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MD4001 > Sleep, EEG > Flashcards

Sleep, EEG Flashcards

1
Q

Define sleep

A

Easily reversible state of inactivity with a lack of interaction with the environment

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2
Q

What is consciousness?

A

Having awareness, with perceptions, thoughts and feelings

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3
Q

What are the two main forms of externally discernible sleep?

A
  • When the eyes move rapidly side to side (REM)

* When they do not (non-REM/ slow wave/ deep sleep)

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4
Q

How does the EEG work?

A
  • Picks up post synaptic activity of synchronised dendritic activity
  • The more neurones that are synchronised, the bigger the peaks on the EEG
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5
Q

Describe stage 1 of sleep

A
  • Stage 1: duration of 1-5 minutes, easily aroused, slow rolling eye movements
  • Some theta waves and higher amplitude waves
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6
Q

Describe stage 2 of sleep

A
  • 10-15 minutes
  • K complexes
  • Sleep spindles
  • No eye movement
  • Body movement remains possible
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7
Q

Describe stage 3 of sleep

A
  • Few mins duration
  • Slower frequency
  • Delta waves appear
  • harder to rouse
  • Few spindles
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8
Q

Describe stage 4 of sleep

A
  • Deepest sleep
  • Hardest to rouse
  • EEG waves at 2Hz and high amplitude - delta waves
  • Lower heart rate and BP
  • 15-30 minutes
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9
Q

Describe REM sleep

A
  • Fast beta waves
  • Rapid eye movement
  • Subject easier to rouse than in stage 4
  • Dreaming recalled
  • Low muscle tone
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10
Q

Typical night sleep

A
  • Several cycles through the 5 stages of sleep
  • Stage 4 is only reached in the initial cycles
  • deepest sleep attained after is stage 3
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11
Q

What is REM characterised by?

A
  • Rapid eye movement
  • Increases in heart rate
  • Increased neuronal activity
  • Increased respiration and oxygen consumption
  • Penile erection
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12
Q

What is the reticular formation?

A

• Diffuse collection of at least 100 networks of neuromodulatory neurones spanning all three divisions of the brainstem

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13
Q

Where do the projections of the reticular formation go to?

A
  • Thalamus
  • Hypothalamus
  • Some brainstem nuclei
  • The cerebellum
  • Spinal cord
  • Cerebral cortex
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14
Q

Where does the reticular formation receive input from ?

A
  • The cerebra (collaterals from the corticospinal pathway)
  • visual and auditory systems
  • Sensory spinal system
  • Cerebellum
  • Certain brainstem nuclei
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15
Q

Describe the neural control of non-REM sleep

A
  • Cortical slow waves caused by hyper polarised thalamus
  • Decreased activity in the arousal centres of the reticulum
  • Sleep spindles and L complexes are caused in part when the thalamic neurones hyperpolarise (due to reduced ascending reticular formation input)
  • Slow wave rhythmicity blocks ascending sensory input
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16
Q

Where are orexinergic neurones

A

In the lateral hypothalamus, they project to the cerebra, arousla nuclei, vneterolateral pre optic nuclei in the anterior hypothalamus

17
Q

VLPO lesion

A

insomnia

18
Q

What is the effect of orexin?

A

Enhance the arousal nuclei and cause indirect inhibition of the VLPO via reciprocal inhibition pathways

19
Q

What is the centre of non REM sleep?

A

Ventrolateral pre-optic nucleus

20
Q

What is the role of the suprachiastmatic nucleus?

A
  • Controls circadian cycle s

* Influences physiological and behavioural rhythms occurring over a 24 hour period including the sleep/wake cycle

21
Q

What resets the clock gene?

A

Receptors in the retina containing melanopsin react to light and synapse directly onto the SCN

22
Q

What causes narcolepsy?

A
  • Onset due to specific loss of the orexin containing neurones in the lateral hypothalamus
  • Thought to be an inherited auto-immune condition linked to chromosome 6
23
Q

How does narcolepsy present?

A
  • Repeatedly falling asleep during the day, regardless of current activity - go straight to REM sleep
  • Limb weakness during emotional episodes
  • Night time or morning wakening accompanied by muscular paralysis
  • Vivid dream recollection just prior to wakening
24
Q

Wha tis the treatment of narcolepsy?

A
  • Modafanil
  • Amphetamines
  • Methylphenidate
  • Sodium oxybate
  • SSRIs and tricyclic antidepressants suppress REM sleep
  • Venlafaxine may help cataplexy
25
Q

Simple partial seizure

A
  • Focal with minimal spread of abnormal discharge

* Normal consciousness and awareness maintained

26
Q

Complex partial seizure

A
  • Local onset then spreads
  • Impaired consciousness
  • Clinical manifestation varies with site of origin and degree of spread
  • Temporal lobe epilepsy most common
27
Q

Secondarily generalised seizures

A
  • Begins focally, with or without focal neurological symptoms
  • Variable symmetry, intensity and duration of tonic (stiffening) and clonic (jerking) phases
  • Typical duration up to 1-2 minutes
  • Postictal confusion and somnolence
28
Q

Generalised seizures

A
  • Noth hemispheres
  • present in 40% of all epileptic syndromes
  • Manifestation of the seizure determine by cortical site at which the seizure arises
29
Q

What are the generalised seizures?

A
  • Absence
  • Myoclonic
  • Clonic
  • Tonic
  • Tonic-clonic
  • Atonic
30
Q

Absence seizure

A
  • Petit-mal
  • Sudden onset and abrupt cessation
  • Consciousness is altered
  • Mild clonic jerking, postural tone changes, autonomic phenomena
31
Q

atonic seizure

A
  • sudden loss of postural tone

* Most often in children

32
Q

Tonic-clonic seizure

A
  • Grand mal
  • Major convulsions with rigidity (tonic) and jerking (clonic)
  • Slows over 60-120 seconds followed by stuporous state
33
Q

Which seizures are non-convulsive?

A

Atonic and absence

34
Q

What is status epilepticus?

A
  • More than 30 minutes of continuous seizure activity
  • Two or more sequential seizures spanning this period without full recovery between seizures
  • Medical emergency
35
Q

What are the targets for AEDs?

A
  • Increase inhibitory neurotransmitter system - GABA
  • Decreased excitatory neurotransmitter system
  • Block voltage gated inward positive currents
  • Increase outward positive current
  • Many AEDs pleiotropic - act via multiple mechanisms

MD4001 (28 decks)

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