Brainstem, arousal, sleep

Question 1

What are consciousness and arousal?

Answer 1

Conscious ness is awareness of both internal and external states - requires both wakefulness (reticular activating system) and awareness (from cerebral cortex)

Arousal is emotional state associated with attaining a goal or avoidance of something noxious.

Question 2

What is the reticular formation? Inputs, outputs, function, transmitter?

Answer 2

Population of specialised interneurones in the brainstem that function to control CVS, resp and micturition but also the arousal of the cortex.

Inputs from sensory system and cortex which regulate the level of arousal

Outputs to thalamus (sensory gating), hypothalamus, basal forebrain nuclei and spinal cord

Function is mostly devoted to arousal - reticular activating system

ACh is main transmitter between neurones from reticular formation to the cortex.

Question 3

Why do anti-muscarinic drugs have drowsiness as a side effect?

Answer 3

• ACh is the main transmitter between the neurones from reticular formation to the cortex hence why anti-muscarinic drugs have drowsiness as a side effect.

Question 4

How does sleep occur?

Answer 4

The neural mechanism of sleep concerns deactivating the reticular activating system (and hence the cortex), and inhibiting the thalamus – remove sensory input from visual system and proprioception, clear mind.

Question 5

How do we go to sleep?

Answer 5

Everything we do to go to sleep aims to reduce stimulation of the reticular system to reduce consciousness – by shutting off the following excitatory sources we reduce the positive feedback on the reticular formation thus reducing consciousness and causing us to go to sleep:
• Sensory inputs – eg we lie down somewhere quiet and comfortable
• Visual inputs via orexinergic neurones – eg we close our eyes
• Cortical inputs – eg we try not think about anything

Question 6

What happens in REM sleep?

Answer 6

• The EEG activity is similar to that seen during arousal but the thalamus is strongly inhibited and so the person is difficult to arouse.
• Glycinergic fibres arising from the reticular formation inhibit the lower motor neurons (reticulospinal tracts) – this leads to low muscle tone.
• Eye movements and some other cranial nerves are preserved (hence rapid eye movement sleep, can also get bruxism).
• Autonomic changes – lose thermoregulation, can get penile erection.

Question 7

What are the outputs of the reticular activating system?

Answer 7

• The thalamus, which then send glutamatergic projections to the cortex
• The hypothalamus, which then send histaminergic projections to the cortex (hence antihistamines cause drowsiness)
• The basal forebrain nuclei, which then sends cholinergic projections to the cortex (hence anticholinergics cause drowsiness)

Question 8

What is insomnia?

Answer 8

Inability to sleep due to excessive cortical stimulation of the reticular formation
Usually psychological cause

Question 9

What is narcolepsy?

Answer 9

Sudden falling of sleep due to loss of orexinergic neurones or mutation in the orexin gene - no input from the visual system to the reticular formation.

Visual input to the hypothalamus is via the hypothalamus – neurons projecting from the hypothalamus to the reticular formation are orexinergic

Question 10

What is sleep apnoes

Answer 10

Compression of airways during sleep
Sensory input (hypoxia) to the reticular formation causes you to wake up
Can interrupt REM sleep

Question 11

What is EEG?

Answer 11

EEG monitors “brain waves” – synchronous electrical activity of the cortex. The cortex has an intrinsic rate of 1Hz.
The EEG can be taken during sleep. There are different stages of sleep (stages 1-4 and REM)

Question 12

What are important waves seen in EEG?

Answer 12

• Beta waves (>14Hz) – seen in alertness and REM sleep
o High frequency (50Hz)
o Mainly parietal and frontal lobes

• Alpha waves (8-13Hz)
o Lower frequency – 10Hz – synchronous
o Seen in wakeful relaxation with closed eyes
o Constant feedback between cortical and thalamic projections

Theta waves (4-7Hz)

Delta waves (<3.5Hz)

Question 13

What are the stages of sleep seen on EEG?

