NS 10: Consciousness and its disturbances Flashcards Preview

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Flashcards in NS 10: Consciousness and its disturbances Deck (53):

change in neurohormone levels associated with depression?

low levels of serotonin and noradrenaline


change in neurohormone levels associated with Alzheimer's Disease?

destruction of ACh secreting cells


change in neurohormone levels associated with schizophrenia?

excessive dopamine


waveforms of EEG characterising relaxed wakefulness?

alpha waves= 8-13 Hz
mainly occipital lobe as not receiving any visual stimuli, awake, quiet, eyes shut


waveforms of EEG characterising mental activity, part. from front of brain?

beta waves= >14Hz, higher frequency
awake, eyes open, frontal and parietal lobes


waveforms of EEG characterising 1st stages of sleep, drowsiness?

theta waves= 4-7Hz
parietal and temporal lobes
children, emotional adults


waveforms of EEG characterising deep sleep?

delta waves= <4Hz
mainly cortical
also seen in serious brain conditions


3 reasons as to why disturbance of consciousness may arise?

-metabolic e.g. hypoglycaemia, uraemia or anoxia (no O2)
-brain stem lesions or pressure on brain stem from any SOL causing raised ICP
-head trauma, which may bruise brain within skull


3 sections to glasgow coma scale?

eye opening, 1-4
motor responses, 1-6
verbal responses, 1-5


max and min scores for glasgow coma scale?



what has control over the sleep-wake cycle?

reticular formation
hypothalamus- inhibits reticular formation to promote sleep


why do we need sleep?

energy conservation
CNS resetting/clearance


neurohormones characterising waking?

5-HT and noradrenaline constantly active
ACh neurones active during a novel input


neurohormones charactersing non-REM sleep?

5-HT and NA inactive
ACh inactive


neurohormones charactersing REM sleep?

5-HT and NA inactive (memory, without emotion?)
ACh fully active


neurohormones charactersing coming out of REM sleep?

increase NA activity


what is AVPU?

system to assess level of consciousness:
V= responds to verbal stimulus
P= responds to pain stimulus
U= unresponsive


scores for eye opening with glasgow coma scale?

4= spontaneously
3= to speech
2= to pain
1= none


scores for verbal resonse with glasgow coma scale?

5= orientated
4= confused
3= inappropriate words
2- incomprehensible
1= none


scores for motor response with glasgow coma scale?

6= obeys commands
5= localises pain
4= flexion to pain
3= flexion/withdrawal
2= extension to pain
1= none


what happens in a subfalcal hernia?

part of the cingulate gyrus is forced into space between falx cerebri (inward folding of meningeal layer of dura mater) and the corpus callosum- connects the 2 cerebral hemispheres.


what happens in an uncal hernia?

the uncus- part of median temporal lobe, is pushed through the tentorial notch*


what happens in pressure coning/tonsillar herniation?

the cerebellar tonsils and possibly the medulla are forced through the foramen magnum
this is induced when lumbar puncture performed in cases of raised IC pressure
usually sudden resp and CVS collapse
pupils may be pin point as PNS overdrive
pons compressed, and subsequently damaged, causing neurological difficulties


what is the locked in state, and why does it occur?

as parts of reticular formation respons for consciousness lie above mid-pons, a lesion just below this e.g. pontine haemorrhage may disrupt descending activating pathways, so ptnt alert and awake, although mute and quadriplegic. Oculomotor pathways often remain intact so patient may only be able to communicate through blinking.


why must a lumbar puncture NOT be done in cases of raised IC pressure?

will cause cerebello-tonsillar herniation, as pressure gradient created down SC as CSF would be give access to atmos pressure, so cerebellar tonsils forced through foramen magnum= coning.


what system activates the cerebral cortex, as occurs in arousal and wakefulness?

ascending reticular activating system (ARAS)


what does the body accumulate during the day which makes you want to go to sleep?

*caffeine blocks adenosine receptors


examples of discrete nuclei embedded in white matter which constitute the reticular formation diffuse modulating system?

raphe nucleus
locus ceruleus
ventral tegmental= all in brainstem
and basal nucleus of Meynert= in basal forebrain


neurotransmitter associated with locus ceruleus?

projections involved in regulation of attention, cortical arousal, and sleep-wake cycle, and learning, memory, anxiety and mood.
NA increases brain responsiveness and speeds information processing.


neurotransmitter associated with raphe nuclei?

5-HT (serotonin)
those near pontomedullary junction are nucleus raphe magnus= projects to SC for modulation of slow pain.
in rostral pons and midprain project to thalamus, limbic system, and cerebral cortex.
Projections involved in sleep-wake cycle, and in control of mood, and certain types if emotional behaviour, especially aggression.


characteristics of REM sleep?

rapid eye movements
decreased tone in almost all muscles so that we don't act out our dreams, except external ocular muscles and diaphragm, descending inhibition of motor neurones
muscle twitches
HR fluctuations, irregular HR and resp rate, and BP, resp, body temp, miosis, penile erection, and clitoral engorgement
BMR increased
EEG patterns similar to that of wakefulness= paradoxical
disturbed by alcohol


charaacteristics of non-REM sleep?

absence of rapid eye movements
reduced body movements
decreased HR and BP, body temp and cerebral blood flor
basal metabolic rate reduced
active body, inactive brain
sleep walking
neuroendocrine= 95% of pit hormones released


why is ACh fully active in REM sleep?

