The Brain & Neuroimaging Flashcards
1
Q
Describe neuroimaging? Give examples of machines used for it?
A
- Divided mainly into structural (spatial) imaging of where things happen in the brain and functional relating to electrochemical and metabolic function of neurons.
- Temporal or time domain neuroimaging
o Electroencephalography (EEG), Magnetoencephalography (MEG) and some Near Infrared Spectroscopy.
o Magnetic Resonance Imaging (MRI) – also fMRI
o Positron Emission Tomography (PET) – fairly invasive
o Single Photon Emission Computed Tomography (SPECT) – similar to PET but less precise
Above 3 provide structural info, blood flow and neurotransmitter specificity in the brain
2
Q
Describe the cerebral cortex?
A
- Human cerebral cortex consists of 3 to 6 layers of neurons
o The phylogenetically oldest part of the cortex (archipallium) has 3 distinct neuronal layers, & is exemplified by hippocampus, which is found in medial temporal lobe - Majority of cortex (neocortex or neopallium) has 6 distinct cell layers & covers most of surface of the cerebral hemispheres.
- Cortex includes 2 general classes of neurons:
o Projection, or principal, neurons (e.g., pyramidal neurons – shaped like pyramid) “project” or send info to neurons located in distant areas of brain
o Interneurons (e.g., basket cells) are local-circuit cells which influence activity of nearby neurons some interneurons look like stars (called stellate cells)
Interneurons are essentially everything else in brain which are modulating output of pyramidal cells - Most principal neurons form excitatory synapses on post-synaptic neurons, while most interneurons form inhibitory synapses on principal cells or other inhibitory neurons
3
Q
Describe neuronal excitability?
A
- Neuron = excitable cell (inside of cell is -ve) – when it depolarises it gets closer to 0 & a little above 0
- Action potentials occur due to depolarisation of neuronal membrane, w/ membrane depolarisation propagating down axon to induce neurotransmitter release at axon terminal
- They occur in an all-or-none fashion as a result of local changes in membrane potential brought about by net +ve inward ion fluxes
o Can’t increase stimulus strength to get a bigger action potential but can stimulate in time (temporal neuronal circuitry) - Membrane potential therefore varies w/ activation of ligand-gated or voltage gated channels (electrochemical signalling)
- Ligand-gated channels conductances are affected by binding to neurotransmitters proteins which alter membranes at synapse region
- Voltage-gated channels (dependent on ions coming in) conductance are affected by changes in transmembrane potential or w/ changes in intracellular ion compartmentalisation (keep neurons excited for longer time)
o Dependent on calcium ions coming in to make it a steady state potential keeping the neuron more depolarised & more excited for a longer period of time - A hyperexcitable state can result from ↑excitatory synaptic neurotransmission, ↓inhibitory neurotransmission
o An alteration in voltage-gated ion channels OR an alteration of intra- or extra- cellular ion concentrations in favour of membrane depolarisation - A hyperexcitable state can also result when several synchronous subthreshold excitatory stimuli occur, allowing their temporal summation (adding together all inputs coming into neuron(s) in time) in post synaptic neurons
4
Q
What are the factors affecting excitability of individual neurons?
A
- Complexity of neuronal activity is partly due to various mechanisms controlling level of electrical activation in one or more cellular regions
- These mechanisms may act inside neuron or in cellular environment, including other cells (e.g., neighbouring neurons, glia, and vascular endothelial cells) as well as the extracellular space, to modify neuronal excitability
o Glia and vascular endothelial cells give neuron energy to act - The inside parts of cell may be termed “neuronal” or “intrinsic,” and the extracellular space is called “extra- neuronal” or “extrinsic.”
5
Q
Describe the array of neurons?
A
- Neurons are connected together in elaborate arrays that provide additional levels of control of neuronal excitability
o An e.g. of a v. basic neuronal network is dentate gyrus & hippocampus (look v similar & act like they are electrically coupled)
o Earliest memories/learning in Hippocampus – when learn new things it is stored here & gyrus) - In dentate gyrus, afferent (sensory) connections to network can directly activate projection cell (e.g., granule cells).
