Sleep and Epilepsy Flashcards

1
Q

Describe the 3 states of consciousness

A
  • wakefulness: alert, able to detect objects and pay attention to them
  • core consciousness: wakefulness plus emotional responses and simple memory
  • extended consciousness: all of the above plus self-awareness, autobiographical memory, language and creativity
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2
Q

What are the 2 main forms of sleep and how can this be measured?

A

REM sleep: eyes move rapidly side to side
Non-REM/slow-wave/deep sleep: when eyes do not move

Neuronal activity during sleep can be measured with an EEG (encephalogram)

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3
Q

Describe how an EEG works

A

Electrodes (19 pairs) are placed as close to the scalp as possible. They have amplifiers which pick up mass interconnected neuronal depolarisation within the brain. Due to many layers of insulation between the electrode and the brain, this means that it requires a lot of simultaneous firing of neurons to generate a depolarisation large enough to be detected by the electrode.

Information from EEGs allows separation of REM and non-REM sleep, and divisions into the 4 stages of sleep

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4
Q

Describe the EEG defined stages of sleep

A

Awake: small amplitude, high frequency waves. Not much synchronicity between adjacent neurons. Can be firing together just not interconnected

Stage 1 (easily roused): slow eye movements, slightly larger amplitude waves in areas

Stage 2 (no eye movement): body movement possible, ‘sleep spindles’ present - fast, large amplitude areas representing half sleep-half wake

Stage 3: slower, high amplitude, low frequency waves.

Stage 4 (deepest sleep): half of waves are 2Hz with very high amplitude (lots of interconnected neuronal synchronicity)

REM: like being awake/stage 1. Very active, clear waves of activity. When dreaming occurs. Not a lot of synchronicity meaning there is a lot of thought going on (repeated on avg 5 times a night with 30mins in between REM sleeps)

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5
Q

Describe the role of the thalamus and reticular formation in sleep

A

The reticular formation interacts with the thalamus to help turn sleep on and off.

Excitation results in activation of the reticular formation which sends excitation signals (depolarisation) to the thalamus resulting in non-rhythmic output from the thalamus to the arousal centres. Activation of the arousal centres (alpha and beta waves) causes active inhibition of the hypogenic (sleep) centres of the brain.

Inhibition acts on the reticular formation to cause decreased excitation (hyperpolarisation) which results in rhythmic output from the thalamus to the cortex which creates more synchronised waves and sends us to sleep.

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6
Q

What is epilepsy, its diagnosis and causes of seizures?

A

Epilepsy is the continuing tendency to have recurrent and unprovoked seizures.

Only certain way of diagnosing is with an EEG. Working diagnosis can be made on the characteristics and classification of seizure, patient’s history and witness accounts of the seizures.

Causes of seizures: epilepsy, alcohol, drug withdrawal, diabetic instability and head trauma

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7
Q

Describe partial/focal seizures

A

Consciousness preserved with positive or negative signs. Symptoms relate to the areas of the brain affected.

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8
Q

What is aura?

A

Brief, simple and partial seizure with no outward behavioural manifestations. It can precede another larger seizure. Causes internal signs such as fear/anxiety.

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9
Q

What are complex partial seizures?

A

Seizures that cause impairment of consciousness. Most common in temporal lobe resulting in damage to the hippocampus pyramidal cells (causing sclerotic tissue)

  • often starts with aura linked to location
  • unresponsiveness
  • automatisms (lip smacking, swallowing etc.) and unusual sounds
  • post-ictal headache
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10
Q

What are generalised seizures?

A

involve the whole brain and alter consciousness with manifestations determined by the cortical sight that the seizure arises from (commonly memory, coordination and vision).

Includes, absence seizures (either sudden onset and absrupt cessation or changes in postural tone with autonomic changes and automatisms), myoclonic seizures (stiffening of muscles and jerking), atonic seizures (sudden loss of postural tone), and tonic-clonic seizures (major convulsions with rigidity and jerking that slows over a few minutes)

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11
Q

Describe the stages of a generalised tonic-clonic seizure (grand mal)

A

Major convulsions with 2 stages:

  • tonic phase: muscles suddenly tense causing person to fall if standing
  • clonic phase: muscles contract and relax rapidly which causes convulsions due to excessive neuronal discharge
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12
Q

Define status epilepticus

A

More than 30mins of seizure activity caused by 2 or more sequential seizures without full recovery between them. Medical emergency.

Requires treatment with diazepam and lorazepam (IV) then phenytoin, fosphenytoin or pheonobarbital once control established

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13
Q

What tests can be done after a seizure to determine if it was epilepsy or not?

A

EEG: check for interictal epileptiform activity (IEA) - characteristic waves and spikes
ECG: check for abnormal function (associations between epilepsy and cardiac problems like arrhythmias and atherosclerosis)
CT: if suspicion of brain tumour. Look for cortical shrinking and scars
MRI: used for identifying scars, reduced perfusion, dysplasia etc.

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14
Q

What are some triggers of a seizure attack

A

Pre-disposition: scar tissue, developmental issues, pyramidal cell damage, decreased regulation of neuronal excitability

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15
Q

What is the treatment of epilepsy and its aims?

A

An anti-epileptic drug (AED) to decrease the frequency and/or severity of the seizures. Treats the symptoms not the cause.

Aim is to:

  • suppress excitatory NT system (inhibit Na+ channels)
  • enhance inhibitory system (GABA) with benzodiazepines
  • increase outward positive current K+
  • block voltage gated inward positive currents (NA+)

Common: sodium valporate, lamotrigine, carbamazepine

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