Sleep, EEG and Epilepsy Flashcards

1
Q

What are the three states of conciousness?

A

1) Wakefulness - alert, can deterct objects and pays attention to them.
2) Core consciousness - wakefulness plus emotional response and simple memory.
3) Extended consciousness - All of the above plus self awareness, autobiographical memory, language and creativity

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2
Q

What is the suggested function of sleep?

A

Processing and storage of memories, recuperation of the bodies immune system and conservation of energy.

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3
Q

What are the two main forms of externally discernible sleep?

A

1) When the eyes move rapidly from side to side (REM sleep) or,
2) When they do not move, then slow wave.

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4
Q

How does the Electroenephalogram work?

A
  • Post synaptic activity of synchronised dendritic activity can be picked up. It doesn’t pick up the post synaptic activity of individual neurons, only those why are synchronised. This synchronisation is either by neuronal interconnections or by pacemaker. It only picks up signals from synchronisation as small individual neuronal activity can’t be picked up due to the many layers of insulation.
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5
Q

What are the functions of the EEG with sleep?

A

It allows for distinguishing between REM and non-REM sleep and for non-REM sleep to be divided into a further four stages.

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6
Q

What are the EEG defined stages of sleep?

A
  • Awake,
  • Stage 1 (easily aroused, slow rolling eye movements),
  • Stage 2 (Sleep spindles, no eye movement but body movement is possible)
  • Stage 3 (Harder to rouse),
  • Stage 4 (deepest sleep, hardest to rouse),
  • REM (subjects easier to rouse than in stage 4, dreaming recalled, low muscle tone)
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7
Q

Describe how the reticular formation and thalamus are involved in arosal

A

With excitatory information comes into the reticular formation it causes it to send excitatory signals to the thalamus which will send a non-rhythmic output to the cortex, increases arousal.
However when there is less sensory information, there is inhibition of the reticular formation which causes it to hyperpolarise and send less excitatory signals to the thalamus. This causes thalamus to send a rhythmic output and slowing of EEG waves in cortex.

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8
Q

What is Epilepsy?

A

A continuing tendency to have recurrent unprovoked seziures.

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9
Q

What is SUDEP?

A

A rare risk of sudden death in epileptic patients. Thought to be due to electrical disruption in the heart.

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10
Q

How is the diagnosis of Epilepsy made?

A

The only method of diagnosis epilepsy for certain is via EEG however most diagnosis is made via history and understanding the characteristics of different types of attacks.

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11
Q

What are the relevant features when taking a history?

A
  • Any aura, warning, fear or Deja Vu from patient,
  • Any abnormal movements such as lip smacking, patting or stroking?
  • After affects? Eg, memory loss, confusion, or headaches.
  • Interictal examination is normal
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12
Q

What are the different classifications of epileptic seizures and their subtypes?

A
  • Partial seziures (focal aware or focal onset impaired awareness seizure).
  • Generalised seizures - always have alteration to conciousness. (absence, myoclonic, clonic, tonic, clonic-tonic or atonic)
  • Unclassified.
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13
Q

What is a simple focal aware seziure?

A

It is where consciousness is preserved with or without symptoms, symptoms relate to the area of brain affected. Symptoms can include:

  • Clonic movements (primary motor cortex),
  • Elaborate motor output (supplementary or pre-motor seziures),
  • Faces or complex scenes from visual association cortex seizure,
  • Contralateral hallucinations from occipital lobe seizure,
  • Music from associative auditory cortex seizure.
  • Roaring or underwater hearing from auditory cortex seizure.
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14
Q

What is aura?

A

Brief, simple partial seziures with no outward behavioural manifestation, it is often a warning sign of a larger seizure. A temporal aura includes visceral discomfort, odour, anxiety or fear.

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15
Q

What is a focal onset impaired awareness seizure

A

Subtype of focal aware, difference from simple. Tend to spread across the brain. Most common is temporal lobe seizure which can result in damage to hippocampus pyramidal cells with sclerotic tissue acting as a foci.

