Brain Shrinkage in M.S.
 

What role does brain shrinkage play in someone dx with M.S.?

Our brains naturally shrink as we age, but does it occur at an accelerated rate with M.S patients?

How does it accelerate with the different forms of M.S.?
RR
SP
PP

Just curious on what others' thoughts are regarding this issue with it's implications with M.S. patients.

:circlelove: Katherine in Oregon

What BRAIN shrinkage???
 

On my last MRI the radiologist wrote "Some moderate brain shrinkage is noted but appropriate for medical condition and age."

You be the Judge.....

jackD
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.http://home.ix.netcom.com/~jdalton/pic049.JPG

jackD, thanks for the chuckle. I needed that! :)

LOL, Jack!!:D

To answer your question...I don't know:confused:

I've had some brain atrophy...not sure what's "normal" for MS patients...I do know it's due to nerve cell death...

I don't know but it sounds like a good excuse for some of the cog fog I have! :D

The normal brain shrinkage that occurs with everyone is accelerated with MS. It has nothing with nerve cell death. Jack, you da man.:D

I must say that I do think that the nerve death is related to the increased loss in volume of the brain because the area of the brain that shows up in a MRI as "enhancing" is REAL inflammation (dying tissue) after which comes the formation of scar tissue which occupies a smaller volume.

Given the number of "enhancing lesions" I had I am very lucky that my brain does not look like a "raisin" in size and shape. I am very glad I have at least a prune size brain.


jackD

Brain atrophy associated with cognitive impairment
 

The main problem associated with Brain atrophy is cognitive impairment.

jackD


Arch Neurol. 2009 Sep;66(9):1144-50.

Cortical lesions and atrophy associated with cognitive impairment in relapsing-remitting multiple sclerosis.

Calabrese M, Agosta F, Rinaldi F, Mattisi I, Grossi P, Favaretto A, Atzori M, Bernardi V, Barachino L, Rinaldi L, Perini P, Gallo P, Filippi M.

Multiple Sclerosis Centre of Veneto Region, First Neurology Clinic, Department of Neurosciences, University Hospital of Padua.

Abstract
BACKGROUND: Neuropsychological deficits in patients with multiple sclerosis (MS) have been shown to be associated with the major pathological substrates of the disease, ie, inflammatory demyelination and neurodegeneration. Double inversion recovery sequences allow cortical lesions (CLs) to be detected in the brain of patients with MS. Modern postprocessing techniques allow cortical atrophy to be assessed reliably.

OBJECTIVE: To investigate the contribution of cortical gray matter lesions and tissue loss to cognitive impairment in patients with relapsing-remitting MS. DESIGN: Cross-sectional survey.

SETTING: Referral, hospital-based MS clinic. Patients Seventy patients with relapsing-remitting MS. MAIN OUTCOME MEASURES: Neuropsychological performance was tested using the Rao Brief Repeatable Battery of Neuropsychological Tests, version A. Patients who scored 2 SDs below the mean normative values on at least 1 test of the Rao Brief Repeatable Battery of Neuropsychological Tests, version A, were considered to be cognitively impaired.

A composite cognitive score (the cognitive impairment index) was computed. T2 hyperintense white matter lesion volume, contrast-enhancing lesion number, CL number and volume, normalized brain volume, and normalized neocortical gray matter volume were also assessed.

RESULTS: Twenty-four patients with relapsing-remitting MS (34.3%) were classified as cognitively impaired. T2 hyperintense white matter lesion volume and contrast-enhancing lesion number were not different between cognitively impaired and cognitively unimpaired patients.

Cognitively impaired patients had a higher CL number (P = .01) and volume (P < .001) and decreased normalized brain volume (P = .02) and normalized neocortical gray matter volume (P = .002) when compared with cognitively unimpaired patients.

Multivariate analysis revealed that age (beta = 0.228; P = .02), CL volume (beta = 0.452; P < .001), and normalized neocortical gray matter volume (beta = 0.349; P < .001) were independent predictors of the cognitive impairment index (r(2) = 0.55; F = 23.903; P < .001).

CONCLUSION: The burden of CLs and tissue loss are among the major structural changes associated with cognitive impairment in relapsing-remitting MS.

PMID: 19752305 [PubMed - indexed for MEDLINE]
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Neurology. 2004 Jul 13;63(1):89-93.

Neocortical volume decrease in relapsing-remitting MS patients with mild cognitive impairment.

Amato MP, Bartolozzi ML, Zipoli V, Portaccio E, Mortilla M, Guidi L, Siracusa G, Sorbi S, Federico A, De Stefano N.

Department of Neurology, University of Florence, Viale Morgagni, 85-50134 Florence, Italy. mariapia.amato@unifi.it

Abstract
OBJECTIVE: To assess neocortical changes and their relevance to cognitive impairment in early relapsing-remitting (RR) multiple sclerosis (MS).

