This is a quote from a transcript on Facebook CCSVI of the media weblink on CCSVI by AAN and MS Society today
"Iron builds in different structures of the brain...there are certain pathways where iron is building in MS...in thalamus and around venous area of pulvinar nucleus of thalamus, thanks to new technology. We need to understand this buildup with disability in MS. " Dr Zivadinov
This is something that I have always wondered about since the time my this symptoms started. Everything that I read seemed to link to the thalamus. I think they might be onto something here.
AIM: In this paper, we seek to determine whether the iron deposition as seen by susceptibility weighted imaging (SWI) in the basal ganglia and thalamus of patients with multiple sclerosis is greater than the iron content measured in normal subjects (individuals unaffected by multiple sclerosis). As increased iron content may result from increased venous pressure, such information would add credence to the concept of Zamboni et al (1) that MS is caused by chronic cerebrospinal venous insufficiency. METHODS: Fourteen MS patients were recruited for this study with a mean age of 38 years ranging from 19 to 66 year-old. A velocity compensated 3D gradient echo sequence was used to generate SW images with a high sensitivity to iron content. We evaluated iron in the following structures: substantia nigra, red nucleus, globus pallidus, putamen, caudate nucleus, thalamus and pulvinar thalamus. Each structure was broken into two parts, a high iron content region and a low iron content region. The measured values were compared to previously established baseline iron content in these structures as a function of age. RESULTS: Twelve of fourteen patients had an increase in iron above normal levels and with a particular pattern of iron deposition in the medial venous drainage system that was associated with the confluence of the veins draining that structure. CONCLUSION: Iron may serve as a biomarker of venous vascular damage in multiple sclerosis. The backward iron accumulation pattern seen in the basal ganglia and thalamus of most MS patients is consistent with the hypothesis of venous hypertension. Haacke EM, Garbern J, Miao Y, Habib C, Liu M. Department of Radiology, Wayne State University, Detroit, MI, USA2 Department of Radiology, the First Affiliated Hospital, Dalian Medical University, Dalian, China Source: Pubmed PMID: 20351671 (01/04/10)
The complete paper is at the MS-MRI site under papers and talks:
This is a piece from Wikipedia about the thalamus
The thalamus has multiple functions. It is generally believed to act as a relay between a variety of subcortical areas and the cerebral cortex. In particular, every sensory system (with the exception of the olfactory system) includes a thalamic nucleus that receives sensory signals and sends them to the associated primary cortical area. For the visual system, for example, inputs from the retina are sent to the lateral geniculate nucleus of the thalamus, which in turn projects to the primary visual cortex (area V1) in the occipital lobe. The thalamus is believed to both process sensory information as well as relaying it—each of the primary sensory relay areas receives strong "back projections" from the cerebral cortex. Similarly the medial geniculate nucleus acts as a key auditory relay between the inferior colliculus of the midbrain and the primary auditory cortex, and the ventral posterior nucleus is a key somatosensory relay, which sends touch and proprioceptive information to the primary somatosensory cortex.
The thalamus also plays an important role in regulating states of sleep and wakefulness. Thalamic nuclei have strong reciprocal connections with the cerebral cortex, forming thalamo-cortico-thalamic circuits that are believed to be involved with consciousness. The thalamus plays a major role in regulating arousal, the level of awareness, and activity. Damage to the thalamus can lead to permanent coma.
Many different functions are linked to various regions of the thalamus. This is the case for many of the sensory systems (except for the olfactory system), such as the auditory, somatic, visceral, gustatory and visual systems where localized lesions provoke specific sensory deficits. A major role of the thalamus is devoted to "motor" systems. This has been and continues to be a subject of interest for investigators. VIm, the relay of cerebellar afferences, is the target of stereotactians particularly for the improvement of tremor. The role of the thalamus in the more anterior pallidal and nigral territories in the basal ganglia system disturbances is recognized but still poorly understood. The contribution of the thalamus to vestibular or to tectal functions is almost ignored. The thalamus has been thought of as a "relay" that simply forwards signals to the cerebral cortex. Newer research suggests that thalamic function is more selective.
In humans, a common genetic variation in the promotor region of the serotonin transporter (the SERT-long and -short allele: 5-HTTLPR) has been shown to affect the development of several regions of the thalamus in adults. People who inherit two short alleles (SERT-ss) have more neurons and a larger volume in the pulvinar and possibly the limbic regions of the thalamus. Enlargement of the thalamus provides an anatomical basis for why people who inherit two SERT-ss alleles are more vulnerable to major depression, posttraumatic stress disorder, and suicide.
