M. Alexander Otto

LAS VEGAS – Treating comorbid depression gives "you the biggest bang for the buck" in the overall care and rehabilitation of patients with chronic pain, according to Dr. Michael Clark, director of Johns Hopkins University’s Chronic Pain Treatment Program in Baltimore.

"When you treat the depression," pain lessens and function improves, regardless of other treatments and the cause of the pain, he said (JAMA 2009;301:2099-110).

Depression is common in chronic pain and generally thought to be its byproduct. But, at least in some cases, the depression comes first and seems to drive the pain. Depression itself increases the risk for chronic pain syndromes and is the best predictor of persistence. Depression is also associated with higher pain intensity and more comorbities (Psychol. Med. 2004;34:211-9).

"We don’t fully understand" the relationship, but pain perception and depression appear to share common brain pathways, which is "probably why there is so much overlap," said Dr. Clark, also vice chairman for clinical affairs in Hopkins’ department of psychiatry and behavioral sciences.

The message for psychiatrists, primary care providers, and others is to "think depression," especially when chronic pain does not improve or gets worse with standard treatments. If patients are depressed, "aggressive treatment to remission is key," he said at the Nevada Psychiatric Association’s Annual Psychopharmacology Update conference.

Tricyclic antidepressants and serotonin–norepinephrine reuptake inhibitors (SNRIs) "are our friends" because they treat depression and, unlike selective serotonin reuptake inhibitors, neuropathic pain, as well.

"Conventional wisdom is that you give low doses of antidepressants to treat pain, and that you don’t need higher antidepressant-type doses. But if you don’t get pain relief at lower doses, there’s nothing to say that you should not give higher doses," he said.

Duloxetine and venlafaxine are good SNRI options; it is easier to achieve a therapeutic dose with duloxetine, but venlafaxine was fewer cytochrome P450 interactions. Bupropion, a norepinephrine and dopamine reuptake inhibitor, seems especially helpful for fibromyalgia cognitive problems, Dr. Clark said.

Given how much they help chronic pain, "you would think antidepressants would be in the water of every pain clinic, but they are not," he said.

Instead, patients often end up in the polypharmacy jungle, prescribed benzodiazepines, sleeping pills, barbiturates, muscle relaxers, and other drugs which "do not help anything and ... mess them up. [Irrational polypharmacy is] a real problem," he said.

So are the ever-increasing doses of opioids likely when comorbid depression goes unrecognized and untreated. "The amount of opioids [these patients] come to us on is huge. It’s not unusual to see people taking 1,000 mg of oxycodone a day or more, and they’re still walking around," he said.

Opioid-induced hyperalgesia is a risk in those situations, but even at lower doses, opioids can do more harm than good in depressed pain patients, worsening their quality of life, disability, and state of mind. "If you want to use them, you’ve got to make sure that your patient doesnot have an active major depression," Dr. Clark said, noting that the goal of his pain program is "to get people off opioids, usually entirely."

If patients "are not doing well and they are on a bunch of stuff, whether it’s opioids or something else, you really have to think about if the medicine they are on could be contributing or causing all of what you see. You really should be taking people off these things and seeing what happens," he said.

Dr. Clark is a consultant for Eli Lilly.

[email protected]

LAS VEGAS – Treating comorbid depression gives "you the biggest bang for the buck" in the overall care and rehabilitation of patients with chronic pain, according to Dr. Michael Clark, director of Johns Hopkins University’s Chronic Pain Treatment Program in Baltimore.

"When you treat the depression," pain lessens and function improves, regardless of other treatments and the cause of the pain, he said (JAMA 2009;301:2099-110).

Depression is common in chronic pain and generally thought to be its byproduct. But, at least in some cases, the depression comes first and seems to drive the pain. Depression itself increases the risk for chronic pain syndromes and is the best predictor of persistence. Depression is also associated with higher pain intensity and more comorbities (Psychol. Med. 2004;34:211-9).

"We don’t fully understand" the relationship, but pain perception and depression appear to share common brain pathways, which is "probably why there is so much overlap," said Dr. Clark, also vice chairman for clinical affairs in Hopkins’ department of psychiatry and behavioral sciences.

The message for psychiatrists, primary care providers, and others is to "think depression," especially when chronic pain does not improve or gets worse with standard treatments. If patients are depressed, "aggressive treatment to remission is key," he said at the Nevada Psychiatric Association’s Annual Psychopharmacology Update conference.

Tricyclic antidepressants and serotonin–norepinephrine reuptake inhibitors (SNRIs) "are our friends" because they treat depression and, unlike selective serotonin reuptake inhibitors, neuropathic pain, as well.

"Conventional wisdom is that you give low doses of antidepressants to treat pain, and that you don’t need higher antidepressant-type doses. But if you don’t get pain relief at lower doses, there’s nothing to say that you should not give higher doses," he said.

Duloxetine and venlafaxine are good SNRI options; it is easier to achieve a therapeutic dose with duloxetine, but venlafaxine was fewer cytochrome P450 interactions. Bupropion, a norepinephrine and dopamine reuptake inhibitor, seems especially helpful for fibromyalgia cognitive problems, Dr. Clark said.

Given how much they help chronic pain, "you would think antidepressants would be in the water of every pain clinic, but they are not," he said.

Instead, patients often end up in the polypharmacy jungle, prescribed benzodiazepines, sleeping pills, barbiturates, muscle relaxers, and other drugs which "do not help anything and ... mess them up. [Irrational polypharmacy is] a real problem," he said.

So are the ever-increasing doses of opioids likely when comorbid depression goes unrecognized and untreated. "The amount of opioids [these patients] come to us on is huge. It’s not unusual to see people taking 1,000 mg of oxycodone a day or more, and they’re still walking around," he said.

Opioid-induced hyperalgesia is a risk in those situations, but even at lower doses, opioids can do more harm than good in depressed pain patients, worsening their quality of life, disability, and state of mind. "If you want to use them, you’ve got to make sure that your patient doesnot have an active major depression," Dr. Clark said, noting that the goal of his pain program is "to get people off opioids, usually entirely."

