Results of my daughter's CT scan...

[browneyesmom]

Not the news for which we were hoping (showed some things related to her corpus callosum we have to pursue to learn what they mean), but it could have been worse (NO tumors; praise God!!). Tomorrow, our pediatrician will get us in with pediatric neurologist for next step...

 

The condition can't be resolved with meds or surgically repaired. Her pediatrician told us that when he called. Apparently, some kids do fine with this condition and others do not. There is *some* possibility of misinterpretation of adult vs. pediatric, but I gather it is a slim chance. He also responded to her dad's question that *maybe* she could outgrow this, but I gathered that was also a slim possibility. Her pediatrician says that given her recent challenges, we can't ignore this and have to see a pediatric neurologist.

 

I was so certain the CT results would be negative but now I am glad that I pressed for it... bless this child, she is going through so much! I know whatever happens, we are in God's hands through this trial...

 

I also heard from someone on Swedo's team who told me that hallucinations are not associated with PANDAS. ??? I later wished I told her to read this forum! In any case, she gave me the name of a psychiatrist in Philadelphia who has worked with PANDAS kids and has done IVIG, so I called and left a message for her. She was honored as one of the best MD's in the country in 2007-2008 by her peers. It is an honor that only about 5% in the country receive. I shared this information with her dad & pediatrician.

 

However, her father (my ex) seems to believe that she is willingly causing these challenges; thus does not want me to have her assessed/treated for conditions for which I believe she needs medical care... mainly, he is VERY opposed to having her see a psychiatrist. We share joint custody for such decisions. My ex did, at one point, tell our pediatrician that he is concerned about our daughter seeing a psychiatrist because at one point when we were still married, I asked him to see one and he was diagnosed as being bi-polar. He said that since then, his colleagues (other psychiatrists/counselors) have agreed with the initial diagnosis and he has found it very hard to shake.

 

He emailed me about legalities of us having to agree & he does not (I'll have to go by the courthouse today to get a copy of the document), even after we spoke to her pediatrician about the abnormalities in the scan and wrote that he suspects the issues are behavioral and recommends that I discipline her during her outbursts/episodes, but he does not agree with me taking her to this MD. We are on totally different pages on this. I am hoping that taking her for assessment is out of his hands. Treatment is likely another issue, but by then, if I have MD opinions, it would be harder for him to fight what is in her best interest... I hope. He also tried *again* to get our pediatrician to discontinue her hypoglycemia diet when we were on the phone, but our pediatrician diplomatically refused - twice... God bless that doctor, he is fabulous and we are so fortunate to have him on her side during this!

[kim]

brqwneyesmom,

 

The condition can't be resolved with meds or surgically repaired. Her pediatrician told us that when he called. Apparently, some kids do fine with this condition and others do not.

 

I'm wondering if this remark was in relationship to the findings regarding the corpus callosum or something else?

 

These are a few things that you might want to become familiar with prior to your appointment with the neuro. I would also request a copy of the test results prior to the appt. so you can get a feel for the terms that he will be using and be able to ask specific questions regarding the results.

 

These studies talk about TS with no emphasis on immune function (except possibly the last one with change in myelination). I guess a better place to look might be in regards to changes in corpus callosum relating to autoimmune disease or immune system function?

 

http://www.psychgenetics.com/pt/re/psychge...1?nav=reference

 

