PNS Flashcards
1
Q
PNS regions
A
- peripheral nerves
- cranial nerves (all but two)
- autonmoic nervous system
2
Q
What is in the PNS
A
- all structures distal to spinal Nerves
- axons of sensory,motor, and autonomic neurons
- specialized sensory endings
- postganglionic autonimic neurons
- cranial nerves
3
Q
Where does the peripheral nervous system start (where does spinal region stop)
A
- where the spinal nerve bifurcates into ventral and dorsal rami
- marks the transition from spinal to peripheral region
4
Q
Peripheral nerve structure: describe from axons to nerve
A
- individual axons are surrounded by the endoneurum and myelin sheath
- bundles of axons = fascicles and fascicles are surrouned by perineurium
- epineurium is the outermost that surrounds the nerve
- Mesoneurium surrounds the nerve trunk and that allows gliding
5
Q
Myelin in the PNS
A
- Surrounds 1 axon = myelinated (schwann cells)
- or surrounds several axons = paritially myelinated or unmyelinated
6
Q
Peripheral nerve blood supply
A
- receive blood supply via arterial branches that enter the nerve trunk
- supples groups of axons
7
Q
Where do peripheral nerves go?
A
- splanchnic –nerves that supply signals and info to and from the visceral organs and blood vessels
- Cutaneous—not purely sensory—they deliver efferent axons to sweat glands and arterioles
- Muscular branches not purely motor –they contain sensory axons from proprioceptive structures.
8
Q
Nerve plexuses
what are they and the types
A
- formed by junctions of anterior rami
- cervical plexus
- brachial plexus
- lumbar plexus
- sacral plexus
9
Q
Cervical Plexus
A
- arises from anterior rami of C1-C4
- lies deep the SCM
- phrenic nerve most important branch as it is only motor supply and sensory nerve for diaphragm
- sympathetic innervation
- cutaneous innervation for posterior scalp to clavicle, anterior neck muscles and diaphragm
10
Q
Brachial plexus
A
- Innervate the upper limb
- sympathetic innervation
- formed by anterior rami of C5-T1
- emerges between the anterior and middle scelenes and then deep to clavicle into axilla
11
Q
Lumbar Plexus
A
- L1-L4
- innervates skin and muscles of anterior and medial thigh
- cutaneous branch to medial leg and foot - saphenous nerve
- sympathetic innervation
- forms in the psoas major muscle
12
Q
Sacral plexus
A
- formed by anterior rami of S1-S4
- innervates posterior thigh, most of leg and foot
- parasympathetic and sympathetic
- only one that has motor, sensory, parasympathetic and sympathetic innervation
13
Q
Peripherl nerve damage: S&S
A
- Sensory
- autonmic
- motor
- Trophic
14
Q
Sensory S&S of peripheral nerve damage
A
- changes include decreased or loss of sensation
15
Q
S&S of peripheral nerve damage
Autonomic
A
- Depends on pattern of dysfunction
- if a single nerve is damaged, autonmic signs usually are observed only if the nerve is completely severed
- signs may include lack of sweating, loss of sympathetic control of smooth muscle in arterial walls
- this can contribute to edema in affected limb
- if many neurons are involved, autonmic problems may include impotence, difficulty regulating blood pressure, heart rate, sweating and bowel and bladder functions
16
Q
S&S of peripheral nerve damage
Motor
A
- paresis/weakening or paralysis
- denervation determined by EMG
- MM atrophy progresses rapidly
17
Q
S&S of peripheral nerve damage
Trophic changes
A
- muscle atrophy
- shiny skin
- birttle nails
- subcutaneous tissue thickens
- tissue ulceration
- poor healing of wounds and infection
- neurogenic joint damage (coming from NS) due to blood supply changes
- loss of sensation and lack of movement
18
Q
Classifications of neuropathies
A
- traumatic myelinopathy
- traumatic axonopathy
- traumatic severance
- multiple mononeuropathy
- polyneuropathy
neuropathy = disease or dysfunction of one or more peripheral nerves
19
Q
Traumatic myelinopathy
A
- Focal compression of a peripheral nerve
- caused by excessive pressure, stretch, vibration and/or friction
20
Q
Traumatic myelinopathy
what happens with a traumatic myelinopathy
as a result
A
- Decreased axonal transport
- decrease epineurial blood flow
- decreased blood flow causes edema/swelling of epineurium and endoneurium
- The edema restricts blood and axoplasmic flow (axon is intact but not working well)
- Perineurium and epineurium thicken
ex: carpal tunnel syndrome
21
Q
Traumatic myelinopathy
what happens with perineurium and epineurium thickening
A
- damages myelin
- decreased nerve conduction velocity = impaired sensation and movement
- ectopic folci develop due to altered gene activity in cell = neurpathic pain
22
Q
What does traumatic myelinopathy interfere with and what functions are intact and recovery
A
- interferes with the function of large diameter axons producing motor, discriminitive touch, proprioceptive and phasic stretch reflex defecits and cause neuropathic pain
- unless injury is unusually severe autonmic function is intact and axons are not damaged
