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Exam 6 Flashcards

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USMLE® Step 1 flashcards
1
Q

Define proprioceptor. List receptors involved. Types of proprioception.

A
  • sense of self – joint angle, muscle length, muscle tension
  • Receptors = joint receptors, muscle spindles, GTOs, skin tactile receptors (Ruffini corpuscles sense stretch of skin)
  • Types = static (joint position), dynamic (joint movement)
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2
Q

Define adequate stimulus

A
  • This refers to the receptor specificity, the type of stimulus a receptor is sensitive to.
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3
Q

Define sensory modality

A
  • vision, hearing, taste, smell, touch, pain, temp, itch, proprioception, vestibular sense
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4
Q

Define receptive field

A
  • region of tissue within which a stimulus can evoke a change in firing rate of neuron
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5
Q

Define graphesthesia

A
  • Sense through which figures/numbers on skin can be recognized.
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6
Q

Define stereognosis

A
  • Ability to recognize objects through touch alone.
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7
Q

Compare and contrast a receptor potential and AP.

A
  • Receptor potential: change in membrane potential by a transducer (converter) mechanism.
  • Stimuli causes receptor potential which is a depolarization. If depolarization reaches threshold, an AP is generated. Rate of AP generation increases as receptor potential rises above threshold.
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8
Q

Describe how nervous system can code for the what, where, intensity and duration of a stimulus.

A
  • What: labeled line principle – chain of interconnected neurons from the sensory receptor sends info to brain to perceive it
  • Where: receptive field in skin (first order) = second order = third order = somatotropic map in brain. Accuracy of location improved by lateral inhibition (touch in surround of receptive field has decreased firing rate compared to center of receptive field)
  • Intensity: a. increasing frequency of nerve fibers impulses from a particular nerve, b. increasing number of nerve fibers
  • Duration: continuous signal during stimulus, having on-off signal
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9
Q

Define the following as it relates to adaptation of receptor, include examples of somatosensory receptors of each type

a. ) Rapidly adapting (aka phasic)
b. ) Slowly adapting (aka tonic)
c. ) Non-adapting

A
  • Definition of receptor adaptation: When stimulus of constant strength is maintained, freq of APs decreases with time.
    a. ) Rapidly adapting (aka phasic): Pacinian, Meissner’s corpuscles. Signal beginning and end of stimulus; signal change in intensity; cannot give continuous signal about stimulus.
    b. ) Slowly adapting (aka tonic): Merkel’s disks. Signals continuous info about stimulus strength and duration; not useful for stimulus duration and low stimulus intensity
    c. ) Non-adapting: Nociceptors. Never completely adapts. Lumped in often with slowly adapting.
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10
Q

Free-nerve endings

A
  • nociception, temp

- crude touch

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11
Q

Merkel’s disks

A
  • static discrimination of shapes, edges, textures

- slow adapting (tonic)

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12
Q

Meissner’s corpuscles

A
  • detection of slippage between skin and object held – grip

- rapidly adapting (phasic)

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13
Q

Pacinian corpuscles

A
  • vibrations transmitted through objects – skilled tool use

- rapidly adapting

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14
Q

Peritrichial nerve endings

A
  • aka hair-end organ, detects movement of objects on body surface via movement of hair
  • rapidly adapting
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15
Q

Classification of nerve fibers. Which is fastest, slowest? What kind of info is carried by each? Which type conducts APs at 100, 50, 20 and 1 m/s?

A
  • I: A alpha – 100 m/s – extrafusal muscle fibers, muscle spindle primary ending (Ia), GTO afferent (Ib)
  • II: A beta – 50 m/s – muscle spindle secondary ending, cutaneous mechanoreceptors (touch) axons
  • III: A delta – 20 m/s – fast pain, some temp receptors
  • IV: C – 1 m/s – slow pain, some temp receptors, SNS, post-G axons
  • note: A fibers myelinated, C fibers not
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16
Q

What is two-point discrimination? Which areas of body show best discrimination? The worst?

A
  • Test of tactile acuity
  • Best = lips, fingertips – high density of receptors and more cortical tissue devoted to analyzing signals
  • Worst = back and calf of leg
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17
Q

Dorsal column.

a. ) What kind of info is carried by this system?
b. ) Where does info in this system cross midline?
c. ) What kind of deficit is associated with damage to this system?

A

a. Fine tactile (two-point), vibratory sense, proprioception
b. Decussation of medial lemniscus in brainstem
c. Lesion = deficit in fine tactile, vibratory sense and proprioceptive discrimination

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18
Q

Anterolateral system.

a. ) What kind of info is carried by this system?
b. ) Where does info in this system cross midline?
c. ) What kind of deficit is associated with damage to this system?

A

a. nociceptive and thermal sensation
b. spinal cord at level of entry
c. lesion = deficit in pain, thermal sensation discrimination

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19
Q

What is the location of the somatosensory cortex? Describe the general organization of this area.

A
  • Location = parietal lobe (SI). BA 3, 1, 2
  • Each area contains separate and complete representation of body. Leg and foot = medial, squashing genitals into corpus callosum. Remainder of body from midline laterally.
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20
Q

In what pathologies is glove-stocking pattern of sensory loss seen?

A
  • Peripheral neuropathies. Tend to target longest nerves first – hands and feet (first). Seen in many pathologies including DM.
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21
Q

Describe Brown-Sequard syndrome

A
  • D/t spinal hemisection
  • Pain/temp loss (contra to lesion)
  • Proprioceptive/fine tactile/vibration loss (ipsi to lesion)
  • Monoplegia (ipsi to lesion) with pos Babinski
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22
Q

Describe symptoms following lesion to cerebral cortex or sensory part of internal capsule

A
  • Loss of fine tactile/vibration/proprioception and pain/temp loss contralateral to lesion
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23
Q

Differentiate between pain and nociception

A
  • Pain: perception of nociceptive sensory info

- Nociception: sensory response to a noxious stimulus, unconscious activity induced by harmful stimulus.

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24
Q

Identify and describe the different components of pain. Provide characteristics and physiological basis for each.

A
  1. ) Sensory (discrimination): perception of external/visceral info providing location, intensity and modality – primary and secondary somatosensory cortices
  2. ) Motivation (affective): emotional and SNS responses with behavior – frontal, limbic, brainstem
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25
Q

Physiologic vs pathologic pain – describe function, fiber types involved, stimuli that elicit response, describe pain

A
  • Physiologic: acute pain critical for survival, warning system. A delta (fast conduction), elicited by mechanical or thermal stimuli. Pain is sharp/prickling/electric/cutting sensation. With healing tissue, pain lessens.
  • Pathologic: chronic pain begins >1 second after stimulus and increases slowly, can become maladaptive (persists when no longer damage). C-fibers (slow conduction), elicited by chemical, mechanical and thermal. Pain is dull/throbbing/aching/nauseating.
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26
Q

Types of pain. Function?

A
  1. ) Nociceptive: “normal” physiologic pain, if chronic = pathologic – warning, protective function
  2. ) Inflammatory: acute or chronic – protective promotes healing
  3. ) Dysfunctional: no lesion found
  4. ) Neuropathic: damage to CNS/PNS, pathologic – no protective function
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27
Q

Origin of pain. Describe and include fiber types found in each.

A
  1. ) Somatic
    a. ) superficial (initial sharp = A delta, delayed = dull/burning = C fibers)
    b. ) deep
  2. ) Visceral
    - C-fibers, poorly localized accompanying other sx such as sweating, BP changes
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28
Q

Physiological steps of pain processing

A
  1. ) Transduction
  2. ) Transmission
  3. ) Modulation
  4. ) Perception
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29
Q

Type of pain receptors? Characteristics?

A
  • Type: mechanical, thermal, chemical

- High threshold (don’t respond to pain all the time), slowly adapting (once activated, keep firing)

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30
Q

Peripheral nociceptive processing

a. ) Mechanism of activation
b. ) What are silent nociceptors?
c. ) Components of inflammatory response?
d. ) Mechanism for primary sensitization
e. ) Describe how peripheral activation can lead to ANS response that contributes to cardinal signs of inflammation

A

a. Stimuli (mechanical, thermal, chemical) opens channel, membrane depolarizes, AP generated. Vasodilation, inflammation response occurs.
b. Silent nociceptors become activated by inflammatory mediators and then respond to typical stimuli of pain.
c. Activators = K, H, substance P (BV dilation), bradykinin, 5-HT; Sensitizers = PGs, LTs, ATP
d. Process of primary hyperalgesia: increased sensitivity to noxious and non-noxious stimuli in area immediately surrounding primary site of damage. How? Chemical-induced (eg. substance P) increased sensitivity; increased receptive field size; activation of silent nociceptors.
e. Adelta and C fibers can activate ANS in cord and ganglia = reflex response leading to redness, heat, swelling and pain – Triple response of Lewis (redness, edema and wheal/flare)

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31
Q

What is allodynia?

A
  • Pain resulting from non-noxious stimulus
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32
Q

What is hyperalgesia?

A
  • An increased response to a stimulus that is normally painful
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33
Q

Fibers responsible for sharp first pain in response to mechanical and thermal stimuli

A
  • A-delta myelinated
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34
Q

Fibers responsible for diffuse second pain in response to mechanical, thermal and chemical

A
  • C fibers unmyelinated
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35
Q

In the following locations, compare and contrast the pain fiber types seen – cutaneous, articular, muscle, viscera

A
  1. ) Cutaneous: A delta and C fiber
  2. ) Articular: 2 x C fibers:1 x A delta
  3. ) Muscle: as in articular
  4. ) Viscera: predominantly C fibers
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36
Q

Identify and describe the synaptic and neuronal arrangement and NTs involved in the spinal processing of nociceptive information.

