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HYMS Y1 > Block 5 W2 > Flashcards

Block 5 W2 Flashcards

1
Q

What is the conus medullar is?

A

Terminal of spinal cord

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2
Q

What is filum terminale?

A

Terminal filament (end of nerves)

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3
Q

What is cauda equina?

A

Collection of nerves - lumbar and sacral

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4
Q

What is white commissure?

A

White matter fibres cross midline

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5
Q

What are 1st order neurones?

A

Convey info from external receptors, run through dorsal root with cell bodies in dorsal root ganglion. PNS

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6
Q

What are 2nd order neurones?

A

Convey info from brainstem or spinal cord and decussates.

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7
Q

What are 3rd order neurones?

A

Convey info from thalamus to primary sensory cortex via internal capsule.

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8
Q

What are the conscious and unconscious tracts?

A

Conscious:

  • dorsal column
  • spinothalamic

Unconscious:

  • spinocerebellar
  • spinotectal
  • spinoreticular
  • spino-olivary
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9
Q

Describe the dorsal column pathway.

A

1st order -> ipsilateral until gracile (medial, lower 1/2) and cuneate (lateral, upper 1/2) nuclei in medulla.

2nd order - decussate as internal arcuate fibres -> medial lemniscus.

3rd order -> medial lemniscus -> thalamus

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10
Q

What info does the PCML pathway convey?

A
  • fine touch
  • pressure
  • vibration
  • proprioception
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11
Q

What is the consequence of lesions in the DCML?

A

Loss of proprioception and fine touch. Patient still able to perform tasks requiring tactile info processing.
Lesion at SC -> sensory loss = ipsilateral.

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12
Q

Describe the spinothalamic pathway.

A

Rise ipsilaterally 1-2 spinal segments then decussates and ascends contra-laterally

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13
Q

What info does the spinothalamic tract convey?

A

Anterior spinothalamic -> crude touch

Lateral spinothalamic -> pain and temperature

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14
Q

What is the consequence of spinothalamic lesion?

A

Contralateral loss of pain and temperature sensations. 2 segment difference (T8 lesion -> loss of sensation below T10).

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15
Q

Describe the spinocerebellar pathway.

A

Dorsal - muscle spindles, Golgi tendon organs enter at T1-L2 -> ipsilateral ascent to inferior cerebellar peduncle (ipsilateral proprioception).
Ventral - decussates -> contralateral ascent.

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16
Q

Describe spine-olivary pathway.

A

Travels to accessory olivary nuclei and cerebellum.

For movement coordination associated with balance e.g. tight rope.

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17
Q

Describe spinotectal pathway.

A

Travels to superior colliculi.

For reflex turning of head and eyes to cutaneous stimuli.

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18
Q

Describe spinoreticular pathway.

A

Travels to reticular activating system.

For arousing consciousness through cutaneous stimulation.

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19
Q

What is the consequence of a brainstem lesion?

A

Pain, temp, touch, position and vibration loss - contralateral.

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20
Q

What is the consequence of spinal cord lesion?

A

Pain and temp - contralateral.

Touch, position and vibration - ipsilateral.

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21
Q

What is Brown-Sequard syndrome?

A

Refers to a hemisection of the spinal cord. Due to traumatic injury and involves DCML and spinothalamic pathways.

DCML - ipsilateral loss of tactile sensation and proprioception.
Spinothalamic - contralateral loss of pain and temp. Ipsilateral hemiparesis.

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22
Q

Define action potential.

A

Rapid change in electrical potential across the plasma membrane of a cell.

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23
Q

Define resting membrane potential.

A

-70mV
Inside of neurone is negatively charged relative to outside.
Set up by electrochemical gradient across cell membrane.

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24
Q

What are ion channels - passive transport?

A

Made up of proteins in plasma membrane.
Allow selective transfer of ions across membrane.
Passive - no energy required.

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25
Q

List ion channel types.

