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Page 4 of 6                 Verma et al. Neuroimmunol Neuroinflammation 2018;5:20  I  http://dx.doi.org/10.20517/2347-8659.2017.65
































                                        Figure 3. Computerized tomography scan of cerebellar calcification

               transfusions. Secondary hypoparathyroidism is a physiological state in which PTH levels are low in response
               to a primary process that causes hypercalcemia.


               The essential capacity of PTH is to keep up the extracellular fluid (ECF) calcium concentration within a
               normal narrow range. The hormone acts directly on bone and kidney and indirectly on the intestine through
               its effects on synthesis of 1,25(OH)2D3 to increase serum calcium concentrations; in turn, PTH generation
               is firmly directed by the concentration of serum ionized calcium. Any tendency toward hypocalcemia, is
               counteracted by an increased secretion of PTH. This in turn: (1) increases the rate of dissolution of bone
               mineral, thereby increasing the flow of calcium from bone into blood; (2) reduces the renal clearance of
               calcium, returning more of the calcium filtered at the glomerulus into ECF; and (3) increases the efficiency of
               calcium absorption in the intestine by stimulating the production of 1,25(OH)2D3.


               Hypocalcemia produces hyperexcitability of nerve fibers with spontaneous and repetitive discharges. As a
               result, patients have perioral and distal numbness and parasthesiae, carpopedal spasm and diffuse muscle
               cramps. Latent tetany can be elicited by hyperventilation, by tapping the facial muscles (Chovstek’s sign)
               or by occluding venous return from arm, resulting in carpopedal spasm (Trousseau’s sign). In severe
               cases laryngeal muscle spasm and convulsions may develop. Respiratory arrest may also occur. Chronic
               hypoparathyroidism is associated with markedly abnormal skeletal microstructure, despite marked increases
               in bone mineral density.

               Increased intracranial pressure, papilledema, and convulsions can also be present, and must be differentiated
                                              [4,5]
               from severe tetany muscular spasms . Rare extrapyramidal signs including parkinsonism and cerebellar
               signs have been reported. Mental changes include irritability, depression, and psychosis. The QT interval on
               the electrocardiogram is prolonged, in contrast to its shortening with hypercalcemia. Arrhythmias occur, and
               digitalis effectiveness may be reduced. Intestinal cramps and chronic malabsorption may also occur.

               Seizures are a frequent complication: they have been reported in 20%-25% of patients with acute
                                                                                    [6]
               hypocalcemia and in 30%-70% of patients with idiopathic hypoparathyroidism . Epileptic seizures may
               happen at any age and usually generalized tonic clonic with loss of consciousness. Non-convulsive status
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