Overview
This lecture covers consciousness as a spectrum, then two major departures from normal waking consciousness: coma (its causes, diagnosis via the Glasgow Coma Scale and EEG, and management) and sleep (its regulating structures, the two major sleep phases and their EEG signatures, the pattern of a night’s sleep, and common sleep disorders). EEG is the thread linking the two halves: the same wave patterns used to describe wakefulness and sleep stages are also used to characterise coma and seizure.
Consciousness
- Definition is difficult; consciousness is better described as a spectrum of levels/states rather than an all-or-nothing property.
- It comprises the experience of the world (internal and external) and awareness of person, place and time.
- It is alterable physiologically, pathologically, and chemically.
- Component processes: arousal, attention, habituation.
Coma
- Definition: deep unconsciousness — unable to react to the environment, not rousable, no sleep-type EEG activity, low brain metabolic activity.
- Abnormal posturing may accompany coma:
- Decerebrate (extension) posturing: arms extended straight at the sides, legs extended.
- Decorticate (abnormal flexion) posturing: arms flexed up onto the chest, legs extended.
Causes of coma
- Focal: trauma, haemorrhage, stroke, tumour, infection/abscess.
- Diffuse processes: trauma, raised intracranial pressure (ICP), toxins, metabolic derangement, hypoxia, infection, seizure, blood pressure disturbance.
- Psychogenic.
Outcomes
- Variable outcomes.
- Persistent vegetative state: no cognitive function, but the patient can breathe and move.
- Brain death.
Coma — diagnosis
- History: friends/family, onset, past medical history (PMHx).
- Examination: trauma, cardiovascular (CVS), neurological (using GCS), eyes.
- Investigation: metabolic, endocrine, toxins, microbiology.
- Imaging: CT / MRI / angiography.
- EEG.
Glasgow Coma Scale (GCS)
Three components are scored and summed:
- Eye opening: spontaneous = 4; to speech = 3; to painful stimulation (e.g. endotracheal suctioning) = 2; none = 1.
- Motor response: follows commands = 6; localises to pain = 5; nonpurposeful (withdrawal) movement to noxious stimulation = 4; abnormal flexion of upper extremities/extension of lower extremities to pain = 3; extension of all extremities to pain = 2; no response to noxious stimuli = 1.
- Verbal response: oriented to person, place and time = 5; converses, may be confused = 4; inappropriate words = 3; incomprehensible sounds = 2; no response = 1.
The GCS score is built from eye, motor, and verbal components scored independently and summed — know each component's individual scoring, not just a total.
Coma — management
- ABC (airway, breathing, circulation).
- Treat the underlying cause.
- Correct electrolytes / metabolic derangement / toxins.
- Reduce intracranial pressure: hyperventilation, diuretics, surgical measures.
- Manage associated problems, e.g. trauma.
- General patient care: positioning/skin care, thermoregulation, bladder care, infection prevention, nutrition.
Electroencephalogram (EEG)
- Scalp electrodes detect cortical activity. Electrodes are placed over sites corresponding to the frontal (Fz, F3, Fp1, F7), parietal (Cz, C3, P3, Pz), temporal (T3, T5), and occipital (O1, O) lobes, referenced to the nasion and inion.
- EEG reflects level of consciousness and cortical activity; it is used to assess seizures and brain death.
Two basic waking patterns
- Alpha: a slow, steady pattern seen when awake, relaxed, with eyes closed, or bored — appears on the trace as a slower, rounded/undulating waveform with intermittent higher-amplitude bursts.
- Beta: a desynchronised pattern reflecting increased arousal and attention — awake, alert, eyes open and concentrating; appears as a faster, lower-amplitude, more uniformly desynchronised waveform.
EEG in seizure
At seizure onset, the trace changes from a low-amplitude baseline to a high-amplitude, rhythmic spike-and-wave pattern, with distinct “wave” and “spike” components visible on the trace.
Slide 5 (posturing images) and the seizure-onset trace (Slide 16) were read visually from labelled illustrations rather than text; no ambiguity was flagged in the transcript, but they are described here as diagrams rather than verbatim text.
Sleep — regulation and function
- Sleep is a cyclical, reversible change in level of consciousness (LOC).
- The sleep/wake cycle is governed by the hypothalamus; arousal involves the reticular activating system (RAS) and medulla/nucleus tractus solitarius (NTS).
- Sleep differs from coma and anaesthesia: in sleep the person is rousable, has characteristic EEG patterns, and maintains a high metabolic rate [slide does not elaborate further on the coma/anaesthesia comparison].
- Structures involved in sleep-wake regulation (from a labelled brain diagram): suprachiasmatic nucleus, preoptic area, brainstem nuclei of the reticular activating system, thalamus, posterior hypothalamus.
