Q J Med 2014; 107:567–569
doi:10.1093/qjmed/hcu010 Advance Access Publication 20 January 2014

Case report
Aggressive gyriform calcifications and seizures after
ischemia stroke in a patient with primary
hyperparathyroidism
From the 1Division of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service
General Hospital, National Defense Medical Center, Taipei, Taiwan and 2Department of Internal
Medicine, Armed Forces Taichung General Hospital, Taichung, Taiwan
Address correspondence to Feng-Chih Kuo, Division of Endocrinology and Metabolism, Department of
Internal Medicine, Tri-Service General Hospital, #325, Section 2, Cheng-Gong Rd., Nei-Hu, Taipei 114,
Taiwan. email: shoummie@hotmail.com

Learning Point for Clinicians
This case highlights that patients with ischemic
stroke concurrent with hypercalcemia caused
by primary hyperparathyroidism should be aggressively treated because long-term hypercalcemia complicated with impaired renal function
may promote cerebral calcification due to elevated blood calcium–phosphate cross-product
levels. Otherwise, hypercalcemia and cerebral
calcification may be predisposing factors of poststroke seizures.

Case history
A 59-year-old man with a history of coronary artery
disease developed a sudden onset of weakness of
his right limbs and an inability to speak, giving an
impression of acute cerebral infarction in the left
middle cerebral artery area. Brain computed tomography (CT) excluded intracranial hemorrhage; he
had a score of 23 on the National Institutes of
Health Stroke Scale. Tissue plasminogen activator
(50 mg) according to the body weight was administrated within 3 h after acute infarction. No hemorrhagic transformation was found in the brain CT
images shown in Figure 1a. However, laboratory
examinations revealed serum total calcium level

of 16.3 mg/dl (4.07 mmol/L) (reference range,
8.6–10.2 mg/dl), phosphate level of 3.7 mg/dl
(1.19 mmol/L) (reference range, 2.7–4.5 mg/dl) and
creatinine level of 2.8 mg/dl (0.7–1.2 mg/dl). High
serum parathyroid hormone (PTH) level of 742 pg/
ml (reference range, 10–69 pg/ml) and the findings
of parathyroid ultrasound imaging confirmed the
diagnosis of primary hyperparathyroidism (PHP)
due to a single parathyroid adenoma. Diuretics,
calcitonin and bisphosphonates were prescribed
to
manage
the
hypercalcemic
crisis.
Parathyroidectomy was postponed due to unstable
vital signs.
Four months later, the patient was admitted to the
emergency department due to the sudden onset of
dyskinesia of the limbs, movements of the eyeballs
upward and a loss of consciousness for approximately 5 min. The brain CT images shown in
Figure 1b revealed encephalomalacic changes
with gyriform calcification over the areas of the
old infarction. Although the patient was undergoing
treatment with bisphosphonates, serum calcium
levels were still between 11.8 and 12.5 mg/dl, with
persistent impaired renal function, and a progressive
increase in PTH levels was observed, which had
increased to 903 pg/ml before surgical intervention.
Parathyroidectomy was performed, and the postoperative PTH level was 6.7 pg/ml; serum calcium and

! The Author 2014. Published by Oxford University Press on behalf of the Association of Physicians.
All rights reserved. For Permissions, please email: journals.permissions@oup.com

Downloaded from https://academic.oup.com/qjmed/article/107/7/567/1556320 by guest on 12 April 2024

T.-J. CHUANG1,2, W.-H. TANG1, Y.-J. HUNG1 and F.-C. KUO1

568

T.-J. Chuang et al.

creatinine levels normalized gradually. Subsequent
brain CT images revealed no increment of gyriform
calcifications, and the clinical frequency and severity of the seizures decreased.

Discussion
Seizure is known to worsen the prognosis of stroke
and complicates the management of an acute
stroke.1 In a recent study, the number of cases
with epilepsy secondary to stroke was approximately 11%, and cortical involvement and large
lesion size increase the risk.1 Moreover, cerebral
calcification may be associated with some neurological
manifestations
including
seizure.2
However, the calcification after ischemic stroke is
rare and is typically discovered years after the
acute event, and this process may be accelerated
by elevated calcium–phosphate cross-product in patients with chronic renal failure.3
PHP is most commonly a result of a single overactive parathyroid gland, and the majority of patients
(>85%) are asymptomatic; this is only definitely
cured by parathyroidectomy.4 However, it may be
associated with some complications such as ischemic stroke and impaired renal function and may
cause progressively elevated hypercalcemia, particularly in those with high PTH levels.4,5 In addition, hypercalcemia caused by PHP may induce
cerebral vasospasm and has been reported to play
a role in the pathogenesis of epileptic discharges
with subsequent seizures.5 In our case, we presented a patient with underlying PHP who suffered

from cerebral infarction with prolonged hypercalcemia and impaired renal function despite undergoing
treatment with bisphosphonates. Four months later,
the patient then developed postinfarction seizure
and intracranial calcification. Intracranial calcification may have been aggravated by persistent elevated calcium–phosphate cross-product levels, and
in combination with hypercalcemia may have
played a role in the development of poststroke epilepsy in this patient. Therefore, patients with ischemic stroke concurrent with symptomatic PHP
should receive parathyroidectomy as early as possible to avoid potential predisposing factors of poststroke seizures to avoid further brain damage.

Acknowledgements
Study concept and design: Y.-J.H. and F.-C.K.;
acquisition of data: T.-J.C., W.-H.T. and F.-C.K.;
analysis and interpretation of data: T.-J.C., W.-H.T.
and F.-C.K.; drafting of the manuscript: T.-J.C. and
F.-C.K.; critical revision of the manuscript for
important intellectual content: T.-J.C., W.-H.T.,
Y.-J.H. and F.-C.K.
Conflict of interest: None declared.

References
1. Wang G, Jia H, Chen C, Lang S, Liu X, Xia C, et al. Analysis
of risk factors for first seizure after stroke in chinese patients.
Biomed Res Int 2013; 2013:702871.

Downloaded from https://academic.oup.com/qjmed/article/107/7/567/1556320 by guest on 12 April 2024

Figure 1. (a) Left fronto-temporo-parietal lobes edema with effacement of sulci and compression of the left lateral ventricle.
(b) Large territorial infarct of the left middle cerebral artery with encephalomalacic change and gyriform calcifications.

Aggressive gyriform calcifications and seizures
2. Anwar ul H, Ibrahim S, Gulab S, Saleem T, Ishaque S. Brain
calcinosis and seizures in an adolescent boy. Clin Pediatr
(Phila) 2010; 49:1160–3.
3. Wityk RJ, Lapeyrolerie D, Stein BD. Rapid brain calcification
after ischemic stroke. Ann Intern Med 1993; 119:490–1.
4. Yu N, Leese GP, Smith D, Donnan PT. The natural history of
treated and untreated primary hyperparathyroidism: the

569

parathyroid epidemiology and audit research study. QJM
2011; 104:513–21.
5. Mitre N, Mack K, Babovic-Vuksanovic D, Thompson G,
Kumar S. Ischemic stroke as the presenting symptom of primary hyperparathyroidism due to multiple endocrine neoplasia type 1. J Pediatr 2008; 153:582–5.

Downloaded from https://academic.oup.com/qjmed/article/107/7/567/1556320 by guest on 12 April 2024