RESUMO
BACKGROUND: Calcified chronic subdural hematoma (CCSDH) is a rare disease for which no standard approach to treatment has been established. Reports covering both burr hole trepanation and craniotomy for CCSDH are rare. Furthermore, infection of CCSDH after the burr hole trepanation has not been reported in the literature. CASE DESCRIPTION: A 61-year-old man presented with left frontotemporoparietal CCSDH demonstrated on computed tomography (CT) scan. The patient underwent 2 separate burr hole trepanations with intraoperative irrigation and postoperative drainage. These procedures led to infection of the CCSDH. The patient eventually underwent an open craniotomy to provide complete removal of the hematoma. CONCLUSIONS: Owing to the complex contents of a CCSDH, burr hole trepanation cannot adequately drain the hematoma or relieve the mass effect. Craniotomy is a much more reliable approach for achieving complete resection of a CCSDH.
Assuntos
Calcinose/cirurgia , Hematoma Subdural Crônico/cirurgia , Infecções Estafilocócicas/terapia , Infecção da Ferida Cirúrgica/terapia , Craniotomia , Desbridamento , Drenagem , Humanos , Masculino , Pessoa de Meia-Idade , Procedimentos Neurocirúrgicos , Staphylococcus epidermidis , Irrigação Terapêutica , Tomografia Computadorizada por Raios X , TrepanaçãoAssuntos
Ependimoma/etiologia , Neurofibromatose 2/complicações , Neoplasias da Medula Espinal/etiologia , Adolescente , Adulto , Ependimoma/diagnóstico , Ependimoma/diagnóstico por imagem , Feminino , Humanos , Neurofibromatose 2/diagnóstico , Neurofibromatose 2/diagnóstico por imagem , Neoplasias da Medula Espinal/diagnóstico , Neoplasias da Medula Espinal/diagnóstico por imagemRESUMO
BACKGROUND: In addition to neurons, all components of the neurovascular unit (NVU), such as glial, endothelial, and basal membranes, are destroyed during traumatic brain injury (TBI). Previous studies have shown that excessive stimulation of calpain is crucial for cerebral injury after traumatic insult. The objective of this study was to investigate whether calpain activation participated in NVU disruption and edema formation in a mouse model of controlled cortical impact (CCI). METHODS: One hundred and eight mice were divided into three groups: the sham group, the control group, and the MDL28170 group. MDL28170 (20 mg/kg), an efficient calpain inhibitor, was administered intraperitoneally at 5 min, 3 h, and 6 h after experimental CCI. We then measured neurobehavioral deficits, calpain activity, inflammatory mediator levels, blood-brain barrier (BBB) disruption, and NVU deficits using electron microscopy and histopathological analysis at 6 h and 24 h after CCI. RESULTS: The MDL28170 treatment significantly reduced the extent of both cerebral contusion (MDL28170 vs. vehicle group, 16.90 ± 1.01 mmÎ and 17.20 ± 1.17 mmÎ vs. 9.30 ± 1.05 mmÎ and 9.90 ± 1.17 mmÎ, both P < 0.001) and edema (MDL28170 vs. vehicle group, 80.76 ± 1.25% and 82.00 ± 1.84% vs. 82.55 ± 1.32% and 83.64 ± 1.25%, both P < 0.05), improved neurological scores (MDL28170 vs. vehicle group, 7.50 ± 0.45 and 6.33 ± 0.38 vs. 12.33 ± 0.48 and 11.67 ± 0.48, both P < 0.001), and attenuated NVU damage resulting (including tight junction (TJ), basement membrane, BBB, and neuron) from CCI at 6 h and 24 h. Moreover, MDL28170 markedly downregulated nuclear factor-κB-related inflammation (tumor necrosis factor-α [TNF-α]: MDL28170 vs. vehicle group, 1.15 ± 0.07 and 1.62 ± 0.08 vs. 1.59 ± 0.10 and 2.18 ± 0.10, both P < 0.001; inducible nitric oxide synthase: MDL28170 vs. vehicle group, 4.51 ± 0.23 vs. 6.23 ± 0.12, P < 0.001 at 24 h; intracellular adhesion molecule-1: MDL28170 vs. vehicle group, 1.45 ± 0.13 vs. 1.70 ± 0.12, P < 0.01 at 24 h) and lessened both myeloperoxidase activity (MDL28170 vs. vehicle group, 0.016 ± 0.001 and 0.016 ± 0.001 vs. 0.024 ± 0.001 and 0.023 ± 0.001, P < 0.001 and 0.01, respectively) and matrix metalloproteinase-9 (MMP-9) levels (MDL28170 vs. vehicle group, 0.87 ± 0.13 and 1.10 ± 0.10 vs. 1.17 ± 0.13 and 1.25 ± 0.12, P < 0.001 and 0.05, respectively) at 6 h and 24 h after CCI. CONCLUSIONS: These findings demonstrate that MDL28170 can protect the structure of the NVU by inhibiting the inflammatory cascade, reducing the expression of MMP-9, and supporting the integrity of TJ during acute TBI.