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

Final Exam Prep Flashcards

1
Q

What are the two major organs in the vestibular system?

A

-Vestibule
-Semi-circular canals

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2
Q

What makes up the vestibule?

A

-Saccule
-Utricle

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3
Q

What makes up the semi-circular canals?

A

-Anterior canal
-Posterior canal
-Horizontal canal

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4
Q

What movements does the vestibule detect?

A

-Linear acceleration (forward or side to side)
-Head displacement to gravity (jumping up and down, flexion, extension, lateral side bending)

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5
Q

What movements does the semi-circular canals detect?

A

-Rotational head movements
-Acceleration of head rotation

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6
Q

What nerve supplies the vestibular system?

A

-CN VIII (vestibulocochlear)
-Vestibular branch supplies vestibular system
-Cochlear branch stimulates the cochlea

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7
Q

What are the major functions of the vestibular system?

A

-Maintenance of balance and stable posture
-Postural reflexes that respond to unexpected perturbations
-A stabilizer, acting to counteract the effects of body movement, gravity, and other external forces

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8
Q

What does each semi-circular canal contain?

A

-Crista ampullaris/ampulla
-Cupula

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9
Q

What does each crista ampullaris contain?

A

-Cupula
-Supporting cells
-Hair cells
-Stereocilia
-Sensory nerve fibers

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10
Q

How does movement effect the cupula, hair cells, and sterocilia?

A

-The head rotates, and the cupula moves in the opposite direction of the head rotation (i.e. head rotates right, cupula moves left)
-Stereocilia get bent in the same direction the cupula moves to
-Stereocilia send excitatory signals to the sensory nerve fibers

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11
Q

What happens to sensory nerve fibers in each semicircular canals during head rotation? What is this phenomenon called?

A

-One side is excited
-The other side is inhibited
-i.e. head rotation to the left, left semi-circular canals are excited, and the right are inhibited
-Called the “push-pull” phenomenon

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12
Q

What is the constant spontaneous firing rate of the vestibular nerve on each side when the head is in a neutral position? What happens when that firing rate changes?

A

-90-100 spikes/sec
-Changes in that firing rate tells the brain what head movement has occured

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13
Q

What are the semi-circular canal (SCC) functional pairs?

A

-The right and left horizontal canals (HSCCs)
-The right anterior and left posterior SCC (RALP)
-The left anterior and right posterior (LARP)
-Functional pairs work in the “push-pull” fashion

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14
Q

What is the function of the otoliths?

A

-Provide information of body position with reference to the force of gravity and linear acceleration
-Are contained within sensory structures called maculae

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15
Q

What age do babies develop otoliths and maculae?

A

4 months

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16
Q

Where are maculae located?

A

In the utricle and saccule

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17
Q

What are otoliths? What is their function?

A

-Otoliths are crystals of calcium carbonate (ear stones)
-Their function is to respond to the changes in gravity and send sensory signals to the brain

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18
Q

What is the structure between the hair cells, stereocilia, and otoliths in the maculae?

A

-Stereocilia project off the hair cells into the otolithic membrane, which is a gel like substance
-The otoliths are attached to the top of the otolithic membrane

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19
Q

How does the sterocilia and otoliths work together to respond to changes in gravity?

A

-When the head flexes forward, the sterocilia responds to the changes in gravity by coming forward with the head
-This displaces the otoliths and a sensory signal is sent to the brain

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20
Q

What movement does the saccule detect?

A

Up and down (flexion and extension of the head)

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21
Q

What movement does the utricle detect?

A

Side to side (side bending of the head)

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22
Q

Where do the sensory signals from the utricle and saccule go to?

A

Straight to the AHC

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23
Q

What does otolith activation help with?

A

Can help increase spatial memory and spatial tasks

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24
Q

What are the four vestibular nuclei? Where are they located?

A

-Superior
-Lateral
-Medial
-Inferior
-They are located on each side of the brainstem at the junction of the pons and medulla, near the 4th ventricle

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25
Q

What are the main vestibular pathways to the spinal cord?

A

-Lateral vestibulospinal tract
-Medial vestibulospinal tract

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26
Q

What is the medial longitudinal fasciculus? What does it help with?

A

-It connects the vestibular nuclei to the cranial nerve nuclei that control eye movement (trochlear nucleus, oculomotor nucleus, and abducens nuclei)
-It helps bring about coordinated movements of the eyes

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27
Q

What nuclei does the medial vestibulospinal tract come from? What about the lateral vestibulospinal tract?

A

-Medial nucleus
-Lateral nucleus

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28
Q

What is the vestibular ocular reflex (VOR)?

A

-While turning head from side to side, focus your eyes on something directly in front of you
-Eyes should move in a smooth and coordinated fashion

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29
Q

What system does the VOR use to coordinate eye movement?

A

-Medial longitudinal fasciculus (MLF)
-Head rotation to the right: excitation of left abducens and inhibition of the left medial rectus and right abducens

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30
Q

What reflex & system is disturbed with concussions? What symptoms occur?

A

-The VOR & vestibular dysfunction is seen
-Dizziness when moving head
-Unable to read books
-Difficult to drive
-Blurry vision

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31
Q

What gives rise to the lateral vestibulospinal tract (LVST)? What is its function? Where does it terminate?

A

-The lateral vestibular nucleus gives rise to the LVST
-It extends throughout the length of the spinal cord and is important in maintaining balance and lower limb extensor tone
-It terminates on the ipsilateral ventral horn of spinal cord

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32
Q

What are the main actions of the LVST? Where does it receive information from?

A

-Automatic postural responses
-Extensor muscle tone
-Innervates extensor muscles of limbs by facilitation to alpha and gamma motor neurons

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33
Q

What gives rise to the medial vestibulospinal tract (MVST)?

A

-The medial vestibular nucleus gives rise to the MVST as well as the inferior vestibular nucleus (semicircular canals)

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34
Q

Where does the MVST extend into? Where does it terminate?

A

-Extends only to the cervical spine and upper thoracic spinal cord
-It terminates bilaterally in the cervical region of the spinal cord connecting with motor neurons that innervate neck muscles and thoracic musculature

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35
Q

What is the action/function of the MVST?

A

-Controls neck and head position
-Provides a stable platform for eye movement and vision
-Mediates postural changes in response to head motion

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36
Q

What are 2 tracts that synapse on the AHC?

A

-Lateral vestibulospinal tract (LVST)
-Lateral corticospinal tract (LCST)

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37
Q

What is the connection between the vestibular system and cerebellum? What information does it send to the cerebellum?

A

-The vestibular nucleus connects to the flocculonodular lobe of the cerebellum
-It sends info directly to the cerebellum to coordinate movements to calculate posture and balance control

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38
Q

What are other outputs/pathways from the vestibular nuclei? What are their functions?

A

-Vestibulo-thalamo-cortical pathways: provides conscious awareness of head position/movement and input to the corticospinal tracts (spatial orientation)
-Vestibulo-ocular pathway: controls the magnitude of muscle responses to vestibular information, including the gain of the VOR. A key pathway in vestibular rehab

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39
Q

How does a peripheral lesion (inner ear) of the vestibular system effect nystagmus and vertigo?

A

-Onset of nystagmus is delayed
-Able to adapt/be treated
-Nystagmus is horizontal or rotatory, not vertical; does not change directions
-Prominent nystagmus is only present if vertigo is also present

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40
Q

How does a central lesion (brainstem or cerebellum) of the vestibular system effect nystagmus and vertigo?

A

-Onset of nystagmus is immediate
-May change directions
-Prominent nystagmus may occur in the absence of vertigo

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41
Q

What are the red flags of central lesions affecting the vestibular system?

A

-Sudden onset of dizziness associated with diplopia, dysphagia, dysarthria, dysmetria
-Blurred vision
-Abnormal eye tracking with oculomotor testing
-Hearing loss without dizziness
-Change in consciousness
-New onset of nystagmus with complaints of dizziness

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42
Q

What are symptoms of peripheral lesions in the vestibular system?

A

-Sudden, notable onset of vertigo often described as “spinning”
-A patient might say “it just hit me out of nowhere and I couldn’t move because the room was spinning round and round”

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43
Q

What is cervicogenic vertigo?

A

-Vertigo that is typically associated with cervical trauma and/or injury (whiplash)
-Symptoms are provoked by moving “the body on the head” rather than moving “the head on the body”
-Impaired cervical kinesthetic sense associated with injury impacts the VOR reflex and dynamic visual acuity, resulting in dizziness
-Manual therapy to decrease pain and increase ROM, joint position, sense retraining, VOR/DVA retraining

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44
Q

What are the three categories of vestibular disorders?

A

-Deficiency
-Distortion
-Fluctuation

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45
Q

What vestibular disorders are in the deficiency category? What are the signs & symptoms of these disorders?

A

-Neuronitis/labyrinthitis (viral infection)
-Acoustic neuroma
-New onset
-Severe
-Complaints of unsteadiness
-Instability that may increase with head movement
-Intense spinning
-Inability to walk
-Difficulty with vision

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46
Q

What vestibular disorders are in the distortion category? What are the signs & symptoms of these disorders?

A

-Benign paroxysmal position vertigo (BPPV)
-Vertigo
-Instability increases in the presence of inappropriate sensory signals (particularly vision)
-Disequilibrium of aging and multisensory disequilibrium

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47
Q

What vestibular disorders are in the fluctuation category? What are the signs & symptoms of these disorders?

A

-Meniere’s Disease
-Migraine
-Dizziness
-Vertigo

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48
Q

What is BPPV?

A

-A mechanical disorder, caused by otoconia displaced from the macula of the utricle into the semicircular canals
-Common in older adults
-Brief episodes of vertigo when the head is moved into certain positions (lying down, rolling over in bed, bending over, looking up)

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49
Q

When does BPPV usually peak?

A

It typically peaks in the 6th and 7th decades of someone’s life

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50
Q

What is the most common cause of vertigo?

A

Peripheral vestibular disorder

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51
Q

What is canalithiasis? What are the signs & symptoms?

A

-A subtype of BPPV
-Caused by debris floating in the semicircular canals
-Nystagmus has a latency between 1-40 seconds and is short in duration (<1 minute)
-Nystagmus fluctuates in intensity
-More treatable than cupulolithiasis

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52
Q

What is cupulolithiasis? What are the signs & symptoms?