- The input can also directly activate local interneurons (bipolar and basket cells), & these may inhibit projection cells in the vicinity (feed-forward inhibition).
- Also, the projection neuron may in turn activate interneurons which in turn act on the projection neurons (feedback inhibition)
6
Q
Describe feedback loops of neurons?
A
- Recurrent inhibition can occur when a principal neuron forms synapses on an inhibitory neuron, which in turn forms synapses back on principal cells to achieve -ve feedback loop
o There are recurrent neurons found in brain, but most common ones are found in spinal cord – these cause recurrent inhibition for mono-synaptic reflex (a 1 synapse reflex which allows you to move or stretch your muscles) - Some interneurons appear to have extensive axonal projections, rather than just local, confined axonal structures
o Output of these interneurons may be more than 1 axon - In some cases, such interneurons may provide a v. strong synchronisation or pacemaker type of activity to large groups of neurons
o When neurons are doing higher order processing, they are not too concerned about ionic flow depolarisation & hyperpolarisation (they are still using these though)
When there is a bigger stimulus, they start by firing & these are V1 cells, they start to fire synchronously towards a particular stimulus - Synchronisation gives percept so that disparate parts of brain will be in synchronous activity (w/ v slight time lag)
7
Q
What is normal synaptic transmission (neurons)?
A
- If there is an inhibitory pre-synaptic terminal:
o Postsynaptic neuron, communicated with by pre-synaptic cell, output is dampened
o Most common inhibitory neurotransmitter is GABA - If it is an excitatory synapse:
o Glutamate is released
o Glutamate not only excited the neuron by sending in sodium channels, but it also opens up voltage gated calcium channels
o N-Methyldiaspartate (NMDA) receptor is one of the glutamate receptor complexes – can be important for changing circuitry – have nanomolar amounts of calcium going into cell & can change cellular circuitry & array & therefore synchronisation
8
Q
Describe the organisation of the neural network and neuronal excitability?
A
- Changes in function of one or more cells within a circuit can significantly affect both neighbouring & distant neurons e.g. sprouting (when have some sort of lesion) of excitatory axons to make more numerous connections can ↑ excitability of network of connected neurons
o This occurs most often after status epilepticus epilepsy – too much synchronisation, only feed-forward inhibition, no feed-back inhibition, entire neural network goes into overdrive, too much calcium going into cells, can be fatal - Loss of inhibitory neurons will also ↑ excitability of the network
- Inhibitory function can also be ↓by a loss of excitatory neurons that activate or “drive” the inhibitory neurons
o E.g. in stroke lose lots of neurons and none of the other neurons in that circuit have the “drive” to function
9
Q
What is electroencephalography (EEG)?
A
- Most common & cheapest form of functional neural imaging
- Recording, from surface of skull, volume currents as well as those that are contributed to by internal neuronal currents over areas of cortex that may or may not be active
- EEG has advantage of high temporal resolution but poor spatial resolution of cortical disorders
- EEG is most important in neurophysiological study for diagnosis, prognosis & tx of epilepsy
- Recording from surface of skull of areas that may or may not be active
- Don’t get a v detailed view – get a gross idea but good picture of functional organisation in px’s brain e.g. in V1
- Gives good picture of functional organisation in px’s brain
10
Q
Describe dipoles (with EEG)?
A
- Dipoles can be electrical or magnetic
- Extracellular dipole generated by excitatory post-synaptic potential at apical dendrite of pyramidal cell
- A dipole: region of +ve charge separated from a region of -ve charge by some distance
o Region of +ve charge is referred to as a source
o Region of -ve charge is referred to as a sink - Many dipoles in the brain
11
Q
How does an EEG scan work? What is the procedure?
