The Sinking Bone Syndrome?

Department of Neurosurgery, Università Politecnica delle Marche, Umberto I General Hospital.
Neurologia medico-chirurgica (Impact Factor: 0.72). 05/2013; 53(5):329-335. DOI: 10.2176/nmc.53.329
Source: PubMed


Bone resorption is a known complication of cranioplasty after decompressive craniectomy (DC). A peculiar group of insidious, progressive, invalidating neurological symptoms was observed in patients presenting with incomplete resorption and abnormal mobility of the re-implanted bone. Such symptoms were similar, but with time more severe, to those encountered in the sinking flap syndrome. Are we facing a sort of Sinking Bone Syndrome? We accurately analyze these cases and review the literature. Over a 7-years period, 312 DCs were performed at our Institution. In 7 patients, headache, vertigo, gait ataxia, confusion, blurred speech, short-term memory impairment, hemiparesis, sudden loss of consciousness, and third cranial nerve palsy were observed in a time period ranging from 18 months to 5 years after cranioplasty. Clinical and neuroradiological examinations were performed to disclose the possible etiopathogenesis of this condition. Collected data showed partial resorption of the repositioned bone and its unnatural inward movements during postural changes. Bone movements were interpreted as the major cause of the symptoms. A new cranioplasty was then performed in every case, using porous hydroxyapatite in 6 patients and polyetherketone implant in the other. Full resolution of symptoms was always obtained 3 to 20 days after the second surgery. No further complications were reported. We believe that long-term follow up in patients operated on by cranioplasty after DC will be needed regularly for years after skull reconstruction and that newly appearing symptoms should never go underestimated or simply interpreted as a long-term consequence of previous brain damage.

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Available from: Roberto Colasanti, Oct 10, 2015
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    ABSTRACT: There is much interest in the use of decompressive craniectomy for intracranial hypertension. Whilst technically straightforward, the procedure is not without significant complications. A retrospective analysis was undertaken of 41 patients who had had a decompressive craniectomy for severe head injury in the years 2006 and 2007 at the two major hospitals in Western Australia, Sir Charles Gairdner Hospital and Royal Perth Hospital. Complications attributable to the decompressive surgery were: herniation of the cortex through the bone defect, 18 patients (51%); subdural effusion, 22 patients (62%); seizures, five patients (14%) and hydrocephalus, four patients (11%). Complications attributable to the subsequent cranioplasty were: infection, four patients (11%) and bone flap resorption, six patients (17%). Syndrome of the trephined occurred in three (7%) of those patients whose bone flap had significantly resorbed. Two deaths (5.5%) occurred as a direct complication of the craniectomy or cranioplasty procedure. I attempted to define what may be regarded as a complication of the decompressive procedure rather than what may be a consequence of the primary pathological process of traumatic brain injury.
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