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.
Showing posts with label medical information. Show all posts
Showing posts with label medical information. Show all posts
Sunday, May 16, 2010
Thursday, April 29, 2010
What is Fahrs syndrome?
Fahrs Syndrome
(Also Called 'Fahrs', 'Familial Idiopathic Basal Ganglia Calcification')
Synonym(s): Familial Idiopathic Basal Ganglia Calcification
What is Fahr's Syndrome?
Fahr's Syndrome is a rare, genetically dominant, inherited neurological disorder characterized by abnormal deposits of calcium in areas of the brain that control movement, including the basal ganglia and the cerebral cortex. Symptoms of the disorder may include deterioration of motor function, dementia, seizures, headache, dysarthria (poorly articulated speech), spasticity (stiffness of the limbs) and spastic paralysis, eye impairments, and athetosis (involuntary, writhing movements). Fahr's Syndrome can also include symptoms characteristic of Parkinson's disease such as tremors, muscle rigidity, a mask-like facial appearance, shuffling gait, and a "pill-rolling" motion of the fingers. These symptoms generally occur later in the development of the disease. More common symptoms include dystonia (disordered muscle tone) and chorea (involuntary, rapid, jerky movements). Age of onset is typically in the 40s or 50s, although it can occur at any time in childhood or adolescence.
Is there any treatment?
There is no cure for Fahr's Syndrome, nor is there a standard course of treatment. Treatment addresses symptoms on an individual basis.
What is the prognosis?
The prognosis for any individual with Fahr's Syndrome is variable and hard to predict. There is no reliable correlation between age, extent of calcium deposits in the brain, and neurological deficit. Since the appearance of calcification is age-dependent, a CT scan could be negative in a gene carrier who is younger than the age of 55.
What research is being done?
The NINDS supports and conducts research on neurogenetic disorders such as Fahr's Syndrome. The goals of this research are to locate and understand the actions of the genes involved in this disorder. Finding these genes could lead to effective ways to treat and prevent Fahr's Syndrome. MORE
(Also Called 'Fahrs', 'Familial Idiopathic Basal Ganglia Calcification')
Synonym(s): Familial Idiopathic Basal Ganglia Calcification
What is Fahr's Syndrome?
Fahr's Syndrome is a rare, genetically dominant, inherited neurological disorder characterized by abnormal deposits of calcium in areas of the brain that control movement, including the basal ganglia and the cerebral cortex. Symptoms of the disorder may include deterioration of motor function, dementia, seizures, headache, dysarthria (poorly articulated speech), spasticity (stiffness of the limbs) and spastic paralysis, eye impairments, and athetosis (involuntary, writhing movements). Fahr's Syndrome can also include symptoms characteristic of Parkinson's disease such as tremors, muscle rigidity, a mask-like facial appearance, shuffling gait, and a "pill-rolling" motion of the fingers. These symptoms generally occur later in the development of the disease. More common symptoms include dystonia (disordered muscle tone) and chorea (involuntary, rapid, jerky movements). Age of onset is typically in the 40s or 50s, although it can occur at any time in childhood or adolescence.
Is there any treatment?
There is no cure for Fahr's Syndrome, nor is there a standard course of treatment. Treatment addresses symptoms on an individual basis.
What is the prognosis?
The prognosis for any individual with Fahr's Syndrome is variable and hard to predict. There is no reliable correlation between age, extent of calcium deposits in the brain, and neurological deficit. Since the appearance of calcification is age-dependent, a CT scan could be negative in a gene carrier who is younger than the age of 55.
What research is being done?
The NINDS supports and conducts research on neurogenetic disorders such as Fahr's Syndrome. The goals of this research are to locate and understand the actions of the genes involved in this disorder. Finding these genes could lead to effective ways to treat and prevent Fahr's Syndrome. MORE
Gene Reviews-updated Sept 2007
Disease characteristics. Familial idiopathic basal ganglia calcification (FIBGC) is a neurodegenerative disorder with characteristic calcium deposits in the basal ganglia and other brain areas visualized on neuroimaging. Most affected individuals are in good health during childhood and young adulthood and typically present in the third to fifth decade with gradually progressive neuropsychiatric and movement disorders. The first manifestations often include clumsiness, fatigability, unsteady gait, slow or slurred speech, dysphagia, involuntary movements, or muscle cramping. Seizures of various types occur frequently. Neuropsychiatric symptoms, often the first or most prominent manifestations, range from mild difficulty with concentration and memory to changes in personality and/or behavior, to psychosis and dementia.
Diagnosis/testing. The diagnosis of FIBGC relies on visualization of bilateral calcification of the basal ganglia on neuroimaging; presence of progressive neurologic dysfunction; metabolic, infectious, toxic, or traumatic cause; and a family history consistent with autosomal dominant inheritance. The gene or genes responsible for FIBGC are unknown. Linkage to chromosome 14q has been established in one family.
Management. Treatment of manifestations: pharmacologic treatment to improve anxiety, depression, obsessive-compulsive behaviors, and dystonia; oxybutynin for urinary incontinence; appropriate antiepileptic drugs (AEDs) for seizures. Surveillance: annual neurologic and neuropsychiatric assessments. Agents/circumstances to avoid: cautious use of neuroleptic medication as it may exacerbate extrapyramidal symptoms. Other: generally poor response of parkinsonian features to levodopa therapy.
Genetic counseling. Familial idiopathic basal ganglia calcification is inherited in an autosomal dominant manner. The proportion of cases caused by de novo gene mutations is unknown. Offspring of an affected individual have a 50% risk of being affected. Prenatal testing is not available. MORE
Diagnosis/testing. The diagnosis of FIBGC relies on visualization of bilateral calcification of the basal ganglia on neuroimaging; presence of progressive neurologic dysfunction; metabolic, infectious, toxic, or traumatic cause; and a family history consistent with autosomal dominant inheritance. The gene or genes responsible for FIBGC are unknown. Linkage to chromosome 14q has been established in one family.
Management. Treatment of manifestations: pharmacologic treatment to improve anxiety, depression, obsessive-compulsive behaviors, and dystonia; oxybutynin for urinary incontinence; appropriate antiepileptic drugs (AEDs) for seizures. Surveillance: annual neurologic and neuropsychiatric assessments. Agents/circumstances to avoid: cautious use of neuroleptic medication as it may exacerbate extrapyramidal symptoms. Other: generally poor response of parkinsonian features to levodopa therapy.
Genetic counseling. Familial idiopathic basal ganglia calcification is inherited in an autosomal dominant manner. The proportion of cases caused by de novo gene mutations is unknown. Offspring of an affected individual have a 50% risk of being affected. Prenatal testing is not available. MORE
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