A
  • Afferent fibers arrive through dorsal horn and the following synapsing occurs:
    a) A delta synapse in lamina I and V (carrying fast, acute pain) with 2nd order neurons
    b) C fibers synapse in lamina II and III (carrying slow, chronic pain) with 2nd order neurons
    c) 2nd order neurons in lamina V = WDR (wide-dynamic range) neurons as they receive both non-noxious (A alpha and beta) and noxious (A delta, C fibers indirectly) input.
  • NTs from A delta and C include: substance P, glutamate and neurokinin A. Glut activates AMPA receptor causing rapid depolarization of 2nd order fiber. Co-release of substance P with glutamate produces complex response allowing glut to act on NMDA receptor as well = long-last depolarization of 2nd order neuron.
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37
Q

Describe central sensitization

A
  • Secondary hyperalgesia = (PNS and CNS event) = prolonged/increased activation of nociceptors in periphery and projection into spinal cord. Wind-up process mediated by substance P, glutamate and other factors causing change in responsiveness of spinothalamic (2nd order) neurons. In case of WDR neurons, allodynia is occurring (pain resulting from non-noxious stimuli) – contributing to neuropathic pain.
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38
Q

Identify the major ascending pathways conveying nociceptive info and describe these wrt:

a. ) location in spinal cord
b. ) projection pathways (from, to)
c. ) sensory modalities conveyed
d. ) what information does the brain get

A
  • Ascending pathway for pain is the ALS (spinothalamic tracts)
    1. ) Paleospinothalamic
    a. medially in anterolateral columns of spinal cord
    b. from: lamina II, III and V to: DM nucleus of thalamus to: limbic system
    c. slow C fiber information carrying second pain
    d. dull, throbbing, poorly localized pain
  1. ) Neospinothalamic
    a. laterally in anterolateral columns of spinal cord
    b. from: lamina I, IV and V to: VPL nucleus of thalamus to: primary sensory cortex
    c. fast A delta fibers carrying first pain
    d. sharp, well-localized pain
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39
Q

Name of tract responsible for descending pain control – a.) motor response to pain and b.) eye movement and regulation of gaze to site of injury

A
  • a.) spinoreticular tract

- b.) spinomesencephalic tract

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40
Q

The sensory/discriminative component of pain is carried by what tract?

A
  • Neospinothalamic tract to somatosensory cortex
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41
Q

The emotional component of pain (affective, cognitive) is carried by what tract?

A
  • Paleospinothalamic tract to limbic system/brainstem
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42
Q

What brain regions are involved in perception of pain (both sensory and emotional/motivational aspects)?

A
  • Sensory aspect: somatosensory cortex
  • Emotional/motivational aspects:
    a. ) anterior cingulate gyrus (most consistent area involved): attention to pain, initiation of behavioral reactions to pain
    b. ) insular cortex: relay to limbic system (learning and pain memory) and hypothalamus
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43
Q

Define gate control theory of pain and describe its postulated mechanisms for modulating nociception and how it may provide a basis for kiss-the-boo-boo, pain control, acupuncture

A
  • Aalpha and beta fibers = low threshold, faster conducting fibers = activate inhibitory interneurons = reduced activation of spinothalamic/reticulothalamic fibers.
  • Adelta and C fibers = high threshold, slower conducting fibers = reduce activation of inhibitory interneurons = reduced inhibition of spinothalamic/reticulothalamic fibers.
  • Therefore kissing, rubbing, touching injury will cause activation of Aalpha/beta fibers first leading to reduced activation of spinothalamic fibers.
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44
Q

Describe sites of descending pain control. Describe mechanisms for action of analgesic meds.

A
  1. PAG (midbrain): activates enkephalin-releasing neurons projecting to raphe nuclei in brainstem, modulating ascending projections
  2. Nucleus raphe magnus (rostral medulla): 5HT projections to dorsal horn of spinal cord
  3. Locus coeruleus (pons): NE projections to dorsal horn of spinal cord
  • TCAs act to reduce reuptake of NE and 5HT
  • Opioids: act enkephalin-releasing sites in dorsal horn of spinal cord, nucleus raphe magnus, PAG and locus coeruleus
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45
Q

Identify and characterize the various types of pain syndromes (referred, projected, neuropathic, phantom, complex regional pain syndrome) and describe the apparent mechanism(s) for these.

A

A.) Referred: localization of pain to a site unrelated and often distant to actual origin. Mechanism: convergence of afferent signal form viscera to spinothalamic neurons receiving other somatic information.

B.) Projected: pain produced by irritation of nerve at ectopic site and localized to site of nociceptors of nerve and along tract of nerve. Mechanism: labeled line theory (chain of interconnected neurons).

C.) Neuropathic: associated with damage or alteration of nervous system, may be induced by otherwise mild stimulus resulting in intense pain. Does not require pathology. Example = diabetic neuropathy.

D.) Phantom: pain/sensations localized to missing areas d/t amputation or deafferented area. Reorganization of spinal cord and cortex thought to contribute to this pain.

E.) Complex regional pain syndrome: continuous burning pain long after seemingly trivial injuries accompanied with dystrophic changes in skin, hairs, nail, muscles and bone. Pain enhanced by SNS activation.

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46
Q

Define alpha motor neuron

A
  • Aka LMN, cell body in spinal cord that exits ventral horn and synapses onto skeletal muscle extrafusal fibers
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47
Q

What are gamma motor neurons?

A
  • Neurons that innervate intrafusal skeletal muscle fibers
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48
Q

What are skeletal-fusimotor neurons?

A
  • Neurons that innervate both extrafusal and intrafusal fibers. This is sometimes called beta innervation
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49
Q

Define motor neuron pool

A
  • All neurons that control one muscle
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50
Q

Define motor unit

A
  • one alpha motor neuron + all skeletal muscle fibers it innervates
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51
Q

Define fibrillation

A
  • spontaneous activity within single muscle fibers, not visible clinically
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52
Q

Define fasciculation

A
  • visible twitches of muscle involving one or more motor units
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53
Q

What size motor units innervate the following

a. ) EOM
b. ) Muscles controlling individual fingers
c. ) Large postural muscle
d. ) Limb muscles affected by polio

A
  • General idea here: many small motor units needed when fine control of muscle must occur
    a. ) small motor units
    b. ) small motor units
    c. ) large motor units
    d. ) polio affects very large motor units
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54
Q

How to increase muscle force production?

A
  • Recruit more motor units

- Increase firing rate of already used motor units

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55
Q

Henneman’s size principle

A
  • Recruitment of motor units from small to large
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56
Q

Describe the effects of LMN damage

A
  1. ) muscle atrophy
  2. ) hypotonia
  3. ) hyporeflexia or areflexia
  4. ) fasciculations
  5. ) fibrillations (possibly d/t upregulation of ACh receptors)
  6. ) paralysis (flaccid) if too many LMNs damaged
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57
Q

Describe the symptoms of disorders of UMNs

A
  1. ) Spasticity: hypertonia, hyperreflexia (overactive DTRs), velocity-dependent tonic stretch reflexes
  2. ) Babinski sign (extensor plantar response)
  3. ) Spastic paralysis (flaccid initially, then spastic)
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58
Q

Describe what happens if spinal cord is transected in terms of:

a. ) What effects are seen immediately? What is spinal shock?
b. ) What effects are permanent?
c. ) How would a patient’s condition change over time?

A

a. ) Spinal shock = flaccid paralysis (no resistance to joint bend), temporary loss of spinal cord reflex including micturition, loss of ANS function below level = hypotension, loss of temp control
b. ) Paralysis is permanent below level of lesion. Also permanent anesthesia below level of lesion.
c. ) Different reflexes return at different rates, patient develops hyperreflexia and hypertonia, Babinski, paralysis remains now spastic

FYI:
- Mechanism: blood supply increases after swelling decreases, hyperexcitability of alpha motor neuron pool d/t loss of descending inhibitory input, supersensitivity, collateral sprouting of afferents from dorsal root

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59
Q

What is the difference between voluntary movement and reflex activity in muscle?

A
  • Voluntary: purposeful movement initiated in response to a specific external stimuli or just because it was willed.
  • Reflex: involuntary, automatic response to external stimuli
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60
Q

Compare and contrast paralysis and paresis

A
  • Paralysis: complete loss of voluntary movement

- Paresis: muscle weakness, partial loss of voluntary movement

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61
Q

ALS affects what neurons

A
  • Both upper and lower MNs
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62
Q

Describe location, structure and innervation of muscle spindle and GTO

A
  1. ) Muscle spindle
    a. ) Location: parallel to extrafusal fibers
    b. ) Structure: fusiform structure
    c. ) Innervation: efferent = gamma motor neuron, afferent = primary ending = Ia fiber (monitors how fast muscle length is changing and current length) and secondary ending = II (gives muscle length, does not emphasize changes)
  2. ) GTO
    a. ) Location: in series with muscle at tendon
    b. ) Structure: ?
    c. ) Innervation: single group Ib fiber (measures muscle force/tension on muscle)
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63
Q

Alpha and gamma motor neurons.

a. ) Which innervates intrafusal muscle fibers?
b. ) Which is larger?
c. ) Describe function of beta-motor neurons/skeletofusimotor fibers.

