Final Exam Prep Flashcards
(505 cards)
1
Q
What are the two major organs in the vestibular system?
A
-Vestibule
-Semi-circular canals
2
Q
What makes up the vestibule?
A
-Saccule
-Utricle
3
Q
What makes up the semi-circular canals?
A
-Anterior canal
-Posterior canal
-Horizontal canal
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)
5
Q
What movements does the semi-circular canals detect?
A
-Rotational head movements
-Acceleration of head rotation
6
Q
What nerve supplies the vestibular system?
A
-CN VIII (vestibulocochlear)
-Vestibular branch supplies vestibular system
-Cochlear branch stimulates the cochlea
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
8
Q
What does each semi-circular canal contain?
A
-Crista ampullaris/ampulla
-Cupula
9
Q
What does each crista ampullaris contain?
A
-Cupula
-Supporting cells
-Hair cells
-Stereocilia
-Sensory nerve fibers
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
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
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
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
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
15
Q
What age do babies develop otoliths and maculae?
A
4 months
16
Q
Where are maculae located?
A
In the utricle and saccule
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
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
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
20
Q
What movement does the saccule detect?
A
Up and down (flexion and extension of the head)
21
Q
What movement does the utricle detect?
A
Side to side (side bending of the head)
22
Q
Where do the sensory signals from the utricle and saccule go to?
A
Straight to the AHC
23
Q
What does otolith activation help with?
A
Can help increase spatial memory and spatial tasks
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
25
What are the main vestibular pathways to the spinal cord?
-Lateral vestibulospinal tract
-Medial vestibulospinal tract
26
What is the medial longitudinal fasciculus? What does it help with?
-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
27
What nuclei does the medial vestibulospinal tract come from? What about the lateral vestibulospinal tract?
-Medial nucleus
-Lateral nucleus
28
What is the vestibular ocular reflex (VOR)?
-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
29
What system does the VOR use to coordinate eye movement?
-Medial longitudinal fasciculus (MLF)
-Head rotation to the right: excitation of left abducens and inhibition of the left medial rectus and right abducens
30
What reflex & system is disturbed with concussions? What symptoms occur?
-The VOR & vestibular dysfunction is seen
-Dizziness when moving head
-Unable to read books
-Difficult to drive
-Blurry vision
31
What gives rise to the lateral vestibulospinal tract (LVST)? What is its function? Where does it terminate?
-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
32
What are the main actions of the LVST? Where does it receive information from?
-Automatic postural responses
-Extensor muscle tone
-Innervates extensor muscles of limbs by facilitation to alpha and gamma motor neurons
33
What gives rise to the medial vestibulospinal tract (MVST)?
-The medial vestibular nucleus gives rise to the MVST as well as the inferior vestibular nucleus (semicircular canals)
34
Where does the MVST extend into? Where does it terminate?
-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
35
What is the action/function of the MVST?
-Controls neck and head position
-Provides a stable platform for eye movement and vision
-Mediates postural changes in response to head motion
36
What are 2 tracts that synapse on the AHC?
-Lateral vestibulospinal tract (LVST)
-Lateral corticospinal tract (LCST)
37
What is the connection between the vestibular system and cerebellum? What information does it send to the cerebellum?
-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
38
What are other outputs/pathways from the vestibular nuclei? What are their functions?
-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
39
How does a peripheral lesion (inner ear) of the vestibular system effect nystagmus and vertigo?
-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
40
How does a central lesion (brainstem or cerebellum) of the vestibular system effect nystagmus and vertigo?
-Onset of nystagmus is immediate
-May change directions
-Prominent nystagmus may occur in the absence of vertigo
41
What are the red flags of central lesions affecting the vestibular system?
-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
42
What are symptoms of peripheral lesions in the vestibular system?
-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"
43
What is cervicogenic vertigo?
-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
44
What are the three categories of vestibular disorders?
-Deficiency
-Distortion
-Fluctuation
45
What vestibular disorders are in the deficiency category? What are the signs & symptoms of these disorders?
-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
46
What vestibular disorders are in the distortion category? What are the signs & symptoms of these disorders?
-Benign paroxysmal position vertigo (BPPV)
-Vertigo
-Instability increases in the presence of inappropriate sensory signals (particularly vision)
-Disequilibrium of aging and multisensory disequilibrium
47
What vestibular disorders are in the fluctuation category? What are the signs & symptoms of these disorders?
-Meniere's Disease
-Migraine
-Dizziness
-Vertigo
48
What is BPPV?
-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)
49
When does BPPV usually peak?
It typically peaks in the 6th and 7th decades of someone's life
50
What is the most common cause of vertigo?
Peripheral vestibular disorder
51
What is canalithiasis? What are the signs & symptoms?
-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
52
What is cupulolithiasis? What are the signs & symptoms?
-A subtype of BPPV
-Nystagmus is immediate and persistent in duration (>1 minute)
-Nystagmus has no change in intensity
-Harder to treat than canalithiasis
53
How is BPPV classified?
-Direction defines the affected canal
-Torsion/rotational: anterior and posterior SCC
-Horizontal: horizontal SCC
54
How do you differentiate between anterior and posterior canal BPPV?
-Anterior canal has down beating torsional nystagmus in Dix Hallpike test
-Posterior canal has up beating torsional nystagmus
55
How do you perform the Dix Hallpike Test?
-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
56
What are the 5 head movements that elicit BPPV symptoms?
-Turning over in bed
-Lying down
-Rising up from supine
-Bending forward
-Reclining head
57
How do therapists examine BPPV?
-Dix Hallpike
-Epley manuever
58
What is disequilibrium of aging vestibular disorder?
-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
59
What are the most common symptoms of disequilibrium of aging vestibular disorder?
-Disequilibrium when walking
-Dizziness
60
What is multisensory disequilibrium vestibular disorder?
-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
61
What is Meniere's disease?
-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
62
What is the patho-mechanism of Meneire's disease?
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
63
What are the signs and symptoms of acute (< 3 days) unilateral vestibular loss (UVL)?
-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
64
What are the signs and symptoms of chronic (> 3 days) unilateral vestibular loss?
-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
65
What is the pathology of UVL from acoustic neuroma? What usually happens after surgical resection? What are the symptoms?
-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
66
What structures are supplied by the anterior inferior cerebral artery?
-Vestibular nuclei
-Trigeminal nuclei
-CN V
-Facial nerve
-Anterolateral tract
67
What is labyrinth?
-Vertigo
-Tinnitus
-Hearing loss
68
What are symptoms associated with AICA?
-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
69
What are symptoms associated with PICA?
-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)
70
What are exams for vestibular dysfunction?
-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
71
What are the inputs to the vestibular system?
-Cortex, cerebellum, reticular formation, extra-pyramidal
-Vision
-Proprioception superficial sensation
-Labyrinth activity
72
What are the outputs of the vestibular system?
