Brain & Development 28 (2006) 607–609 www.elsevier.com/locate/braindev
Case report
Calcified chronic subdural hematoma mimicking calvarial mass: A case report Hu¨seyin Per
a,*
, Hakan Gu¨mu¨ßs a, Bu¨lent Tucer b, Hu¨lya Akgu¨n c, Ali Kurtsoy b, Sefer Kumandasß a
a b
Department of Pediatric Neurology, Erciyes University Medical School, Kayseri, Turkey Department of Pediatric Neurosurgery, Erciyes University Medical School, Kayseri, Turkey c Department of Pathology, Erciyes University Medical School, Kayseri, Turkey
Received 15 June 2005; received in revised form 17 March 2006; accepted 22 March 2006
Abstract Head trauma is a frequent cause of mortality and morbidity in the pediatric population. Chronic subdural hematoma is the most common traumatic lesion in head injury. Chronic subdural hematomas are rare in children older than 2 years old; they are more frequent during adolescence. Calcified or ossified chronic subdural hematoma is a rare entity that usually presents as a space-occupying lesion over the cerebral convexity. Chronic calcified subdural hematomas are reported less than chronic subdural hematomas. In this article, we report a successfully treated patient with surgical removal case of calcified chronic subdural hematoma mimicking calvarial mass. 2006 Elsevier B.V. All rights reserved. Keywords: Calcified subdural hematoma; Calvarial mass; Treatment
1. Introduction
2. Case report
Calcified subdural hematoma is a rare disease, and patients usually present with headaches, seizure or a visible skull deformity. The frequency with which radiologically demonstrable calcification occurs within the membranes of a chronic subdural hematoma (SDH) has been reported to range from 0.3% to 2.7% [1–4]. There are only sporadic reports of calcified subdural hematoma operated upon successfully by authors. The case of calcified subdural hematoma presented here is interesting as it was diagnosed mimicking calvarial mass and was operated upon successfully.
A 3.5-year-old boy was admitted to our pediatric neurology department with a complaint of headache and skull deformities. Ten days before admission, he had fever, weakness and head lumps. He was referred to our department by his pediatrician because of head lumps. On admission his general physical examination was normal except skull deformities. There was no neurological abnormality. The patient’s history, obtained from his family, showed that in the first two years of his life, he had a lot of traumas because of falling and having meningitis. There was no vomiting, nausea, failing, seizure. No surgical intervention had been done until then. No radiological documentation was available. The patient’s hemogram, renal and liver functions, prothrombin time and partial thromboplastin time were in the normal range.
*
Corresponding author. Tel.: +90 352 2246666; fax: +90 352 4375825. E-mail address:
[email protected] (H. Per). 0387-7604/$ - see front matter 2006 Elsevier B.V. All rights reserved. doi:10.1016/j.braindev.2006.03.012
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H. Per et al. / Brain & Development 28 (2006) 607–609
Fig. 1. Plain film radiograph of the skull show a huge calcification extending from the parietal to temporal regions in the right side.
Plain film radiograph of the skull revealed a huge calcification extending from the parietal to temporal regions in the right side (Fig. 1). Unenhanced computed tomography of the brain revealed a mass over the right parieto-temporal area and the mass compressed the brain markedly. The lesion was hypodense on T1 and T2 weighted magnetic resonance imaging (Fig. 2). The patient underwent craniotomy. An organized calcified subdural hematoma was found over the right temporoparietal area and the brain was markedly compressed by
Fig. 3. Calcification area in sclerotic stroma (HEX200).
the hematoma. The dura was tightly adhered to the calcified subdural hematoma; however, the arachnoid membrane over the brain was intact and was not adhered to the hematoma. The calcified subdural hematoma was totally removed. Grossly, the tissue was tan color mass measuring 5 · 4.5 · 1.5 cm with smooth, glistening surface. Microscopically, the lesion was composed of a sclerotic stroma with calcification areas (Fig. 3). Postoperative period was not eventful and the patient was discharged in good condition. At the follow-up on the outpatient clinic, the patient was asymptomatic.
3. Discussion
Fig. 2. Axial T2-weighted MRI of the brain shows a mass with hypodense and hyperdense centrally over the right parieto-temporal area and the markedly compressed brain.
