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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
First sacral root lesion pain is referred to
- Sacro-iliac joint - Posterior thigh - Lateral posterior leg - Posterior heel
26
First sacral root lesion signs
- Triceps surae weakness (sometimes peroneals) | - Weak achilles DTR
27
Spinal dysraphisms
- Developmental abnormalities along the midline of the back - Multi-factorial etiology - Prenatal screening shows increased alpha fetoprotein!!!
28
Spinal dysraphism etiologies
- 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
29
Spina bifida
- 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
30
Spina bifida with meningocele
- Failure of vertebral arches to close - Protrusion of meninges into sac - Symptoms dependent upon degree and level of defect
31
Spina bifida with myelomeningocele
- Protrusion of meninges and spinal cord | - Symptoms dependent upon degree and level of defect
32
Spina bifida clinical recognition
- Symptoms often unilateral - Associated with foot deformities - Accommodative gait disturbances
33
Spina bifida shows decreased
- Proprioception (spinal cerebellar) - Cutaneous sensation - Deep tendon reflexes - Weakness and atrophy of leg muscles
34
Spina bifida dermatological findings
- Nevus flammeus (most common finding) - Capillary angioma - Hypertrichosis at base of spine - Midline lumbosacral lipoma - Lumbosacral sinus
35
Tethered cord syndrome secondary to traction on conus medullaris
- Tight filum terminale - Rests below L2 - Look out for spinal taps
36
Tethered cord syndrome secondary to diastematomyelia
- Division of spinal cord – sagittal plane | - Progressive deterioration if untreated
37
Other dysraphisms
- Anterior cord syndrome - Brown Sequard syndrome - Conus medullaris syndrome - Cauda equina syndrome
38
Anterior Cord Syndrome (spinal thalamic)
- Efferent motor/sharp dull and temperature - Variable motor and LSST loss Preservation of proprioception
39
Brown-Sequard syndrome
- Hemi section of SC - Ipsilateral loss of proprioception and motor - Contralateral loss pain and temperature
40
Conus medullaris syndrome
- Sacral cord injury - Areflexia in bladder, bowel and lower limbs - Variable motor and sensory loss
41
Cauda equina syndrome
- 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
Vascular supply to spinal cord
- One anterior spinal artery to 75% of cord | - Two posterior spinal arteries to 25% of cord
43
Anterior spinal artery supplies
- Corticospinal tract - Lateral spinothalamic tract - Autonomic interomedial pathway
44
Posterior spinal arteries supply
- Dorsal columns
45
Anterior motor horn disease
- Another consideration in patients with weakness without sensory changes - Poliomyelitis - Post-polio syndrome
46
Poliomyelitis
- Initial LMN weakness or paralysis - Replaced by tightening and muscle spasm (spastic paralysis) - Weakness in assymetrical and scattered distribution
47
Post-polio syndrome
- Disruption of agonist-antagonist balance | - Increased deterioration
48
Amyotrophic Lateral Sclerosis (anterior motor horn disease)
- 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
Characteristics of LMN disease (secondary to peripheral nerve pathology)
- Presence of fasciculations and fibrillations - Hypo- or areflexia - Hypotonia or flaccid paralysis - Absent Babinski sign - Diagnosed by sural nerve biopsy!!!