- recovery tends to be complete remyleination before rapdily irrversible damage occurs
23
Q
How movement is important especially with traumic myelinopathy
A
- promotes blood flow: oxygenation of nerves and removal of wast
- promotes axoplasmic flow: keeps axoplasm thin => improves transport
- Axoplasm gets thicker without movement
- Nerve glides can help
24
Q
How do nerves move
A
- Nerves can fold and unfold
as a nerve is stretched:
- viscoelastic tubes formed by endoneurium, perineurium and epineurium stretch
- axons unfold
- fascicles glide along each other
- entire nerve stretches relative to other structures
- if stretch continues tensile stress develops over the nervous tissue
- nerve glides
25
Traumatic axonopathy
- the axon is damaged
- myelin is intact
- crush injury due to dislocation or fracture is often the cause
26
What are signs and symptoms Traumatic axonopathy + recovery
- reflexes, somatosensation and motor function are markedly reduced or absent
- muscle atrophy occurs
- recovery is generally good - axon regrowth typically proceeds at a rate of 1mm/day
- wallerian degeneration distal to lesion
27
What is wallerian degeneration in PNS
- Day 1 axon becomes swollen and irregular
- by day 3-4: axon is fragmented; debris digested by glial cells
- 1 week: entire axon is destroyed; seperated in proximal and distal segments results in death of distal segment - cell body undergoes changes and dies
- Changes in proximal segment: similar to those in distal segment but only extend as far as first node of ranvier
28
Changes that occur in the cell body in response to injury
- retrograde degeneration = chromotaolysis
- may be related to loss of trophic factors
- nucleus moves to one side of cell body
- if axon regenerates and proper connections are restored, chromatolysis stops
- if not cell trophies and dies
- axon re-grows at rate of 1mm/day
29
Chromatolysis
| explain the process
1. normal axon
2. axon severed
3. nucleus moves in cell body/severed axon sprouting occurs
4. sprouts degenerate/axon regenerates
5. chromatolysis ends and either reinnervates the target or is unable to regenerate and dies
30
Traumatic severance
- nerve completely disrupted; excessive stretch or laceration
- immediate loss of sensation/paralysis
- wallerian degeneration begins 3-5 days later
- axons in proximal stumps will begin to sprout - sprounts may enter distal stumps and reach target
31
Recovery from severance
| traumatic severence
- axons in proximal stumps will begin to sprout
- sprouts may enter distal stump and reach target
- stumps may be displaced or scar tissue may be in the way = neuroma
- sprouts may reach inappropriate end organ
32
Neuroma
- if stumps are displaced or if scar tissue intervenes between stumps, sprouts may grow into this tangled mass of nerve fibers
33
Sprouting
- collateral sprouting = a denervated neuron attracks side sprouting from nearby undamaged axons
- regerative sprouting - injured axon issues side sprouts to form new synpase with undamaged neurons
34
Multiple mononeurpathy
- individual nerves affected
- random, asymmetric presentaton of signs
- possible cause = vasculitis
- may result in rupture/need for referral
35
Polyneuropathy
- symmetric involvement of sensory, motor, and autonomic fibers
- often progressing from distal to proximal
- stocking/glove distribution
- *degeneration of distal part of the long acons may occur because of inadequate axonal transport to keep the distal axons viable and because longer axons have more myelin*
36
Common causes of poly neuropathy
- diabtetes
- nutritional deficiences due to alcoholism
- autoimmune disease
- also develops with age
37
What can happen with severe polyneuropathies
| S&S
- trophic changes
- poor healing
- ulceration
- poor sensation and therefore protective sensation
- *most common = diabetic and Gullian Barre*
38
Diabetic polyneuropathy
- axon and myelin damage
- sensation is primarily affected
- decreased ankle reflexes and later strength and joint damage
- decreased balance
- role of PT: strengthen, balance exercises, education etc
39
Gullian barre
- rapid onset, with progressive paralysis
- greater motor effects verus sensory
- distal to proximal sensory loss
- early diagnosis key to preventing res. failure
40
Charcot Marie Tooth disease
- hereditay
- muscle weakness distal to the knee
- atrophy and weakness eventually effect the hands
- sensation to heat, cold, and painful stimuli impaired
- neuropathic pain is common
- muscle weakness in foot drop, steppage gait, frequent tripping, muscle atrophy
- charcot marie foot = pes cavus type position
41
myopathy
- specific to muscle
- peripherl nerve specific to muscle
- random muscle fibers degenerate leaving motor units with fewer muscle fibers
- ex: muscular dystrophy
42
Diagnositcs and clinical testing of the PNS
- EMG or NCS/NCV
- ankle jerk reflex
- imparied vibration sense
- imparied position sense of great toe
- 2/3 signs correlate with electrodiagnostics