Why sleep? (proposed functions, marked as uncertain on the slide)
- Recuperative function.
- Mental development/regeneration, including memory.
- Adaptive function.
- Sleep is not simply rest for the brain — the brain remains highly active during sleep.
Sleep physiology — regulating factors
- Circadian rhythm.
- Light changes, sensed via the suprachiasmatic nucleus.
- “Clock” genes.
- Reticular activating system (RAS), involving multiple nuclei and neurotransmitters.
- Hypothalamus — hypocretin.
- Adenosine.
- Melatonin.
- Serotonin.
Sleep processes and stages
- Sleep is organised and active, not passive.
- Two major phases, which alternate cyclically: REM (rapid eye movement) and non-REM/slow-wave (SW) sleep.
- Each phase has a characteristic EEG pattern.
EEG across states
- Awake, alert: beta rhythm (fast, low amplitude).
- Awake, drowsy: alpha rhythm (slower, rounded).
- NREM Stage 1: theta rhythm.
- NREM Stage 2: sleep spindles and K complexes.
- NREM Stages 3 and 4: delta rhythm (large-amplitude slow waves).
- REM (paradoxical) sleep: pattern similar to the awake beta rhythm.
Slow-wave (NREM) sleep
- Four stages, each with a slow EEG pattern.
- Low metabolic rate.
- Mental activity continues.
- Dreaming is rare.
- Sleepwalking occurs in this phase.
- Proposed (uncertain) function: body repair.
REM sleep
- EEG is desynchronised.
- Rapid eye movements occur.
- Total postural relaxation (muscle atonia).
- Difficult to arouse from REM externally, but the person wakes spontaneously from it.
- Dreaming occurs.
- Proposed (uncertain) function: learning/memory.
Sleep cycle across the night
- The sleeper initially sinks into non-REM sleep, then cycles back to REM.
- Each cycle lasts approximately 90–120 minutes.
- Across the night, non-REM descents become shallower and shorter, while REM periods become more frequent/longer, and waking tends to occur from REM.
- This pattern is shown on a sleep-stage-vs-time graph and on a bar-style hypnogram: both show alternating NREM (stages 1–4)/REM cycling through the night, with progressively shallower non-REM depth and increasing REM later in the night.
Sleep patterns across the lifespan
- Total sleep time varies with age: babies sleep much more, the elderly less.
- Proportion of REM sleep: babies spend over 50% of sleep in REM; adults spend around 20%.
- Stage 4 (deep NREM) sleep decreases with age.
Sleep disorders
- Hypersomnias: apnoea, narcolepsy.
- Insomnia: sleep physiology itself may be normal, with other underlying problems; can arise from disorders of the sleep-wake cycle, psychiatric causes, or lifestyle factors.
- Parasomnias: enuresis, somnambulism (sleepwalking), night terrors.
Self-test
- Why is consciousness described as difficult to define, and what components make up its experience according to the lecture?
- Define coma, including its four defining clinical/EEG/metabolic features.
- Distinguish decerebrate (extension) posturing from decorticate (abnormal flexion) posturing.
- List the three categories of coma causes given in the lecture, with an example of each.
- Distinguish persistent vegetative state from brain death.
- List the five components of the coma diagnostic work-up.
- A patient in coma opens their eyes only to a painful stimulus, extends all four limbs to pain, and makes incomprehensible sounds. Calculate their GCS score, showing each component.
- Describe the four elements of coma management aimed at stabilising and treating the underlying cause (excluding general patient care).
- What does EEG measure, and what three clinical uses does the lecture give for it?
- Distinguish alpha from beta EEG patterns, including the state of the person each is associated with.
- Describe how the EEG trace changes at the onset of a seizure.
- Explain how sleep differs from coma and anaesthesia despite all three involving reduced responsiveness.
- List the five brain structures shown in the sleep-wake regulation diagram.
- List the proposed functions of sleep given in the lecture, noting that they are presented as uncertain.
- List the physiological factors involved in regulating sleep.
- Distinguish the EEG features of NREM stages 1, 2, and 3/4 from each other and from REM.
- Describe the key features of slow-wave (NREM) sleep.
- Describe the key features of REM sleep, including why it is called “paradoxical.”
- Describe the typical progression and duration of a sleep cycle across a night, including how non-REM and REM proportions change.
- How does the proportion of REM sleep and the amount of Stage 4 sleep change from infancy to old age?
- List the three categories of sleep disorder given in the lecture, with an example of each.