A

Leak -> always open and continually leaks ions.
Voltage-gated -> open/close in response to voltage change.
Ligand-gated -> open/close in response to chemical/drug.

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26
Q

What is Na+/K+ pump - active transport?

A

Allows ions to travel across membrane against their concentration gradient.
Active -> requires energy.
3 Na+ out, 2 K+ in.

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27
Q

How is resting potential set up?

A
  1. Low-protein permeability -> negatively charged intracellular proteins can’t leave.
  2. Na+/K+ pump
  3. High K+ permeability -> K+ leaks.
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28
Q

What is the electrochemical gradient?

A

Extracellular charge is positive (high Na+) and intracellular charge is negative (low Na+, high K+).
Overall, more positive outside than inside.

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29
Q

What is the equilibrium potential?

A

Voltage at which ion’s net flow across membrane is 0. Calculated by Nernst equation.
Depends on:
- Valence (charge)
- concentration gradient

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30
Q

Why is KCL used in assisted suicides?

A

Increasing extracellular K+ = resting potential is less negative (depolarisation) -> interferes with cardiac muscle contraction and stops the heart.

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31
Q

What does the Goldman equation depend on?

A

Valence
Concentration gradient
Permeability of multiple ions

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32
Q

Why is resting potential now -80mV, the same as K+ potential?

A

Poor permeability to Na+ allows Na+ to leak back into the cell = -70mV.

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33
Q

Describe the resting state.

A

-70mV

All voltaged-gated Na+ and K+ channels closed.

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34
Q

Describe the depolarisation phase.

A

-55mV (threshold potential)

Voltage-sensitive (fast activation) Na+ channels open.

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35
Q

Describe the repolarisation phase.

A

Absolute refractory period
+40mV
Voltage-sensitive K+ channels open.
Inactivation gate of Na+ channels close.

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36
Q

Describe the hyper-repolarisation phase

A 
Relative refractory phase
-80mV
Voltage sensitive K+ channels remain open.
K+ leak
Fast activation Na+ gate closes.
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37
Q

Summarise the action potential stages.

A

-55 mV: Depolarisation - Voltage-gated Na+ channels open
+40mV: Repolarisation - Na+ channels inactivated (absolute refractory period)
+ 40mV: Repolarisation - Voltage-gated K+ channels open
-80 mV: Afterhyperpolarisation Voltage-gated K+ channels slow to close (relative refractory period)
-70 mV: Resting state - Leaky K+ channels restore RMP

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38
Q

Describe the mechanism of neurone AP transmission.

A
  • Signals arrive via synaptic transmission from presynaptic neurons
  • Electronic potentials spread passively (graded response) from dendrites to soma
  • Negative and positive electronic potentials are integrated (summed) within the soma.
  • Sum of electrotonic potentials reaches axon hillock.
  • If net electric potential > threshold at axon hillock = action potential occurs in an all or nothing response.
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39
Q

What does axon conduction velocity depend on?

A

Axon diameter

Myelination

40
Q

Describe the different stimulus strengths.

A

Subthreshold - magnitude of graded response.

Suprathreshold - freq. of APs increases (same amplitude but fire more rapidly).

41
Q

Describe unmyelinated axon conductance.

A
  • Na+ entry at axon hillock locally depolarises.
  • depolarises adjacent region -> opens voltage-gated Na+ channels.
  • previous Na+ channels inactivate (absolute refractory).
  • 1 way propagation of AP down axon.
42
Q

Describe myelinated axon conductance.

A
  • Na+ entry at axon hillock locally depolarises.
  • myelin sheath insulates axon -> prevents ion leakage.
  • Na+ and K+ channels concentrated at nodes of Ranvier.
  • AP jumps nodes -> saltatory conduction.
43
Q

Describe the action of local anaesthetics.

A

Reversibly prevent transmission of AP within local region.
Blocks voltage-gated Na+ channels
Types:
- esters (cocaine)
- amides (lidocaine)
Local effect prolonged by vasoconstrictors (epinephrine).
Small diameter neurones.

