Hi and welcome,
Unfortunately google searches will just about always bring up MS, CC lesions are most definitely associated with MS but there are many other causes including congenital and birth so it is quite possible the isolated T2 hyper intense lesion in the callosal septal interface that showed up on your brain MRI is something that's always been there.
Without anything else to go by i'd have to assume the lesion is more consistent-suggestive of prenatal development or birth than what is typical when MS is the causation....
"The callososeptal interface is located on the inferior surface of the corpus callosum, where the septum pellucidum abuts it.
It came to radiological attention when T2 hyperintense lesions affecting this region were believed to be specific for multiple sclerosis. This has, as is usually the case, been shown not to be quite as cut and dry, with ischemic lesions also potentially affecting this region 1."
"Lesions of the corpus callosum are uncommon and arise from multiple different etiologies. The lesions can be classified according to underlying pathophysiology 4-6.
agenesis of the corpus callosum
enlarged perivascular spaces
tubonodular pericallosal lipoma: associated with dysgenesis of the corpus callosum
acute disseminated encephalomyelitis
Marchiafava-Bignami disease: demyelination and necrosis, can appear as cystic lesions
progressive multifocal leukoencephalopathy
aspergillosis: can involve corpus callosum 7
transient lesions of the splenium: many underlying etiologies including infectious agents
subacute sclerosing panencephalitis: can involve the corpus callosum in advanced stages 8
tuberculosis: callosal tuberculomas have been reported, although rare 9......."
"The corpus callosum (CC) is the largest white matter structure in the brain, consisting of more than 200–250 million axons that provide a large connection mainly between homologous cerebral cortical areas in mirror image sites. The posterior end of the CC is the thickest part, which is called the splenium.
Various diseases including congenital to acquired lesions including congenital anomalies, traumatic lesions, ischemic diseases, tumors, metabolic, toxic, degenerative, and demyelinating diseases, can involve the splenium of the CC and their clinical symptoms and signs are also variable. Therefore, knowledge of the disease entities and the imaging findings of lesions involving the splenium is valuable in clinical practice. MR imaging is useful for the detection and differential diagnosis of splenial lesions of the CC. In this study, we classify the disease entities and describe imaging findings of lesions involving the splenium of the CC based on our experiences and a review of the literature."
"The corpus callosum is a midline cerebral structure and has a unique embryological development pattern. In this article, we describe the pathophysiology and present imaging findings of various typical/atypical conditions affecting the corpus callosum. Since many of these pathologies have characteristic appearances on magnetic resonance imaging (MRI) and their therapeutic approaches are poles apart, ranging from medical to surgical, the neuroradiologist should be well aware of them.
The corpus callosum is the largest commissure consisting of tightly packed white matter tracts connecting the two cerebral hemispheres. It comprises of four parts (from anterior to posterior): (i) rostrum, (ii) genu, (iii) body, and (iv) splenium.
Various pathologies that can affect the corpus callosum and their characteristic appearances on magnetic resonance imaging (MRI) are illustrated in this pictorial essay. Pathologies of the corpus callosum result in typical symptoms of interhemispheric discoordination.
The etiological spectrum ranges from congenital, demyelinating, inflammatory, trauma to neoplasm and ischemia. Callosal abnormalities developing after ventricular decompression fall under miscellaneous conditions, which have characteristic imaging findings.
After the formation of the massa commisuralis around the 10th week of gestation, the first callosal fibers begin to form. The formation is primarily anterior to posterior, beginning with the genu at 12th week. The rostrum is an exception, as it develops last at 18-20 weeks."
Q: "Also has anyone had a high total protein and elevated SED rate while going through their diagnosis? Possibly a positive ANA? I have both but all other lupus type tests are negative."
A: These are very common blood tests that have no known association with a neurological condition like MS, below is an article that discusses the diagnostic connects see table 1 Conditions Associated With a Change in CRP and ESR to give you some direction.
I hope this helps..............JJ