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OT 6000 > OT 6000 Test 4 > Flashcards

OT 6000 Test 4 Flashcards

1
Q

Cerebellum- pontocerebellar

A

Portion of cerebellum that knows what was intended to do for action

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2
Q

Cerebellum- Spinocerebellar

A

Portion of cerebellum (along with vestibular portion) that knows what actions you are actually doing

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3
Q

Cerebellum- brainstem and motor cortex

A

Make corrections in action to match what was meant to do and what was actually done

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4
Q

Gray matter of cerebellum

A

Gray matter outside of the cerebellum is packed with cell bodies and is responsible for comparing what body is doing to what was actually done

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5
Q

Cerebellar inputs

A
  • *What I am doing
    1. Spinal cord: discriminitive touch
    2. Reticular formation: what is the urgency of the movement?
    3. Vestibular system: inner ear shows head movement and the pull of gravity
  • *What I meant to do
    4. Pontine nuclei: xerox copy coming from cerebral cortex down pons and into the cerebellum
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6
Q

Cerebellar outputs

A
  1. Purkinje cell: takes the result of the processing down to the base of the cerebellum and passes signal to cerebellar nuclei
  2. Cerebellar nuclei: takes signal to brainstem for gross motor UMN’s and to the cerebral cortex for fine motor UMN’s
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7
Q

Vertical divisions of the cerebellum

A
  • Midline vermis: anitomical midline that controls to midline axial skeleton
  • Paravermal hemisphere: controls the most proximal joints (shoulders and hips)
  • Lateral hemisphere: controls the distal muscles
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8
Q

Flocculonodular lobe

A

Lobe of the cerebellum that helps maintain equilibrium

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9
Q

Cerebellar Peduncles (inferior, middle and superior)

A
  • Inferior: brings messages of what I’m actually doing to the cerebellum (input from SC and brainstem)
  • Middle: brings in the xerox copy of what was meant to be done (input from the pontine nuclei)
  • Superior: Takes messages up to the cerebellum to makes corrections if needed (output to brainstem and cerebral cortex)
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10
Q

Functional Divisions of the Cerebellum:

Spinocerebellum division:

A

Vermis and paravermis- core and proximal muscle control (braimstem connection= low voluntary control)

  • Input: spinocerebellar tracts (discriminitive touch and non-conscious proprioception- “what I am actually doing”) and sensorimotor cortex (compares what you meant to do with what you did)
  • Output: Medial division UMN’s of cerebral cortex and brainstem (ipsilaterally)
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11
Q

Functional Divisions of the Cerebellum: Vestibulocerebellum division

A

Flocculonodular lobe- balance and equilibrium

  • input: inner ears
  • output: vestibular nuclei> eye muscles (steady gaze for balance) and postural muscles (keep you upright)
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12
Q

Functional Divisions of the Cerebellum: Cerebrocerebellum division

A

Lateral hemispheres- fine motor control (cortex connection= high voluntary control)

  • Input: cerebral cortex
  • Output: lateral division UMN
  • **passes on the “xerox copy” of movement plan to coordinated movement and timing
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13
Q

Signs of damage in the cerebellum

A
  • Signs are always ipsilateral (same side as damage)

- Often include Ataxia (incoordination due to muscle weakness)

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14
Q

Vermal and floculonodular damage

A

Leads to truncal ataxia- issues controlling the trunk of body

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15
Q

Spinocerebellar damage

A

Leads to gait ataxia-issues controlling the lower trunk directly over hips (wide-base unsteady and staggering).
-runs to spinocerebellum; damage here also leads to limb ataxia: intentional action tremor, dysmetria (impaired ability to hit target) and dysdiadochokinesia (issues with rapid, alternating, reversing movements around joint)

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16
Q

Cerebrocerebellar damage

A

Leads to hand ataxia: issues coordinating fine motor movement in hands

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17
Q

Vestibulocerebellum damage

A

Leads to nystagmus: eye movement problems leading to balance deficits (truncal ataxia) and equilibrium issues

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18
Q

Paravermis and hemisphere damage

A

Leads to dysarthria: disordered production of speech ( speech varies in pitch, volume and rate like a drunk person)

