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Pod Med III > 2) Classification of Nerve Injuries: Hereditary and Acquired > Flashcards

2) Classification of Nerve Injuries: Hereditary and Acquired Flashcards

1
Q

Spinal radiculoptathies result from

A
  • Impingement of the nerve root as it exits the vertebral foramen
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2
Q

Causes of spinal radiculopathies

A
  • Degenerative joint disease
  • Disc herniation
  • Spinal Arthritis
  • Congenital anomalies
  • Infection and neoplasm
  • Acute trauma
  • Mechanical strain
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3
Q

Types of radicular pain

A
  • Local
  • Referred
  • Radicular
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4
Q

Local radicular pain

A
  • Focal irritation of the nerve root
  • Pain is steady and constant
  • Focal tenderness with palpation
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5
Q

Referred radicular pain

A
  • Discomfort from irritation felt in other viscera
  • Upper lumbar irritation: referred to anterior thigh and leg
  • Lower lumbar irritation: referred to buttock, posterior thigh and calf
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6
Q

Radicular pain

A
  • Pain follows the distribution of the nerve
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7
Q

Pain correlates to exercise or particular position?

A
  • Herniated disc
  • Relief with flexed knees
  • More severe when lying down
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8
Q

Family history of back problems?

A
  • Congenital
  • Spina bifida
  • Diastematomyelia (longitudinal split cord formation)
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9
Q

Clinical recognition of radicular pain

A
  • Chronic compression –> edema, demyelination, inflammation
  • Local pain at impingement site
  • Referred pain along myotome or dermatome
  • Symptoms along peripheral course of nerve root
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10
Q

Radiculopathy reflex examination

A
  • Hyporeflexia
  • L3-L4 – Patellar response
  • S1-S2 – Achilles response
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11
Q

Radiculopathy gait evaluation

A
  • Neri’s sign – knees flex with hip extension

- Antalgic gait – possible LLD or postural anomaly

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12
Q

Minor’s sign

A
  • Weight is placed on the unaffected side, hand on back
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13
Q

Radiculopathy physical examination

A
  • Presence of lordosis - spondylolisthesis
  • Presence of kyphosis – osteoporosis
  • Pseudoclaudication (neurogenic claudication)
  • Localized motor dysfunction
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14
Q

Pseudoclaudication (neurogenic claudication)

A
  • Unilateral or bilateral discomfort buttock, thigh or leg
  • Exacerbated by standing or walking
  • Relieved by flexing spine only
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15
Q

Radiculopathy diagnostic tests

A
  • Straight leg raise
  • Lasegue’s test
  • Bowstring test
  • Gaenslen’s test
  • Valsalva maneuver
  • Imaging
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16
Q

Straight leg raise test

A
  • Patient supine
  • Flex hip with knee in full extension
  • Foot pain suggests sciatica or radiculopathy
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17
Q

Lasegue’s Test

A
  • Elevate just below point of pain elicitation
  • Dorsiflex foot
  • Tests for lower lumbosacral nerve root irritation
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18
Q

Bowstring test

A
  • “Root” pain versus hip joint pain
  • Patient supine with hips in full extension
  • Flex knee ⇒ pain ⇒ hip pathology
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19
Q

Gaenslen’s test

A
  • “Root” pain versus Sacro-iliac pain
  • Specifically, Gaenslen’s test can indicate the presence or absence of aSIJ lesion, pubic symphysis instability,hippathology, or an L4 nerve root lesion
  • Twisting of pelvis reproduces sacro-iliac pain
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20
Q

Valsalva maneuver detects

A
  • Presence of space occupying lesion

- Bilateral pressure on jugular veins ⇒ symptoms

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21
Q

Fourth lumbar root lesion pain is referred to

A
  • Proximal down lower back
  • Distal to posterior lateral thigh
  • Anterior leg
  • Medial foot
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22
Q

Fourth lumbar root lesion signs

A
  • Weak quads

- Patellar DTR diminished

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23
Q

Fifth lumbar root lesion pain is referred to

A
  • Sacro-iliac joint and hip
  • Lateral thigh and leg
  • Dorsum of foot
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24
Q

Fifth lumbar root lesion signs

A
  • Weak extensor hallucis longus (maybe peroneals)
  • No reduction of the DTR
  • L5-S1 lesions most common
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25
Q

First sacral root lesion pain is referred to

A
  • Sacro-iliac joint
  • Posterior thigh
  • Lateral posterior leg
  • Posterior heel
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26
Q