Answer 13

• Stage one sleep: alpha waves + theta waves (theta = 5Hz)
• Stage 2/3: a background of theta waves (4-7Hz)
o With kappa complexes
o And sleep spindles – bursts of activity in the thalamus
o Seen in children and during strong emotion in adults (mainly parietal and temporal lobes)
• Stage 4 – delta waves (<3.5Hz) – intrinsic activity of the cortex when devoid of input, seen during sleep and serious brain conditions.

Question 14

What is epilepsy caused by?

Answer 14

Excessive neuronal activity in the brain

Question 15

What are partial seizures? Types?

Answer 15

Affect one hemisphere
o Simple partial – patient retains awareness
o Complex partial – lose awareness, odd behaviours like lip-smacking

Question 16

What are behaviours experienced in partial seizures?

Answer 16

o	Behaviours include:
•	Frontal lobe
•	Abnormal head movements
•	Swearing or shouting
•	Posturing
•	Repeated movements like rocking

• Parietal lobe
• Abnormal sensations
• Feel like part of the body is missing
• Hallucinations
• Cant understand language or reading
• Occipital lobe
• Hallucinations
• Disturbed vision
• Eye pain
• Nystagmus
• Temporal lobe
• Déjà vu
• Strange taste and smell
• Rising sensation in stomach
• Lipsmacking, swallowing or chewing

Question 17

What are generalised seizures?

Answer 17

Affect both hemispheres - cross the corpus callosm

Question 18

What is a tonic-clonic seizure? Another name?

Answer 18

Grand mal seizures
• Tonic – lose consciousness, body stiffens and falls
• Clonic – limb jerking, loss of bladder control, tongue biting, respiratory arrest

Question 19

How is epilepsy diagnosed and managed?

Answer 19

Clinically and with EEG
ABCDE assessment
Oral midazolam (short acting benzodiazepine anaesthetic) or rectal diazepam (long acting benzodiazepine)

IV lorazepam (short acting benzodiazepine) and IV phenytoin

Question 20

What is status epilepticus?

Answer 20

single epileptic seizure lasting more than five minutes or two or more seizures within a five-minute period without the person returning to normal between them

Question 21

What are three mechanisms of altered consciousness

Answer 21

• Diffuse cortical dysfunction – eg metabolic disturbance
• Pressure inhibiting the reticular activating system (RAS) – eg RICP
• Direct lesion in the brainstem damaging RAS – eg infection of brainstem

Question 22

What is brainstem death?

Answer 22

Widespread cortical and brainstem damage, flat EEG

Question 23

What is coma? GCS? Causes?

Answer 23

Widespread brainstem and cortical damage – can see various, disordered EEG patterns.
They are unrousable, don’t respond to stimuli. There is no detectable sleep-wake cycle. (No awareness or wakefulness)
• GCS less than 8/15
• Causes include drug poisoning, hypoxia and stroke
• Prognosis could be recovery, Persistent vegetative state or death

Question 24

What is persistent vegetative state?

Answer 24

Widespread cortical damage with various disordered EEG patterns (like a coma). The differences are:
• Some spontaneous eye opening
• Localize to stimuli via brainstem reflexes
• Sleep-wake cycle is detectable, but impaired awareness

Question 25

What causes locked-in syndrome?

Answer 25

Basilar or pontine artery occlusion – eye movements are preserved; all other somatic motor functions are lost from the pons down.

Question 26

What are causes of RICP?

Answer 26

compensation for expanding mass is by reducing the venous volume and CSF. Causes include:
•	Cerebral oedema
o	Cytotoxic (hypoxia or trauma)
o	Vasogenic (hypertensive encephalopathy)
o	Osmotic (hyponatraemia)
•	Space occupying lesions
o	Tumours
o	Haemorrhages
o	Trauma
•	Hydrocephalus
•	Increased intracranial blood volume
o	Outflow obstruction – venous sinus thrombosis, SOL
o	Vasodilatation (acidosis)