Week 18/19 peripheral nerves Flashcards
What are the steps in the motor neuro exam?
- General inspection.
- Upper limb; pronator drift, tone, power.
- Lower limb; tone, power.
What are you looking for in inspection during a motor neuro exam?
General and limb posture.
MM bulk.
Involuntary movements.
Tremor
Rhythmic oscillation around a joint.
Fasciculations
Involuntary repetitive muscle contractions.
Best seen under tangential lighting.
Tone
Amount of residual resistance offered by a mm when it is moved passively.
How do you assess tone in the upper limb?
Passively rotating the wrist and flexing/extending the elbow.
Rigidity
Constant increased tone that is velocity-independent.
Spasticity
Increased tone that is velocity-dependent (seen in UMN lesions).
Flaccidity
Abnormally decreased mm tone (seen in LMN lesions).
What scale do we use to quantify mm power?
MCR Scale grade 0-5
5: normal strength against resistance
4: reduced strength but can still move against resistance.
4+ strong resistance
4 moderate resistance
4- slight resistance
3: movement against gravity without resistance
2: movement only w/gravity minimized
1: flicker of movement seen or felt in mm or fasciculations observed
0: no movement at all
Clonus
Involuntary rhythmic contractions and relaxations that occur inpatients with UMN lesions.
What are the 3 upper limb reflexes tested?
Biceps
Brachioradialis
Triceps
What lower limb reflexes are tested?
Patellar
Calcaneal
Plantar - looking for inversion and downward toe movement = normal
What is used to quantify DTR results?
DTR grading scale 0-4
0: no reflex
1: diminished
2: normal
3: pathologically brisk
4: pathologically brisk with clonus
Babinski’s sign
Big toe dorsiflexes
Other toes fan out
Indicates UMN lesion
What can be used to illicit a stronger reflex response?
Jendrassik maneuver
hands gripped together, pulling into lateral extension while biting teeth together.
What domains are tested with sensory exams?
Temperature
Pain (sharp vs dull)
Non-discriminative touch (cotton ball)
Vibration (tuning fork on bone)
Proprioception (move joint and get patient to say which direction its moving.)
What are the 2 pathways that sensory information is delivered to the brain?
Spinothalamic tract: non-discriminative touch, temperature, pain.
Posterior column medial lemniscus tract: proprioception, vibration.
How will a nerve root lesion present?
As a dermatomal pattern.
ie; C5 dermatome
How will a lesion at the peripheral nerve level present?
In the peripheral nerve distribution pattern.
ie; radial nerve distribution
What is included in a neurological screening exam?
Language assessment
CN exam
Motor/Sensory
Coordination
Gait
What components are assessed in the language exam?
Comprehension
Naming
Repetition
Which CN are assessed?
All except CNI
How is CNII assessed?
Pupillary light reflex (CN II & III)
Swinging light test
Fundal exam
Visual field testing
Visual acuity assessment
How are CN III, IV, VI assessed?
Smooth pursuit (H pattern)
Saccadic eye movements (horizontal and vertical)
How is CN V assessed?
If no numbness/tingling in face compare sides of face to light touch in all 3 CNV distributions.
Assess for jaw deviation.
How is CN VII assessed?
Eyebrows up and down.
Tightly close eyes and resist passive opening.
Show teeth.
Resist lip separation.
How is CN VIII asssessed?
Close eyes and check to see which ear a noise is heard.
How are CN IX and X assessed?
Say ahhhhh
Look for symmetry in palate elevation and uvula stays midline.
How is CN XII assessed?
Tongue bulk and movement.
Symmetry, strength putting tongue into cheek.
How is CN XI assessed?
SCM resistance.
Traps symmetrical movement.
Scapular winging.
Components of the CNS that could be involved in a neuropathy.
Brain
Spinal cord
Components of the PNS that could be involved in a neuropathy.
Peripheral nerve cell bodies
Nerve Roots
Plexus
Peripheral nerves
Neuromuscular junction
Muscle
UMN vs LMN signs:
1. Tone
2. Reflexes
3. Atrophy
4. Associated features
- UMN - spastic, LMN - flaccid
- UMN - brisk reflexes, LMN - areflexic
- UMN - slight atrophy, LMN - greater atrophy
- UMN - cognitive, language, vision, LMN - fasciculations
Hemi-body weakness and sensory loss are associated with what area?
Brain
Aphasia, visual field defects, cognitive changes (higher function deficits) are associated with what area?
Cortex
CN abnormalities such as double vision, vertigo, swallowing difficulties are associated with what area?
Brainstem
Complete spinal cord injury could result in what?
Bilateral motor weakness.
Bilateral sensory loss.
Bowel/bladder dysfunction.