A

-A subtype of BPPV
-Nystagmus is immediate and persistent in duration (>1 minute)
-Nystagmus has no change in intensity
-Harder to treat than canalithiasis

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53
Q

How is BPPV classified?

A

-Direction defines the affected canal
-Torsion/rotational: anterior and posterior SCC
-Horizontal: horizontal SCC

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54
Q

How do you differentiate between anterior and posterior canal BPPV?

A

-Anterior canal has down beating torsional nystagmus in Dix Hallpike test
-Posterior canal has up beating torsional nystagmus

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55
Q

How do you perform the Dix Hallpike Test?

A

-The patients head is turned 45 degrees toward affected ear in a long sitting position
-The patient is quickly moved into a supine position with her head extended 20-30 degrees and rotated 45 degrees toward their ear
-Wait at least 1 minute to determine if it is cupulolithiasis or canalithiasis

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56
Q

What are the 5 head movements that elicit BPPV symptoms?

A

-Turning over in bed
-Lying down
-Rising up from supine
-Bending forward
-Reclining head

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57
Q

How do therapists examine BPPV?

A

-Dix Hallpike
-Epley manuever

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58
Q

What is disequilibrium of aging vestibular disorder?

A

-No single causative factor
-Disequilibrium on the basis of multiple small summating factors (declining sensory inputs, sensory processing, decrease control mechanisms for balance, and aging musculoskeletal system)
-Gradual worsening of symptoms

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59
Q

What are the most common symptoms of disequilibrium of aging vestibular disorder?

A

-Disequilibrium when walking
-Dizziness

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60
Q

What is multisensory disequilibrium vestibular disorder?

A

-Refers to combined dysfunction of vestibular, visual, and somatosensory systems
-Ex: diabetes can cause vestibulopathy, retinopathy, and peripheral neuropathy (caused by decreased blood flow)
-Any combination of disorders when walking especially in dim lighting and uneven surfaces
-Sensory complaints such as numbness and tingling in feet
-Poor proprioception/vibration sensation
-Poor use of vestibular system
-Poor vision

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61
Q

What is Meniere’s disease?

A

-The triad: tinnitus, hearing loss, and aural fullness
-Episodes of severe vertigo accompanied with vomiting and nausea
-Fluctuating hearing loss especially low frequencies
-Complains of pressure or fullness in head
-May be congenital or due to old ear infection affecting endolymphatic sac

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62
Q

What is the patho-mechanism of Meneire’s disease?

A

Increase volume of endolymph eventually leading to disruption of ionic balance between endolymph and perilymph, which results in spontaneous activation of vestibular receptors unrelated to head movement

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63
Q

What are the signs and symptoms of acute (< 3 days) unilateral vestibular loss (UVL)?

A

-Imbalance
-Assistance with gait
-Increased imbalance with head movement
-Complaints of blurred vision with head movement
-Nystagmus and vertigo
-Vertical diplopia
- + romberg, unable to do sharpened
-Unable single leg stance
-Can’t walk with head movements

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64
Q

What are the signs and symptoms of chronic (> 3 days) unilateral vestibular loss?

A

-Decreased head movement
-Decreased endurance
-Visual dependence
-Blurred vision with head movement
-Negative romberg; + sharpened romberg
-Normal gait
-SOT may be okay if compensated
-Vestibular rehab excellent prognosis for UVL

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65
Q

What is the pathology of UVL from acoustic neuroma? What usually happens after surgical resection? What are the symptoms?

A

-Acoustic neuromas are tumors that grow in the ear
-Pathology: cerebello-pontine angle neoplasm
-Gradual onset
-Surgical resection of tumor usually results in damage to cerebellum and CN VIII
-Symptoms are unilateral hearing loss, disequilibrium with head movement, veering, and tinnitus

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66
Q

What structures are supplied by the anterior inferior cerebral artery?

A

-Vestibular nuclei
-Trigeminal nuclei
-CN V
-Facial nerve
-Anterolateral tract

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67
Q

What is labyrinth?

A

-Vertigo
-Tinnitus
-Hearing loss

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68
Q

What are symptoms associated with AICA?

A

-Labyrinth (problems w/ vestibular system)
-Vestibular nuclei and nerve (lateropulsion towards involved side)
-Cerebellar flocculus and MCP (dysmetria, ataxia)
-Facial paralysis
-Decreased facial sensation
-Abducens nuclei
-Spinothalamic tract
-Spinal tract V

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69
Q

What are symptoms associated with PICA?

A

-Also called Wallenburg’s syndrome or lateral medullary infarction (most common occlusion of vertebral artery)
-Vestibular nuclei
-Dysmetria and gait ataxia
-Anterolateral tract (contralateral reduced pain and temperature of body)
-Ipsilateral decreased pain and temp of face (CN V)
-Solitary and vagus centers in medulla (vomiting and nausea)

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70
Q

What are exams for vestibular dysfunction?

A

-Observation of nystagmus with oculomotor exams
-Dizziness with cervical motions
-Balance dysfunction
-Subjective symptoms
-Caloric stimulation
-Computerized posturography
-Head impulse test
-Rotary chair
-Dix hallpike test

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71
Q

What are the inputs to the vestibular system?

A

-Cortex, cerebellum, reticular formation, extra-pyramidal
-Vision
-Proprioception superficial sensation
-Labyrinth activity

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72
Q

What are the outputs of the vestibular system?

A

-Cortical awareness of head, body, motion
-Control of oculomotor activity
-Control of posture
-Control of motor skill

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73
Q

What is dysarthria?

A

Trouble speaking

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74
Q

What is dysmetria?

A

Issues with coordination

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75
Q

What happens to synapses with repetition?

A

Synapses become “solid” and stronger with repitition

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76
Q

What is synaptic plasticity?

A

-The biological process by which specific patterns of synaptic activity result in changes in synaptic strength and is thought to contribute to learning and memory
-The connection or synapse between two neurons that occur with neuronal activity

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77
Q

What is the mechanism of synapses becoming stronger?

A

The more an activity is done, the amount of neurotransmitters associated with that synapse will increase and so will the receptors

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78
Q

What happens to the number of active brain regions the more an activity is done?

A

The number of active regions are reduced because less energy is required for the same task

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79
Q

What happens to the brain when someone learns a task?

A

When a task is fully learned, only small and distinct regions of the brain show activity

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80
Q

What is long term potentiation (LTP)?

A

The long term increase in synaptic strength

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81
Q

What stimulates long term potentiation?

A

Learning a new task stimulates LTP

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82
Q

What structures play a major role in synaptic stability?

A

-Dendritic spines play a major role in synaptic stability
-Changes in the dendritic spine (getting larger) can create synaptic stability

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83
Q

What can reduce the amount of dendrites in the hippocampus?

A

Stress

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84
Q

What is brain derived neurotrophic factor (BDNF)?

A

Nerve growth factor

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85
Q

What can increase BDNF? What areas of the brain are affected?

A

-Aerobic exercise
-Cerebellum
-Hippocampus
-Spinal cord

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86
Q

What is Hebbian plasticity?

A

-Increases in synaptic strength between neurons that fire together
-“Neurons that wire together, fire together”

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87
Q

What does synaptic strength depend on?

A

It depends on high degree of intense neuronal activity

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88
Q

What are neural networks?

A

Chain of neurons

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89
Q

What is experience dependent plasticity?

A

-Plasticity that is gained through learning & memory
-Requires creating different experiences

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90
Q

What occurs during experience dependent plasticity?

A

-Synthesis of new proteins (receptors)
-Growth of new synapses
-Modification of existing synapses

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91
Q

How many days does it take to learn a task?

A

10 days

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92
Q

What happens when there is repetition of a specific stimulus?

A

-The pairing of pre and post synaptic firing, synthesis, and activation of proteins which alter the excitability of the neuron
-Inhibit or promote growth of new synapses, especially at dendritic spines

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93
Q

What is synaptogenesis?

A

The formation of new synapses

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94
Q

What is experience expectant learning? What is an example?

A

-Learning that will (should) happen no matter what
-Based on our genetics
-Happens early in life (1-3 years)
-Vision and language are experience expectant learning
-The brain expects to be exposed to language and visual stimuli

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95
Q

What happens to rods and cones if we do not get visual stimuli?

A

They will die

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96
Q

What is experience dependent learning? What is an example?

A

-Learning that occurs in response to experiences and complex environmental stimuli over the lifetime
-There is no optimal period (occurs throughout life)
-Unique to individuals
-Development of 2nd language is experience dependent learning

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97
Q

What is the use it or lose it principle in neuroplasticity?

A

-Neuronal circuits not actively engaged in a task for long periods of time will degrade
-Failure to “drive” specific brain functions can lead to functional degradation
-Ex: prolonged tube feedings can lead to the loss of neural circuitry for swallowing

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98
Q

What is the use it or improve it principle in neuroplasticity?

A

-Constraint induced therapy
-Sensory reorganization with sensory discrimination

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99
Q

What is constraint induced therapy? What are the parameters?

A

-Forced use of hemiplegic/affected limb by limiting use of non-affected side
-5 hrs/day and constrain other limb with mitt 90% of time
-Effective 3-21 months post injury
-Mild-moderately impaired individuals can use this
-Must be able to grasp or squeeze a cloth/towel
-Forced use too soon (in the first 7 days) will make the injury worse

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100
Q

What is the specificity principle in neuroplasticity?

A

-Motor skill acquisition is associated with dendritic growth, addition of synapses, and neuronal activity in the cerebellum and motor cortex
-Motor skill acquisition is shown to change activation patterns in motor cortex
-Repetitions of previously learned motor skills does not enhance motor corticalization

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101
Q

What is the repetition principle in neuroplasticity?

A

-Learning a new skill requires repetition to induce neural training
-Must continue performance after learning the skill
-Makes the required skill more resistant to neuronal decay

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102
Q

How much repetition is required to learn a new skill?

A

For adults, between 300-1000 repetitions per day

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103
Q

What will make learning a new skill easier and faster for a patient? What system helps with this?

