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OT 6000 > OT 6000- Test 3 > Flashcards

OT 6000- Test 3 Flashcards

1
Q

Conscious pathway of somatosensation

A

Pathways to Cerebral Cortex is a multi-synaptic pathway of:

  • Dorsal columns: discriminative touch, conscious proprioception
  • Anterolateral columns: discriminative pain and temp.
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2
Q

Dorsal column’s (DCML) three neuron pathway

A
  • 1st order: sensory receptors to caudal medulla.
  • 2nd order: caudal medulla to thalamus (where it crosses the midline; how contralateral stroke symptoms come).
  • 3rd order: thalamus to post-central gyrus of the cerebral cortex.
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3
Q

Muscle cramps

A

Cramp is a muscular phenomenon; spontaneous contraction of motor units with NO neural input.

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4
Q

Cause of muscle cramps

A

An issue of overuse; happens when a motor unit is worked more than it should (connection to ALS; less motor units=more work=more cramps).

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5
Q

Fasciculations

A

Spontaneous depolarization of an ENTIRE motor unit; a twitch
-either benign- no comorbid signs and symptoms- or pathologic- will have comorbid signs and symptoms (ALS has fascilations and muscle weakness).

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6
Q

Fibrillations

A

Spontaneous depolarization of one muscle fiber.

-ALWAYS PATHOLOGICAL; muscle fiber will only contract on its own if its lost its innervation.

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7
Q

Tremors

A

Oscillating movement of body part or limb

-can be resting (Parkinson’s disease) or action (postural, orthostatic)

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8
Q

Decrease or loss of muscle reflexes

A

Signal fails at point of motor neuron damaged. Caused by:

  • One spinal nerve is severed; will create a decrease of reflex
  • One peripheral nerve is cut; will create a complete loss of reflex (a-alphas will be cut off)
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9
Q

Atrophy

A

A marked decrease in muscle mass. Caused by either disuse (mild- still some muscle mass) or denervation (more extreme- complete loss of mass due to loss of nerve supply)

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10
Q

Abnormal muscle tone

A
  • Hypotonic: loss of some alpha motor neurons, and loss of some muscle tone (cut spinal nerve)
  • Flaccidity: completely without resistance to passive stretch and loss of all muscle tone (cut peripheral tone)
  • Flaccid paralysis: paralysis due to loss of lower motor neuron
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11
Q

Motor tracts to the spinal cord

A
  • Cortical origin tract: has the greatest voluntary control over muscle movement
  • Brainstem origin tract: more involuntary muscle movement; can be equipped by cortex when extra muscle is needed
  • Basal Ganglia: in the middle of two tracts and sends movement plans from cortex to brainstem
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12
Q

Upper motor neuron (UMN) locations

A
  • Some end and synapse in spinal cord MEDIALLY: these control PROXIMAL core and posture muscles
  • Some end and synapse in spinal cord LATERALLY: these control DISTAL muscles of limbs/ fractionated movements
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13
Q

Medial group UMN origins

A
  • Cortical origin: More directly control of voluntary movement in proximal muscles
  • Subcortical origin: Supports voluntary movement and is directly guided by medial and lateral cortical pathways.
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14
Q

Lateral group UMN origins

A
  • Cortical origin: direct control of voluntary movement in distal muscles. Influences and guides activity of supporting medial group pathway
  • Subcortical origin: supports and complements direct voluntary control
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15
Q

Reticulospinal motor tract

A
  • Originates in the brainstem= low degree of direct voluntary muscle control
  • Broad distribution to UE and LE muscles (proximally)
  • Helps produce gross limb movements (help picks limb up against gravity)
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16
Q

Medial Vestibulospinal motor tract

A
  • Brainstem origin= low degree of direct voluntary control
  • Projects to neck and upper back muscles to help maintain posture and maintaining upright against gravity
  • ->maintain balance and upright posture against gravity in response to signals from your “inner ear”
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17
Q

Lateral Vestibulospinal motor tract

A
  • Brainstem in origin= low degree of direct voluntary control
  • projects to axial and lower extremity extensors lower trunk and legs) to hold us up against the pull of gravity
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18
Q

