In our Patient, TD presents itself as a long closure of the eye lids as if the Patient was asleep. If you engage the Patient in conversation you find the Patient awake and responding and when you discuss a topic the Patient is excited about, the Patient will open the eyes. Patient is aware that eyes are closed and describes them as being clamped shut.
--gjh
"A common side effect of antipsychotic medications used to treat schizophrenia is a condition called tardive dyskinesia, a movement disorder of the mouth characterized by a constant chewing motion and darting action of the tongue. In a study(1.) of 22 people with schizophrenia and tardive dyskinesia caused by antipsychotic medications, those who took melatonin supplements had significantly reduced mouth movements compared to those who did not take the supplements."
(2.) "antipsychotics produce their effect by reducing DHEA." "DHEA naturally begins to decline around age twenty to twenty-five, and this probably occurs earlier in schizophrenics. In addition to this decline, interference with the availability of DHEA may occur because of another adrenal hormone, cortisol, and, beginning at puberty, the hormone, testosterone."
"In my articles on evolution and sleep at this website, I connect the pineal hormone, melatonin, with DHEA. I suggest melatonin may be involved in producing receptors, chemical doorways, for DHEA. For DHEA to produce its growth promoting activities on neurons, it must have a pathway into the neuron. Melatonin stimulates these receptor at night. I think this pathway is reduced in schizophrenics, because nighttime melatonin is reduced in schizophrenia (Biological Psychiatry 1989, 25: 500). Proper amounts of melatonin are necessary for slow wave sleep to occur; the deepest stage of slow wave sleep is stage 4. Lack of stage 4 sleep is documented in schizophrenia. (sic) ...others think reduced melatonin may be involved in some forms of schizophrenia, however, the investigators do not mention DHEA."
"The drugs used to control schizophrenia, I suggest, actually exert their effects by stimulating DHEA production. That is, "...antipsychotic potencies of most neuroleptic drugs closely correspond to their prolactin-releasing potencies at low doses..." (Biological Psychiatry 1990, 27: 1204). Therefore, it may actually be DHEA that ameliorates schizophrenia upon antipsychotic drug administration. Schizophrenia is thought to result from dopaminergic over-activity; essentially all antipsychotic drugs block postsynaptic dopamine receptors. This increases prolactin release. The dopaminergic agonist, bromocriptine, often used as an anti-prolactin agent, produces hallucinations, delusions, and confused thinking when used in excess."
"Schizophrenia results from lack of cerebral hemisphere growth as a result of severe reductions in DHEA and melatonin during brain growth and development. It is triggered by events later in life that reduce DHEA availability and increase the negative effects of cortisol. I suggest treating schizophrenics with melatonin at night and DHEA during the day may help in some circumstances, depending on the level of damage done by prolonged cortisol exposure."
(3.)"Cortisol also inhibits hippocampal neurogenesis, but DHEA has a stimulatory effect. Cortisol can actually kill hippocampal neurons, and does so increasingly with aging and stress, but this effect can be reversed with melatonin and Insulin-like Growth Factor (IGF-1) [THE JOURNAL OF NEUROSCIENCE; Aberg,MA; 20(8):2896-2903 (2000)]."
Useful Links:
http://www.umm.edu/altmed/ConsSupplements/Melatonincs.html
http://www.anthropogeny.com/Schizophrenia.htm
http://www.benbest.com/nutrceut/melatonin.html
http://www.benbest.com/nutrceut/DHEA.html
(1.)Shamir E, Barak Y, Shalman I, Laudon M, Zisapel N, Tarrasch R, et al. Melatonin treatment for tardive dyskinesia: a double-blind, placebo-controlled, crossover study. Arch Gen Psych. 2001;58(11):1049-1052.