-Cortical awareness of head, body, motion
-Control of oculomotor activity
-Control of posture
-Control of motor skill
73
What is dysarthria?
Trouble speaking
74
What is dysmetria?
Issues with coordination
75
What happens to synapses with repetition?
Synapses become "solid" and stronger with repitition
76
What is synaptic plasticity?
-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
77
What is the mechanism of synapses becoming stronger?
The more an activity is done, the amount of neurotransmitters associated with that synapse will increase and so will the receptors
78
What happens to the number of active brain regions the more an activity is done?
The number of active regions are reduced because less energy is required for the same task
79
What happens to the brain when someone learns a task?
When a task is fully learned, only small and distinct regions of the brain show activity
80
What is long term potentiation (LTP)?
The long term increase in synaptic strength
81
What stimulates long term potentiation?
Learning a new task stimulates LTP
82
What structures play a major role in synaptic stability?
-Dendritic spines play a major role in synaptic stability
-Changes in the dendritic spine (getting larger) can create synaptic stability
83
What can reduce the amount of dendrites in the hippocampus?
Stress
84
What is brain derived neurotrophic factor (BDNF)?
Nerve growth factor
85
What can increase BDNF? What areas of the brain are affected?
-Aerobic exercise
-Cerebellum
-Hippocampus
-Spinal cord
86
What is Hebbian plasticity?
-Increases in synaptic strength between neurons that fire together
-"Neurons that wire together, fire together"
87
What does synaptic strength depend on?
It depends on high degree of intense neuronal activity
88
What are neural networks?
Chain of neurons
89
What is experience dependent plasticity?
-Plasticity that is gained through learning & memory
-Requires creating different experiences
90
What occurs during experience dependent plasticity?
-Synthesis of new proteins (receptors)
-Growth of new synapses
-Modification of existing synapses
91
How many days does it take to learn a task?
10 days
92
What happens when there is repetition of a specific stimulus?
-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
93
What is synaptogenesis?
The formation of new synapses
94
What is experience expectant learning? What is an example?
-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
95
What happens to rods and cones if we do not get visual stimuli?
They will die
96
What is experience dependent learning? What is an example?
-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
97
What is the use it or lose it principle in neuroplasticity?
-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
98
What is the use it or improve it principle in neuroplasticity?
-Constraint induced therapy
-Sensory reorganization with sensory discrimination
99
What is constraint induced therapy? What are the parameters?
-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
100
What is the specificity principle in neuroplasticity?
-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
101
What is the repetition principle in neuroplasticity?
-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
102
How much repetition is required to learn a new skill?
For adults, between 300-1000 repetitions per day
103
What will make learning a new skill easier and faster for a patient? What system helps with this?
-If they are more dedicated and motivated
-Limbic system is involved in this
104
What is the intensity matters principle in neuroplasticity?
-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
105
What should be the repetitions of an exercise to improve neuroplasticity?
A study showed that doubling the # of reps in an upper limb assisted therapeutic intervention resulted in significant improvements in motor function
106
What type of exercise increases neurotrophic factors?
Aerobic exercise increase levels of BDNF
107
What is the type and amount of motor activity intensity critical for?
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
108
What is the salience matters principle in neuroplasticity?
-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
109
How does age affect neuroplasticity?
-Younger brains have more potential for neuroplasticity
-Neurogenesis gets more difficult as we age
110
How much oxygen and nutrients does the brain consume? What nutrients/foods are good for the brain?
-20% of oxygen and nutrients
-Fish, salmon, olive oil
-Vitamin D
-Older people have more difficulty allocating nutrients
111
What is the principle of transference in neuroplasticity?
-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
112
What is the interference principle in neuroplasticity?
-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
113
Does neuroplasticity occur in single synapses or in brain circuits?
Both!!
114
What occurs when multiple brain modalities are used? What is an example?
-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
115
What are the different brain modalities to create neuroplasticity?
-Visual
-Motor
-Cognitive
-Somatosensory
116
What is unconscious motor learning? What structure in the brain is it associated with?
-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
117
What system is the easiest to regain?
The motor system
118
What does memory for coordination of movements involve?
-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
119
What structure in the brain tends to not be as affected by loss of neuroplasticity?
The cerebellum
120
What does rehabilitation build upon?
-Visualization
-Cognitive load
-Coordination and timing
-Communication
121
What is a critical factor in gaining faster over-ground walking speeds?
Speed of walking and training at faster than self-selected speeds
122
What helps increase neuroplasticity in combination with repetition?
Problem solving
123
What does systematic progression of difficulty do to the motor cortex?
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
124
What is meant by the context of the exercise?
-Constantly increasing the difficulty by adding cognitive load, sensory/motor aspects
-Changing or modulating tasks increases the speed of neuroplasticity & learning
125
What happens when there is an increase in white matter?
Processing speed increases
126
What type of matter (white or gray) does neuroplasticity come from? Why?
-Gray matter
-Because neuroplasticity is the result of an increase in receptors and neurotransmitters in the synaptic cleft
127
What does increase of BDNF help with?
-Cognitive function
-Mobility
-Gait
128
What can be used to prime motor rehab post stroke? What does this help with?
-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
129
What are the direct effects of aerobic exercise?
-Increase in neurotrophic growth factos (BDNF)
-Increase in neurotransmitters such as dopamine and serotonin
130
What are the indirect effects of aerobic exercise?
-Increase in physical fitness (cardiorespiratory and muscular)
-Decrease in systemic and CNS inflammation
-Increase in cerebral blood flow
131
What are the three types of ischemic strokes?
-Embolic
-Lacunar
-Athero-thrombotic
132
What is an embolic stroke?
Embolus blocking flow
133
What is a lacunar stroke?
-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
134
What is an athero-thrombotic stroke?
Thrombus blocking blood flow
135
What is the etiology of lacunar strokes?
Chronic hypertension
136
Where do lacunar infarcts usually occur?
-Typically occur in the arteries that supply blood to the internal capsule
-Can also occur in the basilar artery or anterior cerebral artery
137
What are the signs & symptoms of a lacunar stroke?
-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
138
What is the blood supply to the anterior limb of the internal capsule?
It is mainly fed by the lenticulostriate branches of the middle cerebral artery, and sometimes but rarely from ACA
139
What are the lenticulostriate arteries?
Small penetrating arteries that supply blood flow to most of the subcortical structures
140
What is the blood supply to the genu of the internal capsule?
Lenticulostriate branches of MCA
141
What is the blood supply to the posterior limb of the internal capsule?
-Lenticulostriate branches of MCA
-Anterior choroidal artery (AChA) of internal carotid artery
142
What are the clinical findings in internal capsular strokes?
-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)
143
What are watershed areas? What are they causes by?
-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
144
What are transient ischemic attacks (TIA)?
