Child’s Nerv Syst (1997) 13: 415– 417
© Springer-Verlag 1997

Mehmet Turgut
Selçuk Palaoğlu
Süleyman Sağlam

Received: 18 November 1996
M. Turgut (½)1
Department of Neurosurgery,
Adnan Menderes University Hospital,
Aydın, Turkey
S. Palaoğlu
Department of Neurosurgery,
Hacettepe University Hospital,
Ankara, Turkey
S. Sağlam
Department of Neurosurgery,
Hacettepe University Hospital,
Ankara, Turkey

CASE REPORT

Huge ossified crust-like subdural hematoma
covering the hemisphere
and causing acute signs
of increased intracranial pressure

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1

importance of the surgical approach
is stressed, and the rarity of this condition in the neurosurgical literature
is also outlined.
Key words Ossified chronic
subdural hematoma · Epilepsy ·
Computed tomography

Abstract We report the successful
removal of an ossified crust-like
chronic subdural hematoma (SDH)
covering the hemisphere in a
16-year-old boy. In this article, the

Introduction

A review of the literature has revealed that calcified
chronic subdural hematoma (SDH) is relatively common,
but an ossified one is extremely rare, representing
0.3–2.7% of chronic SDHs [5, 6, 14, 16]. There are only
sporadic reports of successful surgical treatment of such
SDHs. We document an additional histologically verified
case of ossified chronic SDH here.

Case report
This 16-year-old boy was admitted to our hospital on 29 December
1992 with complaints of epileptic seizures and dysphasia. In the past,
he had sustained a head trauma with a short period of unconsciousness (10 years before). He was well, and did not have any symptoms
until the last 4 years. Since that time he had suffered from very frequent epileptic attacks which began on the right, and unconsciousness. Because of the epileptic seizures he had been hospitalized in a
local hospital and antiepileptic medication consisting of phenytoin
was begun. Six days before the admission his convulsive seizures

became worse with gradually developing headache, nausea, and
vomiting. On admission he was alert but had dysphasia and a rightsided hemiparesis.
On neurological examination tendon reflexes on the right were
found to be increased and Babinski’s sign was positive on the right.
There was a right-sided spastic hemiparesis, most characteristic in
the hand. There were no disturbances of sensation, but papilledema
and central paresis of the VII cranial nerve were present.
Routine roentgenogram revealed a plate of calcification beneath
the inner table on the right, extending from the frontal to the parietal region (Fig. 1a, b). The sella turcica was normal in size and shape,
and there was no erosion of the clinoids. Electroencephalography
(EEG) was not remarkable apart from some slow wave activity over
the left frontoparietal area. Computed tomography (CT) scan showed
a hyperdense lesion with a hypodense central part (Fig. 2a).
On the basis of the neurological and the radiological findings the
diagnosis of a calcified or ossified chronic SDH was made and we
decided upon an operation. On 31 December 1992, a craniotomy was
made in the left frontoparietal region. When the bone flap was turned
down the dura mater appeared to be normal, but when the dura mater was opened it revealed a stony crust-like hard mass covering the
convexity. The dura mater was carefully dissected back, so that this
subdural mass was exposed in its entirety. Although the mass was
partially adherent to the cerebral cortex, it was easily separated from
the surrounding tissue. Total removal of the mass, which measured
7×6 cm, was accomplished (Fig. 3a). Pathological evaluation of the
specimen after decalcification revealed a hard material with a typi-