METHODS: Conventional MR was acquired in 41 patients with RR MS and 16 demographically matched normal control subjects (NCs). An automated analysis tool was used with conventional T1-weighted MRI to obtain measures of cortical brain volumes normalized for head size. Neuropsychological performance of MS patients was assessed using the Rao Brief Repeatable Battery. Relationship between volumetric MR measures and neuropsychological scores was assessed.

RESULTS: Neuropsychological assessment allowed for the identification of 18 cognitively preserved (MS-cp) and 23 cognitively impaired (MS-ci) MS patients. The whole MS sample showed lower values of normalized cortical volumes (NCVs) than did the NC group (p = 0.01). Upon grouping of MS patients according to cognitive performance, NCV values were lower (p = 0.02) in MS-ci patients than in both MS-cp patients and NCs. Moreover, there were positive correlations between NCV values and measures of verbal memory (r = 0.51, p = 0.02), verbal fluency (r = 0.51, p = 0.01), and attention/concentration (r = 0.65, p < 0.001) in MS-ci patients. Furthermore, NCV values were decreased in patients who scored lower on a greater number of tests (r = -0.58, p < 0.01) in the MS-ci group. None of the neuropsychological measures correlated to NCV values in the MS-cp patient group.

CONCLUSIONS: Cortical atrophy was found only in cognitively impaired patients and was significantly correlated with a poorer performance on tests of verbal memory, attention/concentration, and verbal fluency. Gray matter pathology may contribute to the development of cognitive impairment in MS from the earliest stages of the disease.
PMID: 15249616 [PubMed - indexed for MEDLINE]

I know that when my neuro first looked at the MRI that the former neuro had dxd me based on what he saw, he pointed out some atrophy, said to his assistant, "This is very typical in a brain with MS". Called it some high-falooting thingie and went on...but my heart kind of sank inside...

Early treatment helps
 

There is hope-- early Interferon treatmant may lower the brain atrophy and resulting increased disability.

jackD


Eur J Neurol. 2002 Nov;9(6):645-55.

A 6-year clinical and MRI follow-up study of patients with relapsing-remitting multiple sclerosis treated with Interferon-beta.

Paolillo A, Pozzilli C, Giugni E, Tomassini V, Gasperini C, Fiorelli M, Mainero C, Horsfield M, Galgani S, Bastianello S, Buttinelli C.

Department of Neurological Sciences, University of Rome 'La Sapienza', Viale dell'Università 30, 00185 Rome, Italy.

Abstract
There are few long-term clinical and magnetic resonance imaging (MRI) data on patients treated with interferon-beta (IFN-beta) for relapsing-remitting multiple sclerosis (RRMS).

The aim of this study was to provide clinical and MRI data on 68 patients with RRMS treated over a 6-year period and to investigate whether a baseline MRI predicts their long-term clinical and MRI outcome.

Six MRI scans were performed monthly before treatment and a further 13 scans were performed during treatment with IFN-beta, the last of which 6 years after commencement of treatment.

The relapse rate, disability as measured by the Expanded Disability Status Scale (EDSS), and MRI parameters, including Gd-enhancing lesion load (Gd-LL), T2 hyperintense lesion load (T2-LL) T1 hypointense lesion load (T1-LL) and supratentorial brain volume (SBV) were measured throughout the study.

The mean annual relapse rate over the 6 years was 0.52 (SD 0.67), which is significantly lower (68.6%) than the mean annual relapse rate of 1.6 observed during the 2-year period before the commencement of treatment (P < 0.01).

The median EDSS score increased from 2 to 2.5, remaining stable in 60% of the patients.

From the baseline scan to the final scan, there was a median increase of 7% in the T2-LL and 23.9% in the T1-LL, whilst SBV decreased by 2.7%. The increase in the EDSS over the course of the study was significantly correlated with a reduction in brain volume (r = 0.46, P = 0.001).

Greater brain damage at baseline, as measured by both T2-LL and T1-LL, was significantly associated with an increase in disability over the 6 years (r = 0.44, P = 0.0009; r = 0.50, P = 0.0007, respectively).

This study shows a sustained effect of IFN-beta on the relapse rate, which is lower than during the 2 years before treatment commencement.

More than half the patients showed an improvement or stabilization in the EDSS score.

The increment in disability was correlated with the development of brain atrophy but not with increases in lesion burden.

Finally, the finding that the extent of lesion burden at the baseline was a strong predictor of increasing disability suggests that IFN-beta treatment might have a moderate effect in modifying the multiple sclerosis (MS) disease course over 6 years unless preventive treatment is started early.PMID: 12453081 [PubMed - indexed for MEDLINE]

Brain shrinkage is not that the outer size of the brain gets less, it is the chambers in the center of the brain get larger, so the brain does get smaller from the inside. It is normal with aging, just accelerated with MS. Lesions, black holes, etc. are something else. But, since there is really nothing you can do about it, why worry?