PSYC 301 Unit 3

Disorders of consciousness

Alterations in arousal and/or awareness.

Arousal

Physiological state of being alert and awake.

Awareness

Being responsive to stimuli beyond reflexes.

Coma

Trance or deep sleep. Complete absence of arousal and awareness. No eye opening, even after stimulation. No verbal responses. No motor responses except with posturing towards a painful stimulus.

Unresponsive Wakefulness Syndrome

·        Also known as a vegetative state. Arousal without awareness. Preserved physiological functions (cardiac, respiratory, sleep/wake cycles) without clear signs of awareness of the self or the environment. Only reflexive behaviours. Cannot respond meaningfully.

Terri Schaivo

Entered an unresponsive wakeful state following a cardiac event related to an eating disorder at 26. She could wake or sleep, gag, and swallow food, but had no evidence of awareness. There was a 7-year legal battle between her husband and parents about whether to sustain her life. The expert consensus was that she could not recover, and she died in 2005.

Cognitive Motor Dissociation

People who are awake and aware, but do not behave in any way. Can conduct mental imagery tasks that can be seen in fMRI. Often used as covert consciousness or locked-in syndrome. Some amount estimated 20% of those who appear unaware. Patients in this state are more likely to have functional recovery.

Minimally conscious state

Minimal but inconsistent awareness. Shows some environmentally contingent behaviours not attributable to reflexes. Can be divided into MCS+ with some evidence of language and MCS- without language

Glasgow Coma Scale

Simple standardized way to evaluate the level of consciousness of patients with a brain injury.

Primary headache disorders

The headache itself is the problem and there is no other underlying cause. 38% are tension type, 12% are migraine, and .05% are cluster headaches (trigeminal autonomic cephlalagias).

Secondary headache disorders

The headache is caused by an underlying condition.

Tension-type headaches

Typically bilateral. The head feels full or dull. Mild to moderate in severity. 30 minutes to 7 days. Causes include muscle activation and sensitization of pain receptors. To acutely treat, usually simple pain relief like ibuprofen, but can include antidepressants and other drugs.

Migraines

Unilateral. Throbbing pulsing pain. Mild to severe. Last up to 72 hours. More prevalent in women than in men. There is a genetic component. Causes of migraine are poorly understood. May involve dysfunctional pain signaling in cranial nerves and the brainstem. Triggers can include sleep changes, weather, hormonal changes, caffeine. The acute treatment can be simple pain relief, or triptans. Prevention includes antidepressants, antiepileptics, antihypertensives, and others. Often they have an aura that happens five to 60 minutes before or during a headache attack, which includes muscle weakness, vision changes, and ringing in your ears.

Cluster headaches

Typically unilateral, often near the eye or temple. Burning, sharp or stabbing pain. Often about 30 minutes, but can happen several times within a day. The causes are poorly understood. Trigeminal nerve, histamine, and hypothalamus seem to be involved. The acute treatment involves triptans and high-flow oxygen.

Seizures

A temporary disruption in brain function resulting from abnormal, excessive neuronal activity

Convulsions

Sudden involuntary muscle activities like jerking or shaking.

Epilepsy

A chronic condition of recurrent and unprovoked seizures. Happens at similar rates across genders. Likely a cluster of different syndromes. Most commonly diagnosed in children and in older adults. Typically unprovoked, but can still have internal triggers like stress, tiredness, fever, heat and alcohol. A small amount of people have reflex epilepsies with narrow causes, like music, being startled, flashing lights, tooth brushing, reading, math, or orgasm.

Provoked seizures

Seizures caused by some sort of trigger that are non-epileptic. Can be caused by a traumatic injury, cancer, withdrawal, etc.

Psychogenic non-epileptic seizures

Resemble epileptic seizures in their appearance, unresponsiveness, shaking, or altered awareness, but lack detectable abnormal electrical activity in the brain. Causes are unclear. This is not conscious or voluntary.

Focal seizures

People may be aware of have impaired awareness. There may be motor symptoms or not. There may be non-motor symptoms like changes in emotion, thinking, feeling hot/cold, or being still. Originate within a small group of neurons (the seizure focus). These neurons have enhanced excitability.

Secondary generalization

Sometimes a focal seizure begins to spread to other regions over seconds or minutes. This spread follows the normal connective structure of the brain, especially with white matter tracts.

Primary generalized seizures

Affect both hemispheres simultaneously. Driven by the thalamo-cortical circuits. Awareness is impaired.

