Exam 1 Flashcards
Quiz 1 and this content
where is a medial medullary lesion?
in the rostral medulla
what is the pattern of sensory loss with a medial medullary lesion?
contralateral loss of discriminative touch and proprioception in the body
no loss of somatosensation in the face
why is there no loss of somatosensation in the face with a medial medullary lesion?
bc the trigeminal light touch pathways decussate at the pons above the medulla and goes back up
what is the pattern of somatosensory loss in bilateral polyneuropathy?
“glove and stocking” loss of all modalities following the order of sensory loss bilaterally
starts peripherally and doesn’t affect proximal structures
what is the order of sensory loss?
proprioception, light touch, cold, fast pain, heat, slow pain
what is the pattern of somatosensory loss with a peripheral nerve lesion?
sensory loss in specific areas that follows the peripheral nerve distribution
what are some examples of peripheral nerve lesions?
carpal tunnel syndrome
sciatica
what is the difference b/w a nerve root lesion and a peripheral nerve lesion?
a nerve root lesion will follow the dermatomal pattern of loss and covers a larger area
a peripheral nerve lesion follows the peripheral nerve distribution which tends to be a smaller area
what is the pathophysiology of shingles?
retraction of the herpes zoster virus (chickenpox) in the DRG or sensory ganglia of the CN causes inflammation of the affected nerves
what is the pattern of somatosensory loss in shingles?
dermatomal bc it affects the nerve root
shingles usually affects the ______ dermatome
thoracic
does shingles causes sensory or motor loss or both?
always sensory loss bc the lesion is in the DRG or trigeminal nucleus
what are the s/s of shingles?
eruption of vesicles/clusters of blisters
itching and/or tingling (usually the first sign)
severe burning pain (can last up to 4 wks)
post herpetic neuralgia
what is usually the first s/s of shingles?
itching/tingling
t/f: shingles is usually limited to one or two dermatomes
true
is shingles unilateral or bilateral?
unilateral
what can shingles s/s develop into?
post herpetic neuralgia
what is post herpetic neuralgia?
sharp, electric-shock like pain following the path of the nerve root that can last after the initial s/s are gone
what is the PT’s role in management of shingles?
TENS over nerve root and/or one above or below it to treat the lasting nerve pain
what is pain?
unpleasant physical and emotional experience which signifies tissue damage or the potential for such damage
pain is a ____ and the emotional response to the _____
perception, perception
t/f: pain can result from structural changes in the NS
true
what causes nociceptive pain?
stimulation of free nerve endings
t/f: stimulation of free nerve endings always reaches the brain
false
perception of pain is always in the ____, not in the _____
brain, periphery
t/f: pain is just a physical experience
false
t/f: pain alters physical and psychological processes
true
nociceptors are activated by ______ stimulus and activation of the _____ _____ _____ _____
mechanical, 1st order nociceptive neuron
what are the ascending pathways of pain?
spinothalamic tract
divergent pathways (spinomesencephalic, reticulospinal, spinolimbic)
what are the divergent pathways?
spinomesencephalic, reticulospinal, and spinolimbic
what ascending pathway is well localized fast, discriminitive pain?
spinothalamic
what ascending pathway is slow aching, interpretive pain?
the divergent pathways
what is the pain matrix?
areas of the brain and NS activated when there’s a pain response
network of brain areas that process and regulate pain info
what is the pain response?
something that triggers descending pathways activation
t/f: the pain matrix can create pain perception w/o nociception
true
how does the pain matrix create pain w/o nociception?
activation of an area creates pain w/o peripheral input
maladaptive rewiring of the brain areas involved
what tract is the lateral system of the pain matrix?
the spinothalamic tract
what tract is the medial system of the pain matrix?
the divergent pathways
where in the cortex is the lateral system of the pain matrix?
primary sensory cortex
insula
where in the cortex is the medial system of the pain matrix?
insula or insular lobe
anterior cingulate cortex (ACC)
pre-frontal cortex
what are the subcortical structures of the medial system of the pain matrix?
amygdala
hypothalamus
where in the thalamus is the lateral system of the pain matrix?