Determinant level of spinal cord.
Hemi-cord injury could result in what?
Hemi-body motor weakness.
Hemi-body sensory loss.
Bowel/bladder dysfunction.
Determinant level of spinal cord.
Anterior horn cell dysfunction results in what?
Motor;
segmental weakness,
generalized weakness.
Dorsal root ganglion dysfunction results in what?
Sensory;
non-length dependant sensory loss.
What does the posterior ramus innervate?
Paraspinal muscles.
Sensory of overlying skin.
What does the anterior ramus innervate?
Motor and sensory to limbs and trunk.
Cervical nerve roots emerge from what levels?
C1-C7
Above the vertebra, C1-C8
Thoracic, lumbar, and sacral nerve roots emerge from what levels?
T1-C0
Below the vertebra.
What is the pattern of deficits for radiculopathies?
Dermatomes and myotomes
What is the most common brachial plexopathy?
Upper trunk, C5/C6
Types of peripheral neuropathies.
Mononeuropathy - single nerve distribution.
General neuropathy - length or non-length dependent.
Mononeuritis multiplex - multifocal.
Polyneuropathy - generalized.
Plexopathy.
Radiculopathy.
Approach to localization of peripheral neuropathies
- Motor, sensory, or both?
- UMN vs LMN
- Pattern of abnormalities
- Associated features
How to assess small fiber sensory nerves?
Pinprick
Temperature
How to assess large fiber sensory nerves?
Vibration
Proprioception
Mneumonic for brachial plexus divisions.
Remember To Drink Cold Beer
R Roots; C5-T1
T Trunks; upper, middle, lower
D Divisions; anterior, posterior
C Cords; lateral, posterior, medial
B Branches; nerves
Lumbosacral plexus nerve roots
L1-S3
Upper lumbar plexus; L1-L4
Lower lumbar plexus; L5-S3
Median nerve:
1. Nerve roots
2. Sensory distribution
3. Motor
- C5-T1
- Thumb and lateral 2 1/2 fingers, palm, thenar eminence (palmar cutaneous branch)
- Thumb abduction; abductor pollicis brevis. Thumb opposition; opponens pollicis. Lumbricals. Flexor pollicis brevis. (LOAF)
Ulnar nerve:
1. Nerve roots
2. Sensory distribution
3. Motor
- C8 - T1
- Medial 1 1/2 digits, medial arm and forearm.
- FCU, FDP, Adductor pollicis, Digiti minimi.
Radial nerve:
1. Nerve roots
2. Sensory distribution
3. Motor
- C5 - T1
- Post arm and hand
- Triceps, anconeus, supinator, forearm and hand extensors
Sciatic nerve:
1. Nerve roots
2. Sensory distribution
3. Motor
- L4 - S3
- Tibial/Common peroneal branches, no sensory from Sciatic
Deep peroneal nerve:
1. Sensory distribution
2. Motor
- Web of big toe
- Tib ant, extensors
Superficial peroneal nerve:
1. Sensory distribution
2. Motor
- Lateral and anterior leg, top of foot.
- Peroneals
Polyneuropathy
Dysfunction of many or all peripheral nerves.
Symmetric and distally predominant:
Starts in toes and progress up, when at upper calves fingers get involved.
Gradually progressive.
How do large fiber nerves with a lesion present clinically?
A-Beta
Tingling, numbness
Hypo or areflexia
Decreased vibration and proprioception sensation
Ataxia
How do small fiber nerve lesions present clinically?
A-delta and C
Burning, jabbing, shooting
Decreased pain and temperature sensations
Demylinating polyneuropathy
Destruction of myelin leading to sensory and motor dysfunction.
Globally decreased or absent reflexes.
1. Inherited
2. Acquired: Guillain Barre Syndrome, Chronic inflammatory demyelinating polyneuropathy.
Guillain Barre Syndrome
Medical emergency.
Progression of symptoms <4weeks.
60% have preceding GI or upper resp infection.
CSF = albuminocytologic dissociation (elevated pr w/normal WBC)
Chronic Inflammatory Demyelinating Polyneuropathy
Gradual progress or relaps > 8 weeks of onset.
Symmetric sensory and motor polyneuropathy.
Proximal and distal weakness > sensory loss.
Global decrease/loss of reflexes.
Minimal dysautonomia.
CSF - albuminocytologic dissociation (elevated pr w/normal WBC).
Polyneuropathy investigations
HbA1c, other glucose tests
CBC
TSH
B12
Serum and urine electrophoresis
ANA, CRP, or ESR
(HIV, syphilis)
Mononeuritis multiplex
Asymmetric.
Usually d/t vasculitis.
Stepwise: severe pain followed by weakness and numbness.