Absence seizures

Typically last 10-30 seconds. Impaired awareness with only minor motor manifestations such as blinking for lip smacking. No convulsion, behavioural arrest. Previously petit mal.

Tonic-clonic seizures

Typically 1-3 minutes. Previously grand mal. Loss of consciousness, loss of equilibrium. Major motor symptoms, such as sustained rhythmic jerking movements (clonic), or muscles becoming rigid/tense (tonic).

Normative

Evaluation of right versus wrong. Ought, should.

Descriptive

What is or would be.

Drepetomania

An ‘illness’ causing black slaves to attempt to escape.

Deinstitutionalization

Movement starting in the 50s and 60s to replace long-stay psychiatric facilities with community mental health services. Possible with antipsychotic drugs like chlorpromazine.

Schizophrenia

Splitting of the mind, not between two personalities. Instead between personality, memory, emotion, perception, etc.

Positive symptoms

Something new is present. Mental phenomena that do not occur in healthy people.

Hallucinations

Perceptions without sensory cause. Often auditory. Command hallucinations have a high risk of harm, including suicide.

Delusions

Beliefs that are not realistic or culturally appropriate. Can be quite varied. For example, the world is full of hidden signs, being closely watched, bizarre. Can be culturally specific. For instance, religious people may believe they are a religious figure or that religious figures are talking to them.

Negative symptoms

Resulting from an impairment of normal function. Blunted emotional responses, impoverished content of thought and speech, and reduced social motivation.

Cognitive abnormalities

Disorganization symptoms. Impaired working memory and executive function. Impaired source monitoring (tendency to misattribute own actions and thoughts to external causes, errors confusing imagination and real memory.

Typical

Chlorpromazine, haloperidol. Act on dopamine. Can have movement disorder side effects.

Atypical

Newer. Olanzapine, aripiprazole. Act on dopamine, serotonin and other receptors. Can have metabolic side effects, like weight gain and diabetes.

Reward Hypersensitivity Model of Bipolar Disorder

Being hypersensitive to reward is a trait that predisposes someone to developing BD. Goal attainment can lead to excessive reward states and ultimately (hypo) mania. Goal non-attainment can lead to excessive reward deactivation and a depressive state.

Working memory

Holding and mental working with information in mind.

Inhibitory control

Resisting temptations, not acting impulsively or prematurely, overriding automatic behaviour.

Cognitive flexibility

Fluidly changing perspectives or approaches to solving a problem.

Prefrontal cortex

The non-motor parts of the frontal lobe (depending on who you talk to.)

Abulia

Lack of drive.

Orbitofrontal circuit dysfunction

Impulsive, socially inappropriate, poor safety judgement, difficulty evaluating anticipated rewards and punishments, and don’t learn from mistakes due to diminished guilt and regret.

Dorsolateral circuit dysfunction

Distractible, disorganized, perseverative, difficulty multitasking, poor time management and prioritization.

Medial frontal circuit dysfunction

Bilateral vmPFC lesions lead to emotional dysregulation (loss of empathy and blunted affect), apathy, rigidity in thoughts and actions, poor ability to learn from mistakes, problems thinking ahead, sequencing steps for a task.

ADHD

Key symptoms are extreme inattention, hyperactivity, and impulsivity. Initially characterized as a problem of moral control, but this is not how we think of this today. 5-7% of children and 2-3% of adults receive this diagnosis. Intersects with societal norms, as younger children within a  classroom within a classroom are likely to be diagnosed. There is a rapid rise in adult diagnosis. There is an underdiagnosis of hyperactivity in girls, since presentations vary with gender.

Dual Pathway model of ADHD

Executive circuit (dysfunction: inattention) dlPFC and caudate. Reward circuit (dysfunction: lack of motivation) OFC, ACC, and nucleus accumbens.

Anticipatory ethics

Assessing the potential ethical implications of emerging issues to guide their responsible development.

Volume

Number of data points

Variety

Data may cross different types (structured/unstructured)

Velocity

Pace of data generation.

Veracity

Data quality and accuracy.

Value

Potential to create benefits and insights.

Artificial intelligence

Artificial systems that appear to think like humans (decide, categorize, or recognize).

Automators

Concrete, explainable, consistent algorithms to transform input to output. For example, Deep blue chess program. Doesn’t learn, just follows a set of rules. Might be equivalent to a diagnostic flowchart.

Machine Learning

Systems that can learn from experience or data without direct human programming. A type of AI.

Supervised learning

Trained on known, labelled data.

Unsupervised learning

Identifies patterns in unlabelled data.

Simulators

Emulate natural phenomena. For example, research models of neurons.