Abstract

The aim of this study was to investigate the morphology of the corpus callosum (CC) in Tourette syndrome (TS) and attention deficit hyperactivity disorder (ADHD) to determine whether these conditions affect distinct regional differences.Seventy-seven children and adolescents, aged 6 to 16 years, comprised the four research groups--16 patients with TS, 21 patients with TS plus ADHD, 13 patients with ADHD, and 27 unaffected control subjects. A semiautomated, computer-assisted procedure was used to measure the total area, five subregions, centerline length, perimeter, and bending angle of the CC. MRI data were analyzed using several statistical methods, primarily two-tailed analysis of variance to test the effects of TS and ADHD status, while controlling for the influence of age, gender, and total intracranial area (an estimate of brain size). TS was associated with significant increases in the area of four of five subdivisions, the total area, and the perimeter of the CC. ADHD was associated with a significant decrease in the area of the rostral body. There were no interactions between TS and ADHD factors. These findings suggest that the area of the CC is larger in children with TS, and that this difference is independent of age, handedness, intracranial area, and the diagnosis of ADHD. Our findings support hypotheses that the neurobiologic mechanisms in TS and ADHD involve frontal/subcortical circuits.

 

 

http://www.pubmedcentral.nih.gov/articlere...i?artid=2367151

 

Corpus callosum

The corpus callosum (CC) has been a central focus in studying the biological correlates of TS since the early reports suggesting the presence of abnormal brain lateralization in the disorder. The unilateral character of the initial findings from the basal ganglia—i.e., decreased volumes of the left lenticular nucleus [52] and a loss of the physiological left-greater-than-right asymmetry of the basal ganglia [66]—raised the question of whether individuals with TS would exhibit loss of the normal asymmetric organization of the CNS [75]. In this respect, the CC is a structure of central interest because of the various roles it plays in lateralization of the brain [62]. First, the CC is thought to mirror brain asymmetry and hemispheric specialization [5]. Second, anatomical changes of the CC may represent indirect evidence for alterations in cortical tissue, especially for alterations of the frontal and prefrontal cortical areas, which send widespread, intertwined fibers through the genu and the body of the CC [29].

The first study of the CC in individuals with TS, which included 14 young adults with TS and 14 control subjects, revealed a reduced size of all subregions of the CC in the TS group compared with controls [51]. This study, however, did not include individuals with comorbid ADHD. A second study compared the size of the CC in 16 children with TS, in 21 children with TS-ADHD, in 13 children with ADHD only, and in 21 control children [7]. The group with TS alone had a larger CC on average, whereas the group with comorbid TS-ADHD had an intermediate CC size, and the group with ADHD alone had a reduced CC size. To evaluate the effect of gender on CC size in TS, another study included 10 girls with TS, 9 girls with a comorbid TS-ADHD, and 22 control girls [46]. The absence of differences in CC size across diagnostic groups was interpreted as indicating that differences in the size of the CC in the TS group were restricted to boys. These studies shared the disadvantage of not having realigned midsagittal MR images prior to measuring the CC [59]. The failure to realign midsagittal slices when defining the CC may increase inter-individual differences in measurement of its size, simply because of differences in midline placement of the heads of subjects in the scanner.

The most recent study of CC size [58] examined 158 subjects with TS and 121 controls (5 to 65 years of age) in a cross-sectional design using CCs realigned to true midline. Subjects with TS had smaller overall CCs compared with controls. These reductions in size were found to depend significantly on the age of the subject, with smaller CCs present primarily in children with TS compared with healthy control children and larger CCs primarily in adults with TS compared with healthy adults. The sizes of the CC and its subregions correlated with the severity of motor tics, indicating that a smaller CC may have a protective or compensatory function in subjects with TS. Having a smaller CC could therefore represent a compensatory, plastic response to the presence of tics, similar to the postulated role of the larger prefrontal cortex found in children with TS. Furthermore, CC size correlated inversely with volumes of the prefrontal cortex in both the TS and control groups, although the magnitudes of these inverse correlations were significantly greater in the TS group. This exaggeration presumably represented an adaptive or compensatory process in the brains of individuals with TS, given that smaller CCs and larger prefrontal cortices were both associated with less severe tic symptoms. The putative plastic process that produced a smaller CC may have reduced excitatory input from the CC to the inhibitory GABAergic interneurons in the prefrontal cortex [9, 36]. This postulated reduction in numbers of inhibitory GABAergic interneurons would produce enhanced prefrontal output (because the prefrontal cortex receives less transcallosal inhibition), which in turn may increase the suppression of tics (which are themselves mediated through fronto-striatal connections). Over time, the prefrontal cortex may become hypertrophic because of frequent use, thereby enhancing the prefrontal self-regulatory control in persons with TS. As an alternative explanation, a smaller CC in children with TS may signal a less severe form of TS and produce an outcome with fewer tic symptoms, and hence it could have a protective function in the disorder. A larger CC and smaller prefrontal regions, in contrast, would signal the presence of a more severe form of TS. The positive associations of CC size with tic severity in this study do not support this latter alternative; however, its cross-sectional design prevents definitive support for one or the other of the two hypotheses.