-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
145
What are signs and symptoms of TIA? What are treatments?
-Weakness on one side of the body
-Vision problems
-Slurred speech
-Often resolve within 24 hours
-Treatments include medication, surgery, and lifestyle changes
146
What is cerebral edema?
-Internal pressure within the brain cortex caused by hemorrhage or edema from inflammation
-Serious consequence of stroke and can lead to early mortality
147
What is central perfusion pressure (CPP)? What is the normal values for CPP?
-The net pressure gradient that drives oxygen delivery to cerebral tissue
-Normal CPP is 55-60 mm Hg
148
What is intracranial pressure (ICP)? How is it measured? What are the normal values for ICP in adults?
-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
149
What are abnormal values of ICP that indicate intracranial hypertension?
20-30 mm Hg
150
What is the equation for CPP?
Mean arterial pressure (MAP) - ICP
151
What are brain events that reduce cortical perfusion pressure (CPP)?
-Hemorrhagic stroke
-Tumors
-Infection
152
Why does hemorrhagic stroke reduce CPP?
It leads to increased pressure in the brain and reduces cerebral perfusion
153
Why do tumors reduce CPP?
Brain tumors can create increased cortical pressure and reduce brain perfusion
154
Why does infection reduce CPP? What else can infection cause?
-It causes substantial changes in regulation of cerebral perfusion
-Infection can cause adult brain tumors
155
Are outcomes better with hemorrhagic or ischemic strokes?
Outcomes are typically better with hemorrhagic strokes
156
What sex is more likely to get adult brain tumors?
Males are more likely to get brain tumors than females
157
What is the Goldilocks curve for blood pressure?
-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
158
What has happened to the death rate of stroke patients since the 70's? Why has this change occured?
-Death rate fell 77%
-Greater awareness of symptoms
-Prompt medical attention (60 minutes door to ED)
-IV tissue plasminogen activator (tPA)
159
What is IV tissue plasminogen activator (tPA)? When is it administered?
-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
160
What is earlier treatment of thrombolytic treatment of stroke patients associated with?
-More frequent and independent ambulation at discharge
-Higher discharge rates to home vs SNF
-Reduced mortality and symptomatic intracerebral hemorrhage
161
What is a safe range of systolic blood pressure after a cerebrovascular accident?
Between 140-160 mm Hg
162
When should patients be mobilized after having a stroke?
-Patients should be mobilized 13-24 hours after receiving IV tPA
-Most hospitals follow a 24 hour period
163
What is the recommended dosing for out of bed for stroke patients?
-Early, lower dose out of bed activity is preferable to frequent, higher dose intervention
-First day 10-20 minutes
164
What are the steps involved with preparing patient for out of bed activities?
-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
165
What will the PT assess for a patient post stroke?
-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)
166
When should blood pressure be monitored with stroke patients? What are signs the patients BP has dropped too low?
-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
167
What are general guidelines for BP in post stroke patients?
-Keep systolic under 180
-Diastolic under 105
168
How should PT's assess for neurologic deterioration in stroke patients?
-Ask if they have new headache
-Acute hypertension
-Nausea or vomiting
-Changes in O2 sat
-Excessive SOB
-Syncope
169
What transfers are typically used with stroke patients? What should we protect throughout all of the transfers and why?
-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
170
What are outcome measures typically used for stroke patients in acute care?
-6 minutes
-TUG
-5 times sit to stand
-10 meter walk test
171
How does the sympathetic system effect the heart?
-Increases HR
-Increases BP
172
How does the sympathetic system effect sweating?
Increases sweating
173
How does the sympathetic system effect the eyes?
-Dilates pupils
-Widely opens eyelids
174
How does the sympathetic system effect the digestive system?
-Decreases secretion of digestive juices
-Decreases bowel motility
175
How does the sympathetic system effect blood sugar?
Increases blood sugar
176
How does the sympathetic system effect the lungs?
-Opens airways
-Bronchodilation
177
How does the sympathetic system effect muscle tone?
Increases muscle tone
178
How does the parasympathetic system effect the heart?
-Decreases HR
-Decreases BP
179
How does the parasympathetic system effect sweating?
Decreases sweating
180
How does the parasympathetic system effect the eyes?
-Constricts the pupils
-Relaxes the eyelids
181
How does the parasympathetic system effect the digestive system?
-Increases secretion of digestive juices
-Increases bowel motility
182
How does the parasympathetic system effect blood suagr?
It doesn't/encourages normal blood sugar levels
183
How does the parasympathetic system effect the lungs?
-Bronchoconstriction
-Constricts the airways
184
How does the parasympathetic system effect muscle tone?
Encourages normal muscle tone
185
What are the two divisions of the autonomic nervous system?
-Sympathetic
-Parasympathetic
186
What are the functions of the autonomic nervous system (ANS)?
-A division of the peripheral nervous system that influences organs and tissues
-Maintains homeostasis by regulating temperature and activity of internal organs
187
What does the ANS regulate?
-Circulation
-Respiration
-Digestion
-Metabolism
-Secretions
-Body temp
-Reproduction
188
What regions of spinal nerves does the parasympathetic system come from?
-Cranial nerves
-Sacral nerves
189
What regions of spinal nerves does the sympathetic system come from?
-Thoracic nerves
-Lumbar nerves
190
What is the sympathetic division also known as?
Fight or flight
191
What is the parasympathetic division also known as?
Rest and digest
192
What structures in the brain trigger the fight or flight response?
-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
193
What does the sympathetic trunk consist of?
-Preganglionic sympathetic fiber
-Postganglionic sympathetic fiber
-Collateral ganglion
194
What are Betz cells and where do they originate from?
-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
195
What is the pathway for motor impulses?
-Primary motor cortex
-Through the brain
-To the brainstem
-Midbrain
-Pons
-Medulla
-Through the spinal cord
196
What are the two corticospinal tracts? Where do they cross?
-Lateral corticospinal tract
-Crosses at cervicomedullary junction
-Anterior corticospinal tract
-Stays unilaterally and crosses over at spinal cord level to innervate bilateral sides
197
What is the anterior corticospinal tract? What motor tracts does it contain? What muscles does it innervate?
-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
198
What is an upper motor neuron?
One long axon from the primary motor cortex to the anterior horn cell (CNS)
199
What are upper motor neuron lesions?
Trauma, diseases, or infections occurring in an upper motor neuron that is in the brain or spinal cord
200
What are lower motor neurons?
They involve the anterior horn cell and the peripheral nerves
201
What are lower motor neuron lesions?
Injuries, diseases, or infections associated with the lower motor neurons
202
Do all neurons in the lateral corticospinal tract travel contralaterally?
No, 10% of neurons in the lateral CST travel ipsilaterally and terminate in the ipsilateral spinal cord
203
What is the order that the motor system is activated in?