Medial corticospinal motor tract

A
  • Cortex in origin= high control of direct voluntary muscle control
  • projects to give voluntary control of neck, shoulders and trunk muscles
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19
Q

Lateral Cortiospinal motor tract

A
  • THE MOST IMPORTANT PATHWAY FOR VOLUNTARY MOVEMENT (cortex in origin)
  • used to facilitate fractionated movement of limbs: movement of ANY muscle in ANY combination I want
  • Guiding control of postural support muscles
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20
Q

Pyramids of the medulla

A

Pyramids on bottom of medulla- is where they cross over

  • -Only 90% cross, 10% will not cross
  • because of this, most signs and symptoms will be contralateral, but a very small amount of symptoms in the same side
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21
Q

Discriminative pain and temperature (spinothalamic) three neuron pathway

A
  • 1st order: Free nerve endings to the dorsal root
  • 2nd order: dorsal horn to the thalamus (where synapse crosses and climbs the antereolateral column to the thalamus)
  • 3rd order: Thalamus to the post central gyrus of the cortex
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22
Q

How can you tell if a divergent pain pathway passes through cerebral cortex?

A

If the pathway is a three neuron pathway than it passes through cerebral cortex (spino-emotional pathway).
If the pathway is a two neuron pathway than it will NOT pass through the cerebral cortex (spinoreticular and spinomesencephalic)

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23
Q

Spinoreticular (divergent pain) pathway

A

A two-neuron pathway of pain: starts in the spinal cord and ends in the reticular formation.
This pathway manages arousal levels associated with pain (wakes you up when hurt)

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24
Q

Spinomesencephalic (divergent pain) pathway

A

A two-neuron pathway of pain: starts in the spinal cord and ends in the mid brain.
Has two functions: 1. terminates in area of midbrain that causes head to turn towards pain. 2. activates neurons that go back down the spinal cord to turn off pain to keep it from being so intense it’s disabling.

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25
Q

Spino-emotional (divergent pain) pathway

A

A three-neuron pathway of pain: starts in spine, goes through cerebral cortex and ends in the limbic lobe.
Controls autonomic and emotional response to pain: you get angry when you are hurt and your heart races.

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26
Q

Peripheral sensitization

A

Any injury to the body can result in the sensitization of the pain pathway: lowers the threshold of a AP for pain.
Example: when you get a sunburn and your skin is extremely sensitive and painful.

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27
Q

Neurotransmitters for synapse of the spinothalamic and divergent pathways

A
  • Spinothalamic pathway: glutamate (quick and fast pain; A-delta fibers)
  • Divergent pathway: Substance P (slow and long pain: C-fibers)
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28
Q

Why pain is important to care

A

Pain can be experienced independently of tissue damage, because pain is a perception.
-This is why the first thing therapists should provide is a caring and supportive environment for a patient with chronic pain. This in of itself can help decrease the perception of pain.

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29
Q

When can problems occur with pain?

A
  • When pain severely limits function; A-delta pain can be so severe that pt does not want to move.
  • When pain persists beyond the time necessary or expected for tissue healing.
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30
Q

Referred Pain

A

Pain receptors for visceral organs converge with other pain pathways in more superficial parts of the body. Because of this, pain in organs can be mistranslated by body as pain to superficial body.
-Example: arm pain is a symptom for a heart attack.

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31
Q

Different aspects of pain in the body

A
  1. Sensory-discriminative aspects: you know immediately where you were hurt, what caused it and what type of hurt it was
    - spinothalamic pathway
  2. Motovational-Affective aspects: unconscious change in mood and emotions
    - spinoemotional and spinoreticular pathways
  3. Cognitive-Evaluative aspects: how you evaluate and experience pain and how it affects your life
    - prefrontal lobes of cerebral cortex
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32
Q

Antinociception vs, Pronociception

A
  • Antinocicpetion: Top-down inhibition of pain signals

- Pronociception: top-down amplification of pain signals

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33
Q

Counterirritant

A

Tissue damage is an irritant and it sends signals down pain pathways. Counterirritants (like rubbing where it hurts) activate A-beta gates that activate inhibitory interneurons to close synaptic gates to decrease pain.