If patients "are not doing well and they are on a bunch of stuff, whether it’s opioids or something else, you really have to think about if the medicine they are on could be contributing or causing all of what you see. You really should be taking people off these things and seeing what happens," he said.

Dr. Clark is a consultant for Eli Lilly.

[email protected]

LAS VEGAS – Treating comorbid depression gives "you the biggest bang for the buck" in the overall care and rehabilitation of patients with chronic pain, according to Dr. Michael Clark, director of Johns Hopkins University’s Chronic Pain Treatment Program in Baltimore.

"When you treat the depression," pain lessens and function improves, regardless of other treatments and the cause of the pain, he said (JAMA 2009;301:2099-110).

Depression is common in chronic pain and generally thought to be its byproduct. But, at least in some cases, the depression comes first and seems to drive the pain. Depression itself increases the risk for chronic pain syndromes and is the best predictor of persistence. Depression is also associated with higher pain intensity and more comorbities (Psychol. Med. 2004;34:211-9).

"We don’t fully understand" the relationship, but pain perception and depression appear to share common brain pathways, which is "probably why there is so much overlap," said Dr. Clark, also vice chairman for clinical affairs in Hopkins’ department of psychiatry and behavioral sciences.

The message for psychiatrists, primary care providers, and others is to "think depression," especially when chronic pain does not improve or gets worse with standard treatments. If patients are depressed, "aggressive treatment to remission is key," he said at the Nevada Psychiatric Association’s Annual Psychopharmacology Update conference.

Tricyclic antidepressants and serotonin–norepinephrine reuptake inhibitors (SNRIs) "are our friends" because they treat depression and, unlike selective serotonin reuptake inhibitors, neuropathic pain, as well.

"Conventional wisdom is that you give low doses of antidepressants to treat pain, and that you don’t need higher antidepressant-type doses. But if you don’t get pain relief at lower doses, there’s nothing to say that you should not give higher doses," he said.

Duloxetine and venlafaxine are good SNRI options; it is easier to achieve a therapeutic dose with duloxetine, but venlafaxine was fewer cytochrome P450 interactions. Bupropion, a norepinephrine and dopamine reuptake inhibitor, seems especially helpful for fibromyalgia cognitive problems, Dr. Clark said.

Given how much they help chronic pain, "you would think antidepressants would be in the water of every pain clinic, but they are not," he said.

Instead, patients often end up in the polypharmacy jungle, prescribed benzodiazepines, sleeping pills, barbiturates, muscle relaxers, and other drugs which "do not help anything and ... mess them up. [Irrational polypharmacy is] a real problem," he said.

So are the ever-increasing doses of opioids likely when comorbid depression goes unrecognized and untreated. "The amount of opioids [these patients] come to us on is huge. It’s not unusual to see people taking 1,000 mg of oxycodone a day or more, and they’re still walking around," he said.

Opioid-induced hyperalgesia is a risk in those situations, but even at lower doses, opioids can do more harm than good in depressed pain patients, worsening their quality of life, disability, and state of mind. "If you want to use them, you’ve got to make sure that your patient doesnot have an active major depression," Dr. Clark said, noting that the goal of his pain program is "to get people off opioids, usually entirely."

If patients "are not doing well and they are on a bunch of stuff, whether it’s opioids or something else, you really have to think about if the medicine they are on could be contributing or causing all of what you see. You really should be taking people off these things and seeing what happens," he said.

Dr. Clark is a consultant for Eli Lilly.

[email protected]

LAS VEGAS – Differences in drug responses probably offer the strongest evidence that bipolar disorder and schizophrenia may be separate entities, according to Dr. Charles B. Nemeroff.

The notion that the two are different manifestations of the same disease has gained traction in some quarters because, at least superficially, the two illnesses have quite a bit in common, including age of onset, response to atypical antipsychotics, ventricular enlargement, and shared genetic characteristics.

Early childhood abuse and neglect can increase the risk of both in vulnerable people, as well, and bipolar disorder patients can have auditory hallucinations and paranoid delusions, just as those with schizophrenia do, Dr. Nemeroff said at the Nevada Psychiatric Association’s annual psychopharmacology update.

Indeed, the possibility that they are even on the same spectrum has "implications in terms of current treatment and treatment development," but Dr. Nemeroff said he has his doubts. "The last chapter to this debate has not yet been written," he said.

That both respond to atypicals could be a red herring, for instance. "Imipramine is effective for treating both depression and enuresis, but I don’t think they’re the same thing," said Dr. Nemeroff, Leonard M. Miller Professor and chairman of the department of psychiatry and behavioral sciences at the University of Miami.

Regarding genes, some indeed are associated with both schizophrenia and bipolar disorder, but others appear to increase risk for one but not the other. Overall, genes account for about two-thirds of the risk for bipolar disorder, but only about half the risk for schizophrenia, he said (Neurosci. Biobehav. Rev. 2012;36:556-71).

Bipolar patients also do not lose brain volume over time, unlike patients with schizophrenia, and they often report an early onset of depression, sometimes before puberty. "We often don’t hear that in patients with schizophrenia, even when you talk to family members. There may have been something [odd] going on in those early years, but it doesn’t look like early-onset depression," he said.

Atypicals aside, differences in drug responses probably offer the strongest evidence that the two illnesses are separate entities.

Although of great help in manic patients, anticonvulsants "have no efficacy whatsoever in schizophrenia." Likewise, antidepressants can "rocket" bipolar patients into mania, but "have you ever seen a schizophrenic patient given an antidepressant become acutely manic? I haven’t," Dr. Nemeroff said.

Perhaps the response to lithium is the most telling of all. It remains one of the most effective treatments for bipolar disorder but "just does not work" for schizophrenia, according to numerous trials as both monotherapy and add-on therapy, he said.