Findings of smaller CCs in subjects with TS have recently been extended to the fiber tracts that compose the CC as measured by Diffusion Tensor Imaging (DTI) in 20 boys with TS (5 boys with a comorbid ADHD) and 20 control boys (aged 10–18 years) [57]. DTI measurements [6] showed that boys with TS had lower Fractional Anisotropy values in all regions of the CC. The degree of anisotropy depends both on the number of fibers and on the thickness of the myelin sheaths that surround nerve fibers [48]. Recent studies document the correlation of the degree of myelination with changes of anisotropy, as measured by DTI during brain maturation in infants and toddlers [27]. Thus, these DTI findings again point to the presence of reduced interhemispheric connectivity in children with TS. A comorbid diagnosis of ADHD did not influence the findings, as shown by excluding all individuals with ADHD (and with OCD) from statistical analyses.

The impetus for examining the CC in TS stemmed from previous reports of reduced structural brain asymmetry of the basal ganglia in patients with TS. The hypothesis of abnormal functional brain lateralization, however, has not been confirmed in subsequent studies or in other reports studying anatomical and functional brain lateralization in TS [41, 54, 55]. Reported findings of morphometric and functional deviations of callosal measures [41, 57, 58] are, however, consistent with findings that implicate prefrontal brain regions in tic suppression in TS [53, 54].

 

bolding mine

http://www.pubmedcentral.nih.gov/articlere...i?artid=1738899

 

Corpus callosum signal intensity in patients with bipolar and unipolar disorder

 

Conclusions: The findings suggest abnormalities in corpus callosum white matter in bipolar but not unipolar patients, possibly because of altered myelination. Such abnormalities could lead to impaired interhemispheric communication in bipolar disorder.

[browneyesmom]

Kim,

 

You are such a dear and I am so beat at this point! Thank you for looking up that information for me! Maybe I should have posted more about this, but to be honest, I am still kind of numb and reeling from the news.

 

I already have a copy of the report; I asked our pediatrician to fax it to me and he did so as soon as we got off the phone. I do know what she has, just didn't think many would be familiar with the condition and am still trying to absorb it and wanting to talk with the pediatric neurologist after he looks at the images, which we are also getting from the hospital today, so we will have all of that before the appointment.

 

She has partial ageneis of the corpus callosum (and some related abnormalities) and I have already researched the potential implications. Some kids do ok with the condition and some do not. I was already familiar with what the corpus callosum does as I am an RN, but I have to be honest, right now, I am a Mom first and my mind is kind of spinning at this point, I am so drained with working with her daily on homework, trying to handle the outburst episodes, researching, keeping MD/counselor/ex/school informed, going to appointments, helping her through her worries about all this, managing my own worry and trying to work with my ex on her needing care, while he thinks it is behavioral and wants to utilize discipline to manage the situation... even after talking with the pediatrician and learning the scan shows abnormalities.

 

I absolutely agree... it's important to be prepared for this appointment. Once I get a bit of rest (hopefully this afternoon), I plan to do a bit more research and print some for my records to bring along with me to the appointment. Thanks again!

