ABSTRACT
BACKGROUND: Whether hyperbaric oxygen therapy (HBOT) can cause paradoxical herniation is still unclear. CASE SUMMARY: A 65-year-old patient who was comatose due to brain trauma underwent decompressive craniotomy and gradually regained consciousness after surgery. HBOT was administered 22 d after surgery due to speech impairment. Paradoxical herniation appeared on the second day after treatment, and the patient's condition worsened after receiving mannitol treatment at the rehabilitation hospital. After timely skull repair, the paradoxical herniation was resolved, and the patient regained consciousness and had a good recovery as observed at the follow-up visit. CONCLUSION: Paradoxical herniation is rare and may be caused by HBOT. However, the underlying mechanism is unknown, and the understanding of this phenomenon is insufficient. The use of mannitol may worsen this condition. Timely skull repair can treat paradoxical herniation and prevent serious complications.
ABSTRACT
OBJECTIVE: To investigate whether mammalian target of rapamycin (mTOR) kinase was abnormally activated in maldeveloped balloon cells and dysmorphic neurons of focal cortical dysplasia (FCD) with refractory epilepsy. METHODS: A total of 12 archival cases of FCD typeIIwith medically intractable epilepsy treated between 2008 and 2010 were retrieved. Perilesional brain tissue was used as control specimens (n = 8). The expression of phosphorylated p-AKT (Ser473), p-mTOR (Ser2448) and p-P70S6K (Thr389) was investigated by imunocytochemistry. RESULTS: The expression of p-AKT (Ser473), p-mTOR (Ser2448) and p-P70S6K (Thr389) was found in meldeveloped balloon cells and dysmorphic neurons of FCD. A weak stain in a small amount of pyramid neurons was also found in the control group. CONCLUSION: Abnormal activation of mTOR in maldeveloped balloon cells and dysmorphic neurons of FCD may be a key molecular mechanism underlying the histological changes and repeated seizures.
Subject(s)
Brain Diseases/metabolism , Brain Diseases/pathology , Malformations of Cortical Development/metabolism , Malformations of Cortical Development/pathology , TOR Serine-Threonine Kinases/metabolism , Adolescent , Adult , Child, Preschool , Epilepsy/metabolism , Epilepsy/pathology , Female , Glial Fibrillary Acidic Protein/metabolism , Humans , Immunohistochemistry , Male , Malformations of Cortical Development, Group I , Nestin/metabolism , Neurons/metabolism , Phosphorylation , Proto-Oncogene Proteins c-akt/metabolism , Ribosomal Protein S6 Kinases, 70-kDa/metabolism , Young AdultABSTRACT
OBJECTIVE: To explore the expression and clinical significance of tumor necrosis factor-alpha (TNF-α) and its receptors p55 and p75 in non-specific chronic encephalitis relative intractable epilepsy (NCERE) and non-NCERE. METHODS: Immunohistochemical SABC staining was employed to detect the foci of 24 cases of intractable epilepsy (NCERE, n = 10; non-NCERE, n = 14) and 10 cases of the expression of TNF-α and its receptors p55 and p75 in normal brain tissues (control group) to analyze their clinical significance. RESULTS: All expressions of the control group were negative. TNF-α and its receptors p55 and p75 were differentially expressed in neuron cytoplasm between NCERE and non-NCERE. No statistical significance existed between NCERE and non-NCERE (P > 0.05). There was a positive correlation between the expressions of receptors p55 and p75 (r = 0.897, P < 0.05). CONCLUSION: By binding its receptors and the synergistic effect between receptors p55 and p75, TNF-αis involved in the generation and development of NCERE and non-NCERE. However it appears to have nothing to do with the etiology of epilepsy.
