Emergency. 2017; 5 (1): e65

PH OTO QU I Z

A 41-Year-Old Woman with Seizure
Fatemeh Mohammadi1, Reza Mosaddegh1, Samira Vaziri1∗

1. Emergency Medicine Management Research Center, Iran University of Medical Sciences, Tehran, Iran.

Received: Marchl 2017; Accepted: April 2017; Published online: 15 April 2017

Cite this article as: Mohammadi F, Mosaddegh R, Vaziri S. A 41-Year-Old Woman with Seizure. Emergency. 2017; 5(1): e65

Figure 1: Axial cuts of brain CT scan without contrast.

1. Case presentation

The patient was a 41 year old woman that was brought to

the emergency department (ED) by her husband following

seizure. According to the relatives accompanying her, the

seizure was of tonic-clonic type, had occurred one hour

before presentation to ED, and had lasted 3 minutes. The

patient had been drowsy for about 15 minutes after the end

of the seizure. She had no history of head trauma and did

not mention headache, nausea and vomiting, fever, vision

problems or others. On presentation, amnesia regarding the

things that happened was evident. In her history, she had

a generalized tonic-clonic seizure 4 years back, regarding

which she had not done proper follow up for taking nec-

essary diagnostic measures and had not been treated with

anti-epileptic medication. She had a history of surgery for

removing cold thyroid nodule 20 years ago and was under

calcium treatment for 15 years but she had decided to stop

taking her medications since 5 year ago. She did not have a

history of alcohol or drug abuse. The patient was conscious

∗Corresponding Author: Samira Vaziri; Department of Emergency Medicine,
Firoozgar Hospital, Karimkhan Street, Valiasr Square, Tehran, Iran. Tel:
00989123546849; Email: Samira.vaziri@yahoo.com

and awake on presentation and did not have any spe-

cific clinical complaints. Her vital signs on presentation were

as follows:

Blood Pressure = 120/70mmHg, Pulse Rate = 68/minute,

Respiratory Rate = 16/minute, O2saturation= 98% at air

room, Oral Temperature= 37◦C, and bedside blood sugar in
the normal range.

In head and neck examination, the surgery scar was seen in

the thyroid region. Examination of the thyroid also showed

a nodular surface in palpation. Examination of the heart,

lungs, abdomen and extremities did not have pathologic

findings. Neurologic examinations including evaluation of

cranial nerves, sense and power of the muscles, cerebellar

examination and deep tendon reflexes were normal. Based

on the opinion of the in-charge physician, anti-epileptic

drugs were not prescribed at this stage. Laboratory tests in-

cluding complete blood cell count, liver function tests (LFT),

and level of blood sugar (BS), sodium, potassium, calcium,

phosphorus, magnesium, urea and creatinine electrolytes

were ordered. Considering the full consciousness of the

patient and stability of vital signs and clinical examinations,

by taking safety measures and accompanied by a nurse, the

patient was referred to the radiology unit to undergo a brain

computed tomography (CT) scan, the results of which are

shown in figure 1.

What is your diagnosis?

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F. Mohammadi 2

2. Diagnosis

In the patient’s CT scan, numerous calcifications were de-

tected in the sub-cortical region, cerebellum, and basal gan-

glia. Results of the laboratory tests of magnesium, potas-

sium, sodium, creatinine, urea, LFT, and BS were in the nor-

mal range. However, calcium = 5.9 mg/dl and phosphorus

= 7.8 mg/d were reported. Serum level of parathyroid hor-

mone (PTH) was measured and PTH = 5.2 pg/mL was re-

ported. Considering the history of thyroid surgery and brain

calcinosis in CT scan images as well as hypocalcemia, hyper-

phosphatemia, and low serum level of parathyroid hormone

in the tests, iatrogenic hypoparathyroidism was confirmed.

3. Case fate

Treatment started with prescription of calcium and the pa-

tient received consultation with neurology and endocrinol-

ogy services. In thyroid ultrasonography, a hyperechoic nod-

ule that measured 13×14 with coarse calcification was seen
in the right lobe of the thyroid and a 15×20 nodule was
found in the left lobe of the thyroid. During the hospitaliza-

tion the patient did not have another seizure and was finally

discharged with good general condition and hypopatathy-

roidism diagnosis. She underwent outpatient follow up and

was also put in line for thyroidectomy surgery.