The most common symptom of chronic SDHs is headache, followed by lethargy, confusion, memory impairment, weakness, unconsciousness, gait disturbance and seizures. Chronic calcified SDHs, especially those with a long history, are characterized by slow progress of neurological signs of symptoms. Although the symptoms and signs of calcified chronic SDHs include epileptic seizure, dysphasia, hemiparesis, hemiplegia and behavioral problem, the majority of the cases remain asymptomatic, in spite of a large hematoma [1,2,5,6]. In this report, we present a patient with symptomatic calcified chronic SDH which leads headache and skull deformities and who underwent successful excision and recovered well. The calcified SDH has been associated with brain atrophy, thus a hematoma may not cause a mass effect [2,7]. In addition, a calcified hematoma may sometimes tightly adhere to dura mater and cortex, and dissection of the lesion from the brain may have caused brain
H. Per et al. / Brain & Development 28 (2006) 607–609
contusion or bleeding [2,8]. Therefore, removal of this lesion was not considered necessary or beneficial [7]. However, a calcified SDH can be an active lesion that grows like a neoplasm. As it was in our case, calcified SDH can be considered as calvarial mass. Most calcified SDHs can be diagnosed by CT or MRI and differentiated from the usual chronic SDH by imaging studies and gross pathology. Our patient was diagnosed with calcified SDH because CT and MRI showed a chronic SDH with calcified wall and the calcified SDH had all the characteristics mentioned above except the inner membrane was not adhered to the brain. Children frequently present with asymptomatic head lumps that have been discovered by their parents or by their complaints. Children presents with painful lumps or symptoms of intracranial masses with calvarial involvement. Sometimes the calcified SDH may be confused with other calcified extra-axial space occupying lesions and other occupying lesions, such as calcified epidural empyema, meningioma, calcified arachnoid cyst and calcified convexity dura mater with acute epidural hematoma, dermoid, Langerhans cell histiocytosis, malignant tumors, particularly metastases, posttraumatic masses, angiomas, atretic cephaloceles and sinus pericranii [8,9]. Among these diseases, calcified SDH is most often confused with calcified subdural empyema. Our patient was afebrile and was in good general condition; in addition the operative findings confirmed the lesion was a calcified SDH, not a calcified subdural empyema. The pathogenesis of calcification or ossification of chronic SDHs is still not completely known. Most authors claim that in this process the most important role in the development of calcification and ossification is played by local and metabolic, vascular factors. Calcification occurs between 3 and 12 months after the onset. Calcification of a chronic SDH is more frequent than its ossification, as ossification may be considered a terminal phase of the process. Subdural space created by shunt, craniotomy, or brain atrophy and persisting for a certain period, and additional various brain damage such as microcirculatory disorder, meningitis, encephalitis, or premature delivery may be important in generating calcified or organized SDH [1,2,6,8,9]. We think that meningitis occurred when he was 1.5 years old may have caused the development of SDH apart from trauma. Removal of the calcified SDH reduces the mass effect and cerebral irritation, and increases the cerebral blood flow, thus patients can improve neurologically after surgery. The good postoperative neurological recovery in our patient confirmed that surgery is beneficial for patients with symptomatic calcified chronic subdural hematoma, especially for those with clinical deteriora-
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tion. In symptomatic cases, surgical treatment is considered advisable and careful dissection is necessary because of dense adhesion to the brain surface. Postoperative improvement has been reported in symptomatic patients with ossified or calcified chronic SDHs [2,4,6,10]. Kaspera et al. [9], Iplikc¸iog˘lu et al. [1], Deboits and Lombaerd [5] and Waga et al. [3] believe that in such cases the removal of calcified SDH is not beneficial. Operative treatment should then be limited to middle aged patients and children as well as to the patients with new or increasing neurological deficits, because neurological deficits are caused by cerebral atrophy rather than compression by the hematoma. In summary, we presented a patient with an uncommon calcified chronic subdural hematoma, which was successfully excised resulting in a good recovery. From the literature review and the experience in our patient, we think surgical treatment for calcified SDH is feasible and often results in neurological improvement. In cases of asymptomatic or incidentally found calcified or ossified subdural hematomas of long history and in the cases with longstanding stable neurological deficits, the indications for surgical treatment must be well balanced. In symptomatic cases, surgical removal may be complicated by dense adhesion to the brain surface. Because of this, it is necessary to operate on symptomatic cases.
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