Parkinsonism, iron overload and calcium metabolism

Calcification of the Basal Ganglia and Fahrs syndrome has been linked to a condition called "Parkinsonism", as many of the late onset symproms mimic the effects of Parkinsons disease.However, calcification is not a standard symptom of Parkinsons, and therefore, CBG is not classified under that particular disease. Getting to the bottom of WHAT causes the calcification is the primary objective of research.A decline in ATP production appears to be the most likely culprit, as is an overload of many minerals.There are many possibilities, but until there is a breakthrough, the medical world is left to study and apply their funding to the most appropriate (profitable and prolific?)disease studies.Medical breakthroughs, however are occurring in other areas, as our knowledge and technology increases.In my opinion, it is not unlikely that in the near future we will find that the majority of brain diseases, like Parkinsons, Dementia, Altzheimers, and even MS, are all interlinked.The new study on iron overload on the brain could well apply to CBG, as numerous studies have indicated metal toxicity as a possible cause.

"Disorders of calcium metabolism may occur in association with parkinsonism. Hypoparathyroidism has been reported to cause parkinsonism both in the presence and absence of basal ganglia calcifications. It may occur as a late complication after thyroidectomy[5] and may be responsive to levodopa in some cases.[6] Pseudohypoparathyroidism, characterized by end-organ resistance to normal endogenous parathyroid hormone, may be associated with parkinsonism in up to 4 to 12% of patients, either with or without evidence of basal ganglia calcifications,[7] and may respond partly to normalization of serum calcium.[8] Hyperparathyroidism due to parathyroid adenomas can rarely cause parkinsonism, which is reversible after surgical removal of the tumor.[9] Bilateral subcortical calcification involving the basal ganglia and cerebellum, often labeled as Fahr's disease, represents a heterogeneous collection of disorders that are not associated with a known disorder of calcium metabolism. Movement disorders in Fahr's disease most commonly present as parkinsonism (55%), often in association with dementia, cerebellar signs, or other hyperkinetic movements including chorea, tremor, and dystonia.[10] "
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Hypoparathyroidism and pseudohypoparathyroidism

Physiological intracranial calcification occurs in about 0.3-1.5% of cases. It is asymptomatic and detected incidentally by neuroimaging. Pathological basal ganglia calcification is due to various causes, such as: metabolic disorders, infectious and genetic diseases. Hypoparathyroidism and pseudohypoparathyroidism are the most common causes of pathological basal ganglia calcification. Besides tetany and seizures this condition is presented by parkinsonism and dementia. Such parkinsonism does not respond to drugs containing levodopa. Infections (toxoplasmosis, rubella, cytomegalovirus, cysticercosis, AIDS) give multiple and asymmetric intracranial calcification. Inherited and neurodegenerative diseases cause symmetrical, bilateral basal ganglia calcification which is not related to metabolic disorders. Since adequate treatment of hypoparathyroidism may lead to marked clinical improvement, serum concentration of calcium, phosphorus, and parathyroid hormone (PTH) is suggested to be determined in all individuals with calcification of the basal ganglia to rule out hypoparathyroidism . MORE

From the Department of Internal Medicine, KKGH, Hafr Al Batin, Saudi Arabia
Basak R. OMJ. 24, 220-222 (2009); doi:10.5001/omj.2009.43

Further report on Herpes Simplex and basal ganglia

More reports on herpes virus causing basal ganglia involvement:

"Unusual progression of herpes simplex encephalitis with basal ganglia and extensive white matter involvement'


In herpes simplex encephalitis (HSE), the gray matter of the temporal and frontal lobes is predominantly destroyed by many foci of hemorrhage and necrosis.1 The lesions usually begin either unilaterally or bilaterally in the medial temporal cortex with bilateral spread along limbic pathways to the orbital frontal lobe and insular cortex. Parietal, occipital, brainstem, internal capsule, and cingulate gyrus involvement often occurs with further spread, but the basal ganglia and lobar white matter are relatively spared.2 Here, we report a case of HSE with basal ganglia and white matter involvement evident on MRI during the acute stage, which presented with unusual and severe progression. When there was no response to medical management of HSE, we had to use surgical decompression. Pathological findings of HSE during the acute stage indicated involvement of the white matter. To our knowledge, this is the first report which shows both MR and pathological findings in the white matter during the acute stage of HSE. MORE