A

-If they are more dedicated and motivated
-Limbic system is involved in this

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104
Q

What is the intensity matters principle in neuroplasticity?

A

-Targets speed, accuracy, and controlling phasic and sustained attention
-Neuromodulatory control of learning and subcortical systems that support it
-Working memory (add cognitive aspect)
-Noise/distractor suppression: being able to complete the task with distractions or noise

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105
Q

What should be the repetitions of an exercise to improve neuroplasticity?

A

A study showed that doubling the # of reps in an upper limb assisted therapeutic intervention resulted in significant improvements in motor function

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106
Q

What type of exercise increases neurotrophic factors?

A

Aerobic exercise increase levels of BDNF

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107
Q

What is the type and amount of motor activity intensity critical for?

A

It is critical in modulating the neural environment, and in determining whether the degenerative process or neuronal death cascades predominate during the early stages following brain injury

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108
Q

What is the salience matters principle in neuroplasticity?

A

-Salience=meaningful
-Critical importance of the “task” itself
-Assists in the reorganization of the brain
-Cognitive, emotional, and motivational processes are implemented by overlapping networks of regions that play various roles depending on the task/context
-These networks include prefrontal cortex, cingulate, amygdala, striatum, hypothalamus, hippocampus, insula, and parietal regions

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109
Q

How does age affect neuroplasticity?

A

-Younger brains have more potential for neuroplasticity
-Neurogenesis gets more difficult as we age

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110
Q

How much oxygen and nutrients does the brain consume? What nutrients/foods are good for the brain?

A

-20% of oxygen and nutrients
-Fish, salmon, olive oil
-Vitamin D
-Older people have more difficulty allocating nutrients

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111
Q

What is the principle of transference in neuroplasticity?

A

-The action of transferring something or the process of being transferred
-Training in one area enhances another
-Consider future plans and think positively: have an environment where the patient always feels successful

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112
Q

What is the interference principle in neuroplasticity?

A

-Cognitive, motor, or sensory information that runs “interference” with a planned goal (distractions)
-Enhancement of goal related tasks to reduce outside distractions
-Rest or reduce fatigue
-Ex: TUG with counting down form 100 by 3’s

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113
Q

Does neuroplasticity occur in single synapses or in brain circuits?

A

Both!!

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114
Q

What occurs when multiple brain modalities are used? What is an example?

A

-There is greater neuroplasticity
-Music has been shown to enhance learning
-Rhythmic auditory stimulation has been showing to assist patients with neurological disorders in ambulation

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115
Q

What are the different brain modalities to create neuroplasticity?

A

-Visual
-Motor
-Cognitive
-Somatosensory

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116
Q

What is unconscious motor learning? What structure in the brain is it associated with?

A

-Motor memories that are not easily extinguished, such as driving or riding a bike
-Motor memories related to movement in the cerebellum are very permanent and well designed
-Memories play a role in neuroplasticity

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117
Q

What system is the easiest to regain?

A

The motor system

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118
Q

What does memory for coordination of movements involve?

A

-It involved different types of plasticity in multiple regions including the cortex, hippocampus, and cerebellum
-The cerebellum coordinates a wide variety of signals from the sense and regions of the cortex, involving perception and communication with all aspects of movement

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119
Q

What structure in the brain tends to not be as affected by loss of neuroplasticity?

A

The cerebellum

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120
Q

What does rehabilitation build upon?

A

-Visualization
-Cognitive load
-Coordination and timing
-Communication

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121
Q

What is a critical factor in gaining faster over-ground walking speeds?

A

Speed of walking and training at faster than self-selected speeds

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122
Q

What helps increase neuroplasticity in combination with repetition?

A

Problem solving

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123
Q

What does systematic progression of difficulty do to the motor cortex?

A

Systematically progressing the difficulty of a task results in reorganization of movements in the motor cortex while no progression of difficulty had no effect on cortical motor maps

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124
Q

What is meant by the context of the exercise?

A

-Constantly increasing the difficulty by adding cognitive load, sensory/motor aspects
-Changing or modulating tasks increases the speed of neuroplasticity & learning

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125
Q

What happens when there is an increase in white matter?

A

Processing speed increases

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126
Q

What type of matter (white or gray) does neuroplasticity come from? Why?

A

-Gray matter
-Because neuroplasticity is the result of an increase in receptors and neurotransmitters in the synaptic cleft

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127
Q

What does increase of BDNF help with?

A

-Cognitive function
-Mobility
-Gait

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128
Q

What can be used to prime motor rehab post stroke? What does this help with?

A

-Aerobic exercise should be used before motor training in post stroke patients
-It helps to increase the response to rehabilitation and increases long term potentiation and dendrite formation

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129
Q

What are the direct effects of aerobic exercise?

A

-Increase in neurotrophic growth factos (BDNF)
-Increase in neurotransmitters such as dopamine and serotonin

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130
Q

What are the indirect effects of aerobic exercise?

A

-Increase in physical fitness (cardiorespiratory and muscular)
-Decrease in systemic and CNS inflammation
-Increase in cerebral blood flow

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131
Q

What are the three types of ischemic strokes?

A

-Embolic
-Lacunar
-Athero-thrombotic

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132
Q

What is an embolic stroke?

A

Embolus blocking flow

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133
Q

What is a lacunar stroke?

A

-Plaque blocking blood flow
-Also called lacunar infarct or “small vessel disease”
-Results from the occlusion of small penetrating arteries that provide blood to the brain’s deep structures

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134
Q

What is an athero-thrombotic stroke?

A

Thrombus blocking blood flow

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135
Q

What is the etiology of lacunar strokes?

A

Chronic hypertension

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136
Q

Where do lacunar infarcts usually occur?

A

-Typically occur in the arteries that supply blood to the internal capsule
-Can also occur in the basilar artery or anterior cerebral artery

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137
Q

What are the signs & symptoms of a lacunar stroke?

A

-Pure motor hemiparesis (33-50%)
-Usually involved posterior limb of internal capsule
-Contralateral hemiparesis of face, arm, and leg
-No sensory deficits
-Pt’s typically have problems with their visual field but don’t know it (ask Dr. Rivera to confirm)
-Dysarthria may be present

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138
Q

What is the blood supply to the anterior limb of the internal capsule?

A

It is mainly fed by the lenticulostriate branches of the middle cerebral artery, and sometimes but rarely from ACA

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139
Q

What are the lenticulostriate arteries?

A

Small penetrating arteries that supply blood flow to most of the subcortical structures

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140
Q

What is the blood supply to the genu of the internal capsule?

A

Lenticulostriate branches of MCA

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141
Q

What is the blood supply to the posterior limb of the internal capsule?

A

-Lenticulostriate branches of MCA
-Anterior choroidal artery (AChA) of internal carotid artery

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142
Q

What are the clinical findings in internal capsular strokes?

A

-Weakness of face, arm, or leg
-Pure motor stroke
-One of the classic types of lacunar infarcts
-Upper motor neuron signs
-Mixed sensorimotor (ask Dr. Rivera since info on slide is contradictory)

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143
Q

What are watershed areas? What are they causes by?

A

-Watershed zones are areas for reduced oxygen
-Infarcts in the watershed zones are due to reduced perfusion because of a blockage in the ACA, MCA, or PCA
-Occurs with an internal carotid artery blockage or common carotid artery blockage
-Commonly called watershed infarctions

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144
Q

What are transient ischemic attacks (TIA)?

A

-A stroke that lasts 10 minutes
-Longer than 10 minutes causes cell death
-TIA lasting an hour causes small infarcts, but they can easily recover
-Requires ER visit
-Early warning sign of future strokes
-Typically caused by chronic hypertension

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145
Q

What are signs and symptoms of TIA? What are treatments?

A

-Weakness on one side of the body
-Vision problems
-Slurred speech
-Often resolve within 24 hours
-Treatments include medication, surgery, and lifestyle changes

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146
Q

What is cerebral edema?

A

-Internal pressure within the brain cortex caused by hemorrhage or edema from inflammation
-Serious consequence of stroke and can lead to early mortality

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147
Q

What is central perfusion pressure (CPP)? What is the normal values for CPP?

A

-The net pressure gradient that drives oxygen delivery to cerebral tissue
-Normal CPP is 55-60 mm Hg

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148
Q

What is intracranial pressure (ICP)? How is it measured? What are the normal values for ICP in adults?

A

-Pressure inside the brain/cranium
-Usually measured invasively through an intracranial pressure transduction device
-Most common method is with an intraventricular monitor
-Normal ICP is 5-15 mm Hg

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149
Q

What are abnormal values of ICP that indicate intracranial hypertension?

A

20-30 mm Hg

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150
Q

What is the equation for CPP?

A

Mean arterial pressure (MAP) - ICP

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151
Q

What are brain events that reduce cortical perfusion pressure (CPP)?

A

-Hemorrhagic stroke
-Tumors
-Infection

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152
Q

Why does hemorrhagic stroke reduce CPP?

A

It leads to increased pressure in the brain and reduces cerebral perfusion

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153
Q

Why do tumors reduce CPP?

A

Brain tumors can create increased cortical pressure and reduce brain perfusion

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154
Q

Why does infection reduce CPP? What else can infection cause?

A

-It causes substantial changes in regulation of cerebral perfusion
-Infection can cause adult brain tumors

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155
Q

Are outcomes better with hemorrhagic or ischemic strokes?

A

Outcomes are typically better with hemorrhagic strokes

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156
Q

What sex is more likely to get adult brain tumors?

A

Males are more likely to get brain tumors than females

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157
Q

What is the Goldilocks curve for blood pressure?

A

-It represents how the intensity of exercise effects blood pressure and how blood pressure effects risk or outcomes
-It is a U-shaped curve where the risk is lowest at a blood pressure that is just right, not too high or too low

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158
Q

What has happened to the death rate of stroke patients since the 70’s? Why has this change occured?

A

-Death rate fell 77%
-Greater awareness of symptoms
-Prompt medical attention (60 minutes door to ED)
-IV tissue plasminogen activator (tPA)

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159
Q

What is IV tissue plasminogen activator (tPA)? When is it administered?

