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MD4001 Pathology > Sleep, Wakefulness, Epilepsy and EEG > Flashcards

Sleep, Wakefulness, Epilepsy and EEG Flashcards

1
Q

What is sleep?

A

Usually described in relation to consciousness as an easily reversible state of inactivity with a lack of interaction with the environment

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2
Q

What is unconsciousness?

A

Inconsistant term - can be coma (depressed state of neural activity, absence of wakefulness), sleep (variation in neural activity)

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3
Q

What is consciousness?

A

Having awareness; with perceptions, thoughts and feelings - philosophical and biological aspects

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4
Q

What are the 2 main forms of easily discernable sleep?

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

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

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5
Q

What can neuronal activity during different stages of wakefulness be measured by?

A

EEG (Electroencephalogram)

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6
Q

How does the EEG work?

A
  • Post synaptic activity of individual neurons not picked up
  • Post synaptic activity of synchronised dendritic activity can be picked up
  • Synchronisation is either by neuronal interconnections or by pacemaker
  • The more neurons that are synchronised, the bigger the peaks on the ECG
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7
Q

How many EEG electrodes are there?

A

19

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8
Q

What are the different types of brain wave?

A
  • Beta - Awake with mental activity (14-30Hz)
  • Alpha - Awake and resting (8-13Hz)
  • Theta - Sleeping (4-7Hz)
  • Delta - Deep sleep (<3.5Hz)
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9
Q

What are the 5 stages of sleep?

A

Stage 1-4 + REM

- Waves get longer through each stage until REM where Hz increase and fast beta waves are present. After about 1 hour

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10
Q

What stage of sleep is associated with penile erection?

A

REM

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11
Q

After the first cycle of sleep what is the deepest sleep stage attained?

A

Stage 3 and increasing time spent in REM

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12
Q

What are slow waves thought to be involved in?

A

Inhibiting sections of the relevant cortex

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13
Q

What happens during REM sleep?

A
  • Brain is very active and is most likely to be dreaming (95% likelihood), but the body is effectively paralysed
  • One source of activity is concerened with inhibiting motor output (excepting breathing and eye movement)
  • Body temperature drops as metabolism is inhibited
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14
Q

What is the reticular formation a diffuse collection of?

A

At least 100 networks of neuromodulatory neurons spanning all 3 divisions of the brainstem. It is not homogenous, main NTs are NAdr, 5HT, Ach and has diverse functions (posture, rep, HR and sleep arousal)

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15
Q

What is the reticular formation has projections to what?

A
  • Thalamus
  • Hypothalamus
  • Brainstem nuclei
  • Cerebellum
  • Spinal cord
  • Cerebral cortex
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16
Q

What does the reticular formation receive input from?

A

Cerebra (collaterals from the corticospinal pathways), the visual and auditory systems, sensory spinal systems, the cerebellum, certai brainstem nuclei

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17
Q

Sleep mechanisms rely on communication between what 2 places?

A

Reticular formation and thalamus (being the main relay station to and from the cortex)

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18
Q

Inhibiting and exciting the thalamus does what?

A

Inhibiting:
- Decreases sensory throughput
Exciting
- Increases sensory throughput

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19
Q

What is nonREM sleep characterised by?

A

Synchronised cortical slow waves caused by a hyperpolarised thalamus and decreased activity in the arousal centres of the reticulum

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20
Q

What are Sleep spindles and K complexes?

A
  • Caused in part by inherent rythmicity of thalamic neurons as they hyperpolarise due to reduced ascending reticular formation input. Seen in Non REM stage 2 sleep
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21
Q

What happens as thalamic cells hyperpolarise further?

A

Develop slow wave rhythmicity (due to thalamic interconnections) which serves to block ascending sensory input. This rhythmicity is transmitted to the cortex and due to a strong reciprocity between these two areas, the waves becomes synchronised across the cortex

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22
Q

Where are orexinergic neurons situated?

A

Lateral hypothalamus

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23
Q

When are orexinergic neurons active?

A

During wakefullness

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24
Q

Where do orexinergic neurons project to?

A

The cerebra, the arousal nuclei and the Ventro-lateral pre-optic nucleus in the anterior hypothalamus (VLPO) however the VLPO has no orexin receptors

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25
Q

What do VLPO lesions cause?

A

Insomnia

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26
Q

What is orexin pivotal in?

A

The sleep/awake switch circuitry and adds stability to the mechanism

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27
Q

What nuclei do orexinergic neurons enhance?

A

Arousal nuclei and by doing so cause indirect inhibition of the VLPO via reciprocal inhibition pathways between the arousal centres and the VLPO

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28
Q

Where is the VLPO situated?

