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PHTH 527: Applied Neurosciences I > Exam 2 Prep > Flashcards

Exam 2 Prep Flashcards

1
Q

What is locomotion?

A

An action initiated by the brain, but yet are maintained in its steady-state execution by mostly spinal mechanisms (CPG) with the interaction of peripheral afferent contributions

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2
Q

What is the evidence for CPG in human spinal cord injuries?

A

-Involuntary LE stepping-like movements were expressed spontaneously
-In supine: rhythmic, alternating, and forceful muscle contractions bilaterally
-Rhythmic movements
-Spontaneous rhythmic patterns

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3
Q

What movements does the CPG control?

A

-Protective reflexes
-Locomotion

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4
Q

What is the central pattern generator (CPG)? What is its function?

A

-The rhytmic timing and coordination of muscles generated by the CPG and is located in the spinal cord
-It initiates gait, a locomotor command is generated levels above the spinal cord (brain)

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5
Q

What is the grand initiator of gait that is also involved in the choice and emotion behind gait?

A

-Basal ganglia
-Mesencephalic locomotor region

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6
Q

How is the basal ganglia involved with initiation of gait?

A

It selects the pattern

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7
Q

How is the mesencephalic locomotor region (MLR) involved with the initiation of gait?

A

-It modulates the spinal cord
-Initiates info to the brainstem
-Initiator of neurons

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8
Q

Where does the CPG get sensory feedback from?

A

-Muscle spindle (muscle length)
-Golgi tendon (muscle force)
-Joint receptors

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9
Q

How are the reticulospinal neurons involved in locomotion?

A

They innervate the gamma and alpha motor neurons

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10
Q

What is the order in which locomotion is initiated?

A

-Cortex, basal ganglia, and cerebellum select limb pattern
-Mesencephalic locomotor region initiates the neurons
-Reticulospinal neurons integrate whole body movement and innervate gamma and alpha motor neurons
-Central pattern generator

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11
Q

How does the basal ganglia communicate with the MLR to initiate the gait process?

A

It releases dopamine into the MLR

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12
Q

What are burst generators?

A

They activate synergist muscle at each limb joint and ensure it is appropriately timed

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13
Q

What are locomotor networks composed of?

A

Distributed and interconnected unit burst generators that are selectively recruited to produce specific locomotor patterns

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14
Q

How does alternation of limbs via inhibition and activation of neurons occur?

A

-During locomotion, flexor and extensor neurons receive inhibitory and excitatory input
-Receive inhibitory input from Renshaw cells and reciprocal Ia interneurons

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15
Q

What are Renshaw cells?

A

-A population of inhibitory interneurons that project onto motor neurons
-Can synapse onto two motor neurons

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16
Q

How much does Ia and Ib increase extensor activity?

A

By 50%

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17
Q

How does Ib (GTO) increase extensor activity during gait?

A

It enhances muscular contraction of extensors during the stance phase and resets when activated during the swing phase (ask Dr. Rivera to explain more)

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18
Q

How does Ia (muscle spindle) increase extensor activity during gait?

A

Establishes monosynaptic connection with synergistic alpha motor neurons

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19
Q

How is the hip involved with the step cycle? Why is it important?

A

-The hip movement/position during the step cycle signals which part of the step cycle the limb is at any given moment
-Signals from afferents are influenced by hip position and help regulate the step cycle at the spinal cord level

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20
Q

How are the signals from the hip regarding the step cycle regulated and transmitted to the brain?

A

-The signal is sent to the spinal cord
-Then the signal is transmitted to the cerebellum via the dorsal spinocerebellar tract

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21
Q

Why is loading in mid to terminal stance a key component of sensory input?

A

-The longer the loading and increase in hip extension, the more sensory input
-Provides a greater opportunity for pre-swing and trailing limb
-Leads to greater stride length

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22
Q

How does the hip position regulate the transition from stance to swing phase?

A

Regulates the termination of extensor activity and onset of flexor activity

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23
Q

What is the swing phase mediated by?

A

-The trailing limb, 20-30 degrees of hip extension
-A quick stretch (extension) is needed to activate the muscle spindle
-Aids in the propulsion of the limb in space

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24
Q

What are the three inputs to help in gait training?

A

-Input 1: higher the mid-stance load, the more swing phase is improved
-Input 2: Hip position, hip extension and achieve trailing limb
-Input 3: erect posture

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25
Q

What are the rockers that are essential for smooth gait and that we should consider in gait training?