Constitutional symptoms.
Can affect other organ systems if systemic (rash, resp, GI).
Most common radiculopathies
L5/S1
C5/C6
Cauda equina syndrome
Medical emergency.
Multiple nerve root compression below L1 or L2.
Saddle anesthesia.
Distended atonic bladder with retention or overflow incontinence.
Constipation, fecal incontinence, decreased/absent rectal tone.
Erectile dysfunction.
**URGENT MRI
Electrodiagnostic studies
- Nerve conduction: Sensory or motor
- Needle EMG: can indicate chronicity, myopathy
Only able to study large fibers.
Positive peripheral neuropathy symptoms
Reflect inappropriate spontaneous nerve activity.
Motor: cramps, twitching.
Sensory: tingling, burning, stabbing pain, allodynia, hyperalgesia.
More prominent early on.
Negative peripheral neuropathy symptoms
Reflect reduced nerve activity.
Motor: weakness, atrophy.
Sensory: reduced sensation, numbness, ataxia, imbalance (worse without visual input).
Autonomic peripheral neuropathy symptoms
Cardiac: orthostatic dizziness, labile bp, arrhythmias.
GI: early satiety, bloating, constipation, diarrhea.
Genitourinary: ED, incontinence, retention.
Vasomotor: cold extremities, skin colour changes.
Signs of long standing neuropathy
High arches.
Hammertoes.
Scoliosis.
Ddx for peripheral neuropathy symptoms
CNS (myelopathy).
Motor neuron disease.
NMJ.
Myopathy.
Prototypic polyneuropathy
Length-dependent.
Sensory > distal weakness.
Stepwise approach to peripheral neuropathy
- Is this peripheral neuropathy?
- Localization/pattern of distribution. Is this process length-dependent?
- Nerve fibre involvement: sensory/motor.
- Axonal vs demyelinating.
- Time course.
- Other clues.
Pathogenesis of length-dependent neuropathy
Metabolic function in cell body and axon is impaired.
Defect in production of vital macromolecules seen first in distal axon.
Longest peripheral nerve fibres are sensory.
Large diameter axons with higher metabolic needs (vibration/proprioception) show earliest changes.
What size of nerves carry pain/temp?
Small unmyelinated (some myelinated).
What size of nerves carry vibration and proprioception?
Large myelinated.
Signs and symptoms of length dependent neuropathy.
- Paresthesia in toes, then numbness.
- Progresses proximally.
- When reaching knee starts to manifest “glove and stocking pattern”.
- Motor symptoms develop later; foot, leg, hands after calves involved.
- Reflexes; ankles, then knees, brachioradialis, triceps, biceps.
Causes of distal or length dependent neuropathy
Systemic disorders; diabetes, nutritional deficiencies (B12).
Toxins.
Rheum/CT diseases.
Hereditary.
Idiopathic.
Red flags of axonopathy
Asymmetry.
CN or proximal limb involvement.
Motor > sensory.
Reflex findings overly strong for mild symptoms.
Rapid progression over days-weeks.
What do axonopathy red flags imply?
Different pattern: mononeuropathy multiplex, polyradiculopathy.
Different pathophysiology: demyelination, inflammation, infiltration, infarction.
Signs and symptoms of radiculopathy
Single nerve root distribution.
Presents in myo or derm pattern.
Signs and symptoms of polyradiculopathy
Multiple nerve root distribution.
Signs and symptoms of mononeuropathy
Single nerve distribution.
Signs and symptoms of mononeuropathy multiplex
Multiple named nerve distributions.
Axonal vs demyelinating neuropathy
Need electrodiagnostic study.
Demyelinating: Decreased conduction speed.
Axonal: Decreased amplitude
Clues for demyelination: weakness w/out atrophy, early loss of reflexes, non length-dependent, rapid ascending symptoms, preceding infection.
Medical treatment for GBS
Immunomodulation:
Plasmapheresis (PLEX)
IVIG (Intravenous immunoglobulin)
Features of Charcot-Marie-Tooth (CMT)
Most common hereditary neuropathy.
Can be demyelinating or axonal.
Insidious symmetric progression.
Painless with minimal (+) sensory symptoms.
Hx of clumbsiness.
Severe distal weakness.
High arched feet, hammertoes.
(+) family hx.
What will happen to the distal end of a nerve once an axon is disrupted?
It will ALWAYS degenerate.
Ten test
Compare sensation of light touch between normal and affected areas.
Patient classifies affected area from 0-10 relative to normal area.
Manifestations of distal axonopathy
1st symptom is tingling in toes, followed by numbness.
Glove/stocking pattern.
Motor symptoms later:
Toe weakness/clawed toes,
Weak dorsiflexsion,
Then hands.
