Are black holes associated with neurological issues other than MS?

Here is My Question:
Hi, I was diagnosed with MS in 2018. I had a negative spinal tap so it was a long road of ruling out other possibilities. About every 3-4 months I ended up having a hug episode of denial were I have to do a bunch of research and review my MRIs over and over and try to explain away my symptoms. It is excruciating. I finally told my neuro the other day and she is going to test me for MOG as one last rule out. After looking into it, I read that it is mostly associated with optic neuritis and transverse myelitis but I’ve had neither.

I do have 2 spinal cord lesions and several periventricular lesions, cortical lesions, and lesions in and around the corpus callosum. No intratentorial lesions or cerebellar lesions. I don’t have mobility issues so I think that’s my biggest thing. I also don’t have the usual relapses or suddenly having to go to the hospital and have never had enhancing lesions. I also have black holes on T1 for pretty much all of my brain lesions. I have some mild atrophy too. I have cognitive issues causing me to be on disability and a terrible MS hug pain unless I take trileptal. I have mild nystagmus and a significant tremor. I also have some occasional incontinence. Very bad cold intolerance. And other things. My MS specialist says mine is mold and definitely not primary progressive.

Anyway, what would the differentials for those findings be? Are black holes associated with other neurological issues? Are black holes and white matter lesions like this ever a normal finding? Have you ever seen people not have usual relapses but just have accumulating slow progression in symptoms and no walking issues? Have you ever had an MS patient never have enhancing lesions or optic neuritis?

I’m just looking for differentials to consider if any to discuss with my doctor and wondering if these are ever “normal” to see on an MRI.

P.S. I’m a Nurse Practitioner

Answer:
You raise some very good questions about MS diagnostic criteria. Let me touch on a couple of points and show you where many physicians make mistakes in the interpretation of diagnostic data.

1. The concept of "black holes" emerged as a description of an MRI lesion appearance observed in some MS patients using a 2D (2-dimensional) spin-echo sequence. This was a common imaging sequence used for years on all MRI scanners with imaging usually done before and after the administration of contrast (gadolinium). Several years later it was discovered that if an MS lesion appeared persistently (> 6 months) black on this sequence, the area showed evidence of persistent scaring and tissue destruction when looked at under a microscope. More recently 2D spin-echo sequences have been supplanted by 3D gradient echo images which provide improved tissue resolution with faster imaging time (translation: the radiologists can scan more people and make more money ). Unfortunately, many if not all MS lesions tend to look black on the newer 3D gradient echo images, even though this "black" appearance does not necessarily indicate permanent tissue damage. Many neurologists and radiologists do not understand this problem and refer to these lesions as "black holes", which is clearly a misuse of the term. If you look at your MRI scans or the report, they should list the T1 imaging sequence used. If it is one of the 3D T1 gradient echo images, the two most common are called SPGR and MPRAGE. 
2. Spinal fluid does not have to be abnormal or show the presence of oligoclonal bands for a diagnosis of MS. If this was the case, everyone would have their spinal fluid analyzed to make a diagnosis of MS. In fact, a study in 2017 suggested that spinal fluid oligoclonal bands are mostly observed in people with MS who display Type I pathology, whereas those with Type II or III pathology more commonly do not have CSF oligoclonal bands. The pathology type refers to different mechanisms of injury observed on microscopic analysis of MS brain tissue.
3. lastly, typical MS appearing lesions in the spinal cord, especially when multiple, tend to be very specific for MS when other diagnostic possibilities are eliminated.

Remember, it is generally a good thing not to have typical relapses and typical disease progression with MS. Many patients with more subtle "silent" symptoms do very well over time with a remarkably benign course.

I hope this information helps.

Revere (Rip) Kinkel MD
Director of the Multiple Sclerosis Program
Professor of Clinical Neurosciences
University of California San Diego