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Bloc J - Neuro > Oct17 A1,2-Peripheral Nervous System > Flashcards

Oct17 A1,2-Peripheral Nervous System Flashcards

1
Q

PNS anatomy at the bedside

A 
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
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2
Q

reflex arc def

A

from sensory R to spinal cord interneuron or AHC directly (if monosynaptic reflex) to muscle = the whole arc

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3
Q

what can affect the reflex arc (reflexes) and make reflexes reduced or absent

A

damage anywhere along reflex arc including muscle spindles (sensory axons) inside muscles and includes LMN lesion

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4
Q

5 reflexes usually tested + the muscle involved + nerve root

A
  • 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
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5
Q

UMN lesion (NOT PNS) charact and what happens besides weakness

A

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
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6
Q

LMN lesion charact and what happens besides weakness

A

denervation of muscle leading to irritability (fasciculations) and atrophy

  • decreased bulk (much more than in UMN lesion)
  • fasciculations
  • decreased reflexes
  • Babinski negative
  • normal tone
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7
Q

diff possible locations of LMN problem (which is a PNS problem)

A
  • AHC
  • nerve root
  • peripheral n.
  • NMJ
  • muscle
  • some rare instances where LMN intact and have purely sensory sx with no weakness*
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8
Q

motor unit def

A 
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
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9
Q

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)

A

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)
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10
Q

meaning of radicular weakness

A

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

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11
Q

charact of PNS lesion in AHC

A
  • radicular weakness
  • atrophy
  • fasciculations
  • hyporeflexia
  • NO sensory involvement
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12
Q

charact of PNS lesion in root

A
  • radicular weakness
  • atrophy
  • fasciculations
  • hyporeflexia
  • sensory involvement (occurs in nerve and roots damage bc roots and nerve can carry both motor and sensory info)
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13
Q

charact of PNS lesion in nerve

A
  • nerve weakness
  • atrophy
  • fasciculations
  • hyporeflexia
  • sensory involvement
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14
Q

charact of PNS lesion in NMJ

A
  • 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
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15
Q

charact of PNS lesion in muscle

A
  • 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
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16
Q

weakness patterns depending on where PNS lesion is

A
  • radicular weakness in AHC and root injury
  • nerve weakness in nerve injury
  • fatigue weakness in NMJ lesion
  • proximal weakness in muscle lesion
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17
Q

when m. atrophy in PNS lesion

A
  • yes in AHC, root, nerve and muscle (no inn. or muscle problem)
  • only absent in NMJ lesion (bc muscle still there + still inn.)
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18
Q

when m. fasciculations in PNS lesion

A
  • yes in AHC, root, nerve (bc inn. affected)

- no in NMJ and muscle (bc doesn’t affect inn.)

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19
Q

when hyporeflexia in PNS lesion

A
  • yes in AHC, root, nerve (bc inn. affected)

- no in NMJ, muscle

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20
Q

when sensory involvement in PNS

A
  • yes in root and nerve (bc carry both sensory and motor)

- no in AHC, NMJ and muscle

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21
Q

other clues to PNS injury

A
  • 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)
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22
Q

cranial nerves and PNS

A
  • 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
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23
Q

what does it mean that a muscle is inn by a nerve and also by a root

A

axons of AHC inn. it cross a specific root and a specific nerve

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24
Q

CTS (carpal tunnel syndrome) (mononeuropathy) typical presentation

A
  • 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
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25
Q

how to analyze case for the mononeuropathy presentation

A
  • 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)
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26
Q

what nerve is affected in CTS

A

median nerve

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27
Q

are reflexes (the 5 typically tested) normal or abnormal in CTS

A

normal

-bc we median n. inn. C8-T1 muscles. C8 and T1 reflexes not tested routinely

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28
Q

polyneuropathy def + causes

A

injury to multiple peripheral nn. (usually caused by a diffuse insult)

  • diabetes
  • chemo and toxins
  • leprosy
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29
Q

most common cause of mononeuropathy (meaning focal injury to one peripheral nerve)

A

compression

  • median neuropathy at the wrist (CTS)
  • ulnar neuropathy at the elbow
  • fibular neuropathy at the knee
30
Q

sx of nerve compression

A
  • intermittent pain
  • intermittent paraesthesias (tingling, burning)
  • sensory loss
  • weakness
31
Q

pathophysiology of nerve compression

A
  • irritation
  • demyelination (patho X section of n. shows unmyelinated and myelinated axons)
  • axonal loss
32
Q

does ulnar n. travel in carpal tunnel

A

no, is outside

33
Q

predisposing factors for CTS

A
  • hypoT (causes edema in soft tissues)
  • arthritis (inflam of tendons running in the tunnel)
  • pregnancy (causes edema in soft tissues)
  • certain jobs
34
Q

classical presentation of CTS

A
  • 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
35
Q

ddx of median neuropathy at the wrist

A
  • arthritis

- ulnar neuropathy

36
Q

anatomy of carpal tunnel where median n. passes

A
  • bottom = carpal bones (wrist), width of 4 bones

- top = flexor retinaculum (transverse carpal lig)

