Figure 1
CT axial sections Brain
Unenhanced axial sections through the brain showing bilateral symetrical basal ganglia calcifications
Hypoparathyroidism:Case report
SectionNeuroradiology
Case TypeClinical Cases
AuthorsAsif Alam Khan, Tariq Alam, Sahar Maroof, Rashad Faizi
Connected authors
15 years, male
Clinical History
A 15-year-old male patient with history of seizures and limb spasm presented at our hospital.
Imaging Findings
Diagnostic workup:
After detailed clinical history and examination, various radiological and laboratory investigations can help in reaching the diagnosis.
Laboratory studies reveal hypocalcaemia and hyperphosphataemia with low PTH in the serum, as in our patient.
General radiological findings include generalized osteosclerosis, basal ganglia calcification, calvarial thickening, soft tissue calcifications, and hypoplastic dentition
CT: CT is the imaging modality of choice for showing the intracranial calcifications. Our patients' brain CT examination revealed extensive and symmetrical calcifications of the bilateral basal ganglia (Fig 1). Calcific foci were also seen scattered in the subcortical location of the bilateral cerebral hemispheres (Fig. 2).
On MRI brain examination, bilateral symmmetrical T2 and T1 hyperintense signals seen in the basal ganglia show dropout signals on T* images, corresponding to calcifications seen on CT examinations (Figs. 3-5).
After detailed clinical history and examination, various radiological and laboratory investigations can help in reaching the diagnosis.
Laboratory studies reveal hypocalcaemia and hyperphosphataemia with low PTH in the serum, as in our patient.
General radiological findings include generalized osteosclerosis, basal ganglia calcification, calvarial thickening, soft tissue calcifications, and hypoplastic dentition
CT: CT is the imaging modality of choice for showing the intracranial calcifications. Our patients' brain CT examination revealed extensive and symmetrical calcifications of the bilateral basal ganglia (Fig 1). Calcific foci were also seen scattered in the subcortical location of the bilateral cerebral hemispheres (Fig. 2).
On MRI brain examination, bilateral symmmetrical T2 and T1 hyperintense signals seen in the basal ganglia show dropout signals on T* images, corresponding to calcifications seen on CT examinations (Figs. 3-5).
Discussion
Hypoparathyroidism is an endocrine disorder caused as a result of congenital disorders, iatrogenic causes, infiltration of the parathyroid glands, suppression of parathyroid function, or idiopathic mechanisms. [1]
It clinically presents with neuromuscular signs and symptoms like tetany, carpopedal spasm, and paresthesia.
Laboratory studies reveal hypocalcaemia and hyperphosphataemia with low PTH in the serum as in our patient. [1]
Radiologically hypoparathyroidism causes calcification most often in bilateral basal ganglia. [2] The most common site is often globus pallidus. [3] Calcification can also occur in the cerebellum, subcortical white matter, corona radiata and the thalamus. Cerebral deposition of calcium occurs in many pathological brain processes.
Various terms have been used to describe intracranial calcification including calcification(s) of the basal ganglia, basal ganglia calcification(s), Fahr syndrome, intracranial calcification, pallidal calcification, and striopallidodentate calcinosis. [4, 5]
The immediate treatment is a calcium supplement with supplementation of PTH in cases of acquired hypoparathyroidism. It has a good prognosis if detected early and treated. Since adequate treatment of hypoparathyroidism may lead to marked clinical improvement, determination of serum calcium, phosphorus, and parathyroid hormone is mandatory in all individuals with calcification of the basal ganglia to rule out hypoparathyroidism. [6]
It clinically presents with neuromuscular signs and symptoms like tetany, carpopedal spasm, and paresthesia.
Laboratory studies reveal hypocalcaemia and hyperphosphataemia with low PTH in the serum as in our patient. [1]
Radiologically hypoparathyroidism causes calcification most often in bilateral basal ganglia. [2] The most common site is often globus pallidus. [3] Calcification can also occur in the cerebellum, subcortical white matter, corona radiata and the thalamus. Cerebral deposition of calcium occurs in many pathological brain processes.