"I’ve seen dozens of [bipolar] patients" struggle for years despite treatment with newer agents, but who have never had a lithium trial. When it’s finally tried, they often have "phenomenal response[s]. They became euthymic and remain euthymic for years, and never suffer an episode. I’ve rarely ever seen that with any other treatment for bipolar disorder. [Lithium is] a great drug; it’s also cheap," he said. "Cheap is good for our patients."

Lithium is underused because "nobody’s marketing it to you," he said.

Ongoing monitoring for kidney, thyroid, and other side effects probably puts some psychiatrists off, as well, but it’s really not any more complicated than the ongoing monitoring needed with atypicals and anticonvulsants, he said.

Plus, "there’s pretty good data that if you check TSH [thyroid-stimulating hormone] every 6 months, you’ll be able to catch any incipient hyperthyroidism. Patients who have [thyroid] antibodies at baseline are generally the ones who go on to develop thyroid problems, so you can check that at baseline," he said.

For patients with refractory bipolar depression, "my favorite combination has been lamotrigine and MAO inhibitors," particularly tranylcypromine. "I’ve probably gotten more people [out of] bipolar depression with that – after they’ve been marinated in everything else – than any other strategy besides [electroconvulsive therapy]."

And "lamotrigine doesn’t work in patients with schizophrenia," he noted.

Dr. Nemeroff reported stock ownership, consultant fees, or other income from Allergan, Lilly, Shire, Roche, NovaDel Pharma, BioPharma, AstraZeneca, and other companies.

[email protected]

LAS VEGAS – Differences in drug responses probably offer the strongest evidence that bipolar disorder and schizophrenia may be separate entities, according to Dr. Charles B. Nemeroff.

The notion that the two are different manifestations of the same disease has gained traction in some quarters because, at least superficially, the two illnesses have quite a bit in common, including age of onset, response to atypical antipsychotics, ventricular enlargement, and shared genetic characteristics.

Early childhood abuse and neglect can increase the risk of both in vulnerable people, as well, and bipolar disorder patients can have auditory hallucinations and paranoid delusions, just as those with schizophrenia do, Dr. Nemeroff said at the Nevada Psychiatric Association’s annual psychopharmacology update.

Indeed, the possibility that they are even on the same spectrum has "implications in terms of current treatment and treatment development," but Dr. Nemeroff said he has his doubts. "The last chapter to this debate has not yet been written," he said.

That both respond to atypicals could be a red herring, for instance. "Imipramine is effective for treating both depression and enuresis, but I don’t think they’re the same thing," said Dr. Nemeroff, Leonard M. Miller Professor and chairman of the department of psychiatry and behavioral sciences at the University of Miami.

Regarding genes, some indeed are associated with both schizophrenia and bipolar disorder, but others appear to increase risk for one but not the other. Overall, genes account for about two-thirds of the risk for bipolar disorder, but only about half the risk for schizophrenia, he said (Neurosci. Biobehav. Rev. 2012;36:556-71).

Bipolar patients also do not lose brain volume over time, unlike patients with schizophrenia, and they often report an early onset of depression, sometimes before puberty. "We often don’t hear that in patients with schizophrenia, even when you talk to family members. There may have been something [odd] going on in those early years, but it doesn’t look like early-onset depression," he said.

Atypicals aside, differences in drug responses probably offer the strongest evidence that the two illnesses are separate entities.

Although of great help in manic patients, anticonvulsants "have no efficacy whatsoever in schizophrenia." Likewise, antidepressants can "rocket" bipolar patients into mania, but "have you ever seen a schizophrenic patient given an antidepressant become acutely manic? I haven’t," Dr. Nemeroff said.

Perhaps the response to lithium is the most telling of all. It remains one of the most effective treatments for bipolar disorder but "just does not work" for schizophrenia, according to numerous trials as both monotherapy and add-on therapy, he said.

"I’ve seen dozens of [bipolar] patients" struggle for years despite treatment with newer agents, but who have never had a lithium trial. When it’s finally tried, they often have "phenomenal response[s]. They became euthymic and remain euthymic for years, and never suffer an episode. I’ve rarely ever seen that with any other treatment for bipolar disorder. [Lithium is] a great drug; it’s also cheap," he said. "Cheap is good for our patients."

Lithium is underused because "nobody’s marketing it to you," he said.

Ongoing monitoring for kidney, thyroid, and other side effects probably puts some psychiatrists off, as well, but it’s really not any more complicated than the ongoing monitoring needed with atypicals and anticonvulsants, he said.

Plus, "there’s pretty good data that if you check TSH [thyroid-stimulating hormone] every 6 months, you’ll be able to catch any incipient hyperthyroidism. Patients who have [thyroid] antibodies at baseline are generally the ones who go on to develop thyroid problems, so you can check that at baseline," he said.

For patients with refractory bipolar depression, "my favorite combination has been lamotrigine and MAO inhibitors," particularly tranylcypromine. "I’ve probably gotten more people [out of] bipolar depression with that – after they’ve been marinated in everything else – than any other strategy besides [electroconvulsive therapy]."

And "lamotrigine doesn’t work in patients with schizophrenia," he noted.

Dr. Nemeroff reported stock ownership, consultant fees, or other income from Allergan, Lilly, Shire, Roche, NovaDel Pharma, BioPharma, AstraZeneca, and other companies.

[email protected]

LAS VEGAS – Differences in drug responses probably offer the strongest evidence that bipolar disorder and schizophrenia may be separate entities, according to Dr. Charles B. Nemeroff.

The notion that the two are different manifestations of the same disease has gained traction in some quarters because, at least superficially, the two illnesses have quite a bit in common, including age of onset, response to atypical antipsychotics, ventricular enlargement, and shared genetic characteristics.

Early childhood abuse and neglect can increase the risk of both in vulnerable people, as well, and bipolar disorder patients can have auditory hallucinations and paranoid delusions, just as those with schizophrenia do, Dr. Nemeroff said at the Nevada Psychiatric Association’s annual psychopharmacology update.

Indeed, the possibility that they are even on the same spectrum has "implications in terms of current treatment and treatment development," but Dr. Nemeroff said he has his doubts. "The last chapter to this debate has not yet been written," he said.