[kim]

browneyesmom,

 

How wonderful for you to take the time to post that with everything that you must be going thru right now. I just wanted to send you the biggest cyber hug possible. God is truly with you and your daughter. I can't imagine the relief you must be feeling to get to the bottom of what's going on even if there are unnswered questions at this point.

 

Your daughters condition is all something that we can learn from. I'm so glad you decided on the scan too! With just a quick peak at the condition, it doesn't look like problems with the immune system are altogether ruled out?

 

You get some rest and know that there is support/interest here when you need it.

 

Prayers for you and your daughter!

 

Kim

[EAMom]

Hi Browneyes Mom,

 

I do wonder if the CT Scan findings are a red herring (not relevant to her situaion). If she was affected by this partial agnesis of the corpus callosum, wouldn't you have expected her to have abnormalities all along (since this is a birth defect)? Okay, I have to admit I haven't read Kim's post (I'll read later when my brain feels more awake!) These are the symptoms of Agenesis of the CC on Wiki (okay, we all know Wikipedia can be flawed!). I would imagine those with partial agensis would possibly be less severely affecteted?

 

Signs and symptoms

Signs and symptoms of ACC and other callosal disorders vary greatly among individuals. However, some characteristics common in individuals with callosal disorders include vision impairments, low muscle tone (hypotonia), poor motor coordination, delays in motor milestones such as sitting and walking, low perception of pain, delayed toilet training, and chewing and swallowing difficulties. Laboratory research has demonstrated that individuals with ACC have difficulty transferring more complex information from one hemisphere to the other.[4] They also have been shown to have some cognitive disabilities (difficulty in complex problem solving) and social difficulties (missing subtle social cues), even when their Intelligence Quotient is normal.[4] Recent research suggests that specific social difficulties may be a result of impaired face processing.[5] Unusual social behavior in childhood is often mistaken for or misdiagnosed as Asperger's syndrome or other autism spectrum disorders. Other characteristics sometimes associated with callosal disorders include seizures, spasticity, early feeding difficulties and/or gastric reflux, hearing impairments, abnormal head and facial features, and mental retardation.

 

If your dd is affected by these CC abnormalities, I wouldn't expect her to be a normal, academically gifted, well-adjusted child one month, and suddenly "change" after an infection, then improve on antibiotics, and then regress off of antibiotics. That pattern is PANDAS! I think it is possible that she does have this Partial Agenesis of the CC but she is an individual who is minimally affected (just like how some people with hydrocephalus are normal functioning.)

 

I would just like to add that I think you are doing a fantastic job of handling this situation. PANDAS is tough enough to handle without all this extra stuff going on! I'm also so sorry that your ex is not "on-board" with any of this. That has just got to compound your stress. Hang in there.

[colleenrn]

I wonder if the basal ganglia can be affected by strep antibodies, could it also show up as some kind of abnormality of the corpus callosum? Could this be related to PANDAS? OR like EaMom mentioned, could it be there in addition and unrelated to the PANDAS? I wish you the best of luck! I will be thinking of you.

Colleen

[kim]

Could there be a connection here????? I thought I remembered something about tubulin in relationship to PANDAS

 

 

http://www.jimmunol.org/cgi/content/abstract/178/11/7412

 

Tubulin Is a Neuronal Target of Autoantibodies in Sydenham’s Chorea1

 

http://en.wikipedia.org/wiki/Agenesis_of_the_corpus_callosum

 

The underlying cause may be a dysfunctional molecular mechanism in the primary cilia structures of the cell, organelles which are present in many cellular types throughout the human body. The cilia defects adversely affect "numerous critical developmental signaling pathways" essential to cellular development and thus offer a plausible hypothesis for the often multi-symptom nature of a large set of syndromes and diseases.

 

when you click on cilia in that sentence, you get this

 

The building blocks of the cilia such as tubulins and other partially assembled axonemal proteins are added to the ciliary tips which point away from the cell body.

