HunterThinks.com

Healthcare bụ a nri

Ihe: 18 September 2018
emelitere: 25 September 2018

Therapeutic plan iwebata

My kpọmkwem ọgwụ nsogbu

  1. 5HT2A desensitization.
  2. Low dopaminergic ọrụ.
  3. Hyperactive amygdala.
  4. dysfunctional DMN (Ndabere Mode Network).

na mbụ, sayensị ọgwụ na enweghị a zuru ezu ọkaibe nghọta nke ukwuu mgbagwoju interactions nke neurotransmitters, homonụ, vitamin na ndị ọzọ micronutrients, akụkụ ndị na-amị biochemicals na ndị a na usoro, and the symptoms of improper functioning of these interactions. Ke akpatre 20 afọ, anyị mụtara ọtụtụ ihe, gụnyere na nke a bụ ihe mgbagwoju karịa anyị na-atụ anya na na anyị ka dị n'ụzọ dị ukwuu ịma ihe banyere ndị a Filiks.

My previous diagnoses

si 2007-2014, multiple ọgwụ ọkachamara na-eji ha ọzụzụ, ahụmahụ ha, and my available patient data to diagnose me as well as they could. Ha diagnoses bu olu: ịda mbà n'obi, generalized nchegbu aghara, PTSD, na egwu aghara. Let’s assume that their diagnoses are nti (tụọ ihe n'ezie); n'ihi na diagnoses bu olu, ọ dị mfe iche na nkà mmụta sayensị pụrụ ịdabere (reproducibility). Ka iche na diagnoses ziri ezi. Ha na-adịghị, Otú ọ dị, kpọmkwem.

Ezi ihe nchoputa nke ịda mbà n'obi, ọmụmaatụ, agwaghị anyị otú anyị si emeso ndị ịda mbà n'obi. Talk ọgwụ, na nkà mmụta ọgwụ, na electroconvulsive ọgwụ niile ọrụ maka ụfọdụ ndị ọrịa, ma ọ dịghị nke ha na-arụ ọrụ niile ọrịa. n'ime ọgwụ, ọrịa ike ime ka ọtụtụ ihe, tinyere ụba serotonin, ụba dopamine, ụba micronutrients, ma ọ bụ belata mbufụt (kpọrọ). Ma ọ dịghị nke ndị ọgwụgwọ na-arụ ọrụ maka onye ọ bụla. A ịda mbà n'obi nchoputa bụ mgbe zuru ezu ozi maka achọta ọgwụgwọ. Na n'oge ọ bụla dọkịta chọpụtara m, anyị na-amaghị ezu banyere ahụ mmadụ na-eme ka a ọzọ kpọmkwem nchoputa. Ọzọkwa, ugbu a na anyị maara na ihe banyere otú ihe na-arụ ọrụ, anyị mepụtara na-achọpụta ọrịa ule ma: ma e wezụga n'ihi multiple sessions na fMRI, nke bụ obscenely ọnụ. Na ọbụna njọ, n'ihi na ọ dịghị onye na-atụ anya ngụkọta desensitization nke 5HT2A, ọ dịghị onye kpọmkwem mụọ a na-agwọ. M na-hụrụ atọ ọgwụ mara upregulate 5HT2A. My dọkịta mere ihe magburu onwe ọrụ na ihe ọmụma na-achọpụta ọrịa ngwaọrụ dị ka ha, ma ọ gaara-agaghị ekwe omume ha idepụta a na-agwọ m.

My increased precision is a major breakthrough

Tupu m nwere a kpọmkwem na nghọta nke m ọgwụ nsogbu, m dọkịta nyeere m aka ịchọta ọgwụ site nnwale. ugbu a, M ike ịchọ ọgwụ na lebara a kpọmkwem nsogbu. My nghọta na m dopamine ebighị dị oke obere (na akụkụ n'ihi 5HT2A nsogbu), ọmụmaatụ, mere m ka m kpọrọ bupropion ọzọ. O nyeworo. My two horrible experiences running out of alprazolam were informative: alprazolam enwekwu dopamine na striatum, ma mmetụta bụghị dị ka ibu ma ọ bụ ogologo oge na-adịgide adịgide dị ka bupropion ma ọ bụ modafinil. Gwara m ihe m dopamine etoju ndị ka ala zuru ezu na a obere emeghasịkwa nwere nnukwu mmetụta. Ya mere, M ụba bupropion si 150 mg ugboro abụọ n'ụbọchị ruo ugboro atọ n'ụbọchị. O nyeere melite mgbaàmà m na-atụ anya, na ya mma a mgbaàmà m na-atụghị anya: M nwere agụụ. n'ihi na afọ, m agụụ kemgbe ukwuu n'ime na-adịghị adị, na na na-eme ka o siere m ike na-eri n'ụzọ kwesịrị ekwesị, which makes almost everything else in my life more difficult.

Ọ bụrụ na m nwere ike ịgbanwe ọgwụ, I can improve my symptoms

M ugbu a na-ewere 450 mg nke bupropion kwa ụbọchị, na nke ahụ bụ kacha onunu ogwu n'ihi ihe ọ bụla elu nwere ihe ize ndụ. M nwere ike ịgbanwe ndị ọzọ ọgwụ ka mma m ike ịnagide. Ma, e nwere ọtụtụ ihe mgbochi. Ịba bupropion na modafinil bụ ọnụ. M chọrọ iji kpochapụ venlafaxine, omeprazole, na caffeine, ma n'oge Transition n'ebe ndị ọgwụ, M ga-enwe ọtụtụ nsogbu. Ọ ga-abụ dị ize ndụ m ịgbanwe ndị ọgwụ mgbe enweghị ebe obibi. Ụfọdụ magburu onwe Mmeju, dị ka atọ amino asịd, bụ ọnụ ma nanị dị site mail iji: esiri-enweghị ebe obibi. Caffeine enwekwu dopamine, so I can only stop taking it if I can find other ways to increase my dopamine.

Ọ bụrụ na m chọrọ ịgwọ, M mkpa ka ibu mgbanwe, na n'elu ihe mgbochi na-ọbụna ọzọ mfịna.

Iji nyere aka, click Ebe a.

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