That both respond to atypicals could be a red herring, for instance. "Imipramine is effective for treating both depression and enuresis, but I don’t think they’re the same thing," said Dr. Nemeroff, Leonard M. Miller Professor and chairman of the department of psychiatry and behavioral sciences at the University of Miami.

Regarding genes, some indeed are associated with both schizophrenia and bipolar disorder, but others appear to increase risk for one but not the other. Overall, genes account for about two-thirds of the risk for bipolar disorder, but only about half the risk for schizophrenia, he said (Neurosci. Biobehav. Rev. 2012;36:556-71).

Bipolar patients also do not lose brain volume over time, unlike patients with schizophrenia, and they often report an early onset of depression, sometimes before puberty. "We often don’t hear that in patients with schizophrenia, even when you talk to family members. There may have been something [odd] going on in those early years, but it doesn’t look like early-onset depression," he said.

Atypicals aside, differences in drug responses probably offer the strongest evidence that the two illnesses are separate entities.

Although of great help in manic patients, anticonvulsants "have no efficacy whatsoever in schizophrenia." Likewise, antidepressants can "rocket" bipolar patients into mania, but "have you ever seen a schizophrenic patient given an antidepressant become acutely manic? I haven’t," Dr. Nemeroff said.

Perhaps the response to lithium is the most telling of all. It remains one of the most effective treatments for bipolar disorder but "just does not work" for schizophrenia, according to numerous trials as both monotherapy and add-on therapy, he said.

"I’ve seen dozens of [bipolar] patients" struggle for years despite treatment with newer agents, but who have never had a lithium trial. When it’s finally tried, they often have "phenomenal response[s]. They became euthymic and remain euthymic for years, and never suffer an episode. I’ve rarely ever seen that with any other treatment for bipolar disorder. [Lithium is] a great drug; it’s also cheap," he said. "Cheap is good for our patients."

Lithium is underused because "nobody’s marketing it to you," he said.

Ongoing monitoring for kidney, thyroid, and other side effects probably puts some psychiatrists off, as well, but it’s really not any more complicated than the ongoing monitoring needed with atypicals and anticonvulsants, he said.

Plus, "there’s pretty good data that if you check TSH [thyroid-stimulating hormone] every 6 months, you’ll be able to catch any incipient hyperthyroidism. Patients who have [thyroid] antibodies at baseline are generally the ones who go on to develop thyroid problems, so you can check that at baseline," he said.

For patients with refractory bipolar depression, "my favorite combination has been lamotrigine and MAO inhibitors," particularly tranylcypromine. "I’ve probably gotten more people [out of] bipolar depression with that – after they’ve been marinated in everything else – than any other strategy besides [electroconvulsive therapy]."

And "lamotrigine doesn’t work in patients with schizophrenia," he noted.

Dr. Nemeroff reported stock ownership, consultant fees, or other income from Allergan, Lilly, Shire, Roche, NovaDel Pharma, BioPharma, AstraZeneca, and other companies.

[email protected]

The addition of subthalamic stimulation to medication therapy not only improved the quality of life of patients with early Parkinson’s disease and mild levodopa-induced motor complications but also reduced their subsequent motor disability in a randomized trial conducted in French and German centers.

The combination is already known to help advanced Parkinson’s patients. The new findings suggest that "neurostimulation may be a therapeutic option for patients at an earlier stage than current recommendations suggest," wrote lead author Dr. W.M.M. Schüpbach and coinvestigators in the EARLYSTIM (Controlled Trial of Deep-Brain Stimulation in Early Patients with Parkinson’s Disease) study group (N. Engl. J. Med. 2013;368:610-22 [doi:10.1056/NEJMoa1205158]).

The investigators randomized 127 patients with early motor complications to best-practices drug therapy and 124 to that plus subthalamic neurostimulation.

At the end of 2 years, the combination group reported a 7.8 point quality-of-life improvement on the 100-point Parkinson’s Disease [self-] Questionnaire (PDQ-39) summary index, the study’s primary outcome; medication-only patients reported a 0.2 point drop. The between-group difference in mean change from baseline to 2 years was 8.0 points (P = .002).

The neurostimulation group had better scores on motor disability, too, with a between-group difference on the 70-point Unified Parkinson’s Disease Rating Scale (UPDRS), Part III, of 16.4 points without medication in favor of neurostimulation (P less than .001). Neurostimulation was also modestly superior on activities of daily living (P less than .001) and levodopa-induced motor complications (P less than .001), both also assessed by their appropriate UPDRS sections. The group that received neurostimulation also reported longer times with good mobility and no dyskinesia, as reported in patient diaries (P = .01). Stimulation patients had a 39% reduction in their levodopa-equivalent daily dosages, while drug-only patients had an increase of about 21%.

"Because motor symptoms and quality of life" remained relatively constant in the drug-only group, "the improvement among patients who underwent surgical implantation can be attributed to neurostimulation," wrote the authors of the study, which was funded in part by Medtronic, the manufacturer of the neurostimulation equipment used in the trial.

There were no significant between-group differences at baseline. Patients in both groups were about 52 years old on average, sick for about 7.5 years, and on levodopa for about 5 years. They had levodopa-induced motor complications for an average of about 18 months. Overall, study subjects were a bit younger and less ill than in previous neurostimulation trials, according to the authors.

Sixty-eight patients (55%) in the combination group had serious adverse events; there were 26 serious problems related to the surgery or device, including a brain abscess, but they healed with treatment. Major depression was also more common in the neurostimulation group.

Serious adverse events were noted in 56 of the drug-only subjects (44%), most of which were the result of motor problems and medication side-effects such as impulse control and hallucinations. Those patients made more office visits for health problems, too.

Two patients in the neurostimulation group and one in the medication-only group committed suicide; two in each group made an attempt.

"We hypothesize that the decision to eventually undergo neurostimulation may select a specific subgroup of patients with a higher risk for suicidal behavior than the general population," the researchers wrote.

