Lecture 8: Peripheral Nervous System Disorders Flashcards
UMN lesion
* What are reflexes like? (2)
* What is tone like (2)
* What happens to babinski sign?
* What happens to muscles innervates from these nerves
Reflexes are normal or hyperactive
Tone = spasticity or hypertonicity
Positive babinski sign
Muscle atrophy
LMN
* what are reflexes like? (2)
* What is tone like (2)
* What is babinski sign like?
* What happens to muscles innervated by these nerves
Reflexes are normal or hypoactive
Tone = hypotonicity or flaccidity
Negative babinski sign
muscle atrophy
Spinal region segmental signs occur when what two areas are compromised?
* sensation is lost in what kind of pattern?
* Muscle power is lost in what kind of pattern
* What happens to phasic stretch reflex?
Compromised:
* Nerve roots
* Spinal nerves
Sensation is lost in a dermatomal pattern
Muscle power is lost in a myotomal pattern
Decreased or lost phasic stretch reflex
* where hyporeflexive w/ LMN
Nerve root vs peripheral nerve PNS
Combined sensory and motor monosynaptic stretch reflex
reflex requires sensory and motor to come together and work
* goes to the SC then back to motor units (skips brain)
This is differentiating CNS from PNS
Spinal region/vertical tract signs:
* Where is snsation lost?
* What happens to tone below the level of lesion?
* what happens to muscle power
* if the corticospinal tract is involved what two things hapens?
Sensation is lost below level of lesion (NOT AT LEVEL OF LESION)
KNOW: They’re also going to lose decending control of BP, pelvic viscera and thermoregulation
hypertonia/spasticity
Decrease in muscle power
corticospinal tract invovled = babinski / clonus
Peripheral region lesions produce deficits in the distribution of a peripheral nerve
* What kind of distribution is sensation lost in?
* What is muscle power loss distribution?
* Are there vertical tract signs?
* What happens to phasic stretch reflex? (think patellar reflex)
In a peripheral nerve distribution loss of sensation
Loss/decrease in muscle power in a peripheral nerve distribution
No vertical tract signs - SC unaffected here
Decreased or lost phasic stretch reflex
Dermatomes
L2 spinal cord injury will the pt have hip flexion?
Yes, its loss below the level of the lesion
knowledge check: our damage is in a dermatomal distribution. What is likely injured a peripherl nerve or a spinal nerve
spinal nerve presents in a dermatomal fashion
Complete transection/serverd neuron?
Neurotmesis
Neuropraxia means
Compression
crush or stretch injury of nerve
axonotmesis
Case: A tennis player fell on her shoulder during a tennis match. Her shoulder was tractioned away from her head resulting in a traumatich stretch on the C5 and C6 nerve roots
* Which movements of the arm will likely be weak
* Where are on her arm will she have altered sensation?
* What type of damage in this
Elbow flexion/Wrist extension and down
* for dermatomes / myotomes its at the level of the lesion. This makese sense, if the spinal nerve is impinged it will go out in that pattern
Altered sensation on the side of the arm (learn new dermatomes I guess)
Axonomesis - think stretch
In a spinal cord injury where is the pathology
In a Spinal nerve injury where is the pathology
SC = below level of lesion
Spinal nerve = pathology at level of lesion
* spinal nerves go streaight out to innervate what they need. This makes sense
Case: A 32 year old computer programmer developed 2 months of worsening tingling and numbness in his left fith digit, in the medial aspect of his left fourth digitm and along the medial surface of his left hand and forearm. Symptoms were worse upon awakening in the morning, and were exacerbated after resting his elbows on a hard surface
* which nerve is involved
* What type of dmaage
* Where is the damage coming from?
Nerve = ulnar n
Type of damage = neuropraxia (hes resting his arm down)
Damage is coming from the nerve (peripheral nerve)
Knowledge checK: stretch to nerve = axonomesis
What records the activity of the muscle at rest, with voluntary movement and with e-stim
* looking for damage related to the striated muscle (skeletal muscle)
* EX = myopathy - damage to the muscle or neuromuscular junction
EMG
Measures the conduction time and amplitude of an electrical stimulus along a peripheral nerve (sensory or motor nerves)
* looking for damage to the nerve cell body or the nerve axon
* EX: peripheral nerve injury
Nerve conduction velocity (NCV)
EMG
* Invasive?