A

-First ankle rocker (loading at stance phase)
-Second ankle rocker (tibial advancement over fixed foot)
-Third ankle rocker (metatarsal heads are loaded)

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26
Q

What are common things that happen when someone has a CVA?

A

-Synergistic movement
-Generalized weakness
-Spasticity

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27
Q

What are common gait dysfunctions in CVA patients?

A

-Lack of heel strike
-Knee hyperextension in midstance
-Knee buckling in mid stance
-Absent trailing limb

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28
Q

What are postures that are associated with Parkinson’s disease during gait?

A

-Increased cervical flexion (forward head)
-Increased thoracic kyphosis
-Center of mass out of base of support
-Lack of thoracic rotation and arm swing

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29
Q

What are common gait abnormalities in Parkinson’s disease?

A

-Bradykinesia
-Freezing of gait
-Small steps
-Difficult to initiate gait
-Narrow foot width
-Festination
-Tremors
-Weaving
-Uncoordinated limb movements

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30
Q

What is the definition of pain?

A

Unpleasant or emotional experience associated with, or resembling that associated with, actual or potential tissue damage

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31
Q

What is pain influenced by?

A

-Pain is always a personal experience
-Biological, psychological, and social factors

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32
Q

What is the difference between pain and nociception?

A

-Pain cannot be inferred solely from activity in sensory neurons
-Individual learn the concept of pain through life experiences
-Nociception is the detection of pain via peripheral and central nervous system

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33
Q

What role does pain serve in our lives?

A

It serves as an adaptive and protective role

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34
Q

What can pain have adverse effects on?

A

-Function
-Social and psychological well-being

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35
Q

What are biological factors that can affect pain?

A

-Genetics
-Physiology
-Neurochemistry
-Tissue health

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36
Q

What are social factors that can affect pain?

A

-Socioeconomic status
-Social support
-Social learning
-Skepticism
-Operant

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37
Q

What are psychological factors that can affect pain?

A

-Perceived control
-Self-efficacy
-Catastrophic thinking
-Hypervigilance
-Depression
-Anxiety
-Anger

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38
Q

What is the #1 thing that can help with chronic pain?

A

TENS

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39
Q

How should pain be assessed?

A

-In a comprehensive, safe, ethical, and consistent manner
-Use valid and reliable assessment tools/outcome measures that help determine prognosis
-Consider risks, benefits, costs, and limitations of interventions

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40
Q

What is Article 1 in the International Association of the Study of Pain (IASP)?

A

The right of all people to have access to pain management without discrimination

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41
Q

What is Article 2 in IASP?

A

The right of people in pain to have acknowledgement of their pain and to be informed about how it can be assessed and managed

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42
Q

What is Article 3 in IASP?

A

The right of all people with pain to have access to appropriate assessent and treatment of the pain by adequately trained healthcare professionals

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43
Q

What are risk factors/habits that contribute to chronic pain?

A

-Diet
-Sleep
-Stress
-Physical activity
-Sedentary behavior
-Smoking

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44
Q

What is the first thing to ask patients about and tackle with chronic pain?

A

Sleep!!!

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45
Q

What are the different types of pain fibers?

A

-Delta fibers
-C fibers

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46
Q

What are delta fibers?

A

-Myelinated
-Higher conduction velocity than c fibers
-Mechanical or pressure
-Sharp pain

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47
Q

What are C fibers?

A

-Unmyelinated
-Slow conduction velocity
-Thermal, chemical, or mechanical
-Dull ache

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48
Q

What is the difference between peripheral nerve vs muscle injury?

A

Peripheral
-Burning, tingling, pins and needles
-Arms, legs, feet, and hands
-Follows peripheral nerve
-Tinel’s sign
-Constant pain

Muscle
-Localized
-Palpation of muscle increases pain
-Tender, throbbing, and stiffness
-Increased pain when contracting
-Reduced pain at rest

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49
Q

What substances are constantly released in chronic pain? How does it work?

A

-Glutamate
-Substance P
-They increase the pain perception

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50
Q

How can we help override painful sensations?

A

By giving different sensations

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51
Q

What is acute pain?

A

-Normal response to painful stimulation
-Contributes to survival by protecting the tissue from further damage

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52
Q

What is adaptive pain?

A

Protects tissues and promotes healing

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53
Q

What is maladaptive pain?

A

-Process presenting as a disease
-Represents pathological functioning of the nervous system

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54
Q

What is chronic pain?