- Integrative: a patient is unresponsive, will not open their eyes to any stimulus, and has no sleep-type EEG activity. Using the criteria from the lecture, explain why this points to coma rather than deep sleep, and identify two categories of investigation you would use to work out the cause.
Answers
Reveal answers
- Consciousness is hard to define because it exists on a spectrum of levels/states rather than as a single fixed condition. Its experience comprises awareness of the internal and external world and of person, place, and time, built on the component processes of arousal, attention, and habituation, and it can be altered physiologically, pathologically, or chemically.
- Coma is deep unconsciousness: the patient is unable to react to the environment, is not rousable, shows no sleep-type EEG activity, and has low brain metabolic activity.
- Decerebrate (extension) posturing: the patient lies supine with arms and legs extended straight. Decorticate (abnormal flexion) posturing: the patient lies supine with arms flexed up onto the chest and legs extended.
- Focal (e.g. trauma, haemorrhage, stroke, tumour, infection/abscess); diffuse processes (e.g. trauma, raised ICP, toxins, metabolic derangement, hypoxia, infection, seizure, BP disturbance); psychogenic.
- Persistent vegetative state: no cognitive function, but the patient can breathe and move. Brain death: complete loss of brain function (contrasted with PVS in the lecture as a distinct, more severe outcome).
- History, examination, investigation, imaging, EEG.
- Eye opening to pain = 2; motor extension to pain = 2; verbal incomprehensible sounds = 2; total GCS = 6.
- Follow ABC; treat the underlying cause; correct electrolytes/metabolic derangement/toxins; reduce intracranial pressure (hyperventilation, diuretics, surgical measures).
- EEG uses scalp electrodes to detect cortical activity. It is used to assess level of consciousness/cortical activity, seizures, and brain death.
- Alpha is a slow, steady pattern seen when awake, relaxed, with eyes closed or bored. Beta is a desynchronised, faster, lower-amplitude pattern reflecting increased arousal/attention, seen when awake, alert, with eyes open and concentrating.
- The trace shifts from a low-amplitude baseline to a high-amplitude, rhythmic spike-and-wave pattern, with identifiable spike and wave components.
- Sleep is a cyclical, reversible change in LOC in which the person remains rousable, shows characteristic (sleep-stage-specific) EEG patterns, and maintains a high metabolic rate — unlike coma (not rousable, no sleep-type EEG, low metabolic rate) or anaesthesia.
- Suprachiasmatic nucleus, preoptic area, brainstem nuclei of the reticular activating system, thalamus, posterior hypothalamus.
- Recuperative function, mental development/regeneration (including memory), and adaptive function — all marked with a question mark on the slide as unconfirmed/proposed. The lecture also stresses sleep is not simply brain rest, as the brain stays highly active.
- Circadian rhythm, light changes via the suprachiasmatic nucleus, “clock” genes, the reticular activating system (multiple nuclei/neurotransmitters), hypothalamic hypocretin, adenosine, melatonin, serotonin.
- Stage 1: theta rhythm. Stage 2: sleep spindles and K complexes. Stages 3/4: delta rhythm (large-amplitude slow waves). REM: pattern similar to the awake beta rhythm (desynchronised), distinguishing it from the slow NREM stages.
- Four stages with a slow EEG pattern, low metabolic rate, continuing mental activity, rare dreaming, and the phase in which sleepwalking occurs; proposed (uncertain) function is body repair.
- Desynchronised EEG, rapid eye movements, total postural relaxation (muscle atonia), dreaming, and difficulty rousing the person externally even though they wake spontaneously from it; proposed (uncertain) function is learning/memory. It is “paradoxical” because the EEG resembles the awake state despite the person being asleep and atonic.
- The sleeper first sinks into non-REM sleep, then cycles back to REM, in cycles of about 90–120 minutes. Across the night, non-REM periods become shallower and shorter while REM periods become more frequent and longer, with waking tending to occur from REM.
- REM proportion falls from over 50% of sleep in babies to about 20% in adults. Stage 4 (deep NREM) sleep decreases with age.
- Hypersomnias (e.g. apnoea, narcolepsy); insomnia (e.g. normal sleep physiology with other underlying problems, or disorders of the sleep-wake cycle from psychiatric/lifestyle causes); parasomnias (e.g. enuresis, somnambulism, night terrors).
- Coma is distinguished from deep sleep by being unrousable and showing no sleep-type EEG activity, whereas sleep — even its deepest NREM stages — remains reversible/rousable and shows characteristic sleep-stage EEG patterns (e.g. delta waves), plus a high metabolic rate; coma instead shows low metabolic activity. Given these features, you would investigate with imaging (CT/MRI/angiography) and metabolic/endocrine/toxin/microbiology investigations to find the cause, alongside history and examination.