Tests muscle activity?
Tests nerve activity?
Looking for?
Yes
Tests muscle activity not nerve activity
Looking for motor unit potential
NCV
* invasive?
Tests muscle activity?
Tests nerve activity?
Looking for?
No
Does not test muscle activity but may produce a muscle contraction due to the electricity
Tests nerve activity
CMAP or SNAp (compound motor action potentail or sensory nerve action potential)
notice - nerve conduction velocity is not invasive, you’re not actually stucking a needle into a nerve. its that tool that hes putting over the skin to the right on the picture below
in nerve conduction velocity testing how much of the nerve being blocjed constiutes a block?
40% being blocked
NOTE: EMGs not always invasive, could be a surface electorde
Needle is inserted into the muscle belly at multiple points to get the EMG reading
KNOW: Nerve conduction velocity = asseses the action of nerves not muscles
Cranial nerve function
Know: Cranial nerve disorders = peripherla nerve disorders
Anosmia
* what nerve dysfunction?
* 3 causes
Inability to smell
Olfactor (CN1) dysfunction
causes:
* Common cold
* Trauma to the cribiform plate
* Meningioma
KNOW: The right half of each eyes visual field is recorded by the left half of each retina
* right half of each eye goes to the left vision field
The left half of each eyes visual field is recorded by the right half of each retina
Diplopia
double vision
What nerve is damaged in monocular blindness
optic nerve
Visual field cut/visual loss
Hemianopsia/Hemianopia (hemi meaning half)
* Can can bitemporal (lost the temporal region of each side) but not binasal
* can be homonymous (same visual field in both eyes) - homo means the same
Explain L homonymous Hemianopsia
Explain R homonymous Hemianopsia
* what treatment would you use?
Left Homonymous Hemianopsia
* Means they cant see the left visual field - named for the visual field that they cannot see
* Meaning the right half of each eye isnt working
* Meaning the right optic tract is damaged
Right Homonymous Hemianopsia
* Means they cant see the right visual field
* Meaning the left half of each eye isnt working
* Meaning the left optic tract is damaged
Issue with the left cerebral cortex (stroke)
Have pt do visual scanning
* just tell them to turn their head
* i can scan to take in other side of visual field
* So it is treatable, we can treat someone w/ this
Example of R homonymous Hemianopsia
What homonoys hemianopsia is this
* Which visual field of the right eye is imapcted
* Which visual field of the left eye is imapcted
* which side of each eye is impacted
* Which optic tract is impacted
Remember its named for the side they cannot see. This is left homonyous hemianopsia
* Nasal visual field deficit of the right eye
* Temporal visual field deficit of left eye
Left visual field isnt working (can tell becase they cant see to the left side)
This means the right side of each eye is not working
Meaning the right optic tract is damaged
A lesion in the optic nerve yields what?
Monocular vision (ipsilatearl vision loss)
What is ipsilateral vision loss?
Monocular vision (due to optic n lesion)
A lesion in the optic chiasm yields what kind of vision loss?
Bitemporal hemianopsia aka tunnel vision
* named for what they cant see, so they can’t see the temporal portion bilatearlly
Lesion in the optic tract/optic radiation leads to what?
Homonymous Hemianopsia
the lump near the optic tract = optic radiation
probs go through this at some point - i udnerstand it as of now
quadrent hemianopsia is when there is a partial lesion at the topic tracts (theres to tracts on each side and one has a lesion in it)
What is this?
* where is damage?
Bitemporal hemianopsia
Lesion at the optic chiasm
showing left homonlus hemianopsia
Which nerve supplies most of the ocular muscles
Oculomotor - supplies all extraocular muscles cept superior oblique and lateral rectus
Trochlear nerve (IV) supplies which eye muscle?
* which ways does it move the eye (2)
Supplies:
* Superior oblique muscle
Rotates the eye downward and laterally
Which muscle does the abducent (CN VI) supply?
* which was does it move the eye (1)
Supplies the latearl rectus
Rotates the eye latearlly
what is ptosis?
* which cn is impacted here?
Eye lid drooping
Cranial nerve 3
Patient has lost pupillary function (one is bigger than other) which cn is impacted?
cn3
this is external/latearl strabisumus. Which cn is imapcted?