Department of Neurology, National Hospital Organization Okayama Medical Center, 1711-1 Tamasu Kitaku, Okayama 701-1192, Japan
E-mail: ymanabe@okayama3.hosp.go.jp

©Copyright O. Yoichi et al., 2009
Licensee PAGEPress, Italy
Neurology International 2009; 1:e9
doi:10.4081/ni.2009.e9

American Society of Microbiology article

This article from the american society of Microbiology is very in depth, and covers research into the Human herpesvirus 6 (HHV-6). The research suggest the possibility of HHV- being a co contributor to MS and other brain diseases. Please read the full citation for an overview.

The high fever, characteristic of HHV-6 primary infection, is often accompanied by seizures, and HHV-6 reactivation in immunocompromised patients is associated with severe encephalitis and/or encephalopathy. There have been case reports on immunocompetent and immunocompromised adults with severe CNS disease due to HHV-6 active infection, which was characterized by a fulminant multifocal demyelinating disease (32, 115, 262, 313, 329, 410). The neuroinvasiveness of the virus is proven by the fact that HHV-6 DNA is frequently detected in specimens from divergent regions of the brain (incidence rate of individuals with positive HHV-6 PCR on brain tissue, 32 to 85%) (60, 61, 83, 110, 249). Both A and B variants of HHV-6 have been found in a proportion reflecting their seroprevalence (the B variant being approximately three times more frequent than the A variant). Some patients harbor both variants, though at different locations within the brain (60). However, in a large prospective study including 2,716 children with acute ES, either HHV-6A or HHV-6B DNA, but not both, was detected in the CSF during the active phase (153). In patients with dual infection, only HHV-6A persisted in CSF, which may suggest that HHV-6A has greater neurotropism. Altogether, these studies prove that the brain is an important site for active and latent HHV-6 infection
( Clinical Microbiology Reviews, January 2005, p. 217-245, Vol. 18, No. 1 MORE


0893-8512/05/$08.00+0 doi:10.1128/CMR.18.1.217-245.2005

Copyright © 2005, American Society for Microbiology. All Rights Reserved.)

Could EB and Herpes Zoster be involved?

I read with interest on a site that the EB virus and the related Herpes virus has come under investigation , as to being a possible cause or contributor to the brain calcification process. I will expand on this, but here is just a small snippet;

Herpes zoster:
This can involve any dermatome, including the lower sacral dermatome. However, as lower sacral dermatomal zoster is much less common than genital herpes, so-called "recurrent zoster" is usually recurrent HSV infection.

Prodromal neurological symptoms of herpes zoster comprise pain rather than the typical paraesthesiae of recurrent herpes simplex. The rash of zoster is often intensely pruritic and spreads throughout the dermatome, evolving through papular, vesicular and crusting stages (Box 9). It usually lasts two to four weeks. The most troubling symptom is usually pain, which ranges from mild to severe, and from burning to lancinating (case history, Box 10). Paraesthesiae, or anaesthesia and allodynia (pain induced by touch, often from trivial stimuli), can accompany severe pain. The pain may be self-limited or persist beyond the rash for up to a year ("postherpetic neuralgia").22,25 Another relatively common complication is zoster ophthalmicus (2%–4%), which follows involvement of the first division of the fifth cranial (trigeminal) nerve. It ranges from keratitis to the more severe iritis.26

In about 1% of immunocompromised people with herpes zoster, the virus spreads to the eye, brain or liver. Prolonged pain is uncommon. People with AIDS may have recurrent or prolonged zoster or multiple dermatomal involvement, and zoster in a person at risk of HIV may be an indicator of unrecognised HIV infection.27 Herpes zoster during pregnancy is not associated with intrauterine infection.MORE