34
Q

Four states of dorsal horn processing

A
  1. Normal: you know where you were hurt, synapse faithfully relays information on this
  2. Suppressed: counterirritants can decrease AP in pain pathway
  3. Sensitization: is temporary and neuropathic- synaptic neurotransmitters temporarily increased
  4. Reorganization: is persistent and neuropathic- LTP; permanent change at post-synaptic membrane to change ability to accept synapse
35
Q

Periphery antinociception

A

Periphery has free nerve endings that sense pain, so anything we can do to decrease depolarization of pain receptors will reduce pain.

  • examples: massage, histamine to control inflammation, etc.
  • Periphery is where therapists have the most direct ability to decrease pain.
36
Q

Dorsal horn antinociception

A

Pain can be reduced here by deactivating A-betas which in turn closes pain gateways.
-Examples: E-stim (TENS) and even moving (activates mechanoreceptors)

37
Q

Midbrain descending antinociception

A

Midbrain has a descending pathway of pain and certain meds (and even thought-therapy) can turn off receptors in the spinal cord.

38
Q

Hormonal antinociception

A

Hormonal pathways are mostly autonomic and out of our control, but certain meds, exercises or strong and low rate of TENS may trigger hormonal nociception

39
Q

Amygdala and cortex antinociception

A

Amygdala evaluates everything to see if it’s a threat. If we can convince ourselves through therapy that certain inputs are benign, we can encourage nociception

40
Q

Causes of chronic pain

A
  • Continuing tissue damage
  • Environmental factors: thinking pain into existence through conditioning
  • Sensitization of nociception pathways
  • Dysfunction of endogenous, top-down pain control system
41
Q

Paresthesia

A

Non-painful sensory message that arises in the absence of any sensory receptor stimuli

  • either spontaneous or evoked
  • example: tingly feeling when foot falls asleep
42
Q

Dysesthesia

A

A sensory input that is unpleasant of painful, either evoked or spontaneous

  • Allodynia: unpleasant sensation in response to a generally not unpleasant stimulus (example= skin sensitive to touch after sunburn)
  • Secondary hyperalgesia: pain that is out of proportion to the stimulus creating it
43
Q

Neuropathic pain

A

pain that comes when there is not stimulation of free nerve endings

44
Q

Ectopic Foci

A

A mechanism of neuropathic pain: pain starting in a different location other than nerve endings, such as damaged to a neuron that causes demyelination or degeneration of axon

45
Q

Ephaptic transmission

A

A mechanism of neuropathic pain: pain caused by short circuiting that inappropriately signals a different axon pathway.
-Example: during Guillain-Barre, an AP from a touch neuron can jump to the pain pathway due to short circuit causing pain from light touch

46
Q

Central sensitization

A

A mechanism of neuropathic pain due to a maladaption of the neural pathway: a strong or long-lasting pain signal will cause sensitization to that specific pain pathway due to long term potentiation
-will cause strong pain from small stimulus

47
Q

Structural reorganization

A

A mechanism of neuropathic pain due to a maladaption of the neural pathway: After a long-lasting or extreme stimulus, a central axon of pain may back away from the synapse and attach to to a touch pathway and establish a synapse.
-this will cause a simple touch to cause a pain response

48
Q

Phantom limb sensation

A

After amputation of knee, central neurons may reorganize -via collateral sprouting or denervation hypersensitivity or both- to the touch or pain pathway of the thigh.
-End result: touch/pain of thigh will be translated to touch/pain of missing knee.