Neurostimulation patients had bilateral stereotactic surgery, with the implantation of electrodes (model 3389, Medtronic) and a pulse generator (Kinetra or Soletra, Medtronic). Stimulation was similar in both hemispheres, with a mean strength of 2.8 V, mean stimulation frequency of 142 Hz, and mean pulse duration of 66 microseconds. Stimulation took about 5 months to reach its maximum benefit.

All but 1 of the 50 investigators disclosed some form of financial relationship with Medtronic, including grants, travel funding, and speaker, consultant, data review, and educational-material development fees. One is a Medtronic board member. Part of the lead investigator’s institutional salary is paid by the company. In addition to Medtronic, the German Ministry of Research and the French Programme Hospitalier de Recherche Clinique National helped fund the study.

The addition of subthalamic stimulation to medication therapy not only improved the quality of life of patients with early Parkinson’s disease and mild levodopa-induced motor complications but also reduced their subsequent motor disability in a randomized trial conducted in French and German centers.

The combination is already known to help advanced Parkinson’s patients. The new findings suggest that "neurostimulation may be a therapeutic option for patients at an earlier stage than current recommendations suggest," wrote lead author Dr. W.M.M. Schüpbach and coinvestigators in the EARLYSTIM (Controlled Trial of Deep-Brain Stimulation in Early Patients with Parkinson’s Disease) study group (N. Engl. J. Med. 2013;368:610-22 [doi:10.1056/NEJMoa1205158]).

The investigators randomized 127 patients with early motor complications to best-practices drug therapy and 124 to that plus subthalamic neurostimulation.

At the end of 2 years, the combination group reported a 7.8 point quality-of-life improvement on the 100-point Parkinson’s Disease [self-] Questionnaire (PDQ-39) summary index, the study’s primary outcome; medication-only patients reported a 0.2 point drop. The between-group difference in mean change from baseline to 2 years was 8.0 points (P = .002).

The neurostimulation group had better scores on motor disability, too, with a between-group difference on the 70-point Unified Parkinson’s Disease Rating Scale (UPDRS), Part III, of 16.4 points without medication in favor of neurostimulation (P less than .001). Neurostimulation was also modestly superior on activities of daily living (P less than .001) and levodopa-induced motor complications (P less than .001), both also assessed by their appropriate UPDRS sections. The group that received neurostimulation also reported longer times with good mobility and no dyskinesia, as reported in patient diaries (P = .01). Stimulation patients had a 39% reduction in their levodopa-equivalent daily dosages, while drug-only patients had an increase of about 21%.

"Because motor symptoms and quality of life" remained relatively constant in the drug-only group, "the improvement among patients who underwent surgical implantation can be attributed to neurostimulation," wrote the authors of the study, which was funded in part by Medtronic, the manufacturer of the neurostimulation equipment used in the trial.

There were no significant between-group differences at baseline. Patients in both groups were about 52 years old on average, sick for about 7.5 years, and on levodopa for about 5 years. They had levodopa-induced motor complications for an average of about 18 months. Overall, study subjects were a bit younger and less ill than in previous neurostimulation trials, according to the authors.

Sixty-eight patients (55%) in the combination group had serious adverse events; there were 26 serious problems related to the surgery or device, including a brain abscess, but they healed with treatment. Major depression was also more common in the neurostimulation group.

Serious adverse events were noted in 56 of the drug-only subjects (44%), most of which were the result of motor problems and medication side-effects such as impulse control and hallucinations. Those patients made more office visits for health problems, too.

Two patients in the neurostimulation group and one in the medication-only group committed suicide; two in each group made an attempt.

"We hypothesize that the decision to eventually undergo neurostimulation may select a specific subgroup of patients with a higher risk for suicidal behavior than the general population," the researchers wrote.

Neurostimulation patients had bilateral stereotactic surgery, with the implantation of electrodes (model 3389, Medtronic) and a pulse generator (Kinetra or Soletra, Medtronic). Stimulation was similar in both hemispheres, with a mean strength of 2.8 V, mean stimulation frequency of 142 Hz, and mean pulse duration of 66 microseconds. Stimulation took about 5 months to reach its maximum benefit.

All but 1 of the 50 investigators disclosed some form of financial relationship with Medtronic, including grants, travel funding, and speaker, consultant, data review, and educational-material development fees. One is a Medtronic board member. Part of the lead investigator’s institutional salary is paid by the company. In addition to Medtronic, the German Ministry of Research and the French Programme Hospitalier de Recherche Clinique National helped fund the study.

The addition of subthalamic stimulation to medication therapy not only improved the quality of life of patients with early Parkinson’s disease and mild levodopa-induced motor complications but also reduced their subsequent motor disability in a randomized trial conducted in French and German centers.

The combination is already known to help advanced Parkinson’s patients. The new findings suggest that "neurostimulation may be a therapeutic option for patients at an earlier stage than current recommendations suggest," wrote lead author Dr. W.M.M. Schüpbach and coinvestigators in the EARLYSTIM (Controlled Trial of Deep-Brain Stimulation in Early Patients with Parkinson’s Disease) study group (N. Engl. J. Med. 2013;368:610-22 [doi:10.1056/NEJMoa1205158]).

The investigators randomized 127 patients with early motor complications to best-practices drug therapy and 124 to that plus subthalamic neurostimulation.

At the end of 2 years, the combination group reported a 7.8 point quality-of-life improvement on the 100-point Parkinson’s Disease [self-] Questionnaire (PDQ-39) summary index, the study’s primary outcome; medication-only patients reported a 0.2 point drop. The between-group difference in mean change from baseline to 2 years was 8.0 points (P = .002).

The neurostimulation group had better scores on motor disability, too, with a between-group difference on the 70-point Unified Parkinson’s Disease Rating Scale (UPDRS), Part III, of 16.4 points without medication in favor of neurostimulation (P less than .001). Neurostimulation was also modestly superior on activities of daily living (P less than .001) and levodopa-induced motor complications (P less than .001), both also assessed by their appropriate UPDRS sections. The group that received neurostimulation also reported longer times with good mobility and no dyskinesia, as reported in patient diaries (P = .01). Stimulation patients had a 39% reduction in their levodopa-equivalent daily dosages, while drug-only patients had an increase of about 21%.