First sacral root lesion signs

A
  • Triceps surae weakness (sometimes peroneals)

- Weak achilles DTR

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27
Q

Spinal dysraphisms

A
  • Developmental abnormalities along the midline of the back
  • Multi-factorial etiology
  • Prenatal screening shows increased alpha fetoprotein!!!
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28
Q

Spinal dysraphism etiologies

A
  • Spinal column fails to close due to faulty vertebral development
  • Spinal column closes at 4th intra-uterine week
  • Vertebral column closes by 12th intra-uterine week
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29
Q

Spina bifida

A
  • Incomplete closure of vertebral arches only
  • Occurs in sacral region of 10-25% of population
  • Posterior arches of L5 and S1 are most commonly involved
  • Often an incidental finding
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30
Q

Spina bifida with meningocele

A
  • Failure of vertebral arches to close
  • Protrusion of meninges into sac
  • Symptoms dependent upon degree and level of defect
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31
Q

Spina bifida with myelomeningocele

A
  • Protrusion of meninges and spinal cord

- Symptoms dependent upon degree and level of defect

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32
Q

Spina bifida clinical recognition

A
  • Symptoms often unilateral
  • Associated with foot deformities
  • Accommodative gait disturbances
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33
Q

Spina bifida shows decreased

A
  • Proprioception (spinal cerebellar)
  • Cutaneous sensation
  • Deep tendon reflexes
  • Weakness and atrophy of leg muscles
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34
Q

Spina bifida dermatological findings

A
  • Nevus flammeus (most common finding)
  • Capillary angioma
  • Hypertrichosis at base of spine
  • Midline lumbosacral lipoma
  • Lumbosacral sinus
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35
Q

Tethered cord syndrome secondary to traction on conus medullaris

A
  • Tight filum terminale
  • Rests below L2
  • Look out for spinal taps
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36
Q

Tethered cord syndrome secondary to diastematomyelia

A
  • Division of spinal cord – sagittal plane

- Progressive deterioration if untreated

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37
Q

Other dysraphisms

A
  • Anterior cord syndrome
  • Brown Sequard syndrome
  • Conus medullaris syndrome
  • Cauda equina syndrome
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38
Q

Anterior Cord Syndrome (spinal thalamic)

A
  • Efferent motor/sharp dull and temperature
  • Variable motor and LSST loss
    Preservation of proprioception
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39
Q

Brown-Sequard syndrome

A
  • Hemi section of SC
  • Ipsilateral loss of proprioception and motor
  • Contralateral loss pain and temperature
40
Q

Conus medullaris syndrome

A
  • Sacral cord injury
  • Areflexia in bladder, bowel and lower limbs
  • Variable motor and sensory loss
41
Q

Cauda equina syndrome

A
  • Lumbosacral nerve roots injury
  • Limbs are usually areflexic
    Generally caused by central lumbar disc herniation
  • Areflexia of bladder, and bowel
  • Variable motor and sensory loss
42
Q

Vascular supply to spinal cord

A
  • One anterior spinal artery to 75% of cord

- Two posterior spinal arteries to 25% of cord

43
Q

Anterior spinal artery supplies

A
  • Corticospinal tract
  • Lateral spinothalamic tract
  • Autonomic interomedial pathway
44
Q

Posterior spinal arteries supply

A
  • Dorsal columns
45
Q

Anterior motor horn disease

A
  • Another consideration in patients with weakness without sensory changes
  • Poliomyelitis
  • Post-polio syndrome
46
Q

Poliomyelitis

A
  • Initial LMN weakness or paralysis
  • Replaced by tightening and muscle spasm (spastic paralysis)
  • Weakness in assymetrical and scattered distribution
47
Q

Post-polio syndrome

A
  • Disruption of agonist-antagonist balance

- Increased deterioration

48
Q

Amyotrophic Lateral Sclerosis (anterior motor horn disease)

A
  • Lateral columns and gray matter
  • May be inherited (8 – 10%)
  • Attacks voluntary motor system (somatic nervous system)
  • Corticospinal tract degeneration
  • Alpha motor neurons
  • Demonstrates both upper and lower motor neuron disease
49
Q

Characteristics of LMN disease (secondary to peripheral nerve pathology)

A
  • Presence of fasciculations and fibrillations
  • Hypo- or areflexia
  • Hypotonia or flaccid paralysis
  • Absent Babinski sign
  • Diagnosed by sural nerve biopsy!!!
50
Q

