A catatonic woman awakened after 20 years. Her story may change psychiatry. Washington Post

https://wapo.st/43BZRXH

New research suggests that a subset of patients with psychiatric conditions like schizophrenia may actually have autoimmune disease that attacks the brain.

“The medical team set to work counteracting April’s rampaging immune system and started April on an intensive immunotherapy treatment for neuropsychiatric lupus. Every month for six months, April would receive short, but powerful “pulses” of intravenous steroids for five days, plus a single dose of cyclophosphamide, a heavy-duty immunosuppressive drug typically used in chemotherapy and borrowed from the field of oncology. She was also treated with rituximab, a drug initially developed for lymphoma.”

Long but interesting (not MECFS). Might be of interest to @Jonathan Edwards


Alternative link to the article here (thanks, Arnie Pye):
https://us.knews.media/news/a-catat...ter-20-years-her-story-may-change-psychiatry/

 

It is of interest.

The question I now ask myself is why, when I designed this treatment twenty three years ago, has nobody made any further progress? They may even have gone backwards - using high dose steroids and cyclophosphamide, which are probably unnecessary and are a hang over from the 1980s. Why did it take twenty years even to do good enough trials to show that rituximab worked for lupus?

The medical profession seems to have so little ambition. We should now have risk-free curative treatments for lupus, but nothing has changed.

 

Especially when it comes to people of colour. There has been some suggestion that Black populations have a higher incidence of schizophrenia (or at least, a higher rate of diagnosis).

The story of April hit me hard, because it's that of one of my close school friends. She excelled at everything she did, from art to science to sport, and she was kind, generous, and extremely funny. She was diagnosed with psychosis and then schizophrenia during her teens, and that was the end of her normal life. She's been ill for as long as I have (more than 45 years), but she's endured a double discrimination because of her illness and her race.

I don't know the cause of her illness, but there will be people like her, shining young people who could have changed the world, whose potential was lost even though they have something potentially treatable. It's even more devastating to think that it might have been acted on two decades ago.

 

They aren't even giving her adequate maintenance care!

 

Amazing to me that April's lupus was active only in her brain, and nowhere else.

 

The WaPo story is very scant on details. It’s difficult to say what’s going on or what autoantibodies they have. Neuropsychiatric SLE is a known entity and there is absolutely nothing game changing or informative here other than mid-1990s third rate hospitals in the US being crap at ruling out organic causes of psychosis and shoving people into long-term institutional care.

 

Surely it's costing more money to put someone in care versus treating them --- OK --- no point in saying the blindingly obvious --- barriers to doing the obvious?

 

From the article

@Jonathan Edwards would these abnormalities (or something suggesting them) show up on "routine" bloodwork? such as FBC etc? Or do they need specific tests to be run? Wondering how difficult they are to find.

 

My take on this is it is probably inherent in the human psyche to develope a "theory of mind" in our attempt to understand the people around us.

So we may feel empathy with other people, especially kin but also others and part of the empathy is modelling what we know about them in an image of them retained in our memory, what some might call our "heart". The empathic recollection we have of other people has to be based on our own mental experience i.e. we use our own mind as a way to model other people's minds.

I think the difference between schizophrenia and Parkinson's in this context is that the affects of schizophrenia can be so cruel and deeply disturbing in their nature that it is very hard for anyone who has not experienced it to understand it through reflection on their own psyches. There is also an element of danger perceived to be attributable to schizophrenic people due to unpredictable and misdirected but energetic activity they are capable of, which other people including clinicians want to defend themselves from.

This is not the case with Parkinson's patients who are typically aged and have impaired movement indicating frailty and are not perceived as a threat because they are not strong.

With Parkinson's patients medics can afford to get straight to the issue of improving their situation but with schizophrenics there is the overriding priority of taming their dementia so they are not a danger to themselves or to others which dominates the way they are perceived and treated.

Also because Parkinson's primarily affects movement directly, it is readily perceived as pertaining to the body and control of movement rather than cognition.

With schizophrenia, delusions about the perceived world and consequent incomprehensible behaviour are the primary symptoms, so schizophrenia patients are conceived of has having an illness of cognition, meaning an illness of mind.

IMHO the way we model the mind is instinctively distinct from the way we understand the body because of the way our own brains are arranged which is in turn due to the way they evolved. Which is not exactly the reptile mind so much as the cauliflower mind, in that social awareness must have evolved as an extension of existing behaviour controlling neurological structures, akin to a floret on a metaphysical stalk i.e. distal from the core of our behaviour. Contemplation of mind also retains a distal characteristic because of the importance of physical self awareness and coordination of behaviour to human survival, meaning that physical behaviour has remained the top priority for human cognition and so ruminating on theories of mind is subordinate to the necessity for action because it takes too long in the middle of a fight and this is another reason the theory of mind is compartmentalised in a place apart from the control of the physical body. When adrenalin kicks in and so called fight or flight behaviour dominates, theories of mind are simplified down to enemy or ally so they can be processed expeditiously and reaction times improved. Schizophrenics tend to be seen as enemies because they invoke fear, whereas it is much easier to see a Parkinson's patient as an ally in need of help.

That is because of how we are as human beings and what others' distempers do to us at a cognitive level. So I feel the point I am trying to make is that mind body dualism is not something which will go away, though deep rumination can see inconsistencies in the way it affects our thinking and see through it, that is dependant on peaceful conditions around the thinker permitting such contemplations. Which is why cloistered monasteries developed, later becoming universities as this is the kind of protected environment we need to develope academically. Which is why I believe body mind dualism is intrinsic to the human psyche and can only be reconciled by accepting it as a permanent fixture and handling the conditions we create for ourselves appropriately in that context. If you see what I mean

 

It isn't very clear but if they think she has lupus presumably she has a positive ANA test - which I would have thought was routine as a baseline investigation for a young woman with psychosis.

The more I look at this the more it seems to be an indication of just how backward medicine is. As people have pointed out, picking up cerebral lupus in a patient with psychosis was something expected to be standard in the 19890s. absolutely nothing new. Moreover, it looks as if the 'clever' physician who picked up the problem has completely failed to understand what long term management was needed. They are still working with the treatment of forty years ago. She needed regular B cell monitoring and a regular schedule for retreatment with rituximab from the outset, but clearly the medical team have no clue.

 

The article is quite confusing. I can’t work out what the proposed diagnosis is. Why would it take 70 doctors to diagnose SLE? Then they inform us that the antibodies are actually against glutamate receptors so I’m assuming they’re referring to anti-NMDAR encephalitis. Then we’re told that there are no clinical signs of SLE other than brain involvement which I’m inferring to mean ANA was positive (routine bloodwork) but I assume this was dismissed as an incidental finding in 1990s since there were no other signs of SLE. In 1995 when this was happening the NMDA receptor antibodies hadn’t been discovered yet which would explain why the diagnosis and care she received was so poor. Nonetheless, I’m not sure why they are bringing SLE into it. ANA antibodies are common in this form of autoimmune encephalitis. A recent study suggested 28% had them.