A
- An electrode placed at scalp cannot detect these electrical changes in a single neuron because:
- 1) The potentials are small in magnitude (due to low extracellular resistance)
- 2) There is considerable distance from cell to scalp surface.
- Two cortical properties permit record of brain’s electrical potential
o 1st, pyramidal cells all have same relative orientation & polarity
o 2nd, many cells are synchronously activated cells in dentate gyrus – fire synchronously to generate memories - Summation of dipoles created at each of thousands of neurons creates electrical potential detectable at scalp
- In practice, 20 or more scalp electrodes are placed at specific locations on head to allow simultaneous recording from cortical regions of both hemispheres
o Each electrode detects synchronous activity generated by ~6 cm2 of cortex: the activity is recordable generally at gyral surfaces
Sulci surfaces (valleys) are too deep - Cortex that faces the cortical sulci generally does not contribute to EEG potentials because the cortical dipoles generated in this location cancel each other out
- Electrical field generated by similarly oriented pyramidal cells in cortex (layer 5) & are detected by scalp electrode
12
Q
Describe EEG Waveforms and define the term “Binding”?
A
- EEG waveforms are divided into 5 major frequency bands:
o delta (0– 3+ Hz)
o theta (4–7+ Hz)
o alpha (8–13+ Hz) (v strong in V1 – v related to attention)
o beta (>14 Hz)
o gamma (40 Hz +) (v important to recognise a new stimulus neural binding e.g. happens when look at stereo image) - At 1st glance, normal spontaneous electrical activity detected by EEG appears somewhat chaotic
o However, there is a certain organisation & rhythmicity of the activity that depends on level of alertness or sleep & age of subject. - Physiological basis of some of these rhythms seems to arise from intrinsic pacemaker cells in cortex & thalamus (where LGN hangs out, integrator of sensory info going up to brain & motor info as well as other cortical info coming back down)
o Big area of thalamus called pulvinar which is mostly integrating audio-visual and somatosensory info sent on further to higher order centres - Binding = synchronicity when it is functional
- Several EEG rhythms can be characterized on basis of location, freq & reactivity of activity & clinical state of px
- For e.g., a symmetrical rhythm is observed over posterior head regions during relaxed wakefulness w/ eyes closed – attenuates (gets lower) upon eye opening or mental alerting activities
o This is posterior dominant rhythm or alpha rhythm, as in adults has a freq of 8–13 Hz
o In children it may be in theta range: 4-8Hz
13
Q
What are the EEG Frequencies?
A
- Gamma Band 30-100Hz: thought to integrate or bind spatially separate neuronal populations. Implicated in learning, novel stimulus awareness and ‘consciousness’
- Beta Band 14-30Hz: involved in action and alertness – therefore associated with movement control rhythms which are imposed on spinal neurons
o Usually associated strongly w/ muscular activity - Alpha Band 8-12 Hz: involved in relaxation – appears to be a signature resting rhythm of neurons
- Theta Band 4-8Hz: associated with drowsiness and slipping into sleep
- Delta Band: 0.1-4Hz: associated with deep sleep
o V. slow – v spread out in same period of time
14
Q
Describe EEG & Visual Evoked Potentials (VEPs)?
A
- EEG from over Oz (midline region)(visual cortex)
- Steady state VEP elicited by a 21.2Hz sinusoidal flickering stimulus
o Visual cortical neurons in V1 are frequency tagging or mimicking frequency at which they are being stimulated - Transient VEP waveform elicited by binocular viewing of a patterned stimulus
15
Q
What are transient VEPs? What are pattern VEPs? What are abnormal VEPs?
A
- Transient VEPs are elicited by neurons turning on & off in response to a sudden stimulus
- Because of delay in appearance of next stimulus, visual system is allowed to recover
- Typically, transient VEPs are recorded to either a flash or a reversing checkerboard
- Times are longer for a more complicated pattern/stimulus
Pattern VEPs have different implicit times or latencies to different patterns
Abnormal VEPs – in cavernous sinus meningioma – something growing in brain/pushing on eye
