midterm Flashcards
(315 cards)
1
Q
What is biopsych?
A
The study of psych phenomena in terms of their underlying mechanisms. In other words, asking psychological questions and giving biological answers, which differs from neuroscience which is only concerned with the nervous system.
2
Q
What are neurons?
A
signalling units of the brain. we have one hundred billion. They are unique in their shape. They do not replicate except in two places in the brain where neurogenesis can occur, and we lose about half. This is because neurons would have to connect to the exact same other neurons as their successor to replicate, a task that would be so difficult it is functionally impossible.
3
Q
How can neurons be categorized?
A
Shape, chemistry, Soma shape, function
4
Q
What are the categories of neurons (by shape?)
A
unipolar
one axon extends from cell body
bipolar
two extensions off of cell body–one axon, one dendrite
multipolar
single axon, many dendrites
5
Q
How are neurons categorized by function?
A
motor
coordinates muscle movements
sensory
carries sensory signals
interneurons
increase information processing capacity. These represent the majority of neurons in the body.
6
Q
What do interneurons do?
A
increase information processing capacity. These represent the majority of neurons in the body.
7
Q
How can neurons be categorized by chemistry?
A
The type of neurotransmitter created, eg dopaminergic, etc
Some chemicals are found in different distributions in different neurons, so we could talk about zinc-containing neurons, etc
8
Q
What are the two categories of neurons by soma shape?
A
Granular vs pyramidal cells
9
Q
How many glial cells are there?
A
100 billion to a trillion glial cells in the brain.
10
Q
What do myelinating glial cells do?
A
Myelinating glia put the sheath onto axons. In the PNS, Schwann cells do this–one cell per section of axon, wrapped fully around including nucleus. Oliodendroglia myelinate in the brain–one cell to many different axons, external nucleus.
11
Q
What do Schwann cells do and where do they do it?
A
Schwann cells myelinate the PNS. One cell per section of axon, wrapped fully around including nucleus.
12
Q
What do oligodendroglia do and where do they do it?
A
Oliodendroglia myelinate in the brain–one cell to many different axons, external nucleus.
13
Q
What do astroglia do?
A
In their young form, aid in guiding neurons to make the right connections during development (radial glia) then mature into astroglia and aid in giving the brain structure in adulthood, the “packing peanuts of the brain” that wrap around synapses to keep them compartmentalized, help regulate chemical levels. They support the foundation of the BBB.
14
Q
What do microglia do?
A
are actually phagocytose that eat dead cells) and are not actually glia. Most active during adolescence, after a brain injury.
15
Q
What are axons?
A
Axons speak. There is only one per neuron, and they can extend out very long distances. Their diameter is always the same for each axon, ensuring the action potential is conducted at the same speed unilaterally.
16
Q
What are dendrites?
A
Receive signals–shorter, many branches out from the neuron. They are usually about 1mm. They are covered in spines which enable even more connections. They do not have myelin, and their length usually tapers away from the cell body.
17
Q
What are synapses?
A
the point of communication between two neurons, or a neuron and another cell. They contain the pre-synaptic cleft (axon terminal), post-synaptic cleft (the dendrite bit)
18
Q
What are the four elements involved with the action potential, and what are their charges?
A
K: positive
Na: positive
Cl: negative
proteins: negative
19
Q
Explain the role of membrane permeability in the action potential.
A
for charged particles called ions to get through the cell membrane, they have to travel through specialized ion channels. Some of these channels are static, some are dynamic. The ones that are dynamic are chemically sensitive, some of them are voltage sensitive–will only open up at a certain voltage, for certain chemicals. Ion channels are made of PROTEINS.
20
Q
What does the sodium-potatassium pump do?
A
pumps three sodium out, two potassium in-does not play a major role in the action potential
21
Q
Describe the process of the action potential?
A
Charge rises from resting membrane potential to threshold, causing sodium gates to open. The neuron reaches its peak charge. Potassium gates open, and potassium ions leave the neuron, causing it to overshoot resting potential, have a refractory period, and then resume resting membrane potential.
22
Q
What are the two primary types of cells in the brain?
A
Neurons and glia
23
Q
What is a cation?
A
Positively charged ion
24
Q
What is an anion?
A
Negatively charged ion
25
Where are the four components of the action potential located in the brain?
NaCl is outside, potassium and proteins are inside--like a banana in the ocean!
26
What forces act on sodium during the action potential's conduction?
Sodium wants to get in due EGF and CGF , but the cell membrane won’t let it in.
27
What forces are acting on proteins during the action potential?
Proteins attracted to exterior of the neuron, found in high concentrations in the cell. But they cannot get out because lack of channels and their large size.
28
What forces act on chloride during the action potential?
drawn into the cell by CGF, EGF drawing it out, but cannot move.
29
What forces act on potassium during the action potential?
attracted by CGF in, EGF out. Is allowed to move because neurons have a potassium channel.
30
When does repolarization occur?
RP occurs at the equilibrium of CGF and EGF for potassium because it is the only ion that is free to move.
31
All or none law
Action potential is always the same every time, you either get one or you don’t. Intensity conveyed by frequency or number of activated neurons.
32
What are the stages of synaptic transmission?
Synthesis, prep for release, release, signalling, receptor
33
GABA RECEPTORS
Gaba A, gaba B
34
ACETYLCHOLINE RECEPTORS
Nicatinic and muskarinic receptor
35
DOPAMINE RECEPTORS
D1-5
36
GLUTAMATE RECEPTORS
NDMA, ampa, kianate
37
Metabotropic receptors
Operate on a signalling cascade. Activated receptor couples with g protein > effector molecules (enzymes) > changes the concentration of second messengers > effects mediators. They work by causing reactions in the post-synaptic cell. Effects are long-lasting rather than short-lived, altering cell physiology at a level that can last up to months. Because of their cascading nature, one metabotopic receptor can impact hundreds of mediators.
38
Ionotropic receptors
Open ion channels upon activation causing either excitatory depolarization (Na, Ca) or inhibitory hyperpolarization (k, Cl). This transmission is fast but short-lived. These kinds of receptors are more complex–they use Ligand binding to detect neurotransmitters, pores to let them pass through, and ion selectivity filters to detect specific ions.They can be made from different protein subunits and still functionally work the same–ish. Differences relating to mental disorders can be related to differing structure of ionotopic receptor, impacting frontotemporal dementia, nictotine addiction, depression
39
What ion is most directly responsible for the release of neurotransmitter?
