2 Environmental (External Threats and Stressors) Treatment
4 Allopathic and Non Allopathic Treatments, kinds of doctors (and Treatment Protocols)
Compilation and update of modalities for healing from a stroke
InComplete List of Treatments (by polling)
Julien & Patricia Regimen
Personal Treatment Plan and Recommendations
The 'it's all in your head' - Sheer Willpower Method and Exercise
Back to General Report (Treatment)
Chronic fatigue (Home Button)
+1b Regions Affected by Head Injury (Possible)
+2 Cognition Problems and Compensation
+3 Neurological Dysfunction
+3b Neuroimmune and neuroendocrine processes
1a Decreases in Sphingolipid, glycosphingolipid, phospholipid, purine, microbiome aromatic amino acid and branch chain amino acid metabolites, as well as in flavine adenine nucleotide (FAD) and lathosterol
1 Consistent Abnormalities found in CFS patients
1 Metabolism and Energy Production Dysfunction
2 Effects and Systems Effects
2 Testing, Testing Laboratories, Treatment Centers, Specialists and Clinics
3 Common and Uncommon Causes and Cofactors
3 Drugs used for CFS (and CFS cofactors)
3 Similarly, the HPA axis also interacts with various other glandular systems, among them those producing reproductive hormones, growth hormones, and thyroid hormones. Once activated, the stress response switches off the hormonal systems regulating growth, reproduction, metabolism, and immunity. Short term, the response is helpful, allowing us to divert biochemical resources to deal with the threat.
4 Drugs used for TBI (also helpful for CFS)
4 Immune System Modulators
4 Non Allopathic Treatments of Interest
5 Histaminergic neurons of the hypothalamic tuberomammillary nucleus constitute a major wake‐promoting system
5 Hormone Replacement Therapy (HRT)
Amisulpride (very low dose)
and hippocampus in CFS/ME patients
Atomoxetine (Strattera, Attentin)
Behavioral, Neurobehavioral and Psychiatric changes from head injury
Blood Brain Barrier and disorders
Brain Fog, Confusion, Sensory overstimulation, memory difficulties, pseudopsychopathy, High Effort in processing Planning Administrative Executive Function Planning Anxiety Stress Passive vs Proactive Shy Withdrawn Uncertain w social self esteem and anxiety etc Dysthymia etc
Circuit breaker to room for smartmeter disruption
Cortical Glutathione and Reductions in the levels of cortical GSH
Corticotropin Releasing Factor Receptor type 2 agonist CT38
Doxepin (Sinequan, Sinquan, Zonalon, Deptran, Xepin)
Felbamate (Felbatol, Taloxa)
From CFS Unravelled by Dan Neuffer
HGH (Growth Hormone) and Growth Hormone Deficiency (GHD)
Hypocretin (Orexin) Neurons
Impact of Traumatic Brain Injury on Dopaminergic Transmission
Impact of Traumatic Brain Injury on Neurotransmitter Systems
Impaired Activation of the Hypothalamic-Pituitary-Adrenal Axis
Imunovir (inosine pranoxbex)
Infection-triggered disease onset, chronic immune activation and autonomic dysregulation in CFS point to an autoimmune disease directed against neurotransmitter receptors.
Initiation of Inflammation after TBI
Jaw bone cavitation infection
Lack of Proper Probiotic, Prebiotics and/or Enzymes (in Intestines or diet) and/or fiber
LDN (Low-dose naltrexone)
Leaky gut (intestinal permeability)
Long Term Sequelae of TBI
Metabolic Changes from TBI
Mitochondria in traumatic brain injury and mitochondrial-targeted multipotential therapeutic strategies
Neuroendocrine changes from TBI
One of the most common characteristics of frontal lobe damage is difficulty in interpreting feedback from the environment.
Onset, Patient History of Illness and Triggers
Overexpending for task Drain on resources
Paroxysmal Sympathetic Hyperactivity after Acquired Brain Injury
Peptides LL-37 + BPC-157 1
Pharmacological Medicine for Traumatic Brain-injury Rehabilitation by class
Phenytoin (Dilantin, Hydantin, Phenytek, Epanutin)
post TBI Diabetes Insipidus
Prescriptions used in conjunction
Prolonged acetylcholine-induced vasodilatation in the peripheral microcirculation of patients with chronic fatigue syndrome
Pseudo Neurological Damage (Pre Existing and/or Causal to CFS)
pTBI-CF Factors contributing to chronic fatigue after traumatic brain injury
Rituximab (Rituxan, Ritumax)
Routine cognitive processes are experienced as unduly effortful and Brain Fog
Sleep Disturbance After Traumatic Brain Injury (TBI)
Stemepilepsy Neuron Injected
Suramin (https://www.healthrising.org/blog/category/treatment/drugs/suramin/ "Suramin is anti-purinergic drug usually used to treat African sleeping sickness and river blindness. Dr. Naviauw believes Suranim may be able to turn off the "cell danger response" in ME/CFS and autism. A small Suramin autism trial was successful. ") (2)
syndrome of inappropriate antidiuretic hormone (SIADH)
TBI increases mitochondrial fission and that inhibition of fission improves hippocampal-dependent learning and memory
The primary brain regions sensitive to acute exercise and symptoms of Post Exertional Malaise are the inferior frontal, parietal and cingulate cortices (regions critical for efficient cognitive processing involving processes associated with attention, error detection, and cognitive control/central executive functions)
The stress response and the hypothalamic‐pituitary‐adrenal axis: from molecule to melancholia
Traumatic Brain Injury, Sleep Disorders, and Psychiatric Disorders: An Underrecognized Relationship
Treatment with Flumazenil (GABAA receptor antagonist)
Vasoactive Neuropeptide Dysfunction (including vasoactive intestinal peptide (VIP) and pituitary adenylate activating polypeptide (PACAP))
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