A

-It is a clot buster
-Prevents the stroke from continuing
-Helps to restore blood flow to brains regions affected by stroke, which limits the risk of damage and functional impairments

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160
Q

What is earlier treatment of thrombolytic treatment of stroke patients associated with?

A

-More frequent and independent ambulation at discharge
-Higher discharge rates to home vs SNF
-Reduced mortality and symptomatic intracerebral hemorrhage

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161
Q

What is a safe range of systolic blood pressure after a cerebrovascular accident?

A

Between 140-160 mm Hg

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162
Q

When should patients be mobilized after having a stroke?

A

-Patients should be mobilized 13-24 hours after receiving IV tPA
-Most hospitals follow a 24 hour period

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163
Q

What is the recommended dosing for out of bed for stroke patients?

A

-Early, lower dose out of bed activity is preferable to frequent, higher dose intervention
-First day 10-20 minutes

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164
Q

What are the steps involved with preparing patient for out of bed activities?

A

-Get PT orders from physician
-Review medical chart
-Get proper equipment (wheelchair or chair)
-Blood pressure monitor
-Pillows for UE support of affected side
-Gait belt

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165
Q

What will the PT assess for a patient post stroke?

A

-Shoulder subluxation
-Skin integrity
-Mobility
-Caregiver availability
-Spasticity
-Durable medical equipment/orthosis needs
-Recommendation regarding transition to appropriate level of post-acute care
-Potentially cognition (if no OT’s)

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166
Q

When should blood pressure be monitored with stroke patients? What are signs the patients BP has dropped too low?

A

-During activities
-Laying down to sitting
-After activities (1,2,3, and 5 minutes)
-Rapid large falls in BP can lead to reduced cerebral blood flow
-Eyes will flutter and cognition will change if BP is too low
-High BP has risk for another hemorrhage

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167
Q

What are general guidelines for BP in post stroke patients?

A

-Keep systolic under 180
-Diastolic under 105

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168
Q

How should PT’s assess for neurologic deterioration in stroke patients?

A

-Ask if they have new headache
-Acute hypertension
-Nausea or vomiting
-Changes in O2 sat
-Excessive SOB
-Syncope

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169
Q

What transfers are typically used with stroke patients? What should we protect throughout all of the transfers and why?

A

-Rolling from supine to side lying
-Side lying to sit
-Squat pivot
-Stand pivot
-Need to protect shoulder on hemiplegic side because of risk of subluxation or if it has already subluxed

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170
Q

What are outcome measures typically used for stroke patients in acute care?

A

-6 minutes
-TUG
-5 times sit to stand
-10 meter walk test

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171
Q

How does the sympathetic system effect the heart?

A

-Increases HR
-Increases BP

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172
Q

How does the sympathetic system effect sweating?

A

Increases sweating

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173
Q

How does the sympathetic system effect the eyes?

A

-Dilates pupils
-Widely opens eyelids

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174
Q

How does the sympathetic system effect the digestive system?

A

-Decreases secretion of digestive juices
-Decreases bowel motility

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175
Q

How does the sympathetic system effect blood sugar?

A

Increases blood sugar

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176
Q

How does the sympathetic system effect the lungs?

A

-Opens airways
-Bronchodilation

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177
Q

How does the sympathetic system effect muscle tone?

A

Increases muscle tone

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178
Q

How does the parasympathetic system effect the heart?

A

-Decreases HR
-Decreases BP

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179
Q

How does the parasympathetic system effect sweating?

A

Decreases sweating

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180
Q

How does the parasympathetic system effect the eyes?

A

-Constricts the pupils
-Relaxes the eyelids

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181
Q

How does the parasympathetic system effect the digestive system?

A

-Increases secretion of digestive juices
-Increases bowel motility

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182
Q

How does the parasympathetic system effect blood suagr?

A

It doesn’t/encourages normal blood sugar levels

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183
Q

How does the parasympathetic system effect the lungs?

A

-Bronchoconstriction
-Constricts the airways

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184
Q

How does the parasympathetic system effect muscle tone?

A

Encourages normal muscle tone

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185
Q

What are the two divisions of the autonomic nervous system?

A

-Sympathetic
-Parasympathetic

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186
Q

What are the functions of the autonomic nervous system (ANS)?

A

-A division of the peripheral nervous system that influences organs and tissues
-Maintains homeostasis by regulating temperature and activity of internal organs

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187
Q

What does the ANS regulate?

A

-Circulation
-Respiration
-Digestion
-Metabolism
-Secretions
-Body temp
-Reproduction

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188
Q

What regions of spinal nerves does the parasympathetic system come from?

A

-Cranial nerves
-Sacral nerves

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189
Q

What regions of spinal nerves does the sympathetic system come from?

A

-Thoracic nerves
-Lumbar nerves

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190
Q

What is the sympathetic division also known as?

A

Fight or flight

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191
Q

What is the parasympathetic division also known as?

A

Rest and digest

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192
Q

What structures in the brain trigger the fight or flight response?

A

-The amygdala responds to a stressful event
-The hypothalamus registers the event
-Neural activity combined with released of hormones (norepinephrine and epinephrine) in the bloodstream trigger the fight or flight response

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193
Q

What does the sympathetic trunk consist of?

A

-Preganglionic sympathetic fiber
-Postganglionic sympathetic fiber
-Collateral ganglion

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194
Q

What are Betz cells and where do they originate from?

A

-A type of pyramidal neuron that connects the axon and descend the spinal cord via the corticospinal tract, which synapses directly with the anterior horn cells
-Over 50% of the Betz cells originate in the primary motor cortex

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195
Q

What is the pathway for motor impulses?

A

-Primary motor cortex
-Through the brain
-To the brainstem
-Midbrain
-Pons
-Medulla
-Through the spinal cord

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196
Q

What are the two corticospinal tracts? Where do they cross?

A

-Lateral corticospinal tract
-Crosses at cervicomedullary junction
-Anterior corticospinal tract
-Stays unilaterally and crosses over at spinal cord level to innervate bilateral sides

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197
Q

What is the anterior corticospinal tract? What motor tracts does it contain? What muscles does it innervate?

A

-One long axon from the precentral gyrus to medial motor nuclei
-Contains motor tracts for cevical and upper thoracic cord (trunk)
-Primarily innervates bilateral axial and shoulder girdle muscles

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198
Q

What is an upper motor neuron?

A

One long axon from the primary motor cortex to the anterior horn cell (CNS)

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199
Q

What are upper motor neuron lesions?

A

Trauma, diseases, or infections occurring in an upper motor neuron that is in the brain or spinal cord

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200
Q

What are lower motor neurons?

A

They involve the anterior horn cell and the peripheral nerves

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201
Q

What are lower motor neuron lesions?

A

Injuries, diseases, or infections associated with the lower motor neurons

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202
Q

Do all neurons in the lateral corticospinal tract travel contralaterally?

A

No, 10% of neurons in the lateral CST travel ipsilaterally and terminate in the ipsilateral spinal cord

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203
Q

What is the order that the motor system is activated in?

A

-Posterior sensory cortex sends goals
-Prefrontal cortex plans
-Premotor cortex sequences
-Motor cortex executes the actions

204
Q

What are the 5 steps of voluntary motor activation?

A
  1. Decision made in the frontal lobe
  2. Motor planning areas and command centers activate (Pre-motor and vision)
  3. Motor tract delivers signals to alpha motor neurons
  4. AMNs transmit signals directly to skeletal muscles
  5. Correction/feedback of motor activity in cerebellum and the sensory cortex, regulating the activity in descending motor tracts
205
Q

What are the methods of nervous system muscle activation?

A

-Motor neuron pools
-Systematic method of increasing activation: Henneman’s Size Principle
-Increase the rate of stimulation

206
Q

What is a motor neuron pool?

A

-Groups of muscles that cluster into discrete neurons (AHCs) with a common target
-Link across several spinal nerves
-Receive sensory feedback (proprioceptive) from muscle spindles
-Coordinate with patterns of muscles by segments, sensory and cortical input
-The more motor pools recruited, the more strength there will be

207
Q

What is Henneman’s Size Principle?

A

Arrangement of motor unit activation
-Smallest motor units activated first
-Medium motor units activated second
-Largest motor units activated last
-Motor units receive common neural input and are recruited according to their sizes

208
Q

What are the three types of alpha motor neurons? What is their relative excitabilities?

A

-S type (slow): small and highly excitable
-FR type (fatigue resistant): big and average excitability
-FF type (fatiguable): biggest and low excitability

209
Q

What is the neural activation size principle?

A

-Type I motor units have a low activation threshold with lower force production
-Type II motor units have a high activation threshold but have high force production

210
Q

What do the primary motor cortex and premotor cortex have in common?

A

Both project directly to the spinal cord and are capable of some direct control of movement

211
Q

What is the purpose of the supplementary motor area (SMA)?

A

-Internally generates plan of movement
-Planning of sequences of movement
-Coordination of the two sides of the body such as bi-manual coordination

212
Q

Where does the lateral corticospinal tract decussate?

A

At the cervico-medullary junction in the lower medulla

213
Q

Where does the anterior corticospinal tract decussate?

A

At the spinal cord level

214
Q

Where does the anterior corticospinal tract end? Why does it end there?

A

-It ends at the mid thoracic area
-Because it primarily innervates the bilateral axial and shoulder girdle muscles

215
Q

What is proprioception?

A

Awareness of static joint position

216
Q

What is kinesthesia?

A

Awareness of dynamic joint positions

217
Q

What are free nerve endings?

A

-Unmyelinated
-Pain
-Heat
-Cold

218
Q

What are Delta fibers?

A

-Myelinated free nerve endings
-Carry sharp, stabbing, and pricking pain, or cold
-High threshold
-Immediate pain

219
Q

What are C fibers?

A

-Unmyelinated free nerve endings
-Carry dull, achey pains
-Higher activation threshold than delta fibers
-Polymodal pain receptors (Chemical, heat, mechanical, hypoxia)

220
Q

What is the sizes of axons of different nerve types from smallest to largest? How fast does each travel?

A

-C fibers
-Delta fibers
-Beta fibers (corpuscles)
-Alpha motor neurons
-Axon and speed of transmission have a direct relationship, so the larger the axon, the faster the transmission

221
Q

What is the muscle spindle (MS)?