Calcium
40
Sulci
Crevices in cortex
41
Gyri
sticky-out bits in the cortex
42
Organization of the brain (from inward to outward for the encephalons)
Forebrain, midbrain, hindbrain. 1 diencephalon, tiencephelon, 2 mesencephalon, 3 myencephalon, metencephalon. Derived from anatomy of fetus.
43
What are the stages of signal transmission down a neuron?
Input, integration, conduction, output
44
What does the basal ganglia do?
Motor control, memory
45
Acetylcholine synthesis?
choline and acetyl COA with the enzyme CHAT
46
Serotonin synthesis
tryptophan with the enzyme being 5 hydroxytrotophan (5HTP), turns into AADC, then turns into serotonin
47
Dopamine synthesis
fenylalamine to tyrosine to dopa to dopamine to norepinephrine to epinephrine
48
What is the only family of neurotransmitters which don't get synthesized?
Neuropeptides, which are made from your genes
49
Describe the prep for release stage
To prep for release, transport proteins load neurotransmitters into synaptic vesicles and move these synaptic vesicles to the active zone of the presynaptic membrane.
The action potential arrives, triggering the release of neurotransmitters from vesicles due to the opening of calcium channels. In this area, there are no voltage-gated sodium channels, so sodium rushes in, creating a depolarization. Calcium is attracted to the inside of the cell due to CGF.
Proteins that help hold the synaptic vesicles in place are called the SNARE complex. In response to presence of calcium, one of these proteins pushes the synaptic vesicles to fuse into the presynpatic membrane, and then neurotransmitters spill their contents across the synaptic cleft
50
Release stage of neurotransmission
Dale’s Law (revised): Each neuron can only synthesize a limited and specific number of neurotransmitters, which are released in a specific combination at the synaptic terminals
51
Receptor activation
After neurotransmitters are released across the synaptic cleft, they are detected by specific receptors, specialized for each neurotransmitter. Different subtypes produce different responses in the post-synaptic cell.
52
What are metabotropic receptors also known as?
GCPR
53
Reuptake or destruction
After transmission, neurotransmitters are either reabsorbed or destroyed.
Reuptake
Glutamate reuptake transporters- EAAT, 7 subtypes. EAAT1 is found on astroglia that help keep the synapses separate.
Serotonin’s reabsorbsion is aided by transporters called SERT, which is blocked by SSRIs
Destruction
Specific enzymes will destroy neurotransmitter
54
Synaptic integration
Synaptic integration is when all the signals being received at dendrites are “considered” to decided whether or not to alter their spontaneous firing rate. Two factors in this are temporal summation (time) and spatial summation (space) because as the post-synaptic potential is conducted along the dendrite, it loses its intensity, and PSPs will only be enough to generate another action potential if they intercept at the right time. Generally, PSPs are caused by ionotropic receptors. There are EPSPs (salty milk!) and IPSPs (banana in a swimming pool!)
55
Neurotransmitter subgroups
Biogenic amines (at least one amine group, also known as classical neurotransmitters)
Acetylcholine: important for movement and attention
Monoamines (single amine group)
serotonin (excitatory) and catecholamines
Catecholamines
epinephrine, noraepinephrine, dopamine
Amino acids
glutamate (excitatory)
GABA (inhibitory)- Too much can be lethal, the same neurotransmitter that anesthetics boost
Neuropeptides
Have to be made from our genes
substance p- involved with pain messaging
endorphins
adenosine, nitric oxide
56
Biogenic amines (at least one amine group, also known as classical neurotransmitters)
Acetylcholine
57
Monoamines (single amine group)
serotonin (excitatory) and catecholamines
58
Catecholamines
epinephrine, noraepinephrine, dopamine
59
Amino acids
glutamate (excitatory)
GABA (inhibitory)- Too much can be lethal, the same neurotransmitter that anesthetics boost
60
Neuropeptides
Have to be made from our genes
substance p- involved with pain messaging
endorphins
adenosine, nitric oxide
61
Agonist
An agonist binds to a receptor and causes a response
62
Antagonist
Binds to a receptor and blocks a response
63
PNS
PNS is somatic (musculoskeletal, conscious), autonomic (internal, unconscious). autonomic is parasympathetic and sympathetic
64
CNS
Brain and spinal cord
65
CNS fundamental features
encased in bone, blood brain barrier, primarily just nervous system tissue
66
Spinal cord
White matter, grey matter, and central canal. Canal is shaped like an H, conducts cerebrospinal fluid. Outer parts of spine are myelinated, which is white matter. Inner parts of the spinal cord are mostly neuronal cell bodies and grey matter. Spinal cord is information highway sending motor info and receiving sensory, but reflexes are processed in spine
67
Reflex arc
sensory neuron connects to spinal cord connects to a motor neuron creating a reflex response
68
Fissures
Fissures are especially large sulci
69
Basis for anatomical differentiation in the brain
Visual differences
differences at a cellular level (ratio of parametal to granule neurons)
cell chemistry (neurotransmitters, receptors
reuptake transporters, etc)
the way cells are organized
the way connects to other part of brain function (but this is often more complicated than made out to be and not primary criteria
pattern of interconnectivity with other parts of the nervous system (where a particular neuron’s axons go says a lot about that area of the brain–this is probably the most important thing to look for)
70
dorsal to ventral
Top to bottom
71
Front to back
anterior to posterior, superior-inferior (can also replace dorsal-ventral), rostral-caudal
72
Side to side
Lateral to medial
73
Same-side to different side
ipsilateral to contralateral
74
close to far apart
proximal-distal
75
Structures of the hindbrain
Myelencephalon
Medulla
Metencephalon
Cerebellum
Pons
76
Medulla
Medulla- life-sustaining functions, continuation of the sensory/motor information highway that is the spinal cord
In addition, there are parts of the medulla that are associated with regulating important body processes (heart, breathing, vomiting)
Medullary nucleus are groups of neurons that work together to carry out a common function
77
Cerebellum
Very large structure
Contains lots of neurons
Mainly associated with ability to move in a smooth, coordinated fashion
Handles language and speech, some aspects of how we deal with time
Motor, language, memory
78
Pons
Bulges out of the Medulla
Heavily interconnected with the cerebellum
Nuclei in the pons are the pontine nuclei
These contribute to regulation of arousal, motor
79
Structures of the midbrain
-Tectum (inferior and superior colliculi)
-Tegmentum (red nucleus, substania nigra)
80
Red nucleus
Important for sensorimotor system
81
Superior colliculi
Help with visual tracking
82
Inferior colliculi
Help with tracking by sound
83
How can you remember which colluculi is which?
