Session 10: Consciousness and its Disturbance Flashcards
What is the reticular formation? Describe its roles?
The reticular formation is a network of cells and nuclei (e.g. the raphe nucleus and the nucleus ceruleus) in the central core of the brainstem. The reticular formation functions in sleep regulation, motor control, cardiorespiratory control, autonomic functions, and motivation and reward, differing from other regions of the CNS that may be involved with one primary function. It receives a wide sensory input (the reticular formation is made up of discrete nuclei embedded in the white matter) and control the level of sensitivity (level of conscious awareness) the upper brain receives so that we are able to ignore a constant sensory background but remain acutely sensitive to changes in our surroundings.
These centres also inform the hypothalamus so that autonomic changes are often associated with a new situation as we prepare to fight or flee.
Fibres also descend the spinal cord – the reticulospinal tract – to alter the sensitivity of motor nuclei in the ventral horn – so the reticular formation has projections that travel all the way down to the spinal cord but also up to the cerebral cortexes
What are the two groups the reticular nuclei can be divdied into?
The ascending reticular activating system (ARAS), formed by projections of RF going up to the cerebral cortex, activates the brain to attention (increase levels of consciousness) and a secondary inhibitory area that can decrease the activity of the upper brain effectively altering the level of consciousness.
These centres act by releasing neurohormones such as acetylcholine, serotonin, dopamine, noradrenaline into the extracellular fluid.
Changes in the level of these hormones are seen in the changes of consciousness involved in the sleep/wake cycle.
Describe the ARAS
The ARAS is formed by projection of the reticular formation, having specific effects throughout the CNS to raise levels of consciousness. It acts by filtering incoming signals (gets rid of stuff we don’t need to be aware of – repetitive, continuous stimuli) and is itself inhibited by hypothalamic sleep centres for sleep to occur. So ARAS is inhibited whilst we’re asleep.
NB: LSD (Lysergic acid diethylamide, hallucinogenic psychedelic) acts on this region to inhibit it and reduce the filtering of incoming signals to higher centres of the brain; alcohol, hypnotic (anti-anxiety drugs) and anti-depressants also inhibit this region.
The ARAS has inputs of auditory, nociceptive, visual, somatosensory, visceral and partly olfactory (weakest input), which output to the motor system (fibres – reticulospinal tract - descend in the cord to alter sensitivity of motor nuclei in the ventral horn), autonomic centres (fight/flight response), thalamus and cortex, all to raise the levels of consciousness.
What are the brainstem neurotransmitters? How are they implicated in neurological conditions?
neurones projecting in CNS
- Noradrenaline – low in depression
- 5-HT (serotonin) – low in depression
- ACh – low ACh in Alzheimer’s (associated with destruction of ACh-secreting cells)
- Dopamine – in Parkinson’s (decreased – nigrostriatal pathway affected, in Schizophrenia (excessive dopamine, mesolimbic pathway which is involved in mood and processing).
Describe the activity of the ARAS when we’re awake or in REM sleep
The ARAS neurones stimulate thalamo-cortical neurones when an individual is awake (and REM sleep), stimulating the cortex for consciousness, as well as stimulating inhibitory neurones to act on inhibitory inter-neurones, further stimulating the consciousness of the cortex. Inhibitory inter-neurones are thus switched off. Acetylcholine neurones sensitise the thalamus to sensory signals.
Describe the activity of the ARAS when we’re in non-REM sleep
However, during slow wave sleep the acetylcholine neurones from the ARAS are silent, meaning no thalamo-cortical-neurones are firing and there is significantly reduced consciousness. Cortex is quiet. Inhibitor interneurons are now switched on.
Describe the thalamo-cortical loop
The result is a constant thalamo-cortical loop generated (which can be seen as oscillations on an EEG) with some positive feedback also from the cerebral cortex to the ARAS.
Constant ‘talk’ between these areas produce the electrical patterns seen in the EEG.
Variable neurotransmitters are used to project throughout the CNS and affect the levels of consciousness and the sleep-wake cycle; these centres will release these neurohormones in the extracellular fluid.
Pathological alteration of the level of these chemicals is implicated in disorders of mood and of cognitive ability e.g. excessive levels of dopamine are implicated in schizophrenia, low levels of serotonin (5-HT) in depression whereas Alzheimer’s disease is associated with the destruction of acetylcholine secreting cells.
What is an EEG?
The level of activity in the cortex is reflected in the waveforms of the electroencephalogram (EEG). EEGs are in limited use now due to improved imaging methods (such as fMRI scanning but they work by placing 16-25 electrodes on an individual’s head and measuring electrical activity (both excitatory and inhibitory) of the neurones from the scalp.