-Posterior sensory cortex sends goals
-Prefrontal cortex plans
-Premotor cortex sequences
-Motor cortex executes the actions
204
What are the 5 steps of voluntary motor activation?
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
What are the methods of nervous system muscle activation?
-Motor neuron pools
-Systematic method of increasing activation: Henneman's Size Principle
-Increase the rate of stimulation
206
What is a motor neuron pool?
-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
What is Henneman's Size Principle?
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
What are the three types of alpha motor neurons? What is their relative excitabilities?
-S type (slow): small and highly excitable
-FR type (fatigue resistant): big and average excitability
-FF type (fatiguable): biggest and low excitability
209
What is the neural activation size principle?
-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
What do the primary motor cortex and premotor cortex have in common?
Both project directly to the spinal cord and are capable of some direct control of movement
211
What is the purpose of the supplementary motor area (SMA)?
-Internally generates plan of movement
-Planning of sequences of movement
-Coordination of the two sides of the body such as bi-manual coordination
212
Where does the lateral corticospinal tract decussate?
At the cervico-medullary junction in the lower medulla
213
Where does the anterior corticospinal tract decussate?
At the spinal cord level
214
Where does the anterior corticospinal tract end? Why does it end there?
-It ends at the mid thoracic area
-Because it primarily innervates the bilateral axial and shoulder girdle muscles
215
What is proprioception?
Awareness of static joint position
216
What is kinesthesia?
Awareness of dynamic joint positions
217
What are free nerve endings?
-Unmyelinated
-Pain
-Heat
-Cold
218
What are Delta fibers?
-Myelinated free nerve endings
-Carry sharp, stabbing, and pricking pain, or cold
-High threshold
-Immediate pain
219
What are C fibers?
-Unmyelinated free nerve endings
-Carry dull, achey pains
-Higher activation threshold than delta fibers
-Polymodal pain receptors (Chemical, heat, mechanical, hypoxia)
220
What is the sizes of axons of different nerve types from smallest to largest? How fast does each travel?
-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
What is the muscle spindle (MS)?
-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
How does the muscle spindle work and communicate?
-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
What reflexes test the integrity of the muscle spindle and why?
-Deep tendon reflexes
-Because it causes a quick stretch which makes the muscle contract quickly, which the muscle spindle detects
224
How does the muscle spindle aid in reciprocal inhibition?
-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
What are the two major sensory pathways?
-Anterolateral pathway
-Spinothalamic tract
-Dorsal columns (medial leminiscal pathway)
226
What sensory information goes through the anterolateral pathway?
-Pain
-Temperature
-Crude touch
227
Where does the anterolateral pathway decussate?
Spinal cord
228
What sensory information goes through the medial leminiscal pathway?
-Vibration
-Joint position
-Fine touch
229
Where does the medial leminiscal pathway decussate?
Medulla
230
What is the Golgi Tendon Organ (GTO)?
-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
How does the GTO work?
-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
What are gamma motor neurons?
Type II motor neurons that reset the muscle spindle after activation
233
What does an Upper Motor Neuron UMN) syndrome involve?
-Motor cortex and pathways
-Brainstem
-Cerebellum
-And/or involves the spinal cord and its coordination
234
Where does an UMN injury reside?
-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
Where does and LMN injury reside?
-Anterior horn cell
-Peripheral nerve
236
What causes UMN syndrome?
The result of the disruption of central motor pathways that arise from the cerebral cortex and pathways in spinal cord
237
What are the main motor tracts?
-Corticospinal tracts
-Corticobulbar tracts
238
What are signs of UMN lesions in the brain & brainstem?
-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
What area of the brain is associated with decreased muscular control in UMN syndrome?
Cerebellum
240
What is clonus?
Repeated rhythmic contractions of individual muscle groups
241
What is tone? What is it independent of/exclude?
-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
What does tone reflect?
-Muscle state (relaxation)
-Independent of strength, coordination, or involuntary movement
243
What is the range of muscle tone from least to greatest?
-Flaccidity (LMN)
-Hypotonia
-Normal
-Hypertonia (UMN)
-Rigidity
244
What is hypertonia?
-Increase in passive muscle tightness
-Abnormally increased resistance to an external force about a joint
245
What are the three classifications/subcategories of hypertonia?
-Spasticity
-Rigidity
-Dystonia
246
What is spasticity?
-Velocity dependent increase in tonic stretch reflexes w/ exaggerated tendon jerks, resulting from the hyper excitability of the stretch reflex
-At multiple joints
247
What is rigidity?
-Significant increase in resistance to multidirectional external force about a joint
-Usually seen in end stage Parkinson's Disease
248
What is dystonia?
-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
What are common upper limb postures or synergies that are seen in UMN syndrome?
-Flexed elbow
-Bent wrist
-Pronated forearm
-Clenched fist
-Thumb in palm
250
What is a common synergy pattern for people that have had strokes?
-Upper extremity flexion synergy
-Lower extremity extension synergy
251
What is movement ataxia? What area of the brain is it associated with?
-Loss of coordination, tremors, overshooting, loss of velocity
-Associated with cerebellum
252
What is bradykinesia? What part of the brain is it associated with?
-Slowness of movement
-Associated with the basal ganglia and Parkinson's disease
253
What is the grading system for reflexes?
-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
What are associated movements?
-Moving one part of the body and another limb moves involuntarily
-Loss of complete selective control
255
What is an advanced brain lesion?
-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
What are signs and symptoms of a cerebrovascular accident/stroke?
-Initially flacid
-Later develops spasticity
-Reflexes hyperactive
-Synergistic movements
-Clonus
-Sensory loss
-Cranial nerve changes (facial weakness and vision changes)
-Bladder changes
257
What is a John Doe spinal cord injury?
-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
What are different types of incomplete spinal cord injuries?
-Central cord
-Brown Sequard
-Anterior cord
259
What is Brown Sequard syndrome?
-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
What is a transverse cord lesion?
A complete spinal cord injury, which effects all motor & sensation under the level of injury
261
What is lost on the involved side in spinal cord injuries?
Vibration & proprioception
262
What is lost on the uninvolved side in spinal cord injuries?
Loss of pain & temp.
263
What are signs of lower motor neuron lesions?
-Loss of muscle function (weakness/flaccid)
-Loss of sensation
-Tone: hyporeflexia
264
What are other LMN lesion signs?
-Fibrillations (muscular twitching)
-Fasciculations (worm-like contraction)
-Hypotonia/atonia
265
Where should you test when examining LMN lesions? Why?
-Test above, parallel, & other side of where the lesion is
-Because some peripheral nerve disease spread, like Guillan Barre
266
What are nerve root injuries? How do they occur?
-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
What is Carpel Tunnel Syndrome? What is the clinical presentation?
