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Pseudo and Pseudo-pseudohypoparathyroidism are depicted by a phenotypic spectrum caused by mutations in RNA and they also tend to occur in the same family.

His spasms increased in frequency over the following months, but the patient did not seek further medical attention. The histopathology specimen of the thyroid and parathyroid gland showed chronic lymphocytic thyroiditis and fibro-adipose tissue respectively. Definitive diagnosis of primary familial basal calcification is encephalotis by Proband. Idiopathic calcification of the basal ganglia.

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MRI magnetic resonance imaging Calcified areas in basal ganglia give a low intensity signal on a T2 image and low or high intensity signals on a T1 weighted plane [ 18 ]. A second locus has been identified on chromosome 8 and a third on chromosome 2 [ 8 – 10 ]. The cerebellar lesions are found to be more heterogeneous. Pseudohypoparathyroidism is a condition associated primarily with resistance to the parathyroid hormone and the term Pseudopseudohypoparathyroidism is used to describe a condition where the individual has the phenotypic appearance of Pseudohypoparathyroidism type 1a, but is biochemically normal [ 172433 – 35 ].


Progressive basal ganglia mineralization tends to compress the vessel lumen, thus initiating a cycle of impaired blood flow, neural tissue injury and mineral deposition. Due to the association of mitochondrial myopathy with abnormality in Calcium metabolism and increment in serum lactic acid and CSF protein, it was predicted that Fahr syndrome is also associated with Myopathies.

Fahr’s syndrome: literature review of current evidence

Published online Mar It is characterized by abnormal asep of calcium in areas of the brain that control movements including basal ganglia, thalamus, dentate akep, cerebral cortex, cerebellum, subcortical white matter, and hippocampus [ 5 ].

Journal of molecular neuroscience. The serum concentrations of calcium and phosphorus are normal and there is a normal response to PTH secretion [ 1740 ]. University of Washington, Seattle; Pathological features, being similar in both adults and infants, are not affected by age. Clin Endocrinol Oxf ; 12 4: Literature search was conducted by using the following databases: Establishing the diagnosis of VGKC encephalitis can be difficult.

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Consensus holds that individuals younger than 18 years who are at risk but asymptomatic should not be tested. Most frequently affected area is the lenticular nucleus, especially the internal globus pallidus while Cerebellar gyri, brain stem, centrum semiovale, and subcortical white matter may also affected. Previously, low serum sodium has only been reported in patients with prior evidence of encephalopathy, such as subacute memory impairment or worsening irritability.

The EEG is usually non-specific, with frontotemporal or bitemporal generalized slowing. Faciobrachial dystonic seizures are a well-described feature classically observed in voltage-gated potassium channel autoimmune encephalitis.

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Bangladesh Medical Journal Khulna.

Fahr’s syndrome: literature review of current evidence

Brain CT scan serves as a pre-symptomatic test in at risk individual but its not useful for predicting age of onset, severity, type of symptoms or rate of progression in an asymptomatic individual. These calcifications are generally confined to the Globus Pallidus and do not have associated clinical findings [ 4647 ].

Etiology of this syndrome does not identify a specific agent but associations with a number of conditions have been noted; most common of which are endocrine disorders, mitochondrial myopathies, dermatological abnormalities and infectious diseases.

Motor cortex and hippocampus are the two main cortical targets in LGI1-antibody encepualitis.

Several approaches based on diverse biological theories and small scale clinical experiences have been proposed. New treatment modalities need to be discovered and employed to minimize loss of functionality encephaliits with the disease. Extensive bilateral intracranial calcifications: Available literature concerning Fahr syndrome was analyzed. In a literature review of cases, it was found that 35 Familial bilateral vascular calcification in the central nervous system.

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Calcified areas in basal ganglia give a low intensity signal on a T2 image and low or high intensity signals on a T1 weighted plane [ 18 ]. Calcification seems to be progressive and gradual. No to hattatsu Brain and development.