Neuro - relevant Anatomy and Physiology 2 Flashcards

1
Q

What is Cognition?

A

The integration of all sensory information to make sense of a situation

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2
Q

What is the role of the Hippocampus in memory?

A
  • Formation of memories

- Learning

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3
Q

What is the role of the Cortex in memory?

A

Storage of memories

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4
Q

What is the role of the Thalamus in memory?

A

Searches + Accesses memories

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5
Q

What is the role of the Amygdala and Cingulate gyrus in memory?

A

Emotion + memory

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6
Q

What is the Limbic system?

A

A collection of structures involved in processing emotion and memory

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7
Q

What are the structures of the Limbic system?

A
  • Cingulate gyrus
  • Thalamus
  • Hypothalamus
  • Amygdala
  • Hippocampus
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8
Q

What type of memory loss do people have if they have bilateral hippocampal damage?

A
  • central to learning and the formation of memories*
  • unable to form long-term memories
  • > although immediate (sensory) memory (seconds in length) and intact long-term memory (before the damage) is intact - reflexive memory (motor skills) also remains intact
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9
Q

What is immediate (or sensory) memory?

A
  • a few seconds
  • describes the ability to hold experiences in the mind for a few seconds
  • based on different sensory modalities
  • visual memories decay fastest (<1s), auditory ones slowest (<4s)
  • nb. NOT THE SAME as working memory!!*
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10
Q

What is short-term memory?

A
  • seconds-hours
  • often called working memory
  • used for short-term tasks ie. dialling a phone number, mental arithmetic, reading a sentence
  • associated with reverberating circuits
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11
Q

What is immediate long-term memory?

A
  • hours-weeks
  • ie. what you did last weekend
  • associated with chemical adaptation at the presynaptic terminal
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12
Q

What is long-term memory?

A
  • can be lifelong
  • ie. where you grew up, childhood friends
  • associated with structural changes in synaptic connections
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13
Q

What is Anterograde Amnesia?

Which area is destroyed in this type of amnesia?

A
  • inability to recall events that happen after the injury
  • > depending on the severity of the injury, this can be short-lived or permanent
  • destruction of the Hippocampus (ie. Clive wearing) results in permanent inability to form new memories
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14
Q

What is Retrograde Amnesia?

A
  • can’t remember events leading up to the injury
  • > although recall of events that happened a long time ago are still intact (as they are better rehearsed and more deeply embedded)
  • often presents with anterograde amnesia - however, if only the thalamus is damaged, and the hippocampus is spared, only retrograde amnesia is seen (suggests thalamus is required for “searching” our existing memory bank)
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15
Q

What structural changes are involved at the post-synaptic cell for Long-Term memory?

A

Long Term Potentiation

  • > (“strengthens the synapse”)
  • > a well-established, well-rehearsed pattern of neuronal firing unique to that particular memory
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16
Q

What structural changes are involved at the post-synaptic cell for Immediate Long-Term memory?

A
  • Involves chemical changes in the presynaptic neurones

- Increasing Ca2+ entry presynaptic terminals, increases NT release

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17
Q

What are the 2 main types of Long Term Memory?

A

1 - Declarative or Explicit Memory:

  • Abstract memory for events (episodic memory) and for words, rules and language (semantic memory)
  • Relies heavily on the Hippocampus

2 - Procedural/Reflexive/Implicit Memory:

  • Acquired slowly through repetition -> includes motor memory for acquired motor skills such as playing tennis, and rules-based learning such as, in the UK, always driving on the left
  • Thinking about these skills often impairs performance
  • Based mainly in the Cerebellum
  • Independent of Hippocampus (nb. Clive Wearing)
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18
Q

What is the Papez Circuit?

A
  • If experience is considered useful, the Frontal cortex “gates” the so-called Papez circuit:
  • Hippocampus -> Mammillary bodies -> Anterior Thalamus -> Cingulate gyrus
  • Reverberating activity then continues between the Papez circuit, the Frontal cortex, the sensory and association areas until the consolidation process is complete
  • Different components of the memory are laid down in different parts of the cortex ie. visual component in the visual cortex, auditory in the auditory cortex, etc
  • Recall can be evoked by multiple associations -> many memories have strong emotional components to them ie. pleasant or unpleasant
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19
Q

How does Korsakoff’s syndrome affect memory?