Discriminators

Take an input and assign a label to it. For example, labelling neuroimaging results, identifying seizure foci.

Moral answerability

Duty to explain one’s reasons and actions to others; being answerable. AI processes may be unexplainable to their users.

Predicators

Assign labels that are predictions. For example, calculating disease risk or prognosis.

Culpability

Responsibility based on intention, knowledge, or control. AI introduces potential harms no one person could predict or prevent.

Amalgamators

Aka regurgitators. Generate new output that matches training data. LLMs, case study creators, art generators. Generative AI.

Subjugators

Literary cautionary tales about AGI that operates in its own interest.

Artificial General Intelligence

Flexible, general-purpose, sets and solves its own problems. Essentially AI that has achieved sentience.

Brain-computer interface

Artificial interface with he brain that bypasses natural mechanisms for output, like speech, typing, gesturing, or input like vision, hearing and touch. Brain activity is recorded, then processed using a computer to determine the user’s desired action. A signal is sent out to the application to carry out the desired command. The feedback is provided to the user to indicate their action was successful (might be a feature or naturally build into the action).

Non-invasive

Signal is weaker, dispersed by bone, skin and hair.

Invasive

Typically require craniotomy. Signal is stronger and accuracy can be much higher. Prone to scar tissue build up. Signals can weaken or fail over time.

Electrocorticography (ECoG)

Semi-invasive. Electrodes placed outside the dura mater (epidural) or under the dura mater (subdural). Only performed as part of medically necessary procedures.

Cortical implants

Only well-established invasive recording sensor.

Utah array

First, and most studied, FDA-approved implantable sensor.

Neuropixels

Multi-electode array with hundreds of sensors along a single thin probe. Can record from hundreds of neurons simultaneously. In 2022, tested in 9 patients under anaesthesia receiving brains surgery to test.

Stentrodes

 Made out of wire and electrodes that are threaded into the brain’s blood vessels.

Neural Lace

Many flexible probes inserted via a surgical robot. Pioneered by Elon Musk. Often used on patients with paralysis.

Bidirectional BCI:

Myoelectric prosthesis. Electrodes implanted in motor and somatosensory cortices. Stimulating somatosensory cortex as though the hand is being touched improves task performance.

Volume loss

Overall volume shrinks by 5% per decade after 40 and accelerates after 70. Varies across structures: frontal cortex>basal ganglia>temporal lobe>other.

Neurotransmitter depletion

Dopamine and serotonin levels decline.

Mild Cognitive Impairment (MCI)

Changes in attention and memory serious enough to be noticed by the person, friends and family. Cognitive difficulties in excess of normal aging, but activities of daily living are preserved. 5-15% of people with this will go on to have dementia. Affects 12-20% of individuals 65+.

Dementia

Impairment of multiple cognitive functions and activities of daily living. Progressive decline. A syndrome that can be caused by multiple diseases. Onset in middle-to-late adulthood usually.

Alzheimer’s Disease

Most common cause of dementia. Early symptoms include confusion, irritability, anxiety and deterioration of speech. Later symptoms can include difficulties with simple responses or behaviours like swallowing and speech.

Apo-E status

Everyone carries two of these genes. It plays a role in cholesterol transport and is involved in the normal metabolism of amyloid beta. Multiple alleles. E4 allele can lead to Alzheimer’s.

Neurofibrillary tangles

A tauopathy. Act as prions. Cell structure is compromised. Intracellular.

Tauopathy

Tau proteins are hyperphosphorylated, misfold, and build up.

Amyloid plaques

Beta amyloid proteins take on large, collapsed forms and build up in the extracellular space.

Neurofibrillary (tau) hypothesis

Misfolded tau is the causal agent. Tau pathology correlates with cognitive impairment better than beta amyloid. However, tau mutation alone does not seem to cause plaques.

Amyloid cascade hypothesis

The dominant theory. Holds that amyloid plaques are the primary symptom and cause all others. The evidence is trisomy 21. The problem is high-plaque normals, and amyloid drugs keep failing.

Lithium deficiency theory

Holds that amyloid plaques bind endogenous lithium, reducing its normal function in the brain. Lithium depletion activates microglia, impairing their ability to degrade amyloid. In mice, supplementing with a form of lithium (lithium orotate) that avoids binding to amyloid prevents pathological changes and memory loss. However, there are no human studies yet.

Cholinergic agonists

Can help prevent decline in learning and memory.

NMDA receptor antagonist

Reduces actions of glutamate. Can prevent damage to neurons.