Background Research suggests children with genetic disorders exhibit greater coping skills when they are aware of their condition and its heritability. While the experiences parents have at diagnosis may influence their decision to disclose the diagnosis to their children, there is little research into this communication. The aim of the current study was to examine the relationship between the diagnosis experience and the disclosure experience for parents of children with intellectual disabilities; with a child affected by 22q11.2 deletion syndrome (22q11DS) compared to a group of parents with children affected with other genetic diagnoses, with a similar age of diagnosis (e.g., Fragile X syndrome) and a group where diagnosis generally occurs early (i.e., Down syndrome). Method The sample comprised 559 parents and caregivers of children with genetic developmental disorders, and an online survey was utilised. Items from the questionnaire were combined to create variables for diagnosis experience, parental disclosure experience, child’s disclosure experience, and parental coping and self-efficacy. Results Across all groups parents reported that the diagnosis experience was negative and often accompanied by lack of support and appropriate information. Sixty-eight percent of those in the 22q11DS and 58.3% in the Similar Conditions groups had disclosed the diagnosis to their child, whereas only 32.7% of the Down syndrome group had. Eighty-six percent of the Down syndrome group felt they had sufficient information to talk to their child compared to 44.1% of the Similar Conditions group and 32.6% of the 22q11DS group. Parents reported disclosing the diagnosis to their child because they did not want to create secrets; and that they considered the child’s age when disclosing. In the 22q11DS and Similar Conditions groups, a poor diagnosis experience was significantly associated with negative parental disclosure experiences. In the Similar Conditions group, a poor diagnosis experience was also significantly associated with a more negative child disclosure experience. Conclusions As expected this study highlights how difficult most parents find the diagnosis experience. Importantly, the data indicates that the personal experiences the parents have can have a long-term impact on how well they cope with telling their child about the diagnosis. It is important for clinicians to consider the long-term ramifications of the diagnosis experience and give the parents opportunities; through, for instance, psychoeducation to prepare for telling their child about the diagnosis. Further research is warranted to explore what type of information would be useful for parents to receive.
Cognitive disability is a major contributor to the comorbidities of epilepsy. There is major evidence that confirms that cognitive impairment can appear or worsen with early and chronic progressive neurologic changes in epilepsy. It has been increasingly accepted that comorbidity does not indicate causality. Certainly, cognitive impairment in epileptic patients warrants crucial evaluation and mitigation from the onset of diagnosis and treatment of epilepsy. The concept of a bidirectional nature of cognitive impairment in epilepsy represents a change in the paradigm of the neuropsychology of epilepsy. It has been suggested that both behavioral and cognitive dysfunction associated with epilepsy are not necessarily the consequence of active epilepsy but in fact, can dominate and be associated with factors before the emergence of epilepsy. This review discusses different relations of behavioral and cognitive comorbidities in epilepsy and tries to clarify the nature of the relationship between epilepsy and cognition.
The presence of inflammation is one of the key factors in the onset and progression of various medical disorders and diseases, making it a crucial challenge for treatment. The purpose of this study is to evaluate antioxidant and anti-inflammatory effects of Vinpocetine, using acute models of inflammation; Xylene-, Carrageenan (CGN)-induced inflammation and acetic acid-induced vascularpermeability in mice were used. We also employed molecular docking approach to verify the underlying mechanism of anti-inflammatory activity of Vinpocetine. In a current investigation, Vinpocetine showed anti-inflammatory and antioxidant effects on Xylene-and CGN-induced inflammation in a dose-dependent manner. Vinpocetine reduced inflammatory edema and restored antioxidant tissue balance, probably via suppression of IL-1β, IL-6, TNF-α, MDA and MPO activity, and also through increased non-enzymatic antioxidant (GSH) levels in paw tissue. Histopathological examination showed that Vinpocetine restored normal skin architecture with significant inhibition of tissue edema, congestion, and cellular infiltration in CGN-challenged paw. Mechanistically, Vinpocetine showed downregulation the expression of COX-2 protein, in western blot assessment, that was associated with significant decrease in the level of prostaglandin E 2 (PGE2) levels; a major metabolic product of COX-2 enzyme. Interestingly, Silico study showed that Vinpocetine has strong affinity to COX-2, similar to diclofenac, suggested possible mechanism of downregulation of COX-2 expression. Therefore, Vinpocetine showed antioxidant and anti-inflammatory responses might, in part, due to inhibition of COX-2/PGE 2 pathway.
Sleep is a highly coordinated physiologic state, which is essential for the functional integrity of the neurons and brain. It is crucial for survival. Nonrapid eye movement sleep (NREM) vagal dominance enables the neural/cardiovascular axis to regenerate homeostasis after periods of stress or fatigue during wakefulness. Any reasons for sleep interruption or deprivation like periodic limb movements during sleep (PLMS), insomnia, shift work, and obstructive sleep apnea have a negative effect on cardiovascular homeostasis and restoration. Sleep disorders have a fundamental contribution to cerebrovascular and other cardiovascular diseases. The aim of this review is to highlight the role of sleep disorders in the risk of cerebrovascular ischemic stroke and help both neuropsychiatrists and our community to realize the great value of diagnosis and management of sleep disorders for effective prevention of ischemic stroke and proper care. Further attention and care should be given to the early identification of sleep disorders in risky patients to avoid major cerebrovascular and cardiovascular events.
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