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19
Q

Cerebellar vs. Somatosensory Ataxia

A
  • Cerebellar ataxia: Cerebellum cannot compare and correct information on planned movement
  • ->issues with coordination- eyes open or closed, but will have normal sensation of touch
  • Somatosensory ataxia: information never reaches cerebellum to communicate “what you are really doing.”
  • ->pt with this ataxia will be able to substitute sensory info with visual info- as long as eyes open, balance stays. However; there will be no normal sensation of touch
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20
Q

Basal ganglia overview

A

The “control circuit”- sends output to the cortical UMN’s and the brainstem UMN’s
-This helps plan movement in the cortex of “what I meant to do” compared to “what I want to do”

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21
Q

Motor influence of the basal ganglia

A
  • Influences the cortical UMN’s via the thalamus (BG influence is inhibitory, thalamus’ is excitatory)
  • ->voluntary movement
  • Influences the brainstem via the pedunculopontine nucleus (inhibitory) AND via the midbrain locomotor region (influence becomes excitatory after the locomotor)
  • ->Pedunculopontine “inhibits the inhibitor”- inhibits the reticulospinal tracts that are the postural muscle inhibitors
  • ->Locomotor region is the stepping pattern generator
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22
Q

Components of the basal ganglia

A
  • Substantia nigra: most important component- has the cells which create dopamine, which runs the internal communication and processing in the BG (adjusts and/or inhibits output from BG)
  • Caudate: “what I want to do”
  • Putamen- “what I am doing”
  • Globus pallidus- based on info, what is my movement plan
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23
Q

Basal ganglia input and output

A
  • Input is always excitatory: Glutamate, Acetylcholine and Serotonin
  • Output is ALWAYS INHIBITORY: either inacts GABA or runs it off
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24
Q

Goal-directed behavior loop of basal ganglia

A

Executive functioning: evaluating information for making decisions, planning, choosing actions in context and learning
-found roughly on hairline

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25
Q

Emotional loop of basal ganglia

A

Emotions and motivations that lead to motor plan, reward seeking, making predictions of outcomes and integrating emotions with facial expressions

  • found roughly on forehead
  • damage here leads to impulsive patients
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26
Q

Social behavior loop of basal ganglia

A

Recognizing social cues, regulating self-control, and distinguishes relevant from irrelevant information

  • found roughly behind eyebrows
  • damage here will lead to someone not understanding social boundaries or socially acceptable behavior
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27
Q

Oculomotor loop of basal ganglia

A

Decisions about spatial attention and eye movement and directs eye muscles to “look at” something
-Found roughly on top of head

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28
Q

Motor loop of the basal ganglia

A

Regulates muscle contractions, force of contractions, order of muscle contractions and multi-joint movements (all needed for muscle synergy)

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29
Q

Basal ganglia’s role when initiating plan of movement

A
  1. Suppresses any ongoing motor programs
  2. Facilitates appropriate muscles to move in the way you want
  3. Inhibits muscles that produce unwanted or unnecessary movement
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30
Q

Parkinson’s disease in relation to basal ganglia

A
  • Parkinson’s (a hypokinetic disorder) causes the death of dopamine producing cells in the substantia nigra
  • This death leads to an increase of basal ganglia output, causing:
    1. Too little activation of voluntary muscles
    2. Too much activation of postural and girdle muscles (stiff posture)
    3. Too little activation of locomotor region (stepping pattern generator)
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31
Q

Huntington’s Disease in relation to basal ganglia

A
  • Huntington’s disease is a hyperkinetic disorder which cause the degeneration of basal ganglia and cerebral cortex
  • Dopamine is available but the input into the basal ganglia has diminished, which causes a DIMINISH in basal ganglia output
  • ->this leads to too much activation of voluntary muscles and too little activation of postural and girdle muscles (choreaform, or writhing/twisting, movement is the norm)
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32
Q

Feedforward vs Feedback control of balance

A
  • Freeforward: I anticipate the loss of balance and prepare in such a way that I don’t lose it
  • Feedback: recovering after something has knocked you off balance
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33
Q

Rami classification

A
  • Anterior Rami: all axons that feed arms, legs and front of body
  • Posterior Rami: all axons that feed the back
  • Communicating Rami: take autonomic neurons too and from peripheral synapse
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34
Q