-Injury to the median nerve
-Atrophied thenar eminence
-Weakness or paralysis
-Pain along nerve
-Numbness along nerve
-Sensory loss
-Loss of ROM
268
What are the muscles involved in carpel tunnel syndrome?
-Flexor pollicis brevis
-Opponens pollicis
-Abductor pollicis brevis
269
What muscle testing should be done for a peripheral nerve injury?
-Test muscles on uninvolved side
-Test muscles on involved side
-Test muscles of adjacent peripheral nerves
270
What sensory testing should be done for a peripheral nerve injury?
-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
What are signs and symptoms of injury to the deep fibular nerve/common fibular nerve?
-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
What muscles are involved in common fibular nerve injury?
-Fibularis longus & brevis
-Tibialis anterior, EHL, EDL
273
What are signs and symptoms of a C6 nerve root injury?
-Sensory loss following the C6 dermatome
-Hyporeflexia
-Decreased DTR
-Weakness
-Pain
-Tingling and numbness following C6 distribution
274
What are the muscles involved in the C6 nerve root injury?
-Biceps
-Brachioradialis
-Wrist extensors
275
What is diabetic neuropathy?
-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
What can dysfunction of the basal ganglia and its connectivity lead to?
-Movement disorders (dyskinesias)
-Akinesia
-Bradykinesia
-Hyperkinesia
277
What does dysfunctions in the direct pathway of the basal ganglia lead to?
-Hypokinesia
-Under-stimulation (more inhibition of motor cortex)
-Loss of automatic movements
-PD
-Rigidity
-Bradykinesia
278
What does dysfunctions in the indirect pathway of the basal ganglia lead to?
-Over-stimulation (less inhibition of cortex)
-Hyperkinetic
-Chorea
-Huntington's
279
What is the ranking of basal ganglia movement disorders by movement speed (slowest to fastest)?
-Bradykinesia, hypokinesia
-Rigidity
-Dystonia
-Athetosis
-Chorea
-Ballismus
-Tics
-Myoclonus
-Tremor
280
What is lead pipe rigidity?
-Continous throughout whole movement
-Agonist and antagonist involved
281
What is cogwheel rigidity?
-Ratchet like interruptions as the limb is passively moved
-Normal stretch reflexes
-Shoulders and cervical spine first affected
-Prolonged results in contracture
282
What is the definition of pain?
Unpleasant or emotional experience associated with, or resembling that associated with, actual or potential tissue damage
283
What is pain influenced by?
-Pain is always a personal experience
-Biological, psychological, and social factors
284
What is the difference between pain and nociception?
-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
What role does pain serve in our lives?
It serves as an adaptive and protective role
286
What can pain have adverse effects on?
-Function
-Social and psychological well-being
287
What are biological factors that can affect pain?
-Genetics
-Physiology
-Neurochemistry
-Tissue health
288
What are social factors that can affect pain?
-Socioeconomic status
-Social support
-Social learning
-Skepticism
-Operant
289
What are psychological factors that can affect pain?
-Perceived control
-Self-efficacy
-Catastrophic thinking
-Hypervigilance
-Depression
-Anxiety
-Anger
290
What is the #1 thing that can help with chronic pain?
TENS
291
How should pain be assessed?
-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
What is Article 1 in the International Association of the Study of Pain (IASP)?
The right of all people to have access to pain management without discrimination
293
What is Article 2 in IASP?
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
What is Article 3 in IASP?
The right of all people with pain to have access to appropriate assessent and treatment of the pain by adequately trained healthcare professionals
295
What are risk factors/habits that contribute to chronic pain?
-Diet
-Sleep
-Stress
-Physical activity
-Sedentary behavior
-Smoking
296
What is the first thing to ask patients about and tackle with chronic pain?
Sleep!!!
297
What are the different types of pain fibers?
-Delta fibers
-C fibers
298
What are delta fibers?
-Myelinated
-Higher conduction velocity than c fibers
-Mechanical or pressure
-Sharp pain
299
What are C fibers?
-Unmyelinated
-Slow conduction velocity
-Thermal, chemical, or mechanical
-Dull ache
300
What is the difference between peripheral nerve vs muscle injury?
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
What substances are constantly released in chronic pain? How does it work?
-Glutamate
-Substance P
-They increase the pain perception
302
How can we help override painful sensations?
By giving different sensations
303
What is acute pain?
-Normal response to painful stimulation
-Contributes to survival by protecting the tissue from further damage
304
What is adaptive pain?
Protects tissues and promotes healing
305
What is maladaptive pain?
-Process presenting as a disease
-Represents pathological functioning of the nervous system
306
What is chronic pain?
-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
What does the normal physiologic response to pain involve?
-Injury: physical and chemical
-Response: nerve, vessels, immune cells, prostaglandins
-Nerves release substance P
-CGRP released: vasodilator from sensory nerves
308
What is substance P?
-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
How is substance P correlated with nervous system pain?
-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
What is allodynia?
Pain from "non-painful" stimuli (nociplastic)
311
What is analgesia?
Absence of pain sensation
312
What is hyperalgesia?
Increased sensitivity to painful stimuli
313
What is sensitization?
Increased responsiveness of nociceptive neurons to their normal input, and/or recruitment of a response to normally subthreshold movements
314
How is pain classified?
-Nociceptive
-Neuropathic
-Nociplastic
315
What is neuropathic pain subdivided into?
-Peripheral nerve pain
-Central brain or spinal cord pain
316
What is nociplastic pain subdivided into?
-Peripheral sensitization
-Central sensitization
317
What is peripheral sensitization?
-Increased responsiveness and reduced threshold of nociceptive neurons in the periphery
-Pain felt from a non-noxious stimuli such as a feather
318
What is central sensitization?
-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
What can nociplastic pain cause?
Negative neuroplasticity
320
What is nociceptive pain?
-Pain arising from a noxious stimuli
-Somatic and non-neural
-Localized
321
What is neuropathic pain?
Pain initiated or caused by a primary lesion or dysfunction in the nervous system
322
What is nociplastic pain? What does it cause?
-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
What can cause central sensitization?
Increased responsiveness can be due to dysfunction of endogenous pain control systems such as the spinalthalamic tract & reticular formation off shoots
324
What is the "chemical soup" around an injury?
-Substance P
-CGRP
-Histamine
-Prostaglandin
325
Where can substance P be found in peripheral sensitization?
-Peripheral areas
-Dorsal horn
326
What are the tracts that are invovled in centralized pain?
-Anterolateral
-Spinoreticular
327
What tract synapses onto the brainstem reticular formation (RF)? How is this structure related to pain? What does it connect to?
-Spinoreticular tract
-Awareness and arousal to pain
-Connects to the hypothalamus
328
What tract synapses onto the periaquedcutal gray? Where is this structure located and how does it relate to pain?
-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
Where do the anterolateral and spinoreticular tracts synapse onto before going to the cortex?
