendinous slips from flexor tendons, branching pattern of median nerve
  • Several occupations are suspected to be associated - tasks that require repetitive gripping, holding tools that vibrate, lifting more than 12 kgs, but no conclusive evidence with computer use (report says it does not pose increased risk)
  • Working in extreme cold temperatures
  • Sedentary lifestyle
32
Q

Pathogenesis of carpal tunnel syndrome

A
  • Increased mechanical pressures induce Schwann cells to undergo apoptosis/necrosis, causing demyelination. Proinflammatory cytokines are also involved
  • Demyelination causes neurapraxia
  • Remyelination is not of the same quality, slowing of NCV noted
  • Multiple de- and re-myelination are involved in repetitive motion injuries.
  • If mechanical pressures are high enough, can also cause axonotmesis
  • Both peripheral inflammatory and central changes are responsible for sensory and motor changes, eg, central pain sensitization may cause thermal hyperalgesia
33
Q

Clinical manifestations of carpal tunnel syndrome

A
  • Pain, paresthesia, numbness and weakness in the distribution of median nerve
  • Sensory symptoms precede motor
  • Nocturnal pain is hallmark, pt wake up from painful numbness at night
  • Other positive sensory tests – reduced 2-point discrimination, vibration sense, elevated threshold in monofilament testing
  • Thenar weakness in advanced cases, loss of grip strength, inability to pinch
  • If untreated, can lead to atrophy
34
Q

How would you diagnose carpal tunnel syndrome

A
  • Using Hx, physical exam, electrodiagnostic tests, & provocation tests
35
Q

Lists physical exam or provocation tests used to diagnose carpal tunnel syndrome

A
  • Phalen, Tinel, Durkan’s carpal compression (30secs), Lumbrical incursion tests (make fist w/wrist neutral, pain/parassthesia in 30-40secs)
36
Q

Describe NCV/EmG for diagnosing carpal tunnel syndrome

A
  • Gold standard test for determining CTS
  • Helps with differential diagnosis: rule out other conditions like radiculopathy, brachial plexus injury, myopathy
  • US studies can reveal enlarged median nerve
37
Q

Treatment for carpal tunnel syndrome

A
  • Early management involves ergonomic modifications and lifestyle changes
  • Anti-inflammatory meds: long term use causes gastric side effects without significant improvement in symptoms
  • Corticosteroid injections provide relief up to 1 year
  • Surgical intervention: transverse ligament release; if sensory and motor symptoms have lasted more than 1 year, & if denervation is seen in EMG (fibrillation potentials), return to normal 2-point discrimination and muscle strength in 70% cases
38
Q

Implications for PT for carpal tunnel syndrome

A
  • Icing after long periods of wrist use can reduce pain and swelling
  • Phonophoresis and iontophoresis: to reduce local inflammation and swelling
  • Active ROM exercise of wrist is encouraged as deconditioning exacerbates CTS, but strengthening exercises should be avoided until relief from symptoms are nearly complete
  • Neutral wrist splinting beneficial in severe CTS when worn at night or full time
  • Combination of Cock-up splint along with lumbrical stretches: most effective for functional gains when assessed at 6 months of intervention
39
Q

What is thoracic outlet syndrome (TOS)

A
  • entrapment/compression syndrome caused by pressure on nerve fibers of brachial plexus or vascular structures at some point between the interscalene triangle and inferior border of axilla.
    Vague symptoms, TO anatomy is complex
40
Q

What are the 3 categories of TOS

A
  • Neurogenic (compression of brachial plexus)
  • Vascular (subclavian artery/vein)
  • Nonspecific (Disputed etiology)
41
Q

What are the risk factors for TOS

A
  • Congenital abnormalities and postures associated with growth: cervical rib, elevated 1st rib, scalene muscle anomalies, ‘dropped’ scapula, hypertrophy of cervicoscapular muscles, abnormalities in fascial bands
  • Trauma to shoulder girdle, neck, whiplash injuries
  • Certain occupations (jack hammer operators, heavy weight lifting, dental hygienists), pregnancy/delivery, obesity; many same as CTS
  • Women more than men
42
Q

Pathogenesis of TOS

A
  • Chronic compression of nerves results in ischemia, edema, parasthesia
  • Compression of vascular structures can cause weaker pulse, ischemia, thrombosis, edema (from venous distention)
  • Initially causes neurapraxia, can progress to axonotmesis
43
Q

Clinical manifestations of TOS

A
  • May have vague symptoms, difficult to interpret
  • Pain, tingling, paresthesia in arm, particularly at end of day
  • Can also cause paresis, atrophy in severe cases
  • If upper nerve plexus (C5-7) is involved: pain in neck, radiate to face (sometimes ear), anterior chest, scapula
  • If lower plexus (C7-T1) is involved: pain/numbness in shoulder, arm, ulnar digits of hand
44
Q

What provocation tests can be used for diagnosing TOS

A
  • Adson’s, Wright (hyperabduction)/Allen’s test (alternate ways), Roos elevated arm test
  • Find radial pulse, rotate head, then extend and ext rotate shoulder while extending head
  • Find radial pulse, move shoulder into max abd/ext rot, taking deep breath rotate head
  • Mere obliteration of pulse is not enough, sensory symptoms must be reproduced for TOS
  • Tests used in combination improve diagnosis
45
Q

Describe how to diagnose TOS

A
  • Symptoms of neural involvement: pressure over lateral neck/clavicle elicits pain/tingling; pain with head turned/tilted to opposite side; numbness/hypoesthesia in radial/ulnar nerve distribution; weakness in biceps/triceps/wrist/hand, color and temperature changes
  • Symptoms of vascular involvement: Swelling of arm/hand, discoloration of hand, UE claudication, skin temperature changes, cold intolerance
  • Radiology: presence of cervical rib
  • Electrophysiologic studies: NCV shows decreased amplitude and slowing of velocity, can pinpoint lesion. EMG can detect fibrillation potentials
46
Q

Treatment for TOS

A
  • Postural and breathing ex
  • Nerve stretching exercises
  • Mobilization of 1st rib
  • Strengthening exercise for trapezius, levator scapulae, rhomboids
  • Avoid overhead exercise as they tend to evoke symptoms
  • Surgical management: for refractory cases; scalenotomy, clavicle resection, Pec minor release, 1st rib/cervical rib resection

Clinical Medicine III (20 decks)

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