Plexus damage

A

All plexuses are distal to spinal nerves and proximal to peripheral nerves
-Any damage done to a plexus will be peripheral in nature

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35
Q

Spinal nerve vs peripheral nerve damage

A
  • Damage to one spinal nerve: dermatome pattern of sensation loss (one whole dermatone sensation is lost) and myotomal pattern of motor loss (many muscles weak but not paralyzed)
  • -> example: bulging disc
  • Damage to one peripheral nerve: peripheral pattern of sensory loss (will lose some but not all of dermatome sensation) and peripheral nerve pattern of motor loss (small number of muscles paralyzed)
  • ->example: tunel of Guyon
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36
Q

Peripheral nerve bundles

A
  • Endometrium surrounds individual axon
  • Perineurium surrounds bundles of axons (makes a fascicle)
  • Epineurium surrounds bundles of fascicles
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37
Q

Axons of peripheral nerves

A
  • A-alpha: efferent- extrafusal muscles
  • Ia, Ib, II: afferent- proprioception
  • A-beta: afferent- exteroception
  • A-gamma: efferent- intrafusal muscles
  • A-delta: afferent- pain, temp, viscera
  • B: efferent- presynaptic autonomic
  • C: afferent- pain, temp, visera (dull aching pain)
  • C: efferent- postsynaptic autonomic (sharp pain)
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38
Q

Plexuses

A
  • Cervical= C1-C4
  • Brachial= C5-T1
  • Lumbar= L1-L4
  • Sacral= L4-S4 (only plexus containing CNS AND PNS axons)
  • *One PN gets input from many different spinal levels, one spinal level branches out to many different peripheral nerves
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39
Q

How movement improves nerve health

A
  • Improves blood flow
  • Facilitates gliding of nerves and fascicles
  • Facilitates antereograde and retrograde axoplasmic transport
  • Lack of movement leads to physical stress on neural membrane (Nn get stuck on connective tissue)
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40
Q

Neuropathy classification by number of sick Nn

A
  • Mononeurophathy- one sick nerve. Example: unilateral carpal tunnel
  • Multiple mononeuropathy- several sick Nn. Example: bilateral carpal tunnel
  • Polyneuropathy- many sick Nn. Example: glove sensation loss of fingers, hands and wrists
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41
Q

Traumatic myelinopathy

A

A classification of neuropathy by severity: least severe (prognosis very good)
-caused by compression and ischemia of a nerve that puts the axon to sleep (hand asleep). Usually axon wakes up soon, but if ischemia is prolonged the myelin will die and recovery may take days or weeks

42
Q

Traumatic axonopathy

A

A classification of neuropathy by severity: not severe (prognosis good)
-Axon dies and degenerates distally to point of injury (Wallarian degeneration), but proximal axon survives and regrows (1 in per month)

43
Q

Severence

A

A classification of neuropathy by severity: prognosis “guarded,” but possibly severe
-Axon AND connective tissue tube is cut, proximal may not reconnect or may reconnect to wrong pathway

44
Q

Cauda Equina description

A

Spinal cord ends at L1-L2, cauda equina is portion of spin below this
-Cauda equina contains axons, ventral roots and dorsal roots that are headed down from SC to the body

45
Q

Distinguishing SCI’s by type of damage

A

Level of damage will either be “bony”- damage to the spinal column- or “neuro”- damage to the spinal cord
–>This helps determine what spinal level damage is at

46
Q

Dorsal root organization

A

Dorsal root holds sensory axons:

  • Medial group: do not enter dorsal horn but bypass it straight to the dorsal column to travel up SC (axons of discrimitive touch and conscious proprioception)
  • Lateral group: enter the dorsal horn and synapse there, then cross the midline before traveling up SC (axons of temp and pain)
47
Q

Spinal segment

A

A section of spinal cord that has all of the axons associated with ONE spinal nerve

48
Q

Anterolateral spinal region

A

White matter column and region of pain. Contains:

  • spinothalamic: discriminative pain
  • Reticulospinal- wake up after pain
  • Spinomesincephalic: turn head towards pain
  • Spinoemotional: emotional and autonomic response to pain
49
Q

Lateral spinal region

A

White matter column and region for distal extremity control. Contains:
-Lateral corticospinal: highest level of extremity movement

50
Q

Medial spinal region

A

White matter column and region for proximal muscle control. Contains:

  • medial corticospinal: control of proximal muscles
  • vestibulospinal: keep you up against gravity
  • reticulospinal: helps you pick stuff up against gravity
51
Q

Autonomic spinal region

A

White matter column and region for autonomic control

52
Q

What is located in: dorsal horn, lateral horn and ventral horn?

