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3.2 neuroclin 2 > ADHD 2 > Flashcards

ADHD 2 Flashcards

1
Q

flaw with classical theories of ADHD - frontal cortex and dopamine

A

frontal cortex:
many psychiatric and neurological disorders are associated with frontal cortex dysfunction (from schizophrenia to Parkinson’s disease) - not just ADHD

dopamine:
new drugs (atomoxetine, guanfacine) affect noradrenaline NOT dopamine

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2
Q

ADHD drugs - act on noradrenaline

A

atomoxetine
guanfacine

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3
Q

2 classical theories of ADHD and 1 novel theory

A

classical:

  • frontal cortex dysfunction
  • dopamine

novel:

  • collicular (sensory) hyper-responsiveness
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4
Q

frontline drug treatments of ADHD

A

DL-amphetamine and methylphenidate

these are both class B drugs (Misuse of Drugs Act, 1971) –> therefore have significant abuse potential

therefore an issue that we give these to kids!

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5
Q

novel approach to ADHD treatment

A

several presentations - inattentive, hyperactive/impulsive, combined

may not be productive to look for a single cause or single therapeutic drug action

instead look at specific symptoms not the overall disorder

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6
Q

novel approach to ADHD - symptom of distractability

A

Strauss (1940s/50s) - distractibility as a core symptom of ADHD

DSM-V = “is often easily distracted by extraneous stimuli”

useful focus = neural substrate mediating distractibility is well known (not just in extremes of ADHD, just a general system)

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7
Q

distractibility neural substrates

A

intimately linked with superior colliculus

primitive system - animal response to things around them, both good and bad - pull attention away to other things

can be distracted to important or unnecessary things

superior colliculus = subcortical, dorsal (top/back part) of the brain stem (images on ppt if you want)

idea that SC still appears to be functional in humans as a distractibility circuit

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8
Q

superior colliculus and distractibility circuits

A

SC is part of the visual system
important subcortical visual system

retina projects to the SC
in rats, SC is the biggest area of visual input (not in primates as much)

highly conserved - across many species

humans = SC controls eye movements - idea that the eyes can be moved to new info and pull attention away to it

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9
Q

superior colliculus - collicular lesion and distractibility in rats

A

collicular lesions in rats decrease distractibility

Goodale and Murison (1975)

  • lesion SC in rats
  • rats are trained to run to a set of doors in an arena - one is illuminated - to get a reward (brightness discrimination task)
  • after training, a distraction is added (flashing light or noise)
  • normal SC = attend to distraction, pause, attend to it, or freeze and don’t cross arena (fear)
  • with a SC lesion = don’t respond to it at all
    – go straight across to get their reward
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10
Q

Gaymard et al (2003) - case study lesion to SC

A

lesion in a 51 year old woman which affects the projection from the cortex to the SC (prefronto-tectal tract) on the left hand side

at the inferior colliculus - lost her inhibitory control

SC is often controlled by higher centres - but this lesion interrupts these pathways

she became more distractable on the right visual field (not right eye, right side of both eyes) –> as issue was on the left of the brain

–> left visual field inputs to the right SC
–> right visual field inputs to the left SC

used an anti-saccade paradigm to test:

  • patient fixates on a spot in the middle of a visual field
  • then a target appears - don’t look at it and instead need to look the opposite direction to the target (anti-saccade)
  • target either in left or right visual field

results:

  • measured % errors (error = look at target)
  • target in right visual field = lots of errors
  • target in left visual field = patient did very similar to control

conclusion:

  • cannot resist looking at presented target on the right –> left lesion = distractable (hyperresponsive to target)
  • taking away inhibitory input of colliculus = more responsive = increased distractibility ( look at target not away from it)
  • seemed almost unable to not look at it when presented on the right
  • presented left = able to move eyes and look to the right –> able to not attend to it
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11
Q

distractibility in ADHD and a hyper-responsive colliculus

A

idea that distractibility circuits in the brain are through the SC

increased activity = increased distractibility (less inhibitory control)

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12
Q

how long have vertibrate brains had a SC

A

500 million years

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13
Q

4 types of evidence needed for hyper-responsive colliculus in ADHD

A

hyper-responsiveness in an animal model

is there a “hot line” to the brains interrupt system:

  • need to stop the one activity to be distracted by another
  • continual interruption of what you’re doing to do something else

any collicular impairments in ADHD

do ADHD treatments effect the colliculus

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14
Q

hyper-responsiveness of SC in rats - light flash study

A

study of action potentials in SC in rats when lights of different brightness is flashed

brighter light = more action potentials fired

genetically hypotensive rat = used as an animal model of ADHD

  • shows higher responsiveness to all levels of light brightness than a control rat

peak amplitude = higher at all light levels in GH rats than control

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15
Q

study of the link between distractibility and interrupt systems

A

use tract tracing:

  • anatomical method to look for connections in rat brains
  • anterograde tracing from SC cell body down axons using chemical labelling
  • leave a few weeks and study post mortem - where the label ends up

results = found in STN (subthalamic nucleus)

STN = part of the interrupt system - stops you doing what you are currently doing

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16
Q

STN

A

subthalamic nucleus

interrupt system - stops you doing what you’re doing right now

e.g. Parkinsons = high activity in STN which “jams” brain in an “off” position so they find it hard to move

17
Q

ADHD as a continuum disorder - study in adults

A

difficult to work with kids (ethics) but adults can have ADHD too

ADHD is a continuum disorder (ASRS - adult ADHD rating scale - based on DSM) - find the results in a population fall on a bell curve (normal distribution)

