I had a strange episode the other night.
I woke up and thought I had had a stroke. My legs were like jelly, my arms had no strength, and movement was very slow motion. My brain was functioning quite well, although I had no volume to my speech.
I contemplated ringing the ambulance, but decided to stay calm , breathe deeply and do all the tests the doctors would do to diagnose a stroke. I took an asprin, and lay there slowly trying to regain control. It took 30 minutes, and slowly my strength came back. Was it a panick attack, was it a mini stroke, was it something weird? The CT scan the following morning came back clear, except for a diagnosis of, "normal scan. idiopathic calcification of the basal ganglia.'

Normal, it stated clearly. In fact, it was so normal that my doctor didn't even look at the result, until I brought it up. But when I asked her opinion about it, she didn't have a clue what it was. I have been feeling dizzy, slightly off balance, have aching muscles for 2 years, occasional facial neuropathy, headaches, and strange depression, which I never realy had. I am 52, but the doctors cannot work it out. I should be healthy.

This page will attempt to provide information about this 'rare disease", as I gather data from as many places as possible. It may not be the cause of my present symptoms, but so far in my research, it appears that it will undoubtedly have some effects at one point in my life. If anyone has any information, please add it to the page. Please click on my post headlines to take you direct to the relevant sites.Cheers.

Sunday, May 16, 2010

Wilsons Temperature Syndrome and Hypothyroidism

The articles presented on the WTS site are very interesting, to say the least. Hypothyroidism is a major cause of Calcification of the Basal Ganglia, yet finding thyroid problems seems to be subject to a lot of hit and miss diagnosis. Medicos have concluded that the results from the standard Thyroid tests, are not fully reliable, which is a remarkably important suggestion for those who have been found to have brain calcifications. If a patient has performed all the blood work ups and everything has come up "fine", it takes a dedicated team effort to try to find alternative possibilities , especially for this particular obsure disease. Due to lack of knowledge and lack of time, you doctor may not have heard of any further possible thyroid problems, and will find it easier to refer you to a neurologist or an endocronologist, for further testing.
However, ,as is explicitly explained on the Wilson Temperature Syndrome site, Hypothyroidism is still a high possibility, even though the hormone tests suggest all is well.
A simple method of testing by taking your temperature 3 times a day, for a period of time, could give you a better indication if you, in fact, do have possible thyroid misfunction, which can be corrected by following the W3 protocol. I am going to persue this angle, and will follow up, in time, with the results.
For all the information on WTS, please go to http://www.wilsonstemperaturesyndrome.com/, and decide for yourself  if this could be an approach to investigate.

Thursday, April 29, 2010

The most common ailments as per the Fahrs disease registry

Movement disorder is the most common manifestation of idiopathic basal ganglia calcification, accounting for about 55% of the symptomatic patients. Parkinsonism was seen in 57%, chorea in 19%, tremor in 8%, dystonia in 8%, athetosis in 5%, and orofacial dyskinesia in 3%. Other neurologic manifestations included cognitive impairment, cerebellar signs, speech disorder, pyramidal signs, psychiatric features, gait disorders, sensory changes, and pain.MORE
Idiopathic basal ganglia calcification
Shaheda N Azher and Joseph Jankovic
Last reviewed
October 1, 2009 

ATP- the fuel of life

If ATP depletion is indicated in basal ganglia calcification, new research into understanding the molecule is of great importance. Scientists are at the brink of understanding, as the latest news shows:

ScienceDaily (Mar. 9, 2010) — Researchers at the Louisiana State University Health Sciences Center have figured out how ATP is broken down in cells, providing for the first time a clear picture of the key reaction that allows cells in all living things to function and flourish

"ATP is the fuel of life. It's an energy currency molecule -- the most important source of chemical and mechanical energy in living systems," explains Sunyoung Kim, the associate professor who oversaw the research published Feb. 19 in the Journal of Biological Chemistry. MORE

Where is the Basal Ganglia?

A Professors view

Chorea and the Basal Ganglia

Chorea consists of involuntary, irregular movements that may either take on a "worm-like" appearance called athetosis or a more proximal flinging movement called ballismus
Calcium Metabolism- Hypocalcemia, most frequently in the setting of hypoparathyroidism, can cause chorea, which improves when calcium is corrected

MORE at Medscape

Dystonia and the Basal Ganglia

Dystonia is a movement disorder characterized by involuntary, sustained, patterned, and repetitive muscle contractions leading to twisting movements or abnormal postures. Dystonic movements may be classified by their anatomical distribution or by their clinical characteristics, and can be further categorized as primary (idiopathic) or secondary (symptomatic) in regard to etiology.

Calcium Metabolism. Hypocalcemia from idiopathic hypoparathyroidism may cause paroxysmal dystonia and choreoathetosis, which, rarely, may be kinesigenic. It is associated with basal ganglia calcification on neuroimaging.

MORE at Medscape.

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] "
MORE from Medscape

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