A
  • Dorsal horn: cell bodies of the sensory pathway found here
  • Lateral horn: cell bodies of peripheral autonomic found here (no lateral horns in cervical spine)
  • Ventral horn: cell bodies of LMN,s here (proximal=medial, distal=lateral)
53
Q

How many synapses needed for one A-Alpha?

A

20,000 to 50,000 synapses for one single A-alpha

-takes all input and determines common theme for action

54
Q

Phasic stretch vs withdrawel reflex

A
  • Phasic stretch: stretch of spindles- same muscle you stretch is the one that contracts
  • Withdrawel reflex: pain causes withdrawel that is multi-muscle and multi-segment due to branching pain pathway
55
Q

Bladder control

A
  • Parasympathetic efferent: contracts bladder to empty
  • Sympathetic efferent: Relaxes bladder not to empty
  • Somatic efferent: voluntarily contracts external sphincter
  • Stretch of bladder wall: initiates emptying reflex up through the sacral spinal cord
56
Q

Stretch reflex of bladder

A

Bladder walls stretch as filled, which activates afferent alert to brain to initiate emptying reflex

  • if it is ok to go: higher center relax external sphincter to allow emptying reflex to finish (increasing PNS and decreasing SNS)
  • if it is NOT ok to go: higher centers try to stop emptying reflex by contracting external sphincter (decreasing PNS and increasing SNS)
57
Q

What happens if autonomic nerves are cut at level of bladder reflex?

A
  • If it is a peripheral autonomic nerve, it will cut off the bladder reflex
  • if it is a spinal autonomic nerve, the reflex will increase (can lead to Autonomic Dysreflexia)
58
Q

Touch and proprioception vs pain and temperature tracts- do they cross over?

A
  • Touch and Proprioception only cross over in the medulla, so if there is damage in the spinal cord, the signs and symptoms will be ipsilateral (same side)
  • Pain and temperature cross over at whatever level they enter the cord, so the signs and symptoms will be contralateral (opposite side)
59
Q

Segmental vs tract lesions

A
  • If only one segment is broken, but tract is in tact, there will only be symptoms on THAT SPINAL LEVEL
  • If a tract is broken, there will be symptoms AT AND BELOW that spinal level
60
Q

Segmental pattern lesion- signs and symptoms

A
  • Dermatomal sensory loss
  • Myotomal motor loss: weakness, hypotonia, hyperflexia of reflexes
  • Autonomic loss in that one segment: including red skin and no sweating in that dermatome
61
Q

Tract pattern lesion- signs and symptoms

A
  • Sensory loss in all segments below lesion
  • motor loss in all segments below lesion: paralysis of disuse, hyperflexia of reflexes
  • autonomic loss in all segments below lesion
62
Q

What spinal level would complete destruction of C6 be?

A

C7 and below: because the damage on C6 is what has cut off the signal, so C7 and below have been cut off from signalling higher

63
Q

Anterior cord syndrome

A

Pt able to feel light touch and proprioception, but unable to contract muscles or feel pain below level of SCI

64
Q

Central cord syndrome

A

Inflating syrinx (water balloon of CSF) cuts off the central Nn- pt will begin to lose pain and temp sensation

  • Syrinx damage will begin to ascend if not addressed
  • this will eventually cut off ventral horns and pt will slowly lose motor functions of proximal muscles
  • Dorsal columns usually stay in tact, but if damage unaddressed it could be permanent
65
Q

Brown-Sequard Syndrome

A

Hemi section: left side cut= lose touch and voluntary muscle control on left side, but would lose pain on right side (contralateral)
-vice versa

66
Q

Cauda Equina injury

A

Would lead to DENERVATED paralysis and HYPOFLEXIVE reflexes (cut off reflex loop at the peripheral)