A

a. ) Gamma innervates intrafusal fibers, alpha innervates extrafusal fibers
b. ) Alpha motor neurons are larger
c. ) Innervate both extrafusal and intrafusal muscle fibers

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64
Q

Function of co-activation of alpha and gamma motor neurons

A
  • When extrafusal fibers contract, muscle shortens and spindles would become unloaded.
  • To prevent this, gamma motor neurons are activated with alpha motor neurons and intrafusal spindles contract. Now length of muscle can be sensed.
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65
Q

Describe difference bw static and dynamic sensory information from muscle spindles. What afferent fibers are responsible for each?

A
  • Ia (primary ending) monitors how fast muscle length is changing and current length (dynamic sensing)
  • II (secondary ending) monitors current length, NOT changes (static sensing)
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66
Q

Function of muscle spindle

A
  • Measure length and changes in length of muscle
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67
Q

Function of GTO

A
  • Measures muscle tension
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68
Q

Describe role of gamma motor neurons in controlling muscle spindle response.

A
  • Contract muscle fibers
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69
Q

Draw neuronal circuit for stretch reflex (aka myotactic reflex) specifically the phasic stretch reflex.

A

see image in study guide

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70
Q

Describe how phasic and tonic stretch reflexes work and tell how they are tested.

A
  • Phasic stretch reflex: very brief stretch elicited by tapping on tendon.
    o Group Ia onto alpha motor neuron for extensor and via interneuron onto alpha motor neuron to inhibit flexor muscle
  • Tonic stretch reflex: longer lasting stretch caused by stretching a muscle and holding it at its new longer length
    o Group Ia and II fibers synapse onto alpha motor neuron for extensor. Reflex is used clinically to measure tone. Not very noticeable in neurologically normal patient, exaggerated in Parkinsonism. Velocity-dependent.
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71
Q

Describe reciprocal innervation in spinal cord. Relate to the concept of stretch reflex.

A
  • Refers to the process that takes place during stretch reflex where Group Ia fibers synapse onto alpha motor neuron for extensor (agonist), but also inhibit alpha motor neuron for flexor (antagonist) via an inhibitory interneuron.
  • NB for OMM
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72
Q

Describe how clinicians test muscle tone.

A
  • Tonic stretch reflex – stretching a muscle and holding it at its new longer length
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73
Q

Define term co-contraction and discuss situations where it would be used.

A
  • Simultaneous activation of agonist and antagonists at a joint
  • Used when first learning skilled movements – someone is very stiff at first. Also found in infants/children during postural development.
  • Thought to be inappropriately activated in children with CP
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74
Q

Draw neuronal circuits that include Ib interneuron and describe normal group Ib reflex.

A

see image in study guide

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75
Q

Describe flexion withdrawal and crossed-extension reflexes

A
  • When stepping on injurious stimulus, leg flexes to withdraw (flexor muscle activated, extensor inhibited).
  • In addition, contralateral leg extends (extensor muscle activated, flexor muscle inhibited)
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76
Q

Compare and contrast output of a muscle spindle and a GTO during muscle contraction and passive stretch.

A
  1. Muscle spindle
    - Spinal cord reflex (activation of alpha motor neuron to shorten muscle), also to cerebellum, relayed to cortex for conscious proprioception
  2. GTO
    - Spinal cord reflex (inhibition of alpha motor neuron to prevent increase tension), also to cerebellum and cortex
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77
Q

Discuss feedback system for regulating muscle tension.

A
  • This is the GTO reflex or group Ib reflex
  • When muscle contracts, there is increased tension detected by Ib fiber. This fiber synapses on Ib inhibitory interneuron to inhibit alpha motor neuron to homonymous muscle = decreased tension, therefore decreased action by Ib fiber.
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78
Q

Which is more sensitive to muscle contraction – muscle spindle or GTO?

A
  • GTO

- Muscle spindle more sensitive to passive stretch

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79
Q

Describe clasp-knife response and state when it occurs. Do neurologically intact people have clasp-knife responses?

A
  • Clinician tries to quickly bend patient’s knee (where this phenomenon is most easily demonstrated), resistance to flexion builds up gradually then at certain point, resistance to flexion suddenly decreases. D/t hyperactive stretch reflexes. Can be demonstrated with biceps when attempting to extend elbow.
  • Seen in individuals with UMN lesion.
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80
Q

Define spasticity

A
  • Type of hypertonia often seen with brain trauma, CP, spinal cord injury, may be found in MS
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81
Q

Define clonus

A
  • Oscillation in muscle stretch reflexes, maintained if muscle put under slight stretch
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82
Q

What is Renshaw cell? Function?

A
  • Provides recurrent inhibition in alpha motor neurons (agonist and antagonist)
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83
Q

Describe and give function of:

a. ) utricle and saccule
b. ) semicircular canals
c. ) vestibular hair cells – describe what direction of bending depolarizes and hyperpolarizes
d. ) endolymph

A

a. Otolith organs = utricle and saccule. Each contain macula with hair cells. Organs are sensitive to linear acceleration resulting from gravity (backward/forward tilt, forward acceleration and deceleration). Tonic receptor with tonic firing.
b. Semicircular canals: arranged at right angles to each other, contain hair cells stimulated by angular acceleration. Firing rotate changes on either side when head is rotated, brain compares this. Change firing rate from tonic firing during motion.
c. See a and b for location. Bending towards kinocilium (tallest stereocilia) = depolarization, bending away = hyperpolarization.
d. Endolymph is fluid bathing hair cells and has high concentration of K. When hair cells are bent towards kinocilium, K enters cell depolarizing it. Perilymph has low K.

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84
Q

Describe the VOR (vestibular-ocular reflex) in response to head tile and head turn

A
  • VOR is a response to small head rotations.
  • Eyes move in opposite direction to head turn (slow conjugate movement) to facilitate fixation on a visual target.
  • This is driven by vestibular input and occurs in dark or with eyes closed.
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85
Q

Describe the otolith-ocular reflex

A
  • Aka head tilt/static head reflex

- If head tilted to one side, eyes rotate in opposite direction to maintain visual field in horizontal plane.

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86
Q

Describe what happens to a patient’s eyes when you test them in a vestibular testing chair upon

a. ) first start turning them,
b. ) continued turning
c. ) end of turning
d. ) what is the slow phase of nystagmus
e. ) what is the fast phase of nystagmus
f. ) what do we call what happens at c.). Why do eyes do this?

A

a. ) VOR occurs and eyes slowly turn opposite direction of rotation
b. ) Eyes quickly move back to midline travelling in same direction as rotation – likely driven by normal centers responsible for saccadic eye movement
c. ) Eyes begin slow turn towards direction of rotation with fast movement opposite to the direction of rotation to bring eyes to midline
d. ) Slow phase of nystagmus in both a and c
e. ) Fast phase of nystagmus in both b and c
f. ) Post-rotatory nystagmus. After rotation, patients have illusion they are turning to opposite direction and eyes make those movements.

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87
Q

If a patient is in a coma can they exhibit both fast and slow-phase nystagmus?

A
  • Patients in a coma can have slow movement (VOR), but they don’t make fast movement back to midline.
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88
Q

In the following example, describe what directions the eyes are moving. Patient is sat in chair and a small amount of rotation is applied to the right while patient is asked to fixate one a spot, this causes a. (slow/fast-phase nystagmus) to the b. (right/left). Rotation is continued towards the right a few more times and c. (slow/fast-phase nystagmus) with d. (right-beating/left-beating) is seen. The rotation is ceased and e. (slow/fast-phase nytagmus) is seen to the f. (left/right).

A

a. slow-phase nystagmus
b. left
c. fast-phase nystagmus
d. right-beating
e. /f. both. Slow-phase to right with fast-phase to left.

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89
Q

Describe caloric testing of vestibular function.

a. ) How do eyes move if cold water is put in the canal?
b. ) How do eyes move if warm water is put in the canal?
c. ) What kind of eye movements would you see in a comatose patient?

A
  • Mnemonic: COWS (corresponding to fast phase). Cold water = fast-phase towards Opposite side, Warm water = fast-phase towards Same side. Slow-phase are opposite to fast-phase.
  • Why does this occur? Convection-induced movement of endolymph. Requires intact vestibular system. If patient in coma, slow-phase (run by VOR) is seen, no fast-phase seen. If brainstem lesion, eyes midline.
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90
Q

Physiologic slow-phase nystagmus is run by the VOR. True/False.

A
  • True.
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91
Q

Describe doll’s eye maneuver. When is it performed? What is being tested?

A
  • Way of evaluating brainstem function in an unconscious patient. With pt lying face upwards, open eyes and rotate head side to side. Comatose patient shows slow phase nystagmus set by VOR. Conscious patient can override the VOR.
  • NB: make sure spine is stable prior to doing this.
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92
Q

Give probable cause of BPPV. What symptoms are associated with this problem?

A
  • Otolith detached from membrane of utricle and lodged near an ampulla of posterior semicircular canal making it sensitive to gravity causing abnormal vestibular sensations. This can result from head trauma or viral labyrinthitis.
  • Vertigo episodes lasting 40 seconds or less. No hearing loss. Can accompany nausea and vomiting.
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93
Q

Give probable cause of Meniere syndrome. What symptoms are part of this syndrome?

A
  • Probably d/t imbalance bw production and reabsorption of endolymph.
  • Symptoms = sensation of ear fullness and pressure with transient decreased hearing and tinnitus in ear. Accompanied by severe acute vertigo causing nausea and vomiting.
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94
Q

Define vertigo. Explain why dizziness is an imprecise term.

