Charcot-Wilbrand Syndrome - Physiological Causes

Physiological Causes

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. 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. Patients suffering from Alzheimer's disease as well as Turner syndrome have also described having CWS. In terms of localization, the lesion or damaged tissue is most often localized to the lateral(sides) or mesial(middle) occipitotemporal regions, and typically appears bilaterally(affecting both sides equally). The exact localization however has not been illuminated and can most accurately be summarized as "a lesion in an acute phase affecting the posterior regions”.

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. Early attempts to locate the lesion site responsible for the cessation of dreaming on a universal scale have lead to the parietal lobe with no bias to either side, and single lesions of either hemisphere commonplace. Recent case studies of dream loss have found evidence suggesting that damage to the parietal is not necessary for CWS. Additionally in some of the cases of parietal lobe lesions, the lesion continued into the occipitotemporal regions, further blurring the localization of global dream loss. In almost all cases, dreaming returned within 12 months implying a possibility that site of interest was only connected to the damaged regions, most likely through neural pathways, further complicating localization.