Charcot-Marie-Tooth disease (peroneal muscular atrophy)

A
  • Hereditary, degenerative disorder of peripheral and motor nerves with spinocerebellar tract involvement
  • Slowly progressive disease
  • Starts in feet and legs – progress to upper extremity
  • Cavus foot
  • Affects males > females !!!
51
Q

Charcot-Marie-Tooth disease is characterized by atrophy of

A
  • Peroneal muscles
  • Intrinsics
  • Anterior muscles
52
Q

Charcot Marie Tooth - 1 – “demyelinating” – 50% (most common)

A
  • Early onset, autosomal dominant
  • Trisomy for peripheral myelin protein-22
  • Posterior columns, anterior motor horn, spinocerebellar tract
  • Slow nerve conduction velocities
  • Hypertrophic nerve changes
53
Q

Charcot Marie Tooth - 2 – “neuronal” - 20%

A
  • Adult onset – autosomal dominant
  • Axonal degeneration of peripheral nerve
  • No enlargement of peripheral nerves
54
Q

Charcot Marie Tooth-X – 10-20%

A
  • X-linked inheritance pattern

- Defects in myelin constituent protein connexin 32 (defect in communication between cells)

55
Q

Charcot Marie Tooth – 4 – quite rare

A
  • Autosomal recessive transmission

- Many genetic defects on multiple chromosomes

56
Q

Charcot-Marie-Tooth clinical findings

A
  • Symmetrical, distal involvement
  • Gradual development of Cavus foot deformity
  • Wasting of upper extremity after 10-15 years
  • “Plump” thigh and “slender” leg
  • Prominence of 1st met. = peroneus longus is last to atrophy
  • Clawing of digits = intrinsics are out
57
Q

CMT lower motor neuron lesions

A
  • Flaccid paralysis
  • Fascicular “twitching”
  • Altered Achilles DTR
  • Dorsal column affected (diminished vibration and proprioception)
  • Prolonged NCV
58
Q

CMT treatment options

A
  • Passive stretching
  • Unopposed muscle splinting
  • Soft tissue rebalancing (tendon transfer)
  • Osteotomies
  • Fusion procedures
  • Vitamin E
59
Q

CMT surgical considerations (individualized per deformity)

A
  • Soft tissue procedures
  • Osteotomies
  • Joint stabilization
60
Q

CMT soft tissue procedures

A
  • Plantar medial release

- Tendon transfer

61
Q

CMT osteotomies

A
  • Restoration of bone alignment
62
Q

CMT joint stabilizations

A
  • Triple arthrodesis

- Pan talar arthrodesis

63
Q

Clawed digits in CMT

A
  • Extrinsic motors overpower weakened intrinsics

- Hallux malleus

64
Q

Forefoot cavus deformity in CMT

A
  • Peroneus longus tends to be spared
  • Overpowers weakened anterior tibialis
  • Additional plantarflexion of first metatarsal
  • Increased arch height due to Windlass effect
  • Increased metatarsal declination angles
65
Q

Hindfoot varus in CMT

A
  • Occurs via two mechanisms
  • Subtalar joint inversion – compensation for plantarflexion of first ray
  • Unopposed pull of tibialis posterior
66
Q

Dropfoot deformity in CMT

A
  • Weakness of the anterior tibialis

- Strong superficial and deep posterior compartment motors

67
Q

CMT evaluation

A
  • Determine if upper or lower motor neuron deficit
  • EMG and NCV studies to determine which motor units are functional
  • Laboratory evaluation
  • Flexible versus rigid deformity
  • Presence of ligamentous laxity
68
Q

CMT plantar fascial release

A
  • Steindler stripping

- Release abductor hallucis fascia if tight

69
Q

CMT correction of hallux malleus

A
  • Jones tenosuspension

- Hallux IPJ fusion

70
Q

CMT tibialis posterior tendon transfer

A
  • Split tendon transfer

- “Bridle” procedure (interosseous or circumtibial)

71
Q

CMT peroneus longus tendon transfer

A
  • Weakens pull of tendon

- Empowers peoneus brevis

72
Q

CMT osseous and fusion procedures are done as an adjunct to

A
  • Soft tissue rebalancing
73
Q

CMT osseous procedures (names)

A
  • Digital correction
  • Dorsiflexory osteotomy of first metatarsal
  • Dwyer osteotomy
  • Samilson osteotomy
  • Biplanar calcaneal osteotomy
74
Q

CMT fusion procedures

A
  • Triple arthrodesis
  • Pan-talar arthrodesis
  • Procedures are often staged
75
Q

Roussy-Levy Syndrome

A
  • Static tremor of hands!!!!
  • “Forme fruste” of Charcot-Marie-Tooth
  • Hereditary areflexic dystasia
  • Familial pes cavus
  • Extension of the digits
  • DTR absent
  • Prolonged NCV of involved muscles
  • Positive Romberg’s
  • Kyphoscoliosis
76
Q

Most common of all hereditary ataxias

A
  • Friedreich’s Ataxia!!!!!

