Oct17 A1,2-Peripheral Nervous System Flashcards
PNS anatomy at the bedside
one spinal segment has sensory info coming in (dorsal root) and motor info going out (ventral root) -descending axons -motor neuron in ventral horn (anterior horn cell) -ventral rootlets and root -mixed peripheral n. -NMJ -muscle \_\_\_\_\_\_\_\_\_\_\_\_ -sensory R -mixed peripheral n. -cell body of sensory R in DRG -dorsal root and rootlets -interneurous (connect to AHCs) and-or ascending axons
reflex arc def
from sensory R to spinal cord interneuron or AHC directly (if monosynaptic reflex) to muscle = the whole arc
what can affect the reflex arc (reflexes) and make reflexes reduced or absent
damage anywhere along reflex arc including muscle spindles (sensory axons) inside muscles and includes LMN lesion
5 reflexes usually tested + the muscle involved + nerve root
- biceps (biceps m.): biceps tendon. root C5
- triceps (triceps m.): triceps tendon. root C7
- brachioradialis (brachioradialis m.): brachioradialis tendon. root C6
- patellar (knee) (quadriceps m.): patellar tendon: L3/4.
- achilles (ankle) (gasctrocnemius m.): achilles tendon: S1
UMN lesion (NOT PNS) charact and what happens besides weakness
leads to loss of control of LMN (bc UMNs are normally a brake on reflexes)
- increased tone
- increased reflexes
- positive Babinski
- normal m. bulk (or slightly decreased)
- NO fasciculations
LMN lesion charact and what happens besides weakness
denervation of muscle leading to irritability (fasciculations) and atrophy
- decreased bulk (much more than in UMN lesion)
- fasciculations
- decreased reflexes
- Babinski negative
- normal tone
diff possible locations of LMN problem (which is a PNS problem)
- AHC
- nerve root
- peripheral n.
- NMJ
- muscle
- some rare instances where LMN intact and have purely sensory sx with no weakness*
motor unit def
one LMN (AHC or motor cranial nerve neuron), its axon, branches of the axon and muscle fibres it innervates -a n. contains axons of many motor units
how to identify where the lesion is in the PNS (once distinguished LMN from UMN lesion and know it’s LMN that caused the lesion)
find where it is in the 5 locations based on variations in these 5 things
- weakness
- atrophy
- fasciculations
- hyporeflexia
- sensory involvement (for this one, think what is purely motor and what is not)
meaning of radicular weakness
weak muscles are all inn. by same AHC or root at the same level
-diff from nerve weakness, which is a pattern of weakness in muscles all inn. by one nerve
charact of PNS lesion in AHC
- radicular weakness
- atrophy
- fasciculations
- hyporeflexia
- NO sensory involvement
charact of PNS lesion in root
- radicular weakness
- atrophy
- fasciculations
- hyporeflexia
- sensory involvement (occurs in nerve and roots damage bc roots and nerve can carry both motor and sensory info)
charact of PNS lesion in nerve
- nerve weakness
- atrophy
- fasciculations
- hyporeflexia
- sensory involvement
charact of PNS lesion in NMJ
- fatigue weakness (get more and more weak as use this muscle, as do activity)
- NO atrophy (bc connections still there)
- NO fasciculations (bc still connections)
- NO hyporeflexia
- NO sensory involvement
charact of PNS lesion in muscle
- proximal weakness (just bc muscle dz affect proximal muscles (shoulder and hip girdle) most of the time)
- atrophy
- NO fasciculations
- NO hyporeflexia
- NO sensory involvement
weakness patterns depending on where PNS lesion is
- radicular weakness in AHC and root injury
- nerve weakness in nerve injury
- fatigue weakness in NMJ lesion
- proximal weakness in muscle lesion
when m. atrophy in PNS lesion
- yes in AHC, root, nerve and muscle (no inn. or muscle problem)
- only absent in NMJ lesion (bc muscle still there + still inn.)
when m. fasciculations in PNS lesion
- yes in AHC, root, nerve (bc inn. affected)
- no in NMJ and muscle (bc doesn’t affect inn.)
