The Science

In this article, the futility of current medical therapy is discussed along with a recommendation for a new approach that targets inflammation, mitochondrial function and Neuro Active Steroid support. 

Pooled clinical and neuropathology data from three prospective cohort studies indicate that TBI with LOC is associated with risk of Lewy body accumulation, progression of parkinsonism, and Parkinson’s disease, but not dementia, Alzheimer’s disease, neuritic plaques, or neurofibrillary tangles.

This article describes how hyperprolactinemia can be secondary to hyperplasia of the pituitary gland.

This review attempts to summarize our current knowl- edge of the mechanisms used by glial cells to control GnRH neuronal activity and secretion.

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Targeting inflammatory responses may be a potential treatment strategy for targeting neurons-psychiatric disorders. 

The findings of this pilot study provide prelimi- nary evidence suggesting that some of the cognitive impairments observed in persons who are GHD/GHI after TBI may be partially reversible with appropriate GH replacement therapy.

Clomiphene was effective at interrupting the chronicity of cluster headaches in all patients while noted to be safe and well tolerated. 

The study shows that ibuprofen use results in selective transcriptional repression of endocrine cells in the human testis. This repression results in the elevation of the stimulatory pituitary hormones, resulting in a state of compensated hypogonadism, a disorder as- sociated with adverse reproductive and physical health disorders.

This pilot study suggests that testosterone levels may be important in the recovery of patients with traumatic brain injury, treated at an in-patient rehabilitation hospital.

This review summarises current evidence regarding the role of NO in the regulation of cerebral blood flow at rest, under physiological conditions, and after brain injury, focusing on subarachnoid haemorrhage, traumatic brain injury, and ischaemic stroke and following cardiac arrest.

Microglia-regulated mechanisms may underlie the differential susceptibility to stress and con- sequently the vulnerability to diseases triggered by the experience of stressful events, such as major depression.

Impact on Hormonal Environment and Gender Identity