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Tuesday, May 16, 2017

Psychosocial Impact of Multiple Sclerosis: Challenges and Solutions

Multiple sclerosis (MS) is a disease of the central nervous system characterized by an immune-mediated attack on the myelin and oligodendrocytes, resulting in inflammatory lesions, astrocytic scarring, and axonal loss. It is estimated that more than 300,000 people in the United States have MS, and there is some epidemiologic evidence that the incidence is increasing in women. Symptoms of MS are wide ranging in nature and severity and may or may not include disturbances in gait, balance, vision, bladder and/or bowel function, sensation, sexual function, psychiatric status, and cognition. The course of MS is highly variable, although the expected life span is decreased only by a few years.

Psychosocial Challenges

MS is an unpredictable, potentially disabling disease. Although outcomes can be estimated in large epidemiologic studies and follow-up studies from large clinical trials, it is very difficult to predict long-term outcomes for a given individual. This uncertainty represents a challenge to the coping capacity of persons with MS. There are a number of specific psychosocial challenges, including clinical depression, anxiety, sexual dysfunction, cognitive changes, and demoralization and grief associated with MS-related losses.

Clinical Depression and Grief

Depression is the most common psychiatric disorder in MS. Major depression is a serious psychiatric disorder that is distinguished from minor depression, discouragement, and grief by the persistence, severity, and number of symptoms.

According to the Diagnostic and Statistical Manual for Mental Disorders, 4th edition, text revision, a diagnosis of major depression requires an individual to have a sad or irritable mood most of the day and nearly every day for at least 2 weeks. In addition, there must be 4 other symptoms present during this time, which may include:

  • anhedonia (loss of interest in the things one is usually interested in and capable of doing);
  • feelings of worthlessness or excessive/inappropriate guilt;
  • significant increase or decrease in appetite with weight gain or loss;
  • change in sleep patterns (waking up 2-3 hours earlier than usual, or increase in number of hours of sleeps each day, by several hours or more);
  • recurrent thoughts of death or suicidal feelings and thoughts;
  • fatigue;
  • attentional impairment; and
  • sexual dysfunction.

Some of the symptoms associated with major depression are also associated with MS. Consequently, it's important to differentiate between social withdrawal associated with depression (due to loss of interest in usual social activities) and the inability to socialize in one's usual manner due to MS symptoms or impairments. If the persistent and severe mood changes that characterize major depression are not present, such symptoms are most likely due to MS.

Major depression among those with MS is consistently related to a loss in the perceived quality of life and is associated with decreases in self-care, including adhering to disease-modifying medications in MS, the failure of which may lead to long-term disease morbidity. In contrast to clinical depression, normal grief tends to occur after a loss (eg, recent exacerbation that produced permanent neurologic impairments). Grief is not associated with significant sustained impairments in function and is not typically associated with anhedonia.

In MS there is increased suicidal risk. One study that evaluated death records in MS found that suicide rates in MS patients were up to 7.5 times greater than in the general population. These findings are supported by other studies that show that suicidal ideation and lifetime suicidal intent among individuals with MS were approximately 18% and 28% respectively.

Evidence from several studies suggests that many MS patients who experience major depression are not treated or are significantly undertreated for their depressive symptoms. The latter studies highlight the need for increased systematic screening in MS for depression. Decreases in depression in MS patients receiving treatment for depression have also been associated with decreases in in-vitro antigen-specific and non-antigen-specific TH1-mediated interferon-gamma production, which may reflect an underlying inflammatory component associated with major depression in MS.

Because numerous studies estimate that between 36% and 60% of MS patients will experience an episode of major depression at some point during their lifetime, it is imperative to screen for depression during visits. Recommendations for screening have included the use of self-report scales, such as the Beck Depression Inventory II, Patient Health Questionnaire, and Chicago Multiscale Depression Inventory. One study found that simply asking the following questions was able to detect the presence of a major depressive episode with high sensitivity and specificity:

During the past 2 weeks, have you often been bothered by feeling down, depressed, or hopeless?
During the past 2 weeks, have you often been bothered by little interest or pleasure in doing things?
Several randomized trials in MS have indicated that depression can be treated successfully with a variety of antidepressant medications, cognitive-behavioral therapy, or both. The relative effect sizes of antidepressant therapy and cognitive-behavioral therapy on depression in MS have been found to be similar, so individuals can be offered a choice. However, in patients with severe depression, mental health professionals consider antidepressant therapy the first line of treatment, with psychotherapy serving as an important adjunctive therapy. There is some evidence that offering both antidepressant treatment and psychotherapy will confer improved long-term outcomes over either treatment alone.


The prevalence rates of clinically significant symptoms of anxiety in MS vary from 12% to 90% with most studies indicating 30% to 50%. Risk factors for anxiety disorders in MS patients have included female sex, time since diagnosis, comorbid diagnosis of depression, limited social support, and disability status. MS patients report significantly more anxiety than do healthy controls, with anxiety symptoms associated with fatigue, sleep disturbance, problem-solving deficits, pain, and disability status. It is possible that screening assessments or targeted interventions can be put into place based on the findings about prevalence rates or predictors of anxiety.