A

-Sensory proprioceptor in the muscle belly
-Intrafusal muscle fibers (muscle spindle) connects w/ extrafusal muscle fibers
-Efferent info is sent from MS to muscle

222
Q

How does the muscle spindle work and communicate?

A

-Transmits information of the length of the muscles as well as the speed of the muscle contraction
-Sends info to the cerebellum
-Unconscious sensation
-Plays a vital role in regulating the contraction of muscle

223
Q

What reflexes test the integrity of the muscle spindle and why?

A

-Deep tendon reflexes
-Because it causes a quick stretch which makes the muscle contract quickly, which the muscle spindle detects

224
Q

How does the muscle spindle aid in reciprocal inhibition?

A

-The muscle spindle synapses onto two motor neurons
-One synapses directly onto the motor neuron of the agonist muscle
-The other synapses onto an inhibitory interneuron, then the interneuron synapses onto the motor neuron of the antagonist muscle to force it to relax

225
Q

What are the two major sensory pathways?

A

-Anterolateral pathway
-Spinothalamic tract
-Dorsal columns (medial leminiscal pathway)

226
Q

What sensory information goes through the anterolateral pathway?

A

-Pain
-Temperature
-Crude touch

227
Q

Where does the anterolateral pathway decussate?

A

Spinal cord

228
Q

What sensory information goes through the medial leminiscal pathway?

A

-Vibration
-Joint position
-Fine touch

229
Q

Where does the medial leminiscal pathway decussate?

A

Medulla

230
Q

What is the Golgi Tendon Organ (GTO)?

A

-Encapsulated receptor located at musculoskeletal junction
-In series w/ extrafusal muscle fibers
-3-50 GTO per muscle fiber
-Innervated by afferent fiber branches, Ib, by which the distal parts of the tendon-spindle are inneravted
-Detects tension in the tendon

231
Q

How does the GTO work?

A

-Detects small change in muscle force (<1g of force)
-Compensates for fatigue in motor units
-Can shut things down to avoid injury by inhibiting muscle contraction
-Reflex regulation of alpha motor neuron
-Context/task dependent because it helps us estimate how much force we need to perform a task

232
Q

What are gamma motor neurons?

A

Type II motor neurons that reset the muscle spindle after activation

233
Q

What does an Upper Motor Neuron UMN) syndrome involve?

A

-Motor cortex and pathways
-Brainstem
-Cerebellum
-And/or involves the spinal cord and its coordination

234
Q

Where does an UMN injury reside?

A

-Injury resides in several areas of the brain and spinal cord
-Major areas are located in the motor cortex or brainstem
-Also involved motor pathways from the major brain areas and the spinal cord involving motor output

235
Q

Where does and LMN injury reside?

A

-Anterior horn cell
-Peripheral nerve

236
Q

What causes UMN syndrome?

A

The result of the disruption of central motor pathways that arise from the cerebral cortex and pathways in spinal cord

237
Q

What are the main motor tracts?

A

-Corticospinal tracts
-Corticobulbar tracts

238
Q

What are signs of UMN lesions in the brain & brainstem?

A

-Spasticity
-Weakness, loss of selective control (pathologic synergies) which can lead to contractures
-Hyperactivity; increase in deep tendon reflexes, clonus, and rigidity
-Loss of upright control

239
Q

What area of the brain is associated with decreased muscular control in UMN syndrome?

A

Cerebellum

240
Q

What is clonus?

A

Repeated rhythmic contractions of individual muscle groups

241
Q

What is tone? What is it independent of/exclude?

A

-Resistance to passive stretch as a patient is attempting to maintain a relaxed state of muscle activity
-Independent of joint, skeletal, or ligamentous abnormalities

242
Q

What does tone reflect?

A

-Muscle state (relaxation)
-Independent of strength, coordination, or involuntary movement

243
Q

What is the range of muscle tone from least to greatest?

A

-Flaccidity (LMN)
-Hypotonia
-Normal
-Hypertonia (UMN)
-Rigidity

244
Q

What is hypertonia?

A

-Increase in passive muscle tightness
-Abnormally increased resistance to an external force about a joint

245
Q

What are the three classifications/subcategories of hypertonia?

A

-Spasticity
-Rigidity
-Dystonia

246
Q

What is spasticity?

A

-Velocity dependent increase in tonic stretch reflexes w/ exaggerated tendon jerks, resulting from the hyper excitability of the stretch reflex
-At multiple joints

247
Q

What is rigidity?

A

-Significant increase in resistance to multidirectional external force about a joint
-Usually seen in end stage Parkinson’s Disease

248
Q

What is dystonia?

A

-A state of abnormal muscle tone resulting in muscular spasm and abnormal posture, typically due to neurological disease or a side effect of drug therapy
-Usually associated w/ basal ganglia & Huntington’s disease

249
Q

What are common upper limb postures or synergies that are seen in UMN syndrome?

A

-Flexed elbow
-Bent wrist
-Pronated forearm
-Clenched fist
-Thumb in palm

250
Q

What is a common synergy pattern for people that have had strokes?

A

-Upper extremity flexion synergy
-Lower extremity extension synergy

251
Q

What is movement ataxia? What area of the brain is it associated with?

A

-Loss of coordination, tremors, overshooting, loss of velocity
-Associated with cerebellum

252
Q

What is bradykinesia? What part of the brain is it associated with?

A

-Slowness of movement
-Associated with the basal ganglia and Parkinson’s disease

253
Q

What is the grading system for reflexes?

A

-4 Absent
-3 Just elicit able
-2 Low response
-1 Moderately low
0 Normal
+1 Brisk
+2 Very brisk
+3 Exhaustible clonus
+4 Continuous clonus

254
Q

What are associated movements?

A

-Moving one part of the body and another limb moves involuntarily
-Loss of complete selective control

255
Q

What is an advanced brain lesion?

A

-Severe injury in the brain (usually from stroke)
-Causes severe motor disruption “posturing”
-All limbs are “fixed” on a posture w/ limited limb movements
-Associated w/ rigidity (severe increase in tone)
-Flexion and extension synergies

256
Q

What are signs and symptoms of a cerebrovascular accident/stroke?

A

-Initially flacid
-Later develops spasticity
-Reflexes hyperactive
-Synergistic movements
-Clonus
-Sensory loss
-Cranial nerve changes (facial weakness and vision changes)
-Bladder changes

257
Q

What is a John Doe spinal cord injury?

A

-When a whole vertebrae shatters
-The broken pieces irritate the spinal cord
-It doesn’t typically sever the spinal cord
-Mostly from high speed accidents

258
Q

What are different types of incomplete spinal cord injuries?

A

-Central cord
-Brown Sequard
-Anterior cord

259
Q

What is Brown Sequard syndrome?

A

-Lesion on hemisection of spinal cord
-Ipsilateral UMN signs below the level of lesion
-Ipsilateral loss of tactile, vibration, proprioception loss 1-2 levels below lesion
-Contralateral pain and temp. loss below lesion
-Ipsilateral loss of all sensation
-Ipsilateral LMN signs

260
Q

What is a transverse cord lesion?

A

A complete spinal cord injury, which effects all motor & sensation under the level of injury

261
Q

What is lost on the involved side in spinal cord injuries?

A

Vibration & proprioception

262
Q

What is lost on the uninvolved side in spinal cord injuries?

A

Loss of pain & temp.

263
Q

What are signs of lower motor neuron lesions?

A

-Loss of muscle function (weakness/flaccid)
-Loss of sensation
-Tone: hyporeflexia

264
Q

What are other LMN lesion signs?

A

-Fibrillations (muscular twitching)
-Fasciculations (worm-like contraction)
-Hypotonia/atonia

265
Q

Where should you test when examining LMN lesions? Why?

A

-Test above, parallel, & other side of where the lesion is
-Because some peripheral nerve disease spread, like Guillan Barre

266
Q

What are nerve root injuries? How do they occur?

A

-An injury to the nerve right at the nerve root (when it exits the spinal cord)
-Common causes are foraminal stenosis and herniated discs

267
Q

What is Carpel Tunnel Syndrome? What is the clinical presentation?

A

-Injury to the median nerve
-Atrophied thenar eminence
-Weakness or paralysis
-Pain along nerve
-Numbness along nerve
-Sensory loss
-Loss of ROM

268
Q

What are the muscles involved in carpel tunnel syndrome?

A

-Flexor pollicis brevis
-Opponens pollicis
-Abductor pollicis brevis

269
Q

What muscle testing should be done for a peripheral nerve injury?

A

-Test muscles on uninvolved side
-Test muscles on involved side
-Test muscles of adjacent peripheral nerves

270
Q

What sensory testing should be done for a peripheral nerve injury?

A

-Ask about pain
-Test sensation to uninvolved side first, then involved side
-Test sensation in the involved sensory distribution
-Test sensation of adjacent peripheral nerves

271
Q

What are signs and symptoms of injury to the deep fibular nerve/common fibular nerve?

A

-Numbness and tingling
-Shooting pain along the nerve
-Pain w/ nerve tapping
-Pain at rest
-Hyperreflexia
-Muscular weakness
-Sensory loss in common fibular distribution

272
Q

What muscles are involved in common fibular nerve injury?

A

-Fibularis longus & brevis
-Tibialis anterior, EHL, EDL

273
Q

What are signs and symptoms of a C6 nerve root injury?

A

-Sensory loss following the C6 dermatome
-Hyporeflexia
-Decreased DTR
-Weakness
-Pain
-Tingling and numbness following C6 distribution

274
Q

What are the muscles involved in the C6 nerve root injury?

A

-Biceps
-Brachioradialis
-Wrist extensors

275
Q

What is diabetic neuropathy?

A

-Length dependent (distal)
-Blood vessels in distal extremities deteriorate which cuts off the blood supply to the nerves
-Follows a glove and stocking presentation
-Polyneuropathy (many nerves involved)

276
Q

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

A

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

277
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

278
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

279
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

280
Q

What is lead pipe rigidity?

A

-Continous throughout whole movement
-Agonist and antagonist involved

281
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

282
Q

What is the definition of pain?

A

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

283
Q

What is pain influenced by?

