Lecture 3 Peripheral Neuropathy

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PT546 Neuropathology Flashcards on Lecture 3 Peripheral Neuropathy, created by Mia Li on 28/01/2018.
Mia Li
Flashcards by Mia Li, updated more than 1 year ago
Mia Li
Created by Mia Li over 6 years ago
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Which part of the nervous system is involved in peripheral neuropathy? 1. motor CN (sensory and special) 2. peripheral nerve (motor AND sensory, also both spinal nerve roots) 3. autonomic system
What if UMN sign is present when patient is referred for peripheral neuropathy? RED FLAG! not purely peripheral!!!!!
Peripheral neuropathy: clinical presentation from the motor perspective 1. weakness 2. fasciculations 3. atrophy 4. areflexia
Peripheral neuropathy: clinical presentation from the sensory perspective: If peripheral nerve: cutaneous sensory loss in peripheral nerve pattern If polyneuropathy: stocking-glove pattern If spinal nerve root: dermatomal pattern
Peripheral neuropathy: clinical presentation from the autonomic perspective: 1. flushing (redness) 2. change in HR, BP, Breathing pattern 3. incontinence/retention; constipation/diarrhea 4. dry eyes/ mouth
T/F: diabetic neuropathy typically starts with sensory disturbance and works its way from proximal to distal. F. (distal - proximal)
The easiest way to distinguish GBS from CIDP is by considering: Timeline
What are the 4 major categories of neurons? 1. neuronal degeneration (as in ALS) 2. Wallerian degeneration (axon cut at midway) 3. segmental demyelination (axon is still intact) 4. axonal degeneration (from distal - proximal)
Among all 4 types of degenerations, which ones causes more atrophy? Wallerian and axonal (because nothing gives muscle input)
Define neuronal degeneration: cell body damage with degeneration of axons
Define Wallerian degeneration: damage to axon at a specific point with distal degeneration
Define segmental demyelination: injury to myelin sheath WITHOUT injury to axon
Define axonal degeneration Diffuse axonal damage (starting distally)
Steps of acute axonal insult at a specific point 1. initial injury 2. macrophage recruitment with Wallerian degeneration 3. Schwann cell alignment and axon regeneration 4. Successful target reinnervation
T/F: basement membrane typically stays intact after wallerian degeneration. T.
Cause of mononeuropathy 1. nerve entrapment 2. repetitive motion injury 3. trauma
Causes of polyneuropathy 1. infectious diseases (HIV) 2. Inflammatory diseases (AIDP/GBS, CIDP) 3. Systemic disease (DM, critical illness, Vit D deficiency) 4. Genetic disorders (Charcot Marie Tooth) 5. Toxins (chemo, alcohol)
What is the single most important diagnostic test for eval of neuropathy, which can determine whether it is primarily axonal, demyelinating or mixed. EMG/ NCV
What should be done to rule out GBS and CIDP? Lumbar puncture
Another name for Guillain-Barre Acute inflammatory demyelinating polyneuropathy
What mostly happens before GBS? acute infection
Is sensory affected in GBS? Yes. May have numbness/tingling in hands and feet.
Most common symptoms for GBS - muscle weakness - usually begins in legs and ascends - may cause severe respiratory muscle weakness - areflexia
What are some medical treatment for GBS? plasma exchange IVIG
More (male/female) are affected in GBS. Male
What are some variations of GBS? 1. acute MOTOR axonal neuropathy (AMAN) acute MOTOR SENSORY axonal neuropathy (AMSAN)
T/F: GBS is autoimmune. T.
About ___% GBS has a preceding infection. 60%
Which structure is affected in GBS? - myeline of peripheral nerves - nerve cell and axons are SPARED
For GBS, symptoms takes ______ to onset, it progresses rapidly for _____ to reach nadir and plateaus in about _________. In _______, some patient can recover fully. For GBS, symptoms takes 1-3 wks to onset, it progresses rapidly for1-4 wks to reach nadir and plateaus in about 2-4 weeks. some patient can recover fully.
Onset of GBS: symettrical or asymmetrical? Symmetrical
Can there be CN involvement in GBS? Yes
Can there be autonomic dysfunciton in GBS? Yes.
