PNS disorders Flashcards

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1
Q

Nerve anatomy

A
  • endometrium: around axon
  • perineurium: around a bundle of axons (fascicles)
  • epineurium: around a bundle of fascicles)
  • epieneural sheath: around a nerve (has blood vessels)
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2
Q

What can be damaged in the PNS and what degeneration occurs

A
  • can occur to myelin, axons, different CT etc
  • damage to an axon = anything distally will degenerate and can have some healin g
  • wallerian degeneration (distal degeneration)
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3
Q

Effects of Aging on the PNS

A
  • number of fascicles
  • effect on CT
  • cross sectional area
  • myelinated and non-myelinated fibers
  • blood vessels = plaques
  • processing speed of nociceptive signals
  • protein production
  • motor units decrease
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4
Q

Aging neuropathy

A
  • loss of motor and sensory cell bodies
  • fibers and receptors decrease
  • nerve damage from a lifetime of trauma
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5
Q

Classification of nerve injury/neuropathy

A
  • Demyelination: neurapraxia (least sever/grade 1)
  • Axonotmesis: degeneration; damage to axon but CT is intact (stage 2)
  • Stage 3: damage to axon and endoneurium
  • stage 4: damage to axon, perineurium
  • stage 5: neutromesis: complete severance of axon; damage to all layers of CT
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6
Q

Neuropathy types

A
  • mononeuropathy: one nerve
  • polyneuropathy: more than 1 nerve
  • myopathy: muscle signs and symptoms
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7
Q

Signs and symptoms of peripheral nerve pathology

A
  • loss of sensory function
  • paresis or paralysis
  • vascular control and sweating (dry skin, scaly, blue etc)
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8
Q

Mechanical injuries to PNS

A
  • median neuropathy
  • thoracic outlet syndrome
  • tardy ulnar palsy/retroepicondylar palsy
  • Saturday night palsy/sleep palsy (radial nerve)
  • parsonage-turner syndrome
  • morton neuroma
  • idiopathic fascial paralysis/bell palsy
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9
Q

Thoracic outlet syndrome

A
  • can be nerve or vascular
  • can cause changes peripheral
  • brachial plexus involvement due to compression in thoracic outlet
  • pain, paresthesia, motor weakness
  • raynauds
  • color, temperature changes, ischemia and trophic changes
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10
Q

Tardy ulnar palsy

A
  • ulnar nerve
  • could occur after a fracture, direct force or trauma
  • leads to benediction hand
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11
Q

Charcot-marie tooth disease

A
  • Hereditary motor and sensory neuropathy
  • progressive muscular (peroneal) atrophy
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12
Q

Clinical manifestations of Charcot-marie tooth disease

A
  • distal symmetrical weakness, atrophy, and diminished DTR
  • weak DF, evertors
  • steppage gait
  • progression causes wasting in intrinsics of hands and eventually forearm
  • poor proprioception and cutaneous sensation (risk of falls)
  • pes cavus (high arch) and hammer toes
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13
Q
  • Saturday night palsy/sleep palsy
A

(radial nerve)
- in radial groove
- wake up/slept on arm wrong

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14
Q

parsonage-turner syndrome
- what is it + a differential diagnosis

A
  • neuralgia amyotrophy affecting LMN of brachial plexus
  • Differential: cervical radiculopathy, rotator cuff, TOS
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15
Q
  • morton neuroma
A
  • benign mass between 2nd and 3rd metatarsals that presses on the nerve
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16
Q
  • idiopathic fascial paralysis/bell palsy
A
  • facial nerve compression
  • facial nerve motor for facial expression
  • can be caused by an exposure to virus/infection
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17
Q

Hammer toe

A
  • extended MTP and flexion of PIP
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18
Q

Metabolic neuropathies

A
  • diabetic neuropathy
  • alcoholic neuropathy: over consumption for long time
  • chronic renal failure: changes in electrolytes
  • stocking and glove pattern
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19
Q

Diabetic neuropathy etiology

A
  • hyperglycemia
20
Q

Diabetic neuropathy risk factors

A
  • type 1 - 54%
  • type 2 - 30 %
21
Q

Diabetic neuropathy types

A
  • rapidly reversible neuropathy (acute and goes away)
  • generalized symmetric polyneuropathies
  • focal neuropathies
22
Q

Diabetic neuropathy treatmetn

A
  • general-control hyperglycemia
  • specific-symptomatic management
  • meds include anticonvulsants and antidepressants (treat the pain/is not reversible)
23
Q

Gullian Barre syndrome

A
  • inflammatory infectous disorder
  • typicall follows bacterial/viral infection
  • more common in males than females
  • Radipdly ascending bilateral symmetric motor weakness and distal sensory impairments
  • paresthesia in toes that quickly spreads to leg within hours or days
24
Q

Postpolio syndrome/postpolio muscular atrophy

A
  • had pollio and stays dormit
  • muscular atrophy
  • can be asymtomatic
  • nonparayltic infection that produced GI, flu-like symptoms and muscular pain
  • virus invades anterior horn cell bodies
25
Q