49
Q

Central sensitivity syndrome

A

Top-down reorganization of a pain pathway (brain’s influence) that causes an increase in antinociception and a decrease in pronociception through LTP.
-Through targeted therapy focused on acknowledgement, support and education, we can help re-wire the brain after this syndrome develops

50
Q

Motor system pathways

A
  1. Decision (cerebral hemisphere)> motor planning areas (pre-motor cortex)> upper motor neurons (tracts)> spinal interneurons> lower motor neurons> skeletal muscles
  2. Decision (cerebral hemisphere)> control circuits (basal ganglia and cerebellum)> upper motor neurons> lower motor neurons> skeletal muscles
51
Q

Components of a sarcomere

A

Sarcomere: the contractile units of a muscle

  • Z line: are the physical ends of a sarcomere
  • M line: are the structural protein that myosin are hung on
  • Titin: are the structural protein that extend from one sacromere to the other; resists stretch that would otherwise pull sarcomere apart.
  • Myofilaments: actin and myosin: actin grabs onto myosin to make a bridge; actin then climb down myosin to physically shorten sarcomere
52
Q

How sarcomeres contract

A
  1. Action Potential on A-alpha
  2. Acetylcholene creates an excitatory postsynaptic potential to begin muscle contraction
  3. This opens membrane to dump out Ca++
  4. Ca++ activates actin
  5. Actin climbs on myosin to shorten sarcomere
  6. Muscle contracts
53
Q

Total muscle resistance to stretch

A
  • Titin can reach its elastic limit (contractures can play a part in this)
  • Active contraction: crossbridges are being formed and actin crawls down myosin either voluntarily or involuntarily (involuntary= Parkinson’s)
  • Weak actin/myosin bonds: muscle not moved, for long= actin and myosin can stick together
  • Proprioceptive information- especially that from muscle spindles, can influence the stiffness of a muscle by depolarizing motor neurons
54
Q

How can the number of sarcomeres adapt to length?

A

Our muscles are dynamic and respond to position and stretch; the number of sarcomeres is related to length muscle is stretched.

  • if a muscle is kept in flexed position for too long, the number of sarcomeres will decrease causing contractures
  • we can increase the number of sarcomeres through lots of movement and continuous stretching of that limb through splints
55
Q

Cocontraction

A

Cocontraction: two muscles contracted at the same time

  • Static cocontraction: will lock segment or joint through equal opposing muscle contractions
  • Dynamic cocontraction: opposing muscles are playing off each other to allow body segment to move, but under control
56
Q

Myotome organization

A

Myotome is all muscles innervated by a single spinal level

  • almost all muscles are in more than one myotome
  • Different movements are asociated with each myotome
57
Q

Alpha-gamma coactivation

A

Allows muscle to contract (alpha) and keeps the spindle sensitive (gamma)

58
Q

Slow twitch motor unit

A
  • Red motor unit due to oxidative metabolism
  • is innervated by small A-alphas
  • Lower tension, more fatigue resistant (think marathon)
59
Q

Fast twitch motor unit

A
  • Is white; glycolytic metabolism instead of oxidative
  • lnnervated by larger diameter A-alphas
  • high tension and less fatigue resistance (think sprinting)
60
Q

Henneman’s size principal

A
  • Order of recruitment: your body recruits slow twitch muscles first and will only recruit fast twitch if needed because of the energy needed for depolarization is higher
  • UNLESS you are in fight or flight, in which case the order of recruitment is reversed
61
Q

Muscle fibers per motor unit

A
  • Gross motor control (gastroc)= 2,000 muscle fibers per axon: lots of strength, not much control
  • Fine motor control (extraocular)= 2.5 muscle fibers per axon: less strength, but allows for much control
62
Q

Reciprocal inhibition

A

If an agonist is facilitated, than the antagonist is inhibited to get movement around a joint
-happens consciously and unconsciously

63
Q

Normal muscle synergies

A

A group of muscles that work together under good voluntary control in any pattern desired for function

64
Q

Abnormal muscle synergies

A

A group of muscles that work together under limited voluntary control in a limited number of patterns that may or may not contribute to function

65
Q

Spinal reflex pathway

A

Stimulus at sensory organ> afferent pathway> connection of afferent to efferent> efferent pathway> effector organ

66
Q

Multi-segment withdrawal

A

allows for multisegment reflex in response to damaging stimulus:
-because pain neurons send branches one level above and below, this allows movement of more than one body segment at a time (example: hip and knee withdrawal after stepping on tack)

67
Q

Helpful abbreviations for understanding motor tracts

A
  • cortico= beginning in cortex (voluntary)
  • reticulo= beginning in reticular formation in brainstem (mostly involuntary) and medial in formation (core/proximal muscles)
  • vestibulo= beginning in vertibule of brainstem (mostly involuntary)
68
Q

Nonspecific motor tracts

A

Nonspecific motor tracts lower the threshold for all other motor neuron pathways so it is easier for UMNs to activate LMNs.