In humans, vision is superior to hearing
84
Structures of the forebrain
Diencephalon
Thalamus
Subregions: thalamic nuclei
Hypothalamus
Subregions: hypothalamic nuclei
Hypothalamus controls endocrine system
Telencephalon
-Cortex
85
Thalamus
Sensory processing
86
Hypothalamus
Structure below the thalamus (hypo means below)
Subregions: hypothalamic nuclei
Ventromedial nucleus creates feeling of fullness, Latero hyothalamic area creates feeling of hunger.
Differentiate by where they are located
Hypothalamus controls endocrine system through its control of the pituitary gland
Controls pituitary gland (master gland)
This allows hypothalamus to regulate life-sustaining behaviours: feeding behaviour, fighting, fear, sexual behaviours (four F’s)
87
RAS
RAS related to arousal and sleep/wake cycle, this is the part of your brain that gets damaged when you have a concussion.
Synapses spread widely throughout forebrain
Pontine nuclei related to this system
88
Cortex
Comprised of parietal, occipital, frontal, temporal lobes, divided by the pattern of sulci and gyri
89
Gray matter
Neuronal cell bodies
90
White matter
Myelinated axons
91
Frontal lobe
Movement (contains motor cortex on precentral gyrus)
The amount of sensitivity a body part has to manipulation is determined by the amount of space it takes up in motor cortex. Top to bottom it is organized feet, hip, trunk, arms, hands, face, tongue, larynx.
More anterior part is the prefrontal cortex which contributes to executive functions, personality
92
Parietal
Somatosensory cortex (post-central gyrus)–results in perception of a part of our body
amount of cortex devoted to area determines sensitivity
Area behind that contributes to awareness of where our body is (which is really just a calculation)
So also important for math functions
Damage to this lobe will lead to hemispatial neglect
93
Occipital
Visual functions
94
Temporal
Hardest to characterize in a functional way
Parts of temporal lobe that are important for emotional processing, memory
95
How are the two hemispheres of the brain connected?
Right and left are connected via the corpus callosum
Pathways between right and left are called commissural pathways, eg, thalamic commisure
Callosum is biggest example of this–massive bundle of myelinated axons
96
To what extent can brain function be lateralized?
Some functions can be lateralized, for example for most people language is more on the left than right side
97
Subcortical structures
Basal ganglia- motor control, memory
Wraps around the thalamus like earmuffs
Amygdala- emotional cognition
Ability to have emotional response to something–eg fear response
Hippocampus - memory
Involved in declarative memory
episodic memory (events), semantic memory (facts)–but not procedural memory
98
Subtypes of somatosensation
Organic sense (enteroception)
Perception of body’s internal state (eg, if you have a heart attack, you can feel it). Relatively weak compared to other somatosensory senses).
Kinesthesia (proprioception)
What is happening in our muscles and joints
Cutaneous sense (exteroception)
Perception of what’s happening on the skin
Types of sensation given by the cutaneous sense include touch (pressure), temperature, pain, itchy/tickly
Audition
Travels through the ear in the form of soundwaves
Vestibular sense (equilbrioception)
Balance, or our perception of gravity’s impacts on our inner ear
99
Layers of the skin (top to bottom)
Stratum corneum: layer of dead skin cells on the skin’s surface. This is what you remove when you exfoliate
Epidermis is below stratum corneum
Below the epidermis is the demis
Below the dermis is the subcutaneous layer
100
What sense do mechanoreceptors contribute to?
Cutaneous sense
101
Mechanoreceptors
subtype of somatosensory receptor designed to detect mechanical force. They also include additional tissue and cells, forming a structure that is corpuscular (small mass of tissue) in nature. These mechanoreceptors will respond to physical force on the skin. Mechanoreceptors all have a receptive field: this is small and precise for superficial receptors, and larger and broader for deeper mechanoreceptors–with a concentrated heart.
102
Merkel’s disks
Superficial and highly sensitive, but slow-adapting when it comes to desensitization, making them worse at detecting pressure changes
103
Meisnner’s disks
Superficial and fast-adapting
104
Ruffini endings
In the middle-to-deeper regions of the dermis. Slow-adapting. Primarily tell you when something is touching you, and need strong pressure to be triggered.
105
Pacinian corpuscules
Located at the bottom of the dermis and very large. Less sensitive (need stronger pressure to trigger), but fast-adapting.
106
What is glabrous skin and how does it relate to sensation?
The areas of our bodies that are most sensitive are glabrous (not hairy), e.g. face, fingers. Mechanoreceptors, especially superficial ones, are more likely to be found in glabrous skin. However, mechanoreceptors do not account for all of somatosensory experience.
107
Free nerve ending (FNE)
No additional tissue (non-corpuscular)
Axon-like structure
Some more superficial, some deeper
Contribute additional depth to sense of touch
Hair shafts have FNEs wrapped around them
Contribute to aspects of pressure sensation in glabrous skin
Mostly detect pain, temperature
May contribute to itchiness and tingling and are activated by non-mechanical information
108
How does sensory information get to the brain?
Axons come out from ganglia in the spinal cord, continue to the skin, then branch back in
Receptor axons > dorsal root ganglia > dorsal part of the spinal cord > CNS
OR Axons > cranial ganglia > CNS
109
Dorsal column medial lemniscus
Mechanoreceptor > Dorsal root ganglion > Continues up spinal cord without switching sides > heads up to the medulla, where it synapses in nucleus cuneus and nucleus gracilus (nuclei of dorsal columns) > ascends medial lemniscus > Ventroposterior (VP) thalamus > Thalamic neuron up to post-central gyrus. This pathway supports well-localized mechanical touch.
110
Spinothalamic path
For less localized information, like temperature and pain. Primarily this information is coming from FNEs > Travels to spinal cord > Synapses to spinal neuron, crosses over > Travels up to the brain via spinothalamic tract > travels to VP thalamus > Postcentral gyrus
111
What is a ganglia?
Group of neurons outside the brain
112
Dermatomes
Areas of the body connected to specific nerves. In a clinical setting, this allows us to map out the area that has been damaged if a patient has a loss of sensory information.
113
How is the post-central gyrus organized?
Grey matter is organized in six distinct layers (columnar organization)
From the midline downward, it is organized as such: feet, lower legs, knees, hips, core, chest, shoulder, neck, arm, hand, face, mouth, tongue, vocal cords. Smaller columns will respond to different types of sensation, such as pain, temperature, pressure.
Size of an area devoted to a certain body part determines its sensitivity
114
What different types of itchiness exist?
