Gadolinium-Induced Psychosis. An important, one of many, forms of cognitive impairment.

There are numerous patterns of brain dysfunction observed in GDD. Brain Fog is the most common form described and is primarily a cognitive cerebrum effect. Patient ambulatory Instability which is also very common, primarily reflects cerebellar dysfunction (will discuss later). It is uncertain how much of these conditions reflect direct deposition in brain tissue or systemic (or local) cytokine effects. My opinion a combination of all 3. DIrect neurons deposition has not been clearly shown on pathology specimens reported in the literature, so I am unsure of how much of this occurs, I suspect relatively little, as I have previously reported. Maybe 1-5% of brain deposition is actually in the neurons (brain cells) themselves. Supporting evidence for my theory is that recovery from cognitive dysfunction tends to occur fairly early in the chelation management of patients.

A relatively uncommon but important manifestation of cognitive impairment is true psychosis, a cerebrum effect. The psychosis often exhibits paranoia as the dominant feature.. It is not clear to me that pure Gd toxicity can result in psychosis or if it requires a co-effector such as Mercury or even other Tcell dysregulators like mold. Mercury/Gd combo pack is likely the most common cause of GDD psychosis. As with other GDD symptoms there can be spontaneous worsening and improving of psychosis, with occasional near complete improvement. Spontaneous near complete improvement, as with other GDD symptoms, occurs not uncommonly after 1 GBCA injection (probably atleast 1/3) but progressively rare/ to not occuring as the number of GBCA injections increase.

Unfortunately this condition is probably essentially never considered in a patient presenting (usually by family) to the ER with the history of psychotic thinking or severe paranoia. A number of GDD sufferers have been admitted to psych wards (often involuntarily) and I believe to the present time the diagnosis is never suspected. Most of the adminssions are probably not because of frank psychosis, but because the subject is complaining too much of brain fog... and is a woman.

To expand on Gd and heavy metal toxicity as a cause of many forms of brain dysfunction, it is tragic that this is rarely considered. I suspect that heavy metal toxicity is a relatively common cause for a variety of common brain disturbances, probably depression most commonly. The tragedy is that a number of these individuals with heavy metal toxicty, are readily diagnosable and readily treatable..

DIagnosis: For GDD quite simple as the patient had an MRI with Gd in the recent past, and devloped new symptoms shortly after. From few anecdotal reports to me it appears that frank psychosis with paranoia may be an escalatory step in the timeline of symptoms of GDD, where other symptoms appear earlier and frank psychosis may develop 2-5 months after GBCA. My experience is too limited to know if this is the common presentation form. No history of GBCA administration then mercury is classic for brain dysfunction, but lead may be even more common by virtue of the fact that everyone has lead in them, and not everyone has mercury. These sufferers are a risk for self-harm and also to be victims of predation of various forms, from individual predators to cults. As with other psychosis their actions cannot be considered the actions of a rational person or their conscious attempt to create chaos. This is a sickness like any other, such as diabetes.

24 hr urine pre-provocation/chelation may or may not show elevation of the responsible metal, but post-chelation with an effective chelator (I prefer iv DTPA if Gd or lead is suspected) will show elevation. I always perform both of these together, by which I mean always. The critical observation is that the symptoms of psychosis/paranoia increase following chelation, when the offending metal is increased in quantity postchelation. I consider it essential to always give pre-chelation and post chelation steroid to keep the flare of GDD symptoms (and in this case of psychosis symptoms) short-lived and manageable.

Among the tragedies is if undiagnosed then psychosis may persist indefintiely. The treatment with DTPA chelation with steroids often shows early and drammatic response of cognitive impairment findings, with notable improvement even observed after just 1 chelation. Chelation therapy in a psychotic patients requires close observation of the patient. A critical apsect of success is repeat chelation, and likely a minimum of 5 chelation sessions spaced 1-4 weeks apart (with no missing of sessions) is required to bring it fully after control. 1 chelation and then stopping because ' chelation has made the person crazier' is one of the worst thing that can be done, as they represent a danger to themselves and to others. 3 chelation sessions will show notable improvement consistently, and 5 will show durabable and effective improvement for most.

Consider Gd or other heavy metals as a cause for psychosis. Relatively easy to diagnose with pre- and post-chelation 24 hour urines and observation, and are highly treatable. These are not a psychosis that needs to be managed forever with antipsychotoic drugs. Caution that these individuals require careful monitoring in the early sessions of chelation, because in the early Gd removal and later Gd re-equilibration Flare phases they can be a danger, and they may have a tendency to not continue with chelation, when chelation is the only effective treatment for them. Ideal would be, if GDD individuals are admitted to a psychiatric ward they be chelated early after admission, and receive at least 3 chelation sessions, so a 2-3 week stay. This is how psychiatric admissions should be occurring with GDD patients

Richard Semelka, MD