(2.)James Michael Howard - http://www.anthropogeny.com/Schizophrenia.htm
(3.) Chapter 3 -- Learning, Memory and Plasticity, by Ben Best
http://www.benbest.com/science/anatmind/anatmd3.html
One Patient's story of non clinical and clinical diagnosis of Schizophrenic like symptoms, attempts at vitamin therapy approach, seizure activity present. We searched for answers & much of our research was beneficial in chronological context. Taken out of context, the information may not provide an accurate understanding/solution. Psychiatric illness was ruled out. This blog indicates how we arrived @ the current treatment -vitamin therapy. Diagnosis given: Fronto-temporal dementia.
LOW HISTAMINE
- This LOW HISTAMINE schizophrenia supplement schedule was developed to improve the quality of life of our family member-referred to as Patient. Once the FTD diagnosis was agreed, the patient was in late stages and soon hospitalized. The only supplement that was to have significant impact on FTD was DHEA in the early stages. THIS is not a recommendation and we make no claims this protocol will work for you. Always check with a qualified Doctor when making changes to your recovery protocols.
- 100mg L-Carnosine AM - scavenger of oxidative stress (ROS & alpha-beta unsaturated aldehydes), improves processes affected with autisim, found highly concentrated in muscle and brain tissue, quickly metabolizes blood levels of stress produced Cortisol returning levels to normal, too much Carnosine may cause hyperactivity.
- 100mg R-ALA (RLA) PM - Powerful antioxidant, reverse cognitive dysfunction, increases glutathione, "recycles" other key antioxidants such as vitamin C, vitamin E, and glutathione, promotes glucose metabolism, proven effective for treating diabetic neuropathy, prevents nerve damage from oxidation.
- 2mg Melatonin PM-ONLY - counteracts TD, Improves sleep quality of chronic schizophrenia patients, suppresses prolactin release, necessary for SWS-REM sleep, stimulates endorphin production (updated from 1mg 12-9-06)
- 5mg DHEA AM Androgen occurring naturally in humans and synthesized from cholesterol. 5mg maintenance dose-no higher. Patient responded to larger 50mg dose in the past but then had significant side effects. Goal is to balance or restore normal level. Body does not upregulate its own levels when taken orally, so max total levels should not exceed natural 15 mg in body daily.
- 100mg CoQ10 AM Many useful antioxidant activities especially Schizophrenia, neuroprotective effects, potent free radical scavenger in lipid and mitochondrial membranes (increased from 30mg on 2-15-07)
- 800mg EPA-protein AM Balance with DHA
- 200mg Vitamin B6 Pyridoxine AM Counteracts Kryptopyrrole, break down and use fats, proteins, and carbohydrates, to make red blood cells and antibodies, to help the digestive and nervous systems function, maintain healthy skin. Converts to coenzyme P5P in body
- 800mg DHA-protein AM Balance with EPA
- 500mg per meal Vitamin B3 Niacin (no flush-slow release) AM Opens Capillaries, take after each meal, Removes voices, Needed for Omega EFA conversions to prostaglandins.
- 50-80mg Zinc AM Positive Factor for TD, inverse of Copper, Works closely with B6, promotes normal metallothionein, commonly out of balance with Copper
- 200mcg-600mcg Selenium AM Antidote for Mercury, Antioxidant, Antidepressant, Improves Prostaglandins
- 30mg Chelated Manganese PM Prevents Tardive (TD), increases elimination of copper and helps return copper levels to normal. Do not take with Calcium.
- 5,000mcg Vitamin B12 AM Improves RBC flow through Capillaries
- |AVOID| 200mg SAM-e (S-adenosylmethionine) Treats Undermethylation, was tested on this Patient and did not respond well, maintains cell membrane structure, substances vital to transmitting nerve impluses that influence mood and emotion
- |AVOID| 100mg L-Theanine - inhibits glutamic acid excitotoxicity, promotes GABA production, decreases serotonin and increases dopamine (BAD FOR PATIENT), promotes alpha wave production associated with alert relaxation (non drowsy), improves immune system response by boosting capacity of T cells, crosses blood brain barrier.
- Exercise & Diet - 30 minutes of walking per day
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