There are different types of itchiness: scabs healing, clothing, chemically induced itch powder
115
What types of nerves are responsible for itchiness?
May arise through particular combinations of somatosensation (eg, a particular ratio of activation)
One type of FNE may especially contribute
Sensitivity to itchiness can vary
Pacinian corpuscles relate to clothing-induced itchiness: therefore, by avoiding movement, itchiness can be reduced
116
How does somatosensory decline contribute to increased risk of falling?
Somatosensory information about pressure on the soles of the feet is important for balance/positioning. Other sensory systems also decline with age, and this may be effected too.
117
How are mechanoreceptors impacted by aging?
Their density decreases in elderly people
118
What are some tests of somatosensory acuity?
Monofilament test: Narrow rods have to be pressed a certain amount before they bend
Vibrating machines (more complex, costly)
Two-point discrimination: Two prongs move closer together or further apart. The subject is tested on their ability to distinguish the two rods as separate stimuli. In an older population, this gap has to get wider.
119
What syndrome occurs with partial spinal cord injury?
Brown-Sequard syndrome (spinal cord hemisection)
120
What are the symptoms of Brown-Sequard syndrome?
Patients show a loss of motor function on the right side of the body and ipsilateral loss of fine touch, vibration; contralateral loss of pain and temperature
121
Why is lack of nociception not a good thing?
Lack of nociception is typically comorbid with other neurological disorders (not perfectly selected). Because of pain’s role in triggering postural adjustments, avoiding accidents, and learning lessons, individuals with this disorder have worse health.
122
What are some subtypes of pain?
Somatic pain (skin)
Visceral pain (internal organs)
Neuropathic pain (pain despite no signal giving reason for its activation)
123
What somatosensory sense is pain a subtype of?
Exteroception (cutaneous sense)
124
What are pain receptors called?
Nociceptors
125
What type of nerve ending are nociceptors?
FNEs
126
Types of pain you can experience
Pinching
Extreme temperature
Chemical-based pain (acid)
Internal pain (tissue damage)
Inflammation
127
Types of nociceptors
Myelinated A-delta type fibres
Thermal nociceptors
Polymodal (thermal-mechanical) nociceptors
Unmyelinated C-type fibres
Myelinated A-alpha fibres
Fibres from fastest to slowest: A-alpha > A-beta > A-delta > C-type
128
Myelinated A-delta type fibres
These fibres transmit faster signals due to their myelin, these fibres give a precise and intense sensation
129
Thermal nociceptors
Respond to both heat and temperature, which past a certain threshold feel the same
130
Polymodal (thermal-mechanical) nociceptors
Activated by mechanical force, to some extent temperature, pressure, chemical signals
131
Unmyelinated C-type fibres
These fibres are smaller and transmit 10x slower than myelinated fibres
Only one general variety, polymodal
Responsible for lower-intensity, persistent pain like chronic pain
132
What is the adaptive function of thermal nociceptors?
When these fibres signal, the brain cannot tell what sensation causes this–it’s just an action potential. The only way that the type of pain can be distinguished is the activation of different nociceptors. This is the adaptive function of thermal nociceptors.
133
Pain fibres from fastest to slowest
A-alpha > A-beta > A-delta > C-type
134
Transduction
Turning stimuli into action potentials
135
What kind of info do pain receptors have to convey?
have to signal not just the pain event but the damage it caused and the body’s response to the damage.
136
How many receptors may be involved with pain transduction?
As many as 8
137
How are pain receptors activated?
Receptors generally activated by a pain event that causes it to change its shape, leading to a sodium or calcium-caused depolarization
138
Capsaicin/vanilloid/TRPV1(Transient receptor potential vanilloid 1)
Activated by capsaicin (the spicy component of hot peppers), high temps, or changes in pH as well as other mechanical stimuli, chemical signals
Can be used as an analgesic because it stays locked onto receptors, blocking other signals for hours after initially causing pain.
139
Capsazepine
Capsazepine is an antagonist which binds to the receptor without activating it at all. However, it does not stay at the receptor for as long.
140
What trait may be at the root of polymodal receptors' function?
Polymodal capacities may originate from FNEs having multiple nocireceptors
141
How do prostaglandins cause inflammation?
Prostaglandins activate when tissue becomes inflamed, then bind to and activate receptors, produce intracellular signalling molecules, bind to capsaicin receptors, making them more sensitive
142
What is the lateral path (in the context of neuroanatomy of pain)
Another way of saying the spinothalamic tract
143
What is the medial path (neuroanatomy of pain)
Goes up the spinal cord, crosses over, travels to the brain
Spinoreticular
Synapses with RAS at various points > VP thalamus > somatosensory conrtex
Spinomesencephalic
Synapses on neurons in mesencephalon > go up to VP thalamus > somatosensory cortex
144
Where do emotional, cognitive, and sensoery aspects of pain live?
The sensory aspect of pain exists in the primary and secondary somatosensory cortex, the emotional aspect of pain exists in the cingulate and insular cortices (awareness that “this hurts!”, irritability), and the cognitive aspect of pain exists in the prefrontal cortex (“How am I going to stop this pain? How long is this pain going to last?).
145
Is pain hierarchical? Describe the study that looked at this
One study had participants all put their hands into a bucket of ice water while under a PET scanner
One group was hypnotized to experience the pain as less intense, one group was hypnotized to experience the pain as less unpleasant
“less unpleasant” group experienced less activation in the cingulate and insular cortices, and the “less intense” group experiences less somatosensory cortex activation
“less unpleasant” group did not differ from the control of cingulate and insular cortices activation (and vice versa for “less intense”)
146
How is pain often studied?
With thermal stimuli, which typically won't cause tissue damage
147
What evidence is there (based on common sense) that a network for pain modulation exists in the brain?
Pain experience is subjective and individual. How we experience pain often depends on context: what is pleasurable in one context (eg whipping) is horribly unpleasant in another context.
In high-stress situations such as battles, sports games, fights for survival, we can be entirely numb to pain for an extended period of time.
148
Gate control theory of pain
the gate control theory of pain was proposed in the 60s by Melzak. The basic idea was that there was some kind of gating mechanism at the spinal cord, where pain signals entered the CNS. The gate is open under normal circumstances, allowing you to experience pain–but in extreme circumstances, can close and block signals.