VPL/VPM
where in the thalamus is the medial system of the pain matrix?
midline
intralaminar nuclei
where in the brainstem is the medial system of the pain matrix?
periaqueductal gray
reticular formation
ventral medulla
what is the lateral system of the pain matrix?
discriminative info about location, timing, and intensity of pain/damage
what does the insula contribute to?
cognitive, evaluative interpretation of the pain; strong connection to the limbic system
what is the role of the medial system of the pain matrix?
to provide meaning to the pain; emotional interpretation
what is the role of the anterior cingulate cortex (ACC)?
complex cognitive processing
impulse control
sympathy/empathy
decision making
what is the role of the pre-frontal cortex?
decision making
which system of the pain matrix has more connections in the brain?
the medial system
what is the role of the amygdala?
to ascribe meaning to the pain
what is the role of the reticular formation?
to direct attention to the pain
what is the role of the PAG?
release of endogenous opioids that have an important role in modulating pain (suppression of pain)
what are the 3 pain responses?
reflex movements
autonomic responses
muscles guarding
what are reflex movements?
removing the limb from the painful stimuli
w/drawal reflex
what are the autonomic responses?
increased internal temperature
increased BP
increased HR
increased RR
what is muscle guarding?
reflex to protect the area
the pain matrix generates a ____ ____ response to regulate/modulate pain signals
top down
what is antinociception?
transmission of nociceptive info that can be suppressed at several locations in the NS
what are the 5 levels of antinociception from most peripheral to most cortical?
- periphery
- dorsal horn
- neuronal descending system
- hormonal system
- amygdala and cortical level
how does antinociception work in the periphery?
decreased activation of nociceptors and 1st order nociceptor fibers
what are examples of peripheral antinociception?
anti-inflammatory drugs
topical menthol rubs and capsaicin
local anesthetics
how do anti-inflammatory drugs work?
they decrease the synthesis of prostaglandins that are created from arachidonic acid in the inflammatory response
pain is decreased bc the 1st order neuron isn’t activated as much
how do topical menthol rubs and capsaicin work?
they desensitize nociceptive fibers
how do local anesthetics decrease pain?
they block Na+ channels in neurons to prevent APs (opening of Na+ channels is what initiates APs)
how does antinociception work in the dorsal horn?
decreased relay of nociceptive info to 2nd order neurons
what are examples of antinociception in the dorsal horn?
gate-theory/counterirritant theory
high frequency, low intensity TENS
what is gate theory/counterirritant theory?
in modulated pain, A beta fibers (DCML) synapses on and excites the inhibitory interneuron on the C fibers for pain
mechanical info that isn’t pain activates the inhibitory interneuron to lessen pain
the use of an inhibitory interneurons as a gate
what is high-frequency, low intensity TENS?
treatment of non-chronic LBP
fast frequency competes with the pain signal to lessen it’s effects
how does antinociception work in the fast-acting neuronal descending system?
the PAG activates the ventromedial medulla which activates the raphespinal tract to release serotonin to block pain transmission and lessen pain
the locus coerulus releases NE to inhibit spinothalamic activity and suppress the release of nociceptive transmitters
what structures are involved in the fast acting neuronal descending system?
PAG
rostral ventromedial medulla
raphespinal tract
locus coerulus in the pons
how does the ceruleospinal tract inhibit spinothalamic activity?
binds to afferent nociceptive neurons to suppress APs
how does antinociception work with hormonal control?
endogenous analgesic hormones (endogenous opioids) are released by the periventricular zone (PVZ), pituitary gland, and adrenal medulla
where are the receptors for endogenous opioids?
PAG
rostral ventromedial medulla
dorsal horn
what are the endogenous opioids?
endorphin, enkephalin, and dynorphin
how do we activate the hormonal controls?
with pain
what are ways the hormonal controls are used?
low-frequency, high-intensity TENS
runner’s high
how does low-frequency, high-intensity TENS work?
it activates mechanoreceptors and nociceptive fibers
controlled discomfort to treat chronic pain
endogenous opioids system kicks in with nociceptive stimulation
why is low-frequency, high-intensity TENS used to treat chronic pain?
bc you can’t just stimulate mechanoreceptors to relive their pain as the pain isn’t nociceptive, it has to be higher up
how does runner’s high work in the hormonal control system?