3
this is internal or medial strabismus. Which cn is impacted?
cn6
Knowledge check: Right hemonomous hemianopsia, which field is missing
* This means the right visual field is lost
* Meaning the left side of each eye is imapcted
* right temporal visual field loss
* left nasal visual field loss
* talking about from the prospective of the visual field
What disease has a brief paroxsyms (sudden attack) of excruciating pain
* triggers
* Least impact on what division of this nerve?
Trigeminal Neuralgia
Least impact on the opthalamic division of this nerve
Triggers: Chewing, smiling, talking, yawning, hot or cold fluids in the mouth, blowing the nose, brushing teeth, or completely spontaneous onset
This is bells palsey. Which side is impacted?
Right side is imapcted. You can see that the muscles arent moving
which nerve is imapcted w/ bells palsy?
Cranial nerve 7
Is cognition impacted in bells palsey?
* is sensation to the face impacted?
Nope, just muscles of facial expression (because the facial nerve is imapcted)
Sensation to the face is not imapcted. Thats the trigeminal nerve
NOTE: Its a viral infection, typically after some infection taht stays dorment
* treated well w/ medication, but if you dont have emds quickly symptoms can be irreversible
NOTE: if the vestibulocochlear nerve is impacted
Vestibular n: symptoms
* Nystagmus
* vertigo
Cochlear nerve: symptoms:
* deafness
* Tinnitus
Ramsay Hunt Syndrome: JB
* Which nerves are impacted (2)
* What recovers better, facial m’s or hearing?
Nerves impacted
* Facial
* Vesitbulocochlear
Usually consists of acute facial paralysis accompanied by ear pain and blisters on the external ear
In some cases, blsiters in the mouth and problems with balance, gaze, stability, vertigo, hearing, and rarely tinnitus may also occur. Facial muscle control recovers fully in mild to moderate cases but remains impaired 6 months post onset in serve cases
With early treatment with corticosteriods and antiviral durgs is provided, motor and vestibular recovery is good, but hearing tends not to recover
NOTE: This is a pretty intense diagnosis
NOTE: CN’s don’t cross or decusate because they’re considered LMN’s
which diagnosis is vestibulochochlear and facial nerve?
Ramsey Hunt
Does Guillain-Barre syndrome affect the CNS or PNS
Affects the PNS
* myelin damage and axon destruction
Whats desotroyed in guillan barre UMN or LMN
LMN
What typically happens 1-3 weeks prior to guillain barre
* autoimmune of immune regulated?
* male or female more?
infection
* most common is respiratory infection or GI
* Lymphocyte mediated autoimmune reaction
very rare 1-2 per 100,000 cases males more afected
KNOW: w/ GNS we have acute demyelination
* autoimmune
Does GBS move proximal to distal or distal to proximal
* is onset symmetrical or assympetrical
* is progression fast or slow
distal to prxoimal
symmetrical
Pregression is fast: hours –> 1 week
Full function to respiratory dependent quadriplegia
What is Nadir w/ GBS?
* How quickly does it occur?
Nadir typically occurs in less than 4 weeks
Nadir = point when the syndrome progression ahs eached its most intense and then stabilized
Sub types of GBS
What is loss like w/ GBS? What about return?
Loss: rapid loss distal to proximal
return proximal to distal
Clinical amnifestation w/ GBS
What two important things do we need to know w/ GBS scale?
0 = normal
6 = death
What is the prognosis w/ GBS like?
good w/ high likelihood of recovery
KNOW: w/ GBS requiring mechanical ventilation increases mortality and complications –> poor prognosis
Who has the fastest recovery w/ GBS?
Children
KNOW: Demyeliantion process stop and remyelination beings after a few weeks w/ GBS
How long does it take to recovery from GBS?
weeks - years for full recovery
Acute phase of GBS
* lasts how long
Onset of symptoms with rapid progression until no more deteriation occurs, lasting up to 4 weeks
Plateau phase of GBS lasts how long?
Symptoms constant from acute phase and do not change; days to weeks
Recovery phase of GBS lasts how long
Patients condition bengins to improve; lasts few days to few weeks to 2 years
Poor outcome for GBS
* older than 40-50
* extended mechanical ventilation
* A long period before recovery beings (time for more demyleination)
* 5-10% of pts die in the acute phase
medical treatment w/ GBS
* IVIg, plasmapheresis, corticosteriods
Chronic demyelination of PNS with exacerbations
Chronic inflammatory demyelinating Polyneuropathy
is Chronic inflammatory demyelinating Polyneuropathy
* an UMN or LMN disorder?