[Dedee]

Well I can't add anything to the wonderful infomation you have already gotten regarding your physical findings. However, I just wanted to throw in my two cents on the whole ex-husband issue. I am sure this is hard enough to get through without having to convince him that these issues are valid and worthy of persuing. I rember in the begining I had to convince my husband somewhat before he was on board. That was stressful enough and not near what you are going through. I hope it doesn't come to it, but you may need to consult with your attorney. I feel certain with the physical findings that you have to support your decisions, you have the upper hand on this issue. It is so unfortunate that you would have to stress about this in addition to everything else. I can't imagine. But you need to have the freedom to make medical decisions for your child without defending everything to someone who is obviously bringing in their own personal issues. This is confusing enough. Let's not muddy the water anymore with his hang ups. You are doing a great job! Keep up the good work!

 

Dedee

[colleenrn]

http://www.ncbi.nlm.nih.gov/pubmed/10390719

 

The authors previously found significant abnormalities in the region of the corpus callosum (CC) connecting ventral prefrontal cortex and striatum in pediatric OCD patients compared to controls that correlated significantly with OCD symptom severity.

 

The striatum is part of the basla ganglia. The basal ganglia is affected by the strep antibodies, which cause the tics/OCD/etc... This does not seem like it would be a coincidence, IMO.

 

Colleen

[colleenrn]

http://books.google.com/books?id=RJOy1vy2R...1&ct=result

 

This is another article about MRI results in children with OCD, showing an increase in size of the corpus callosum.

 

Colleen

[kim]

I can't find anything relating to PANDAS (only SC). The SC study talks about reactivity in the caudate and putamen.

[browneyesmom]

Oh my! Thank you for all this information!! Unfortunately, I barely slept last night after receiving the results of the scan and I had a minor surgical procedure today that is still kind of tender, so I am too tired and distracted by yesterday's news to make heads or tails of it at the moment. I will review all this again tomorrow after I get some rest.

 

Did I post yet that her appointment with the pediatric neurologist will be on April 3? I'm trying to keep it as light as possible; told her I'd take her out to lunch afterward at this neat restaurant we will be near, where we haven't eaten in a long time. I emailed her a link to the menu to help occupy (ok, distract... hey, whatever works to help her through it!) her until then.

 

I'll try to reply to what I am able to process for now...

 

Did someone post about the CC being larger maybe being related to PANDAS? The CC in her case is not larger, but apparently, smaller... or part of it is missing. I have not yet viewed the scan myself, only the report... but you know, I think I will see if I can look at the images on this disc or not. Might have to have special software to do that, so maybe I will have to wait until we get to the appointment to see it.

 

Agenesis of the CC is a condition, according to our pediatrician and what I read last night, that can affect some kids, does not affect other kids at all, and in some cases, does not show up for the first few years... which might be the case for our daughter. That we don't yet know and it is one of the things I will be asking the pediatric neurologist.

 

I also do not think this is the "full" answer to what is happening with her and I am still inclined to believe that PANDAS plays a role here. I am thinking at this point, that this is something in addition to it, but I don't really know yet... maybe it is related in some way... just trying to learn all I can right now... again.

 

I have to say again, how blessed I am to have been led to this forum! I was feeling so drained after the news of the scan and you have all been so kind and helpful. What a wealth of information and support!!! Thank you for the blessing you are!

[browneyesmom]

I spoke with my best friend on the phone this afternoon. I felt a bit better after we talked and I told her that I have to have faith that we are in God's hands and He is faithful and will take care of us and handle all of this somehow. I shared that with my daughter before she left for with her dad and it seemed to comfort her a bit.

 

Yes, just getting to the bottom of sorting out WHAT is causing WHAT here will be a huge relief. Then we will finally be able to know what we are fighting and move forward with making some decisions for her.

 

I will update as we learn more... I know everyone here is seeking to learn all we can.

 

... and thanks for the hug, Kim... I sure needed that today!! Here's one right back to you!!