"Because motor symptoms and quality of life" remained relatively constant in the drug-only group, "the improvement among patients who underwent surgical implantation can be attributed to neurostimulation," wrote the authors of the study, which was funded in part by Medtronic, the manufacturer of the neurostimulation equipment used in the trial.

There were no significant between-group differences at baseline. Patients in both groups were about 52 years old on average, sick for about 7.5 years, and on levodopa for about 5 years. They had levodopa-induced motor complications for an average of about 18 months. Overall, study subjects were a bit younger and less ill than in previous neurostimulation trials, according to the authors.

Sixty-eight patients (55%) in the combination group had serious adverse events; there were 26 serious problems related to the surgery or device, including a brain abscess, but they healed with treatment. Major depression was also more common in the neurostimulation group.

Serious adverse events were noted in 56 of the drug-only subjects (44%), most of which were the result of motor problems and medication side-effects such as impulse control and hallucinations. Those patients made more office visits for health problems, too.

Two patients in the neurostimulation group and one in the medication-only group committed suicide; two in each group made an attempt.

"We hypothesize that the decision to eventually undergo neurostimulation may select a specific subgroup of patients with a higher risk for suicidal behavior than the general population," the researchers wrote.

Neurostimulation patients had bilateral stereotactic surgery, with the implantation of electrodes (model 3389, Medtronic) and a pulse generator (Kinetra or Soletra, Medtronic). Stimulation was similar in both hemispheres, with a mean strength of 2.8 V, mean stimulation frequency of 142 Hz, and mean pulse duration of 66 microseconds. Stimulation took about 5 months to reach its maximum benefit.

All but 1 of the 50 investigators disclosed some form of financial relationship with Medtronic, including grants, travel funding, and speaker, consultant, data review, and educational-material development fees. One is a Medtronic board member. Part of the lead investigator’s institutional salary is paid by the company. In addition to Medtronic, the German Ministry of Research and the French Programme Hospitalier de Recherche Clinique National helped fund the study.

Bronchiectasis alone predicted mortality in patients with moderate to severe chronic obstructive pulmonary disease, independent of pulmonary function and other risk factors, a study by Spanish investigators has shown.

That finding means that "bronchiectasis could be a new prognostic factor" for COPD, the study’s authors predicted.

Confirmation of bronchiectasis "would have a major clinical impact," because high-resolution CT can readily diagnose the condition, and effective therapy is available to treat the chronic bronchial inflammation and infection that plague patients, said lead investigator Dr. Miguel Angel Martínez-García of the Polytechnic and University La Fe Hospital in Valencia, Spain, and his colleagues (Am. J. Respir. Crit. Care Med. 2013 Feb. 7 [doi:10.1164/rccm.201208-1518OC]).

Conceivably, those patients could be "subject to different diagnostic and therapeutic approaches and, therefore, define a new phenotype": COPD with bronchiectasis, Dr. Martínez-García said.

Bronchiectasis is already known to be associated with worse exacerbations, more frequent bacterial colonizations, and greater degrees of impairment in COPD patients. But its relationship to mortality – or its utility as a prognostic factor – hasn’t been demonstrated until now, the researchers noted.

The investigators followed 115 patients with moderate to severe COPD and with bronchiectasis and 86 COPD patients without bronchiectasis for a median of 48 months. A total of 43 patients (37%) died in the bronchiectasis group, but only 8 patients (9%) in the nonbronchiectasis group died. COPD exacerbations were the most common cause of death.

COPD patients with bronchiectasis were 2.5 times more likely to die than those without bronchiectasis, after adjustment for factors such as dyspnea, body mass index, the presence of potentially pathogenic respiratory microorganisms, and other potential confounders (hazard ratio, 2.54; 95%CI: 1.16-5.56; P = .02).

Patients with bronchiectasis also presented with "a more severe form of COPD in clinical and functional terms, as well as a greater concentration of parameters of systemic inflammation and a greater presence of" potentially pathogenic microorganisms (PPMs) in their airways, the investigators said.

Bacterial respiratory colonization and subsequent inflammation probably play an important role in dilating the bronchioles and causing bronchiectasis – which leads to more colonization and a vicious cycle. But that cycle might "be broken by the early identification of this subgroup of patients" and the use of oral moxifloxacin or inhaled antibiotics, they said.

A total of 59% (68) of patients with bronchiectasis, but only 20% (17) of those without it, had PPM respiratory isolates, most commonly Haemophilus influenzae, followed by Pseudomonas aeruginosa.

Most of the patients were men and, on average, around 70 years old and overweight. Overall, they had an average smoking history of 60.7 pack-years and had COPD for more than decade. A minority of patients had tuberculosis histories or active pneumonia.

The authors said they had no relevant financial disclosures. Praxis Pharmaceutical funded the study.

[email protected]

Bronchiectasis alone predicted mortality in patients with moderate to severe chronic obstructive pulmonary disease, independent of pulmonary function and other risk factors, a study by Spanish investigators has shown.

That finding means that "bronchiectasis could be a new prognostic factor" for COPD, the study’s authors predicted.

Confirmation of bronchiectasis "would have a major clinical impact," because high-resolution CT can readily diagnose the condition, and effective therapy is available to treat the chronic bronchial inflammation and infection that plague patients, said lead investigator Dr. Miguel Angel Martínez-García of the Polytechnic and University La Fe Hospital in Valencia, Spain, and his colleagues (Am. J. Respir. Crit. Care Med. 2013 Feb. 7 [doi:10.1164/rccm.201208-1518OC]).

Conceivably, those patients could be "subject to different diagnostic and therapeutic approaches and, therefore, define a new phenotype": COPD with bronchiectasis, Dr. Martínez-García said.

Bronchiectasis is already known to be associated with worse exacerbations, more frequent bacterial colonizations, and greater degrees of impairment in COPD patients. But its relationship to mortality – or its utility as a prognostic factor – hasn’t been demonstrated until now, the researchers noted.