A
  • World is spinning around or that one’s head or body is whirling.
  • Dizzy = light-headed, faint
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95
Q

Give three major roles for vestibular system. What sensory systems help the vestibular system fulfill these roles?

A
  1. ) Subjective awareness of body position and movement of body in space
  2. ) Postural tone and equilibrium
  3. ) Stabilization of eyes in space during head movements.
    - This system works in conjunction with visual and proprioceptive system
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96
Q

List main inputs and outputs of vestibular nuclei. Assign function to each output.

A
  • Input:
    a. neck proprioceptors and motor commands to bend neck
    b. cerebellum
  • Output:
    a. medial and lateral vestibulospinal tracts
    o Medial = control neck muscles and head position
    o Lateral = control of limb and trunk muscles for maintenance of balance and posture
    b. MLF to motor nuclei of EOM for VOR
    c. higher centers via thalamus to cerebral cortex – conscious awareness of body orientation and motion
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97
Q

Function of medial system motor pathways

A
  • Control of posture and locomotion – mainly axial and proximal muscles
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98
Q

Lateral vestibulospinal tract function

A
  • Facilitates motor neurons of extensor muscles (limb / trunk muscles)
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99
Q

Medial vestibulospinal tract function

A
  • Reflex head movements in response to vestibular stimuli, adjusts head in response to postural changes
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100
Q

Medullary reticulospinal tract (aka lateral reticulospinal tract) function

A
  • Many functions. Considering just skeletal muscle: facilitates motor neurons to flexors and inhibits extensors
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101
Q

Reticulospinal system function

A
  • integrates vestibular and other sensory input, activating locomotion and controlling its speed
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102
Q

Tectospinal (aka colliculospinal) tract function

A
  • Coordinates head and eye movements
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103
Q

Sensory input for the following reflexes. Where do these act – neck or limb?

a. vestibulocolic (vestibulo-cervical)
b. vestibulospinal
c. cervicocolic
d. labyrinth righting

A

a. ) vestibular system to neck, reflex controls head position
b. ) medial controls head/neck, lateral controls limb/trunk
c. ) neck muscles acting on neck muscles – synergistic with vestibulocolic reflex
d. ) same as vestibulocolic

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104
Q

Describe asymmetrical and symmetric tonic neck reflex. What kind of patient would exhibit these reflexes?

A
  • Asymmetrical: primitive reflex in young infants to about 6 months. If head is turned to one side, limbs on that side extend and limbs on other side flex. Fencer’s pose. Persists in CP children.
  • Symmetric: appears in infants around 4-6 months and disappears before age 1. When neck is extended, upper limbs extend and lower limbs flex. Persists in children with cerebral damage.
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105
Q

What is tonic labyrinthine reflex?

A
  • Tilting head back while lying supine causes back to stiffen or arch back, legs to extend and arms to flex. Found in newborns. In CP, this persists.
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106
Q

Compare and contrast feed-forward and feedback mechanisms for controlling posture.

A
  • Feed-forward (aka anticipatory): anticipate or predict effect of disturbance (environmental or motor command), apply corrective action before error in posture and before environmental disturbance of motor command
  • Feedback (aka compensatory): correction applied after error is detected, rapid and improves with practice and learning
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107
Q

Give location of stepping pattern generators (SPGs). What do SPGs do?

A
  • SPGs in spinal cord.
  • SPGs control stepping movements at hip and knee. They are networks of spinal interneurons which elicit alternating patterns of flexion and extension at knee and hip. These are activated by descending input. Coordination through commissural fibers.
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108
Q

Discussing swinging room experiment. Which age group, toddlers or adults was most strongly affected by visual stimulus?

A
  • Room approaches subject, they will assume they are falling forward and sway backward
  • Room moves away from subject, they will assume they are falling backward and swap forward.
  • Toddlers are more strongly affected and will either fall forward or backward.
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109
Q

List sensory systems involved in the control of posture.

A
  • Vestibular system: detect body sway through head motion
  • Proprioceptive: muscle spindles, GTOs, joint receptors
  • Cutaneous receptors: touch and pressure
  • Visual
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110
Q

Define posture and describe three behavioral functions of postural adjustments.

A
  • Posture = overall position of body and limbs relative to each other and orientation of these structures in space
  1. ) support head and body against gravity or other forces
  2. ) keep C of G aligned and balanced over base
  3. ) stabilize supporting part of body during movement of other parts
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111
Q

Describe decerebrate and decorticate postures. Describe briefly the lesions that cause each of these.

A
  • Decerebrate: extension of all four limbs and neck. Lesion to upper pons and also to caudal red nucleus above vestibular nuclei = facilitate motor neurons of the extensor muscles through lateral vestibulospinal and pontine reticulospinal tracts.
  • Decorticate: arms flexed, legs extended when lying on back with head straight forward. Lesion to internal capsule releases vestibulospinal and tonic neck reflexes, also upper midbrain/diencephalon lesions. If head is turned, the asymmetrical tonic neck reflex is initiated.
112
Q

Describe how adjustment of posture occurs during platform tilting and translation

A
  • Tilt back: toes lifted = gastroc stretched, stretch reflex destabilizes postures, continued tilt causes this reflex response to decrease over repeated trials to allow for forward sway
  • Translate backward: person leans forward stretching gastroc = stretch reflex opposes body way, this reflex occurs progressively earlier with repeated trials
113
Q

Why could a dorsal rhizotomy be useful in treating subject with decerebrate rigidity or CP child with lower limb spasticity?

A
  • Prevent afferent muscle spindle fiber from driving stretch reflex, therefore decreasing spasticity.
  • Dorsal rhizotomy is an attempt to open up gamma loop and decrease its effect.
114
Q

State the origins, terminations and functions of the following pathways

a. corticospinal
b. corticonuclear (aka corticobulbar)
c. rubrospinal

A

a. ) Corticospinal
- Lateral corticospinal: cortex (forearm and hand) – medulla (decussate into pyramids) – synapse with LMNs in ventral horn
- Medial corticospinal: cortex (axial and proximal limb) – pyramids – decussate in spinal cord before synapsing onto LMNs (or interneurons) in ventral horn
- Function: fractionated movement of skeletal muscle for regions (see above).

b. ) Corticonuclear: cortex (head and neck) – genus of internal capsule – crus cerebri (midbrain) – motor nuclei of CNs V, VII, IX, X and XII. Function = control of muscles of head and neck. Not eyes.
c. ) Rubrospinal: red nucleus – decussates midline and then intermingles with lateral corticospinal tract – distal and proximal muscles of UE. Function questioned, voluntary movement of arm, hand and fingers. Insignificant is lesioned.

115
Q

True/false. Corticospinal tracts contain sensory information.

A
  • True. Not sure what. Corticonuclear also has sensory.
116
Q

Does the corticonuclear tract control eye movements?

A
  • No. Projection from frontal and parietal eye fields to horizontal and vertical gaze centers of reticular formation.
117
Q

List effects of lesions in the corticospinal tract

A
  • Weakness and Babinski
  • Difficult for just this tract to be affected in real life.
  • No spasticity seen in monkey studies.
118
Q

Location and functions of the following areas. Lesion here would result in?

a. ) motor cortex
b. ) premotor cortex
c. ) supplementary motor area
d. ) frontal eye fields

A

a. BA4 in precentral gyrus of frontal lobe. Function = control of skeletal muscle of body. Lesion = paresis, hypotonia (spasticity if other motor cortical areas damaged), permanent deficit in fine fractionated finger movements.
b. BA 6 lateral anterior to primary motor cortex. Function = visually guided movement, grasping and reaching, uses visual info about object to control task movement. Lesion = difficulty learning a new task involving specific stimulus with required movement.
c. BA 6 medially anterior to primary motor cortex. Function = planning/preparing for sequential motor acts. Lesion = problems initiating or suppressing movement – not paralysis.
d. BA 8/6 anterior to premotor cortex. Function = voluntary and memory guided eye movements through projections to vertical and horizontal gaze centers and superior colliculus. Lesion = deficit in ability to make saccades that are not guided by external target – to a remembered target, cannot voluntarily direct their eyes away from stimulus in visual field.

119
Q

Infarct of anterior cerebral artery affects what areas?

A
  • Supplies leg area of primary motor cortex, most of the supplementary motor area and cingulate gyrus
120
Q

Infarct of middle cerebral artery affects what areas?

A
  • Supplies trunk, hand and face area of primary motor cortex and all of the premotor area
121
Q

Define quadriplegia (aka tetraplegia), paraplegia, monoplegia

A
  • Quad: paralysis of all four limbs – transection in high cervical spine
  • Para: paralysis of legs – transection below cervical spine
  • Mono: paralysis of a limb
122
Q

Explain the crossed paralysis found with some brain stem lesions

A
  • Lesion to brainstem will typically affect the exiting cranial nerve (LMN) ipsilateral to lesion, but then also the uncrossed descending (eg. corticospinal) tract causing contralateral deficit
123
Q

Describe effects of lesion in the internal capsule

A
  • Corticonuclear in genu
  • Corticospinal in posterior limb
  • Stroke involving lenticulostriate artery can produce pure motor signs contralateral to lesion
124
Q

Effect of lesions of UMNs in motor cortices on the control of upper and lower facial muscles. Compare this to effect of damaging facial nucleus or facial nerve.