149
Describe the brainstem-spinal cord analgesic circuit
PFC, amygdala, signal to the PAG that "now is not a good time to feel pain" , turning off the "off switch for the off switch and activating circuit > PAG signals to Raphe nucleus > Raphe nucleus signals to spinal cord > inhibitory interneurons connect with the ascending pain circuit and block it from firing with the release of endorphins
150
Describe the effects of opiate drugs
Endorphins or opiate drugs work by turning off the off-switch of the off-switch, so your body’s own endorphins will be mixed with those of the drug.
151
Local neuron
neuron whose cell body and axon are located within the same structure
152
How do opiods work?
Analgesic drugs like opioids use this pathway to block pain transmission. Endorphins or opiate drugs work by turning off the off-switch of the off-switch, so your body’s own endorphins will be mixed with those of the drug.
153
What are opiod drugs?
Endorphin agonists related to opium
154
List common opioid drugs
Morphine, heroin, fentanyl, dilaudid (hydrocodone), oxycontin (oxycodone), codeine, demerol (meperidine), Darvon (propoxyphene)
155
Why do opoid drugs have such a potential for abuse?
Removing pain is reinforcing, and their ability to engage the body's natural pan relieving circuits makes their impact incredibly powerful
156
Common opiod drugs
Morphine, heroin, fentanyl, dilaudid (hydrocodone), oxycontin (oxycodone), codeine, demerol (meperidine), Darvon (propoxyphene)
157
What is the most problematic opiod?
Fentanyl
158
How much stronger is fentanyl than morphine?
50-100x
159
Why is fentanyl stronger than morphine?
Penetrates BBB more effectively
160
Why does fentanyl's potency make it more dangerous?
Because the required dose for an effect is so small, it is easy to overdose on accidentally. If someone is illicitly making drugs and accidentally spills fentanyl into their other drugs, it only takes a little bit to cause problems.
161
What drug is even stronger than fentanyl?
Car fentanyl, 10k times stronger, used to tranquilize elephants
162
How many overdose deaths occur in Canada?
2-3k annually
163
How much higher is the overdose death rate in the US?
3-5x higher
164
Other names for fentanyl
Sublimaze, Actiq, Instanyl, “apache”, “china girl”,”goodfellas”
165
What percent of OD deaths involve fentantyl?
70-90%, the majority
166
Naloxone
Narcan
167
What is the mechanism of naloxone?
Binds to endorphin receptors and stops anything from activating them
168
What is the experimental use of naloxone?
Allows us to see experimentally if something is related to endorphinergic neurons by disabling them and seeing if an effect is still seen on pain releif for things like acupuncture, hypnosis, sex
169
What are endorphin receptors known as?
Opiate receptors
170
Are endorphin receptors metabotropic or ionotropic? Excitatory or inhibitory?
metabotropic, inhibitory
171
Subtypes of opiate receptors?
mu, delta, kappa, NOP receptor
172
Subtypes of endorphins?
Enkephalin
Dynorphins
Endorphins
Endomorphin
Nociceptin
173
What family of neurotransmitters do endorphins belong to?
Neuropeptides
174
Which endorphins have strongest impact on pain?
Endorphin, endomorphin
175
Enkephalin (example, receptor type)
Met-enkephalin
Activates Delta receptor most strongly
176
Dynorphins (example, receptor)
Dynorphin B, Kappa receptor
177
Endorphins (receptor, example)
Beta-endorphin
Activates Mu receptor most strongly
178
Endomorphin (example, receptor type)
Endomorphin 1
Activates Mu receptor most strongly
179
How does nociceptin differ from other neurotransmitters?
Reduces ability of brainstem-spinal cord analgesic circuit to reduce pain (anti-analgesic)
180
Nociceptin receptor
Activates NOP receptor, also known as ORL-1 (orphanin-like), orphanin FQ (metabotropic) as are all receptors for neuropeptides. Like other endorphin receptors, it is inhibitory.Activates NOP receptor, also known as ORL-1 (orphanin-like), orphanin FQ (metabotropic) as are all receptors for neuropeptides. Like other endorphin receptors, it is inhibitory.
181
Why do opiod drugs have side effects?
Endorphins potently reduce pain, but they are also involved in breathing, gastrointestinal processes, and arousal. This is why side effects of opioid drugs include depressed breathing (potentially leading to death), constipation, and unconsciousness if dose is too high.
182
NSAID meaning
Non steriodal anti-inflammatory--steriods decrease inflammation, NSAIDs have this same effect without steriods
183
NSAID examples
Ibuprofen, aspirin
184
How do NSAIDs work
These drugs also reduce inflammation, without steriods, due to their nonspecific inhibition of COX (cyclooxygenase), an enzyme involved in inflammation, so inflammation signals are blocked.
185
Role of two different COX enzymes
COX-1 is involved with mucus production including mucus lining in your stomach. Because NSAIDs also inhibit this COX, NSAIDs can cause stomach issues like ulcers with constant use
COX-2 is involved with pain
186
Acetaminophen
Despite being around for a long time, we do not totally understand the mechanism of acetaminophen
Can block COX-2 a little bit, but not enough to account for its analgesic effects
Does not impact COX-1 so is a good alternative for those who experience stomach issues with NSAIDs, while still inhibiting pain at about the same level
187
Celebrex (celecoxib)
Has the same effects of NSAIDs without the impacts on the stomach, but is much more expensive and must be prescribed
188
How do anaesthetics and anticonvulsants reduce pain?
Block action potentials from firing entirely, stopping pain neurons from talking to the brain
Anticonvulsants block signals by general inhibition of GABA inhibitory interneurons
Because GABA is so widespread, this produces widespread side effects including lethargy and reduced arousal
189
Example of an anesthetic?
Lidocaine
190
Antidepressants, pain releif
Can also reduce pain signalling
We don’t even understand how they reduce depression, let alone pain
Might be used for chronic, low-level pain
191
Cannabinoids
eg Cannibidiol
Cannabinoid receptors interact with pain, but mechanism is not really understood
Can take the edge off of low level chronic pain
192
Phantom limb pain
After losing a limb, a person continues to feel pain from that limb as if it is still there. Initially, clinicians documented this in case studies before realizing it was a common phenomenon experienced by most amputees.
193
Bailey & Moersch (1941), phantom limb pain
Wrote a case report on the experience of phantom limb pain for patients in which they recognized how common it is as a phenomenon which at the time was inexplicable
194
What did Bailey & Moersch describe specifically about phantom pain?
Describe how common phantom sensation is
Focus on pain, since that's of the greatest clinical importance
Discuss the various treatments which have failed to improve pain
195
How common is phantom limb pain?
Depending on how it is operationalized, experienced by 80-100% of amputees
196
Is there any body part which you can lose and not have phantom pain?