A

-Pain that lasts longer than 3 months
-Tissue is no longer in protective mode but has a maladaptive process
-Tissue is healed
-May involve alternative neuro pathways

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55
Q

What does the normal physiologic response to pain involve?

A

-Injury: physical and chemical
-Response: nerve, vessels, immune cells, prostaglandins
-Nerves release substance P
-CGRP released: vasodilator from sensory nerves

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56
Q

What is substance P?

A

-Neuropeptide
-First responder to stress or pain in periphery
-Released by a variety of cells (sensory neurons of the epithelium, muscle, joint, glia)
-Immediate and ongoing
-Causes vasodilation & histamine release

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57
Q

How is substance P correlated with nervous system pain?

A

-Highly correlated with nervous system pain
-Associated with glutamate
-Released in tissue
-Released in dorsal root ganglion and dorsal horn
-Released for our protection so we don’t move or touch the painful area

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58
Q

What is allodynia?

A

Pain from “non-painful” stimuli (nociplastic)

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59
Q

What is analgesia?

A

Absence of pain sensation

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60
Q

What is hyperalgesia?

A

Increased sensitivity to painful stimuli

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61
Q

What is sensitization?

A

Increased responsiveness of nociceptive neurons to their normal input, and/or recruitment of a response to normally subthreshold movements

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62
Q

How is pain classified?

A

-Nociceptive
-Neuropathic
-Nociplastic

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63
Q

What is neuropathic pain subdivided into?

A

-Peripheral nerve pain
-Central brain or spinal cord pain

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64
Q

What is nociplastic pain subdivided into?

A

-Peripheral sensitization
-Central sensitization

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65
Q

What is peripheral sensitization?

A

-Increased responsiveness and reduced threshold of nociceptive neurons in the periphery
-Pain felt from a non-noxious stimuli such as a feather

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66
Q

What is central sensitization?

A

-Increased responsiveness of nociceptive neurons in the central nervous system to their normal or subthreshold afferent input
-Pain associated with fear and other cognitive issues

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67
Q

What can nociplastic pain cause?

A

Negative neuroplasticity

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68
Q

What is nociceptive pain?

A

-Pain arising from a noxious stimuli
-Somatic and non-neural
-Localized

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69
Q

What is neuropathic pain?

A

Pain initiated or caused by a primary lesion or dysfunction in the nervous system

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70
Q

What is nociplastic pain? What does it cause?

A

-Pain that arises from altered nociception despite no clear evidence of actual tissue damage
-This pain causes activation of peripheral nociception despite no evidence of disease or lesion of the somatosensory system

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71
Q

What can cause central sensitization?

A

Increased responsiveness can be due to dysfunction of endogenous pain control systems such as the spinalthalamic tract & reticular formation off shoots

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72
Q

What is the “chemical soup” around an injury?

A

-Substance P
-CGRP
-Histamine
-Prostaglandin

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73
Q

Where can substance P be found in peripheral sensitization?

A

-Peripheral areas
-Dorsal horn

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74
Q

What are the tracts that are invovled in centralized pain?

A

-Anterolateral
-Spinoreticular

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75
Q

What tract synapses onto the brainstem reticular formation (RF)? How is this structure related to pain? What does it connect to?

A

-Spinoreticular tract
-Awareness and arousal to pain
-Connects to the hypothalamus

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76
Q

What tract synapses onto the periaquedcutal gray? Where is this structure located and how does it relate to pain?

A

-Located in the midbrain
-Modulation & perception of pain
-Lessen or increases pain perception
-Key in defensive behaviors
-Elevates HR, BP, and RR
-Defense mechanism for future pain

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77
Q

Where do the anterolateral and spinoreticular tracts synapse onto before going to the cortex?

A

-They both synapse on the thalamus
-Then they synapse onto the cortex

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78
Q

What structures in the brain are involved in central sensitization?

A
  1. Thalamus to
    -Anterior cingulate cortex (ACC)
    -Amygdala
    -Prefrontal cortex
  2. Hypothalamus
    -Hippocampus
    -Amygdala
    -ACC
  3. Hippocampus
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79
Q

What is the descending pathway? How does it modulate pain?

A

-Catecholinergic pathway
-The cortex sends info to the periaqueductal gray
-The periaqeductal gray provides endogenous opioids and serotonin
-The periaqueductal gray sends info to the Nucleus Raphe which inhibits the dorsal horn
-Inhibition of the dorsal horn inhibits pain and inhibits substance P

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80
Q

What are other factors that can affect pain?

