distal (tripping over toes) and proximal (more neurons) motor neuropathy
sensory: pain, tingling
acute (tingling for a little) vs. chronic
feel like stabbing, piercing
what are physical clues that suggest neuropathy?
sensation: (vibration/proprioception), pain
trophic: imbalance of neuronal innervations in muscle of joints
backward/lateral spine curvature
joint disease related to nerves
what do large myelinated axons vs. small myelinated axons affect?
large (vibration/proprioception-spatial orientation)
small (pain and temp)
types of neuropathy
cell body damage of the motor neuron (movement destroyed) or dorsal root ganglion (sensation destroyed)
traumatic, toxic, metabolic
length dependent, symmetric, distal
hereditary or inflammatory
non-length dependent (patchy is inflammatory, diffuse is hereditary)
compound muscle action potential (CAMP)
neuron to motor muscle (proximal to distal)
sensory nerve action potential (SNAP)
distal nuron to proximal)
when stimulation is further from the muscle what is the latency?
what is latency
how rapidly nerve conducting impulse
what happens to EMG in axon degeneration?
amplitude is down, NCV is stable
action potential is variable (signal may or may not get through)
when further away from the muscle stimulated, amplitude decrease and increase in latency)
goes down from arm to palm
goes to motor neuron (up), fire and depolarize and send another signal down (f-wave)
possible causes of demyelination?
some antigen initiates immune response
resulting antigen receptors cross react with self-protein that mimics the antigen
self-protein may be inhibited or the containing cells destroyed
self protein that binds with bad antigen receptors
what are molecular mimicry examples?
MS, GBS, CIDP
how many % patients have the classic triad of CIDP
slow nerve condition velocity
increase CSF protein
demyelination on nerve biopsy
what is the only way to see pathology of the disease?
point of EMG
whether it is truly a peripheral neuropathy and whether the neuropathy is demyelinating
what happens as disease prolongs?
patents develop secondary axonal degeneration
multifocal conduction block or temporal dispersion of CMAP/SNAP
absent ro prolonged F-wave latency
neuropathy in EMG
decrease conduction velocity
increased distal latency
increase F-wave latency
clinical criteria for neuropathy
two or more months, hypo/areflexia, motor/sensory involvement, more than 1 limb
cytotoxic chemo drug used as immunosuppressant
antimetabolite drug that interferes with the purine pathway and therefore with DNA synthesis in cell division; it causes inhibition of proliferating lymphocytes and is often used as steroid-sparing agent.
decrease in RBC (anemic) and WBC (susceptible to infection)
IVIg (intravenous immunoglobulin)
IVIg is a preparation of human polyclonal IgG obtained from plasma of several thousands of healthy donors
anti-inflammatory activity when used in high dose and immunomodulation
gamma (second therapy)
alkylating agent that can be given orally or by intravenous injection to deplete T and B lymphocytes
pure motor CIDP treatment
IVIg, since deterioration has been reported with steroids, as in MMN
catheter entered target vein but was first tunneled under the skin for a few inches
reduced infection risk
Interferon beta 1a
released by host cells in response to the presence of several pathogens
a virus-infected cell will release interferons causing nearby cells to heighten their anti-viral defenses.
type of cytokine
Interferon beta balances the expression of pro- and anti-inflammatory agents in the brain, and reduces the number of inflammatory cells that cross the blood brain barrier
first study sarah was in
flulike side effects
patient with cancer during sarah's plasma replaced in oncology unit
sarah worked at a book store
decreased conduction velocity
increase distal latency
increased F wave latency
most common preceding infection in GBS
excessive amounts of monoclonal gamma globulin, IgM produced by b cells, it is the first to appear in response to an antigen
what changes in CNS occur with patients with CIDP?
changes in white matter
treatment for CIDP
block immune process
interferons (activate against bad antigens)
decoy molecules to sop up antibody
random set of antibodies to neutralize immune factors causing damage
activates complement cascade and provides antibodies capable of neutralizing many microorganisms, toxins