A
  • Volitional movements of upper face controlled bilaterally by fibers from cortical motor areas. Lower face by contralateral motor cortices. This refers to UMNs.
  • Lesion to cortex unilaterally = upper face movement still functions. Lower face deficit contralateral to lesion.
  • LMN (facial nerve) and nucleus damage would = ipsilateral deficit to entire face.
125
Q

Define akinesia

A
  • lack of movement
126
Q

Define chorea

A
  • Brief, sudden, random, twitch-like movements of limbs or facial muscles.
127
Q

Define bradykinesia

A
  • Slowness in execution of movement
128
Q

Define athetosis

A
  • Dyskinesia with slow, writhing movements
129
Q

Define hemiballismus/ballismus

A
  • Involuntary, violent, flinging movements of a limb while patient is awake. If one-sided = hemi.
130
Q

Define dyskinesias

A
  • involuntary movements
131
Q

Define freezing of gait

A
  • sudden inability to start walking or just stop moving forward while walking
132
Q

Define festinating gait

A
  • Manner of walking in which person’s speed increases in an unconscious effort to catch up with displaced C of G. Common in PD.
133
Q

Structures composing basal ganglia. What is the striatum? Corpus striatum

A
  • Caudate
  • Putamen
  • Globus Pallidus (internal and external segments) – aka pallidum aka paleostriatum
  • Subthalamic nucleus
  • Substantia nigra (pars reticulata and compacta)
  • Nucleus accumbens (ventral striatrum)
  • note: putamen + caudate = striatum
  • note: corpus striatum = striatum + globus pallidus
134
Q

Is GABA inhibitory or excitatory?

A
  • inhibitory
135
Q

Is Glutamate inhibitory or excitatory?

A
  • excitatory
136
Q

Describe symptoms of PD

A

Note: first 4 are cardinal

  • rhythmic tremor at rest
  • hypertonia – cog-wheel characteristics
  • bradykinesia can evolve into akinesia
  • mask-like facies
  • flexed posture
  • shuffling steps in absence of arm swing
  • reduced blinking
  • small handwriting
  • loss of automaticity of movement
  • freezing of gait: suddenly be unable to start walking or just stop moving forward while walking
137
Q

Which transmitter system is most severely damaged in PD. Damage to which part of the basal ganglia causes PD?

A
  • Degeneration of DA projection from substantia nigra (zona compacta) to striatum.
138
Q

Symptoms of HD

A
  • Chorea, dementia, voluntary movements slower than normal
139
Q

Location of lesion causing hemiballismus

A
  • Subthalamic nucleus contralateral to symptom
140
Q

List functional loops of basal ganglia and give cortical area involved and general function of each loop.

A
  1. ) Body movement loop
    - Cortical area: primary motor, premotor and supplementary motor cortices
    - Basal ganglia: putamen
    - Function: selectively activates some movements, suppresses other
  2. ) Oculomotor loop
    - Cortical area: FEF, supplementary eye field
    - Basal ganglia: caudate (body)
    - Function: control of saccadic eye movements
  3. ) Prefrontal loop
    - Cortical area: dorsolateral prefrontal cortex
    - Basal ganglia: anterior caudate
    - Function: initiation and termination of cognitive processes such as planning, attention and working memory
  4. ) Limbic loop
    - Cortical area: anterior cingulate and orbital frontal cortices
    - Basal ganglia: ventral striatum (with nucleus accumbens)
    - Function: regulation of emotional behavior and motivation (? Drug addiction)
141
Q

NTs important in the following pathways/structures

a. ) Nigrostriatal pathway
b. ) Corticostriate pathway
c. ) Striatum to GPe and GPi

A

a. Nigrostriatal = SNc to neostriatum (striatum) = release of DA, which has excitatory or inhibitory effects depending on receptor type
b. Excitatory glutamate
c. Inhibitory GABA

142
Q

Main afferents and efferents to/from basal ganglia are to what structures?

A
  • Afferents to striatum = putamen + caudate

- Efferents from globus pallidus (internal segment) and substantia nigra (pars reticulata)

143
Q

True / False. All parts of basal ganglia are inhibitory.

A
  • False. Subthalamic nucleus is excitatory (Glut). DA released from substantia nigra is inhibitory or excitatory depening on receptor type it binds. Rest are inhibitory GABA.
144
Q

What is tardive dyskinesia?

A
  • Tardive = iatrogenic disorder d/t tx with drugs affecting DA (they have too much DA). Most common sign is continual chewing with intermittent protrusions of tongue, lip, smacking and facial grimacing.
145
Q

Functions of cerebellum

A
  • Coordination of motor acts, planning sequential movements
  • Posture regulation
  • Control of muscle tone
  • Motor learning
  • Some cognitive functions (verb generation)
146
Q

Vestibulocerebellum. What anatomical area does this correspond to? Function? Lesion symptoms?

A
  1. Vestibulocerebellum (floccular-nodular lobe): equilibrium, gait/posture, control of eye movements coordinated with head, role in visual guidance of eye movements
    - Lesion = ataxic gait, eye movement disorder (deficits in smooth pursuit, cerebellar nystagmus. Clinically difficult to tell difference between lesion here and vestibular apparatus. Fall ipsilateral to lesion. Compensate by having a wide-based stance.
147
Q

Spinocerebellum. What anatomical area does this correspond to? Function? Lesion symptoms?

A
  1. Spinocerebellum (vermal and paravermal parts):
    - Vermal: regulates axial and proximal musculature (medial descending systems), concerned with ongoing motor execution and regulation of muscle tone, control of saccades and smooth pursuit
    - Lesion: deficits in accuracy of saccades and smooth pursuit eye movements.
  • Paravermal part: regulates distal limb muscles (lateral descending systems), concerned with ongoing motor execution and regulation of muscle tone
  • Lesion: hypotonia, dysmetria, intention tremor, pendular reflexes, affects limbs ipsilateral to lesion.
148
Q

Cerebrocerebellum. What anatomical area does this correspond to? Function? Lesion symptoms?

A
  1. Cerebrocerebellum aka pontocerebellum (lateral part of hemisphere): role in preparation for movement, especially multi-joint movement, timing functions
    - Lesion: delay in initiating and terminating movements, problem with multi-joint movements, impairments of highly skilled sequences of learned movements, affect on ability to judged elapsed time in non-motor tasks
149
Q

Do cerebellar lesions cause ipsilateral or contralateral symptoms.

A
  • Ipsilateral
150
Q

State which cell type is the source of axons leaving the cerebellar cortex. Which cerebellar cortex cell makes excitatory synapses?

A
  • Purkinje = only cell to project out of cerebellar cortex (inhibitory)
  • Granule cell makes excitatory synapse with Purkinje.
151
Q

Describe the difference between mossy fibers and climbing fiber input onto Purkinje fibers.

A
  • Mossy fiber input (from spinal cord and brainstem) results in smaller EPSPs which must sum via spatial and temporal summation onto granule (aka parallel) cell to causing a single AP in a Purkinje cell
  • One AP in climbing fiber (from inferior olivary nuclei) is enough to cause Ca2+ spike in Purkinje cell. Purkinje cell only receives one climbing fiber with multiple synapses.
  • This setup is basis of motor learning.
152
Q

Cells with input onto the Purkinje cells, effect?

A
  • Granule (aka parallel) = excitatory – these cells are excited by mossy fibers, inhibited by Golgi cell (excitatory feedback by granule cells)
  • Stellate = inhibitory – these cells are excited by granule cells
  • Basket = inhibitory – these cells are excited by granule cells
153
Q

Cerebellum and MS

A
  • MS: cerebellum itself, cerebellar peduncles or brainstem pathways to/from cerebellum
154
Q

Deficiency of which vitamin is associated with atrophy of the anterior lobe of the cerebellum?

A
  • Thiamine (B1) associated with long term alcoholism.

- Difficulty walking, leg control in general. Control of arms, head is less affected.

155
Q

Genetic disease of cerebellum

A
  • Friedreich ataxia: recessive, progressive spinocerebellar ataxia caused by TNR (c/s 9 GAA)
156
Q

Abnormalities resulting from cerebellar damage

A
  • Ataxia
  • Dysmetria (hyper/hypo)
  • Dysdiadochokinesia
  • Dysarthria
  • Intention tremor
  • Static tremor: tremor when pt is holding limb up against gravity
  • Titubation: tremor of entire trunk of head during stance and gait (midline lesion)
  • Cerebellar nystagmus
  • VOR can be suppressed by visual fixation. This suppression can be impaired by certain cerebellar lesions (esp vestibulocerebellum)
  • Hypotonia
  • Pendular muscle stretch reflexes
  • Asynergia (bw/ muscles)
  • Rebound phenomena: inability of agonist and antagonist muscles to adapt to changes in load
157
Q

Types of brain waves. Describe what each is associated with? Include frequency.

A
  1. ) Alpha (8-13 Hz): state of relaxed wakefulness, eyes closed, non-novel sounds
  2. ) Beta (13-30 Hz): alert state, eyes open, response to sensory stimuli, mental concentration
  3. ) Theta (4-7 Hz): sleep
  4. ) Delta (0.5-3.5 Hz): sleep
158
Q

Which brain wave is the fastest? Slowest?

A
  • Beta:alpha:theta:delta
159
Q

Why brain wave has a very low frequency below 3.5 Hz?

A
  • Delta
160
Q

Which brain wave is characteristic of an awake, alert adult whose eyes are open?

A
  • Beta
161
Q

Which brain wave is characteristic of an awake, relaxed adult with eyes shut?

A
  • Alpha
162
Q

What stage of sleep has highest percent of time spent in delta waves?