-They both synapse on the thalamus
-Then they synapse onto the cortex
330
What structures in the brain are involved in central sensitization?
1. Thalamus to
-Anterior cingulate cortex (ACC)
-Amygdala
-Prefrontal cortex
2. Hypothalamus
-Hippocampus
-Amygdala
-ACC
3. Hippocampus
331
What is the descending pathway? How does it modulate pain?
-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
What are other factors that can affect pain?
-Drug abuse
-Financial difficulties
-Cultural barriers
-Litigation
-Language barriers
-Lack of health insurance
333
What are some non-pharmacologic ways of managing pain?
-Exercise
-Patient education
-Taping
-PT/OT
-ROM exercises
-Weight loss
334
What is the best thing a PT can do for someone with chronic pain?
-Listen to them!!!
-Acknowledge their pain
-Promote socialization and activity (hobbies, altruism, family, etc.)
335
What does effective pain education involve?
-Listening
-Pain science concepts
-Patient understanding
-Reflective questions
-Validation
-Tailored to education level
-Ongoing process
-Individualizing
336
What is the pain reduction theory?
-Providing a different stimulus that utilizes the dorsal column pathway
-Providing a different sensation, the dorsal column will inhibit the pain pathway
337
What is the gate control theory?
-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
Can negative neuroplasticity be reversed?
It can be reversed, but most of the time, not fully
339
How can NSAIDs help in pain reduction?
-Reduces prostaglandins
-Prostaglandins plays a role in the peripheral and central sensitization process
340
What is Capsaicin? How is it used to treat pain? How long does it take to work?
-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
Are there any side effects to Capsaicin? What conditions is it good for?
-No side effects
-Good for arthritis and muscular pain
342
What are some common pain/chronic pain conditions?
-Phantom limb pain
-Hand shoulder syndrome (post mastectomy)
-Pelvic pain
-Chronic low back pain
-Autoimmune conditions
-Fibromyalgia
343
What pain condition automatically gets placed in the sensitization category? Is it peripheral or central sensitization?
-Fibromyalgia
-Almost always in both peripheral and central
344
How does phantom limb pain occur?
-The person is missing sensory input to the somatosensory cortex
-The brain perceives it as pain
-Negative neuroplasticity
345
What is chronic regional pain syndrome (CRPS)?
-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
What kind of pain is CRPS?
Allodynia
347
What are treatments for CRPS?
-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
What is the efferent sympathetic fibers formed by?
Formed by gray matter in the thoracic and lumbar spinal cord
349
How does the sympathetic division effect blood flow to the muscles and heart?
-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
What nerve provides about 75% of the parasympathetic outflow?
Vagus nerve (CN X)
351
What cranial nerves are involved in the parasympathetic system? Where does the other portions of the parasympathetic system come from?
-CN III (oculomotor)
-CN VII (facial)
-CN IX (glossopharyngeal)
-Sacral nerves
352
What are the functions of the parasympathetic system?
-Pupillary response
-Stimulates saliva
-Constricts bronchi
-Peristalsis/secretion
-Bile release/liver
-Bladder contracts
-Constricts pupil
353
What nerve in the parasympathetic system controls the bladder and reproductive system?
Pelvic splanchnic nerve
354
What are the ganglionic neurons in the parasympathetic system? What are their target organs?
-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
What kinds of receptors are part of the autonomic nervous system?
-Mechanoreceptors
-Chemoreceptors
356
Where are autonomic pressure receptors found?
-Aortic baroreceptors
-Carotid sinuses
-Lungs
357
Where are the autonomic stretch receptors found?
Respond to distention in the veins, bladder, or intestines
358
Where are the autonomic chemoreceptors found?
-Carotid and aortic bodies (responds to oxygen)
-Medulla (respond to hydrogen ions and carbon dioxide)
359
What is the afferent information from the heart?
Baroreceptors in carotid and aortic bodies which send information to the medulla along CN IX and X
360
What is the efferent information to the heart?
-Efferent to spinal cord-sympathetic trunk: accelerates HR
-Efferent parasympathetic directly to SA node: slows HR
361
What neurotransmitters does the sympathetic system use?
-Acetylcholine
-Norepinephrine
362
What neurotransmitters does the parasympathetic system use?
Acetylcholine
363
What are cholinergic agonists? What do they do? What condition might they be used for?
-A group of medicines that mimic the actions of acetylcholine
-Increases transmission
-Can be used for myasthenia gravis since they lose acetylcholine
364
What are anticholinergics? What do they do? What condition might they be used for?
-Drugs that block the action of acetylcholine
-Decreases sweat and peristalsis
-Bronchodilator
-Can be used for COPD
365
How does diaphragmatic breathing affect the ANS and stress? What technique can be used?
-Deep breathing stimulates the parasympathetic nervous system
-4-7-8 technique (in 4, hold 7, out 8)
-Reduces cortisol (stress hormone)
-Increases attention
366
What are common pathologies of the autonomic nervous system?
-Spinal cord injury above T6
-Parkinson's disease
-Postural orthostatic tachycardia syndrome
367
What happens to the autonomic nervous system if someone has a spinal cord injury above T6?
-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
How does Parkinson's affect the ANS?
-Dysautonomia: GI system, temperature dysregulation, pupillary
-Orthostatic hypotension (from levodopa)
-Sympathetic innervation (blood pressure drops)
369
What are symptoms associated with postural orthostatic tachycardia syndrome (POTS)?
-Cardiac instability
-Fainting
-Postural hypotension
-Weakness
370
What can timely out of bed and upright activity prevent in patients with CVA? What is a potential complication of early out of bed?
-DVT
-Pulmonary emboli
-Pneumonia
-Falls
-11% of patients experienced progression of lesion with early OOB
371
What should be monitored with patients with CVA during OOB and upright activities? What activity should we avoid during early OOB activities?
-Orthostatic hypotension
-High intensity exercise should be avoided in the acute phase following a CVA (wait at least 3 months)
372
What are common characteristics of gait in patients with CVA?
-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
What are common assistive devices for people with CVA?
-Hemi-walker
-Cane
-Quad cane
374
What kind of gait pattern is usually seen in a patient with a CVA who used a cane?
-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
What hemisphere in the brain is associated with language and processing? What lobes are the language areas in?
-Left hemisphere
-Frontal and temporal lobes contain the language centers
376
What hemisphere of the brain is considered the dominant hemisphere?
The left hemisphere
377
What is the function of the right hemisphere?
-Spatial awareness
-Body awareness
378
If someone has a right hemisphere CVA, what symptom would they most likely experience?
Neglect
379
What is the function of Broca's area? Where is it located?
-Expressive language and the ability to produce language
-Inferior frontal lobe in the left hemisphere
380
What is the function of Wernicke's area? Where is it located?