the endogenous analgesic hormones system is activated and released opioids to suppress pain
what is stress induced antinociception?
stress suppressing nociceptive pain with the activation of the sympathetic NS in response to pain
activation of the raphespinal tract and PVZ w/ the release of endogenous alalgestics that bind to opioid receptors in the pain matrix and SC
how does antinociception in the amygdala and cortex work?
it is responsible for the emotional aspects of pain
what happens at the amygdala level of antinociception?
emotional aspects of pain where upsetting experiences outside of pain makes pain worse
what happens at the cortical level of antinociception?
expectations, distraction, and placebo can suppress pain
what is pronociception?
increased pain intensity
what are the 3 levels of pronociception?
- periphery
- psychiatric influence
- pain matrix
what is peripheral pronociception?
edema and endogenous chemicals sensitize free nerve endings
increased edema=____ pain
increased
what is the psychiatric influence of pronociception?
stress, anxiety, and depression intensify pain
how does the pain matrix contribute to pronociception?
it can produce pain in the absence of nociceptive input
what is normal sensory processing in the dorsal horn?
perceiving nociceptive info as nociceptive
what is suppressed sensory processing in the dorsal horn?
gate control theory
use of high-frequency, low-intensity TENS
what is sensitized (acute) sensory processing in the dorsal horn?
pain w/o nociceptive input
increased NT=increased receptor binding
what is reorganized (persistant) sensory processing in the dorsal horn?
long term potentiation
structural changes resulting in persistant increase in sensitivity
allodynia vs hyperalgesia
what is acute pain?
nociceptive pain from a nociceptive stimulus leading to a potential/actual tissue damage
what is chronic pain?
pain most/every day for the past 3 months
can be nociceptive or non-nociceptive
can the pain in nociceptive chronic pain be eliminated when the trigger is eliminated?
yes!
what are types of non-nociceptive chronic pain?
neuropathic pain
central sensitivity syndromes
pain syndromes
t/f: there is no active tissue injury in non-nociceptive chronic pain
true
what is somatic pain?
localized pinprick, stabbing, or sharp pain from a delta fiber activity in the periphery
what is visceral pain?
generalized aching, pressure, or sharp pain from c fiber activity and involved deeper innervation
what is neuropathic pain?
radiating or specific pain described as burning, prickling, tingling, electric shock-like, or lancinating pain from dermatomal or non-dermatomal mechanisms
what is central pain?
thalamic pain
what kind of pain is associated with MS, GBS, and carpal tunnel syndrome?
neuropathic pain
what are some causes of nociceptive pain?
burns
mechanical LBP
cancer
arthritis
trauma
metabolic disease
infection
soft tissue injuries
what is referred pain?
pain at another location from the actual site of origin
inflammation of the viscera and the brain’s misinterpretation of the nociceptive signal
what pain requires a referral somewhere else when presented in PT?
referred pain
what are the symptoms of neuropathic pain?
paresthesia
dysesthesia
allodynia
hyperalgesia
what is paresthesia?
numbness
what is dysesthesia?
abnormal sensation
what is allodynia?
pain w/non-nociceptive signals
what is hyperalgesia?
excessive pain response to nociceptive signals
what are the 4 mechanisms that produce neuropathic pain?
ectopic foci
ephaptic transmission
allodynia
hyperalgesia
what is ectopic foci?
demyelinated axon creates AP itself
very sensitive channels that fire APs w/o stimulation from the soma
what is ephaptic transmission?
abnormal signaling b/w adjacent demyelinated axons w/o synapses
cross-talk
what cellular changes are associated with central sensitization?
increased spontaneous activity with no stimulus
increased responsiveness to afferent inputs due to a lowered activation threshold
prolonged after-discharge in response to repeated stimuli
expansion of receptive fields to a greater area around the injury
what sites generate neuropathic pain?
periphery
dorsal horn
CNS
what damages to neurons can cause neuropathic pain?
stroke
diabetes
MS
viral infection (GBS)
what are the peripheral generations of neuropathic pain?
complete or partial damage to a nerve
what does complete nerve severance cause?
lack sensation from the nerve’s receptive field
sometimes paresthesia and pain
what does partial damage to a nerve cause?
allodynia
electric shock-like sensations
what causes peripheral neuropathic pain?
