Large Bilateral Calcified Subdural Hematomas

A 7-year-old boy presented with a spastic quadriparesis and learning difficulties that had been detected at 2 years old. He had undergone a ventriculoperitoneal shunt insertion for malformative hydrocephalus at a different neurosurgical institution 4 years prior to his visit to our clinic. He was followed regularly as an outpatient and continued to be well except for a retarded psychomotor development. He was admitted to our department for episodic diffuse headache that had lasted for almost 9 months. Pain was well tolerated; however, 1 month prior to admission additional seizure was reported. There were no associated symptoms of nausea or diminished vision. At admission he was conscious and spastic with mental retardation. Cranial computed tomography scan scan showed a large bilateral fronto-temporoparietal heterogeneous polylobulated lesion with important peripheral calcifications consistent with calcified chronic subdural hematomas (CSDH). The hematomas were biconvex with a mild shift of the midline from left to right (Figure A,B). On magnetic resonance imaging, both collections were heterogeneous and the peripheral calcifications appeared as a low-intensity curve on T2-WI (Figure C,D). Hemispheric lobes had an atrophic appearance bilaterally. In addition, an extensive extracerebral fluid accumulation was noted around the hematomas. In view of the clinical condition of the patient, antiepileptic drugs and analgesics were prescribed with a good control. The decision to not treat was based on an assessment that surgery carried too high a risk of possible complications without the guaranteed benefit of satisfactory improvement of seizure and headache. Calcified CSDH is an unusual phenomenon, rarely observed as a long-term complication in patients with ventricular shunting for hydrocephalus. When the intracranial pressure is reduced secondary to the overdrainage of cerebrospinal fluid,a partial collapse of the brain may occur. This collapse results in widening of the subdural space and stretching of the bridging veins, which increase the risk of occult hemorrhage. The pathogenesis of calcified CSDH is unclear, the hemorrhage is thought to progress from hyalinization to calcification but it has been found that it takes at least 6 months for calcification to develop. A variety of clinical presentations have been reported in the literature from asymptomatic to acute intracranial pressure. Bilateral calcified CSDH is more rare, classically named “armored brain,” where another concentric skull appears to be inside the cranium on the computed tomography scan scan. Calcification can occur in both the parietal and visceral capsules as well as in the hematoma itself as seen in our patient. To our knowledge, only one other paper showed MR imaging findings of Calcified CSDH: T1-WI showed organized or partially calcified subdural hematoma as a characteristic heterogeneous web-like appearance. On T2-WI, a hypointense curve was seen in the periphery of hematoma. Most authors recommend the surgical procedure for calcified CSDH only when there is an acute or progressive neurological deficit that can be clearly attributed to the calcified hematoma. From Department of Neurosurgery, Mohammed V Military Teaching Hospital, Rabat, Morocco. ISSN 0017-8748 doi: 10.1111/j.1526-4610.2011.01865.x Published by Wiley Periodicals, Inc. Headache © 2011 American Headache Society