Cognitive neuroscience of dreams
Both patients had undergone damage to posterior parietal regions, one of which involved predominately the left side of the parieto-occipital areas.
[2] Reconstructing the dream from memory while awake might affect the accuracy of recall because the subject may report more information than actually experienced, and sequence of events may be reordered.
[3] Similarly, the laboratory environment may alter the content of dreams recalled from spontaneous awakenings at the end of a night's sleep, as indicated by high frequency of laboratory references in morning spontaneous awakenings in REM and NREM dream reports.
Many investigators used small samples for sleep studies and statistical parametric mapping (a technique for examining differences in brain activity recorded during functional neuroimaging experiments).
Measures of global brain activity like electroencephalogram (EEG) voltage averaging or cerebral blood flow cannot identify small but influential neuronal populations like the locus coeruleus, the raphe nucleus and the pedunculopontine tegmental nucleus, which reveal mechanistic and functional details in dreaming.
Eugene Aserinsky and Nathaniel Kleitman observed REM sleep and concluded that it was the physiological manifestation of dreaming.
[9] Dream imagery can change quickly and is regularly of a bizarre nature, but reports also contain many images and events that are a part of day-to-day life.
[5] Dreams are also characterized by a lack of "orientational stability; persons, times, and places are fused, plastic, incongruous and discontinuous".
[5] Aserinsky and Kleitman's discovery prompted further research into the brain mechanism involved in REM sleep (and by their assumption, dreaming).
It was found that REM is generated by a small region of cells located in the brain stem called the pons (it sits slightly above the spinal cord at the nape of the neck).
Cholinergic activation of these higher areas was thought to result in the meaningless images that make up our dreams.
The formation of the Activation-Synthesis Model put forth by Allan Hobson and McCarley in 1975 rested largely on these discoveries.
Their model posits that dreams are actively generated by the brain stem and then passively synthesized by the forebrain.
A main problem with obliterating REM sleep is that the associated area, the brain stem, is responsible for consciousness.
A dopaminergic pathway runs from the ventral tegmental area, ascends through the lateral hypothalamus, various basal forebrain areas (nucleus basalis, stria terminalis, shell of nucleus accumbens) and terminates in the amygdala, anterior cingulate gyrus and frontal cortex.
Furthermore, chemical stimulation of the pathway (with L-DOPA for example) increases the frequency and vividness of dreams without affecting REM sleep.
[10] The mesolimbic and mesocortical pathways are considered the seeking areas or the motivational command centers of the brain.
[6] Transection or inhibition of the dopamine pathway also reduces some positive symptoms of schizophrenia, many of which have been likened to dream-like states.
[10] Further evidence that dreaming can occur independently of REM sleep is found in the occurrence of nocturnal seizures during NREM that often present themselves as nightmares.
[6][10] The evidence of the involvement of mesolimbic and mesocortical dopaminergic pathways suggests that dreaming occurs when a motivational component is activated.
[10] This is an area of grey cortex towards the back of the brain involved in the highest levels of perceptual processing.
Furthermore, there is inactivation of the reflective system in the limbic brain which leads the dreamer to mistake the dream for reality.