37
Q

dx of median neuropathy done how

A
  • clinical hx

- EMG helps CONFIRM the dx

38
Q

tx of CTS (median neuropathy at the wrist)

A
  • none
  • wrist splints (piece of plastic to avoid flexion)
  • surgery (cut flexor retinaculum)
  • steroid injection
39
Q

pathophysiology of ulnar neuropathy at the elbow

A
  • stretching around the elbow

- compression in ulnar groove (cubital canal)

40
Q

imp thing in hx for ulnar neuropathy at elbow

A

sleeping position

  • ask about it
  • look for atrophy
41
Q

ulnar neuropathy at elbow, main sx to think about

A
  • in 10% of pts, numbness of medial two digits (4,5) specifically
  • in 90% of pts, numbness in 5 fingers
42
Q

stereotypical presentation of ulnar neuropathy at the elbow

A
  • 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)
43
Q

dx of ulnar neuropathy at the elbow

A
  • 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)
44
Q

ddx of ulnar neuropathy at the elbow

A

C8 radiculopathy

45
Q

tx of ulnar neuropathy at the elbow

A
  • change sleeping position or precipitating factors
  • elbow padding
  • rarely surgery
46
Q

how to diff C8 radiculopathy (affects axons to median and ulnar nn) and ulnar neuropathy

A
  • 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)
47
Q

general use of an EMG

A
  • helps confirm a diagnosis that has already been made

- helps localization process and tells you what’s going on

48
Q

polyneuropathy typical pres

A
  • 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
49
Q

how localization of polyneuropathy is done

A
  1. know PNS prob bc loss reflexes + muscle atrophy
  2. can be AHC, root, nerve, NMJ, muscle
  3. motor and sensory sx so root or nerve
  4. bilateral symmetrical, length-dependent so likely peripheral n
50
Q

list of etiologies of length-dependent polyneuropathy

A

long list

-most common cause is diabetes

51
Q

why reflexes abnormal in length-dependent polyneuropathy

A

damage or interruption to reflex arc

52
Q

EMG utility in length-dependent polyneuropathy

A
  • dx can be made without it
  • helps show severity
  • can show if a demyelinating neuropathy is present (much smaller list of etiologies)
53
Q

pathophgy of length-dependent polyneuropathy

A
  • 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)
54
Q

main goal in length-dependent polyneuropathy dx

A

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
55
Q

serious things in length-dependent polyneuropathy

A
  • 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)
56
Q

amyotrophic lateral sclerosis (ALS) (or Lou Gehrig’s disease) clinical pres

A
  • 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*
57
Q

how localize lesion in amyotrophic lateral sclerosis (ALS) (or Lou Gehrig’s disease)

A
  1. PNS prob bc LMN (atrophy and fascic)
  2. can be AHC, root, nerve, NMJ, muscle
  3. fasciculations present = AHC, root or nerve
  4. normal sensation so prob in AHC
    * widespread weakness and not just focal (nerve or root) helps confirm lesion is in AHC*
58
Q

why may the reflexes be normal in amyotrophic lateral sclerosis (ALS) (or Lou Gehrig’s disease)

A
  • damage not severe enough yet (some intact motor axons)

- combination of partial UMN and LMN damage seen with ALS helps preserve clinically visible reflexes

59
Q

EMG use in amyotrophic lateral sclerosis (ALS) (or Lou Gehrig’s disease)

A
  • can show features strongly suggesting ALS but not needed for dx
  • helps prove there is no sensory loss (which can be missed clinically)
60
Q

what does amyotrophic lateral sclerosis (ALS) (or Lou Gehrig’s disease) do

A

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)
61
Q

ddx of amyotrophic lateral sclerosis (ALS) (or Lou Gehrig’s disease)

A
  • spinal muscular atrophy
  • other genetic causes
  • polio
  • west nile virus
62
Q

cause of amyotrophic lateral sclerosis (ALS) (or Lou Gehrig’s disease)

A
  • 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
63
Q

Guillain-Barré syndrome (GBS) possible pres

A
  • 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)
64
Q

what EMG shows in GBS

A
  • diffuse prob affectig PNS (all 4 extremities motor and sensory)
  • shows demyelination
65
Q

GBS localization done how

A
  1. PNS bc absent reflexes + weakness + bilateral in UL and LL
  2. absent reflexes = AHC, root or nerve
  3. abnormal sensation = root or nerve
66
Q

on top of localization, what also makes you suspicious of GBS

A
  • diffuse (arms and legs), acute, progressive

- increased CSF protein

67
Q

why reflexes absent in GBS

A

reflex arc (sensory and motor neurons) damaged and the damage is extensive

68
Q

GBS cause

A
  • 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
69
Q

classical things in GBS

A
  • 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
70
Q

GBS management

A
  • 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

Bloc J - Neuro (60 decks)

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