•Depression in epilepsy patients is not only extremely common, but is often poorly recognized and inadequately treated.
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•Depression can have significant consequences including increased medical utilization, poor quality of life, social disability,
and mortality.
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•Etiology of depression is multifaceted with prominent psychosocial determinants. Salient medical issues include iatrogenic
causes, especially side effects of antiepileptic drugs (AEDs). In addition, seizures with increased frequency and with ‘forced
normalization’ can be associated with mood disturbance.
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•After a thorough search for correctable causes, treatment should not be delayed, and should include both psychotherapy and
pharmacologic therapies.
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•Antidepressants remain the mainstay of pharmacologic intervention with the selective serotonin reuptake inhibitors (SSRIs)
considered first-line treatment. Venlafaxine, nefazadone, and tricyclic antidepressants (TCAs) can also be used, but with
some important caveats.
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•Decreasing the seizure threshold is a common side effect of all antidepressants, but the risk can be minimized and should
not prevent vigorous treatment of the depressive state.
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Other side effects present with varying frequency from the common (eg, sexual dysfunction as seen with SSRIs) to uncommon withdrawal reactions and rare complications of serotonin syndrome.
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•Depression must also be considered a recurring disease, and when a successful regimen is ascertained, adequate continuation
of treatment is a necessity.
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•Care must be taken to treat the patient until complete resolution is achieved. Many patients with a major depressive disorder
(MDD) will improve with inadequate treatment, but remain encumbered by a smoldering, low-level dysthymia that, in itself,
can severely restrict the patient’s quality of life.
The purpose of this study is to measure soluble CD14 (sCD14) levels in sera from newborn with sepsis, to compare it with other markers, and to study its evolution in Gram-negative and Gram-positive sepsis. Forty normal newborns were included (26 were full term and 14 were preterm infants), 20 babies had a positive blood culture (11 Gram-positive and 9 Gram-negative) and 16 cases were suspected of having sepsis based on clinical and laboratory findings, but a negative blood culture. Interleukin-6 (IL-6), sCD14, and tumour necrosis factor-α (TNFα) were measured by enzyme immunoassay, and fibronectin (FN) and C-reactive protein (CRP) by radial immunodiffusion. Neonates with a positive blood culture had increased levels of sCD14(3.20 ± 1.26μgml-1, p < 0.001), CRP(69 ± 46 μgml-1, p < 0.001)and IL-6 (134 ± 150 pg ml-1, p < 0.001), and decreased values of FN (12.3 ± 6.6 mg ml-1, p < 0.001). TNFα levels were also high (160 ± 37 pg ml-1), but this increase was not statistically significant. Newborn infants suspected of having sepsis but a negative blood culture had similar but milder abnormalities. Soluble CD 14 levels correlated with CRP values; however, there was no correlation between sCD 14, TNFα and IL-6. Neonates with sepsis by Gram-positive bacteria had lower sCD14 levels than patients with Gram-negative sepsis (2.63 ± 1.2 versus 4.04 ± 1.0μgml-1, p < 0.05). In conclusion, the sCD14 level is increased in newborn infants with sepsis, and this is higher in infections by Gram-negative bacteria, suggesting a different contribution of monocyte and macrophage cells. In contrast, IL-6, TNFα, CRP and FN values are similar in infections by Gram-positive and Gram-negative bacteria. 相似文献
Androstene-3beta, 17alpha-diol (17alpha-AED) inhibits DNA synthesis and induces apoptosis in several myeloid cancer cell lines. The purpose of this study was to determine if 17alpha-AED inhibition of human breast carcinoma cell proliferation is dependent on the estrogen or androgen receptor. At concentrations of 12.5 to 50 x 10(-9) M 17alpha-AED inhibited the proliferation of ZR75-1, estrogen receptor-positive (ER+) cells, by 54% to 68%. Further, 17alpha-AED inhibited MDA-MB231, estrogen receptor-negative (ER-) cells, by 33.6% to 56.0%. The inhibitory effect was dose dependent with a minimal effective inhibitory dose at 12.5x10(-9) M for both cell lines. Both 17beta-AED and estradiol potentiate the inhibitory effect of 17alpha-AED on ER+ cells at lower doses (3.13 to 6.25 x 10(-9) M) where 17alpha-AED alone was not inhibitory. The inhibitory action of 17alpha-AED on human mammary carcinomas appears to be independent of either the alpha estrogen or the androgen receptors. 相似文献
The acetylcholinesterase (AChE) inhibitors sarin and pyridostigmine bromide (PB) have been proposed as causes of neurobehavioral dysfunction in Persian Gulf War veterans. To test possible delayed effects of these agents, we exposed rats to low (subsymptomatic) levels of sarin (0.5 LD50 s.c. 3 times weekly) and/or PB (80 mg/L in drinking water) for 3 weeks. Controls received saline s.c. and tap water. At 2, 4 and 16 weeks after exposure, regional cerebral blood flow (rCBF) and glucose utilization (rCGU) were measured in conscious animals with the Iodo-14C-antipyrine and 14C-2 deoxyglucose methods, respectively.
Two weeks after exposure, PB+sarin caused significant rCBF elevations, but no changes in rCGU, in neocortex, with lesser effects on allocortex. Four weeks after exposure, the same general pattern was found with sarin. Only a few changes were found at 16 weeks post-treatment. The predominant effects of sarin or PB+sarin on rCBF at earlier times after treatment are consistent with the well known direct cerebral vascular effect of cholinergic agonists. The lack of changes in rCBF and rCGU observed at 16 weeks after treatment does not support the hypothesis that repeat exposure to low-dose cholinesterase inhibitors can generate permanent alterations in cerebral activity. 相似文献
OBJECTIVE: Neurologic complications after repair of acute type A aortic dissection remain significant. The use of power M-mode transcranial Doppler monitoring to verify cerebral blood flow during these repairs might decrease cerebral ischemia by correcting malperfusion. The purpose of this study was to analyze the use of power M-mode transcranial Doppler monitoring during repairs of acute type A dissection with regard to neurologic outcome. METHODS: We performed a prospective study of patients undergoing repairs of acute type A aortic dissection. Repairs included profound hypothermic circulatory arrest and retrograde cerebral perfusion. Patients in whom transcranial Doppler monitoring was used to monitor cerebral blood flow and modify operative technique during repair (study group) were compared with those without monitoring and modification (control group). RESULTS: Between September 2001 and October 2003, we repaired 56 cases of acute type A dissection. Power M-mode transcranial Doppler monitoring was used in 50% (28/56) of cases. Power M-mode transcranial Doppler monitoring altered operative cannulation and guided retrograde cerebral perfusion flow in 28.5% (8/28) and 78.6% (22/28) of cases, respectively. Two patients presented with preoperative stroke, one in each group. One operative death occurred in each group. In-hospital mortality and the occurrence of new stroke were not significantly different between the 2 groups. Temporary neurologic dysfunction occurred less often in the study group (14.8% [4/27] vs 51.8% [14/27], P = .008). CONCLUSIONS: Identification of cerebral malperfusion requires cerebral monitoring. By ensuring cerebral blood flow by using power M-mode transcranial Doppler monitoring and correcting cerebral malperfusion by modifying operative technique, neurologic outcome was improved during repairs of acute type A aortic dissection. 相似文献