* s it linked to infection?
* How long can it be present prior to diagnosis?
* Is it symmetrical
LMN w/ no known cause
thought to be immune mediated neuropathy
Progresses over weeks to months, gradual/progressive sensory and motor loss of peripheral nerves
NOt linked to infection (unlike GBS)
May be present years prior to diagnosis
People who do not recover from GBS may develop CIDP
Symmetricall both distal and proximal
Autoimmune: attacks the myelin
Recovery is possible; relapses common
Inisital s/s of Chronic inflammatory demyelinating Polyneuropathy
Inital rapid loss distally, may or may not progress proximally
progressive paresthesia and paresis
areflexia
may or may not have autonomic dysregulaton or cranial nerve palsies
Can you have PT while in an active Chronic inflammatory demyelinating Polyneuropathy
exacerbation?
No!!!
Multifocal Motor Neuropathy
* Motor or sensory?
* Symmetrical?
* How does it progress?
Pure motor disorder
Asymmetrical
Distal to proximal; usually starts in the hands/wrists
Knowledge check: Not favoriable recovery from GBS if on ventilator
Attacks the ACh receptor of the neuromusuclar junction
* Immune regualted or auto?
* Age of onset per sex
* what gets weak with this
* What is myasthenic risis?
Myasthenia Gravis
Autoimminue
Age of onset:
* Women under 40
* Men over 60
Results in muscle weakness
Myasthenic crisis: muscles of breathing not working
Signs of MG
What is onset like w/ MG?
* how does it spread?
* What incrases episiodes
* what % of peopel get remission from this?
Onset is sudden
Spread generally from head to toe (starting in face, then head/neck)
Increased episodies/itnensity w/ any physical/emotional stress
20% experience a remission of some or all symptoms for up to 5 years
Meds:
* Cholinesteras inhibitors
* Immunosupressamts
Other treatment:
* Plasmaphoresis
* IV-ig
knowledge check: Which neurotransmitter is affected in MG?
ACh
Charcot-Marie-Tooth Disease
* which muscles are affected w/ this? - causing what?
* Are their sensory symptoms w/ this
* age of onset?
* Where does it normally start? Where does it progress?
* What does it attack? (CNS vs PNS)
* Which kind of nerves are imacted first?
* What happens to the foot? (what kind of abnormaltities)
Causes paresis of muscles distal to the knee, with resulting foot drop, a steppage gait, frequent tripping and muscle atrophy
Significant numbness is unusual
Onset usually in adolescence to early adulthood
usually starts in feet/legs, later progresses to hands/arms
Normally attacks either the peripherl nerves or the myelin surrounding the nerves?
Longer nerves impacted first
Can occur secondary to neuropathy - charcot foot comprises patholgic fracture, joint dislocation and if left untreated, disability joint deformity
Foot deformities include high arches and hammer toe deformity
* Hammer toe is flexion of the proximal interphalangaeal joint
Therapy involves strengthening, stretching, conditioning, and joint, muscle and skin protection
What is the foot abnormalitty with charcot-marie tooth disease?
High arches
Poliomyeltitis turns into post-polio syndrome years later
* new neuro symptoms affecting polio survivors 15-30 years after intital infection
* releated to severity of inital illness, releated to burden over time in surviving anterior horn cells
This is a LMN disorder
NOTE: w/ post polio syndrome there are less total nerves innervating the muscle fibers
know that intital severity of polio determine the liklihood of getting post polio syndrome
Do you get UMN or LMN s/s w/ post polio syndrome?
Criteria for getting post polio syndrome = intital strength improvement after paralysis, at least 15 years (typically 23-35 years) of stability
for post polio syndrome
PPS
Moderate resistance exercise for PPS is indicated and can increase strength in muscle w/ a MMT grade of _?
3/5
* meaning they can move the muscle in its full ROM
* need to wait until the muscle has antigravity strength until stressing w/ PPS
Knwoledge check: know that PPS is directly releated to the severity of intital onset of polio
