норм исследований по NMDA при быстром поиске не попалось, за потенциально интересные статьи просят деньги:
NMDA for depression
predictors of clinical improvement to ketamine in depression
короче, если очень хочется, сам экпериментально устанавливаешь оптимальную дозу кетамина и вперед.
Я помню где-то видел сравнение действия кетамина СИОЗС. Они там даже что-то общее нашли, вроде какой-то адренорецептор который реагирует и на то и на другое схожим образом.
Вообще NMDAr самый изучаемый благодаря его уникальной функции в ЦНС. Реально только два заболевания прямо непосредственно связанны со степенью его активности это шизофрения и эпилепсия. Блокада вызывает кататано-онейроидный психоз, чрезмерная активация судорожный припадок, все. А вообще исследований о том на сколько он активен когда на дворе март месяц тьма. Если откроете неврологию, любую, реально пох, абсолютно любую, будь-то ЧМТ, инсульт, Альцгеймер или олигофрения - тонны информации.
многие психиатры из этих ссылок говорят медленно, не понятно почему.
Заразились от пациентов.
Про борнавирус и антивоспалительную терапию, как всегда на закуску и без практического применения.
У шизофреников бывает как избыточное метилирование, так и недометилирование, которое гораздо тяжелее “закручивания хвостов”.
Исходное интервью - дурное, если такие неначитанные профессора учат, то понятно какие психиатры получаются.
Кризис - есть, но выходить из него не хотят, психиатрам так лучше, кризис - он для больных и родственников.
кстати, о кетамине и депрессии.
что не находилась на пабмеде, есть в евровики:
Antidepressant use When treating patients suffering from complex regional pain syndrome (CRPS) with a low-dose (subanesthetic) ketamine infusion, it was observed that some patients made a significant recovery from associated depression . This recovery was not formally documented, as the primary concern was pain management. It was not possible to quantify to what degree depression recovery was secondary to the patient’s recovery from CRPS. One trial administered a short-term ketamine regimen to patients with severe depression, with the dose carefully monitored to prevent hallucinogenic side effects. The patients’ normal medications were continued as it was feared that stopping them might result in severe depressive episodes. Before and following each treatment with ketamine, at patient clinic visits, the Beck Depression Inventory (BDI) and the Hamilton Rating Scale for Depression (HAMD-17) were obtained. Two of the patients demonstrated significant, long-term improvement. [ 71 ] Another small study found that ketamine significantly improved treatment-resistant major depression within hours of injection. [ 72 ] The improvement lasted up to one week after the single dose. [ 73 ] These patients were previously treatment resistant, having tried an average of six other treatments that failed.The researchers apparently attribute the effect to ketamine being an NMDA receptor antagonist . [ 74 ] Those findings of Zarate et al. corroborate earlier findings by Berman et al. . [ 75 ] However Zarate et al. do raise some concerns about their results due to a possible lack of blinding, because of the inebriating effects of low dose ketamine infusion, and it is recommended that future studies include an active placebo .
These findings are corroborated by Liebrenz et al., who successfully, according to an attending doctor, treated a patient with a treatment-resistant major depression and a co-occurring alcohol and benzodiazepine dependence by giving an intravenous infusion of 0.5 mg/kg ketamine over a period of 50 minutes and Goforth et al. who helped a patient with severe, recurrent major depressive disorder that demonstrated marked improvement within 8 hours of receiving a preoperative dose of ketamine and one treatment of electroconvulsive therapy with bitemporal electrode placement. [ 76 ] [ 77 ]
However, a new study in mice by Zarate et al. shows that blocking the NMDA receptor is an intermediate step. According to this study, blocking NMDA increases the activity of another receptor, AMPA , and this boost in AMPA activity is crucial for ketamine’s rapid antidepressant actions. NMDA and AMPA are receptors for the neurotransmitter glutamate . The glutamate system has been implicated in depression recently. This is a departure from previous thinking, which had focused on serotonin and norepinephrine . The glutamate system may represent a new avenue for treatment and research. [ 78 ]
Krystal et al. retrospectively compared the seizure duration, ictal EEG, and cognitive side effects of ketamine and methohexital anesthesia with ECT in 36 patients. [ 79 ] Ketamine was well tolerated and prolonged seizure duration overall, but particularly in those who had a seizure duration shorter than 25 seconds with methohexital at the maximum available stimulus intensity. Ketamine also increased midictal EEG slow-wave amplitude. Thus, a switch to ketamine may be useful when it is difficult to elicit a robust seizure. Faster post-treatment reorientation with ketamine may suggest a lower level of associated cognitive side effects.
Kudoh et al. investigated whether ketamine is suitable for depressed patients who had undergone orthopedic surgery. [ 80 ] Depressed mood, suicidal tendencies, somatic anxiety, and hypochondriasis significantly decreased in the active group as compared with the control. The group receiving ketamine also had significantly lower postoperative pain.
Acute administration of ketamine at the higher dose, but not imipramine , increased BDNF protein levels in the rat hippocampus . The increase of hippocampal BDNF protein levels induced by ketamine might be necessary to produce a rapid onset of antidepressant action in rats.
шикарные сцылы:
при биполярных депрессиях
про BDNF, о котором недавно говорили
быстрый кетамин
ЭСТ