The investigators followed 115 patients with moderate to severe COPD and with bronchiectasis and 86 COPD patients without bronchiectasis for a median of 48 months. A total of 43 patients (37%) died in the bronchiectasis group, but only 8 patients (9%) in the nonbronchiectasis group died. COPD exacerbations were the most common cause of death.

COPD patients with bronchiectasis were 2.5 times more likely to die than those without bronchiectasis, after adjustment for factors such as dyspnea, body mass index, the presence of potentially pathogenic respiratory microorganisms, and other potential confounders (hazard ratio, 2.54; 95%CI: 1.16-5.56; P = .02).

Patients with bronchiectasis also presented with "a more severe form of COPD in clinical and functional terms, as well as a greater concentration of parameters of systemic inflammation and a greater presence of" potentially pathogenic microorganisms (PPMs) in their airways, the investigators said.

Bacterial respiratory colonization and subsequent inflammation probably play an important role in dilating the bronchioles and causing bronchiectasis – which leads to more colonization and a vicious cycle. But that cycle might "be broken by the early identification of this subgroup of patients" and the use of oral moxifloxacin or inhaled antibiotics, they said.

A total of 59% (68) of patients with bronchiectasis, but only 20% (17) of those without it, had PPM respiratory isolates, most commonly Haemophilus influenzae, followed by Pseudomonas aeruginosa.

Most of the patients were men and, on average, around 70 years old and overweight. Overall, they had an average smoking history of 60.7 pack-years and had COPD for more than decade. A minority of patients had tuberculosis histories or active pneumonia.

The authors said they had no relevant financial disclosures. Praxis Pharmaceutical funded the study.

[email protected]

Bronchiectasis alone predicted mortality in patients with moderate to severe chronic obstructive pulmonary disease, independent of pulmonary function and other risk factors, a study by Spanish investigators has shown.

That finding means that "bronchiectasis could be a new prognostic factor" for COPD, the study’s authors predicted.

Confirmation of bronchiectasis "would have a major clinical impact," because high-resolution CT can readily diagnose the condition, and effective therapy is available to treat the chronic bronchial inflammation and infection that plague patients, said lead investigator Dr. Miguel Angel Martínez-García of the Polytechnic and University La Fe Hospital in Valencia, Spain, and his colleagues (Am. J. Respir. Crit. Care Med. 2013 Feb. 7 [doi:10.1164/rccm.201208-1518OC]).

Conceivably, those patients could be "subject to different diagnostic and therapeutic approaches and, therefore, define a new phenotype": COPD with bronchiectasis, Dr. Martínez-García said.

Bronchiectasis is already known to be associated with worse exacerbations, more frequent bacterial colonizations, and greater degrees of impairment in COPD patients. But its relationship to mortality – or its utility as a prognostic factor – hasn’t been demonstrated until now, the researchers noted.

The investigators followed 115 patients with moderate to severe COPD and with bronchiectasis and 86 COPD patients without bronchiectasis for a median of 48 months. A total of 43 patients (37%) died in the bronchiectasis group, but only 8 patients (9%) in the nonbronchiectasis group died. COPD exacerbations were the most common cause of death.

COPD patients with bronchiectasis were 2.5 times more likely to die than those without bronchiectasis, after adjustment for factors such as dyspnea, body mass index, the presence of potentially pathogenic respiratory microorganisms, and other potential confounders (hazard ratio, 2.54; 95%CI: 1.16-5.56; P = .02).

Patients with bronchiectasis also presented with "a more severe form of COPD in clinical and functional terms, as well as a greater concentration of parameters of systemic inflammation and a greater presence of" potentially pathogenic microorganisms (PPMs) in their airways, the investigators said.

Bacterial respiratory colonization and subsequent inflammation probably play an important role in dilating the bronchioles and causing bronchiectasis – which leads to more colonization and a vicious cycle. But that cycle might "be broken by the early identification of this subgroup of patients" and the use of oral moxifloxacin or inhaled antibiotics, they said.

A total of 59% (68) of patients with bronchiectasis, but only 20% (17) of those without it, had PPM respiratory isolates, most commonly Haemophilus influenzae, followed by Pseudomonas aeruginosa.

Most of the patients were men and, on average, around 70 years old and overweight. Overall, they had an average smoking history of 60.7 pack-years and had COPD for more than decade. A minority of patients had tuberculosis histories or active pneumonia.

The authors said they had no relevant financial disclosures. Praxis Pharmaceutical funded the study.

[email protected]

The DSM-5 is expected to place obsessive-compulsive disorder and posttraumatic stress disorder into their own diagnostic categories, removing them from the family of anxiety disorders, according to Dr. Daniel S. Pine.

Setting trauma-related and obsessive-compulsive spectrum disorders off on their own makes sense because the "longitudinal outcomes, comorbidities, familial aggregations, and underlying biology" suggest the conditions are different from anxiety disorders, said Dr. Pine, chief of the section on development and affective neuroscience at the National Institute of Mental Health in Bethesda, Md.

This new approach also makes sense because the disorders that will be left in the anxiety category – generalized, social, separation, panic, and phobic anxieties – are pretty much treated the same way. "Nothing in the treatment literature suggests we should approach any of these [problems] differently from any of the others," Dr. Pine said at a psychopharmacology update sponsored by the American Academy of Child and Adolescent Psychiatry.

Overall, such problems "are incredibly common [in children]. One in three will, some time in their adolescence, have an anxiety disorder." They go away in most, but the minority in whom they persist "account for the majority of chronic mood and anxiety disorders" in adults, he said.

It’s probably the same for "substance abuse, conduct problems, personality disorders, eating disorders, mood disorders," and other problems. Children who don’t overcome those issues are the "precursors for adults who have a problem," Dr. Pine said.

"The hope of neuroscience is that it will give us better clues about" which anxious children will progress, he said. "We’re very bad at predicting that right now." Children who are worse seem to do worse over time, but beyond that, gender, age, type of anxiety disorder, and other factors do not seem to predict persistence into adulthood, he said.

