Cranial and Peripheral Nerve Disorders Flashcards
What are the 3 pathological processes behind peripheral nerve disease/injury?
1) wallerian degeneration
2) segmental demyelination
3) axonal degeneration
What is destroyed with wallerian degeneration?
axons and myelin distal to injury degenerate d/t transection of nerve
Can wallerian degeneration improve?
endoneurium (nerve sheath) doesn’t regenerate but forms a tube direction regeneration
What type of cells do the myelinating in the PNS?
schwann cells = myelinate the peripheral nerves
Describe the layers of protections for a neuron.
epineureum = surrounds entire spinal nerve perineureum = surrounds a fascicle in the spinal nerve endoneureum = surrounds a myelinated/unmyelinated neuron
T/F: Neurons in the PNS typically don’t regenerate.
false, they can
- it’s in the CNS that neurons typically don’t regenerate d/t oligodendrocytes, the enviro, etc
What helps clean up neuronal cell damage in the PNS?
macrophages, schwann cells
How fast does an axon regenerate?
1mm/day
What are the three types of traumatic nerve injury, least issue to most issue?
1) neuropraxia (transient loss of function; conduction block ischemia)
2) axonotomesis (injury to nerve interrupting axon causing wallerian degeneration distal to lesion; regeneration possible
3) neurotomesis: cutting of nerve with severance of all structures; reinnervation typically requires surgery
What remains intact in neuropraxia?
everything: axon and endoneurium are all good, just myeline is squished/compressed
- think about radial nerve compression at night, causes wrist drop when you wake up
- this is a rapid reversal case cause it goes away when you move
What remains intact in axonotmesis? What issues occur?
endoneurium still intact!!
- only myelin/axon interrupted
- so since everything still contained, regeneration is possible
BUT distal end: terminal bulbs die off since no complete connection; wallerian degeneration occurs
Crush injuries and displaced bone injuries often have what kind of nerve damage?
axonotmesis (endoneurium intact, axon disrupted)
Wallerian degeneration occurs in which of the three nerve injury types?
axonotmesis
neurotmesis
What is intact with neurotmesis?
nothing: endoneurium is damaged, no pathway for axon to regrow and find its terminal bulbs (wallerian degeneration occurs)
- worse case: epineurium is damaged, indicating NO growth potential
- if perineurium is split, poor growth may occur
- fair growth with only endoneurium involved
What is polyneuropathy?
bilateral, symmetrical involvement of peripheral nerves
- degeneration usually occurring more in legs, distal to proximal
In segmental demyelination, does wallerian degeneration occur? In what disease do we see this occur?
no
See this is GBS
What is the pathological process behind peripheral neuropathy?
axonal degeneration: degeneration of axon/myelin, progressing proximal to distal
A disease with involvement of nerve roots is indicated by what term?
radiculopathy
The nerve roots coming off the spinal cord exit to form peripheral nerves through what foramen?
intervertebral foramen
A dorsal ramus carries what kind of information?
both sensory and motor
- it’s the dorsal branch off of the spinal nerve (which was the joining of the ventral/dorsal root)
ventral root + dorsal root = spinal nerve -> dorsal and ventral rami
Are axons damaged in segmental demyelination?
NO just demyelinated (like in GBS)
What does the term neuropathy mean?
any disease of the nerves characterized by deterioration of nerve function
What is the pathologic process for peripheral neuropathy?
axonal degeneration -> degernation of axon/myelin from distal to proximal
Do people with LMN disorders have muscle weakness? What kind?
yes, rapid and atrophy and fatigue
- in a root-innervated pattern
Your patient comes in with LMN disease. What types of sensory deficits might you see in her?
- sensory loss (including proprioception) in same areas of motor weakness
- hypersensitivity of neurons (hyperalgesias, pins/needles)
T/F: autonomic dysfunction is present in those with LMN issue.
true (edema from poor vasomotor tone, orthostatic hypotension)
Your patient comes in with a diagnosis of postpolio syndrome. What are some symptoms you might expect?
myalgias since it’s an inflammatory myopathy
What diagnostic tests can be done to confirm peripheral nerve disorders?