Distal reflexes first, then ascending.
Classic polyneuropathy presentation
Length dependent.
Evolves over months-years.
Deviation from this implies different localization/pattern or pathophysiology.
Principles of managing peripheral neuropathy
- Treat underlaying cause.
- Treat neuropathic pain.
- Bracing/orthotics.
- Multidisciplinary team.
- Education and counselling.
- Avoid neurotoxins.
What % of pain reduction is clinically important, resulting in “moderate relief” or “much improved”
30% reduction.
Pharmacologic management of neuropathic pain algorhythm
- Gabapentinoids/TCAs/SNRIs
- Tramadol/Opioids
- Cannabinoids
- 4th line agents
Hallmarks of a “run of the mill” polyneuropathy
Length dependent.
Slow progression.
Minimal disability.
Clinical features of GBS
Sensory:
Numbness/tingling in feet that ascend to arms.
Face/trunk involvement.
Neuro pain in back/limbs.
Large fiber > small fiber impairment.
Motor:
Distal > proximal weakness.
Weakness in legs that ascends to arms, trunk, head & neck.
Facial weakness in 50%.
Opthalmoplegia/ptosis in 5-15%.
Respiratory:
Respiratory failure in 33%.
Autonomic:
Hypo/Hypertension.
Arrhythmia.
Approach to distinguish between radiculopathy and mononeuropathy.
Examine:
Mm groups.
Reflexes.
Sensation.
Unique irritative signs.
How do axons receive nutrients?
Blood-nerve barriers.
Microvascular blood supply to the nerve.
Between the inner perineurium and endoneurium.
Classification of traumatic nerve injuries (levels of injury)
Neurapraxia - only myelin damaged.
Type II axonotemesis - axon damaged.
Type III axonotemesis - endoneurium is disrupted.
Type IV axonotemesis - perineurium and endoneurium are disrupted.
Neurotemesis - all three connective tissue layers are disrupted (epi, peri, & endo).
Classification of peripheral nerve fibers from largest to smallest (slowest to quickest)
MYELINATED
Aa: motor to skm.
Aa Ia: sensory from mm spindle.
Ab Ib: sensory from Golgi and Ruffini.
AB II: sensory from skin.
Ay: motor to intrafusal fibres.
Ad III: Sensory from free nerve endings and hair follicles.
B: Preganglionic autonomic fibres.
UNMYELINATED
C: Sensory from free nerve endings for pain/temp, smell, autonomomic fibres.
Motor unit
Single a-motor neuron and all innervated muscle fibres.
What is the NMJ made up of?
Presynaptic terminal.
Synaptic cleft.
Post synaptic terminal.
How is ACh released?
Exocytosis d/t Ca2+ and SNARE proteins.
How does botulinum toxin affect mm ctx?
Blocks SNARE protein in NMJ to cause temporary paralysis.
Myasthenia gravis
Autoimmune neuromuscular disorder wehre ab’s attack Ach receptors in the NMJ.
Malignant hypothermia
Mutation in Ryanodine Receptor 1 channel that leads to sustained mm ctx.
What is the role of the Ryanodine Receptor 1 in mm ctx?
AP moves down T-tubule.
Ca2+ released from SR.
Ca2+ binds to ryanodine receptor 1 on SR causing more Ca2+ to be released.
Ca2+ binds to actin.
Mechanism of mm spindle
Sensory input from mm spindle (intrafusal mm) via Aa Ia fibres to dorsal horn.
Dorsal horn to ventral horn.
Aa motor neurons contract extrafusal mm AND
Ay motor neuron maintains coactivation of mm spindle
Type I muscle fibres
Slow twitch.
More mitochondria.
Oxidative metabolism.
Endurance.
Type II muscle fibres
Fast twitch.
Glycolytic pathway.
Fatigue easily.
Several subtypes.
Pathophysiology of myasthenia gravis
Autoantibodies against ACh receptors.
Clinical presentation of MG
Fluctuating ptosis and diploplia.
Fatigueable weakness.
Respiratory weakness.
Examination for MG
Upgaze for 1 minute.
Count backwards outloud from 100.
Repeated strength testing.
Ice pack.
Curtain sign.
Positive symptoms for muscle disorder.
Cramps.
Contractures.
Hypertrophy.
Myalgia.
Myoglobinuria.
Stiffness.
Negative symptoms for muscle disorder
More common than positive symptoms.
Weakness.
Fatigue.
Exercise intolerance.
Muscle atrophy.
Lateral femoral cutaneous neuropathy.
1. Site of compression
2. Sensory
3. Motor
- Inguinal ligament
- lateral and anterior thigh
- No motor, only sensory