when hyporeflexia in PNS lesion
- yes in AHC, root, nerve (bc inn. affected)
- no in NMJ, muscle
when sensory involvement in PNS
- yes in root and nerve (bc carry both sensory and motor)
- no in AHC, NMJ and muscle
other clues to PNS injury
- bilateral limb symptoms and signs and NOT at a level (cerebral = unilateral, spinal = bilateral below a level)
- length-dependent sx (bc longest axons = higher injury risk) like sx first in feet, then knees, and then hands. note still can have dz afecting all peripheral nn
- nerve or root territories sx (CNS = body region sx like arm or hand, as in stroke). some muscles. same idea for sensory loss
- face is spared (facial (bulbar) lesions = brainstem lesion. CNs are short and more protected so rarely injured. can still be injured, bc once exit brainstem are in PNS)
cranial nerves and PNS
- nucleus and axons travelling TO or FROM the nucleus are part of PNS even though nucleus + part of axons are within the brainstem (CNS)
- same thing for AHCs and sensory axons in the spinal cord
what does it mean that a muscle is inn by a nerve and also by a root
axons of AHC inn. it cross a specific root and a specific nerve
CTS (carpal tunnel syndrome) (mononeuropathy) typical presentation
- numbness of left hand
- sx resolve after 5-15 min
- come during the day
- mostly first 3 digits
- sometimes same thing in right hand
- mild atrophy and weakness of left abductor pollicis brevis
- all other mm normal, reflexes normal
- pinprick sensation mildly reduced over tip of left index finger and, to lesser extent, middle finger and thumb
how to analyze case for the mononeuropathy presentation
- atrophy and weakness = LMN (AHC, root, nerve or muscle)
- sensory symptoms so root or nerve
- very focal (one muscle distally and distal region) so is a mononeuropathy (eliminate root bc root prob often prixmal AND distal prob)
what nerve is affected in CTS
median nerve
are reflexes (the 5 typically tested) normal or abnormal in CTS
normal
-bc we median n. inn. C8-T1 muscles. C8 and T1 reflexes not tested routinely
polyneuropathy def + causes
injury to multiple peripheral nn. (usually caused by a diffuse insult)
- diabetes
- chemo and toxins
- leprosy
most common cause of mononeuropathy (meaning focal injury to one peripheral nerve)
compression
- median neuropathy at the wrist (CTS)
- ulnar neuropathy at the elbow
- fibular neuropathy at the knee
sx of nerve compression
- intermittent pain
- intermittent paraesthesias (tingling, burning)
- sensory loss
- weakness
pathophysiology of nerve compression
- irritation
- demyelination (patho X section of n. shows unmyelinated and myelinated axons)
- axonal loss
does ulnar n. travel in carpal tunnel
no, is outside
predisposing factors for CTS
- hypoT (causes edema in soft tissues)
- arthritis (inflam of tendons running in the tunnel)
- pregnancy (causes edema in soft tissues)
- certain jobs
classical presentation of CTS
- waking at night with pain and numbness, shake hands to relieve
- waking in AM with persistent numbness, resolves after 30-60 min
- situational daytime sx (driving, phone, etc) involving FLEXION
- weakness eventually (abductor pollicus brevis, part of thenar eminence, for thumb abduction (lift up to ceiling when arm flat with palm facing up))
- slow progression of path and sx over time
ddx of median neuropathy at the wrist
- arthritis
- ulnar neuropathy
anatomy of carpal tunnel where median n. passes
- bottom = carpal bones (wrist), width of 4 bones
- top = flexor retinaculum (transverse carpal lig)
dx of median neuropathy done how
- clinical hx
- EMG helps CONFIRM the dx
tx of CTS (median neuropathy at the wrist)
- none
- wrist splints (piece of plastic to avoid flexion)
- surgery (cut flexor retinaculum)
- steroid injection
pathophysiology of ulnar neuropathy at the elbow
- stretching around the elbow
- compression in ulnar groove (cubital canal)
imp thing in hx for ulnar neuropathy at elbow
sleeping position
- ask about it
- look for atrophy
ulnar neuropathy at elbow, main sx to think about
- in 10% of pts, numbness of medial two digits (4,5) specifically
- in 90% of pts, numbness in 5 fingers
stereotypical presentation of ulnar neuropathy at the elbow
- waking at night with sx and shake the hands to relieve (like carpal tunnel)
- persistent numbness in medial 1.5 digits
- daytime sx from leaning on elbow
- weakness (finger abduction, weak grip)
- can be asx (in diabetic elderly with muscle wasting)
dx of ulnar neuropathy at the elbow
- clinical hx
- exam more helpful (more likely to notice atrophy and weakness bc finger abduction (FIRST DORSAL INTEROSSEUS AND ABDUCTOR DIGITI MINIMI) is more used than thumb abduction)
ddx of ulnar neuropathy at the elbow
C8 radiculopathy
tx of ulnar neuropathy at the elbow
- change sleeping position or precipitating factors
- elbow padding
- rarely surgery
how to diff C8 radiculopathy (affects axons to median and ulnar nn) and ulnar neuropathy
- both have weakness of first dorsal interosseus and abductor digiti minimi but only C8 radiculopathy has weakness of abductor pollicus brevis
- both have fifth finger and medial hand numbness but only C8 radiculopathy has medial forearm numbness. (bc covered in the dermatome of C8)
general use of an EMG
- helps confirm a diagnosis that has already been made
- helps localization process and tells you what’s going on
polyneuropathy typical pres
