Charcot–Wilbrand syndrome

[1] The name of this condition dates back to the case study work of Jean-Martin Charcot and Hermann Wilbrand, and was first described by Otto Potzl as "mind blindness with disturbance of optic imagination".

[2][3] MacDonald Critchley, former president of the World Federation of Neurology, more recently summarized CWS as "a patient loses the power to conjure up visual images or memories, and furthermore, ceases to dream during his sleeping hours".

[citation needed] In patients with loss of visual imagery during sleep, instances of acute-onset brain damage such as thrombosis, hemorrhage, trauma, and carbon monoxide poisoning in particular have been indicated as possible motivators for CWS.

[2] Additionally, some slower progressing conditions, namely tumor growth (neoplasm) in brain tissue and abnormal embryonic development (dysgenesis) of the corpus callosum, have been associated with this syndrome.

[5] Similarly, in patients with complete loss or suppression of dreaming there is typically an association with focal, acute-onset cerebral lesions like hemorrhage, thrombosis, or trauma.

In almost all cases, dreaming returned within 12 months, implying a possibility that the site of interest was only connected to the damaged regions, most likely through neural pathways, further complicating localization.

[10] A polysomnography test (PSG) records the biological changes during sleep through monitoring the brain (Electroencephalography, EEG), eye movement (Electrooculography, EOG), heart rhythm (electrocardiogram, ECG), and muscle activity (Electromyography, EMG).

[12] Recently fMRI has come to the forefront of dream research because it does not require the use of dyes or isotopes and allows for brain blood flow and related activity to be monitored during sleep.

Specifically analysis of dreaming patients have revealed increased blood flow/oxygen utilization by network consisting of the pontine tegmentum, thalamus, amygdala, basal ganglia, anterior cingulate and occipital cortex.

The specific mechanism for deactivation of the prefrontal cortex is unclear due to the complexity of the acetylcholine activation pathway and its expanse into variety of other cortical areas.

[citation needed] The diagnosis criteria for posttraumatic stress disorder (PTSD) involve hyper-arousal, disturbed sleeping, and traumatic nightmares with numerous REM-related sub-symptoms.

[citation needed] Major depression which is believed to be modified by acetylcholine systems, is a functional disorder pertaining to the same neuronal structures that regulate dreaming.

[citation needed] In 1883 Jean-Martin Charcot encountered a patient who most likely had posterior cerebral artery thrombosis (not confirmed with autopsy)[2] and lost the ability to consciously reproduce images from his dreams while awake.

[6] His resulting contribution to the formulation of the syndrome lies on the lack of ability to re-visualize dream imagery and does not imply their complete absence, but a general state of visual amnesia.