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Objective To investigate the clinical characteristics and imaging features of radiation-induced hypopituitarism (RIH) in nasopharyngeal carcinoma (NPC) patients after radiotherapy.Methods Retrospective study was performed on the clinical data of 9 NPC patients (7 males and 2 females), diagnosed as RIH after radiotherapy in our hospital from 2000 to 2009; their clinical manifestations, anterior-pituitary hormone levels, cranial MRI features and follow-up results were analyzed. Results The interval between complications after radiotherapy and diagnoses of RIH varied from 10 months to 15 years.Multiple hormone deficits appeared in 5 patients; thyrotropin deficiency and hyperprolactinemia were the most common complications, followed by adrenocorticotropic hormone (ACTH) insufficiency.Typical radiological imaging of the pituitary gland displayed partially empty sella and atrophy of pituitaly gland,which was demonstrated in 2 patients.Five patients got improvement after hormone replacement therapy. Conclusion Radiation-induced hypopituitarism may occur in NPC patients; most patients are subclinical without typical radiological alterations in MRI for pituitary.Routine evaluation of adenohypophysis function is necessary for early detection of hormone deficiency and early hormone replacement treatment.
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Objective To explore the best operation time and approach, and the improvement mechanism of radiation encephalopathy in patients with nasopharyngeal carcinoma. Methods The data of 9 patients with radiation encephalopathy after radiotherapy for nasopharyngeal carcinoma who admitted to our hospital from January 1996 and December 2008 were retrospectively analyzed. The neurological manifestations, imaging, neurosurgery strategies and pathological features of the patients were collected and analyzed. The efficacy and the follow-up results were compared. Results MRI showed such typical encephalopathy as severe edema or necrosis in the temporal lobe in most patients adopted radiotherapy; edema and necrosis in the brain tissues, hyaline degeneration and blocking in the small blood vessels were showed by pathologic examination. Some patients manifested as having unilateral edema or liquefactive necrosis in the brain with marked mass effect. After the surgery, the edema in the patients' brain was alleviated; 8 patients got improvement and discharged from the hospital in 2-3 weeks with stable vital signs. Eight patients achieved complete remission of headache with 1 having mild headache. Conclusion When medical treatment is not effective in patients who developed edema or liquefactive necrosis after radiotherapy, neurosurgery is a good therapeutic strategy, which can alleviate the symptoms, help clarify the diagnosis and guide the follow-up treatment.
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Objective To observe the effects of lithium chloride (LiCl) on neural cell apoptosis, inflammatory response and expression of nuclear factor kappa B (NF-κB) protein in rats with intracerebral hemorrhage (ICH). Methods Fifty-four male SD rats were randomized into sham-operated, ICH and LiCl treatment groups (n=18), and in the latter two groups, ICH was induced by injection of collagenase Ⅳ into the internal capsule, and phosphate buffer solution was injected in the sham-operated group. Seven days before ICH, the rats in LiCl group received intraperitoneal injection of 1 mmol/kg LiCl once daily till the rats were sacrificed. Brain tissue specimens were collected at 1, 3, and 7 d after ICH to observe neural cell apoptosis, inflammatory response and expression of NF-κB in rat brain using terminal dUTP nick end-labeling (TUNEL), HE staining and immunohistochemistry, respectively. Results Compared with the ICH model group, the rats in LiCl treatment group showed significantly reduced number of TUNEL-positive cells in the brain tissues around the hematoma at 1, 3, and 7 days after ICH (P<0.05). NF-κB protein expression was observed 1 day after ICH, which reached the peak level on day 3 and lowered 7 days after ICH. LiCl treatment significantly lowered the expression of NF-κB protein in comparison with that in ICH group (P<0.05) and obviously ameliorated the inflammatory responses in the brain tissues. Conclusion LiCl provides neuroprotection against ICH by inhibiting neural cell apoptosis and reducing inflammatory response through down-regulation of NF-κB expression.
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Objective To observe neural stem cell activation and proliferation in situ afterintracerebal hemorrhage (ICH) and its effect on the neurological function of the injured adult rats.Methods Seventy-two adult rats were randomized into ICH and sham operation groups (n=36). In theICH group, type Ⅳ collagenase was injected into the internal capsule through a microinfusion pump toinduce intracerebral hemorrhage, and the rats in the sham operation group received only phosphate buffersolution injection. The neurological functions of the rats were observed by rotarod motor test on days 1, 7,14, 21, 28, and 35 after the injection. One day before sacrifice, the rots were subjected to intraperitonealBrdU injection to label the regenerated cells, and immunohistochemistry was used to detect theexpressions of nestin and BrdU in the brain tissue. Results No nestin- or BrdU-positive cells werefound in the brain of the rats in the sham operation group. In rats with ICH, nestin- and BrdU-positivecells were found predominantly in the basal ganglion around the hematoma, in the ependyma and near thesubventricular zone (SVZ) in the brain; the number of the positive cells increased significantly 7 daysafter ICH, peaked on day 14 and then significantly reduced on day 28. The rats exhibited no obviousimprovement of the impaired motor function over the period from day 1 to 35 after ICH. Activation andproliferation of the neural stem cells was not obviously related to the recovery of the neurologicalfunctions. Conclusion Endogeneous neural stem cells in the brain are activated in rats after ICH, butthese stem cells possess rather limited capacity of proliferation and can not sufficiently compensate forICH-induced neurological function impairment.