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16
Q

What are the stages of a focal onset impaired awareness seizure?

A
  • Aura which is linked to location.
  • Unresponsiveness then,
  • Automatisms (lip smacking, patting ect )and unusual sounds,
  • Occasional autonomic responses (tachycardia and pupil dilation)
  • Post Ictal headache is common.
    These can evolve into generalised seizures which involve the whole brain.
17
Q

Describe the features of Absence seizures (petit mal)

A

Most typical form - Sudden onset, abrupt cessation, brief duration and the attack may be associated with mild clonic jerking of eyelids.
More Atypically - Postural tone changes, autonomic phenomena, automatisms and characteristic 2.5-3.5hs Spike and wave patter

18
Q

What are features of myoclonic seziures?

A

Myoclonic jerking. It must be treated differently as treating with carbamazepine will make them worse.

19
Q

What are atonic seizures?

A

Sudden loss of postural tone which is more often seen in children but is generally rare.

20
Q

What are tonic-clonic seizures (grand mal)

A

Major convulsions with rigidity (tonic) and jerking (clonic). Slows over 60-120 seconds followed by stuporous state (post-ictal depression)

21
Q

What are the two stages of major convulsions?

A

1) Tonic phase which is where muscles tense up, causing person to fall if standing.
2) Clonic phase which is where muscles will start to contract and relax rapidly causing convulsions (motor manifestations which is due to excessive neuronal discharge)

22
Q

What is Status Epilepticus?

A

More than 30 minuets of continuous seizure activity. Can be two or more sequential seizures spanning this period without full recovery. It IS a medical emergancy

23
Q

Name some other causes of seizures

A

Alcohol and drug withdrawal, diabetic instability or blow to the head.

24
Q

What are some non-invasive tests that help confirm an epilepsy diagnosis?

A

ECG - check for abnormal function.
EEG - Interictal EEG as unlikely to be able to do an EEG whilst patient is having an attack.
CT scan - however normally not done unless there is suspicion of a brain tumour and MR scan not available.
MRI - Identify area of scarring, reduced perfusion, dysplasia or areas of cortex damage

25
Q

What are some attack triggers and pre-disposition?

A

Pre-disposition can be scar tissue, developmental issue, pyramidal cell damage or sub-optimal regulation of neuronal excitability.
Triggers - Tiredness, alcohol, certain drugs (tricyclics) or change of medication.

26
Q

What are the cellular mechanisms of siezures?

A

EPSPs, Na+ influx, Ca++ currents of paroxysmal depolarisation. This allows for drug therapy to be developed to prevent seizures. Can’t cure Epilepsy

27
Q

What are the targets of AEDs?

A

Supress excitatory neurotransmitter system bt inhibiting Na channels.
Enhance inhibitory neurotransmitter system via GABA (benzodiazapeines),
- Block voltage gated inward positive currents,
- Increase outward positive current.

28
Q

Name the AEDs that act primarily on Na channels

A
  • Phenytoin and Carbamazepine - Only block voltage gated Na channels at high firing frequency.
  • Oxcarbazepine - Blocks Voltage gated Na channels and effects K+ channels.
  • Zonisamide - blocks voltage gated sodium channels and T-type calcium channels.
  • Lamotrigine - Inhibits voltage gated Na channels. Best starting drug
29
Q

What are the commonly used antiepileptic drugs?

A
  • Sodium Valproate (teratogenic),
  • Lamotrigine,
  • Carbamazepine,
  • Oxcarbazepine (better tolerated),
  • Levetiracetam,
  • Topiramate,
30
Q

What drug is used in abscent seizures?

A

Ethosuximide.

31
Q

What is the treatment of status epilepticus?

A

IV diazepam or lorazepam followed by phenytoin, fosphenytoin or phenobarbital when control is established.