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| Question | Answer |
| 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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