A

Anterior hypothalamus

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29
Q

What is the centre of non-REM sleep promotion?

A

VLPO

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30
Q

What does the VLPO have inhibitory projections to?

A

Major direct arousal centres (red), and is active during sleep

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31
Q

What does the VLPO innervate?

A

Neurons in the lateral hypothalamus (including the orexin neurons (green)), and inter-neurons in the MRF cell groups (yellow) (PPT and LDT)

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32
Q

What does the extended VLPO (eVLPO) promote?

A

REM sleep

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33
Q

What is the VLPO reciprocally inhibited by?

A

Projections (NA GABA and 5-HT) from the arousal centres

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34
Q

What does the suprachiasmatic nucleus (in the hypothalamus) control?

A
  • Circadian cycles

- Influences many physiological and behavioral rhythms occuring over a 24 hour period, including the sleep/wake cycle

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35
Q

What receptors in the retina react to light and synapse directly onto the SCN resetting the clock gene?

A

Melanopsin

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36
Q

How long is the “free running” of the SCN clock gene?

A

Gives a periodicity of about 24.5 hours

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37
Q

What is the circadian cycle re-set by?

A

A variey of zeitgebers (time givers in German), the most dominant of which is the light dark cycle

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38
Q

What is narcolepsy due to?

A
  • Due to specific loss of the orexin containing neurons in the lateral hypothalamus
  • Though to be an inherited auto-immune condition linked to chromosome 6
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39
Q

What are the tetrad of symptoms associated with sleep disorders?

A
  • Repeatedly falling asleep during the day, regardless of current activity (go straight into REM sleep)
  • Limb weakness during emotional episodes (mild to extreme cataplexy)
  • Night time or morning wakening accompanied by muscular paralysis (sleep paralysis)
  • Vivid dream recollection just prior to wakening (hypanagogic hallucinations)
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40
Q

How is Narcolepsy treated?

A
  • Modafanil
  • Amphetamines
  • Methylphenidate
  • Sodium oxybate (GHB)
  • SSRIs and tricyclic antidepressants suppress REM sleep
  • Venlafaxine may help cataplexy
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41
Q

What are some sleep disorders?

A
  • Narcolepsy
  • Insomnia
  • Sleep apnoea (XS daytime sleepiness)
  • REM sleep disorder
  • Somnambulism
  • Epilepsies
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42
Q

How is sleep apnoea treated?

A

Respiratory support overnight with increased oxygen pressure

43
Q

What is REM sleep disoreder associated with?

A

PArkinsons

44
Q

How common is epilepsy?

A

0.5% of the population

45
Q

What is the overall lifetime risk of seizure?

A

1 in 50

46
Q

What is epilepsy?

A

Continuing tendency to have seizures

47
Q

What are seizures?

A

Sudden discharges of abnormal electrical activity

48
Q

What is the risk of sudden death in epileptics?

A

1 in 1000 epileptics

49
Q

What is the DVLA rule for driving with seizures?

A

Cannot drive within 6 months of having a seizure

- 2 attacks = 1 year off driving

50
Q

What is the most important part of an epilepsy diagnosis?

A

History

51
Q

What is the commonest lobe to have abnormal electrical activity?

A

Temporal lobes - control sense of smell, taste and emotion

- Abnormal taste or smell or feeling of fear may precede a seizure

52
Q

What factors are important in diagnosing epilepsy?

A
  • History (patient and witness)
  • Aura/warning
  • Abnormal movements (myoclonic jerks esp morning)
  • colour
  • Position
  • When?
  • After effects?
53
Q

How is epilepsy diagnosed?

A
  • Examination usually normal
  • Investigations include ECG, EEG, MRI
  • Put all information together to come up with best diagnosis, seizure semiology
  • Partial, simple or complex
  • Generalised, primary or secondary
54
Q

What can cause the abnormal electrical activity that can cause a seizure?

A
  • Areas of abnormal neuronal migration

- Islands of nerve cells in white matter

55
Q

What cells control memory?

A

Temporal lobes contain very big cells called pyramidal cells - can cause hippocampal sclerosis

56
Q

What is the difference between a partial and simple seizure?

A

Partial: Abnormal electrical activity from one spot of the brain
Generalised: Abnormal electrical activity from all over the brain

57
Q

What is a todds paralysis?

A

Seizure is followed by a brief period of temporary paralysis

58
Q

What is the difference between partial simple and partial complex seizures?

A
  • Simple partial seizures, patients retain awareness

- Complex partial seizures, they lose awareness

59
Q

What is a simple secondary seizure?