- Hereditary spinocerebellar ataxia

77
Q

Friedreich’s Ataxia involves

A
  • Spinocerebellar tract
  • Lateral spinothalamic tract
  • Dorsal columns
78
Q

Friedreich’s Ataxia signs

A
  • Broad-based gait

- Ask them to do heel-to-toe test

79
Q

Friedreich’s Ataxia incidence

A
  • Males = females
  • Frataxin protein defect!!!
  • Abnormally high iron content –> free radicals –> neural and muscular tissue damage
80
Q

Characteristics of Friedreich’s Ataxia

A
  • Cerebellar symptoms initially unsteady gait
  • Delayed motor milestones
  • Progressive thoracic scoliosis (90%)
  • Decreased dorsal column sensation
  • Staccato speech
  • Cardiac failure causes death
  • Positive Romberg’s sign
81
Q

Dejerine-Sottas Syndrome

A
  • HMSN type III
  • Hypertrophic neuropathy
  • Autosomal recessive
82
Q

Dejerine-Sottas hypertophic neuropathy

A
  • Proliferation of Schwann cells of perineural sheath

- Onion bulb appearance!!!

83
Q

Dejerine-Sottas onset

A
  • Infancy
  • Poor walking
  • Lightning paresthesia
  • Posterior auricular nerve affected
84
Q

Sensory modalities affected in Dejerine-Sottas syndrome

A
  • ALL SENSORY MODALITIES
  • Stocking/glove decrease in light touch and sharp/dull
  • Positive Romberg’s sign
  • Progressive muscle weakness
  • Decreased deep tendon reflexes
  • Impaired pupillary response
  • Coarse muscle fibrillations
85
Q

Dejerine-Sottas management

A
  • Accommodative
  • Insensate foot measures (preventing injury)
  • Night Splinting and passive muscle stretching (prevent development of contracture deformities)
86
Q

Riley-Day syndrome

A
  • Familial dysautonomia
  • COMPLETE INDIFFERENCE TO PAIN
  • Autosomal recessive – Ashkenazi Jews (Max)
87
Q

Riley-Day syndrome characteristics

A
  • Decreased mental abilities
  • Emotional lability
  • Orthostatic hypotension and resting tachycardia
  • Poor thermal regulation, excessive sweating
  • Deep tendon reflexes absent or hyporeflexic
  • Absent fungiform papillae on tongue!!!
88
Q

Key difference between Dejerine-Sottas and Riley-Day

A
  • Autonomic dysfunction
89
Q

Riley-Day management

A
  • Insensate foot measures

- Addressing autonomic dysfunction

90
Q

Guillain-Barre Syndrome(Landry’s Ascending Paralysis)

A
  • Symmetrical sensory and motor paresis
  • Acute inflammatory demyelinating polyneuropathy
  • Acute flaccid paralysis
91
Q

Guillain-Barre Syndrome(Landry’s Ascending Paralysis) incidence

A
  • 1.5/100,000
92
Q

Guillain-Barre Syndrome(Landry’s Ascending Paralysis) etiology

A
  • Associated with Campylobacter jejuni

- Schwann cell surface is targeted

93
Q

Guillain-Barre Syndrome(Landry’s Ascending Paralysis) characteristics

A
  • Distal limbs usually first involved (moves proximally/Ascending)
  • Roughly symmetrical distribution
  • Variable autonomic involvement (loss of tendon reflexes)
94
Q

Guillain-Barre Syndrome(Landry’s Ascending Paralysis) maximum disease progression

A
  • Two weeks (75%)

- CSF has increased protein with monocyte presence

95
Q

Guillain-Barre Syndrome(Landry’s Ascending Paralysis) treatment

A
  • Immunomodulation (IgG infusions)
  • Plasmaphoresis (effectiveness of this treatment supports the molecular mimicry theory)
  • Palliative management

Pod Med III (8 decks)

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