67
Q

Spastic bladder vs flaccid bladder

A
  • Spastic bladder: reflex loop in tact but cognitive or higher level function cut off, stopping it from emptying; when bladder is full, signal to empty bladder will be released but won’t reach cortex
  • Flaccid bladder: cauda equina damaged, SC will never know that bladder is full so the bladder will continue to fill until in overflows
68
Q

Most common causes of SCI

A

MVA
Sports injuries
Falls
Penetrating wounds (gun shot, stabbing)

69
Q

Neurological level of SCI

A

Lowest (most caudal) level with normal sensory and motor function (at least 3/5 MMT)

70
Q

Autonomic dysfunction after SCI

A

Autonomic function will be cut off to whole body after SCI: loss of blood shunting, loss of ability to sweat and impaired capacitance (leads to low BP) and muscle pumping (leads to blood pooling in extremities)

71
Q

Cranial nerve axon insulation

A

1 and 2 are insulated by oligodendrocyte because they are found entirely in head. The other 10 are insulated by Schwann cells because they are in the brainstem

72
Q

Cranial nerve introduction

A

Cranial Nerves:

  1. Are peripheral sensory nerves (damage leads to SAME SIDE signs and symptoms)
  2. Are lower motor neurons
    3: Gets input from UMN’s of the corticobrainstem tract
73
Q

CN I- Olfactory- function and location

A
  • Function: smell
  • Location: buried in the bone of the sinus- pokes out of the nasal sinus
  • Tracts to: Amygdala (primal brain- assesses smells as threat) and parahippocampal gyrus
74
Q

CN I dysfunction

A

Anything that traumatizes the brain can sheer off these Nn by shaking skull (like a MVA)

  • Loss of smell
  • This will change taste of food (may be first sign of damage)
75
Q

CN II- Optic- function and location

A
  • Function: vision

- Location: bundle of axons that live in the retina

76
Q

CN’s III (oculomotor), IV (trochlear) and VI (abducens) function

A

All work to move the eyes

  • IV: allows you to look down and in, as if looking at tip of nose
  • VI: abducts in a straight plain- look to the side in a straight plain
  • III: does EVERYTHING ELSE for eye movement- straight up, straight down, adduction, ect.
77
Q

CN V- Trigeminal- function

A

Very large in diameter because it innervates face, which has a high density of sensory neurons
Has sensory and motor functions:
-Motor: chewing and speaking (mandible movement)
-Sensory: all sensation in front of face (think Kenny from South Park)- discriminative touch, proprtioception (mandible), discriminitive pain, divergent pain

78
Q

CN V- dysfunction

A
  • Sensory loss- same side as damage
  • loss of blink reflex
  • jaw weakness
  • trigeminal neuralgia: pain in CN V from non-painful stimulus (like wind blowing in face)
79
Q

CN VII- Facial- function

A
  • Some sensory from tongue, pharynx and ear
  • Taste in anterior 2/3 of tongue (sweet, salt and sour)
  • ALL muscles of facial expression
  • Gland control- salivary, nasal and lacrimal
80
Q

CN VII dysfunction

A
  • Ipsilateral (same side) symptoms, usually of facial control
  • Bell’s Palsy: damage to LMN decrease facial expression: paresis of all facial muscles on ipsilateral side of face (eyes can’s close tight and smile is droopy)
81
Q

CN VII damage vs Stroke symptoms

A
  • Lower facial droop with upper face still in tact= CVA (1/4 face weakness)
  • Both upper and lower face drooping= Bell’s Palsy (1/2 face weakness)
82
Q

CN VIII- Vestibulocochlear- function

A
  • Transduction of sound
  • Converts air waves to water waves- this creates action potentials
  • ->air pressure> vibration> connector bones> push on inner ear> creates water waves in inner ear> shake hair cells back and forth> this creates AP to brain
  • ->One end of cochlea is wide (slow and low frequency), and one side is narrow (fast and high frequency)
83
Q

Inferior colliculus, reticular formation function, and temporal lobe (CN VII)

A
  • Inferior colliculus: automatically turns head towards sound
  • Reticular formation: helps modulate arousal in response to sounds (why loud noises wake you up and soft noises put you to sleep)
  • Temporal lobe: makes sense of sound coming into the brain (passes through thalamus)
84
Q