ASRS is not a diagnostic tool - idea that lots of people have high traits of ADHD but no diagnosis

continuum disorder = symptoms grade into normal population (everyone is distractible, some more tho) –> therefore not categorical - where is the line to distinguish between people

can study a subclinical population - high traits but no ADHD diagnosis

18
Q

colliculus function - layers, responses

A

SC is a visual area
BUT also is involved in multisensory integration

SC has 7 layers
shallower layers are purely visual
deeper layers are multisensory - visual, auditory, and somatosensory converge onto a common pool of neurons here

supra-additive response (mixed modalities gives bigger response than just adding individual responses together) - enhanced response to multisensory if they are close together in space and time

19
Q

studying collicular impairments in ADHD - simultaneous judgement

A

Panagiotidi et al (2017)

simultaneity judgement task:

  • participants given multisensory stimuli (auditory beep and visual pattern)
  • at a range of stimulus onset asynchronies (SOAs)
  • determine if auditory or visual were at same or different times

measure = proportion of trials that are reported as simultaneous

compared high and low ADHD (ASRS) groups

results:

  • bell curve shape - both ends are less likely to be thought to have been presented together as the SOA is larger
  • 0s is the middle of the curve (simultaneous presentation)
  • in high ADHD group, always perceive as ore distinct stimuli - less viewed as simultaneous –> could this be the cause of distraction
  • low ADHD - perceive much more as simultaneous stimuli
  • low ADHD curve appears to be ontop of high ADHD curve

view as more separate = could be more distracting –> less cohesive

20
Q

effect of amphetamines on colliculus

A

amphetamine used on rats

reduces superior colliculus’ response to visual stimuli with higher doses

21
Q

anatomical link between colliculus and and dopamine
pathway and how it has been seen

A

colliculus mediates distractibility and dopamine neurons

The tectonigral projection:

  • a direct pathway from the deep layers of the colliculus to the ventral midbrain
  • terminates on dopamine and non-dopamine neurons

electron microscopy has shown this - terminal of axon from colliculus with dopamine neuron

bouton and dendrite together

22
Q

link between colliculus and dopamine - light flash study methods

A

dopamine and reward - this is really linked to sensory system

colliculus is a primary source of visual input to dopamine neurons

study:

  • anaesthetise a rat
  • flash a light in its eye - with colliculus asleep or when it is awake
  • single unit recording of dopamine neurons
  • look at effect on responses of dopamine neurons to visual stimulation

awakened deep layers of the colliculus with bicuculline (GABA antagonist - prevents neurotransmitter from getting access to receptor)

23
Q

light flash study results - visual activation of dopamine neurons

A

record cells in colliculus (multi-unit) and dopamine cell (single cell)

flash a light and measure response:

pre-drug baseline = no light response in deep layers (superficial layers of colliculus always respond - visual only)

after bicuculline = colliculus (deep layers) starts to “see” light - responds to light stimuli
dopamine neurons also respond to the light

24
Q

how to measure dopamine levels in very specific brain areas

A

can use electrodes (amperometry) in the forebrain to measure dopamine levels in a very small area

by establishing a small voltage which changes chemical composition of dopamine through oxidation

results in dopamine releasing electrons which is measured by electrode

visual activation of dopamine neurons via the input from the colliculus leads to dopamine release in the forebrain

25
Q

light flash study - effect of dopamine release in the forebrain

A

no electrochemical response to light without collicular bicuculline - wake up colliculus

nomifensine:

  • selective DA re-uptake inhibitor
  • increases amplitude and duration of light response

what this shows:

  • colliculus can change level of activity in dopamine system
  • connectivity chain is very important into the forebrain
  • indication that dopamine theory and colliculus hyper-responsiveness MAY be related
26
Q

where are hotspots for prescribing methylphenidate in england

A

northwest and southeast

27
Q

retrograde vs anterograde tracing

A

anterograde tracing = cell body to terminal - direction of action potential
retrograde tracing = to find cells of origin = opposite to action potential

28
Q

cerebral cortex dysfunction and ADHD - how they find the link to colliculus

A

use retrograde tracing - inject into SC to find cells of origin which project into deeper layers of SC (link to dopamine)

want to find origins from cortex - cortical projections

found they come from almost all areas of cortex - including frontal

all areas of frontal cortex in rats project into SC

29
Q

can the cortex cause change in DA neurons via superior colliculus

barrel cortex study in rats - method

A

would show a chain of command through these ( cortex changes DA via SC)

effects of local chemical manipulation of colliculus (to “wake it up” on responses of dopamine neurons to barrel cortex stimulation

method:

  • anesthetise a rat
  • stimulate the sonatosensory cortex and see if the DA neurons change activity
  • then wake the SC and see if that changes the effect of cortical stimulation on DA
  • light flash used as control (seen in previous studies)

results:
when SC is asleep:

  • SC = no reaction to light flash and very small reaction to barrel cortex stimulation
  • DA neuron = no reaction to flash or stimulation

when SC is awake:

  • SC = large increase in activity from light flash and barrel cortex stimulation
  • DA neuron = massive increase in DA from light flash, barrel cortex stimulation also increases DA

conclusions:

  • functional from cortex to DA via colliculus
  • the same can happen in reverse e.g. stimulation leads to decrease in DA

3.2 neuroclin 2 (12 decks)

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