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Clinical Symptoms of Hypocalcemia
Most of the symptoms and signs of hypocalcemia occur as a result of increased neuromuscular excitability (tetany, paresthesia, seizures, organic brain syndrome) or because of deposition of calcium in soft tissues (cataract, calcification of basal ganglia).
The most prominent symptom of severe hypocalcemia is tetany. Tetany is a condition characterized by a state of spontaneous tonic muscular contraction. Overt tetany is often preceded by tingling paresthesias in the fingers and about the mouth. However, the classic muscular component of tetany is carpopedal spasm, which causes a painful contraction of the hand. Carpopedal spasm begins with adduction of the thumb, followed by flexion of the finger joints and wrists, which produces a posture known as the main d’accoucheur posture.[iv][iv] Although the hands are most often involved, tetany can occur in other muscle groups, including the laryngeal muscles, which can obstruct breathing. When tested electromyographically, tetany appears as repetitive motor neuron action potentials usually grouped as doublets.
Patients with hypocalcemia are also predisposed to developing focal or generalized seizures. Two distinct types of seizure activity are associated with low calcium levels. Hypocalcemia decreases the excitation threshold for pre-existing subclinical epilepsy. Here, the attacks are indistinguishable from seizures that occur in individuals with normal calcium levels. EEG findings may remain abnormal after treatment of hypocalcemia event through the number of seizures is reduced. In addition, the neuronal irritability caused by hypocalcemia may occur in the central nervous system, including brain cells.
Other central nervous system effects of hypocalcemia include pseudotumor cerebri, papilledema, and confusion, lassitude and organic brain syndrome. Twenty percent of children with chronic hypocalcemia develop mental retardation.[v][v]
Patients with long-standing hypoparathyroidism or pseudohypoparathyroidism often have calcified basal ganglia. This usually doesn’t cause symptoms, but it can result in a number of motor disorders.
Patients with hypocalcemia may also experience cardiac, ophthalmologic, and dermatologic effects. The cardiac effects are manifested as a delay in repolarization with a prolonged QT interval. Cataract is common in patients with chronic hypocalcemia, and its severity is correlated with the duration and level of hypocalcemia. Patients with hypocalcemia often have dry and flaky skin as well as brittle nails. A dermatitis known as impetigo herpetiformis or pustular psoriasis is often associated with hypocalcemia. Chronic hypocalcemia may affect the ectoderm, producing dry skin, coarse hair and brittle nails. In children, delayed dentition, dental caries and enamel hypoplasia may occur. Alopecia, a disorder characterized by patchy hair growth, may also be seen.
Psychological Manifestations of Hypoparathyroidism
The chronically low levels of calcium seen in hypoparathyroidism contribute to hyperirritability, fatigue, and anxiety. [vi][vi] Organic brain syndrome, psychosis and psychoneurosis have been associated with hypoparathyroidism, and abnormal intelligence has been noted in some children.[vii][vii]
In Neurology and General Medicine, Dr. Michael Maninoff writes that hypocalcemia produces varied alterations in mental status ranging from dementia to frank psychosis.[viii][viii]
The clinical textbook, Robbins Pathologic Basis of Disease, lists mental changes in hypothyroidism as “ranging from irritability to depression to frank psychosis.”[ix][ix]
Dr. Maninoff adds that although convulsions are well-recognized symptoms of hypocalcemia, seizures are usually generalized and patients do not develop epilepsy. Furthermore, intracranial calcifications are a common feature of hypoparathyroidism. This usually doesn’t cause symptoms, but it may cause tremor and symptoms of parkinsonism. Increased cranial pressure is also common in hypoparathyroidism.
Diagnosis
The diagnosis of hypoparathyroidism must be considered when serum calcium levels are low and phosphorus levels are high in the presence of normal serum creatinine and magnesium, and in the absence of a source of massive phosphate leakage into the circulation. Hypoparathyroidism can then be confirmed by tests for parathyroid hormone and 1,25-(OH) vitamin D. In hypoparathyroidism levels of parathyroid hormone are low or undetectable and vitamin D levels are reduced.
Response to treatment can be measured by routine measurements of calcium and vitamin D. Cholecalciferol (vitamin D3) and calcium are both routinely employed to correct the hypocalcemia, which in turn, may influence levels of parathyroid hormone.