CN VIII- dysfunction

A
  • Conductive hearing loss: affects the conversion of air waves to water waves
  • Sensorineural hearing loss: receptor cells not creating action potentials (can be caused by death of hair cells)
  • Tinnitus: extra action potentials from the inner ear- signals when there is no stimulus, due to inner ear irritation (especially hair cells)
85
Q

CN IX- Glossopharygeal- function

A
  • Taste in back 1/3 of taste (bitter)
  • begins the swallow and gag reflex
  • somatosensation from soft palate, and pharynx
  • parotid salivary glands: releases saliva to mush food for swallow
  • Carotid sinus: stretch receptor to determine BP
86
Q

CN IX- dysfunction

A
  • Unable to swallow or gag normally

- cannot release saliva to mush food

87
Q

CN X- Vagus- function

A
  • Sensory and motor innervation for all muscles of pharynx and larynx
  • innervates viscera in thorax and abdomen
88
Q

CN X- dysfunction

A
  • Difficulty speaking: hoarse voice (vocal folds cannot come together)
  • Difficulty swallowing- cannot close flap over wind pipe (leads to aspiration)
  • Poor digestion (can lead to constipation)
  • Asymmetric elevation of soft palate (unable to resonate voice normally)
89
Q

CN XI- Spinal Accessory- function and dysfunction

A
  • Function: Elevates upper trapezius and sternocleidomastoid

- Dysfunction: will lead to neck weakness

90
Q

CN XII- Hypoglossal- function and dysfunction

A
  • Function: controls extrinsic muscles of tongue
  • Dysfunction: difficulty speaking T, D, and TH sounds, issues swallowing (pushing food back to throat) and tongue weakness (will point to side of damage)
91
Q

Cranial nerves- three stages of swallowing

A
  • Oral stage: V- mastication, VII- lips and cheeks keep food in, XII- move food from side to side and to back of mouth
  • Laryngeal/Pharyngeal stage: IX- senses food for need to swallow, X- closes flap of windpipe to begin swallowing
  • Esophageal stage: X- finishes swallowing
92
Q

Cranial nerves for speaking

A
  • CN X: Larynx- keeps vocal folds together. Soft palate- resonating cavity
  • CN V: jaw- move for air to enter mouth and tongue to move
  • CN VII: lips: come together to make mechanical sounds for speech
  • CN XII: tongue- T, D, TH sounds of tongue on hard palate
93
Q

Functions of peduncles

A
  • Middle peduncles: what I meant to do
  • Inferior peduncles: what I am really doing
  • Superior peduncles: change movement if needed to correct
94
Q

Areas of brainstem

A
  • Base of brainstem: primarily motor “descending” tracts
  • Tegmentum: sensation tracts, including pain
  • Tectum: The “roof” of the fourth ventricle, holds the colliculi together
95
Q

Superior vs inferior colliculi

A
  • Superior: turns head towards VISUAL response

- Inferior: Turns head towards AUDITORY response

96
Q

Four outputs of the reticular formation

A
  1. Up to the head- regulates consciousness, arousal and sleep wake cycle
  2. All three horns of the spinal cord- dorsal, lateral and ventral horns
    - Dorsal horn: influences synapse of pain- descends to turn pain signal down
    - Lateral horn: autonomic and visceral control from pons and medulla down to SC
    - Ventral horn: cell bodies of LMN’s- slightly depolarizes LMN’s to help them reach fight or flight
97
Q

Damage to vertical tracts of brainstem

A

Will produce contralateral signs and symptoms, as opposed to spinal segments which lead to ipsalateral signs and symptoms

98
Q

Vertebral artery stroke on one side

A

Will have symptoms on OPPOSITE side of body, but SAME side of face as damage.

99
Q

Disorders of specific brainstem regions

A
  • Vertical tracts for body- contralateral signs and symptoms
  • Cranial nerves- ipsilateral signs and symptoms
  • Cerebellum- ipsilateral signs and symptoms
  • Autonomic- ipsilateral signs and symptoms
100
Q

Four D’s of brainstem dysfunction

A
  • Dysphagia (damage to IX or X)- issues swallowing
  • Dysarthria (damage to V, X, VII, or XII)- difficulty with speech production
  • Diplopia (damage to III, IV or VII)- double vision
  • Dysmetria (damage to cerebellum)- cannot hit target

OT 6000 (8 decks)

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