Algebraic sum of the electrical activity (both excitatory and inhibitory) of neurones, from scalp.
Useful in epilepsy, brain damage etc.
How are the different waveforms of EEGs classified?
Alpha waves (8-13 Hz, 50μV): typical of relaxed wakefulness. Seen when awake, quiet and eyes shut (mainly occipital lobes), whereby there is a constant feedback between cortical and thalamic projections.
Beta waves (>14 Hz) recorded during mental activity, particularly from the front of the brain – seen when awake and eyes open (mainly parietal and frontal lobes)
Theta waves (4-7 Hz): typical of a drowsy state of the first stages of sleep. Also seen in children, concentrating or mediating adults (mainly parietal and temporal lobes). High amplitude, slow frequency (slower response).
Delta waves (<3.5 Hz): characteristic of deep sleep and in serious brain conditions (mainly cortical). High amplitudes, low frequency.
What does consciousness require? Give examples of altered states of consciousness and what is meant by coma?
Consciousness: requires adequate function of both the cerebral cortex and ARAS
Examples of altered states:
- Locked in Syndrome: cortex is ok but brainstem damage (only movement is movement of the eyes in response to stimuli)
- Persistent Vegetative State (brainstem intact so can breathe unaided, cerebral cortex damaged).
- Brain death: both are damaged (could be due to hypoxia etc)
Coma:
- A state of unconsciousness from which the person cannot be roused using pain, sound, light. Patient does not initiate any voluntary movement.
- Causes: intoxication (drugs of abuse or misuse), metabolic (hypothermia etc), neurological (strokes, intracranial bleeds), trauma
- Evaluation: e.g. Glasgow coma scale, scans, blood work, history, EEG etc.
- NB: ~20% of comas are due to hypoxia.
Why do we need sleep? Describe control of the sleep-wake cycle
Why do we need sleep?
- Energy conservation (although largely disputed these days)
- CNS resetting/clearance (one idea is glial cells wash out CSF to get rid of wastes)
- Memory formation and consolidation (particularly occurs during dream sleep).
- Homeostasis: reduced sleep switches on bad genes (associated with diabetes, poor immunity etc).
Control of Sleep-Wake Cycle
- Reticular Formation keeps us awake
- Hypothalamus (inhibits RF to promote sleep)
- Biological clocks (feel most sleepy between 2&6am, 2&4pm)
- Caffeine is an adenosine antagonist – interrupts the stimuli for sleep
Sleep appears to be important for resetting the CNS (improving rhythm and removing thought), good memory (converting short term to long-term memory) and homeostasis. The control of sleep is heavily influenced by the reticular formation and the hypothalamus (acting to inhibit the reticular formation to promote sleep).
How does an EEG show sleep?
The EEG shows characteristic changes during sleep giving occasional large amplitude waves – sleep spindles.
In deep sleep, blood flow and the metabolic rate of the brain is reduced (non-REM) sleep. [REM = Rapid Eye Movement]
Periodically, however the brain becomes very active, blood flow increases and the deep sleep pattern of the EEG is interrupted by the appearance of a wakeful pattern in the EEG. This stage is accompanied by rapid eye movements, giving REM sleep, often called paradoxical or wakeful sleep.
During REM sleep, the motor system (except those nerves controlling muscles of breathing and eye movements) is largely inhibited
Describe Non-REM sleep
Non-REM sleep is slow wave sleep, where there is an “active body and inactive brain” which is made up of 4 (deeper) stages. It is restorative and has a large part in neuroendocrine functioning, with over 95% of pituitary output occurring in non-REM sleep. Sleepwalking, bedwetting in children occurs during non-REM sleep. During non-REM sleep, there is decreased cerebral blood flow, O2 consumption, body temperature, blood pressure, respiratory rate and BMR (decreased metabolic activity).
Describe REM sleep
REM sleep is an “active brain and inactive body” state and on EEG will appear as if awake (same projections between reticular formation, thalamus and cortex seen). EEG waves spread from pons to thalamus then occipital lobe. REM sleep is where an individual is difficult to disturb and commonly dreams, as the brain is very active. During REM sleep, there is irregular heart rate and respiratory rate, increased BMR (20% higher than in daytime), descending inhibition of motoneurones (respiratory, extraocular and some muscles of the inner ear – to maintain pressure – are exempt), and penile erection (can be used to distinguish is dysfunction is psychological or physiological). Alcohol reduces REM sleep.
Describe the pharmacology of sleep and what happens during a night’s sleep
Pharmacology of Sleep: Cholinergic neurones in reticular activating system are active when awake and REM sleep, and cholinergic and serotonergic (5-HT) neurones together switch on REM sleep whilst noradrenergic neurones switch off REM.
