Hi - I have just got the results of a MRI scan and I was wondering if anyone could help me interpret them. I will be seeing my GP to find out more info, however, I usually don't think of what to ask when I am there because I have not considered all the information beforehand, so that is why I am posting this question.
A brief bit of history about me that may be relevant…. I am a 45 yo woman and am relatively healthy (Crohn’s disease, Osteopenia and overweight). I had the tests done so as to see if there was any indication of brain damaging causing reduced executive function and/or attention deficit disorder. As a child I had severe dyslexia, did not speak till I was 4 and few people could understand me till I was 8. I had very poor coordination and used to fall over a lot. Once I reached about 8 years of age I went to boarding school which took me away from a very abusive family situation. Once at boarding school my problems went away – my speech and movement were normal and my dyslexia became quite mild. Recently I have been finding it more difficult than normal to do the more complex organisational tasks. The difficulty is relatively mild – I still work as a senior policy officer in a government department, but am finding it harder to do my work than I used to.
I would greatly appreciate it if anyone could review the MRI results below and let me know if they have any relevance to the questions below.
Thank you for any information you are able to provide.
The questions I have about my results are:
1. Is this anything I should worry about?
2. Could this be responsible for causing reduced executive function?
3. Could this be an indication of Attention Deficit Disorder?
4. Could this be an indication of brain damage causing my early coordination/speech problems?
5. What happens within the subcortical white matter and pons?
In the body of the report it mentioned the following:
On FLAIR weighted imaging, there are several small foci of T2 hyperintensity within the periventricular white matter in keeping with very mild chronic small vessel ischaemic change. These tow foci are essentially located within the left frontal lobe.
On gradient echo there is a focus of haemosiderin deposition within the subcortical white matter of the right frontal lobe. This area of haemosiderin measures 8mm. There is a further focus of haemosiderin deposition measuring 1-2mm within the subcortical white matter of the right frontal lobe anteriorly and within the pons. There is possibly a smaller focus of haemosiderin deposition within the right parietal lobe anteriorly.
No hydrocephalus is seen. No abnormal vasogenic oedema is demonstrated. Incidental septum cavum pellucidum et verge is noted.
On sagittal imaging the corpus callosum is intact. The midline structures are otherwise normal. There is a prominent cisterna magna an incidental finding. No Chiari abnormality is seen. The pituitary fossa and clivus are of normal signal.
There is no evidence for restricted diffusion.
Conclusion: There are several small foci of haemosiderin deposition within the subcortical white matter and pons. The most likely differentials for this include incidental multiple cavernomas. Amyloid is felt less likely given the lack of deep white matter/chronic small vessel ischaemic change demonstrated elsewhere.