The point-prevalence of clinically significant anxiety was found to be 25% in one study, which was 3 times the rate of clinically significant depression in the sample. Females were significantly more anxious than males, and anxiety comorbid with depression was associated with increased thoughts of self-harm, more somatic complaints, and greater social dysfunction.

Social anxiety has also been found to be common. In one study, 30.6% of serial clinic patients met criteria for social phobia (fear and avoidance of social situations) on the Social Phobia Inventory, which was not associated with severity of disability. The presence of social phobia was associated with reduced health-related quality of life. To date, no treatments for social phobia in MS have been reported in the literature.

Injection phobia is also fairly common in MS. This is a problematic symptom, as most disease-modifying therapies are delivered by injection and require a schedule of either subcutaneous or intramuscular injections ranging in frequency from daily to weekly. Patients with injection phobia often select a family member/friend/other to conduct the injection, which is strongly linked to poor long-term adherence.

Cognitive-behavioral therapy for the treatment of injection phobia in MS patients was successful in one small sample pilot study published to date. In this study, 8 patients who could not self-inject due to phobia were able to do so within 7 treatment sessions, and 7 of 8 patients continued to self-inject at 3-month follow up. Given poor long-term adherence associated with non-self-injection, it is advisable to treat injection phobia early.

The MS literature cites the treatment of generalized anxiety with psychopharmacologic agents, including benzodiazepines and SSRI's. To date, one randomized clinical trial of short-term (6 weeks) cognitive-behavioral therapy reported clinically significant reductions in anxiety (and comorbid depression) with treatment (cognitive-behavioral therapy combined with progressive deep-muscle relaxation training adapted for patients with MS) relative to non-treatment (MS clinic services only). This study also reported that treated patients showed increases in coping behaviors that were associated with better emotional management and problem-solving behaviors. More recently, a 1-year, open-label trial of escitalopram in women with relapsing-remitting MS reported reduced risk for relapses associated with stressful life events; results will need to be replicated in larger samples with better controlled studies.

Cognitive Dysfunction in MS

Prevalence studies report that 43% to 65% of persons diagnosed with MS have objective cognitive impairments on neuropsychological tests. The prevalence rates range widely, in part due to sampling and other study design issues. Studies that focused on community samples of MS patients and excluded clinic patients report lower rates, while studies that sampled clinic patients report higher rates.

The types of cognitive impairments identified in MS are wide ranging and have included slowed processing speed, impairments in verbal and visual memory, various aspects of attention, visual-spatial judgment, verbal fluency, and executive function. Cognitive impairments can occur very early in MS, and several studies have identified impairments in patients with clinically isolated syndrome before meeting the criteria for clinically definite MS. The severity of cognitive impairment in MS also ranges widely, mirroring the variability of other clinical symptoms. Most patients have multifocal impairments with relatively good preservation of premorbid language abilities and some aspects of reasoning skills. Occasionally the severity is extreme, with the obvious presence of a dementia. Natural history studies are few but have indicated that patients identified with a focal cognitive impairment are likely to have progression of that impairment longitudinally and to develop additional impairments.

Cognitive impairments have been found to be highly associated with employment problems, social problems, difficulties in activities of daily living, and quality of life. The presence of a cognitive impairment cannot be predicted from the overall severity of disability, as numerous studies report the relationship between them to be quite modest. Cognitive impairments correlate better with a variety of MRI metrics, including T2 lesion load, T1 "black hole" lesions, cerebral atrophy, diffusion tensor imaging, and diffusion-weighted imaging studies. Third-ventricle width has been highly associated with the presence of cognitive impairments, probably due to the relationship between proximal thalamic and other structures that are highly related to cognitive function. Overall, studies have indicated that measures of atrophy account for more variance in cognition than does lesion burden.

The literature on the treatment of cognitive impairments is relatively sparse. Symptomatic treatment studies are inconclusive or largely negative. There are few large-scale, well-controlled, or well-designed studies on cognitive rehabilitation to date, although preliminary studies have found that verbal learning and memory can be improved objectively. Evidence from substudies of clinical trials of disease-modifying therapies indicates that cognitive impairments can be prevented or delayed. Studies of beta-interferon 1a and 1b found fewer cognitive deficits at the end of trials in patients randomly assigned to active treatment arms, although substudy data from a clinical trial of glatiramer acetate did not find differences between groups. Differences in results between disease-modifying therapies must not be overinterpreted, however, because these trials were not designed or powered to evaluate cognitive outcomes as either primary or secondary endpoints. Future studies that are designed and powered for that purpose will shed better light on the impact of disease-modifying therapy on cognition.

This article was originally published in Medscape by authors: Frederick W. Foley, PhD, faculty and disclosures

Sunday, May 14, 2017

The motherlode of 'mother love' chemicals

The feel-good brain chemical dopamine appears to play a role in the development of a healthy bond between a mother and baby, a new study suggests.

Dopamine may motivate moms to do more for their children because it makes mothers feel better, researchers said.