  • Turned on by limbic system (emotional and autonomic) to get you ready for action
  • descend from brainstem and control broad faciliation of lower motor neurons in spinal cord
69
Q

Corticobrainstem tracts

A
  • These are the UMN of cranial nerve control
  • High degree of motor control (descend from cortex)
  • Control muscles of face, tongue, throat and part of neck
70
Q

Cortical areas in front of pre-central gyrus

A
  • Premotor area: controls anticipatory postural control (sets posture so you can move and act without falling over)
  • Supplementary motor area: allows for sequential movement and bimanual activities. Can be activated just by thinking about moving (good for therapy if body schema is intact)
71
Q

Three broad conditions of UMN damage

A
  1. UMN completely cut off from LMN (example= complete SCI)
  2. UMN in tact but tonically overactive (example= Parkinson’s)
  3. Cortical UMN damage but brainstem UMN undamaged (example= Stroke: when they want to move gross motor kicks in through brainstem, but fine motor gone due to cortical loss; arm flexed and leg extended)
72
Q

Paralysis vs Paresis

A
  • Paralysis: all motor neurons are cut off from SC, so UMN are still alive in the brain but cannot make connection to LMN that are still connected to muscles
  • Paresis (seen is stroke): cortical UMN damaged but brainstem intact. Creates weak, gross movement (no fine motor, fractionated movement)
73
Q

Reflexes after SCI

A

When spinal level is cut off, spinal reflexes below that level get stronger
-Babinski response: toes curling up in strong force instead of curling down with stimulus (indicates UMN damage= enhanced cutaneous response)

74
Q

Muscle stretch Hyperreflexia

A

When UMNs are cut off from connection to a reflex synapse, you see an exaggerated stretch reflex

  • is velocity dependent; repeats itself as long as stimulus is maintained
  • -spasticity= muscle stretch hyperflexia
75
Q

Clonus

A

Rhythmic, repeating (usually involuntary) contraction of a single muscle group in response to a quick stretch
-can be unsustained (happens a few times and stops) or sustained (keeps on going- ALWAYS pathological)

76
Q

Where do the discriminative pain and touch pathways cross over?

A
  • Discriminative touch: the caudal medulla
  • Discriminative pain: after the dorsal horn, at the same spinal level at which the peripheral pain neuron entered the spinal cord
77
Q

Adaptive changes inside the muscle in response to non-use (myoplasticity)

A
  • Atrophy: atrophy of disuse: still has nerve supply, but there is a loss of neuromuscular excitation and decrease in muscle tone
  • Increased stiffness: actin and myosin begin sticking together causing stiffness in muscle
  • Contractures: loss of sarcomeres due to prolonged position: cannot stretch to physiological length
78
Q

Atrophy in relation to location of motor neuron

A
  • Damage to upper motor neurons leads to atrophy of disuse

- Damage to lower motor neuron leads to atrophy of denervation (more extreme)

79
Q

Temporary hypotonia

A

During spinal shock after spinal damage, there are no reflexes present (hypotonia). After some time these reflexes will become hypersensitive due to lack of messages

80
Q

Decerebrat vs Decorticate rigidity

A
  • Deceberate: “without head”- UMN’s are too active to contract extensors of arms and legs
  • ->this is a very extreme injury because most of the head has been cut off due to damage
  • Decorticate “without cortex”- UMNs are overactive to flex arms and extend legs
  • ->is more common but less serious than decerebrat
81
Q

Abnormal synergies

A

Often seen in stroke patients: extended legs and flexed arms (reflects bodies desire to pick up body and hold things against gravity)
-the higher the effort of action, the more the lack of controlled movement appears (why we grade down therapy)

OT 6000 (8 decks)

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