Trigeminal Neuralgia/tic douloureux

A
  • intense paroxysms of lancinating pain within nerve distribtuion (face)
  • can arise from herpes zoster, MS, vascular lesions or tumors
  • sudden onset of sharp knifelike pain/lightning bold
26
Q

Human immunodeficiency Virus Advenaced disease (AIDS) - PNS symptoms

A
  • peripheral neuropathy,
  • disease or drug indiuced myopathy
  • MSK pain syndrome
    occur in advanced stages of HIV
27
Q

Vasculitic Neuropathy

causes

A
  • primary cause: inflammation and necrosis of blood vessel walls
  • secondary: process associated with autoimmune responses, infections, toxins or drug exposure
  • peripheral nerves or even in CNS can sustain ischemia
28
Q

herpes zoster/postherpetic neuralgia

A
  • occurs in dermatomal pattern
  • painful, sensory symptoms
  • red lesions
29
Q

Paraneoplastic neuropathies

A
  • associated with carinomas
  • numbeness/paresthesias initialy assymetric but progress
  • weakness that is generally related to inability to sustain contraction secondary to proprioceptive feedback
30
Q

Lead neuropathy

A
  • primarily affects neurons innervating muscules in UE
  • wrist drop,
  • trouble grasping
31
Q

Pesticides and organophosphates

A
  • inhibit cholinesterase activity = creating an acute cholinergic crisis
  • nausea/vomiting
  • diarrhea
  • muscule fasciculations
  • weakness
  • paralysis
  • sudden paralysis of respiratory musculature
32
Q

Myasthenia Gravis

A
  • motor end plate disorder (NMJ)
  • autoimmune
  • number of ACh receptors are decreased and others are flattened
33
Q

myasthenia gravis cardinal features

A
  • muscule weakness and fatigability
  • normal neurological findings
  • eyes dont close
  • speech is nasal
  • aspiration of food (controlling epiglottis is hard)
34
Q

4 categories of myasthenia gravis

A
  • ocular,
  • mild generalized
  • acute fulminating
  • later severe
35
Q

myasthenia gravis diagnosis

A
  • immunological: presence of anti-ACh receptor antibodies
  • Pharmacologic: tensilon inhitis AChE (leaves ACh in junction)
  • electrophysiological testing = normal EMG at rest
36
Q

myasthenia gravis treatment

A
  • ACh
  • surgical removal of thymus = successful in 85%
  • immunosuppressants
  • long-term corticosteriods
37
Q

What is Complex regional pain syndrome/reflex sympathetic dystrophy

A
  • sensory, autonomic, motor and dystrophic signs and symptoms with or without known trauma
38
Q

CRPS 1

A
  • formerly RSD
  • there was a known injury
  • absence of known traumatic nerve injury
39
Q

CRPS 2

A
  • formerly causalgia
  • known traumatic nerve injury
40
Q

CRPS-NOS

A
  • no other explanation
41
Q

Complex regional pain syndrome/reflex sympathetic dystrophy: etiology/pathogenesis

A
  • may follow medical procedures or injury
  • no apparent soft tissue inflammaiton
  • represents a reflex neurogenic inflammation
  • migrains
42
Q

CRPS: stage 1

A
  • acute inflammation: denervation and sympathetic hypoactivity
  • begins up to 10 days following injury and lasts 3-6 months
43
Q

CRPS: stage 1 signs and symptoms

A
  • Abnormalities in pain
  • pain: more severe than expected; burning or aching character; increased by dependent position
  • hyperalgesia (lower pain threshold)
  • allodynia: all stimuli = pain
  • hyperpathia: threshold to pain increased once exceeded sensation intensity increased more radiply than expected
  • edema: soft and localized
44
Q

CRPS: stage 2

A
  • dystrophic paradoxic sympathetic hyperactivity
  • occurs 3-6 months after onset of pain and lasts about 6 months
45
Q

CRPS: stage 2 Signs and symptoms

A
  • skin color and temperature changes
  • pain: worsens, constant, burnging and aching
  • allodynia, hyperalgesia and hyperpathia almost always present
  • edema: becomes thicker and more fibrotic causing joint stiffness
  • vasomotor/thermal changes: neither warm nor cold
  • skin: thin, glossy, cool and sweating, thin ridgiied nails
  • osteoporosis,cyctic and subchondral bone erosion
46
Q

CRPS: stage 3

A
  • atrophic
  • begins about 6-12 months
47
Q

CRPS: stage 3 signs and symptoms

A
  • **Edema, Vasomotor and sudomotor abnormalities and motor dysfunction and trophic changes **
  • pain: spreads proximally occasionally to entire skin surrounding face and plateaus joint stiffness progresses
  • edema: hardens
  • vasomotor/thermal: sympathetic NS regulation is decreased and affected extremity, affected limb is cooler
  • skin: thin, shiny, cyanotic and dry
  • fingers and toes are involved extremity are atropic
  • fascia is thickened and contracutres may occur
  • demineralization and ankylosis