And this may not end when babies get older. "It is very likely that the processes we observed between mothers and their infants continues through the life span as their children grow," said study co-author Lisa Feldman Barrett. She's a psychology professor at Northeastern University in Boston.

"It may also be the case that this process supports people as they provide care and nurture to one another in close relationships," she added.

Previously, research has linked mother-baby bonding to the hormone oxytocin.

In this study, the researchers wanted to learn more about what goes on in the brain that helps motivate mothers to take care of their babies.

"Newborns are completely helpless and rely on their parents for survival. A mother must figure out if her infant is hungry, tired, uncomfortable, or lonely to provide appropriate care. So mothers must be highly motivated to care for their infants," Barrett pointed out.

Previous research in rodents has suggested that the brain chemical dopamine is key to bonding between mothers and infants, said study lead author Shir Atzil. She's a post-doctoral fellow at Massachusetts General Hospital in Boston.

"Rat mothers who are highly motivated to care for their pups secrete more dopamine in response to their pups. But the chemical basis of mother-infant bonding in humans was still a mystery," Atzil said.

For the new study, the researchers enlisted 19 mothers (aged 21 to 42) and their babies (aged 4 months to 2 years). The investigators video-recorded the mothers interacting with their babies to see how they got along. Then the researchers had the moms undergo brain scans as they watched videos of their babies or other babies.

The brains of the mothers secreted more dopamine when they watched their own babies, Atzil said. Judging by the videos of the mothers and babies interacting, she said, "mothers who secrete more dopamine were more likely to provide optimal care for their infants, were more sensitive to their infants' needs, and adjusted their own behavior to meet those needs."

Atzil said the research shows how important dopamine is in optimal maternal caregiving. Conversely, the study also gives clues to what might be going wrong in mothers who don't or can't properly care for their babies.

"Mothers who were less responsive to their infants also secreted less dopamine when watching films of their infants. This provides us with hints as to what goes wrong in a mother's brain when she is struggling to provide for her infant," Atzil said.

What does this mean in the long term?

Barrett said the researchers suspect that the brains of the infants themselves develop at a higher level when their mother does a better job of caring for them.

"An infant is not born with a fully developed brain," she said. "Its wiring develops over a number of years, and normal brain development requires responsive caregivers. Infants who do not receive the normal care they require are more likely to do poorly at school, have lower achievement levels, and are at risk for mental and physical disease as adults."

What about fathers and others who take care of babies who aren't their biological mothers? They may also feel a dopamine boost from taking care of an infant, but future research is needed to know for sure, Barrett said.

Paul Zak, founding director of the Center for Neuroeconomics Studies at Claremont Graduate University, said the study results may seem obvious. Of course women who bond more with their babies "have stronger responses in the brain to their infants in areas that make it feel good to care for them and in areas associated with emotional connection," he said.

Still, he said, the study authors connected all this to how the mothers bonded with their babies in a way that's "important and convincing."

Zak pointed out, however, that the study is small so it may not apply to all mothers.

And he added that it's not clear if "great moms are born that way or become that way," since the study can't show whether some mothers are primed for better bonding before their child is born.

The study was published online Feb. 13 in the Proceedings of the National Academy of Sciences.

More information: Lisa Feldman Barrett, Ph.D., professor, psychology, Northeastern University, Boston; Shir Atzil, Ph.D., post-doctoral fellow, Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Boston; Paul Zak, Ph.D., chairman and professor, economics, and founding director, Center for Neuroeconomics Studies, Claremont Graduate University, Claremont, Calif.; Feb. 13, 2017, Proceedings of the National Academy of Sciences, online. www.pnas.org/cgi/doi/10.1073/pnas.1612233114

Journal reference: Proceedings of the National Academy of Sciences via Medical Xpress

Tuesday, May 2, 2017

Child molestation is not a joke: Hadiqa Kiani on Yasir Hussain's slip of tongue

The tasteless joke made by the show’s host Yasir Hussain on the 5th Hum Awards when Ahsan Khan won the award for his role in critically acclaimed serial Udaari, left many furious.

While Jibran Nasir slammed the Lahore Se Aagay actor’s crass humour on Twitter, Hadiqa Kiani also gave her two cents on the matter.

The Dupatta singer, who was present at the award ceremony, took to Twitter to expressed her feeling about the very delicate issue Udaari showcased and how Yasir’s joke ruined it all.

She wrote, “I guess I was lucky enough to have left the award show before this disgusting joke was cracked. This is exactly what’s wrong with out society, people think it’s okay to stoop so low and speak in such a foul manner. I’m not putting the blame exclusively on Mr Yasir Hussain, but on everyone in the room who sat in that room and laughed along… you all deserved to be questioned.”

“Staying silent in the face of rape culture is bad enough…but to laugh along and encourage it? Despicable. God, when especially honouring Ahsan and the whole Udaari team for shedding light on such an issue…all of it was just tainted by that joke. So, in case you need to be reminded, child molestation is not a joke, it is a serious crime that violates BASIC human rights. Disgusted,” she further added.

Here’s the original post:

Muniba Mazari, too condemned the crude joke and posted:

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