A
  • Stage 4 (deep sleep): > 50% of period characterized by delta waves
163
Q

During which stage of sleep is there intense descending inhibition of spinal motor neurons?

A
  • REM sleep
164
Q

Which stage of sleep is least likely during the first 60 minutes of normal adult sleep?

A
  • REM. This doesn’t usually occur until 90 mins or more into sleep.
165
Q

What sleep stage is associated with penile erection or clitoral engorgement?

A
  • REM
166
Q

Describe various sleep stages. What are the characteristics wave patterns?

A
  • Stage 1: transition from awake-sleep – theta waves prominent
  • Stage 2: light sleep – K complexes, sleep spindles
  • Stage 3: moderately deep sleep – some delta waves (not > 50%)
  • Stage 4: deep sleep – delta waves (> 50%)

Note: Non-REM sleep = stages 1-4

167
Q

When is stage 4 sleep present?

A
  • Appears primarily in first half of sleep period
168
Q

What happens to REM sleep throughout the night?

A
  • It lengthens
169
Q

What brain waves are not present at birth?

A
  • Delta waves. Increase in amplitude over first year of life, greatest amount ages 3-11. Begins to decline in adolescence and throughout life.
170
Q

How much of sleep is REM sleep in adult?

A
  • ~ 20-25%
  • Older adults = 15-20%
  • Newborns get about 50% of their sleep with REM.
171
Q

Describe physiological changes during non-REM sleep

A
  • Decrease body temp and BMR
  • Decrease HR and BP
  • Decrease RR
  • Muscles relaxed, postural adjustments every 20 minutes
  • GH release
172
Q

Characteristic features on EEG during REM sleep

A
  • Sawtooth waves
173
Q

Which sleep stage is associated with dreaming?

A
  • Both. REM dreams longer more visual and emotional than dreams of non-REM
174
Q

Neurons involved in atonia of REM sleep

A
  • Pontine neurons excite glycinergic neurons in medullary reticular area – medullary reticulospinal tract = post-synaptic inhibition of motor neurons
175
Q

During what stage of sleep is it harder to wake someone up?

A
  • Threshold for arousal increases as EEG frequency decreases

- Therefore stage 4 = hardest

176
Q

Describe physiological changes during REM sleep

A
  • Irregular heart beat and respiration
  • Penile erection or clitoral engorgement
  • Depressed muscle tone except for EOM and respiration
177
Q

Describe various sleep theories.

A
  • Sleep can increase interstitial space in brain and contribute to removal of potentially neurotoxic waste products.
  • Sleep for learning-dependent synapse formation.
178
Q

Which brain areas and NTs are most closely associated with sleep and arousal?

A
  1. ) Wakefulness:
    - Cholinergic neurons (pons-midbrain junction) high firing rates during wake
    - Locus coeruleus: NE
    - Raphe: 5HT
    - Histaminergic neurons of posterior hypothalamus (TMN)
    - Orexin (hypocretin) from lateral hypothalamus excite LC, raphe and TMN
  2. ) Sleep:
    - Cholinergic neurons (pons-midbrain junction) decrease firing rates during sleep (high again during REM)
    - Low firing of LC and raphe
    - Low-firing of TMN
    - VPLO (hypothalamus): periodically inhibit the above structures (TMN and brainstem nuclei (cholinergic, LC and raphe nuclei) for non-REM sleep
    - Melatonin
179
Q

Describe sensory evoked potentials. How are they measured? What is their clinical significance?

A
  • Measured and extracted from EEG recordings through averaging
  • Useful for evaluating demyelinating diseases such as MS
180
Q

Location of primary biological clock.

A
  • SCN: suprachiasmatic nucleus of hypothalamus
181
Q

Where is melatonin synthesized and released? Role in sleep?

A
  • Pineal gland indirectly controlled by SCN

- Sleep promoting by modulating brainstem circuits that control sleep-wake cycle

182
Q

What are parasomnias? Examples

A
  • Disorders of sleep cycle and other non-sleep dysfunctions associated with sleep
  • Examples: wetting/nocturnal enuresis, walking (Somnambulism), sleep terrors, REM sleep disorder, sleep apnea
183
Q

Symptoms of narcolepsy. What causes it?

A
  • Sleep attacks
  • Cataplexy (abrupt attack of muscle weakness and hypotonia often triggered by emotional stimulus)
  • Hypnagogic hallucinations
  • Rapid onset of REM with sleep
  • Sleep paralysis
  • Cause: reduction of absence of orexin (hypocretin) producing cells – probably d/t autoimmunity
184
Q

Describe characteristics of types of epilepsy/seizure (what is the difference between these)

A
  • Seizure = symptom (excessive abnormal electrical discharge of neurons)
  • Epilepsy: disease characterized by tendency to have repeated seizures
  1. Generalized seizure
    a. ) Tonic-Clonic seizure (fka grand mal)
    - LOC, tonic period = increased muscle tone, clonic = jerky movements, post-ictal state = confusion

b. ) Absence seizure (fka petit mal)
- transient LOC (seconds), 3/second spike and some pattern on EEG, begin in childhood rarely persist, muscle tone maintained rarely falls, subtle motor manifestations, no post-ictal state

  1. Focal/partial seizure
    a. ) Simple partial
    - no LOC, limited symptoms with small part of cortex involved

b. ) Complex partial
- affect consciousness, usually temporal or frontal, patient continue to perform motor behaviors, verbal/motor automatisms (lip smacking, chewing, patting, picking at clothing) can occur, hallucinations

185
Q

What type of epilepsy is characterized by EEG record of 3/second spike and dome pattern?

A
  • Absence seizure (fka petit mal)
186
Q

What is status epilepticus?

A
  • Recurrent or continuous motor seizures with little or no recovery bw attacks.
  • This is medical emergency.
187
Q

What is the dominant cerebral hemisphere?

A
  • Language hemisphere, usually left
  • Non-dominant = spatial abilities, comprehension of complicated patterns, control of affective components of language (prosodic – rhythms, timing, stress and patterns).
188
Q

Hemisphere typically involved in lexical and syntactic language

A
  • Left hemisphere
189
Q

Hemisphere typically involved in emotional coloring of language

A
  • Right hemisphere
190
Q

Hemisphere typically involved in writing

A
  • Left hemisphere
191
Q

Hemisphere typically involved in speech

A
  • Left hemisphere

- Rudimentary speech in right hemisphere

192
Q

Hemisphere typically involved in spatial abilities

A
  • Right hemisphere
193
Q

Function of posterior parietal cortex. Lesion here results in?

A
  • BA 5/7
  • Goal directed movements
  • Lesion:
    a. ) In non-dominant hemisphere = neglect syndrome of which there are different kinds. Personal, spatial, representational. Asomatognosia.
194
Q

Define asomatognosia

A
  • When pt has lack of awareness of condition of all or part of his body. Verbal asomatognosia is when pt verbally denies that his arm belongs to him.
  • D/t lesion to posterior parietal cortex in non-dominant hemisphere.
195
Q

Test used to determine hemisphere dominance for language

A
  • Wada test
196
Q

What is Broca’s aphasia?

A
  • aka expressive/motor/non-fluent aphasia
  • Lesion to BA 44/45 (frontal lobe)
  • Halting speech, tendency to repeat words/phrases, disordered syntax/grammar, disordered structure of words, comprehension intact
  • Patients aware of language difficulties
197
Q

What is Wernicke’s aphasia?

A
  • aka receptive/sensory/fluent aphasia
  • Lesion to BA 22 (posterior temporal gyrus)
  • Fluent speech, little spontaneous repetition, syntax adequate, grammar adequate, contrived/inappropriate words, comprehension not intact
  • Usually not aware of difficulties
198
Q

What is conduction aphasia?

A
  • Caused by interruption of connections b/w Broca’s and Wernicke’s
  • Comprehension normal for simple sentences and speech is fluent but patient used many paraphasia (incorrect or senseless words). Ability to repeat is lost.
199
Q

What is global aphasia?

A
  • Most severe aphasia.
  • Patients cannot produce understandable speech or comprehend spoken or written language.
  • May have automatic speech, can sing previously learning melody/lyrics.
200
Q

Alexia

A
  • disruption in ability to read
201
Q

Agraphia

A
  • disruption in ability to write
202
Q

How does right cerebral hemisphere lesion affect language function?

A
  • Expression and recognizing emotion in speech is associated with this hemisphere.
  • Lesion causes aprosidia = loss of emotional expression in speech. Speak in monotone regardless of circumstances. May have problems interpreting emotional tone of others speech. Can have trouble understanding jokes – awful!
203
Q

Define astereognosis

A
  • Inability to identify objects by feeling them

- Lesion in somatosensory cortices in parietal lobe

204
Q

Agnosia

A
  • Term for inability to recognize objects by a particular sensory modality (auditory, visual etc.)
205
Q

Split brain patients have a hard time naming objects in what hand?

A
  • Left hand
206
Q

Fibers connecting Broca’s and Wernicke’s areas

A
  • Arcuate fasciculus
207
Q

Describe affective components of language. Which hemisphere is usually responsible for these components?

A
  • Components: prosodic elements (rhythms, timing, stress and patterns)
  • Non-dominant, typically right
208
Q

Describe prefrontal lobe syndrome.