A

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

284
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

285
Q

What role does pain serve in our lives?

A

It serves as an adaptive and protective role

286
Q

What can pain have adverse effects on?

A

-Function
-Social and psychological well-being

287
Q

What are biological factors that can affect pain?

A

-Genetics
-Physiology
-Neurochemistry
-Tissue health

288
Q

What are social factors that can affect pain?

A

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

289
Q

What are psychological factors that can affect pain?

A

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

290
Q

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

A

TENS

291
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

292
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

293
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

294
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

295
Q

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

A

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

296
Q

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

A

Sleep!!!

297
Q

What are the different types of pain fibers?

A

-Delta fibers
-C fibers

298
Q

What are delta fibers?

A

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

299
Q

What are C fibers?

A

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

300
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

301
Q

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

A

-Glutamate
-Substance P
-They increase the pain perception

302
Q

How can we help override painful sensations?

A

By giving different sensations

303
Q

What is acute pain?

A

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

304
Q

What is adaptive pain?

A

Protects tissues and promotes healing

305
Q

What is maladaptive pain?

A

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

306
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

307
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

308
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

309
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

310
Q

What is allodynia?

A

Pain from “non-painful” stimuli (nociplastic)

311
Q

What is analgesia?

A

Absence of pain sensation

312
Q

What is hyperalgesia?

A

Increased sensitivity to painful stimuli

313
Q

What is sensitization?

A

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

314
Q

How is pain classified?

A

-Nociceptive
-Neuropathic
-Nociplastic

315
Q

What is neuropathic pain subdivided into?

A

-Peripheral nerve pain
-Central brain or spinal cord pain

316
Q

What is nociplastic pain subdivided into?

A

-Peripheral sensitization
-Central sensitization

317
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

318
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

319
Q

What can nociplastic pain cause?

A

Negative neuroplasticity

320
Q

What is nociceptive pain?

A

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

321
Q

What is neuropathic pain?

A

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

322
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

323
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

324
Q

What is the “chemical soup” around an injury?

A

-Substance P
-CGRP
-Histamine
-Prostaglandin

325
Q

Where can substance P be found in peripheral sensitization?

A

-Peripheral areas
-Dorsal horn

326
Q

What are the tracts that are invovled in centralized pain?

A

-Anterolateral
-Spinoreticular

327
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

328
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

329
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

330
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
331
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

332
Q

What are other factors that can affect pain?

A

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

333
Q

What are some non-pharmacologic ways of managing pain?

A

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

334
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.)

335
Q

What does effective pain education involve?

A

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

336
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

337
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

338
Q

Can negative neuroplasticity be reversed?

A

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

339
Q

How can NSAIDs help in pain reduction?

A

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

340
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

341
Q

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

A

-No side effects
-Good for arthritis and muscular pain

342
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

343
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

344
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

345
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

346
Q

What kind of pain is CRPS?

A

Allodynia

347
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)

348
Q

What is the efferent sympathetic fibers formed by?

A

Formed by gray matter in the thoracic and lumbar spinal cord

349
Q

How does the sympathetic division effect blood flow to the muscles and heart?

A

-Prioritizes sending blood to the skeletal muscles and heart in times of emergency
-Vasodilation in heart and skeletal muscles
-Vasoconstriction to vessels of skin to minimize bleeding

350
Q

What nerve provides about 75% of the parasympathetic outflow?

A

Vagus nerve (CN X)

351
Q

What cranial nerves are involved in the parasympathetic system? Where does the other portions of the parasympathetic system come from?

A

-CN III (oculomotor)
-CN VII (facial)
-CN IX (glossopharyngeal)
-Sacral nerves

352
Q

What are the functions of the parasympathetic system?

A

-Pupillary response
-Stimulates saliva
-Constricts bronchi
-Peristalsis/secretion
-Bile release/liver
-Bladder contracts
-Constricts pupil

353
Q

What nerve in the parasympathetic system controls the bladder and reproductive system?

A

Pelvic splanchnic nerve

354
Q

What are the ganglionic neurons in the parasympathetic system? What are their target organs?

A

-Ciliary ganglion: intrinsic eye muscles
-Pterygopalatine and submandibular ganglion: nasal, tear, and salivary glands
-Otic ganglion: parotid salivary gland
-Intramural ganglia: visceral organs of neck, thoracic cavity, and abdominal cavity
-Intramural ganglion: visceral organs in inferior portion of abdominal cavity and pelvic cavity

355
Q

What kinds of receptors are part of the autonomic nervous system?

A

-Mechanoreceptors
-Chemoreceptors

356
Q

Where are autonomic pressure receptors found?

A

-Aortic baroreceptors
-Carotid sinuses
-Lungs

357
Q

Where are the autonomic stretch receptors found?

A

Respond to distention in the veins, bladder, or intestines

358
Q

Where are the autonomic chemoreceptors found?

A

-Carotid and aortic bodies (responds to oxygen)
-Medulla (respond to hydrogen ions and carbon dioxide)

359
Q

What is the afferent information from the heart?

A

Baroreceptors in carotid and aortic bodies which send information to the medulla along CN IX and X

360
Q

What is the efferent information to the heart?

A

-Efferent to spinal cord-sympathetic trunk: accelerates HR
-Efferent parasympathetic directly to SA node: slows HR

361
Q

What neurotransmitters does the sympathetic system use?

A

-Acetylcholine
-Norepinephrine

362
Q

What neurotransmitters does the parasympathetic system use?

A

Acetylcholine

363
Q

What are cholinergic agonists? What do they do? What condition might they be used for?

A

-A group of medicines that mimic the actions of acetylcholine
-Increases transmission
-Can be used for myasthenia gravis since they lose acetylcholine

364
Q

What are anticholinergics? What do they do? What condition might they be used for?

A

-Drugs that block the action of acetylcholine
-Decreases sweat and peristalsis
-Bronchodilator
-Can be used for COPD

365
Q

How does diaphragmatic breathing affect the ANS and stress? What technique can be used?

A

-Deep breathing stimulates the parasympathetic nervous system
-4-7-8 technique (in 4, hold 7, out 8)
-Reduces cortisol (stress hormone)
-Increases attention

366
Q

What are common pathologies of the autonomic nervous system?

A

-Spinal cord injury above T6
-Parkinson’s disease
-Postural orthostatic tachycardia syndrome

367
Q

What happens to the autonomic nervous system if someone has a spinal cord injury above T6?

A

-Loss of autonomic drive from carotids to cardiac centers
-Autonomic dysreflexia: sends wrong info to heart and there is no parasympathetic control of sympathetic, which can be life threatening

368
Q

How does Parkinson’s affect the ANS?

A

-Dysautonomia: GI system, temperature dysregulation, pupillary
-Orthostatic hypotension (from levodopa)
-Sympathetic innervation (blood pressure drops)

369
Q

What are symptoms associated with postural orthostatic tachycardia syndrome (POTS)?

A

-Cardiac instability
-Fainting
-Postural hypotension
-Weakness

370
Q

What can timely out of bed and upright activity prevent in patients with CVA? What is a potential complication of early out of bed?

A

-DVT
-Pulmonary emboli
-Pneumonia
-Falls
-11% of patients experienced progression of lesion with early OOB

371
Q

What should be monitored with patients with CVA during OOB and upright activities? What activity should we avoid during early OOB activities?

A

-Orthostatic hypotension
-High intensity exercise should be avoided in the acute phase following a CVA (wait at least 3 months)

372
Q

What are common characteristics of gait in patients with CVA?

A

-Hip circumduction
-Foot drop in early to late swing
-Limited hip or knee flexion during swing
-Foot flat contact
-Knee hyperextension
-Trendelenburg
-Knee buckle
-Talocrural joint dysfunction

373
Q

What are common assistive devices for people with CVA?

A

-Hemi-walker
-Cane
-Quad cane

374
Q

What kind of gait pattern is usually seen in a patient with a CVA who used a cane?

A

-Two point step to pattern (cane and affected leg, then unaffected leg step to)
-Three point step to pattern (cane, affected leg, unaffected leg step to)

375
Q

What hemisphere in the brain is associated with language and processing? What lobes are the language areas in?

A

-Left hemisphere
-Frontal and temporal lobes contain the language centers

376
Q

What hemisphere of the brain is considered the dominant hemisphere?

A

The left hemisphere

377
Q

What is the function of the right hemisphere?

A

-Spatial awareness
-Body awareness

378
Q

If someone has a right hemisphere CVA, what symptom would they most likely experience?

A

Neglect

379
Q

What is the function of Broca’s area? Where is it located?

A

-Expressive language and the ability to produce language
-Inferior frontal lobe in the left hemisphere

380
Q

What is the function of Wernicke’s area? Where is it located?

A

-Language comprehension
-Temporal lobe in the left hemisphere

381
Q

What structure connects the Broca and Wernicke areas?

A

White matter called the arcuate fasciculus

382
Q

What is the blood supply to the Broca area, Wernicke area, and arcuate fasciculus?

A

-Broca: Middle cerebral artery superior division
-Wernicke: MCA inferior division
-Arcuate fasciculus: MCA superior & inferior divisions

383
Q

What is aphasia? What is affected?

A

-A deficit in language processing caused by dysfunction of the dominant hemisphere (left)
-Aphasia is a disorder of language so both spoken and written language are affected

384
Q

What is expressive aphasia? What are the signs and symptoms?

A

-Also called Broca’s aphasia
-Caused by lesions in the inferior frontal gyrus of the left hemisphere from an infarct of the left MCA superior division
-Decreased fluency of spontaneous speech
-Short phrase length
-Telegraphic speech with lack of grammatical structure
-Naming difficulties
-Comprehension is relatively intact
-Reading and writing is slow and effortful
-Frustration and depression is common since individual is aware of the deficit

385
Q

What is receptive aphasia? What are the signs and symptoms?

A

-Also called Wernicke’s aphasia
-Lesion in the superior posterior portion of the temporal lobe caused by infarct of the L MCA inferior division
-Impaired comprehension
-Lacks response to questions
-Speech has normal fluency and grammatical structure
-The speech is empty and meaningless
-Naming impaired with aphasia
-Commonly associated with visual field cut
-Patients are unaware of deficits

386
Q

What happens if there is an occlusion of left stem MCA?