-Language comprehension
-Temporal lobe in the left hemisphere
381
What structure connects the Broca and Wernicke areas?
White matter called the arcuate fasciculus
382
What is the blood supply to the Broca area, Wernicke area, and arcuate fasciculus?
-Broca: Middle cerebral artery superior division
-Wernicke: MCA inferior division
-Arcuate fasciculus: MCA superior & inferior divisions
383
What is aphasia? What is affected?
-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
What is expressive aphasia? What are the signs and symptoms?
-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
What is receptive aphasia? What are the signs and symptoms?
-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
What happens if there is an occlusion of left stem MCA?
-Global aphasia
-R hemiplegia
-Frontal-temporal-parietal lesion
-Speaking, listening, & reading impaired
-Limited speech
-Impaired auditory comprehension
-Brain damage is massive
387
What is the recovery of aphasia like? What is the time frame?
-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
What are some tips for working with people with aphasia?
-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
What spatial problems commonly occur in people that have non-dominant hemisphere strokes?
-Left sided neglect is closely related to right temporo-parietal function and posterior parietal cortex
-Right MCA stem stroke
390
How does neglect often manifest?
-It manifests as a sensory deficit and a failure to pay sufficient attention to sensory input
-Lateralization of attention (selective or directed attention)
391
What is typically the cause of severe right neglect?
A bilateral lesion
392
What is hemi-neglect syndrome?
-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
What are tasks that are a common difficulty in patients with non-dominant hemisphere lesions?
-Visual-spatial analysis
-Construction abilities
-These patients also often present with severe personality and emotional changes
394
What are interventions for spatial/hemi-neglect?
-Forced use
-Constraint induced used
-Patching the unaffected eye so they are forced to use affected eye
395
What is the association cortex?
-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
Where does the unimodal motor association cortex project into? What is its function?
-It projects predominantly to the primary motor cortex
-It is important for formulating the motor program for a complex action involving multiple joints
397
What does the heteromodal association cortex project/connect to?
-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
What is the association cortex divided into?
-Frontal heteromodal association cortex (prefrontal cortex)
-Motor association cortex (unimodal)
-Somatosensory association cortex (unimodal)
-Lateral parietal and temporal heteromodal association cortex
399
What is the function of the frontal part in the association cortex? When does the frontal lobe mature in females and males?
-Executive function
-Complex behavior
-Motor planning
-Females: 18
-Males: 25
400
What is the function of the temporal part in the association cortex?
Recognition
401
What is the function of the parietal part in the association cortex?
-Attention
-Awareness
402
What is the function of the association cortex?
-Higher order sensory processing
-Motor planning
-Language processing and production
-Visual-spatial orientation
-Socially appropriate behavior
403
What are the 3 major divisions of the frontal lobe? What is another division?
-Primary motor cortex
-Premotor cortex
-Prefrontal association cortex
-Frontal eye fields ( state of enlightenment)
404
What is the premotor cortex responsible for?
-Planning movements
-Speech
405
What is the prefrontal association cortex responsible for?
-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
How is the frontal eye fields connected to the superior colliculus?
They work together to help to alert you to things such as car accidents
407
What is the function of the frontal lobe?
-Being socially apprpriate
-Restraint
-Initiative
-Order
-Working memory (i.e. where did I park)
408
What are the subcortical connections of the prefrontal association cortex?
-Amygdala
-Thalamus
-Hippocampus
-Basal ganglia
-Hypothalamus
409
Who was Phineas Gage?
-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
What is the function of the dorsolateral prefrontal cortex?
-Regulation of attention and behavior
-Attention and working memory
-Cognitive control
-Executive functions
411
What is the function of the orbitofrontal prefrontal cortex?
-Impulse control
-Social judgement
-Involvement in associating things
-Rewards
-Cognition
-Personality
-Involved in conscious reappraise strategies to emotional regulation
412
What structures are involved in working memory?
-Prefrontal cortex
-Amygdala: emotional memory
-Hippocampus: long term memory
-Cerebellum: procedural memory
412
What is short term memory?
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
What is the function of the amygdala?
-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
What is the function of the hypothalamus in relation to the limbic system?
-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
What is the function of the hippocampus in relation to the limbic system?
-Required for the formation of conscious memory
-Facilitate learning and memory processing
416
What is the function of the prefrontal cortex in relation to the limbic system?
-Modulation of emotions
-Inhibitory inputs to the amygdala
-Component in traumatic brain injury (loss of emotion modulation)
417
What are the main structures in the limbic system? What are the substructures?
Main Structures
-Hippocampus
-Hypothalamus
-Amygdala
Substructures
-Cingulate cortex
-Thalamus
418
What is the function of the limbic system?
-Emotion
-Behavior
-Memory
-Motivation
-Olfaction
-Decision making
419
What is the limbic system also called?
The primitive brain
420
What is the function of the thalamus in relation to the limbic system?
Relays information from sensory organs to cerebral cortex
421
What is the function of the cingulate cortex in relation to the limbic system?
-Primary cortical component of the limbic system
-Involved in emotional and cognitive processing
422
What are the diencephalic structures of the limbic system?
-Anterior thalamic nuclei
-Hypothalamus
423
What are the fiber tracts connecting the limbic system?
The fornix
424
How is the olfactory bulb involved with the limbic system?
-It is not an actual part of the limbic system, smells trigger feelings
-We associate certain smells with feelings and memories
425
How fast do autonomic reactions with the limbic system occur?
Within 100-500 milliseconds
426
What area of the brain is the limbic system primarily associated with?
-Involves multiple brain structures primarily the prefrontal cortex
-Involves behavior
427
What is apraxia? Are lesions that cause apraxia localized?
-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
Do patients with aphasia often have apraxia?
Typically one third of patients with aphasia also have apraxia
429
What is dyspraxia?
-Movement based problem
-Clumsy, unable to manipulate objects properly
430
What is preservation? What can be the cause of this?
-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
What is ideation apraxia?
The individual cannot recall how to perform everyday activities (i.e. using toothbrush to brush hair)
432
What is attention deficit hyperactive disorder (ADHD)? What are signs and symptoms?
-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
What are the three layers of tissue in the visual system?
-Retina (part of CNS)
-Uveal tract
-Sclera
434
What structures are part of the retina?
-Optic disc
-Fovea
435
What are the three components of the uveal tract?
-Choroid
-Ciliary muscle
-Iris
436
What is the function of the choroid?
Rich capillary bed for nourishment of photoreceptors
437
What is the function of the ciliary muscle?
-Surrounds the lens
-Adjusts the lens
438
What is the function of the iris?
Pupillary constriction
439
What is the sclera?
Outermost fibrous tissue
440
What is the cornea?
Outer structure that permits the flow of light into the eye
441
What is the function of the vitreous humor?
Contains phagocytic cells to pick up debris
442
What is the fovea? What is its function?