A

-Drug abuse
-Financial difficulties
-Cultural barriers
-Litigation
-Language barriers
-Lack of health insurance

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81
Q

What are some non-pharmacologic ways of managing pain?

A

-Exercise
-Patient education
-Taping
-PT/OT
-ROM exercises
-Weight loss

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82
Q

What is the best thing a PT can do for someone with chronic pain?

A

-Listen to them!!!
-Acknowledge their pain
-Promote socialization and activity (hobbies, altruism, family, etc.)

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83
Q

What does effective pain education involve?

A

-Listening
-Pain science concepts
-Patient understanding
-Reflective questions
-Validation
-Tailored to education level
-Ongoing process
-Individualizing

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84
Q

What is the pain reduction theory?

A

-Providing a different stimulus that utilizes the dorsal column pathway
-Providing a different sensation, the dorsal column will inhibit the pain pathway

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85
Q

What is the gate control theory?

A

-Same as pain reduction theory?
-When pain and touch fibers are stimulated at the same time, gate for pain will be closed and pain is not felt

86
Q

Can negative neuroplasticity be reversed?

A

It can be reversed, but most of the time, not fully

87
Q

How can NSAIDs help in pain reduction?

A

-Reduces prostaglandins
-Prostaglandins plays a role in the peripheral and central sensitization process

88
Q

What is Capsaicin? How is it used to treat pain? How long does it take to work?

A

-Chemical from chili peppers
-Binds to open c fiber receptors, which allows calcium ions to flow into the fiber causing desensitization
-It depletes substance P
-It can take several weeks to work

89
Q

Are there any side effects to Capsaicin? What conditions is it good for?

A

-No side effects
-Good for arthritis and muscular pain

90
Q

What are some common pain/chronic pain conditions?

A

-Phantom limb pain
-Hand shoulder syndrome (post mastectomy)
-Pelvic pain
-Chronic low back pain
-Autoimmune conditions
-Fibromyalgia

91
Q

What pain condition automatically gets placed in the sensitization category? Is it peripheral or central sensitization?

A

-Fibromyalgia
-Almost always in both peripheral and central

92
Q

How does phantom limb pain occur?

A

-The person is missing sensory input to the somatosensory cortex
-The brain perceives it as pain
-Negative neuroplasticity

93
Q

What is chronic regional pain syndrome (CRPS)?

A

-There is an injury to the hand/foot/arm/etc.
-Pain impulse sent to the brain
-This triggers an impulse in the sympathetic nervous system which returns to the original site of injury
-Sympathetic impulse triggers inflammatory response and vessels to spasm and swell
-This causes increased pain, burning, and red mottling skin
-Incorrect response in autonomic nervous system

94
Q

What kind of pain is CRPS?

A

Allodynia

95
Q

What are treatments for CRPS?

A

-Deep pressure (wrapping with ace bandage) to reduce sensory input for 20-30 minutes
-Movement (increased use of muscle spindles, increases blood flow)
-Tactile information (self initiated, skin movement)

96
Q

What population are cerebellar tumors in?

A

Typically only in children

97
Q

How common are cerebellar strokes?

A

Cerebellar artery strokes are very rare

98
Q

How does the cerebellum communicate with the cortex?

A

Through the thalamus

99
Q

What is the cerebellum responsible for?

A

-Motor coordination and correction of movements
-“Motor memory”
-Maintenance of balance/posture: vestibular info/proprioception
-Coordination of multiple motor groups
-Muscle spindle feedback
-Postural adjustments
-Sensory processing
-Adaptability
-Automatic responses
-Modifies motor activity

100
Q

How does the cortex communicate with the cerbellum?

A

It sends signals directly to the cerebellum

101
Q

What is the cerebellum also known as?

A

The “Little Brain”

102
Q

How does the cerebellum play a role in motor learning?

A

-It adapts and fine tunes motor programs to make accurate movements through a trial and error process (ex: learning to hit a baseball)

103
Q

How is the cerebellum involved in cognition?

A

It is involved with language

104
Q

How is the cerebellum related to the eyes?

A

-Controls eye reflexes
-Fixation on target and eye coordination

105
Q

How is the cerebellum involved in accuracy of timing movements?

A

-Predicts the sensory outcome of our movements/actions
-Controls timing of on and off muscle activation and direction of movement

106
Q

How much of the brain’s volume does the cerebellum make up? How much of the brains neurons are in it?

A

-10% of the brains volume
-Over 50% of the total number of neurons in the brain are in the cerebellum

107
Q

What sensory feedback does the cerebellum receive?