A

-Global aphasia
-R hemiplegia
-Frontal-temporal-parietal lesion
-Speaking, listening, & reading impaired
-Limited speech
-Impaired auditory comprehension
-Brain damage is massive

387
Q

What is the recovery of aphasia like? What is the time frame?

A

-A slow process that involved helping the individual and family understand the nature of aphasia and learning compensatory strategies for communication
-Most recovery happens in the first 2-3 months after a stroke
-If symptoms persist after 2-3 months, complete recovery is unlikely

388
Q

What are some tips for working with people with aphasia?

A

-Draw or write things down on paper
-Be patient
-Speak simply, clearly, and slowly
-Be sure that the person understands your request
-Treat the person with aphasia as an intelligent adult, especially because it doesn’t affect thinking skills

389
Q

What spatial problems commonly occur in people that have non-dominant hemisphere strokes?

A

-Left sided neglect is closely related to right temporo-parietal function and posterior parietal cortex
-Right MCA stem stroke

390
Q

How does neglect often manifest?

A

-It manifests as a sensory deficit and a failure to pay sufficient attention to sensory input
-Lateralization of attention (selective or directed attention)

391
Q

What is typically the cause of severe right neglect?

A

A bilateral lesion

392
Q

What is hemi-neglect syndrome?

A

-Processing deficit
-Loss of representation of space on left
-Inattention to space to the left (will draw one side of the clock)
-Anosognosia (unawareness of the illness)
-MCA stem infarct right parietal or frontal cortex
-Improvement seen with return of spatial attention in a few weeks
-Poor outcome with no return or change in 4 weeks

393
Q

What are tasks that are a common difficulty in patients with non-dominant hemisphere lesions?

A

-Visual-spatial analysis
-Construction abilities
-These patients also often present with severe personality and emotional changes

394
Q

What are interventions for spatial/hemi-neglect?

A

-Forced use
-Constraint induced used
-Patching the unaffected eye so they are forced to use affected eye

395
Q

What is the association cortex?

A

-It includes most of the cerebral surface of the human brain
-It is largely responsible for the complex processing that goes on between the arrival of input in the primary sensory cortices and the generation of behavior

396
Q

Where does the unimodal motor association cortex project into? What is its function?

A

-It projects predominantly to the primary motor cortex
-It is important for formulating the motor program for a complex action involving multiple joints

397
Q

What does the heteromodal association cortex project/connect to?

A

-Bidirectional connections with both motor and sensory association cortex of all modalities and bidirectional connection with the limbic system
-This arrangement allows the heteromodal association cortex to perform the highest-order mental functions

398
Q

What is the association cortex divided into?

A

-Frontal heteromodal association cortex (prefrontal cortex)
-Motor association cortex (unimodal)
-Somatosensory association cortex (unimodal)
-Lateral parietal and temporal heteromodal association cortex

399
Q

What is the function of the frontal part in the association cortex? When does the frontal lobe mature in females and males?

A

-Executive function
-Complex behavior
-Motor planning
-Females: 18
-Males: 25

400
Q

What is the function of the temporal part in the association cortex?

A

Recognition

401
Q

What is the function of the parietal part in the association cortex?

A

-Attention
-Awareness

402
Q

What is the function of the association cortex?

A

-Higher order sensory processing
-Motor planning
-Language processing and production
-Visual-spatial orientation
-Socially appropriate behavior

403
Q

What are the 3 major divisions of the frontal lobe? What is another division?

A

-Primary motor cortex
-Premotor cortex
-Prefrontal association cortex
-Frontal eye fields ( state of enlightenment)

404
Q

What is the premotor cortex responsible for?

A

-Planning movements
-Speech

405
Q

What is the prefrontal association cortex responsible for?

A

-Largest association area of the frontal lobe (30% of the brain)
-Main functions include restraint, initiative, and order
-The executer
-Higher consciousness
-Decision making
-Integrates different sources of information
-Judgement of context
-Attention, abstraction, self awareness, decision making, social judgement

406
Q

How is the frontal eye fields connected to the superior colliculus?

A

They work together to help to alert you to things such as car accidents

407
Q

What is the function of the frontal lobe?

A

-Being socially apprpriate
-Restraint
-Initiative
-Order
-Working memory (i.e. where did I park)

408
Q

What are the subcortical connections of the prefrontal association cortex?

A

-Amygdala
-Thalamus
-Hippocampus
-Basal ganglia
-Hypothalamus

409
Q

Who was Phineas Gage?

A

-A railroad foreman that had an iron rod driven through his frontal lobe
-He lacked emotional control
-Unable to stick to plans
-Personality change: used lots of profanity

410
Q

What is the function of the dorsolateral prefrontal cortex?

A

-Regulation of attention and behavior
-Attention and working memory
-Cognitive control
-Executive functions

411
Q

What is the function of the orbitofrontal prefrontal cortex?

A

-Impulse control
-Social judgement
-Involvement in associating things
-Rewards
-Cognition
-Personality
-Involved in conscious reappraise strategies to emotional regulation

412
Q

What structures are involved in working memory?

A

-Prefrontal cortex
-Amygdala: emotional memory
-Hippocampus: long term memory
-Cerebellum: procedural memory

412
Q

What is short term memory?

A

It acts as a “scratch pad” for temporary recall of the information which is being processed at any point in time and has been referred to as the brains “post it note”

413
Q

What is the function of the amygdala?

A

-Appraisal of emotions
-Preferential activation in threatening and social situations
-Part of the limbic system
-Required for fear condition and accurate emotion recognition
-Survival

414
Q

What is the function of the hypothalamus in relation to the limbic system?

A

-Physiological context of emotions
-ANS, endocrine functions on emotions; changes in BP and HR
-Primary output to the limbic system
-Connected to frontal lobe, brain stem, hippocampus
-Appetite, sexual response, circadian rhythm

415
Q

What is the function of the hippocampus in relation to the limbic system?

A

-Required for the formation of conscious memory
-Facilitate learning and memory processing

416
Q

What is the function of the prefrontal cortex in relation to the limbic system?

A

-Modulation of emotions
-Inhibitory inputs to the amygdala
-Component in traumatic brain injury (loss of emotion modulation)

417
Q

What are the main structures in the limbic system? What are the substructures?

A

Main Structures
-Hippocampus
-Hypothalamus
-Amygdala

Substructures
-Cingulate cortex
-Thalamus

418
Q

What is the function of the limbic system?

A

-Emotion
-Behavior
-Memory
-Motivation
-Olfaction
-Decision making

419
Q

What is the limbic system also called?

A

The primitive brain

420
Q

What is the function of the thalamus in relation to the limbic system?

A

Relays information from sensory organs to cerebral cortex

421
Q

What is the function of the cingulate cortex in relation to the limbic system?

A

-Primary cortical component of the limbic system
-Involved in emotional and cognitive processing

422
Q

What are the diencephalic structures of the limbic system?

A

-Anterior thalamic nuclei
-Hypothalamus

423
Q

What are the fiber tracts connecting the limbic system?

A

The fornix

424
Q

How is the olfactory bulb involved with the limbic system?

A

-It is not an actual part of the limbic system, smells trigger feelings
-We associate certain smells with feelings and memories

425
Q

How fast do autonomic reactions with the limbic system occur?

A

Within 100-500 milliseconds

426
Q

What area of the brain is the limbic system primarily associated with?

A

-Involves multiple brain structures primarily the prefrontal cortex
-Involves behavior

427
Q

What is apraxia? Are lesions that cause apraxia localized?

A

-A dominant syndrome
-Inability to carry out an action in response to a command in absence of comprehension deficit and weakness of incoordination
-Lesions that cause apraxia are not well localized and can be caused by lesions in different locations

428
Q

Do patients with aphasia often have apraxia?

A

Typically one third of patients with aphasia also have apraxia

429
Q

What is dyspraxia?

A

-Movement based problem
-Clumsy, unable to manipulate objects properly

430
Q

What is preservation? What can be the cause of this?

A

-This activity tends to occur in persons with apraxia
-Performing an action over and over again
-Not having enough GABA or glutamate can cause this

431
Q

What is ideation apraxia?

A

The individual cannot recall how to perform everyday activities (i.e. using toothbrush to brush hair)

432
Q

What is attention deficit hyperactive disorder (ADHD)? What are signs and symptoms?

A

-Brain disorder characterized by poor attention span and hyperactivity
-Involves delays in the dorsolateral prefrontal cortex
-35% of children with ADHD will not graduate from high school
-Hyperactivity is the first symptom to be noticed in infants, excessive energy and talk excessively
-Treatments: stimulants of the dopamine and norepinephrine system to increase attention and concentration

433
Q

What are the three layers of tissue in the visual system?

A

-Retina (part of CNS)
-Uveal tract
-Sclera

434
Q

What structures are part of the retina?

A

-Optic disc
-Fovea

435
Q

What are the three components of the uveal tract?

A

-Choroid
-Ciliary muscle
-Iris

436
Q

What is the function of the choroid?

A

Rich capillary bed for nourishment of photoreceptors

437
Q

What is the function of the ciliary muscle?

A

-Surrounds the lens
-Adjusts the lens

438
Q

What is the function of the iris?

A

Pupillary constriction

439
Q

What is the sclera?

A

Outermost fibrous tissue

440
Q

What is the cornea?

A

Outer structure that permits the flow of light into the eye

441
Q

What is the function of the vitreous humor?

A

Contains phagocytic cells to pick up debris

442
Q

What is the fovea? What is its function?

A

-Center of the macula (part of the retina)
-A small depression or pit
-Responsible for sharp vision or details
-Carries 50% of the information from optic nerve

443
Q

What are the two types of photoreceptors in the retina? What are their functions?

A

-Rods: allow us to see in the dark
-Cones: allow us to see in the light
-Process of activation, then sends info to optic nerve

444
Q

What does the primary visual pathway involve?

A

-CN II
-Optic tract
-Optic radiation

445
Q

Where does the optic tract decussate? Does all of it cross over?

A

-Decussates at optic chiasm
-Only 60% crosses over at optic chiasm

446
Q

What is the main target of the optic tract? How much of the tract synapses onto this target?