ectopic foci and ephaptic transmission
what is tinel’s sign?
tapping an injured nerve can elicit pain/tingling
mechanical stimulus elicits pain
what is deafferentation?
disruption in afferent fibers and signals
when peripheral sensory information is completely absent, neurons in the CNS that formerly received information from the body part may become _____ ______
abnormally active
what are the central responses to deafferentation?
phantom pain
central pain
small fiber neuropathy
what is phantom pain/sensation?
pain coming from a limb that is no longer there due to structural reorganization that occurs
what allows a cut axon to still send potentials?
ectopic foci and ephaptic transmission
what is a common treatment of phantom sensation?
mirror therapy
what is central pain caused by?
CNS lesion
what is central pain?
an area of the body deafferentated by a lesion causing burning, shooting, aching, freezing, tingling pain
similar to phantom sensation
what are causes of central pain?
SCI
stroke
MS
how does a SCI lead to central pain?
spontaneous activity of the VPL thalamic nucleus (spinothalamic and DCML)
when does a stroke lead to central pain?
following a lateral medullary lesion or ventroposterior thalamic lesion
what is small fiber neuropathy?
damage to C fibers and loss of nociceptors
partial deafferentation and central sensitization
what are some examples of small fiber neuropathies?
polyneuropathies
post herpetic neuralgia
what do central sensitivity syndromes do?
disrupt top-down regulation of pain
decreased antinociception
increased pronociception
what set of symptoms occur in central sensitization syndromes?
hypersensitivity to lights, sounds, touch, and scents
what are the 4 central sensitization syndromes?
fibromyalgia
episodic tension type headache
migraine
chronic whiplash associated disorder
what is fibromyalgia?
increased glutamate in the SC leads to amplified neural responses
decreased pain inhibition
what are the s/s of fibromyalgia?
widespread pain and stiffness
fatigue
impaired concentration and memory
impaired sleep
functional impairment
what is an episodic tension type headache?
bilateral supersensitivity of the nociceptive pathway to nitric oxide (vasodilation/constriction)
moderate
triggered by fumes, mold, light, or noise
no nausea or vomiting
t/f: episodic tension type headaches often involved nausea and vomiting
false
what are migraines?
unilateral hypersensitivity and amplification of nociceptive signals in the trigemino-thalamo-cortical pathway
severe pulsating
what are the s/s of a migraine?
nausea, vomiting, photophobia (light sensitivity), and/or phonophobia (noise sensitivity)
what is chronic whiplash associated disorder?
allodynia and hyperalgesia around the neck exacerbated by cervical movements
overstretch of nerves/shear force to nerves combined with tissue vulnerability
t/f: chronic whiplash associated disorder can be worsened by stress
true
what are red flags with headaches?
onset of paralysis/reduced level of consciousness
what are the signs that a headache may be caused by excessive intracranial pressure?
headache present at waking
pain triggered by coughing, sneezing, or straining
vomiting
worse when lying down
what are signs that a headache may be caused by serious intracranial disease (encephalitis, meningitis)
progressive worsening over days or weeks
necks stiffness and vomiting
rash and fever
history of cancer or HIV infection
what are signs that a headache may be caused by hemorrhage?
headache following head injury
abrupt onset
history of HTN and hyperglycemia
what are pain syndromes?
involve other body systems in addition to the pain system
disorder/dysfunction of anti/pronociception
what are 2 examples of pain syndromes?
CRPS
chronic LBP syndrome
what is CRPS?
progressive regional pain syndrome affecting somatosensory, autonomic, and motor systems following trauma
what are the s/s of CRPS?
vascular and trophic changes
muscle atrophy
edema
what is the primary precipitating factor for CRPS?
disuse of limbs
what is stage 1 CRPS?
severe burning/aching pain that increases w/ slight touch/breeze
fluctuation in skin temp
rapid growth of hair and nails
changes in skin color, appearance, and texture (pale, red, blotchy, thin, and dry)
hyperhydrosis (excessive sweating)
what is stage 2 CRPS?
increased level of pain
continued skin changes (blue, cold, shiny, dry, and flaky)
brittle and cracked nails
hair growth slows down
stiff joints
muscle weakness
lasts 3-6 months
what is stage 3 CRPS?
