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J Neurol Neurosurg Psychiatry. 2007 May; 78(5): 542–543.
PMCID: PMC2117812

Armoured brain: case report of a symptomatic calcified chronic subdural haematoma

We present the case of a patient with a symptomatic calcified chronic subdural haematoma (CSDH), or a so‐called “armoured‐brain”, who was admitted to our hospital with clinical signs of tentorial herniation.

Figure 11 shows the computed tomography image of this 67‐year‐old male patient who presented with a Glasgow Coma Score of E1M5V1 and a bilateral oculomotor paresis. Uncal herniation due to a bilateral calcified CSDH can be clearly appreciated. The patient's medical history showed meningitis at the age of 3 months, resulting in hydrocephalus and mental retardation. His family had noticed numerous falls and frequent headaches over the past 3 months. Furthermore, 6 months previously, he was diagnosed with focal epilepsy due to a left hemisphere infarction.

figure jn108662.f1
Figure 1 Computed tomography scan of a patient with armoured brain at admission. Note the uncal herniation and cortical compression due to a bilateral calcified chronic subdural haematoma.

Bilateral CSDH can be treated by bilateral burr hole craniostomy combined with irrigation.1,2 However, we thought that abrupt decompression by two‐sided burr hole craniostomy in this case posed too great a risk for recurrence of haematoma or for reversing the downward into an upgrade herniation. Therefore, we treated the patient with corticosteroids and mannitol for the first 24 h to prepare him for surgery, during which he regained consciousness (Glasgow Coma Score E4M6V4) and pupillary reactivity to light. Then, we performed a left‐sided twist drill craniostomy with controlled drainage via an external catheter, placed in the subdural space, for 48 h (volume 150 ml). Postoperatively and after catheter removal, the patient further recovered and showed no clinical signs of increased intracranial pressure. He was able to carry out his usual duties and activities, and could be discharged after 5 days. A postoperative computed tomography scan directly after catheter removal showed adequate brain expansion (fig 22),), although an enlarged subdural space remained, creating the potential for haematoma reaccumulation.2 Indeed, 6 weeks after surgery, the patient again became lethargic, and follow‐up computed tomography scanning once again showed bilateral CSDH increase and herniation. At this point, a bilateral small (ca. 4 cm) frontotemporal craniotomy was performed, through which the subdural haematoma was rinsed. The fibrous, calcified inner membrane was not surgically removed. One day postoperatively the patient again recovered his normal performance status, and postoperative computed tomographic scanning before discharge after 7 days (fig 33)) for a second time showed adequate brain expansion.

figure jn108662.f2
Figure 2 Postoperative computed tomography scan after subdural catheter removal.
figure jn108662.f3
Figure 3 Postoperative computed tomography scan after the second surgical intervention via a small bilateral craniotomy. “Armoured brain” or “Matrioska head” appearance, showing adhering calcification extending ...

An adhering calcification extending to the cerebral cortex corresponding to the inner membrane of a CSDH has been termed “Matrioska head”3 or “armoured brain”.4 These names well reflect the computed tomogram, where another concentric skull appears to be inside the cranium. The frequency with which radiologically demonstrable calcification occurs within the membranes of a CSDH has been reported to be in the range from 0.3% to 2.7%.5 Although usually seen in subdural haematomas resulting from trauma, it has also been reported in postmeningitic subdural effusions as in the present case.6 An “armoured brain” seems more common in children, but it has been reported in all age groups. The interval between haematoma occurrence and the development of calcification varies from 6 months to many years.5,6 In this case, we suspect that the CSDH might have been present since childhood. The mechanism underlying the calcification remains unclear, and the clinical presentation varies from patients who are asymptomatic to those with signs of raised intracranial pressure as well as seizures and mental retardation.6 Surgical removal of the calcification is difficult and could damage the underlying cortex, and hence should not be performed routinely.5 The treatment of a symptomatic expanding haematoma in these cases presents the treating doctor with a difficult problem, and may require a somewhat different approach from usual.


Competing interests: None declared.


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