A

-Major target is dorsal lateral geniculate nucleus (LGN) in the thalamus
-90% synapse here

447
Q

What is the secondary target of the optic tract?

A

Optic radiation onto the visual cortex

448
Q

When does the optic nerve become the optic tract?

A

After the optic nerve passes through the optic chiasm, it becomes the optic tract

449
Q

What is a good way to see if there is a horizontal lesion across the whole brain? Why?

A

Testing CN II because it spans the whole horizontal portion of the brain

450
Q

Where is the visual cortex located?

A

Thalamus

451
Q

How does the pupillary light reflex work?

A

-CN II sends info from retina to the pretectum
-Info is relayed to the Edinger Westphal Nucleus and is relayed bilaterally
-Contains pre ganglionic parasympathetic fibers via CN III
-Terminates in ciliary ganglion: post ganglionic to iris
-Constricts pupillary constrictor muscles to decrease pupil size by pulling the lens to allow less light in

452
Q

What half of the retina does not cross over/decussate?

A

Temporal half of the retina

453
Q

What part of the visual field does the temporal half of the retina provide?

A

It provides the nasal visual field

454
Q

What half of the retina decussates at the optic chiasm?

A

The nasal half decussates at the optic chiasm

455
Q

What part of the visual field does the nasal half of the retina provide?

A

It provides the temporal visual field

456
Q

What is the monocular visual field?

A

-Closing one eye
-Each eye visualizes a visual field: divided into quadrants

457
Q

What is the binocular field?

A

-Two foveas focus on two visual hemi fields
-Temporal fields more extensive than nasal

458
Q

What is left homonymous hemianopsia? What causes it?

A

-Defect in the right optic tract which receives information from the left nasal retina and right temporal retina
-Deficiit of bilateral visual fields: visual field cut
-Lesion is after decussation
-Caused by strokes, tumors, or TBI

459
Q

What is monocular visual loss?

A

-Loss of all visual fields in one eye
-Caused by a lesion in the optic nerve before it decussate
-Caused by tumors, TBI, or glaucoma

460
Q

What are the two types of neuronal transmission?

A

-Electrical
-Neurotransmitters

461
Q

How is electrical neuronal transmission carried out?

A

-Information is processed electrically
-Ionic current flows passively through synaptic junction

462
Q

What is an advantage to electrical neuronal transmission?

A

The main advantage of electrical synapses is that the signal transduction occurs at a very high speed through the gap junctions

463
Q

How is neurotransmission carried out?

A

-Neurons communicate with each other by secreting and responding to neurotransmitters (chemicals)
-Medication influences the chemical interactions between neurons

464
Q

How do ions move through the synaptic membrane? What do they move in response to?

A

-They move through the synaptic membrane via channels or pumps
-They move in response to passive forces (channels) or active transport pumps (requires energy)

465
Q

What is post synaptic receptor transport?

A

-Receptors are anchored to post synaptic membrane
-G-protein coupled receptors
-May directly open channels or indirectly open channels (via second messenger)

466
Q

What are the two main types of channels?

A

-Non-gated: open all the time (leaky)
-Gated: generally have two states, open or closed

467
Q

What are voltage gated ion channels?

A

-Open in response to changes in electrical charge across the membrane
-Changes in positive and negative ions (Na+, K+, Ca+, Cl-)
-Ex: voltage gated calcium channels

468
Q

What do calcium channel blockers do?

A

-They target voltage gated calcium channels in the heart
-Nifidepine
-Lowers blood pressure

469
Q

What are modality gated channels?

A

-Sensory
-Activated by stimuli
-Close in the absence of stimuli
-Touch receptors of skin
-Hearing and balance (inner ear)
-Temperature changes (skin)
-Chemicals
-Pain sensations
-Stretch receptors in muscles

470
Q

What is the Na+-K+ pump?

A

-Channel that requires ATP
-20-40% of synapses are pumps
-Moves ions against concentration or electrical gradients
-Maintains concentration gradients
-Pumps 3 Na+ out for every 2 K+ in

471
Q

What is a neurotransmitter?

A

-A chemical substance that is released at the end of a nerve fibers by the arrival of a nerve impulse and by diffusing across the synapse or junction
-Causes the transfer of the impulse to another nerve fiber, muscle fiber, or some other structure

472
Q

What are neuromodulators?

A

-Are NOT released into the synaptic cleft
-Released into extacellular fluid
-Acts on multiple neurons at the same time
-Act more slowly and effects last longer
-Act in conjunction with neurotransmitters
-Substance P is a neuromodulator

473
Q

What are the cholinergic neurotransmitters?

A

Acetylcholine (ACh)

474
Q

What are the amino acid neurotransmitters?

A

-Aminobutyric acid (GABA)
-Glutamate (Glu)
-Glycine (Gly)
-Aspartate

475
Q

What are the amine neurotransmitters?

A

-Dopamine (DA)
-Histamine
-Norepinephrine (NE)
-Serotonin (5-HT)
-Melatonin

476
Q

What are the peptide neurotransmitters?

A

-Endorphines
-Enkephalines
-Substance P

477
Q

What is another neurotransmitters that does not fall in the main categories of neurotransmitters?

A

Nitric oxide (NO)

478
Q

What are the strictly excitatory neurotransmitters?

A

-Acetylcholine
-Glutamate
-Aspartate
-Nitric oxide

479
Q

What neurotransmitters are both excitatory and inhibitory?

A

-Dopamine
-Norepinephrine
-Histamine (mostly inhib.)
-Endorphines (mostly inhib.)
-Enkephalines (mostly inhib.)

480
Q

What neurotransmitters are strictly inhibitory?

A

-GABA
-Glycine
-Serotonin

481
Q

What is the most widespread excitatory neurotransmitter?

A

-Glutamate
-It provides 90% of excitatory function in the brain

482
Q

What is glutamate associated with? What happens when glutamate levels are too high?

A

-Attention, learning, and function
-High levels leads to cell death by setting off inflammation (too many calcium ions entering cells causing excitotoxicity)

483
Q

How does glutamate play a role in neuroplasticity?

A

-It is responsible for sending signals between nerve cells, and under normal conditions, it plays an important role in learning and memory
-Essential role in neuroplasticity
-The form of plasticity known as long term potentiation takes place at glutamatergic synapses in the hippocampus, neocortex, and other parts of the brain

484
Q

What is GABA? What is its function?

A

-Gamma aminobutyric acid
-Main inhibitory neurotransmitter
-Counters glutamate
-Activation of GABA induces sleep patterns
-Found throughout the brain and spinal cord

485
Q

What is Gabapentin? What does long term use cause?

A

-Anti-seizure medication
-Also used for neuropathic pain
-Similar structurally to GABA
-Inhibition of nerve communication
-Long term use causes decreased levels of glutamate

486
Q

What are uses of the neurotransmitter GABA?

A

-Neuropathic pain management
-Anti-spasticity medication
-Anti-seizure medication

487
Q

What is the function of acetylcholine?

A

-Facilitatory
-Released in the neuromuscular junction
-ANS preganglionic and postganglionic neurons
-Receptors: nicotinic, muscarinic

488
Q

What is the function of dopamine?

A

-Generally excitatory
-Movement
-Memory
-Rewards and motivation
-Involved in addiction
-Limbic (happiness)
-Retina
-Found in CNS (brain stem, basal ganglia, substantia nigra)

489
Q

How do drugs of abuse such as cocaine and other amphetamines affect the reward pathways?

A

-They affect the reuptake leading to longer dopamine acticity, which produces euphoria
-Requires more drugs/higher doses to produce the same effect

490
Q

What causes Parkinson’s disease?

A

Loss of dopaminergic neurons in the substantia nigra

491
Q

What is the function of serotonin?

A

-Generally inhibitory
-Associated with mood, appetite, and sleep
-90% located in the GI tract, 10% in the brain
-Often used for depression (tricyclic anti-depression medication)
-Also used for pain reduction (slow acting)

492
Q

What are low levels of serotonin associated with? What medication can help?

A

-Depression
-Prozac is a selective blocker of serotonin reuptake resulting in serotonin remaining in synapses longer

493
Q

What is the function of norepinephrine? Where is it found?

A

-Distinct pathways to many locations in the brain, including the cerebral cortex, limbic system, and spinal cord
-Works at the areas in the brain that works with attention and responding
-Hormone and neurotransmitter
-Found in smooth muscle, ANS, and brain stem

494
Q

What are common antidepression medications?

A

-Tricyclic antidepressants (TCA)
-Serotonin-norepinephrine reuptake inhibitors (SNRI)
-Effexor
-Cymbalta
-These drugs keep neurotransmitters in the synpatic cleft longer

495
Q

What is Ritalin?

A

-ADHD medication
-Increases norepinephrine and dopamine

496
Q

How does norepinephrine affect the amygdala?

A

It affects the amygdala which is involved in control of attention and responses

497
Q

What neurotransmitters are involved in fight or flight? How do they affect the organs?

A

-Epinephrine and norepinephrine
-Increases HR
-Triggers the release of glucose from energy stores
-Increases blood flow to skeletal muscle

498
Q

What is substance P? Where is it found? What do high levels lead to?

A

-Facilitatory
-Found in spinal cord, basal ganglia, and limbic system
-High levels lead to inflammation and can contribute to fibromyalgia, and changes the perception of pain

499
Q

What medication attacks substance P?

A

Motrin

500
Q

What are endorphins? When are they released?

A

-Endogenous neuropeptides
-Releases positive feelings
-They are produced by the central nervous system and the pituitary gland
-They are released during aerobic exercise

501
Q

What is brain derived neurotrophic factor? What causes the release of BDNF?

A

-BDNF
-Protein from the neurotrophin family
-Acts on neurons in CNS and periphery
-Exercise induced neurogenesis
-Aerobic exercise at 65-85% of max HR causes release of BDNF

502
Q

How does BDNF affect the hippocampus?

A

Associated with higher learning and memory

503
Q

How does BDNF affect the cortex?

A

Facilitates nerve growth, differentiation of synapses

504
Q

How does BDNF affect the basal forebrain?

A

Helps with long term memory

PHTH 527: Applied Neurosciences I (5 decks)

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