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

has been also reported. Seizures may be the presenting symptoms preceding other signs of hypocalcemia
such as chorea and tetany. Several types of partial motor seizures including jacksonian seizures may also be
observed. If not treated the results of these convulsions may be very serious. Seizures are thought to occur
[7,8]
due to hypocalcemia and intracranial calcification that occur in vascular and perivascular locations .
Early EEG changes associated with hypocalcemia include evolution from alpha through theta and delta
dominance. Runs of higher amplitude theta activity also appear and a very marked response to over
breathing occurs. Other EEG findings (generalized spikes, sharp-waves burst of delta activity with sharp
[9]
components). Generalized paroxysmal discharges and absence status epileptic have also been reported . No
correlation was found between calcium level and EEG changes and these changes typically revert to normal
with correction of the serum calcium levels.

[10]
Eaton et al. in 1939 first described basal ganglia calcification (BGC) in association with chronic
hypoparathyroidism. Pathogenesis is obscure, but its occurrence with hypocalcemia signifies an important
role of increased calcium-phosphorus complex formation. Radiological studies have found that calcification
encompassing cerebral veins most habitually happen in the lentiform (putamen and globus pallidus) and
the caudate cores of the basal ganglia; however, the factors that predispose individuals to basal ganglia
[11]
calcification have not been identified . Other areas affected by BCG include the thalamus, dentate nuclei,
cerebral cortex, gray-white junctions, and the cerebellum [10,12] . Such intracranial calcification occurs in 0.3%
to 1.5% of patients with hypoparathyroidism, and is often detected incidentally [13,14] . Treatment involves
replacement with vitamin D or 1,25(OH)2D3 (calcitriol) combined with a high oral calcium intake. For
many patients, vitamin D in doses of 40,000-120,000 U/day (1-3 mg/day) combined with ≥ 1 g elemental
calcium is satisfactory. Many physicians now use 0.5-1 mg of calcitriol in management of such patients,
especially if they are difficult to control. It is critical to monitor therapy closely since overtreatment may
[15]
result in hypercalciuria, hypercalcemia, renal stones, and nephrocalcinosis. Modi et al. reported among 70
patients, seizures were present in 64.3% of patients with idiopathic hypoparathyroidism and they responded
to antiepileptic drugs (AEDs) and calcium/1a(OH)D3 during the follow-up and it was possible to withdraw
AEDs in 71% of patients.

In both of our patients’ basic investigations were not done before starting the antiepileptic drugs due to
lack of facilities in this rural and remote part of country. Hypoparathyroidism is a rare yet treatable cause
for seizures. For any patient having new onset seizures even in the elderly population basic investigations,
including calcium profile, may uncover the hidden etiology.

The diagnosis of idiopathic hypoparathyroism is often missed if presentation is in elder age group. The
objective of this report is to increase awareness of such a rare, reversible cause of seizures and to consider
hypoparathyroidism in the work up of these patients.

DECLARATIONS
Authors’ contributions
Both the case workup and treatment: Verma A
Manuscript writing: Kumar A

Financial support and sponsorship
None.

Conflicts of interest
There are no conflicts of interest.