What is the Golden standard diagnostic test for GBS? - Lumbar puncture (elevated protein levels in CSF with normal cell count) elevated protein = myeline breakdown normal cell count = not infection
Timeline for CSF protein level changes -starts to rise a few days after onset - peaks in 4-6 weeks
What do you look for in blood tests of GBS patients? infectious agents
What is a good test to do to rule out competing diagnoses in GBS patients? Spinal cord imaging (R/O acute SCI)
Which tests can be done at the plateau stage of GBS? - EMG - NCV
What might happen if you perform EMG test right after diagnosis of GBS? may not show any abnormality for up to 2 weeks (due to length of nerve)
What can you expect in a patient's EMG, who has plateaued in GBS? - decreased interference pattern due to less MU recruitment
What do you expect to see in a GBS patient's NCV test? - slowed nerve conduction - minimal sensory slowing - prolonged distal latencies
What are some competing Dx of GBS? - Acute SCI - Brain stem ischemia - Myasthenia Gravis - Botulinum intoxication - CIDP
What are the medical management options for GBS? - IVIG (5 days) - Plasmapheresis (5-6 exchange over 1-2 weeks)
Does steroidal use help with GBS? No (but able to treat CIDP)
T/F: GBS cannot recover. F. Most patients return to normal function.
___% regain full strength in 1 year. 60% patients
Does GBS re-occur? No
Severe motor problems persist in ___ patients. 14%
What are some negative prognostic factors? 1. old age 2. requiring ventilation 3. rapid progression (<7 days) 4. axonal injury
After schwann cell recovery, there are (more/less) nodes along a single axon. More. (hence slower conduction)
What is a result for collateral sprouting in early recovery? Very large MU
Speed of axonal regrowth 1 mm per day
T/F: GBS patients usually do not have pain. F. muscle belly pain.
What is a precaution during clinical management of GBS patients? - over-stretching - over-working
T/F: both GBS and CIDP are autoimmune diseases. T.
T/F: GBS and CIDP have the same mechanism of axonal degeneration. F. Demyelination, not axonal problem.
How to differentiate CIDP from GBS? Timeline
Which of the following is a typical progression of CIDP? A. stepwise progression with periods of plateau B. Steadily declining course C. Course with recurrent episodes All of above.
Which one has more sensory involvement, GBS or CIDP? CIDP.
Signs and symptoms of CIDP: 1. Gradual progressive weakness over at least ________. 2. _____ reflex 3. flaccid muscle 4. (motor/sensory/autonomic) involvement 5. possible cranial and respiratory muscle weakness 1. Gradual progressive weakness over at least 2 months 2. decreased/ absent reflex 3. flaccid muscle 4. motor, sensory, and autonomic involvement 5. possible cranial and respiratory muscle weakness
What are some diagnostic studies in CIDP? - EMG - NCV - LP (elevated protein but no increase in cell count)
How will EMG be like in CIDP patients? fibrillations and positive sharp waves (denervation)
How does NCV look like in CIDP patients? slowed velocity (both motor and sensory)
What are some competing diagnosis of CIDP? 1. multifocal stroke 2. motor neuron disease 3. polyradiculopathy 4. inflammatory myopathy 5. neuromuscular junction disease 6. DM, B12 deficiency 7. multiple sclerosis 8. Tabes dorsalis
Medical management options for CIDP Prednisone IVIG (5 days) Plasmapheresis (6 exchanges over 7-10 days.
T/F: the relapse rate for CIDP is low. F. It is high.
Most common cause of neuropathy? DM
____% DM patients are likely going to develop polyneuropathy. 50%
Typical presentation of DM-PN - distal to proximal - symmetric (stocking-n-glove) -sensory + motor - autonomic neuropathy
How long does the progression of DM-PN take? months to years
Onset of DM-PN: (sudden/ insidious) insidious
Which one comes first in Dm-PN, sensory or motor loss? Sensory
What tests are needed to diagnos DM-PN? 1. EMG 2. NCV 3. Glucose tolerance test
What is special about EMG results in DM-PN patients? - mixed evidence of acute denervation and re-innervation - fibrillations (acute) - polyphasic and giant motor units (re-innervation) - changes in interference pattern (chronic)
What is the expected NCV results in patients with DM-PN? - slowed conduction velocity (both sensory and motor) - Sensory changes precede motor changes
What are some competing diagnoses of DM-PN? - any chronic sensorimotor neuropathy - all causes of small-fiber neuropathy, autonomic neuropathy/ radiculopathy/ plexopathy/ mononeuropathy - myopathy - stroke - Carpal Tunnel Syndrome - cervical/ lumbar radiculopathy
What are the most important medical management for DM-PN patients? - glucose control - medication for neuropathic pain - prevention of ulcers - manage autonomic symptoms
Special sensory tests for DM-PN patients. Monofilament test for protectives sensation
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