Re: Dura - brain SPECT, CFS- ERIC

[Guest guest]

--- In infections , " Hodologica "

<usenethod@y...> wrote [iN PART]:

> Have you seen Fallons chronic lyme SPECT study - I believe the one

I'm

> thinking of is the one copied below. I dont know the first thing

about

> the tech or the abnormalities; I only paid attention to the nice

low p

> value Fallon derived, presumably from some sort of matrix of the

SPECT

> signal intensities at various sites in the brain.

YES, THIS IS A DESCRIPTIVE PAPER -- JUST NOTING THE VARIOUS SIGNS

AND SYMPTOMS IN NEURO/PSYCH Bb. AS FALLON HIMSELF SUGGESTS, SPECT

IS GOOD FOR FOLLOWING TREATMENT PROGRESSION AS ABNORMAL SPECTS

GENERALLY NORMALIZE AS TREATMENT WORKS. SPECT IS NOT A GOOD

DIFFERENTIAL DIAGNOSTIC TOOL HOWEVER -- AGAIN, CANNOT DISCRIM AMONG

CHANGES SEEN IN Bb, VASCULITIS, LUPUS, ETC. ALSO, THIS IS WHY I

OBJECT TO DR'S GETTING SPECTS DONE ON THEIR PATIENTS AND

SAYING " VOILA! YOU HAVE LYME! " THE BEST YOU CAN DO IS SAY THAT

WITH THE CLINICAL OBSERVATIONS, TEST DATA, AND SPECT INFO, THE DATA

ARE CONVERGING ON THE DIAGNOSIS OF LYME. THE PATTERN SEEN

IN " TYPICAL NEURO LYME " IS NOT DIAGNOSTIC.

>

> What do depression-ologists of the CBT persuasion think of the

SPECT

> results in that disease and other primary psych dx's? Do they have

> hold of anything hefty to back the hypothesis of such changes being

> produced in the brain by the mind, or do they rather dispute the

> consistency of the findings in the first place?

BY cbt I ASSUME YOU MEAN COGNITIVE BEHAVIORAL THERAPY? FIRST, ERIC,

LET ME CLARIFY, I am not A CLINICIAN! MY PHD IS IN THE RESEARCH END

OF THINGS. HOWEVER, FROM THAT PERSPECTIVE I CAN TELL YOU THAT THERE

ARE STUDIES LOOKING AT THE NEURO RAMIFICATIONS OF THERAPY IN GENERAL

(I DON'T KNOW THE CBT THERAPY STUFF SPECIFICALLY). IN SHORT, YOU

CAN FIND MEASURABLE NEURO DIFFERENCES (NOT NECESSARILY IMAGING DIFFS

HOWEVER) BEFORE AND AFTER THERAPY. THESE RESULTS ARE NOT CONSISTENT

AND THE PRIMARY DIAGNOSIS IS IMPORTANT.

What about the atrophy

> of the hippocampus in depression, is that noncontroversial?

DATA RE: HIPPOCAMPAL ATROPHY IN DEPRESSION IS VARIABLE. HIPPOCAMPAL

ATROPHY WITH STRESS AND PARTICULARLY IN PTSD PATIENTS IN PRETTY

SOLID. THE DEPRESSION/HIPPOCAMPUS DATA THUS FAR ARE MUDDIED BECAUSE

NOT ALL CONTROL FOR AGING (AFFECTS HIPPOCAMPAL VOLUME) OR CO-

EXISTING LONG TERM STRESS/PTSD DIAGNOSIS. I SUSPECT IT IS THE

STRESS/AGE FACTORS THAT ARE RESPONSIBLE FOR ANY CORRELATION BETWEEN

DEPRESSION AND AGING. HIPPOCAMPUS/MEMORY STUFF IS MY PRIMARY AREA

OF EXPERTISE.

>

> Is the question of demonstrating patient benefit from CBT as

fraught

> as I think it is - without actually reading anything, I'll admit? I

> mean, doesnt it seem like CBT could change ones response to

questions

> used to quantify depression, and even change clinical signs such as

> posture and eye contact, without changing ones actual experience?

Do

> any studies purport to show brain changes by imaging as an

objective

> index of the payoff of CBT? If brain changes after CBT cannot be

> demonstrated, is that percieved as slightly embarrassing by those

who

> hold CBT to be effective?

SEE ANSWER ABOVE. BRAIN CHANGES (E.G., NEUROTRANSMITTER LEVELS,

NEURONAL DNA CHANGES, SOME IMAGING STUDIES) SHOW PRE/POST TREATMENT

CHANGES. NEED TO CONSULT LIT. FOR SPECIFICS ON CBT IN PARTICULAR.

>

> What about a disorder like PTSD which presumably is generally

accepted

> as being caused by experience rather than, say, infection - I

think it

> is associated with increased urinary catecholamine levels by at

least

> some studies... any brain imaging abnormalities in that disease?

LOTS OF DATA HERE. THIS IS WHERE THE HIPPOCAMPAL ATROPHY DATA COME

IN -- MRI, PET, fMRI. NOW WHAT IS UNCLEAR IS WHETHER THE

HIPPOCAMPUS ATROPHIES IN RESPONSE TO STRESS-RELATED CHANGES (E.G.,

CORTISOL HOMEOSTATIC CHANGES) OR WHETHER THOSE WITH HIPPOCAMPAL

ATROPHY ARE MORE LIKELY TO GET PTSD. ALAS, NO VOLUNTEERS TO GET

HIPPOCAMPAL ATROPHY AND THEN STRESS THEM VS. SHAM ATROPHY GROUP!