Whereas the hysterias involved at their source a narrowing of the field of consciousness, the psychasthenias involved at root a disturbance in the fonction du reél (function of reality), a kind of weakness in the ability to attend to, adjust to, and synthesise ones changing experience (cf. executive functions in todays empiricist psychologies). Carl Gustav Jung later made the hysteric and the psychasthenic states the prototypes of what he described as extroverted and introverted personalities.Karl Jaspers preserves the term "neurasthenia", defining it in terms of "irritable weakness" and describing phenomena such as irritability, sensitivity, a painful sensibility, abnormal responsiveness to stimuli, bodily pains, strong experience of fatigue, etc. This is contrasted with "psychasthenia", which, following Janet, he describes as a variety of phenomena "held together by the theoretical concept of a diminution of psychic energy." The psychasthenic person prefers to "withdraw from his fellows and not be exposed to situations in which his abnormally strong complexes rob him of presence of mind, memory and poise." The psychasthenic lacks confidence, is prone to obsessional thoughts, unfounded fears, self-scrutiny and indecision. This state in turn promotes withdrawal from the world and daydreaming, yet this only makes things worse. "The psyche generally lacks an ability to integrate its life or to work through and manage its various experiences; it fails to build up its personality and make any steady development." Jaspers believed that some of Janets more extreme cases of psychasthenia were cases of schizophrenia. References


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A favorable outcome is more likely if a kidney transplant is complemented by a liver transplant, given the disease originates in the liver. Controversy
Perhaps the key difficulty in understanding pathogenesis of primary hyperoxaluria, or more specifically, why AGXT ends up in mitochondria instead of peroxisomes, stems from AGXTs somewhat peculiar evolution. Namely, prior to its current peroxysomal destiny, AGXT indeed used to be bound to mitochondria. AGXTs peroxisomal targeting sequence is uniquely specific for mammalian species, suggesting the presence of additional peroxisomal targeting information elsewhere in the AGT molecule. As AGXT was redirected to peroxisomes over the course of evolution, it is plausible  that its current aberrant localization to mitochondria owes to some hidden molecular signature in AGXTs spatial configuration unmasked by PH1 mutations affecting the AGXT gene. References
External links

GeneReviews/NIH/NCBI/UW entry on Primary Hyperoxaluria Type 1