2.5 Consciousness Flashcards
NREM sleep makes up __% of sleep
75%
Which arm of the autonomic nervous system is more active during NREM/REM sleep?
NREM: Parasympathetic
REM: Sympathetic
REM sleep makes up __% of sleep
25%
What happens to sensation during REM/NREM sleep?
NREM: Limited/absent
REM: Vivid, internally generated
Describe muscle activity during REM sleep
Movements are commanded, but none are carried out
Why is REM sleep called paradoxical sleep?
EEG looks more awake than asleep.
Oxygen consumption of brain during REM vs NREM
REM: Elevated
NREM: Decreased
How are muscles paralyzed during REM sleep?
Glutamatergic neurons in the brainstem activates neurons in the medulla. They release GABA, inhibiting the activity of skeletal muscles.
Describe the four stages of NREM sleep
Stage 1: Hypnagogic hallucinations
Stage 2: Harder to awaken
Stage 3: Few eye and body movements
Stage 4: Sleep talking
Describe the sleep cycles
Move from stage 1 to stage 4 of NREM. Back up to stage 1 sequentially, and into REM. This is one sleep cycle.
With each cycle, we spend less time in N3 and N4, and longer in REM.
Describe the two mechanisms by which neurons can create synchronous rhythms
- Central pacemaker (orchestra conductor)
- Inhibiting/exciting one another (all playing)
Gamma EEG waves
Conscious perception/problem solving
Beta EEG waves
Waking state; alertness
Alpha/Mu EEG waves
Quiet waking state. Relaxed, lucid, calm.
Theta EEG waves
Deep relaxation/light sleep; meditation
Delta EEG waves
Deep sleep
What EEG waves can be found in someone who is awake/in REM sleep?
Beta waves (gamma can also be found in wakefulness)
What EEG waves can be found in someone who is in Stage 3/Stage 4 NREM sleep?
Delta waves
What EEG waves can be found when we are drowsy/relaxed?
Alpha waves
What EEG waves are most prominent in Stage 1 NREM sleep?
Theta waves
What happens to EEG activity between Stage 1 and Stage 2 sleep?
- More theta
- Increased amplitude
- Sleep spindles (inhibit cognitive processes)
- K complexes (memory consolidation)
This part of the reticular formation is responsible for promoting wakefulness…
Ascending reticular activating system (ARAS)
How is the ARAS activated?
By the release of a peptide called orexin from the lateral hypothalamus
In order to fall asleep, we need to inhibit ARAS. How is this done, and by what system?
VLPO (Ventrolateral preoptic area) releases GABA to inhibit ARAS modulatory neurons
How does adenosine progressively make us sleepier?
Takes foot of ARAS accelerator (reduces orexin release).
Puts foot on ARAS brake (increases GABA release from VLPO)
How does caffeine make us less sleepy?
Binds to adenosine receptors
Give some examples of zeitgebers
- Sunlight
- Food
- Exercise
- Social interactions
Describe how the suprachiasmatic nucleus regulates sleep/wake cycles in response to sunlight
- Increases Orexin release from LH
- Decreases GABA release from VLPO
- Decreases melatonin release from pineal
Why is melatonin called the dracula hormone?
- Released in response to dark
- Inhibited release in response to light
How is it thought that melatonin makes us sleepy?
- Decreases orexin from LH
- Increases GABA from VLPO
Define consciousness
Full awareness of the self and one’s relationship to their environment
Define coma
Patient has closed eyes and is unable to interact with their environment (GCS 8 or less)
What are the two main components of consciousness?
- Arousal
- Awareness
Which neuroanatomical areas are responsible for arousal?
Thalamic/extrathalamic ascending systems
What is the relationship between awareness and arousal in terms of interdependence?
Awareness requires arousal, but arousal does not require awareness.
Describe the structure of the neuroanatomical regions responsible for awareness
- Distributed neuronal circuits
- Modular in nature
- Loop from thalamus and cortex
Lesions in which brain areas can lead to coma?
- Cortex
- Thalamus
- Brainstem
What is brain death? How is it different from death?
- Permanent loss of all brain activity
- Occurs when a patient dies whilst on life support; if life support is removed, the patient will die.
