Shifts of attention are useful for many daily tasks, such as finding your keys, playing video games, learning, personality and flexibility and efficiency.
Patients with attentional deficits have damage to the frontoparietal network, causes:
- Visual Neglect
- Balint’s syndrome
Neglect
- Hemispatial unilateral neglect: left side of the visual field is neglected, due to right inferior lobe damage. Right side neglect is less common due to processing of right space by both hemispheres
- Ideational apraxia: misuse of tools, due to left inferior parietal lobe damage
- Can become covertly aware of stimulus
- Neglect also happens for mental imagery and emotional content may implicitly affect behavior
- Theory: right hemisphere damaged, left hemisphere takes over and receives all attention over-focus of right visual field
- Patients often have anosognosia
Neglect is different from hemianopia (V1 damage). Difficult to differentiate though (but hemianopia patients often know something is wrong).
Balint’s syndrome
- Bilateral damage to dorsal posterior parietal cortex and lateral occipital cortex
- Optic & oculomotor apraxia: motor (arm&gaze) guidance to objects is impaired
- Simultanagnosia: difficulty handling two objects at a time
Parietal lobe damage: deficits in attention and changing the allocation of attention
Frontal lobe damage: deficits in control & initiating the changes in attention
Frontalparietal network = attentional control
There is first activity in frontal areas, then in parietal areas.
- cue: frontal activity
- reorienting: parietal activity
The TPJ (temporo-parietal junction) is specifically important for bottom-up processing of attention.
During visual search you use a lot of bottom-up attention.
- Pop-out search: automatically grabs your attention
- Conjunction: top-down attention. You have to steer your gaze

When searching for something, you are always driven by both pop-out and conjunction search. Reorienting during both types of visual search is coded in the intraparietal sulcus (IPS).
Default-mode network: active in rest. Decreased activity in the frontoparietal network means increased activity in the default-mode network (inverse coupling) --> Posterior cingulate cortex
EEG reflects sleep stages:
- Relaxed: alpha activity
- Stage 1 – drowsy: theta activity
- Stage 2-3 – sleep: theta/delta
- Stage 4 – deep sleep: delta
- REM sleep: rapid eye movements
Sleep neurotransmitters:
- Acetylcholine – memory consolidation
- Noradrenaline / Norepinephrine – arousal
- Serotonin --> melatonin – motivation, sleep onset, internal clock
- Raphe nuclei, pineal gland
- Histamine – vigilance, alertness
- Orexin/hypocretin – stable sleep, appetite
- Cortisol – awakening response
- Glutamate – GABA (sleep duration)
Awake: all neuron types are active
Beginning of sleep: all less active
Before REM sleeps: noradrenaline active (to reactivate REM)
During REM: acetylcholine active

Consciousness can be seen as ‘being awake’ or as ‘being aware or being self-aware’.
Changing awareness over time:
- Attentional blink
- Change blindness
- Bi-stable perception (e.g. monocular rivalry or binocular rivalry).
There is a BOLD response during a change in awareness.
How do we know what they see when there is no report? Use objective signals such as pupil size.
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