Hi Andreas,
thank you for your suggestions.
We have tried to overcome the problem of dehydration by scanning patients
that were not in acute starvation/dehydration. Only few patients were
admitted in hospital at the time of scanning and they have been scanned
after reydration. And few (2 or 3 in a group of 29) used vomiting to
control weight. No patients used laxatives or diuretics. All the other
patients were on outpatient treatment and their weight was stable or
increasing at the time of scanning. We found no correlation with present
weight/BMI and connectivity in this brain area. ON the contrary we found a
correlation with total weight loss and with some measures of cognitive
functioning (visuo-spatial abilities).
However, we will look at bioimpedenziometry data (that measures body
water) and electrolytes and we will check this point.
thank you again and let me know if you have any other idea

Cheers
Angela



> Hi,
>
>>and is usually reversible
> than it's no atrophy but 'pseudoatrophy', no?
> Did you control for hydration status using serum electrolytes and ADH
> levels, for example? AN patients often do not only starve but may engage
> in thristing or 'intoxicate' themselves with water (to feel less hungry
> and to weight more at the therapeutic weight check). When they purge using
> laxatives or vomiting, they may nevertheless dehydrate. It is an extremly
> hard population to deal with, even at the scientific level;), because
> their physiology is so deranged.
> Now - part of the pseudoatrophy may simply be loss of water. Usually that
> prevails (only very young AN patients tend to starve on food and fluid
> intake) and it may explain reversibility. Short term volume changes in the
> magnitude of 0.5-1% have been documented due to de/rehydration using SIENA
> (http://www.ncbi.nlm.nih.gov/pubmed?term=duning%20dehydration%20neurology).
> If the neurons are 'closer' to each other due to dehydration, you may
> expect an artificial increase in functional activations.
> Ok, very over-simplicistic explanation. It's just unpredictable. In
> essence, I argue that you must control for de-/rehydration for being able
> to interprete your data.
> Cheers,
> Andreas
> ________________________________________
> Von: FSL - FMRIB's Software Library [[log in to unmask]] im Auftrag von
> Angela Favaro [[log in to unmask]]
> Gesendet: Montag, 28. Februar 2011 15:33
> An: [log in to unmask]
> Betreff: Re: [FSL] relationship between resting state and brain atrophy
>
> Hi Stijn,
>
> I will carefully read your paper. In the meantime, a quick answer to your
> questions.
> My data about brain atrophy are corrected for age, education, handedness
> and ICV. All subjects are female. GM is decreased because of prolonged and
> severe undernutrition in AN and is usually reversible. So I think it is a
> bit different situation from aging.
> I am studying connectivity using resting state fMRI and I have used ICA
> and dual regression.
> My question is if there are other situations where an increase in
> connectivity (functional not structural) is present in atrophic areas of
> the brain.
>
> AN and control groups differed significantly on this and the connectivity
> of the AN group significantly correlates (on a voxel basis) with the total
> amount of weight loss (a negative correlation!). A similar correlation is
> present in healthy subject, but it is unsignificant at cluster-based
> correction.
> Thank you for your interest and let me know what you think about it
>
> Angela
>
>
>> Hi Angela,
>>
>> Interesting to have a topic on interpretation of results. It's always
>> good
>> to share some knowledge and discuss. I did some research on healthy
>> brain
>> aging.
>>
>> Your analysis is on gray matter in various area's as you state. First
>> you
>> notice a significant loss of gray matter in the patient group, which is
>> interesting. Are you sure about matching your groups on age, gender,
>> handedness, education, IQ and such? Variables may influence your
>> results.
>> Another question is on normalizing your results. Different subjects have
>> different intra-cranial volume (ICV). To make sure you compare
>> correctly,
>> you should normalize the specific areas to the ICV.
>> It is known that gray matter volume decreases in healthy aging (and
>> cerebrospinal fluid increases). Different structures in the brain age
>> differently. There is a theory based on the frontal-occipital way of
>> aging
>> where the frontal part ages quicker than the occipital part. Consider
>> checking my paper on healthy aging:
>> http://www.ncbi.nlm.nih.gov/pubmed/20483378
>>
>> How do you define the connectivity in the GM areas you investigated?
>> Usually connectivity (like FA, MD, ADC) is investigated in white matter.
>> In this respect I can't say what's right. Your finding might be a
>> compensation mechanism of the brain, getting less matter but 'better'
>> connections. If you assume that the increase of connectivity is
>> presented
>> because of the atrophy, you might check for a relation with illness
>> duration/age of onset/severity. A hypothesis like "A longer the illness
>> duration makes an increase of connectivity" can be used. And is the
>> increase in connectivity significant between your two groups?
>>
>> Let me know what you think!
>>
>> Kind regards,
>>
>> Stijn Michielse
>> Research Assistant
>> Dept. Psychiatry and Neuropsychology
>> Maastricht University
>> E-mail: [log in to unmask]
>>
>> ------------------------------------------------------------------------------------------
>> Hi FSL masters,
>> I (again) need some advice on analyses/interpretation of my data.
>> I am analysing a sample of patients with atrophy of GM in various brain
>> areas due to malnutrition and weight loss (it is a sample of anorexia
>> nervosa subjects). I have used ICA and dual regression to identify
>> networks and analyse differences between patients and controls.
>>
>> I have found an increase in connectivity in areas that (on a voxel based
>> morphometry) have a significant loss of GM.
>> Is this a contradictory finding? Is it possible to observe an increase
>> of
>> connectivity as a 'compensation' of brain atrophy? Or may I consider
>> this
>> finding as an increase of connectivity due to the psychiatric illness
>> observable despite atrophy?
>> It is not easy to disentangle the effects of weight loss, brain atrophy
>> and what is due to (or at the origin of) the psychiatric disorder
>>
>> I know that interpretation is up to me (and my clinical data), but I am
>> wondering if something similar has been observed in other patients
>> populations with brain atrophy.
>>
>> thank you for any help!
>>
>> Angela
>>
>> Angela Favaro, MD, PhD, MSc
>> Psychiatric Clinic
>> Department of Neurosciences
>> via Giustiniani 3
>> 35128 Padova
>> Italy
>>
>>
>