A

Partial seizure that becomes generalised

60
Q

What lobe is the most common site of complex partial seizures?

A

Temporal (presence common)

61
Q

Describe generalised seizures?

A
  • Both hemispheres are widely involved from the outset

- Manifestations of the seizure are determined by the cortical site at which the seizure arises

62
Q

How common are generalised seizures?

A

Present in 40% of all epileptic syndromes

63
Q

What are the different types of generalised seizures?

A
  • Absence seizure
  • Mycolonic seizure
  • Atonic seizures
  • Tonic-clonic seizures
64
Q

What is an absence seizure?

A

Type of generalised seizure. Sudden onset abrupt cessation; brief duration, consciousness is altered; attack may be associated with mild clonic jerking of the eyelids or extremities, postural tone changes, autonomic phenomena and automatisms (difficult diagnosis from partial); characteristic 2.5-3.5 Hz spike-and wave pattern

65
Q

What is a myoclonic seizure?

A

Type of generalised seizure
Myoclonic jerking is seen in a wide variety of seizures but when this is the major seizure type it is treated differently to some extent from partial leading to generalised

66
Q

What are atonic seizures?

A

Sudden loss of postural tone; most often in children but may be seen in adults

67
Q

What are tonic-clonic seizures?

A

Major convulsions with rigidity (tonic) and jerng (clonic), this slows over 60-120 sec followed by stuporous state (post-ictal depression)

68
Q

What are the major two phases of generalised tonic-clonic seizures?

A

Tonic phase:
- Muscles will suddenly tense up, causing the person to fall to the ground if they are standing

Clonic phase:
- Muscles will start to contract and relax rapidly, causing convulsions

69
Q

What are convulsions?

A
  • Motor manifestations
  • May or may not be present during seizures
  • Excessive neuronal discharge
70
Q

In what seizures do convulsions appear?

A

Simple partial and complex partial focal neuronal discharge includes motor centres; they occur in all generalised tonic-clonic seizures regardless of the site of origin

71
Q

WHat type of seizures are non-convulsive?

A

Atonic and absence seizures

72
Q

What is status epilepticus?

A
  • More than 30mins of continous seizure activity
  • Two or more sequential seizures spanning this period without full recovery between seizures
  • Medical emergency
73
Q

What are antiepileptic drugs?

A
  • Drug which decreases the frequency and/or severity of seizures in people with epilepsy
  • Treats the symptoms of seizures, not the underlying epileptic condition
  • Goal - maximise quality of life by minimising seizures and adverse drug effects
  • Currently no “anti-epileptogenic” drugs available
74
Q

What percentage of people with epilepsy can become seizure free with drug therapy?

A

Just under 60% - in another 20% the seizures can be drastically reduced
- 20% of epileptics seizures are refractory to currently available AEDs

75
Q

What should be considered when choosing an antiepileptic drug?

A
  • Seizure type
  • Epilepsy syndrome
  • Pharmacokinetic profile
  • Interactions/other medical conditions
  • Efficacy
  • Expected adverse effects
  • Cost
76
Q

What are the targets of AEDs?

A
  • Increase GABA (inhibitory NT)
  • Decrease Glutamate (excitatory NT)
  • Block voltage-gated inward positive currents - Na+ or Ca2+
  • Increase outward positive current - K+
  • Many AEDs pleiotropic - act via multiple mechansims
77
Q

What is the brain’s main excitatory NT?

A

Glutamate

78
Q

What are the 2 groups of glutamate receptors?

A
  • Ionotropic - fast synaptic transmission

- Metabotropic - slow synaptic transmission

79
Q

What are the 2 major glutamate receptors?

A

NMDA and AMPA

- work through Na+ K+ interaction

80
Q

What AEDs act primarily on Na+ channels?

A

Phenytoin, carbamazepine
- Block voltage-dependant Na+ channels at high firing frequencies - use dependant
Oxcarbazepine
- Blocks voltage-dependant Na+ channles at high firing frequencies
- Also effects K+ channels
Zonisamide
- Blocks voltage-dependant Na+ channels and T-type Calcium channel
Lamotrigine

81
Q

What is the commonest AED?

A

Lamotrigine

82
Q

What is phentoin effective in?

A

Many forms of epilepsy but not absence seizures

- Also used as antidysrhythmic

83
Q

What are current commonly used AEDs?

A
  • Lamotrigine
  • Sodium Valproate
  • Carbamazepine
  • Oxcarbazepine
  • Levetiracetam
  • Topiramate
84
Q

What are older AEDs less used?