What is a minimally conscious state?
- No ability to follow instruction or communicate
- Appears to have awareness of surroundings
Minimal = only just passing = can do it, but can’t follow INSTRUCTIONs (maybe better…)
What is a vegetative state?
Complete unawareness of the self and the environment — but seems to be awake.
Awake but not aware (like the microbiome of on a piece of brocolli)
Locked in syndrome
- Alert wakefulness
- Inability to move or speak
What is akinetic mutism?
- Very infrequent movement or speech
- Well preserved eye movements; can speak or move occasionally if directed
What is the role of the hypothalamus in the baroreceptor response to low BP?
Stimulates vasopressin release -> fluid retention -> increase BP
Define syncope
Sudden, transient loss of consciousness due to cerebral hypoperfusion
List some different causes of syncope by category
- Reflex (e.g. vasovagal)
- Cardiac (e.g. structural heart disease, arrhythmia)
- Neurologic (e.g. CVA)
- Psychogenic (e.g. anxiety)
- Other (e.g. anaemia)
PRNC= Prank = Face syncope = first cause in acronym
Which type of syncope has the worst prognosis
Cardiac origin (e.g. arrhythmia, structural heart disease)
Vasovagal syncope mechanism
- Higher cortical sites trigger exaggerated sympathetic activity
- Followed by increased parasympathetic tone
- Bradycardia, dilation of blood vessels
- Cerebral hypoperfusion -> syncope
Vasodepressor vs cardioinhibitory vasovagal syncope
Vasodepressor: loss of arterial blood pressure
Cardioinhibitory: Bradycardia/asystole
(In most vasovagals, both are involved)
Prodromal symptoms of vasovagal syncope
- Sweating
- Dizziness
- Epigastric discomfort
- Nausea
Describe the mech of how increased intrathoracic pressure can cause situational syncope
- Increased ITP
- Vena cava compression
- Decreased venous return
- Decreased intra-aoritc pressure (baroreceptors)
- SNS activation
- When pressure released: increased PNS activation
- Bradycardia
- Cerebral perfusion down
- Bye bye
Is orthostatic hypotension/syncope associated with increased vagal response?
- No
- Rather, an insufficient baroreceptor-mediated sympathetic response to standing
Why are older adults at increased risk of orthostatic syncope?
- Decreased baroreceptor responsiveness
- Polypharmacy
What are some reasons why pregnancy can increase likelihood of syncope?
- Progesterone lowers BP
- Dehydration (e.g. morning sickness)
- Iron deficiency anaemia
Can hypoglycaemia cause syncope?
- Not often — only in old patients on glucose-lowering drugs for diabetes.
- It mimics syncope, but does not have to have cerebral hypoperfusion
True or false: hyoglycaemic crisis causes no change (or an increase) of postural tone
True
True or false: syncope in the presence of cardiac cause is more sinister than vasovagal syncope
True. Not good.
Syncope red flags
- Occurs during exercise
- Pupils aren’t equal in size
- Precipitated by severe headache
- Double vision
- Back/abdo pain (aortic dissection)
Explain how raised ICP can cause a vicious cycle
Raised ICP -> Lowered CPP -> Hypoxia -> Oedema -> raised ICP -> death
Investigations for a comatose patient
- EUC/LFT, glucose, creatinine
- ABG, CRX, ECG (if o2 concerns)
- Lumbar puncture (exclude meningitis)
- Toxicology (?Alcohol/drugs)
- CT/MRI
Other than brain masses/lesions/infections, what are some other causes of coma?
- Organ failure
- Epilepsy
- Psychogenic
- Metabolic
Patient has focal neuro dysfunction, progression, localising deficit, and coma. Is the lesion supra or infratentorial?
Supratentorial
Patient has immediate coma, pupil/occulomotor/respiratory abnormality. Is the lesion supra or infratentorial?
Infra
Delirium associated with a coma, and seizures. What is the common cause?
Metabolic
Describe treatment of patient with coma
- ABC (Airway, breathing, circulation)
- Get to scanner as fast as possible
- If structural: neurosurg registrar. If metabolic: medical registrar.
(Basically: keep them alive, work out what’s wrong, then find who can fix it)