A

-Vestibular
-Muscle proprioceptors (spindle and GTO)

108
Q

How does the cerebellum modulate commands to motor neurons?

A

It compensates for shifts in body or changes in load upon muscles

109
Q

What are the different lobes of the cerebellum?

A

-Anterior
-Posterior
-Flocculonodular

110
Q

What are the different zones of the cerebellum? Where are they located in relation to the vermis?

A

-Intermediate zone (just lateral to the vermis)
-Lateral hemisphere (most lateral zone to the vermis)

111
Q

What does the primary fissue separate in the cerebellum?

A

It separates the anterior and posterior lobes of the cerebellum

112
Q

What does the posterolateral fissure of the cerebellum separate?

A

It separates the intermediate zone from the lateral hemisphere

113
Q

What is the function of the flocculonodular lobe in the cerebellum?

A

-It is the major transport for vestibular information to the cerebellum
-Responsible for equilibrium,balance, and posture

114
Q

What is the function of the lateral hemisphere of the cerebellum?

A

-Planning and initiating of movements
-Motor planning for extremities

115
Q

What is the function of the intermediate hemisphere of the cerebellum?

A

Distal limb coordination

116
Q

What is the function of the vermis?

A

Proximal limb and trunk control

117
Q

What are the deep cerebellar nuclei (DCN)? Are they inputs or outputs to the cerebellum?

A

-Purkinje (output)
-Climbing fibers (input)
-Mossy fibers (input)

118
Q

What are the main cerebellar unconscious input pathways?

A

-Vestibular feedback
-Visual motor and sensory feedback

119
Q

What is the superior colliculus involved in?

A

-Learning and memory connections
-Visuospatial and steering

120
Q

What is the dorsal spinocerebellar tract?

A

-Carries proprioceptive information from muscle spindles and golgi tendon organs from ipsilateral trunk and lower limb to cerebellum
-Carries touch and pressure sensation from lower extremities and trunk

121
Q

What is the ventral spinocerebellar tract?

A

-Carries info regarding coordinated movement and posture of the entire lower limb and GTO
-Only to lower extremities (L2 and below)

122
Q

What is the rostral spinocerebellar tract?

A

-Carries info regarding coordinated movement and posture for the entire upper limb
-Above C8

123
Q

What is the cuneo spinocerebellar tract?

A

-Large, myelinated axons
-Carries unconscious proprioception, touch, and pressure sensation
-Above C8

124
Q

What is a commonality amongst all of the spinocerebellar tracts?

A

They all carry unconscious perception

125
Q

What are the cerebellum outputs?

A

-Red nucleus
-Ventrolateral nucleus of thalamus

126
Q

What does the red nucleus communicate with?

A

-The red nucleus receives info from the cerebellum
-Then it sends info directly to the spinal cord
-Motor relay system

127
Q

What does the ventrolateral nucleus (VLN) of the thalamus communicate with? What is the function of it?

A

-Receives info from the cerebellum
-Sends info to the pre motor cortex, supplementary cortex, and prefrontal association area
-Aids in postural control, smooth movements, and provides feedback for errors

128
Q

How do cerebellar injuries present and why?

A

-They always present unilaterally
-The spinocerebellar tracts either stays unilaterally or crosses over twice

129
Q

What is decomposition of movement?

A

-Patients with cerebellar dysfunction are unable to produce coordinated, smooth movements
-The loss of feedforward mechanism (spindle & GTO) does not allow for temporal timing of the activated muscles, sequence of activation, force or awareness in space

130
Q

What is an intention tremor?

A

-When someone is moving volitionally, such as moving their hand towards a target, there is a tremor that increases more as the hand gets closer to the target

131
Q

What is one of the most common signs of cerebellar dysfunction?

A

Ataxic movement

132
Q

What is the Romberg & Sharpened Romberg test?

A

-Romberg is standing with feet together or semi-tandem and eyes open for 10 seconds, then eyes closed for 10 seconds
-Sharpened Romberg is standing tandem with eyes open for 10 seconds, then eyes closed for 10 seconds

133
Q

What are different cerebellar exams?

A

-Finger to nose
-Heel to shin
-Dysdiadochokinesia (RAM)
-Tandem walking
-Romberg
-Rapid finger tapping movements

134
Q

What is dysrhythmia?

A

Abnormal timing

135
Q

What is dysmetria?

A

Overshooting or past pointing

136
Q

What is dysdiadochokinesia?