Any body part connected to exteroceptive system (ears, nose, etc) will cause phantom pain when lost
197
Will you experience phantom pain if you are born without a limb?
No, but you can if you have an amputation as a child
198
What could confound the rates at which people report having phantom limb pain?
Social desirability bias
199
What kind of phantom sensations can you experience?
Pain, temp, itching, etc--anything you can normally sense
200
How do phantom sensations feel to the sufferer
Completely real, although they don't change from moment to moment the same way normal sensation does
201
What is universally true about phantom pain?
normal, diverse, and feels completely real
202
How long can phantom pain last/how can it develop after onset?
Phantom limb expresses differently in terms of time of onset and its longevity: some amputees experience it immediately and have it gradually taper off, some will experience it for years after an amputation, getting gradually more intense, etc
203
What was the earliest hypothesis of phantom limb pain?
Residual nerve activity hypothesis
204
Residual nerve activity hypothesis
Because the cell body is found in the dorsal root ganglion, the residual nerves in a stump are still capable of firing even after their receptors have been severed.
To treat phantom limb, nerves could be severed at the DRG.
205
Neuroma
Activity from the axonal stump in the residual nerve theory of phantom limb pain
206
How was the residual nerve activity theory proven false?
Proven false as severing nerves at DRG did not provide more than moderate relief for some patients, and did not eliminate pain entirely
207
Describe the somatotopic map reorganization hypothesis of phantom limb pain
The idea that phantom limb pain is caused by the brain reorganizing in the somatosensory cortex after amputation
208
What was the dominant dogma of neuroscience in the 1980s
In the 1980s, the dominant dogma of neuroscience was that neuroplasticity only existed in children, with the exception of brain areas which incorporate learning (ie, motor learning, etc)
209
Merzenich monkey finger stimulation study
Stimulated the fingers of monkeys every day for an hour for three months and found the area devoted to the fingers expanded in size, implying neuroplasticity existed in adults
210
Critique of Merzenech monkey finger stimulation study
neuroplasticity did not occur under normal or natural circumstances, and therefore may only have happened in response to extreme stimuli
211
Nursing rats study
In response to critique of Merzenich's finger stimulation study, this study aimed to see if somatosensory area for the breast of a rat increased after breastfeeding, which indicated neuroplasticity in adults was naturally occuring
212
Merzenich amputation study
Amputated the fingers of monkeys and found that the somatosensory area of the finger beside the amputated finger expanded into the area previously devoted to the amputated finger
213
Critique to Merzenich amputation study
Human exceptionalism- would same results be found in humans?
Observed change was very small
Would results apply for a larger amputation, like losing a leg or arm?
214
Why was it difficult to study neuroplasticity in adults in the 80s
Due to ethical constraints and recruitment issues, hard to get human data in this area. As well, at the time, it was difficult to record human brains with the same degree of acuity that animal brains could be recorded
215
Mogilner et al 1993, Syndactyly study
Found that somatosensory mapping changed after individuals with webbed fingers had surgery to separate fingers so they were separate units in the somatosensory cortex, not one cohesive structure
216
Critique of Mogilner et al 1993, Syndactyly study
Syndactyly is pathological, what about normal humans?
217
What imaging technique was used in Mogilner et al 1993, Syndactyly study
fMRI
218
What are other examples of adult somatosensory neuroplasticity in normal adults?
Musicians, Braille readers
219
Neuroplasticity and musicians
Horn players have larger somatosensory areas devoted to their hands than age-matched controls
Guitar players will be more sensitive in their fretting hand than in their strumming hand
220
Braille readers, neurplasticity
Somatosensory area devoted to fingers is larger in the reading hand
221
Pons: arm amputations in monkeys study
Found that after an arm amputation in monkeys, the somatosensory area devoted to the face encroached on the arm area
222
In what other areas has neuroplasticity after amputation been shown?
In the secondary somatosensory cortex, the same effect was observed with the foot area moving into the hand area after a hand amputation
Plasticity was also observed in the axons leading to the somatosensory cortex
The VP thalamus (which is also mapped out for different body parts, and will have the same “invading” effect happen post-amputation)
Evidence for plasticity in key areas of the brainstem and other areas
223
What was the understanding of adult neuroplasticity by the late 90s and 2000s?
Every area of the brain is capable of plasticity
Plasticity can be caused by events such as amputation
224
Ramachandran, Q-tip experiment
By stimulating the face of hand amputees, he was able to map out the areas of the face which corresponded to specific secondary phantom hand sensation
225
Describe current understanding of phantom limb?
stimulation is coming from somatopically adjacent body parts
Stump activity does not contribute much;
Stump stimulation can cause phantom sensation
When adjacent areas “invade” into area that is no longer connected to the body, columnar organization means that this mapping is not always neat, and sometimes can expand into pain regions, etc
226
Do we understand the underlying mechanism of somatopic reorganization?
The underlying mechanisms (ie, why is the face area invading the hand area?) are still unknown
227
What does phantom limb sensation indicate?
When someone experiences phantom limb immediately after amputation, this tells us that somehow these neurons are still getting activated, which contradicts the logical assumption that nervous system activity on this pathway would be decreasing
228
Describe the proposed mechanism by Ramachandran for phantom limb pain
When no stimuli is activating neurons, they release factors that aid in drawing other neurons to them to make new connections (axonal sprouting) to adjacent regions
Dendrites are also capable of sprouting
This process is slow and takes time, so it does not account for the immediate onset of phantom limb, but it does explain its capacity to change
229
What explains the immediate onset of phantom limb?
Even before the loss of a limb, we see some crossover between adjacent somatosensory areas
Normally, your sensory input from an area would drown out this “noise”, like someone whispering in a crowded room (unmasking of silent synapses)
However, when a limb is lost and sensory input decreases, this “noise” becomes much more noticeable, accounting for the immediate onset of phantom limb
230
What percent of phantom limb sufferers experience pain?
50%
231
What is the impact of artificial limbs on phantom pain?
Can be helpful but not reliably so
232
Why might artificial limbs help phantom limb?
The limb creates sensation at the stump which may activate the neuromas present there, preventing axonal branching
233
How effective is mirror box therapy?
Can sometimes help but not reliably and more effective for some types of pain than others
234
Describe how mirror box therapy works?
Box with a mirror in the middle and a curtain over top
Patient places limbs inside the box with curtain covering their stump
In the mirror, they see the illusion of two limbs
Amputee can make different motions depending on the nature of their pain (unclenching their hand if they’re experiencing phantom tightness, etc) and will look at the mirror for an extended period of time
235
What may explain how mirror box works?