 

browneyesmom,

 

How wonderful for you to take the time to post that with everything that you must be going thru right now. I just wanted to send you the biggest cyber hug possible. God is truly with you and your daughter. I can't imagine the relief you must be feeling to get to the bottom of what's going on even if there are unnswered questions at this point.

 

Your daughters condition is all something that we can learn from. I'm so glad you decided on the scan too! With just a quick peak at the condition, it doesn't look like problems with the immune system are altogether ruled out?

 

You get some rest and know that there is support/interest here when you need it.

 

Prayers for you and your daughter!

 

Kim

[kim]

BEmom,

 

Please don't feel any pressure to respond. I'm sure you are doing tons of your own research.

 

I did want to leave you a few studies that I thought were interesting in one respect or another.

 

The first one talks about a few chromosomes (i bolded them). 8 and 11 caught my eye. They are both implicated in a benign bony tumor that my oldest son has. Another child on this forum had one of these tumors on his wrist (this child clearly had PANDAS symptoms) another mom reported something similar on her daughters spine (?) but we never really determined if it was just a calcification or a similar tumor. Pretty sure that I have seen double ureters mentioned here too. Also 11p11,12 were implicated in a large autism study recently. When I pulled up a page on agenesis of the corpus callosum and 11p11 this is what I got. You can look at the other headlines. Just interesting! While one person might have a deletion another might have a translocation etc. Not saying this one chromosome means anything, just suspicious that it is involved in some of our situations (probably along with other genetics and environmental stuff). If these are involved for any of our kids, it seems it's usually a mild/very mild set of symptoms compared to the known syndromes that are assoc. Gotta run right now, i'll post the others with comments a little later.

 

http://www.google.com/search?hl=en&rls...art=10&sa=N

 

Information Centre for Rare Diseases and Orphan Drugs :corpus callosum agenesis double urinary collecting system corpus callosum agenesis .... deletion 11p11 p12 deletion 11p13 deletion 11q partielle ...

 

http://www.ncbi.nlm.nih.gov/pubmed/3310713...ogdbfrom=pubmed

 

Seven hundred five cases of agenesis of the corpus callosum (ACC) are reviewed from the literature (n = 660) and from our own observations (n = 45). The diagnosis was made or confirmed using neuroradiological techniques (n = 519) and necropsy or surgery (n = 231). Association with abnormalities often of chromosomes 8, 11, 13-15 and 18 suggests their involvement in abnormal corpus callosum (CC) morphogenesis. Four syndromes (e.g. Aicardi, acrocallosal, Andermann and Shapiro) are characterized by ACC, while others are only sporadically associated (e.g. fetal alcohol syndrome, Dandy-Walker syndrome, Leigh disease, Arnold-Chiari II syndrome). In non-Aicardi patients, the male-to-female ratio was 3:2 and X-linked recessive inheritance is postulated to play a role in some cases. Common abnormalities in acallosal patients included: mental retardation (MR), 73% [corrected]; seizures, 42%; ocular anomalies, 42%; gyral abnormalities, 32%; hydrocephalus, 23%; other central nervous system (CNS) lesions, 29%; costovertebral defects, 24%. Developmental disabilities are not attributable to absence of the CC per se, but due to other CNS malformation or dysfunction, which may be genetic or non-genetic. Future research using recombinant DNA techniques will enable isolation and identification of specific chromosomal defects in those cases with a genetic abnormality.

 

looks like i've got a few more minutes so.... REVERSABLE was interesting here. Made me wonder if PANDAS related exacerbation could change the image? Could swelling compress the CC?

 

2520al.pdf+corpus+callosum+abnormality+hypoglycemia&cd=7&hl=en&ct=clnk&gl=us

 

Acute, isolated, focal, and reversible abnormali-ties of the corpus callosum, have been reported on diffusion weighted images (DWI) in various med-ical conditions : encephalopathy with seizures(Maeda et al., 2003; Tada et al., 2004), non-epilep-tic patients receiving anti-epileptic drugs for any reasons(da Rocha et al., 2006), systemic lupus,hypoglycemia, and various types of infections suchas influenzae (Bulakbasi et al., 2006), herpes virus(Kato et al., 2003), rotavirus, or Legionnaire’s dis-ease (Bulakbasi et al., 2006), and even in a case offever of unexplained origin (Shimizu et al., 2007).