4. Discussion

Hypoparathyroidism is an endocrine disorder that occurs

due to various reasons including genetic, autoimmune, id-

iopathic, or iatrogenic causes (1). Damage to parathyroid

glands following surgery in the neck area and particularly

thyroidectomy, is the most common etiology detected for

this problem that despite taking all the precautious measures

and proper skill of the surgeon happens temporarily in 20-

30% of the cases and permanently in 1-7% (2). Hypoparathy-

roidism after thyroid surgery happens due to direct damage

to the parathyroid glands or as a result of damage to its blood

supplying vessels (3, 4).

Neuromuscular symptoms are the most common clinical

manifestations of hypoparathyroidism. Patients usually

present with complaints of paresthesia, muscle cramps,

tetany, and carpopedal spasm. However, it may also man-

ifest as seizure, neurocognitive disorder, bronchospasm,

laryngospasm, or cardiac rhythm disorders (3, 5). Chronic

hypocalcemia due to hypoparathyroidism caused by surgery

can be subclinical for long periods of time (6). Seizure and

psychological disorders in this disease occur due to hypocal-

cemia and are reversible after correction of calcium. Cogni-

tive and extrapyramidal disorders are seen due to advanced

calcification of brain tissue, usually in late diagnosis cases.

Manifestation of hypocalcemia symptoms in patients who

undergo total thyroidectomy occurs more rapidly compared

to those who undergo sub-total thyroidectomy and due to re-

moval of more thyroid tissue and more damage to parathy-

roid glands, the drop in calcium is also more rapid (7). Hy-

perphosphatemia caused by hypoparathyroidism can lead to

ectopic calcification in kidney, eye, vessels, and brain in the

long run (2). Observation of calcinosis in brain imaging of

a patient with a history of thyroidectomy should make the

physician suspicious of hypoparathyroidism and guide them

towards doing more evaluations (6). However, calcification

of basal ganglion has numerous causes; the most common of

which is calcium and phosphorus imbalance, yet some peo-

ple develop this problem without an apparent cause, which

is called Fahr syndrome (8). Initially, serum levels of calcium,

phosphorus, and parathormone hormone should be mea-

sured. If hypocalcemia, hyperphosphatemia and low level of

parathormone are detected, it is necessary to measure serum

levels of ionized calcium and magnesium in the next step. If

serum magnesium level is normal and serum level of ionized

calcium is low, the diagnosis is confirmed (9). Hypomagne-

siumia is one of the rarest and reversible causes of hypothy-

roidism that has a completely different treatment compared

to post-surgery hypoparathyroidism (2).

The treatment for this problem in ED is prescription of cal-

cium. For this purpose it has been recommended to use cal-

cium gluconate and avoid injection of calcium chloride due

to potentially sclerosing to veins (9). Anti-epileptic drugs

alone are not effective in controlling the seizure caused by

electrolyte imbalances and rapid identification and correc-

tion of these imbalances, if present, is necessary for con-

trolling seizure and preventing brain disorders (10). About

54% of the patients need anti-epileptic drugs for control-

ling seizure. Phenytoin is epileptogenic in presence of

hypocalcemia, since it induces liver enzymes and increases

metabolism of vitamin D to its inactive form. Therefore, it

is better to use other anti-epileptic drugs in these patients if

needed (5, 11).

When encountering patients with seizure presenting to ED,

taking accurate history and especially asking about their his-

tory of thyroid surgery can lead to clinical suspicion to hy-

poparathyroidism. Confirming or ruling out this diagnosis

can be easily and rapidly done via measuring serum levels

of calcium and phosphorus. By detecting hypocalcemia and

hyperphosphatemia, instead of unnecessary prescription of

anti-epileptic drugs, proper treatment can be done.

5. Appendix

5.1. Acknowledgements

We would like to express our special thanks to Emer-

gency and Neurology department staff of Firoozgar Hospital,

Tehran, Iran.

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3 Emergency. 2017; 5 (1): e65

5.2. Conflict of interest

None declared.

5.3. Funding and support

None declared.

5.4. Authors’ contributions

The authors meet the four criteria for authorship All authors

passed four criteria for authorship contribution based on

recommendations of the International Committee of Medi-

cal Journal Editors.

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	Case presentation
	Diagnosis
	Case fate
	Discussion
	Appendix
	References