NCV testing (measuring time of conduction from place to place)
EMG (needle in muscle looking at motor unit potentials)
T/F: Cranial nerves are part of the CNS.
false, they’re peripheral
What are some causes of trigeminal neuralgia?
compression on basilar artery or cerebellopontine tumor
- or degeneration, unknown etiology
Exacerbations of trigeminal neuralgia?
stress, cold -> causes spasms of pain along trigeminal nerve distribution, restricted to one side of face
- relieved by relaxation
T/F: those with trigeminal neuralgia have good motor control of facial muscles.
true, motor control is normal
- just a neurogenic pain issue
What mode of relief can you give these patients?
TENS
Bell’s palsy involves what cranial nerve?
CN VII -> unilateral facial paralysis
What is recovery time for Bell’s palsy?
several weeks/months
T/F: Full sensation is present in Bell’s palsy
true (that’s from trigeminal)
Etiology of Bells palsy?
acute inflammatory process causing compression of CN VII
What should you assess for with Bell’s palsy?
1) drooping of mouth, eyelids that don’t close
2) taste to ant. 2/3rds of tongue
3) facial expression muscles
PT treatment of bells palsy includes what?
1) providing active facial muscle exercises
2) e- stim to maintain tone/support facial muscle fxn
3) protect cornea with eye patching; decrease droop stretching with facial sling (no lacrimal gland right now)
4) functional retraining; easier foods to eat, one sided chewing, etc
What is Bulbar palsy, and what are typical deficits?
bulbar palsy = weakness/paralysis of motor nuclei (face, tongue, larynx, pharynx)
- difficulties with swallowing, phonation, coughing
What does your pharynx do?
promotes swallowing
What type of disease is GBS?
LMN disease, characterized by acute demyelination of both cranial and peripheral nerves
- often occurs after recovery from infectious illness (respiratory/gastrointestinal)
In GBS, is it more sensory or motor involvement?
motor more, but also sensory
What is the prognosis with GBS?
85% make full recovery, rarely any die
- recovery slow though, 6mo - 2 years
In what direction do symptoms occur with GBS?
distal to proximal
What are especially important to check in your assessment of a patient with GBS?
MMT Cranial nerve function Sensory Skin integrity (d/t prolonged hospitalization) Vitals and reflexes Respiratory function
What should you avoid with exercise prescription for patients with GBS?
over fatiguing exercise, as that can delay recovery
Is ALS a disorder of UMN or LMN?
BOTH
- degeneration of anterior horn cells and descending corticobulbar/corticospinal tracts
Prognosis of ALS?
death in 2-5 years
You have an evaluation of a patient with ALS. What symptoms might you expect?
LMN issues: muscle weakness/atrophy, fasciculations
UMN issues: spasticity, hyperreflexia
bulbar issues (dysphagia, dysphonia) near end
autonomic dysfunction
pain
You have an evaluation of a patient with ALS. What symptoms might you expect?
LMN issues: muscle weakness/atrophy, fasciculations
UMN issues: spasticity, hyperreflexia
bulbar issues (dysphagia, dysphonia) near end
autonomic dysfunction
pain
What is PTs role in ALS?
1) maintain respiratory function (cough production, breathing technqiues, chest stretching)
2) prevent indirect impairments for as long as possible
3) energy conservation
T/F: overwork damage can occur in ALS
true, so only give mild resistance exercises to muscles with 3/5 or above
What is postpolio syndrome?
new, slowly PROGRESSIVE muscle weakness in people that had polio before and were functioning for awhile
What is the reticular formation and what does it do?
in brainstem and responsible for wakefullness/alertness, sexual functioning
What are some symptoms that characterize postpolio syndrome?
myalgia
weakness/atrophy in asymmetrical distribution
abnormal fatigue with poor recovery with rest
cold intolerance
concentration/memory difficulty
For which PNS diseases should you really be focusing on energy conservation teaching as well as respiratory function focus and limiting high intensity training?
post polio
GBS
ALS
When is exercise contraindicated for those with post polio?
severe atrophic polio
