The worst category of GDD are subjects with chronic progressive GDD. A condition which is essentially as severe as NSF and can also be fatal. To refresh your memories from an early blog this is the categorization of GDD I have previously described: 1. probably many cases of GDD-type symptoms spontaneously resolve (to a great extent). I suspect that maybe 20% of all individuals who undergo GBCA injection, have prominent symptoms but they resolve in 24 hours, and these individuals blend in with the group of GSC subjects. 2. Maybe 1 % have bonafide GDD but largely resolve at 1 month. 3. Maybe 0.1 % have bonafide GDD but largely resolve by 3 months. 4. Probably 0.05% have bonafide GDD but resolv

How can we minimize the chance of getting GDD when we undergo GBCA-enhanced MRI? I have always loved the quote from Shakespeare in the play Julius Caesar, Cassius speaking to Brutus: The fault, dear Brutus, is not in our stars, But in ourselves. I think this applies to most things, but certainly to this condition. This I take to mean that it is not our fate that things happen, it is do to us and what we do. The two critical things we have control of are: 1. do not be dehydrated before and for atleast 2 days after GBCA injection. 2. do not be in a state of self-determined metabolic acidosis. In practical terms that everyone can understand, these are the two commandments: 1. make sure to drink

There are 2 components to treating GDD: i) removing the Gd, and ii) treating the host response. Removing the Gd is the most obvious and straightforward, so treatment begins with focusing on that. Patients basically fall into two groups: 1) those relatively easy to treat, and 2) those that are challenging. In group 1, the largest subgroup are patients who have received only linear agents and are beyond 1 year after the most recent GBCA administration. In those patients often just a regimen designed to remove Gd may be sufficient. In group 2, the 3 largest subgroups are: a) those who have received the most recent GBCA within 6 months, b) those who have received macrocyclic agents, and c) those

Sufferers from GDD should familiarize themselves with this term: Disease Modifying AntiRheumatic Drugs (DMARDs), and the drugs that are members of this heterogenous group. If chelation and chelation with mild autoimmune disease therapy does not work, they may require one, or a combination of these agents (excerpted from Wikipedia): At this early juncture, it appears from preliminary work that TNF-alpha and IL-6 may be integral in the mediation of GDD. I am in the process to see if any sufferer has been placed on these drugs, probably for a concurrent auto-immune disease, such as rheumatoid arthritis. So I do not know which agent or combination of agents works effectively. If you are on any

The main feature shown with NSF has been disease distribution that primarily affects the lower arms and hands, and the lower legs and feet, what has been termed 'glove and sock' distribution. Winter is coming, so glove and sock is an appropriate subject matter. Like with NSF, GDD also shows 'glove and sock' distribution in the subacute stage. GDD also shows a number of other A symptoms (symptoms that are more specific): brain fog, skin burning, pin and needles, boring bone pain, and B symptoms (seen with many diseases): vision problems, gastrointestinal abnormalities. The A symptoms are essentially identical to other heavy metal toxicities, lead being the classic. Also they share the B sympt

Placebos are extremely important aspect of essentially all health care. Usually when a physician uses the term 'placebo' it is considered derogatory, and maybe often that is the intention. From my perspective, placebo effect, both positive and negative, are powerful tools. Essentially when placebos have effect, it actually is a reflection that the mind is effecting the body function to heal itself (positive placebo) or make itself sicker (negative placebo). Let us begin the discussion with negative placebo. Negative Placebo. I start with negative placebo because this is what radiologists deal with all the time on a daily basis. For the 30 + years I have been involved in Radiology this has be

I've had several requests to discuss the subject of children and GDD. I have to preface this by saying I have minimal knowledge of this, so this is one of my blogs which is highly speculative. Surprisingly there is little contact I receive regarding children and GDD, and little in the patient activist internet and Face book sites. This leads me to believe that it is relatively rare (although not impossible, as a few parents have contacted me about their children). How is that possible, especially when we hear in the news about children who are grossly affected with neurological deficits, delayed maturation, spasticity secondary to lead, when symptoms from lead seem so similar to gadolinium i

Is it important if Gd is in the intact chelate or if it is unchelated? It appears clear with NSF that it is important if Gd is in the intact chelate (should not get NSF) or unchelated (may cause NSF), and with GSC (notably Gd deposited in brain), however it does not appear to be important in acute hypersensitivity reactions or GDD. In many respects my current thinking is that GDD is essentially a hypersensitivity reaction which over time recruits chronic immune cells into the response. After decades of recognizing the existence of acute hypersensitivity reactions to Gd it is not clear what cells of acute reactions are responding to: is it the intact GBCA, is it released Gd, or something els