- During waking: 5-HT/NA constantly active, ACh neurones active during a novel input
- Non-REM sleep: 5-HT and NA inactive, ACh inactive
- REM sleep: 5-HT inactive, NA inactive (it’s suggested things are stored as memory without emotion – so things look better the next day), ACh fully active (stimulating cortex to process information)
- Coming out of REM: Increase NA activity, ACh active
- NB: all this work has been done in animal models so far, not humans
During a night’s sleep, the type of sleep occurring alters. Non-REM normally occurs in the first hours and you get more and more REM sleep throughout the night. Children have lots of REM sleep, elderly people have very little.
What are possible immediate treatments?
Hypoxia => high flow oxygen
Hypoglycaemia => glucose IV
Fitting => Lorazepam (benzodiazepam) IV (to bring brain’s metabolic requirement down to normal, reduce chances of brain damage)
Opiates OD => Naloxone IV+IM (specific antagonist at opioid receptors).
NB: for some overdoses, it’s not appropriate to give an antidote e.g. in a benzodiazepine OD such as valium, giving flumazenil can cause negative consequences (e.g. seizures)
How would you measure eye opening?
Spontaneous: 4
On Command: 3
In response to pain: 2
No eye opening: 1
NB: can be voluntarily controlled if patient doesn’t want to speak to you so may not be reflective of brain function)
How would you measure motor responses?
Obeys Commands: 6
Localises response to pain: 5 (e.g. purposely moves an arm to remove the cause of central painful stimulus – but does not respond to a verbal stimulus)
Withdraws in response to pain: 4 (patient flexes or bends the arm towards the source of the pain but fails to locate the source of the pain – no wrist rotation)
Flexion response to pain (abnormal flexion): 3 (patient flexes or bends the arm; characterised by internal rotation and adduction of the shoulder and flexion of the elbow, much slower than normal flexion)
Extensor response to pain: 2 (extends the arm by straightening the elbow and maybe associated with internal shoulder and wrist rotation – moves towards painful stimulus - ABNORMAL)
No response to painful stimuli: 1
How would you measure verbal responses?
Orientated place/time/person: 5
Confused conversation: 4
Inappropriate word use: 3
Non-speech sounds only: 2
No vocalisation: 1
NB: can also be voluntarily controlled.
What is meant by Patterns of Change
Patterns of Change – need to do serial measurements of the GCS
- More important than any one measurement
- Reflection of global brain function
- Change in GCS = change in brain function
- A head trauma injury e.g. baseball bat blow could cause GCS to drop from 15 to 3. After a period of time, the ARAS corrects itself and the patient gradually comes round – GCS returns to 15. So it is reassuring if the GCS is increasing. Patient is recovering.
- But if the patient starts getting drowsy after a period of full consciousness (lucid interval) and GCS drops to 13/15, this indicates a process going on that is impairing global brain function – need to find out what’s going wrong urgently. Patient needs urgent intervention.
- A lucid interval followed by drowsiness is typical of a patient with an extradural haematoma. There isn’t really a primary brain injury - the brain isn’t damaged – but the extradural haematoma from the meningeal artery started expanding, compressing the brain => raised ICP, impairing level of consciousness. If we don’t treat the haematoma, this could eventually lead to death. If we treat the haematoma, patient would recover because brain itself is not injured.
- If a patient is knocked out and gradually comes round very slowly, this is evidence of a primary brain injury because brain is recovering really slowly. They probably don’t have a secondary process e.g. haematoma forming because level of consciousness is improving so there’s probably not something making it worse.
- A CT scan is always needed for a patient with a decreasing level of consciousness to work out what’s going on!
What are the three types of intracranial haemorrhage?
Cerebrovascular accidents are one of the commonest causes of death in this country. The blood supply to the brain is vulnerable to trauma to the head, certain disease processes e.g. hypertension, and to the normal ageing processes.
Bleeding into the head is particularly dangerous because as the cranium is effectively a closed box, such a bleed raises intracranial pressure leading to a variety of neurological signs.
There are broadly 3 kinds of intracranial haemorrhage
- Extradural (epidural) haemorrhage: following a blow to the head, blood from torn meningeal arteries accumulates between the endosteal layer of the meninges and the calvaria
- Subdural haemorrhage: following a blow that causes the brain to move within the skull (e.g. as in boxing), blood collects in the subdural space following the rupture of a vein.
- Subarachnoid haemorrhage: this kind of bleed usually follows the rupture of an aneurysm (pathological dilation of a blood vessel) although may be linked to other kinds of head trauma. Blood collects below the arachnoid layer of the meninges