44
Q

What is carbamazepine?

A

Treats epilepsy and nerve pain.

Prolongs inactivated state of Na+ channel and absolute refractory period.

45
Q

What is multiple sclerosis?

A

Autoimmune disease - demylination as T cell attack myelin sheath causing inflammation, lesions and scarring in axon bundles -> APs can’t propagate as fast.

46
Q

What is tetrodotoxin?

A

Product of symbiotic bacteria of pufferfish.
Blocks fast voltage-gated Na+ channels.
Death by respiratory paralysis.

47
Q

Define pain.

A

Unpleasant sensory and emotional experience associated with actual or potential tissue damage -> psychological emotional experience.

48
Q

Define nociception.

A

Neural processes of detecting, encoding and processing noxious stimuli - physiological response.

49
Q

What are the advantages of pain?

A
  • early cue
  • protective
  • educational -> avoid harmful situations and changes our behaviour
  • prevents infections
  • prevents bedsores
50
Q

What are the disadvantages of pain?

A
  • No useful function in chronic, rheumatic, cancer, neuropathic, amputation pain.
  • Persists after tissue heals.
51
Q

What is acute pain?

A
  • pain resolves when injury heals
  • recent with well-defined onset
  • ends in days or weeks
  • vital warning function
  • forces rest and avoidance of further pain
  • treatable
52
Q

What is chronic pain?

A
  • pain persists with ill-defined onset
  • longer and unpredictable duration
  • no apparent biological function
  • resting doesn’t improve pain
  • persists after tissue heals
  • poorly treatable
53
Q

What are nociceptor?

A

Sensors found in most body tissue that respond to noxious stimuli.
Unspecialised nerve cell endings.
Brain has no no nociceptors.

54
Q

What are the types of nociceptors?

A 
Thermal - burning, frost
Mechanical - pinch, incision
Chemical - capsaicin
Polymodal - all (most nociceptors are polymodal)
Sleeping/silent - inflammation
55
Q

Describe the primary afferent fibres.

A

Large diameter - rapidly conducting afferents (Aa and Ab) associated with low-threshold mechanoreceptors e.g. touch.
Small diameter - slow conducting afferents (Ad and c) associated with nociceptors and thermo-receptors.

Polymodal nociceptors have c fibres.

56
Q

Describe the difference between first and second pain.

A

First - fast (Ad fibres), sharp, easily located, rapid, short duration, mechanical and thermal nociceptors.

Second - slow (c fibres), dull, aching, burning, poorly localised, slow, long duration. polymodal nociceptors.

57
Q

Describe the transduction of pain.

A

Different noxious stimuli open different receptor channels.

  1. receptors at nociceptor free endings are selectively activated by noxious stimuli -> generates receptor potential.
  2. depolarises membrane, opening Na+ channels -> generating AP.
  3. AP enters spinal cord via dorsal root ganglion.
  4. voltage-gated Ca2+ channels trigger release of NT (glutamate and substance P) -> activates 2nd order neurones in spinal cord -> ascends to brain.
58
Q

What is congenital analgesia?

A

Mutation in genes encoding Na+ channels specific to nociceptors.
Inability to feel pain.
Associated symptoms:
- recurrent bruises, cuts, burns, eye damage (pain ignored -> dangerous)
- limb and joint deformity as improperly healed bones causing chronic infection (osteomyelitis)
- missing body parts
Reduced life expectancy

59
Q

Where does the termination of primary afferents occur in the spinal cord?

A
  • Ad and C fibres enter dorsal horn and innervate laminae I and II.
  • 2nd order neurones take info to laminae IV-VI.
    Also cross the midline and ascend to brain.
60
Q

Describe the spinothalamic pathway.

A

Sensory inputs cross at spinal cord and ascend on opposite side.
Info relayed via medulla to thalamus.
Pain relayed from thalamus to primary somatosensory cortex.

61
Q

Describe the ascending pathway of pain.