A

Rapid alternating movements

137
Q

What are common postural dysfunctions in patients with cerebellar disorders? What do these dysfunctions cause?

A

-Loss of automatic movements
-Loss of ankle & hip strategies
-Static and dynamic postures
-Causes high fall risk

138
Q

What is hypotonia?

A

Low tone from loss of muscle spindle and GTO input

139
Q

What is slow generation of force?

A

Unable to produce timely force generation

140
Q

What is loss of rapid alternating movements?

A

Inability to produce rapid movement patterns and alternating movements

141
Q

What are deficits in motor learning?

A

Loss of the ability to anticipate or correct feedback because of loss of proprioceptive, sensory, and muscle force

142
Q

What is the clinical presentation of peripheral nerve injury?

A

-Atrophied muscle
-Weakness or paralysis
-Pain along nerve distribution
-Numbness along nerve
-Sensory loss (light touch, position sense) along nerve
-Loss of ROM over time

143
Q

What is the clinical presentation of carpel tunnel syndrome/median nerve injury?

A

-Atrophy of thenar eminence
-Pain along median nerve
-Positive Tinel’s sign

144
Q

What is the clinical presentation of C6 nerve root injury?

A

-C6 myotome and dermatome pattern
-Muscles: biceps, brachioradialis, wrist extensors

145
Q

What are signs and symptoms of spinal nerve root injuries?

A

-Hyporeflexia
-Decreased DTR
-Weakness
-Sensory loss
-Pain
-Numbness and tingling following dermatome pattern

146
Q

What side should always be tested first during myotome/dermatome testing?

A

Uninvolved side

147
Q

What is the clinical presentation of injury to common fibular/peroneal nerve?

A

-Sensory loss in common fibular distribution (dorsum of foot and lateral portion of shin and leg)
-Hyporeflexia
-Muscles: fibularis longus and brevis, tibialis anterior, EHL, EDL, fibularis tertius

148
Q

What are some big differences between lower motor neuron injuries and upper motor neuron injuries?

A

Lower motor neuron
-Hyporeflexia
-Loss of muscle tone
-Rapid muscle wasting

Upper motor neuron
-Hyperreflexia
-No loss of muscle tone
-Maintained muscle mass
-Contralateral symptoms to lesion

149
Q

How is the basal ganglia involved in motor control?

A

-Eye movement (helps us plan where to look)
-Associative function
-Limbic system

150
Q

What structures make up the basal ganglia?

A

-Caudate
-Putamen
-Globus pallidus
-Subthalamic nucleus
-Substantia nigra

151
Q

What is the basal ganglia?

A

-The basal ganglia is a collection of gray matter nuclei
-Contains a variety of complex excitatory and inhibitory connections, utilizing different neurotransmitters

152
Q

How are the caudate and putamen separated?

A

-Separated by penetrating fibers of the internal capsule but remain joined by cellular bridges

153
Q

What are the functions of the basal ganglia?

A

-Initiates and integrates behavior and movement
-Removes unwanted and inappropriate movement
-Plans motor activity
-Regulates motor habits
-“Rewards and motivation”
-Associations with attention

154
Q

What influences the basal ganglia and how does it influence other structures?

A

-The cerebral cortex directly influences the basal ganglia
-The basal ganglia influences the cortex via the thalamus
-It also influences the motor system through spinal cord pathways

155
Q

What is the basal ganglia circuitry to the brainstem?

A

-Reticulospinal tract
-Vestibulospinal tract

156
Q

Where do skilled movements arise from in the motor cortex?

A

-Corticospinal tracts
-Brainstem

157
Q

How do we select/initiate motor programs?

A

-Basal ganglia to brainstem
-Basal ganglia to thalamus

158
Q

What motor pathways come from the spinal cord?

A

-Central pattern generation
-Muscle movement
-Reflexes

159
Q

How is the basal ganglia intimately connected to the cortex?

A

Through parallel loops

160
Q

What are the parallel loops subdivided into?

A

-Motor
-Associative (cognition)
-Limbic

161
Q

What can dysfunction of the basal ganglia and its connectivity lead to?

A

-Movement disorders (dyskinesias)
-Akinesia
-Bradykinesia
-Hyperkinesia

162
Q

What are non-motor loop pathologies of the basal ganglia?

A

-Emotional, cognitive, and psychiatric deficits
-OCD
-Tourette’s
-ADHD

163
Q

What does functional data suggest about the basal ganglia?