Vision contributes to our perception of our limbs (hand-eye coordination)
236
Why is movement such an important and under-studied topic in psychology?
Movement is the reason we have a complex nervous system--plants don't have a nervous system and are unable to move, seasquirts digest their nervous system once they settle down, etc
Everything the nervous system does fundamentally funnels into movement
237
Why is it called the sensorimotor system?
Because sensation informs movement
238
Examples of sensorimotor system changing over time?
You can become a better guitar player or develop sloppier writing
239
What is the effect of practise over time on brain activation when performing a task?
When we first attempt a movement, it produces a lot of brain activation. The longer we practise, the less activation is produced
240
What type of cell comprises muscles?
Muscle fibres
241
What are the two specialized proteins that enable muscles to contract?
Actin and myosin
242
Motor unit
motor neuron in the spinal cord whose axon synapses on muscle fibre(s). This synapse is called the neuromuscular junction and is critical for generating movement
243
What neurotransmitter gets released at the neuromuscular junction and what type of receptor is it?
Acetylcholine, ionotropic nicatinic receptor
244
What charge do muscle cells have?
Muscle cells are polarized and negatively charged on the inside
245
What determines the level of fine motor control we have over a certain area?
Motor units can be synapse onto many muscles fibres (back muscles) or few muscle fibres (fingers) allowing for the differing ability for fine motor control in different areas
246
Is there a signal that gets sent allowing muscle fibres to elongate?
Muscle cells are not capable of signalling to elongate, just to contract. Muscle relaxation is either caused by gravity, or by opposing muscle groups (bicep, tricep) or joints that move in opposite directions
247
How many motor units do we have?
Millions
248
What types of muscles do animals and humans have?
Smooth muscles, cardiac muscles, striated muscles (fast and slow)
249
Smooth muscles
Less power, more endurance
Located in internal organs like the intestines
250
Striated muscles
More power, less endurance
Fast contract quickly
Slow contract more slowly
251
Cardiac muscles
Heart muscle is powerful and has the endurance of a smooth muscle
252
Myasthinia gravis
Autoimmune disorder in which immune system attacks nicotinic receptors at the neuromuscular junction
253
How many Canadians are impacted by Myasthinia gravis?
1 in 5-6k
254
Symptoms of myasthinia gravis
Loss of ability to contract muscles leads to weakness, fatigue, and postural changes, droopiness of the face, struggles with blinking–sometimes more on one side than another.
255
Where is precentral gyrus located
In front of the central sulcus
256
What does a larger area representing a certain region mean in the somatosensory cortex
Like in the sensorimotor cortex, a larger area representing a body part means there are more motor units representing it and therefore it is capable of more fine motor control
257
Are there multiple maps in the somatosensory cortex?
The multiple maps, like in the somatosensory cortex, are not seen in the sensorimotor cortex with the exception of the hands, which have two areas giving both feedback from muscles and feedback from skin which enables stereognosis (identifying objects by touch), astereognosia is the inability to do this
258
Stereognosis
Identifying objects from touch
259
What is the role of the precentral gyrus
Initiate consciously controlled movements
260
What lobe is precentral gyrus
frontal
261
What lobe is postcentral gyrus
parietal
262
outside of the brain, what can signals from the precentral gyrus control?
with a BCI, machines like exoskeletal legs, etc
263
monkey prosthetic arm experiments
Monkeys have been able to control prosthetic arms with their brains to gain a reward (such as experiments involving Belle the monkey)
264
Supplementary motor cortex
area of the secondary motor cortex, plans out the specific muscles which need to be activated to initiate a specific movement, which would be impossible to do in the primary motor cortex reliably
265
what brain areas might be activated when trying to execute a complex movement
When movement is complex to initiate, we see activation in the secondary motor cortex before there is activation in the primary motor cortex
266
three secondary motor cortex areas
Supplementary motor cortex
Premotor area
Cingulate areas
267
where is posterior parietal cortex located
Somatosensory association cortex
268
role of posterior parietal cortex
Tells you where your body is in relation to the world around you before initiating movement (visual-spatial processing)
Communicates with secondary motor areas and more anterior parts of the PFC
269
what brain area is damaged in apraxia
posterior parietal cortex
270
Apraxia
Occurs after brain trauma. Deficit in the execution of consciously controlled movements (unconscious movements do not require the posterior parietal cortex)
271
What other condition can be caused by damage to the posterior parietal cortex
Hemispatial/contralateral neglect
272
hemispatial neglect symptoms
Damage to right posterior parietal cortex creates neglect for that side of the world
273
Role of prefrontal cortex in movement
The “command centre” of movement. The PFC decides what the goal is rather than determining specific muscle groups or commanding them to move itself
274
What part of the brain informs the prefrontal cortex (sensorimotor system)
posterior parietal cortex
275
pathway of a motor action occuring
PFC decides to execute movement > secondary motor areas, figure out how to execute movement > primary motor area signals for movement
276
clinical use of BCI
may be useful for people with spinal cord paralysis or any other situation in which the brain can signal but the body can’t move
Could also help different brain areas communicate in disorders where this is impaired, or in any loss of connection (helping patients with ALS or other similar disorders learn to speak again)
277
Non clinical use of BCI
Useful for brain-computer or brain-machine interactions, like playing video games, turning off a light cube, making the bunny ears move in that video, controlling a virtual environment, etc
278
when were BCIs first conceptualized
BCIs were first conceptualized in the 60s-70s during the computing revolution.
279
What impaired BCI research catching on in 60s-70s
Poor knowledge of the brain (compared to modern day)
Computers couldn’t take the amount of data necessary for this complex process
Even if they had been able to read and process brain activity, what would they use it to control? Tech like robot prosthetics did not exist at this point
It took until about the year 2000 for research on this topic to take off, and it has exponentially increased since then
280
different mechanisms for recording brain activity
eeg, ecc, intracortical array, meg, fmri, fnirs
281
pros and cons of EEG
Electroencephalography, records brain activity through electrodes placed on the surface of the skull
Pros Cheap, good temporal (time) accuracy, durable, cheap, portable, noninvasive
Cons Poor spatial accuracy (microphone over a stadium)
282
pros and cons of ECC
Achieves better fidelity by implanting electrodes directly in brain tissue
Pros Great temporal resolution, highly portable, decent spatial resolution
Cons Modest expense (surgery, both to extract and implant), invasive, less durable (electrodes do not always last long in the brain environment),
283
Pros and cons of Intracortical electrical array (microelectrode array)
Array of tiny electrodes implanted into the brain
Pros: Excellent spatial and temporal resolution, portable
Cons: More expensive than other electrode technology, poor durability
284
Pros and cons of MEG (magnetoencephalography)
ecords the magnetic fields generated by electrical activity
Pros: Ok spatial resolution, great temporal resolution, noninvasive, durable
Cons: Non-portable and very expensive
285
fMRI pros and cons
Records changes in bloodflow in the brain which indicate where activity is occuring. Same as a regular MRI with altered information processing.
