Neuro - relevant Anatomy and Physiology 2 Flashcards
What is Cognition?
The integration of all sensory information to make sense of a situation
What is the role of the Hippocampus in memory?
- Formation of memories
- Learning
What is the role of the Cortex in memory?
Storage of memories
What is the role of the Thalamus in memory?
Searches + Accesses memories
What is the role of the Amygdala and Cingulate gyrus in memory?
Emotion + memory
What is the Limbic system?
A collection of structures involved in processing emotion and memory
What are the structures of the Limbic system?
- Cingulate gyrus
- Thalamus
- Hypothalamus
- Amygdala
- Hippocampus
What type of memory loss do people have if they have bilateral hippocampal damage?
- 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
What is immediate (or sensory) memory?
- 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!!*
What is short-term memory?
- 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
What is immediate long-term memory?
- hours-weeks
- ie. what you did last weekend
- associated with chemical adaptation at the presynaptic terminal
What is long-term memory?
- can be lifelong
- ie. where you grew up, childhood friends
- associated with structural changes in synaptic connections
What is Anterograde Amnesia?
Which area is destroyed in this type of amnesia?
- 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
What is Retrograde Amnesia?
- 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)
What structural changes are involved at the post-synaptic cell for Long-Term memory?
Long Term Potentiation
- > (“strengthens the synapse”)
- > a well-established, well-rehearsed pattern of neuronal firing unique to that particular memory
What structural changes are involved at the post-synaptic cell for Immediate Long-Term memory?
- Involves chemical changes in the presynaptic neurones
- Increasing Ca2+ entry presynaptic terminals, increases NT release
What are the 2 main types of Long Term Memory?
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)
What is the Papez Circuit?
- 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
How does Korsakoff’s syndrome affect memory?
- Vitamin B1 deficiency
- Leads to damage of Limbic system structures
- Leads to loss of ability to consolidate memories
How does REM sleep affect memory?
- 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)
How does Alzheimers disease affect memory?
- 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
What is the difference between Coma and Sleep?
- 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)
What are the main molecules involved in Sleep?
- DSIP -> (Delta) Sleep Inducing Peptides
- Adenosine
- Melatonin
- Serotonin
- > (precursor to melatonin)
What gland releases Melatonin?
Pineal gland
What is Orexin released from?
What is its purpose?
- The Hypothalamus
- required for wakefulness
What happens in defective Orexin signalling?
Narcolepsy
What is Melatonin released from?
What inhibits and stimulates its release?
- released from the SCN
- 24-hr circadian rhythm
- inhibitory neurones in the SCN are stimulated by light, darkness removes that inhibition
What are Alpha waves associated with?
- associated with relaxed awake state
- high frequency, medium amplitude waves
What are Beta waves associated with?
- associated with alert awake state
- very high frequency, low amplitude waves
What are Theta waves associated with?
- associated with early sleep
- low frequency waves which can vary enormously in amplitude
What are Delta waves associated with?
- associated with deep sleep
- very low frequency but high amplitude waves
What are the stages of the Sleep cycle?
5 stages
- 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
Which stages of the sleep cycle does Sleep walking/talking occur?
- Stage 3 and 4
- (known as Deep Sleep -> delta waves: low frequency, high amplitude waves)
Which stages of the sleep cycle does dreaming/nightmares occur?
- during REM sleep
low amplitude, high frequency waves -> eerily similar to awake state
What is Deep sleep associated with?
- 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)
What is REM sleep associated with?
- 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)
What part of the sleep cycle do night terrors occur in?
- Deep delta sleep
early in the night
What part of the sleep cycle does sleep walking (sommambulism) occur in?
- exclusively in non-REM sleep
- > mainly stage 4 sleep (deep delta sleep)
What is the pathophysiology of Narcolepsy?
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
What is sensory transduction?
What encodes the stimulus intensity?
- 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
Describe the major pathway by which information from the body about pain and temperature reaches consciousness
- 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
Describe the major pathway by which information from the body about touch and limb position reaches consciousness
- 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
Why does pain originating from the viscera often result in sensation being referred to a somatic structure from the same dermatome?
“Referred pain”
- 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
Describe the gate control hypothesis for pain modulation
- 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”
Which descending pathways from the CNS are responsible for controlling pain?
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”)
What determines the acuity of receptive fields?
- Density of innervation
- Size of Receptive fields
What type of fibres are mechanoreceptive fibres?
- > A-alpha and A-beta fibres
- > large diameter, myelinated fibres
- > proprioceptive fibres ie. muscle spindles, GTOs
What type of fibres are thermoreceptive and nociceptive fibres?
- > A-Delta and C fibres
- > A-Delta = small diameter, myelinated fibres -> cold, “fast” pain, pressure
- > C = small diameter, unmyelinated fibres -> warmth, “slow” pain
What is the sensory homunculus?
- 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
What is the mechanism of action of NSAIDs as an analgesic?
- Prostaglandins sensitise nociceptors to bradykinin
- NSAIDs inhibits COX enzyme which converts arachidonic acid to prostaglandins
- Therefore, NSAIDs work well against pain associated with inflammation
What is the mechanism of action of Local Anaesthetics?
- Blocks Na+ action potential and therefore blocks all axonal transmission
What is the mechanism of action of TENS?
- “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
What is the mechanism of action of Opioids?
- 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)