A
  • Vitamin B1 deficiency
  • Leads to damage of Limbic system structures
  • Leads to loss of ability to consolidate memories
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20
Q

How does REM sleep affect memory?

A
  • Subjects deprived of sleep show impairment in memory consolidation for complex cognitive tasks
  • Dreaming may enable memory consolidation -> reinforce weak circuits
  • Pt’s with Korsakoff’s or Alzheimer’s have greatly reduced REM sleep (cholinergic neurones responsible for REM)
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21
Q

How does Alzheimers disease affect memory?

A
  • Severe loss of cholinergic neurones throughout the brain, including the Hippocampus
  • Gross impairment of memory
  • Some improvement in Alzheimer’s may be seen with anti-cholinesterases, but underlying degeneration continues
  • Unknown cause
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22
Q

What is the difference between Coma and Sleep?

A
  • Coma = state of unconsciousness from which individual can be aroused by normal stimuli, light, touch, sound, etc
  • Sleep = state of unconsciousness from which individual can be aroused by normal stimuli, light, touch, sound, etc (predictable and cyclical)
23
Q

What are the main molecules involved in Sleep?

A
  • DSIP -> (Delta) Sleep Inducing Peptides
  • Adenosine
  • Melatonin
  • Serotonin
  • > (precursor to melatonin)
24
Q

What gland releases Melatonin?

A

Pineal gland

25
Q

What is Orexin released from?

What is its purpose?

A
  • The Hypothalamus

- required for wakefulness

26
Q

What happens in defective Orexin signalling?

A

Narcolepsy

27
Q

What is Melatonin released from?

What inhibits and stimulates its release?

A
  • released from the SCN
  • 24-hr circadian rhythm
  • inhibitory neurones in the SCN are stimulated by light, darkness removes that inhibition
28
Q

What are Alpha waves associated with?

A
  • associated with relaxed awake state

- high frequency, medium amplitude waves

29
Q

What are Beta waves associated with?

A
  • associated with alert awake state

- very high frequency, low amplitude waves

30
Q

What are Theta waves associated with?

A
  • associated with early sleep

- low frequency waves which can vary enormously in amplitude

31
Q

What are Delta waves associated with?

A
  • associated with deep sleep

- very low frequency but high amplitude waves

32
Q

What are the stages of the Sleep cycle?

5 stages

A
  • Stage 1: slow-wave, non-REM, s-sleep, slow eye movements, light sleep, early in the sleep cycle -> Theta waves
  • Stage 2: eye movements stop, frequency slows further but EEG shows bursts of rapid waves called “sleep spindles”
  • Stage 3: high amplitude, very slow delta waves -> spindle activity declines
  • Stage 4: exclusively delta waves
  • from stage 4 sleep, move back up through stage 3 and stage 2 before entering REM sleep*
  • REM sleep: rapid eye movements -> low amplitude, high frequency waves eerily similar to awake state
33
Q

Which stages of the sleep cycle does Sleep walking/talking occur?

A
  • Stage 3 and 4

- (known as Deep Sleep -> delta waves: low frequency, high amplitude waves)

34
Q

Which stages of the sleep cycle does dreaming/nightmares occur?

A
  • during REM sleep

low amplitude, high frequency waves -> eerily similar to awake state

35
Q

What is Deep sleep associated with?

A
  • Stage 3 and 4
  • Delta waves
  • First hours of sleep
  • Sleep walking/talking
  • V active Hippocampus
  • Decreased vascular tone (BP), respiratory and BMR (hence drop in body temp)
36
Q

What is REM sleep associated with?

A
  • cholinergic pathways
  • > anticholinesterases increases time spent in REM sleep
  • rapid eye movements
  • dreaming
  • inhibitory projections from pons to spinal cord: inhibition of skeletal muscles -> prevents acting out of dreams
  • mimics beta waves (associated with highly alert, awake state)
  • % of time in REM sleep declines as you get older -> important for neuronal spasticity (may be the reason why you get cognitive decline as you grow older)
37
Q

What part of the sleep cycle do night terrors occur in?

A
  • Deep delta sleep

early in the night

38
Q

What part of the sleep cycle does sleep walking (sommambulism) occur in?