A
  • personality changes including loss of sense of social propriety (conforming) and sense of responsibility
  • planning deficits
  • perseveration: tendency to continue with one form of behavior when situation requires new changed response
  • frontal release signs: primitive reflexes come back
  • lack of ambition
  • akinetic mutism: become motionless and mute even though they could if they wanted
  • profoundly apathetic
  • abulia (loss or impairment to perform actions/make decisions)
209
Q

Types of prefrontal dysfunctions and symptoms? Do you think we need to know this?

A
  1. ) Dorsolateral prefrontal area: issues with executive function, planning, choosing goals, monitoring execution, perseverate
  2. ) Orbitofrontal area: disinhibition, ignore social conventions, impulsive, unconcerned about consequences (Mignon)
  3. ) Medial frontal/anterior cingulate gyrus
    - apathy, slowing of cognition, abulia (decrease in will/motivation), akinetic mutism (motionless/mute)
210
Q

Define and characterize the concept of emotion

A
  • Combination of subjective feelings (conscious fear, anxiety, happiness etc.) and associated physiological states (unconscious, autonomic, endocrine, somatic motor etc.)
211
Q

Identify and describe the main functions of the limbic system and associate them with one or more major anatomic structures of the limbic system

A
  • Emotional responses
  • Certain types of memory
  • Homeostasis (repro drive, eating/drinking, endocrine, ANS reg)
212
Q

Identify functional role of hypothalamus

A
  • ANS function, reproductive drive, endocrine/hormonal regulation, eating, drinking, sleeping
213
Q

Identify functional role of amygdala

A
  • Fear response, facial expression interpretation, homeostasis (conditioning of ANS), sensory perception (hallucinations if malfunction), motivation and emotion, memory and learning
214
Q

Identify functional role of limbic cortex

A
  • conscious, rational mind
215
Q

Identify functional role of hippocampus

A
  • Sensory processing (novelty detection)
  • Homeostasis (HPA axis)
  • Learning/memory
216
Q

Identify functional role of nucleus accumbens

A
  • Brain reward system
217
Q

How does amygdala interact with cerebral cortex and hypothalamus to produce emotional behaviors?

A

see image in study guide

218
Q

How is fear conditioned?

A
  • When conditional stimulus (neutral) is paired with unconditional stimulus (aversive), animal begins to respond to conditional stimulus with fear behaviors in absence of unconditional stimulus.
  • CS/US acts on thalamus (auditory, somatosensory) and cortices which interacts with amygdala. Amygdala outputs onto hypothalamus, activating visceral motor effector system to prepare body for action.
219
Q

Partners of amygdala in fear response

A
  • Hippocampus provides context (memory, learning)

- Medial prefrontal cortex (regulation – whether you express fear or not, how much)

220
Q

Mirror neurons – what are they? Function in limbic system?

A
  • Subset of neurons in premotor area activated when performing action itself and when observing another living creature perform that same action.
  • In limbic system – might contribute to neural basis of empathy.
221
Q

How does the brain reward system work in regards to drug addiction?

A
  • Structures = nucleus accumbens, frontal cortex, VTA (ventral tegmental area)
  • NT: dopamine from VTA to nucleus accumbens
  • Works through reinforcement of limbic loop promoting activation of motor programs to acquire beneficial rewards
  • Drug addiction: alters neuromodulatory influence of DA.
222
Q

Clinical manifestations of lesion of components of limbic system

A
  • Schizophrenia
  • Depression, mood disorders
  • Addiction
  • Autism
  • PTSD
  • OCD
  • Korsakoff’s syndrome (immediate memory disorder)
  • Kluver Bucy syndrome
  • AD
  • FTD
223
Q

NT of mesolimbic system

A
  • DA
224
Q

Mesolimbic system

A
  • VTA (ventral tegmental area)

- Nigrostriatal projection

225
Q

What structures assign emotional significance to what’s experienced?

A
  • Higher limbic structures
226
Q

Define learning and memory

A
  • Learning: new info is acquired by nervous system and adaptive changes are produced
  • Memory: encoding, storage (as interpreted) and retrieval of learned info
227
Q

Characterize the major forms of memory and major brain regions involved in processing these types

A
  1. Declarative (aka explicit): semantic (facts), episodic (events)
    - Area = medial temporal lobe (hippocampus + surrounding), diencephalon (basal forebrain, thalamus)
  2. Non-declarative (aka implicit):
    - Skilled movements and habits: striatum (procedural), motor cortex, cerebellum, spinal reflex circuits
    - Priming: neocortex
    - Associative learning: emotional responses (amygdala, limbic), skeletal musculature (cerebellum, spinal reflex circuits)
    - Non-associative learning: complex pathways
228
Q

Types of learning

A
  • Associative: passive, operant (reinforcement – neg or positive)
  • Non-associative, simple: habituation, sensitization
  • Non-associative, complex: imprinting, observational (vicarious)
229
Q

Major steps of memory processing and formation

A
  • Acquisition into short-term memory
  • Rehearsal
  • Encoding/consolidation into long-term memory (codification throughout cortex)
  • Retrieval from long-term into short-term
  • Memory extinction
    3 steps overall = acquisition, storage, extinction
230
Q

Temporal categories of memory

A
  • Short-term memory
  • Working memory (may be subcategory under short-term)
  • Long-term
231
Q

Domains of memory

A
  • Cognitive: recall, calculate, discuss, analyze, problem solve
  • Psychomotor: dance, swim, ski etc.
  • Affective: like something or someone
232
Q

Various physiological mechanisms for learning and memory formation

A

1.) Recurrent circuits: pos feedback system, persistent neural activity, short term, rapid extinction, proposed for working memory

  1. ) Synaptic plasticity: strengthening or weakening of synaptic transmission
    a. ) Short-term: habituation/sensitization
    b. ) Long-term (LTP): enduring increase in synaptic efficacy results from high-frequency stimulation of afferent pathway. NMDA-R dependent in some types.

3.) Synaptogenesis: changes in numbers of active synapses

233
Q

Major disturbances and diseases that can occur in memory and learning processes

A
  1. ) Working memory disorders: AD, MS, schizo, OCD, FTD
  2. ) Procedural memory: PD, HD, OCD, depression
  3. ) Episodic memory: AD, FTD, MS
  4. ) Semantic memory: AD, encephalitis
234
Q

Mechanism of fear extinction

A
  • Prefrontal cortex blocks fear response to conditional stimulus
235
Q

Amnesia types. Describe what defect is

A
  • Anterograde: inability to form new declarative (semantic, fact) memories, defect in consolidation, hippocampal damage, does not affect procedural memory
  • Retrograde: inability to recall previously stored memories, issue in cortex/forebrain
236
Q

Symptoms of AD

A
  • Aphasia, apraxia, agnosia, amnesia (anterograde in early stages, retrograde in late stages)
237
Q

State the normal human hearing range. Range of frequencies to which humans are most sensitive.

A
  • 20 Hz to 20 kHz (people over ~25 cannot hear usually above 16 kHz
  • Most sensitive range from 1-4 kHz
238
Q

Describe how normal range of hearing changes with age. Describe presbycusis.

A
  • Hearing loss occurs as one ages. First loss is higher frequency. Can be genetic component.
239
Q

How is dB scale used to measure sound level?

A
  • sound pressure level measured in dB and is in relation to a reference pressure, 0 dB = pressure of sound = reference pressure, negative dB = sound pressure less than reference pressure
240
Q

Describe how sound energy is transformed into neural signals.

A
  • Ossicular system: air in outer ear has low impedance (resistance to movement) and fluid in inner ear has high impedance. To enable transmission of sound from air to fluid, middle ear increases the pressure felt at TM to a higher pressure at oval window.
  • What happens after here I’m not exactly sure☺
  • Organ of Corti contains auditory hair cells. Endolymph found in cochlear duct scala media with high conc of K. Perilymph found in scala vestibule, tympani surrounding lower part of hair cells.
  • At the end of this system, afferents take signal away in CN VIII
241
Q

What produces endolymph?

A
  • Stria vascularis
242
Q

Describe middle-ear attenuation reflex. Which muscles are involved? What CNs are involved? Give possible functions for the reflex. What is the hyperacusis?

A
  • Stapedius muscle (CN VII) and tensor tympania (CN V) contract in response to loud noise
  • Most pronounced for frequencies below 1 kHz believed to aid in understanding speech in noisy environment.
  • Hyperacusis = painful sensitivity to moderate and even low intensity sounds
243
Q

Disorder causing hyperacusis

A
  • Bells palsy – CN VIII – stapedius
244
Q

Function of outer vs inner hair cells

A
  • Outer: contract and expand in response to small electrical currents, thought to sharpen frequency-resolving power of cochlea by expanding and contracting and thus changing stiffness of tentorial membrane. Through olivocochlear bundle (from superior olivary nucleus).
  • Inner: what we hear with
245
Q

Explain the place principle for the determination of sound frequency. Relate this concept to the traveling wave on the basilar membrane and the tonotopic map of the cochlea. What frequencies cause firing from nerves from base of cochlea? What frequencies maximally stimulate the apex of the cochlea?

A
  • Traveling wave of endolymph starts at stiffer part of basilar membrane
  • Basilar membrane varies in width and stiffness. Near stapes or base of cochlear – membrane narrow/stiff; near helicotrema or apex – membrane is wider/floppy.
  • Therefore a tonotopic map is created as basilar membrane is tuned at different areas for different frequencies. High frequencies are coded for at stapes/base; low frequencies coded for at apex/helicotrema.
246
Q

Auditory pathway. Clinical implication.