-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
What are the two types of photoreceptors in the retina? What are their functions?
-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
What does the primary visual pathway involve?
-CN II
-Optic tract
-Optic radiation
445
Where does the optic tract decussate? Does all of it cross over?
-Decussates at optic chiasm
-Only 60% crosses over at optic chiasm
446
What is the main target of the optic tract? How much of the tract synapses onto this target?
-Major target is dorsal lateral geniculate nucleus (LGN) in the thalamus
-90% synapse here
447
What is the secondary target of the optic tract?
Optic radiation onto the visual cortex
448
When does the optic nerve become the optic tract?
After the optic nerve passes through the optic chiasm, it becomes the optic tract
449
What is a good way to see if there is a horizontal lesion across the whole brain? Why?
Testing CN II because it spans the whole horizontal portion of the brain
450
Where is the visual cortex located?
Thalamus
451
How does the pupillary light reflex work?
-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
What half of the retina does not cross over/decussate?
Temporal half of the retina
453
What part of the visual field does the temporal half of the retina provide?
It provides the nasal visual field
454
What half of the retina decussates at the optic chiasm?
The nasal half decussates at the optic chiasm
455
What part of the visual field does the nasal half of the retina provide?
It provides the temporal visual field
456
What is the monocular visual field?
-Closing one eye
-Each eye visualizes a visual field: divided into quadrants
457
What is the binocular field?
-Two foveas focus on two visual hemi fields
-Temporal fields more extensive than nasal
458
What is left homonymous hemianopsia? What causes it?
-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
What is monocular visual loss?
-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
What are the two types of neuronal transmission?
-Electrical
-Neurotransmitters
461
How is electrical neuronal transmission carried out?
-Information is processed electrically
-Ionic current flows passively through synaptic junction
462
What is an advantage to electrical neuronal transmission?
The main advantage of electrical synapses is that the signal transduction occurs at a very high speed through the gap junctions
463
How is neurotransmission carried out?
-Neurons communicate with each other by secreting and responding to neurotransmitters (chemicals)
-Medication influences the chemical interactions between neurons
464
How do ions move through the synaptic membrane? What do they move in response to?
-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
What is post synaptic receptor transport?
-Receptors are anchored to post synaptic membrane
-G-protein coupled receptors
-May directly open channels or indirectly open channels (via second messenger)
466
What are the two main types of channels?
-Non-gated: open all the time (leaky)
-Gated: generally have two states, open or closed
467
What are voltage gated ion channels?
-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
What do calcium channel blockers do?
-They target voltage gated calcium channels in the heart
-Nifidepine
-Lowers blood pressure
469
What are modality gated channels?
-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
What is the Na+-K+ pump?
-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
What is a neurotransmitter?
-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
What are neuromodulators?
-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
What are the cholinergic neurotransmitters?
Acetylcholine (ACh)
474
What are the amino acid neurotransmitters?
-Aminobutyric acid (GABA)
-Glutamate (Glu)
-Glycine (Gly)
-Aspartate
475
What are the amine neurotransmitters?
-Dopamine (DA)
-Histamine
-Norepinephrine (NE)
-Serotonin (5-HT)
-Melatonin
476
What are the peptide neurotransmitters?
-Endorphines
-Enkephalines
-Substance P
477
What is another neurotransmitters that does not fall in the main categories of neurotransmitters?
Nitric oxide (NO)
478
What are the strictly excitatory neurotransmitters?
-Acetylcholine
-Glutamate
-Aspartate
-Nitric oxide
479
What neurotransmitters are both excitatory and inhibitory?
-Dopamine
-Norepinephrine
-Histamine (mostly inhib.)
-Endorphines (mostly inhib.)
-Enkephalines (mostly inhib.)
480
What neurotransmitters are strictly inhibitory?
-GABA
-Glycine
-Serotonin
481
What is the most widespread excitatory neurotransmitter?
-Glutamate
-It provides 90% of excitatory function in the brain
482
What is glutamate associated with? What happens when glutamate levels are too high?
-Attention, learning, and function
-High levels leads to cell death by setting off inflammation (too many calcium ions entering cells causing excitotoxicity)
483
How does glutamate play a role in neuroplasticity?
-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
What is GABA? What is its function?
-Gamma aminobutyric acid
-Main inhibitory neurotransmitter
-Counters glutamate
-Activation of GABA induces sleep patterns
-Found throughout the brain and spinal cord
485
What is Gabapentin? What does long term use cause?
-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
What are uses of the neurotransmitter GABA?
-Neuropathic pain management
-Anti-spasticity medication
-Anti-seizure medication
487
What is the function of acetylcholine?
-Facilitatory
-Released in the neuromuscular junction
-ANS preganglionic and postganglionic neurons
-Receptors: nicotinic, muscarinic
488
What is the function of dopamine?
-Generally excitatory
-Movement
-Memory
-Rewards and motivation
-Involved in addiction
-Limbic (happiness)
-Retina
-Found in CNS (brain stem, basal ganglia, substantia nigra)
489
How do drugs of abuse such as cocaine and other amphetamines affect the reward pathways?
-They affect the reuptake leading to longer dopamine acticity, which produces euphoria
-Requires more drugs/higher doses to produce the same effect
490
What causes Parkinson's disease?
Loss of dopaminergic neurons in the substantia nigra
491
What is the function of serotonin?
-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
What are low levels of serotonin associated with? What medication can help?
-Depression
-Prozac is a selective blocker of serotonin reuptake resulting in serotonin remaining in synapses longer
493
What is the function of norepinephrine? Where is it found?
-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
What are common antidepression medications?
-Tricyclic antidepressants (TCA)
-Serotonin-norepinephrine reuptake inhibitors (SNRI)
-Effexor
-Cymbalta
-These drugs keep neurotransmitters in the synpatic cleft longer
495
What is Ritalin?
-ADHD medication
-Increases norepinephrine and dopamine
496
How does norepinephrine affect the amygdala?
It affects the amygdala which is involved in control of attention and responses
497
What neurotransmitters are involved in fight or flight? How do they affect the organs?
-Epinephrine and norepinephrine
-Increases HR
-Triggers the release of glucose from energy stores
-Increases blood flow to skeletal muscle
498
What is substance P? Where is it found? What do high levels lead to?
-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
What medication attacks substance P?
Motrin
500
What are endorphins? When are they released?
-Endogenous neuropeptides
-Releases positive feelings
-They are produced by the central nervous system and the pituitary gland
-They are released during aerobic exercise
501
What is brain derived neurotrophic factor? What causes the release of BDNF?
-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
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How does BDNF affect the hippocampus?
Associated with higher learning and memory
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How does BDNF affect the cortex?
Facilitates nerve growth, differentiation of synapses
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How does BDNF affect the basal forebrain?
Helps with long term memory