If there is iron deposition issues in the thalamus it could be effecting/causing/influencing our most common MS symptoms. Hopfully the research can shed some light on this possibility.
Thanks for posting. The thalumus seems to be an important little connector for a lot of things. It will be interesting to see how this research evolves.
Interestingly, BNAC has also been involved in research on iron and MS.
http://www.bnac.net/?page_id=473 lists several recent studies:
Cox JL, Kennedy C, Zivadinov R. Quantification of regional iron content, as measured by susceptibility-weighted imaging (SWI), in brains of multiple sclerosis patients and normal controls. Mult Scler 2009;15 (Suppl 2):P372:S104.
Schirda C, Dwyer MG, Magnano C, Bergsland N, Wack D, Hussein S, Cox JL, Zivadinov R. Scan-rescan reproducibility of focal iron deposition detection in patients with multiple sclerosis and normal controls. Mult Scler 2009;15 (Suppl 2):P373:S105.
Schirda C, Magnano C, Nayyar NS, Cox JL, Dwyer MG, Zivadinov R. Contrast enhanced susceptibility weighted imaging (SWI) increases detection of iron deposition in patients with multiple sclerosis. A pilot study. Neurology 2009;72 (Suppl 3):P03.065, A139.
And a more recent article about a small study with a CCSVI link:
Zivadinov R. et al. Chronic cerebrospinal venous insufficiency and iron deposition on susceptibility-weighted imaging in patients with multiple sclerosis: a pilot case-control study. http://www.ncbi.nlm.nih.gov/sites/entrez
AIM: Chronic cerebrospinal venous insufficiency (CCSVI) is a vascular phenomenon recently described in multiple sclerosis (MS) that is characterized by stenoses affecting the main extracranial venous outflow pathways and by a high rate of cerebral venous reflux that may lead to increased iron deposition in the brain. Aim of this study was to investigate the relationship between CCSVI and iron deposition in the brain of MS patients by correlating venous hemodynamic (VH) parameters and iron concentration in deep-gray matter structures and lesions, as measured by susceptibility-weighted imaging (SWI), and to preliminarily define the relationship between iron measures and clinical and other magnetic resonance imaging (MRI) outcomes. METHODS: Sixteen (16) consecutive relapsing-remitting MS patients and 8 age- and sex-matched healthy controls (HC) were scanned on a GE 3T scanner, using SWI. RESULTS: All 16 MS patients fulfilled the diagnosis of CCSVI (median VH=4), compared to none of the HC. In MS patients, the higher iron concentration in the pulvinar nucleus of the thalamus, thalamus, globus pallidus, and hippocampus was related to a higher number of VH criteria (P<0.05). There was also a significant association between a higher number of VH criteria and higher iron concentration of overlapping T2 (r=-0.64, P=0.007) and T1 (r=-0.56, P=0.023) phase lesions. Iron concentration measures were related to longer disease duration and increased disability as measured by EDSS and MSFC, and to increased MRI lesion burden and decreased brain volume. CONCLUSION: The findings from this pilot study suggest that CCSVI may be an important mechanism related to iron deposition in the brain parenchyma of MS patients. In turn, iron deposition, as measured by SWI, is a modest-to-strong predictor of disability progression, lesion volume accumulation and atrophy development in patients with MS.
Although not formally diagnosed, I have many features of MS. My 1.5, no contrast MRI showed no MS lesion, but did point to chronic microvascular disease. I read this info with interest, as my stiffness and balance problems came on with a vengeance a month after completing a series of 14 weekly iron shots (relating to gyn problems which were resolved surgically). Could this iron loading be connected with my symptoms?
The iron shots that you describe are to correct a mineral imbalance. They wouldn't cause chronic microvascular disease, or MS.
The iron accumulation that is described in CCSVI is thought to come from a venous insufficiency in the jugular veins, causing blood to back up in the brain. They speculate that this backup causes iron deposition in the brain itself, causing the axons to break and the immune system to attack the myelin.
At this point, it's all speculation - they're not even sure that CCSVI is connected to the MS disease process.
However, chronic microvascular disease is basically neurological damage, caused by 'mini-strokes' in the brain. MS disease activity is neurological damage, but it comes from a different source. So it's no surprise that your symptoms mimic MS.
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