A

-It is involved in both the preparation and execution of movements, motor control, and learning of motor sequences and habit (implicit learning aka learning yourself)

164
Q

How is the basal ganglia related to turning?

A

-It helps us decide where and when to turn based on perceptual decisions
-BG dysfunction creates gait deficits and can make turning hard for people w/ Parkinson’s

165
Q

How does the basal ganglia help us turn?

A

-Planning of cervical and trunk rotation
-Changes the angles of hip rotation, while anticipating any environmental disruptions

166
Q

What are the two motor loops?

A

-Body movement loop
-Oculomotor loop

167
Q

What are the two non-motor loops?

A

-Prefrontal loop
-Limbic loop

168
Q

Is the direct pathway of the basal ganglia more inhibitive or excitable?

A

More inhibitive

169
Q

Is the indirect pathway of the basal ganglia more inhibitive or excitable?

A

More excitable

170
Q

What does dysfunctions in the direct pathway of the basal ganglia lead to?

A

-Hypokinesia
-Under-stimulation (more inhibition of motor cortex)
-Loss of automatic movements
-PD
-Rigidity
-Bradykinesia

171
Q

What does dysfunctions in the indirect pathway of the basal ganglia lead to?

A

-Over-stimulation (less inhibition of cortex)
-Hyperkinetic
-Chorea
-Huntington’s

172
Q

What is the ranking of basal ganglia movement disorders by movement speed (slowest to fastest)?

A

-Bradykinesia, hypokinesia
-Rigidity
-Dystonia
-Athetosis
-Chorea
-Ballismus
-Tics
-Myoclonus
-Tremor

173
Q

What is ballistic movements?

A

-Flinging with large amplitude
-Hemiballismus: unilateral flinging contralateral to lesion

174
Q

What is a common cause of ballistic movements?

A

Infarct of the subthalamic nucleus

175
Q

What are tics?

A

-Involuntary small jerks or yelling
-Tourette’s syndrome
-4 times more in girls
-Increased in ADHD
-Symptoms come and go

176
Q

What are tremors?

A

-Both agonist and antagonist involved
-Bidirectional movement
-Asymmetrical
-“Pin rolling”
-Resting tremor and intention tremor
-Resting tremor is commonly seen in Parkinson’s

177
Q

What is lead pipe rigidity?

A

-Continous throughout whole movement
-Agonist and antagonist involved

178
Q

What is cogwheel rigidity?

A

-Ratchet like interruptions as the limb is passively moved
-Normal stretch reflexes
-Shoulders and cervical spine first affected
-Prolonged results in contracture

179
Q

What is Parkinson’s disease? What are the signs and symptoms?

A

-Loss of dopaminergic neurons & production in the substantia nigra
-Festinating gait (slow & shuffling, difficult to initiate)
-Difficulty turning corners
-Stooped forward & kyphotic
-Gait impediments coincide with visual, decision making, and motor control deficits
-Freeze with impediments/objects in path
-Resting tremors
-“Reptillian stare”/no expression

180
Q

What symptoms in Parkinson’s disease can present themselves 5 years before the onset of motor symptoms?

A

-Sleep issues/insomnia
-GI issues

181
Q

Where does gait originate from?

A

-Brainstem and descends to spinal cord
-Descending pathways come from mesencephalic locomotor region and lateral hypothalamus
-The MLR project into neurons in the pons and medulla , then project into the spinal cord to activate the CPGs involved in locomotion

182
Q

How does the Mesencephalic Locomotor Region (MLR) and lateral hypothalamus help in gait?

A

It helps us plan and initiate walking

183
Q

What is the Mesencephalic locomotor region (MLR)?

A

Area of the brainstem that is implicated in the control of gait and balance

184
Q

What is the pedunculopontine nucelus (PPN)? How is it related to Parkinson’s disease?

A

-Located in the MLR
-Plays a crucial role in appearance of axial symptoms in PD
-Dysfunction of cholinergic neurons in the PPN is what causes the axial symptoms in PD

185
Q

How does deep brain stimulation help PD patients?

A

Because it activates the MLR and PPN, which helps to alleviate locomotor symptoms

186
Q

What is labile presentation? What patient population is it commonly seen in?

A

-Awake, but not engaged
-Seen in PD

187
Q

What other additional basal ganglia diseases are there?

A

-Brain anoxia (cerebral palsy, common in babies before 1970)
-Huntington’s disease
-Stroke

188
Q

Where are cranial nerves located? What part of the nervous system are they apart of?

A

-Around the brainstem area
-PNS

189
Q

How many cranial nerves are there?