A
  • Fibers cross at level of cochlear nucleus, nucleus of lateral lemniscus and inferior colliculus.
  • Deafness in one ear is therefore usually the result of issue proximally to ear. More distally means crossing has occurred and you need to have more extensive damage to brainstem, likely interfering with both ears.
247
Q

How is sound localized?

A
  • LSO: compare loudness of sound arriving in each ear
  • MSO: compare time of arrival

• medial and lateral superior olive

248
Q

Types of deafness, explain, give causes

  1. Conductive
  2. Sensorineural
  3. Central hearing loss
A
  1. Conductive
    - Impaired sound transmission in external / middle air
    - Otosclerosis, FB, otitis media w/effusion, damage to TM, cerumen impaction
  2. Sensorineural
    - Loss of cochlear hair cells or damage to nerve
    - Ototoxic drugs, noise exposure, vestibular schwannoma, Meniere’s
  3. Central hearing loss
    - Lesion to central auditory nuclei and pathway (retrocochlear lesions)
    - MS
249
Q

Describe the following hearing tests

a. brainstem auditory evoked response (BAER)
b. evoked otoacoustic cortex
c. audiometry

A

a. ) BAER: test to measure brain wave activity in response to clicks or certain tones
b. ) Emissions of pure tones in response to auditory stimulus – screen for sensory hearing loss of greater than 30 dB
c. ) Audiometry: measures hearing thresholds at specific frequencies

250
Q

Location of primary auditory cortex

A
  • Temporal lobe, BA 41

- BA 42 = association area

251
Q

List the five primary sensations of taste. Be able to state which taste sensation is elicited by discussed substances.

A

Sour - intensity of sensation depends on amount of hydrogen ion, caused by acids, e.g. HCl

Salty - caused by ionized salts e.g. – NaCl

Sweet - not caused by any one class of chemicals – e.g. some members of classes: sugars, glycols, alcohols, amino acids, inorganic salts of lead

Bitter - not caused by any one class of chemicals - almost all though organic substances e.g. alkaloids - quinine, caffeine, strychnine, nicotine

Umami - elicited by monosodium glutamate, glutamate, and other amino acids. Taste common to protein rich foods like meat and cheese.

252
Q

List which cranial nerves are involved in transmitting taste information. State which cranial nerve innervates the anterior 2/3 of the tongue. State which innervates the back of the tongue. Which innervates the soft palate, the epiglottis and esophagus?

A

Anterior 2/3 of tongue - CN VII chorda tympani branch

Posterior 1/3 of tongue - CN IX

Soft palate - CN VII (greater superficial petrosal branch)

Epiglottis and esophagus - CN X

253
Q

Classify taste receptor cells. Classify olfactory receptor cells. Is either receptor a neuron? What is the average life span of taste receptor cells?

A

Taste cells arise from basal epithelial cells and are stimulated by taste. Taste cells last 10 days to 2 weeks.

Olfactory receptor neuron (ORN) - bipolar nerve cell – new ORN are generated continuously from dividing stem cells which are maintained among the population of basal cells.

Both are neurons and would lose sensation if damaged.

254
Q

Give the probable biological roles of taste and olfaction.

A

Taste: edibility, diet selection, taste aversion

Olfaction: smelling danger I guess

255
Q

Describe bait-shyness. How can this phenomenon be clinically significant?

A

If an animal feels sick after eating, assumption by the brain is that (most) novel food is responsible. Animal “loses its taste” for that food. Clinically significant for chemo patients because a lot of things will make them sick so you might work with a nutritionist so you can plan times of eating so they don’t lose taste for everything/lose weight.

256
Q

Define the following terms:

a. Hyposmia
b. Anosmia: specific anosmia and general anosmia
c. Parosmia
d. Hypogeusia
e. Ageusia
f. Parageusia

A

Hyposmia – impaired sense of smell

Specific anosmia – specific scent that a person can’t smell (can have normal odor sensation but less sensitive to specific smell)

General anosmia – complete loss of the sense of smell

Parosmia – perversion of sense of smell

Hypogeusia – decreased taste sensation

Ageusia – absence of taste

Parageusia – perversion of the sense of taste; a bad taste in the mouth

257
Q

Match positions in visual field to retinal location. Match retinal location to projection area

A
  • review slides 32-35 of this powerpoint (images)
258
Q

Describe difference b/w locations of rods and cones. Describe functional differences b/w rod and cone vision. Which receptor mediates scotopic vision? Mesotopic? Photopic vision?

A
  • Rods function in differentiating B&W, peripheral vision, night vision. They are found more eccentric from the fovea.
  • Cones function in color vision. They are found more centrally and in highest concentration at the fovea.
  • Scotopic vision (low to no light, no color vision) is mediated by rods only.
  • Mesotopic vision (starlight and moonlight) is mediated mostly by rods and starts having some cones.
  • Photopic vision (indoor lighting and sunlight) is mediated dominantly by cones and this is where rods start becoming bleached.
259
Q

What are the types of photopigments found in rods and cones?

A
  • Rods have rhodopsin only (retinal + rod opsin).
  • Cones have 3 kinds of photopigments, each containing retinal and an opsin (blue, red and green)
  • Rare specialized ganglion cells (intrinsically photosensitive ganglion cell) contain melanopsin
260
Q

Describe the electrophysiological changes that occur when a photoreceptor is stimulated by light.

A
  • Photoreceptors hyperpolarize to light
  • in darkness, calcium and sodium come in (because cGMP holds the channels open) and keep rods and cones depolarized
  • in light, cGMP that was holding channels open is reduced to calcium and sodium stop coming in and instead potassium continues to leave unmatched, leading to hyperpolarization
261
Q

Define receptive field for visual neurons. What type of field does the bipolar and retinal ganglion cells have? Do they respond more to stationary or moving light sources?

A
  • the area of the retina from which the neuron can be influenced
  • bipolar cells have receptive fields with a center – surround organization, meaning they will respond more to a properly positioned spot of light (or dark spot in light) than to even illumination
  • retinal ganglion cells also have center-surround type receptive fields
  • moving light sources will affect both these cells more than a stationary one which fills the center and surround portion of their receptive fields
262
Q

Which retinal cell type can produce AP, which are output cells, which capture photons?

A
  • only ganglion cells (which are the output cells of the retina) can produce an action potential since their axons form the optic nerve/chiasm/tract
  • rods and cons are the photoreceptor cells which capture photons
263
Q

Functions of retinal projections to the SCN, pretectal nuclei, LGN and superior colliculi

A
  • Projection to SCN = circadian rhythms
  • Pretectal nuclei = reflex constriction of pupil to bright light
  • LGN = actually how you see (relays to visual cortex and receives input form visual cortex – 90% retinal axons terminate here)
  • Superior colliculus = orients movement of head/eyes to visual/auditory/somatic stimuli (can be reflex)
264
Q

Functions of the dorsal and ventral visual streams to higher visual areas? What is the clinical significance of having different pathways for different aspects of vision?

A
  • 2 main visual pathways from striate cortex to higher order visual areas
  • ventral visual stream (MT) goes to parietal lobe. This stream functions in spatial vision (high level form vision, selective for shape/color/texture, faces)
  • dorsal visual stream (V4) goes to temporal lobe. This stream functions in object recognition (analysis of motion and relative positions of objects in visual scene, selective for direction and speed of movement)
  • clinical significance: restricted cortical lesions have resulted in different kinds of selective visual deficits (limited visual agnosias instead of full vision losses when lesions occur)
265
Q

Color blindness terminology. Location of genes for cone pigments. What do we use to test for color blindness?

A
  • red-green colorblindness = missing EITHER red or green cone
  • no true color vision if missing BOTH red and green cones (= monochromatopsia/achromatic)
  • genes for red and green are on the X-chromosome (hence why it sucks to be dudes cause they’re so susceptible to these disorders)
  • gene for blue cone pigment is on an autosomal chromosome (Chr 7)
  • rhodopsin gene is on autosomal chromosome (Chr 3)
  • Ishihara chart (colored numbers)
266
Q

Mechanisms for depth perception. Which are monocular and which require vision in both eyes?

A
  • stereoscopic vision requires binocular vision, binocular disparity for near objects
  • monocular depth cues include size of image of known objects on the retina and motion (or monocular movement) parallax
267
Q

Define strabismus. Describe how it can result in suppression of visual image from one eye.

A
  • strabismus = squint or cross-eyedness
  • young children tend to use one eye for fixation and eventually suppress vision from the other eye; the brain learns to ignore the suppressed eye which develops amblyopia (less vision in one eye)
268
Q

Describe visual field losses associated with specific visual pathway lesions.

A
  • see slides 38 and 39
269
Q

Which type of vit deficiency can cause night blindness?

A
  • Vit A: retinal is part of rhodopsin (rod pigment)
270
Q

Define accommodation

A
  • ciliary muscle contract (PSNS activation) = lens spherical

- focus light from closer objects, therefore used for near vision

271
Q

Define presbyopia

A
  • near point of vision recedes, impaired near vision
272
Q

Define blind spot

A
  • area on retina that don’t have receptors, therefore no vision in this area – optic disk
273
Q

Define fovea

A
  • central pit with closely packed cones located in center of macula lutea (pigmented area on retina for high-acuity vision) on retina
274
Q

Define binocular disparity

A
  • difference in image location of an object seen by left and right eyes, stereopsis (perception of depth and 3D structure from binocular vision)
275
Q

Define prosopagnosia

A
  • Problem visually identifying faces
276
Q

Define scotoma

A
  • visual field defect, blind area either natural or caused by disease

Medical Physiology (10 decks)

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