A

Noxious stimuli activate nociceptors and spinal neurones that project to higher brain centres including thalamus (perception), cortex (localisation), limbic system (emotional)

62
Q

Describe the nociceptive pathway for face and head.

A
  1. info enters at pons via CN 5, 7, 9, 10.
  2. small diameter afferents descend in spinal trigeminal tract to brainstem
  3. synapse with 2nd order neurones in medulla
  4. axons then ascend contra laterally to thalamus in trigeminothalamic tract
  5. projects to cortex via ventral posteromedial nucleus
63
Q

What is dissociated sensory loss?

A

Unilateral spinal lesion -> sensory loss of touch, proprioception on same side and pain, temp on opposite side.

64
Q

Describe the gate theory.

A

Local interneurones in spinal cord act as gate.
Co-activation of Aa/b and C fibres suppresses projection of C fibres.
Explains why pain reduced by stimulating mechanoreceptors e.g. rubbing.

65
Q

What can suppress pain?

A

Perception of pain modulated in higher brain centres -> strong emotions, stress and stoic determination suppresses pain e.g. soldiers and placebo effect.

66
Q

Define hyperalgesia.

A

Increased sensitivity (reduced threshold) to pain from stimulus that normally provokes pain.

67
Q

Define allodynia.

A

Pain from stimulus that doesn’t normally provoke pain e.g. light touch

68
Q

What are the chemical modulators of pain?

A

Tissue damage and inflammation triggers release of substances that can sensitise peripheral nociceptors and induce hyperalgesia e.g. substance P, prostaglandins, bradykinin, histamine

69
Q

Differentiate between primary and secondary hyperalgesia.

A

Primary - occurs in site of the tissue damage.

Secondary - occurs around the site of tissue damage.

70
Q

What is fibromyalgia?

A

Chronic widespread pain and allodynia.
Other symptoms: fatigue, IBS, headache, muscle stiffness.
Mainly affects females.
Treatments: analgesics, antidepressants, counselling and exercise.

71
Q

What is referred pain?

A

Caused by convergence of nociceptor inputs from viscera and skin.
Few neurones specialised for visceral pain so nociceptive afferents from viscera and skin enter SC through same route and target overlapping populations of spinal neurones.
Cross-talk -> visceral nociceptor activation is perceived as cutaneous sensation.

72
Q

Give examples of referred pain.

A

Angina - pain localised to upper chest wall, left arm and hand.
Appendicitis - pain referred to umbilicus.
Bladder pain - perineum.
Ureter - lower abdomen and back.
Prostate - lower trunk and legs.

73
Q

What is phantom limb?

A

Sensation that a missing limb is still attached to body and moving appropriately (80% amputees).

74
Q

What is phantom limb pain?

A

Chronic pain in phantom.

Stabbing/burning pain or phantom limb contorted in uncomfortable position.

75
Q

What are the treatment for phantom limb pain?

A

Pain associated with central brain changes - re-organisation of somatosensory map.

Mirror therapy.

76
Q

Give an overview of pain relief treatments.

A

Pharmacological (opioids, NSAIDs)
Stimulation (TENS, acupuncture, physiotherapy)
Psychological (placebo, hypnosis)
Neurosurgery (hemisection, rhizotomy)

77
Q

What are opioids?

A

Any substance that produces morphine-like effects.
Produces profound analgesia.
Binds opioid receptors in brain (mu, delta, kappa).
Brain has endogenous opioids e.g. endorphins, enkephalins.

78
Q

Describe the nociceptive descending pathway.

A

Periaqueductal grey matter and raphe nuclei decrease NT release from nociceptive primary afferents by binding opioids with opioid receptors.

Placebo and acupuncture effects occurs though stimulation of endogenous pain relief systems.

79
Q

List common clinical opioids.