A
  • exclusively in non-REM sleep

- > mainly stage 4 sleep (deep delta sleep)

39
Q

What is the pathophysiology of Narcolepsy?

A

Dysfunctional Orexin release from the Hypothalamus

  • > less orexin produced from the Hypothalamus -> less inhibition of melatonin from the Pineal gland -> more Melatonin produced!
  • > enters directly into REM sleep with no warning
40
Q

What is sensory transduction?

What encodes the stimulus intensity?

A
  • All sensory receptors transduce their adequate stimulus into a depolarisation, the receptor (generator) potential
  • The size of the receptor potential and the frequency of APs encodes intensity of the stimulus
41
Q

Describe the major pathway by which information from the body about pain and temperature reaches consciousness

A
  • Thermoreceptive and Nociceptive fibres (A-Delta and C fibres)
  • synapse in the Dorsal Horn (spinal cord)
  • 2nd order fibres decussate in the midline in the spinal cord
  • project up through the contralateral spinothalamic tract to the reticular formation, thalamus and cortex
42
Q

Describe the major pathway by which information from the body about touch and limb position reaches consciousness

A
  • Mechanoreceptive fibres (A-alpha and A-Beta fibres)
  • project straight up through ipsilateral dorsal columns
  • synapse in cuneate and gracile nuclei (medulla)
  • 2nd order fibres decussate in the medulla, and project to the reticular formation, thalamus and cortex
43
Q

Why does pain originating from the viscera often result in sensation being referred to a somatic structure from the same dermatome?

“Referred pain”

A
  • Due to convergence between 2 nociceptors of the 2 different regions (ie. skin on shoulder and heart)
  • Interpreted by the brain as coming from the same place
44
Q

Describe the gate control hypothesis for pain modulation

A
  • Activity in A-Beta fibres (from fine touch) activates inhibitory interneurones
  • Inhibitory interneurones release opioid peptides (endorphins) that inhibit transmitter release from A-Delta/C fibres (pain and temp) hence “closing the gate”
  • The same inhibitory interneurones are also activated by descending pathways from PAG and NRM, hence also “closing the gate”
45
Q

Which descending pathways from the CNS are responsible for controlling pain?

A

Peri-Aqueductal Grey Matter (PAG) + Nucleus Raphe Magnus (NRM)

-> activate inhibitory interneurones that release opioid peptides and inhibits transmitter release from A-Delta/C fibres (“closing the gate”)

46
Q

What determines the acuity of receptive fields?

A
  • Density of innervation

- Size of Receptive fields

47
Q

What type of fibres are mechanoreceptive fibres?

A
  • > A-alpha and A-beta fibres
  • > large diameter, myelinated fibres
  • > proprioceptive fibres ie. muscle spindles, GTOs
48
Q

What type of fibres are thermoreceptive and nociceptive fibres?

A
  • > A-Delta and C fibres
  • > A-Delta = small diameter, myelinated fibres -> cold, “fast” pain, pressure
  • > C = small diameter, unmyelinated fibres -> warmth, “slow” pain
49
Q

What is the sensory homunculus?

A
  • Ultimate termination of afferent fibres in the somatosensory cortex of the postcentral gyrus
  • endings are grouped according to the location of the receptors
  • extent of representation in the homunculus is related to the density of receptors in each location
50
Q

What is the mechanism of action of NSAIDs as an analgesic?

A
  • Prostaglandins sensitise nociceptors to bradykinin
  • NSAIDs inhibits COX enzyme which converts arachidonic acid to prostaglandins
  • Therefore, NSAIDs work well against pain associated with inflammation
51
Q

What is the mechanism of action of Local Anaesthetics?

A
  • Blocks Na+ action potential and therefore blocks all axonal transmission
52
Q

What is the mechanism of action of TENS?

A
  • “like a technological version of ur mum rubbing your sore arm to make it better”
  • Uses direct electrical stimulus to activate A-beta fibres (mechanoreceptors), which will activate inhibitory interneurones and “close the gate” to A-delta/C fibres
53
Q

What is the mechanism of action of Opioids?

A
  • ie. Morphine, Codeine
  • reduces sensitivity of nociceptors
  • blocks NT release in the dorsal horn (hence epidural administration)
  • activates descending inhibitory pathways (from the PAG and NRM)