Proposed hypotheses include a functional role for PrPC in metal metabolism, and loss of this function due to aggregation to the disease-associated PrPSc form as the cause of brain metal imbalance.
The cause of brain involvement in this patient despite an initial improvement of visceral lesions with the appropriate treatment [ 21], is difficult to explain.
6 27–29 These vascular risk factors could be the cause of brain lesions, not yet recognised clinically, and earlier studies have shown associations between cerebrovascular risk factor burden and a broad range of cognitive abilities.
Theories for the cause of brain cell loss have suggested a role for factors such as tau-protein abnormalities (Liou et al. 2003), metals (Casadesus et al. 2004), vascular factors (Fernando & Ince 2004), and viral infections (Ringheim & Conant 2004).
However, since the cause of brain cancer is still unclear, we could not definitively state a minimum latency period, and therefore considered several periods between 1 and 10 years, similar to other studies.
The cause of brain edema following HSES remains unclear, however, Unterberg et al. reported that brain edema of traumatic brain injury was associated with various mediators including cytokines, lactate, free oxygen radicals, etc. [ 30].