A
  • morphine sulphate
  • diamorphine
  • codeine
  • fentanyl (operative)
  • pethidine (obstetrics)
  • tramadol (opioid effect + enhances serotinergic and adrenergic pathways)
  • naloxone (antagonist)
80
Q

What are upper motor neurones?

A
  • CNS
  • origin in cerebral cortex, cerebellum and brainstem
  • form descending tracts
  • projects to LMN in brainstem or spinal cord.
81
Q

What are lower motor neurones?

A
  • brainstem cranial nerve nuclei or spinal anterior horn
  • PNS -> cranial nerves and spinal nerves
  • projects to muscle.
82
Q

What are ventromedial UMNs involved in?

A

Postural and girdle muscles e.g. trunk and proximal limbs.

For righting movements and posture.

83
Q

What are dorsolateral UMNs involved in?

A

Distal muscles, elbow to finger, knees to toes.

For fine movement.

84
Q

What are the tracts of ventromedial and dorsolateral?

A

Ventromedial:

  • anterior corticospinal
  • vestibulospinal
  • reticulospinal
  • tectospinal

Dorsolateral:

  • lateral corticospinal
  • rubrospinal
85
Q

Describe the reticulospinal tract.

A
  • Function - increased extensors and decreased flexors. For automatic posture and gait-related movements -> adapts to environ.
  • Arise - pontine and medullary reticular formation (arousal)
  • Rise ipsilaterally (no decussation).
  • Polysegmental
86
Q

Describe the tectospinal tract.

A
  • Function - orienting and flinching movements, ballistic reaching. Coordination of head and eye movement.
  • Arise - superior colliculus (tectum) -> cervical spinal cord. Proximal shoulder girdle muscle and neck.
  • Decussates midbrain -> dorsal tegmental decussation.
87
Q

Describe the vestibulospinal tract.

A
  • Function - increased gravity stance and increased extensors.
    Medial VST:
  • arise -> medial and inferior vestibular nuclei -> cervical and thoracic cords.
  • for positioning of head and neck.
    Lateral VST:
  • arise -> lateral vestibular nuclei -> all SC
  • for balance.
88
Q

What are the effects of lesions on the ventromedial tracts?

A
  • loss of righting reactions
  • loss of navigational control
  • axial immobility and forward slump
  • can’t reach out (no extensor action)
  • can flex elbow and individual digits.
    e. g. pianist - can’t walk but can play but needs support as slumps forward.
89
Q

Describe the rubrospinal tract.

A
  • Functions - increased flexors and active in swing phase. Control and coordination of movement.
  • Arise - red nucleus -> cervical segments.
  • Mesencephalic decussation (midbrain)
90
Q

What does injury to rubrospinal tract cause?

A

Impaired distal arm and hand movement, intention tremors and decorticate posturing.

91
Q

Describe the origin and decussation of the corticospinal tract.

A

Arises -> premotor cortex, primary motor and sensory cortex -> contralateral anterior horn. Corticospinal and corticobulbar tracts.
Posterior limb of internal capsule.
- Pyramid decussation -> 90% contralateral LCST, 10% ipsilateral ACST.

92
Q

What is the function of the corticospinal tract?

A
  • voluntary skilled motor activity e.g. writing and typing.
  • independent flexion of single distal joint
  • not fully myelinated until 2 years.
  • small % dorsal grey projection -> write through pain.
93
Q

What are the consequences of transections above and below decussation?

A

Above -> contralateral spastic paresis and + babinski’s.

Below -> ipsilateral spastic paresis and babinski’s.

94
Q

What does injury to corticospinal tract cause?

A
  • normal walking and navigation, righting reactions and axial posture
  • arms hang limply (loose fine control)
  • reach by shoulder circumduction
  • elbow inactive and fingers flex together
    e. g. pianist - can’t lift elbow or fingers individually but flexes together.
95
Q

Define brainstem death.

A

Irreversible loss of capacity for consciousness (pontine reticular activating system), combined with irreversible loss of capacity to breathe (medullary cardioresp. centres).

HYMS Y1 (25 decks)

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