A
  • Phenytoin
  • Ethosuxamide
  • Phenobarbitone
  • Vigabatrin
  • Tiagabine
85
Q

What are the features of Lamotrigine?

A
  • Inhibits Na+ channels
  • Broad therapeutic profile
  • Main s0de-effects are hypersensitivity reactions
86
Q

What are the features of sodium Valproate?

A
  • Chemically unrelated to other antiepileptic drugs
  • MOA not clear, causses GABA increase in brain. Weak inhibition of GABA transaminase, some effect of Na+ channels
  • Side effects: Tetratogenicity and foeatla syndrome AVOID IN PREGNANCY, liver damage
87
Q

What AED must be avoided in pregnancy?

A

Sodium Valproate

88
Q

What are the features of Carbamazepine?

A
  • Derivative of tricyclic antidepressants
  • Effective particularly in partial seizures; also useful in trigeminal neuralgia
  • Strong enzyme-inducing agent; therefore, many drug interactions
  • Unwanted side effects principally sedation, ataxia, mental disturbances, water retention
89
Q

What are the features of Oxacarbazepine?

A
  • Newer drug, closely related to Carbamazapine, approved for monotherpay, or add-on therapy in aprtial seizures
  • May also augment K+ channels
  • Some induction of P450 but much less than that seen with CBZ
  • Sedating but otherwise less toxic than Carbamazapine
90
Q

What ar ethe features of Levetriacetam?

A
  • Probably inhibits presynaptic CA
  • Analogue of piracetam, a drug used to improve cognitive function
  • Useful in partial seizures and generalised seizures now
  • Can use psychiatric side effects
91
Q

What are the features of Topiramate?

A
  • Compex actions not fully understood
  • Risk of teratogenesis
  • Need to slow titration to avoid cognitive side effects
92
Q

What are the features of tigabine?

A
  • GABA uptak inhibitor
  • Side-effwects are dizziness and confusion
  • Licensed for partial seizures
93
Q

What are the feautures of Zonisamide?

A

Blocks Na+ channels, can cause anorr=exia and somnolence

94
Q

How does Phenytoin (old) act?

A
  • Mainly by use-dependant block of Na+ channles
  • Interactions are common
  • Plasma conc varies needs to be monitored
  • Unwanted side-effects of confusion, gum hyperplasia, skin rashes, anaemia, teratogenesis, cerebellar syndrome, osteoperosis
95
Q

What was ethmosuximide (old) used to treat?

A

Absense seizures in children, may exacerbate other forms

- Acts by blocking T-type Calcium channels

96
Q

What are the side-effects of ethosuximide (old)?

A

Relatively few unwanted side-effects, mainly nausea and anorexia

97
Q

Features of phenobarbitone?

A
  • Rarely used, but ppl stil on it
  • Enzyme inducing
  • Very long half life
  • Osteoperosis
98
Q

What is the treatment for status epilepticus?

A
  • First line: IV benzodiazepines
  • Followed by phenytoin, fosphenytoin, or phenobarbital (longer acting) when control is established
  • If still not working pateint to be paralysed and ventilated
  • Medical emergency
99
Q

What are some rarely used AEDs?

A

Felbamate
- Use limited to intractable disease high risk of hypersensitivity reactions, aplastic anaemia

Vigabatrin

  • Inhibits GABA transaminase
  • Effective in patients who are unresponsive to conventional drugs
  • Side-effects of drowsiness, behavioural and mood swings, retinal loss, now rarely used
100
Q

What are gabapentin and its second generation derivative Pregabalin used to treat?

A
  • Act specifically on Calcium channel subunits called alph2delt1. Unclear how this action leads to antiepileptic effects, but inhibition of NT release may be one mechanism
  • Used in add-on therapy for partial seizures and tonic-clonic seizures
  • Less sedating than classic AEDs
  • Now mainly used in neuropathic pain
101
Q

When is neurosurgery considered in treatment for epilepsy?

A
  • Partial seizures
  • When at least 3 AEDs have been tried
  • Temporal lobe lesions or tumour causing attack
  • Work-up includes detailed electrophysiology
  • Certain seizure comes from lesion
  • Ideally non-dominant hemisphere
  • fMRI, specialist centre
102
Q

What is Baclofen?

A
  • Selective agonsit on GABA(B) receptor occur in spinal cord
  • Reduces spasticity
  • Effective in spinal cord lesions and MS NOT epilepsy
103
Q

What are scars on the brain most commonly due to?

A

Lack of O2 probably pre-natally or around time of birth

MD4001 Pathology (18 decks)

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