A

12

190
Q

How are cranial nerves identified by?

A

Roman numerals

191
Q

What tract do cranial nerves use to communicate with the cortex?

A

Corticobulbar tract

192
Q

What is cranial nerve I (CN I)? What is its function?

A

-Olfactory
-Sense of smell
-Interaction w/ memory

193
Q

What is cranial nerve II (CN II)? What is its function?

A

-Optic nerve
-Visual info from retina to optic nerve to optic chiasm

194
Q

What cranial nerves are all involved in/responsible for coordinated eye movement?

A

-CNIII
-CNIV
-CNVI

195
Q

What is cranial nerve III (CN III)? What is its function?

A

-Oculomotor
-Pupillary constriction
-Innervates muscles surrounding the eye
-Superior rectus
-Medial rectus
-Inferior oblique
-Inferior rectus

196
Q

What response should be seen during the pupillary eye reflex test if CN III is intact? What is seen if it is not intact?

A

-Direct and consensual responses should be seen
-If direct is not seen, it is ipsilateral CN III is not intact
-If consensual response is not seen, contralateral CN III is not intact

197
Q

What is not intact if both consensual and direct responses are not seen when doing the pupillary eye reflex?

A

CN II

198
Q

What is cranial nerve IV (CN IV)? What is its function?

A

-Trochlear nerve
-Innervates the superior oblique muscle around the eye
-Medially rotates the eye

199
Q

What is cranial nerve VI (CN VI)? What is its function?

A

-Abducens nerve
-Abducts the eye
-Innervates the lateral rectus muscle

200
Q

What is cranial nerve V (CN V)? What is its function?

A

-Trigeminal nerve
-Provides sensation for face, mouth, and nasal cavity
-Innervates the temporalis muscle and muscles of mastication (masseter)

201
Q

What is cranial nerve VII (CN VII)? What is its function?

A

-Facial nerve
-Wrinkles forehead, nose, and brings eyebrows upward
-Purses lips
-Smiling
-Provides sensation to anterior 2/3 of tongue (taste)

202
Q

What is Bell’s Palsy?

A

-Unilateral injury to the facial nerve
-Causes facial drooping, smoothing of forehead, eyebrow droop, and drooping of the corner of the mouth on one side

203
Q

What is cranial nerve VIII (CN VIII)? What is its function?

A

-Vestibulocochlear
-Splits into two branches: vestibular and cochlear
-Vestibular branch: balance, semicircular canals, acceleration, saccule and utricle, gravity
-Cochlear branch: auditory sensation

204
Q

What is cranial nerve IX (CN IX)? What is its function?

A

-Glossopharyngeal
-Motor: dilates pharynx
-Visceral motor: salivation from parotid gland
-Visceral sensory: carotid sinus
-Sensory: posterior 1/3 of tongue

205
Q

What is cranial nerve X (CN X)? What is its function?

A

-Vagus nerve
-Mixed motor and sensory
-Regulates SA node & HR, decreases BP
-Causes vasovagal syncope
-Regulates breathing
-Regulates intestine and stomach peristalsis

206
Q

What is cranial nerve XI (CN XI)? What is its function?

A

-Spinal accessory
-Innervates the SCM and trapezius muscles

207
Q

What is cranial nerve XII (CN X)II? What is its function?

A

-Hypoglossal
-Innervates muscles of the tongue

208
Q

What is a pneumonic to help remember cranial nerves in the correct order (CN I- CN XII)

A

Only one of the two athletes felt very good, victorious, and happy

-Only (olfactory)
-One (optic)
-Of (oculomotor)
-The (trochlear)
-Two (trigeminal)
-Athletes (abducens)
-Felt (facial)
-Very (vagus)
-Good (glossopharyngeal)
-Victorious (vestibulocochlear)
-And (accessory)
-Happy (hypoglossal)

209
Q

What drugs work on the spinal cord and brain to alter descending modulation/pain?

A

-Anticonvulsants
-Opioids
-Tricyclic/SNRI Antidepressants

210
Q

What drugs work on the dorsal horn to alter central sensitization/pain?

A

-Anticonvulsants
-Opioids
-NMDA-receptor antagonists
-Tricyclic/SNRI antidepressants

211
Q

What drugs work on the peripheral nervous system to alter peripheral sensitization/pain?

A

-Local anesthetics
-Topical analgesics
-Anticonvulsants
-Tricyclic antidepressants
-Opioids

PHTH 527: Applied Neurosciences I (5 decks)

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