50
Charcot-Marie-Tooth disease (peroneal muscular atrophy)
- 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
Charcot-Marie-Tooth disease is characterized by atrophy of
- Peroneal muscles - Intrinsics - Anterior muscles
52
Charcot Marie Tooth - 1 – “demyelinating” – 50% (most common)
- 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
Charcot Marie Tooth - 2 – “neuronal” - 20%
- Adult onset – autosomal dominant - Axonal degeneration of peripheral nerve - No enlargement of peripheral nerves
54
Charcot Marie Tooth-X – 10-20%
- X-linked inheritance pattern | - Defects in myelin constituent protein connexin 32 (defect in communication between cells)
55
Charcot Marie Tooth – 4 – quite rare
- Autosomal recessive transmission | - Many genetic defects on multiple chromosomes
56
Charcot-Marie-Tooth clinical findings
- 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
CMT lower motor neuron lesions
- Flaccid paralysis - Fascicular “twitching” - Altered Achilles DTR - Dorsal column affected (diminished vibration and proprioception) - Prolonged NCV
58
CMT treatment options
- Passive stretching - Unopposed muscle splinting - Soft tissue rebalancing (tendon transfer) - Osteotomies - Fusion procedures - Vitamin E
59
CMT surgical considerations (individualized per deformity)
- Soft tissue procedures - Osteotomies - Joint stabilization
60
CMT soft tissue procedures
- Plantar medial release | - Tendon transfer
61
CMT osteotomies
- Restoration of bone alignment
62
CMT joint stabilizations
- Triple arthrodesis | - Pan talar arthrodesis
63
Clawed digits in CMT
- Extrinsic motors overpower weakened intrinsics | - Hallux malleus
64
Forefoot cavus deformity in CMT
- 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
Hindfoot varus in CMT
- Occurs via two mechanisms - Subtalar joint inversion – compensation for plantarflexion of first ray - Unopposed pull of tibialis posterior
66
Dropfoot deformity in CMT
- Weakness of the anterior tibialis | - Strong superficial and deep posterior compartment motors
67
CMT evaluation
- 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
CMT plantar fascial release
- Steindler stripping | - Release abductor hallucis fascia if tight
69
CMT correction of hallux malleus
- Jones tenosuspension | - Hallux IPJ fusion
70
CMT tibialis posterior tendon transfer
- Split tendon transfer | - “Bridle” procedure (interosseous or circumtibial)
71
CMT peroneus longus tendon transfer
- Weakens pull of tendon | - Empowers peoneus brevis
72
CMT osseous and fusion procedures are done as an adjunct to
- Soft tissue rebalancing
73
CMT osseous procedures (names)
- Digital correction - Dorsiflexory osteotomy of first metatarsal - Dwyer osteotomy - Samilson osteotomy - Biplanar calcaneal osteotomy
74
CMT fusion procedures
- Triple arthrodesis - Pan-talar arthrodesis - Procedures are often staged
75
Roussy-Levy Syndrome
- 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
Most common of all hereditary ataxias
- Friedreich's Ataxia!!!!! | - Hereditary spinocerebellar ataxia
77
Friedreich's Ataxia involves
- Spinocerebellar tract - Lateral spinothalamic tract - Dorsal columns
78
Friedreich's Ataxia signs
- Broad-based gait | - Ask them to do heel-to-toe test
79
Friedreich's Ataxia incidence
- Males = females - Frataxin protein defect!!! - Abnormally high iron content --> free radicals --> neural and muscular tissue damage
80
Characteristics of Friedreich's Ataxia
- 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
Dejerine-Sottas Syndrome
- HMSN type III - Hypertrophic neuropathy - Autosomal recessive
82
Dejerine-Sottas hypertophic neuropathy
- Proliferation of Schwann cells of perineural sheath | - Onion bulb appearance!!!
83
Dejerine-Sottas onset
- Infancy - Poor walking - Lightning paresthesia - Posterior auricular nerve affected
84
Sensory modalities affected in Dejerine-Sottas syndrome
- 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
Dejerine-Sottas management
- Accommodative - Insensate foot measures (preventing injury) - Night Splinting and passive muscle stretching (prevent development of contracture deformities)
86
Riley-Day syndrome
- Familial dysautonomia - COMPLETE INDIFFERENCE TO PAIN - Autosomal recessive – Ashkenazi Jews (Max)
87
Riley-Day syndrome characteristics
- 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
Key difference between Dejerine-Sottas and Riley-Day
- Autonomic dysfunction
89
Riley-Day management
- Insensate foot measures | - Addressing autonomic dysfunction
90
Guillain-Barre Syndrome(Landry’s Ascending Paralysis)
- Symmetrical sensory and motor paresis - Acute inflammatory demyelinating polyneuropathy - Acute flaccid paralysis
91
Guillain-Barre Syndrome(Landry’s Ascending Paralysis) incidence
- 1.5/100,000
92
Guillain-Barre Syndrome(Landry’s Ascending Paralysis) etiology
- Associated with Campylobacter jejuni | - Schwann cell surface is targeted
93
Guillain-Barre Syndrome(Landry’s Ascending Paralysis) characteristics
- Distal limbs usually first involved (moves proximally/Ascending) - Roughly symmetrical distribution - Variable autonomic involvement (loss of tendon reflexes)
94
Guillain-Barre Syndrome(Landry’s Ascending Paralysis) maximum disease progression
- Two weeks (75%) | - CSF has increased protein with monocyte presence
95
Guillain-Barre Syndrome(Landry’s Ascending Paralysis) treatment
- Immunomodulation (IgG infusions) - Plasmaphoresis (effectiveness of this treatment supports the molecular mimicry theory) - Palliative management

Pod Med III (8 decks)

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