Complex PTSD vastly widened the definition of potential stressor events by calling them adverse events, and deliberating dropping reference to life-threatening, so that experiences can be included such as neglect, emotional abuse, or living in a war zone without having specifically experienced life-threatening events. By broadening the stressor criterion, an article published by the Child and Youth Care Forum claims this has led to confusing differences between competing definitions of complex PTSD, undercutting the clear operationalization of symptoms seen as one of the successes of the DSM.There are no known case reports with prospective repeated assessments to clearly demonstrate that the alleged symptoms followed the adverse events. Instead, supporters of complex PTSD have pushed for recognition of a disorder before conducting any of the prospective repeated assessments that are needed. See also
References
Further reading
External links
Post-traumatic stress at Curlie
APA practice parameters for assessment and treatment for PTSD (Updated 2017)
Thiamine is first metabolised to its more active form, thiamine diphosphate (TDP), before it is used. The body only has 2–3 weeks of thiamine reserves, which are readily exhausted without intake, or if depletion occurs rapidly, such as in chronic inflammatory states or in diabetes. Thiamine is involved in:
Metabolism of carbohydrates, releasing energy. Production of neurotransmitters including glutamic acid and GABA. Lipid metabolism, necessary for myelin production. Amino acid modification. Probably linked to the production of taurine, of great cardiac importance. Neuropathology
The primary neurological-related injury caused by thiamine deficiency in WE is three-fold: oxidative damage, mitochondrial injury leading to apoptosis, and directly stimulating a pro-apoptotic pathway. Thiamine deficiency affects both neurons and astrocytes, glial cells of the brain. Thiamine deficiency alters the glutamate uptake of astrocytes, through changes in the expression of astrocytic glutamate transporters EAAT1 and EAAT2, leading to excitotoxicity. Other changes include those to the GABA transporter subtype GAT-3, GFAP, glutamine synthetase, and the Aquaporin 4 channel. Focal lactic acidosis also causes secondary oedema, oxidative stress, inflammation and white matter damage. Pathological anatomy
Despite its name, WE is not related to Wernickes area, a region of the brain associated with speech and language interpretation.In most, early lesions completely reversed with immediate and adequate supplementation.Lesions are usually symmetrical in the periventricular region, diencephalon, the midbrain, hypothalamus, and cerebellar vermis. Brainstem lesions may include cranial nerve III, IV, VI and VIII nuclei, the medial thalamic nuclei, and the dorsal nucleus of the vagus nerve.