Brain shrinkage

Müller M, Esser R, Kötter K, Voss J, Müller A, Stellmes P.Third ventricular enlargement in early stages of multiple sclerosis is a predictor of motor and neuropsychological deficits: a cross-sectional study. BMJ Open. 2013 Sep 10;3(9):e003582. doi: 10.1136/bmjopen-2013-003582.

OBJECTIVES:Whether transcranal sonography (TCS) depicted third ventricular enlargement as a sign of brain atrophy is predictive for neuropsychological deficits in mildly affected patients with multiple sclerosis (MS).
PARTICIPANTS: Fifty-four patients with MS (16 men, 38 women, mean age 40±10 years, mean disease duration 6±5 years; mean Expanded Disability Status Scale 2±1.3) and 33 healthy controls (12 men, 21 women; 38±11 years) underwent clinical examination, an assessment of the third ventricle width by means of TCS and the Brief Repeatable Battery of Neuropsychological tests for MS, the 25-Feet Foot Walk test, the 9-Hole PEG test, the Beck Depression Inventory and a quantitative fatigue assessment. Statistical analysis was performed with univariate correlation and thereafter by stepwise regression analysis.
RESULTS: Patients’ mean third ventricular width (3.9±1.6 mm) was significantly wider compared to controls (3.4±0.8 mm). MS duration, third ventricle width and quantitative fatigue assessment as baseline variables, an increasing third ventricle width significantly correlated with the target variables worsening of motor deficits (p<0.002), worsening of verbal recall (p<0.04) and of visual spatial recall (p<0.005). Severity of depression and of fatigue was unrelated to third ventricular width.
CONCLUSIONS: In this cohort of patients with MS with mild disease, third ventricular enlargement was indicative for motor deficits and cognitive impairment, even after considering fatigue as a relevant comorbidity. Third ventricular enlargement by means of TCS seems to be a useful, clinically meaningful parameter to stage patients’ disease severity. Follow-up studies must show whether an intra individual future third ventricular increase indeed signals larger cognitive impairment.
The brain ventricles are fluid filled sinues that appear to enlarge as the surrounding tissue shrinks. This enlargement is associated with worse brain functions, future work need to determine how predictive this will be loss of brain function

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  • Prof G

    I read your post regarding Laquinimod and wonder if you can help me understand some basics.

    If Laquinimod has a neuroprotective capability. Shouldn't laquinimod be a standard treatment for RRMS'ers? Since RRMS'ers end up as SPMS'ers it's difficult for me to understand why not use Laquinimod as a first line treatment?

    I guess the likelyhood to delay the disease must be better the earlier Laquinimod is administered ( if it delays brain-atrophy and delay EDSS progression )

    Can you please comment? Maybe I miss something?

  • Perfect logic…but is it business sense. This is where TEVA is

    For RRMSer the target was to effect relapses, once your drug fails to affect relapses it fails. This is because if you do a trial you have to say what it is going to work on before you start. This is to stop companies cherry picking postivie sound bites from otherwise failed studies

    Would they need more trials to do atrophy as the target I suspect so. But I agree start protecting nerves ASAP.

    But as lacquinimod is not affecting relapse that much why not put in on top of a drug that does.

    • So would this cover my question of a few days ago to the blog 'is laquinimod the new wonder drug that progressive….'ie that NICE could refuse the use of laquinimod for RRMSers as it is n't very good re relapses even though it seems quite an effective neuroprotectant.

    • That would not be very wise of NICE in case Laquinimod provides real neuroprotection. NICE should in that case choose Laquinimod as the preferred DMT or at least in a combination with other DMT's as Gilenya in cases with more frequent relapses.

      If it will be possible to alter the course of the disease ( in my view i.e to stop or slow down brain atrophy ) that would be a true revolution in the treatment paradigm.

      What do you say?

  • It's always the third ventricle that we hear about but I don't understand what makes the third ventricle different than the other ventricles. Wouldn't atrophy show enlargement of all the ventricles equally?

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