[kim]

On this one, I was questioning the sensitivity of the scan. With the info on how WELL your daughters brain works, prior to the all of the strep problems, it would seem that the ability of her brain 1/2's to communicate has been functioning very well!

 

http://www.ncbi.nlm.nih.gov/pubmed/1900153...Pubmed_RVDocSum

 

 

Variability of homotopic and heterotopic callosal connectivity in partial agenesis of the corpus callosum: a 3T diffusion tensor imaging and Q-ball tractography study.Wahl M, Strominger Z, Jeremy RJ, Barkovich AJ, Wakahiro M, Sherr EH, Mukherjee P.

Department of Radiology and Biomedical Imaging, University of California, San Francisco, San Francisco, CA 94143-0628, USA.

 

BACKGROUND AND PURPOSE: Little is known about the anatomic connectivity of callosal axons in individuals with partial agenesis of the corpus callosum (pAgCC). We used tractography based on both diffusion tensor imaging (DTI) and high angular resolution diffusion imaging (HARDI) to investigate interhemispheric white matter connectivity in pAgCC. MATERIALS AND METHODS: DTI and HARDI were performed at 3T on 6 individuals with pAgCC and 8 control subjects. For HARDI analysis, a Q-ball reconstruction method capable of visualizing multiple intravoxel fiber orientations was used. In both DTI and HARDI, whole-brain 3D fiber tractography was performed by using deterministic streamline algorithms. Callosal fibers were then segmented to identify separately connections between homologous cortical regions (homotopic fibers) and nonhomologous regions (heterotopic fibers) by using manually drawn regions of interest. RESULTS: In control individuals, we observed densely connected homotopic fibers. However, in individuals with pAgCC, we identified not only homotopic connections but also heterotopic connections in 4 of 6 subjects. Furthermore, the observed homotopic connections in pAgCC did not necessarily correlate with the position or size of the residual callosum. The nature of homotopic and heterotopic connectivity varied considerably among subjects with pAgCC, and HARDI recovered more callosal fibers than DTI. CONCLUSION: Individuals with pAgCC demonstrate a remarkable diversity of callosal connectivity, including a number of heterotopic tracts that are absent in healthy subjects. The patterns of their callosal connections cannot be predicted from the appearance of their callosal fragments on conventional MR imaging. More tracts and more extensive fibers within tracts are recovered with HARDI than with DTI.

 

 

I believe some of these same cellular and molecular mechanisms are reponsible for the way infections and viruses affect the cells.

 

 

http://www.ncbi.nlm.nih.gov/pubmed/1535542...ogdbfrom=pubmed

 

Mechanisms regulating the development of the corpus callosum and its agenesis in mouse and human.Richards LJ, Plachez C, Ren T.

The University of Maryland School of Medicine, Department of Anatomy and Neurobiology and Programs in Neuroscience and Membrane Biology, Baltimore, MD 21201, USA. lrich001@umaryland.edu

 

The development of the corpus callosum depends on a large number of different cellular and molecular mechanisms. These include the formation of midline glial populations, and the expression of specific molecules required to guide callosal axons as they cross the midline. An additional mechanism used by callosal axons from neurons in the neocortex is to grow within the pathway formed by pioneering axons derived from neurons in the cingulate cortex. Data in humans and in mice suggest the possibility that different mechanisms may regulate the development of the corpus callosum across its rostrocaudal and dorsoventral axes. The complex developmental processes required for formation of the corpus callosum may provide some insight into why such a large number of human congenital syndromes are associated with agenesis of this structure.