416

Fig. 1a, b Skull X-ray. a Anteroposterior and b lateral projections of plain X-ray film,
showing calcification extending
from frontal to parietal region
in the left side. Note that there
was a highly brachycephalic
cranium in addition to the obvious abnormality
Fig. 2a, b CT scan. a Preoperative CT scan showing a huge
mass with high density over the
left hemisphere. The central
part of the lesion is low density.
The lateral ventricle and the
sulci are almost completely
obliterated on the affected side.
There was midline shift from
left to right. b Postoperative
CT scan demonstrating some
decrease in midline shift with
complete disappearance of the
mass shown in a
Fig. 3 a Photograph of specimen removed at operation
(scale in cm). b Photomicrograph of subdural mass removed at operation, showing
a typical structure of bone and
Haversian canals (haematoxylin-eosin, ×40)

cal bone structure and with formation of Haversian canals surrounded by osteoblasts (Fig. 3b).
A postoperative CT scan 4 days after the initial scan demonstrated complete disappearance of the mass (Fig. 2b). By the time of discharge from hospital there were signs of rapid recovery from the focal neurological deficits. With an antiepileptic drug, phenytoin
200 mg/day orally, no epileptic seizures have occurred since the operation. When the patient was seen in the outpatient clinic 13 months
later, he was neurologically intact.

Discussion

Although many techniques for the management of chronic
SDH have been advocated in the literature, the pathogenesis of calcification or ossification of chronic SDH remains
unclear. According to some authors, metabolic, vascular
and/or some local factors play a part in this process [1, 13].

417

The interval between the initial traumatic event and the
development of calcification is generally longer than
6 months [1, 5, 6]. After hyalinization and calcification,
the irritation of tissue probably results in the process of
ossification, which takes many years in most of the published cases [1, 5, 7, 10]. Calcification of a chronic SDH
is more frequent than its ossification, as ossification may
be considered a terminal phase of the process. Fortunately,
the ossified mass was removed with ease without causing
bleeding in our case and in all those documented in the literature.
Clinically, chronic SDH usually presents in one of three
ways [2, 3, 8–11, 15]: (1) symptoms of raised intracranial
pressure (ICP); (2) fluctuating drowsiness; and (3) progressive dementia. However, in some cases no special pattern
is produced by this lesion, as in our case. In our case there
were symptoms of elevated ICP and progressive neurological deficits suggesting a cerebral stroke. We think that, in
this case, either pressure or vascular compromise secondary to the initial trauma or epileptic seizures was responsible for the neurological symptoms. By contrast, Kotwica
and Brzezinski [8] reported that there was no brain damage in their patients with chronic SDHs. They suggest that
the capsule of the hematoma plays an important part in the
incidence of epilepsy in chronic SDH, and it was developed in 7% of them [8]. McKissock et al. [12] also stated
that such a clinical presentation is uncommon and usually
associated with a poor prognosis. Our result is at odds with
these conclusions; our patient was well after the total removal of the subdural ossified mass.

At present, CT is the method of choice for determination of the location and age of any chronic SDH [3, 7, 11].
The CT appearance of our case was highly characteristic
for an ossified chronic SDH: CT revealed a huge ossified
crust-like mass covering the hemisphere, discrediting the
clinical diagnosis of cerebral stroke made because of the
rather sudden onset of the symptoms. In fact, the patient’s
symptoms are possibly related to Todd’s palsy, a focal deficit after seizures, which usually resolves completely with
time. Focal neurological deficits may result from the reduction in cerebral blood flow within the area of the brain compressed by a chronic SDH [4, 8]. Recently, Kotwica and
Brzezinski [9] also reported that young patients had a higher
incidence of such neurological syndromes than do older patients. On the other hand, İplikçioğlu et al. [7] suggest that
the removal of a calcified or ossified hematoma is neither
necessary nor beneficial in these patients. Our experience
is the opposite: progressive focal deficits in a young patient
sometimes need a surgical procedure. During the operation,
moreover, care had to be taken to prevent a new SDH that
could have arisen from an injury to the vascular structures
situated between the ossified hematomas and the cortex.
The results of our own and others’ experience with
chronic SDHs are as follows. The most interesting fact is
that the rather acute onset of clinical symptoms in our case
suggested a false diagnosis of cerebral stroke initially. Second, the CT scan is always sufficient to determine the correct preoperative diagnosis in the cases of chronic SDHs.
Third, it is stressed that early diagnosis and proper surgical treatment are vital, especially in some younger patients.

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