Pros: Unlike EEG, does not just record from superficial brain regions, durable, noninvasive
Cons: Poor-ish spatial resolution, poor temporal resolution, not portable, expensive
286
Pros and cons of fNIRS
Shoots laser beams through the head, and by analyzing which beams make it through to the back of the head can detect changes in bloodflow (functionally the same as MRI)
Pros: noninvasive, durable, portable, cheap-ish but more than electrodes
Cons: poor spatial resolution, maybe better than EEG a little bit, poor temporal resolution
287
Why is it important to know all the different methods of imagining the brain
Over time, these technologies could be improved by research to make one clear perfect solution. Until then, it makes sense to consider all of them.
288
what demands does the computer component of BCI have to fulfill
After brain activity is recorded, something needs to analyze it
Computer needs to be able to distinguish the spontaneous firing rate from normal brain activity (feature extraction)
Then, the computer needs to convert this into an output message (feature translation)
This output could go to to your own body, or to anything controlled by a machine
289
An ionotropic receptor can be thought of as a(n)
Chemically gated ion channel
290
Are there any encephalons where you wouldn't find neurons from the RAS
no
291
In the directional terminology used by neuroanatomists, your left amygdala and hippocampus are considered to be ______________ to one another.
ipsilateral
292
When a new neurotransmitter receptor is discovered, it is found that its activation leads to an decrease in concentration of chemical Y in post-synaptic neurons. Chemical Y is likely
A second messenger
293
What is the most commonly used technology to record brain activity in a BCI?
EEG is most commonly used technology, which has been improving such that it can accommodate a larger number of electrodes
Some research combines techniques which supplement each others’ strengths and weaknesses. Depending on the context for use, this can be effective (EEG + fNIRS, EEG + MEG)
294
Pragmatics aside, which technique for recording brain activity has the best result?
MEA has the best results aside from pragmatics. The durability of this technology has improved, and electrodes can last up to 15 months
295
extrinsic operations (BCI)
Brain activity outputs to an external device
296
intrinsic operations (BCI)
clinically intrinsic operations could be useful for modifying brain activity or allowing for communication between brain areas
297
what could BCIs functioning intrinsically accomplish
modify brain circuits, modify memories, emotions, restore communication between brain areas (in disorders like aphasia), modify circuits involved with storing memories
298
How does electrode technology need to improve for BCIs?
Electrodes need to be improved in BCI technology: smaller, more stable when implanted
299
What advancement has been made for electrode technology?
Synchron has developed tiny electrodes which can be implanted via vascular surgery, which is cheaper and less invasive than brain surgery
300
How does computer analysis need to improve for BCIs?
Algorithms need to learn how to improve at feature extraction, which AI may be able to accelerate
Accuracy rate needs to improve, ideally to that
Decrease the time required for training
301
Neuroethical considerations for BCIs?
Privacy, safety, legal/social, security concerns
302
Privacy concerns for BCIs
Ultimate potential for privacy violations given the level of data collected
Companies could use this to know exactly what users are thinking
303
Security concerns for BCIs
A BCI meant to control either you or the external world could be compromised
A compromised BCI could tell you what to think, a power that could be abused by dictatorial leaders
Could create mental illness or delusions instead of removing them
304
Safety concerns for BCIs
There is inherent danger to modifying or reading brain activity (seizures, epilepsy, brain damage, unwanted psychological or behavioural output)
305
Legal/social concerns for BCIs?
Our legal code rests upon the notion of free will
If BCI use becomes widespread, what does this mean for the concept of personal responsibility when malfunctioning BCI could be blamed?
Would using a BCI to rehabilitate criminals be ethical?
What about the ethics of using a BCI to enhance performance (for example, enhancing memory for school)
306
Equity implications of BCIs?
Equity implications: BCIs serve to increase existing socioeconomic inequalities if not made available for everyone
307
National interests implications of BCIs
impact international security, economic integration
A country with widespread BCI access may become the next superpower. Right now, China is investing heavily in BCIs while the West has been cutting public investment in research
Could amplify international inequalities as well
308
Use of BCIs for neuroprosthetics
Clinical use was early impetus for BCI development. Neuroprosthetics have been successfully used in research
Neuroprosthetics could be used either for amputees, people with paralysis, or anyone whose nervous system has been compromised
Willesy et al were successfully able to create a BCI that converted motor cortex activity to finger movements controlling a joystick
309
Clinical uses of BCIs
Neuroprosthetics, compromised communication, neurorehabilitation, cognitive and emotional health, biofeedback, or any other miscellaneous intrinsic operations
310
Use of BCIs for individuals whose communication ability has been compromised
BCI could be used to restore communication where it has been compromised, even for communication which would be “telepathic”
AI could assist this, such as a Handwriting BCI which uses a language AI to correct typos
311
Why is it easier to develop typing/writing BCIs than speech BCIs?
Typing/writing BCIs are relatively easy to develop compared to ones which handle speech, since they only have to interpret 26 signals rather than thousands of words in a person’s vocabulary
312
Neurorehabilitation use of BCIs
Though unnecessary in mild cases, for severe cases of impairment (ie, after a stroke) BCIs could be used to aid rehab
Patients who were given a BCI controlling exoskeletal legs were able to learn to control these, which serendipitously enhanced control of their OWN legs
This phenomenon may be able to be generalized to all neurorehabilitation
313
Biofeedback use of BCIs
Could analyze brain activity and relate it to anxiety levels
Could help get you into a sleep state by monitoring brain activity and providing feedback
Could help you in generating brain patterns which enable you to better remember information
Biofeedback BCIs are currently being sold by Bitbrain
314
Can BCI modify the brain itself?
Change the way you think for clinical purposes by modifying endogenous circuits
If this tech becomes powerful enough, beyond tweaking natural patterns of brain activity it could implant patterns of activity to create emotions like happiness
Oishi et al, 2019 used BCIs to implant something artificial in an individual’s brain, resulting in cognitive/emotional changes, though perhaps not practically or at scale
315