Various terms have been used to describe intracranial calcification including calcification(s) of the basal ganglia, basal ganglia calcification(s), Fahr syndrome, intracranial calcification, pallidal calcification, and striopallidodentate calcinosis. [4, 5]
The immediate treatment is a calcium supplement with supplementation of PTH in cases of acquired hypoparathyroidism. It has a good prognosis if detected early and treated. Since adequate treatment of hypoparathyroidism may lead to marked clinical improvement, determination of serum calcium, phosphorus, and parathyroid hormone is mandatory in all individuals with calcification of the basal ganglia to rule out hypoparathyroidism. [6]
Differential Diagnosis List
Basal ganglia calcifications secondary to hypoparathyroidism
Hyperparathyroidism
Familial idiopathic cerebral calcification (Fahr’s syndrome)
Birth anoxia
Carbon monoxide intoxication
Lead poisoning
Final Diagnosis
Basal ganglia calcifications secondary to hypoparathyroidism
References
[1] Ravi Kanth Jakkani, MD, FRCR; Jyoti Sureka, MD, FRCR; and John Mathew, MD, DNB (2011) Spondyloarthropathy occurring in long-standing idiopathic hypoparathyroidism. Radiology Case Reports Volume 6, Issue 4
[2] Girija AS (2000) Idiopathic hypoparathyroidism with extensive intracranial calcification associated with kinesogenic choreoathetosis. J Assoc Physicians India Sep;48(9):938-939 (PMID: 11198806)
[3] Vakaet A, Rubens R, de Reuck J, vander Eecken H (1985) Intracranial bilateral symmetrical calcification on CT-scanning. A case report and a review of the literature. Clin Neurol Neurosurg 103-111 10.1016/0303-8467(85)90106-4 (PMID: 4028584)
[4] Koller WC, Cochran JW, Klawans HL. (1979) Calcification of the basal ganglia: computerized tomography and clinical correlation. Neurology Mar;29(3):328-333 (PMID: 571978)
[5] Harrington MG, Macpherson P, McIntosh WB, Allam BF, Bone I (1981) The significance of the incidental finding of basal ganglia calcification on computed tomography. J Neurol Neurosurg Psychiatry Dec;44(12):1168-1170 10.1136/jnnp.44.12.1168 (PMID: 7334414)
[6] Litvin Y, Rosler A, Bloom RA (1981) Extensive cerebral calcification in hypoparathyroidism. Neuroradiology 21(5):271-272 10.1007/BF02100158 (PMID: 7266863)
Case information
| URL: | https://www.eurorad.org/case/12995 |
| DOI: | 10.1594/EURORAD/CASE.12995 |
| ISSN: | 1563-4086 |
License
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
Figure 2
CT brain axial sections
CT axial setions of brain showing subcortical and bilateral symmetrical basal ganglia calcifications
Figure 3
T2 weighted MR axial sections through brain
T2 weighted MR axial sections through brain revealed bilateral symmetrical hyperintense basal ganglia
Figure 4
T1 weighted MR images through brain
T1 hyperintense signals in bilateral basal ganglia
Figure 5
T2* images through brain
T2* image through brain showing drop out signals in bilateral basal ganglia, corresponding to calcifications seen on CT
CT axial sections Brain
Unenhanced axial sections through the brain showing bilateral symetrical basal ganglia calcifications
FMIC
FMIC
CT brain axial sections
CT axial setions of brain showing subcortical and bilateral symmetrical basal ganglia calcifications
fmic
fmic
T2 weighted MR axial sections through brain
T2 weighted MR axial sections through brain revealed bilateral symmetrical hyperintense basal ganglia
fmic
fmic
T1 weighted MR images through brain
T1 hyperintense signals in bilateral basal ganglia
FMIC
FMIC
T2* images through brain
T2* image through brain showing drop out signals in bilateral basal ganglia, corresponding to calcifications seen on CT
FMIC
FMIC