- sensory loss and pain in both feet
- pins and needles sensation worse in evening
- trouble feeling floor when walking
- hard to feel water temp
- mild weakness of toe extension
- extensor digitorum brevis m not isible
- absent reflexes at ankle
- absent pinprick sensation in toes but improves as move up ankles (gradient)
- absent vibration sensation at toes
how localization of polyneuropathy is done
- know PNS prob bc loss reflexes + muscle atrophy
- can be AHC, root, nerve, NMJ, muscle
- motor and sensory sx so root or nerve
- bilateral symmetrical, length-dependent so likely peripheral n
list of etiologies of length-dependent polyneuropathy
long list
-most common cause is diabetes
why reflexes abnormal in length-dependent polyneuropathy
damage or interruption to reflex arc
EMG utility in length-dependent polyneuropathy
- dx can be made without it
- helps show severity
- can show if a demyelinating neuropathy is present (much smaller list of etiologies)
pathophgy of length-dependent polyneuropathy
- longer nerves (axons) ore susceptible so usually worse distally. feet then knees then fingers
- positive sx and THEN sensory loss (negative sx) and THEN motor (LMN)
main goal in length-dependent polyneuropathy dx
long ddx so want to narrow it by looking for unusual pattern
- pure motor
- sensory ataxia
- mononeuritis multiplex (only sensory) = many peripheral nn
- autonomic
- hereditary
- demyelinating (on EMG)
- anything that is not distal, symmetrical, motor and sensory
serious things in length-dependent polyneuropathy
- unusual pattern (lof of involvement of upper limbs) (unless explained by CTS and ulnar neuropathies)
- mononeuritis multiplex (potential serious, rapidly progressive causes like vasculitis)
- rapid progression (months instead of years)
- length-dependent polyneuropathy without clear etiology (not diabetes or toxins like chemo)
- problem other than PNS (like hyper-relfexia = UMN)
amyotrophic lateral sclerosis (ALS) (or Lou Gehrig’s disease) clinical pres
- weakness
- no pain and no sensory loss
- atrophy
- fasciculations
- normal tone
- normal reflexes
- can present as foot drop, weakness of ankle dorsiflexors, inversion, eversion and plantarflexion*
how localize lesion in amyotrophic lateral sclerosis (ALS) (or Lou Gehrig’s disease)
- PNS prob bc LMN (atrophy and fascic)
- can be AHC, root, nerve, NMJ, muscle
- fasciculations present = AHC, root or nerve
- normal sensation so prob in AHC
* widespread weakness and not just focal (nerve or root) helps confirm lesion is in AHC*
why may the reflexes be normal in amyotrophic lateral sclerosis (ALS) (or Lou Gehrig’s disease)
- damage not severe enough yet (some intact motor axons)
- combination of partial UMN and LMN damage seen with ALS helps preserve clinically visible reflexes
EMG use in amyotrophic lateral sclerosis (ALS) (or Lou Gehrig’s disease)
- can show features strongly suggesting ALS but not needed for dx
- helps prove there is no sensory loss (which can be missed clinically)
what does amyotrophic lateral sclerosis (ALS) (or Lou Gehrig’s disease) do
motor neuron dz
- degeneration of AHC (LMNs)
- often involves UMNs too but initially LMN only
- combination of UMN and LMN signs is very suggestive of ALS
- spasticity and increased reflexes (CNS = UMN things seen)
ddx of amyotrophic lateral sclerosis (ALS) (or Lou Gehrig’s disease)
- spinal muscular atrophy
- other genetic causes
- polio
- west nile virus
cause of amyotrophic lateral sclerosis (ALS) (or Lou Gehrig’s disease)
- unknown
- some familial cases with mutation of superoxide dismutase
- could be oxidative stress in susceptible cell types
- steadily progressive dz
- pts die of resp failure after 2-5 yrs
Guillain-Barré syndrome (GBS) possible pres
- weakness and tingling in both feet
- worsened over several days
- leg weakness, difficulty walking and standing
- normal CNs, no facial weakness
- normal bulk and tone
- loss of power proximally and distally
- mostly normal sensation
- reflexes not obtained (meaning ABSENT)
- ACUTE presentation (started 1 week ago)
what EMG shows in GBS
- diffuse prob affectig PNS (all 4 extremities motor and sensory)
- shows demyelination
GBS localization done how
- PNS bc absent reflexes + weakness + bilateral in UL and LL
- absent reflexes = AHC, root or nerve
- abnormal sensation = root or nerve
on top of localization, what also makes you suspicious of GBS
- diffuse (arms and legs), acute, progressive
- increased CSF protein
why reflexes absent in GBS
reflex arc (sensory and motor neurons) damaged and the damage is extensive
GBS cause
- syndrome that includes multiple diff autoimmune dz
- pattern and severity of motor and sensory sx depends on Ag involved
- axonal forms are more severe than demyelinating forms
- cause is probably post infectious autoimmune
- one axonal form related to campylobacter jejuni
classical things in GBS
- ascending paralysis with absent reflexes (sublte tingling and weakness start in feet, spreading upwards)
- albumino-cytological dissociation in CSF (high protein and normal cell count in CSF)
- need high index of suspicion to dx it + pt coming back in few days will be helpful to see progression
GBS management
- medical emergency, outcome depends on early tx
- IVIG or plasma exchange (NOT steroids)
- monitor resp fct and watch for deterioration (resp weakness bc of damage to phrenic nn)
- GBS is SOMETIMES reversible