allows information processing, can sort through memories


what is the decorticate response?

cortex is effectively isolated from the lower brain and SC due to severe injury to head or a large infarct which destroys the connections between the thalamus and the cortex. Cerberal hemispheres, thalamus or internal capsule may be damaged. Lower limbs extend but arms flexed as brainstem reticular inhibiting centres are intact. Patient will be unconscious but able to respond to painful stimuli= decorticate responses.
Hands are clenched into fists and feet turned inwards, also known as mummy baby.
descending tracts e.g. rubrospinal (flexor muscle tone) and reticulospinal (automatic movements) from red nucleus in midbrain and reticular formation in brainstem respectively, intact, no inhibition on their function.
May be seen in certain classes of people living with disability.


what is the decerebrate response?

marked increase in muscle tone with involuntary tonic extension of upper and lower limbs.
head arched back
occurs if damage affects lower parts of brain/brainstem, so lose inhibition from reticular formation on descending motor tracts.
Patients respond by reflexive extension to pain.
Damage, in particular, at level of red nucleus at mid-collicular level.
It is characteristic of pontine damage
It is commonly seen in uncal or tonsilar herniation
Decerebrate posturing is only seen in the acutely ill.


when is decerebrate posturing commonly seen?

in uncal or tonsilar herniation
so only seen in the acutely ill


why is uncal/transtentorial herniation a life-threatening development, and what signs may the patient have on examination?

pressure on brainstem breathing centres
patient may have difficulty breathing, mid-point or dilated non-reactive pupils and ptosis due to oculomotor nerve damage.
usually reduced consciousness and decerebrate rigidity= upper and lower limbs in involuntary tonic extension as loss of inhibition on descending motor tracts from reticular formation in brainstem.


importance of cholinergic neurones in pons and midbrain, forming part of reticular system?

these project to thalamus and regulate excitability of thalamic nuclei. Those in the basal nucleus of Meynert project to areas of cerebral cortex and play major role in cortical excitability, memory and learning.
Degeneration of these in Alzheimer's may be resonsible for their impaired cognitive functioning.


which areas of reticular formation are associated with dopamine production?

substantia nigra= dopaminergic projections to caudate nucleus and putamen, degeneration results in Parkinson's disease.
Ventral tegmental area= dopaminergic neurones to accumbens, amygdala, and prefrontal cortex. Increased dopaminergic activity in accumbens nucleus caused by psychostimulant drugs e.g. amphetamines and cocaine coincides with its reward and pleasure functions.


where are the neurones located that chiefly regulate REM sleep?

at midbrain-pontine junction


where are neurones located that chiefly regulate NREM sleep?

anterior hypothalamic nucleus in hypothalamus, preoptic area and medulla
95% of pituitary hormones are released in NREM sleep so not having enough sleep damages homeostasis.
anterior hypothalamic sleep centre can facilitate sleep by inhibiting arousal centres in posterior hypothalamus, so bilateral lesions of anterior hypothalamic sleep centre results in insomnia.


where do lesions occur that interrupt ascending reticular activating system causing a coma?

paramedian tegmental lesions in rostral midbrain


various functions of reticular formation?

sleep regulation
motor control
cardio/resp control
autonomic functions
motivation and reward


function of ascending reticular activating system?

=projections of reticular formation in brainstem which is responsible for keeping us awake, filters out unimportant sensory info, and is inhibited by hypothalamic sleep centres (anterior hypothalamic sleep centre?)
*Taking LSD switches off filtering system so signals and clearer, more intense, get hallucinations, can't cope with vol of info.


what inhibits the ascending reticular activating system?

hypothalsmic sleep centres
sleeping tablets


what is happening within the ascending reticular activating system when we are awake, and in REM sleep?

stimulation up to cortex from thalamus
inhibitory pathway inactive, so no inhibition on thalamo-cortical projections
ACh neurones sensitise thalamus to sensory signals
brain active


what is happening within ascending reticular activating system in non-REM (slow wave) sleep?

no excitation to thalamus and cortex, ACh neurones quiet, so they can't inhibit the inhibitory interneuone, this is therefore active, inhibiting thalamo-cortical projections.

however, cerebral cortex is capable of overiding pathway e.g. in stress, which keeps you awake, =+ve feedback mechanism.


what is EEG?

algebraic sum of electrical activity, both inhibitory and excitatory, of neurones from scalp.


characteristics of EEG waveforms when awake with eyes open?

high frequency, low amplitude
electrical activity all over brain as responding to lots of different stimuli, in different directions so can cancel each other out so very low amplitude


how doe EEG waveforms change between NREM and REM sleep?

NREM starts off with theta waves in stage 1, which have lower amplitude than alpha waves. As progress through stages of NREM sleep, amplitude becomes greater and frequency less, so stage 4= delta waves, but in REM sleep, looks like you're awake with eyes open= low amplitude high frequency waveform.


what is obstructive sleep apnoea?

loss of tone of upper resp tract muscles in sleep e.g. palatal muscles, closure of airways, patient actually stops breathing- 1 min or more, waking them up in sleep repetitively, so end up tired during day. Snore.
RFs= obesity, smoking....
can use continuous +ve airway pressure therapy to treat- keep airways open


what is parasomnia?

sleep paralysis*


what is hypersomnia?

daytime sleepiness e.g. with OSA, or narcolepsy= sudden and spontaneous episodes of sleep at any time during day, begins with REM phase of sleep.