too painful to move affected limb
muscle atrophy of affected limb
arthritic changes
very blue, thin, shiny skin
involvement spreads through entire limb
osteoporosis
what are aggregating factors of CRPS?
psychologic and physiologic stimuli
what is chronic LBP syndrome?
change in LBP etiology from tissue damage to central sensitization and deconditioning
what are s/s of chronic LBP syndrome?
pain matrix dysfunction
muscle guarding
abnormal movement
disuse atrophy
decreased pain threshold
what can be done at the cortical level to manage chronic LBP syndrome?
placebo, distraction, positive outlook and expectations, and motivation
what can be done at the hormonal level to manage chronic LBP syndrome?
endogenous opioid release with exercise
what are the sex differences in pain perception?
women are more sensitive to pain than men
women are at a greater risk for developing chronic pain
what may account for the differences in pain perception b/w the sexes?
hormones-testosterone is associated with opiate-mediated pain relief
_____ lean mass may alleviate pain by _____ ascending nociceptive signals
increased, decreasing
where are the cell bodies of LMNs located?
in the ventral horn of the SC
a lesion inside the foramen would lead to a _____ pattern of loss
dermatomal/myotomal
a lesion outside the foramen would lead to a _____ pattern of loss
peripheral
what are the signs of a LMN lesion?
hypotonicity
decreased/loss of reflexes (hyporeflexia)
neurogenic atrophy
fasciculation/fibrillation
paralysis and paresis
what is muscle tone?
resistance to muscle stretch in resting muscle
what factors contribute to muscle tone?
descending motor commands
proprioceptive info
weak cross bridge binding
titan
what is hypotonia?
low muscle tone
abnormally low resistance to passive motio
resting tension is close to none
what is flaccidity?
more severe absence of resistance to passive movement
why can hypotonicity lead to injury?
ligament laxity and hypermobility puts the joints at risk for injury
lack of voluntary motor control
what 2 things can phasic stretch reflex/DTR determine?
- determine integrity of monosynaptic reflex and SC at dif segmental levels
- determine excitability of the alpha motor pool
diminished input from motor neurons to skeletal muscles leads to what?
hyporeflexia
what is neurogenic muscle atrophy?
loss of muscles bulk due to motor neuron axons dying so that there is no nerve stimulus to muscles
denervation of skeletal muscles
what is neurogenic muscle atrophy associated with?
LMNs
is neurogenic muscle atrophy rapid or slow?
rapid
why does denervation occur in neurogenic muscle atrophy?
bc the ground motor neuron is trying to innervate a lot more fibers and it can’t support them so they die leaving only one type of fibers
what is the series of events in neurogenic muscle atrophy?
lack of neural stimulation and contraction–>lack of gene expression–>changed protein production–>rapid atrophy
what will a muscle biopsy show in LMN lesion?
change in protein production in the muscle
what is fasciculation?
spontaneous quick twitch of single motor unit (one motor neuron and all fibers it innervates) that can be seen
t/f fasciculation is always pathologic
false, it is only pathologic when there is atrophy
what may cause fasciculation?
too much caffeine
fatigue
what is fibrillation?
spontaneous contraction of muscles fibers that can’t be observed with the eyes
dispersed ACh receptors (bc of muscles not getting enough ACh) become hypersensitive to any ACh
t/f: fibrillation is always pathologic
true
what is fibrillation a sign of?
denervation/electrolyte imbalance
what is the difference b/w paralysis and paresis?
paralysis: completely severed nerve with no way of signals to get to muscles
paresis: cut a few fibers weakening muscles
how do we measure muscle strength?
MMT and dynamometer
what movement is produced by the C5 myotome?
elbow flexion
what movement is produced by the C6 myotome?
wrist extension
what movement is produced by the C7 myotome?
elbow extension
what movement is produced by the C8 myotome?
flexion of the tip of the middle finger
what movement is produced by the T1 myotome?
finger abduction
what movement is produced by the L2 myotome?
hip flexion
what movement is produced by the L3 myotome?
knee extension
what movement is produced by the L4 myotome?
ankle dorsiflexion
what movement is produced by the L5 myotome?
great toe extension
what movement is produced by the S1 myotome?
ankle plantarflexion