As with adults, selective serotonin reuptake inhibitors (SSRIs) "are extremely good" for treating anxiety in children, and "there’s particularly good" evidence for fluvoxamine, fluoxetine, paroxetine, and sertraline. Across studies, the number needed to treat is about three, which is "about as good a treatment as we can get," he said, noting that SSRIs are "much better treatments" for anxiety than for depression (J. Am. Acad. Child Adolesc. Psychiatry 2003;42:415-23).

But because anxiety disorders are transient in most children and the effect of SSRIs on developing brains is unknown, children "deserve a trial off medication" after a year of treatment, he said.

There’s also "very good evidence" that cognitive-behavioral therapy (CBT) helps anxiety, too, though it might be a bit slower than SSRIs. Combining the two also is a possibility. In one 12-week study (N. Engl. J. Med. 2008;359:2753-66), it was clear that combination treatment was the best, Dr. Pine said.

Despite the value of treating anxiety with SSRIs, it is important to remain vigilant of the increased risk of suicidal ideations and attempts that accompany use of these medications in children and adolescents. "You really are obliged to spend a fair amount of time reviewing with parents the nature of that risk," he said.

Dr. Pine said that he had no financial disclosures.

[email protected]

The DSM-5 is expected to place obsessive-compulsive disorder and posttraumatic stress disorder into their own diagnostic categories, removing them from the family of anxiety disorders, according to Dr. Daniel S. Pine.

Setting trauma-related and obsessive-compulsive spectrum disorders off on their own makes sense because the "longitudinal outcomes, comorbidities, familial aggregations, and underlying biology" suggest the conditions are different from anxiety disorders, said Dr. Pine, chief of the section on development and affective neuroscience at the National Institute of Mental Health in Bethesda, Md.

This new approach also makes sense because the disorders that will be left in the anxiety category – generalized, social, separation, panic, and phobic anxieties – are pretty much treated the same way. "Nothing in the treatment literature suggests we should approach any of these [problems] differently from any of the others," Dr. Pine said at a psychopharmacology update sponsored by the American Academy of Child and Adolescent Psychiatry.

Overall, such problems "are incredibly common [in children]. One in three will, some time in their adolescence, have an anxiety disorder." They go away in most, but the minority in whom they persist "account for the majority of chronic mood and anxiety disorders" in adults, he said.

It’s probably the same for "substance abuse, conduct problems, personality disorders, eating disorders, mood disorders," and other problems. Children who don’t overcome those issues are the "precursors for adults who have a problem," Dr. Pine said.

"The hope of neuroscience is that it will give us better clues about" which anxious children will progress, he said. "We’re very bad at predicting that right now." Children who are worse seem to do worse over time, but beyond that, gender, age, type of anxiety disorder, and other factors do not seem to predict persistence into adulthood, he said.

As with adults, selective serotonin reuptake inhibitors (SSRIs) "are extremely good" for treating anxiety in children, and "there’s particularly good" evidence for fluvoxamine, fluoxetine, paroxetine, and sertraline. Across studies, the number needed to treat is about three, which is "about as good a treatment as we can get," he said, noting that SSRIs are "much better treatments" for anxiety than for depression (J. Am. Acad. Child Adolesc. Psychiatry 2003;42:415-23).

But because anxiety disorders are transient in most children and the effect of SSRIs on developing brains is unknown, children "deserve a trial off medication" after a year of treatment, he said.

There’s also "very good evidence" that cognitive-behavioral therapy (CBT) helps anxiety, too, though it might be a bit slower than SSRIs. Combining the two also is a possibility. In one 12-week study (N. Engl. J. Med. 2008;359:2753-66), it was clear that combination treatment was the best, Dr. Pine said.

Despite the value of treating anxiety with SSRIs, it is important to remain vigilant of the increased risk of suicidal ideations and attempts that accompany use of these medications in children and adolescents. "You really are obliged to spend a fair amount of time reviewing with parents the nature of that risk," he said.

Dr. Pine said that he had no financial disclosures.

[email protected]

The DSM-5 is expected to place obsessive-compulsive disorder and posttraumatic stress disorder into their own diagnostic categories, removing them from the family of anxiety disorders, according to Dr. Daniel S. Pine.

Setting trauma-related and obsessive-compulsive spectrum disorders off on their own makes sense because the "longitudinal outcomes, comorbidities, familial aggregations, and underlying biology" suggest the conditions are different from anxiety disorders, said Dr. Pine, chief of the section on development and affective neuroscience at the National Institute of Mental Health in Bethesda, Md.

This new approach also makes sense because the disorders that will be left in the anxiety category – generalized, social, separation, panic, and phobic anxieties – are pretty much treated the same way. "Nothing in the treatment literature suggests we should approach any of these [problems] differently from any of the others," Dr. Pine said at a psychopharmacology update sponsored by the American Academy of Child and Adolescent Psychiatry.

Overall, such problems "are incredibly common [in children]. One in three will, some time in their adolescence, have an anxiety disorder." They go away in most, but the minority in whom they persist "account for the majority of chronic mood and anxiety disorders" in adults, he said.

It’s probably the same for "substance abuse, conduct problems, personality disorders, eating disorders, mood disorders," and other problems. Children who don’t overcome those issues are the "precursors for adults who have a problem," Dr. Pine said.

"The hope of neuroscience is that it will give us better clues about" which anxious children will progress, he said. "We’re very bad at predicting that right now." Children who are worse seem to do worse over time, but beyond that, gender, age, type of anxiety disorder, and other factors do not seem to predict persistence into adulthood, he said.

As with adults, selective serotonin reuptake inhibitors (SSRIs) "are extremely good" for treating anxiety in children, and "there’s particularly good" evidence for fluvoxamine, fluoxetine, paroxetine, and sertraline. Across studies, the number needed to treat is about three, which is "about as good a treatment as we can get," he said, noting that SSRIs are "much better treatments" for anxiety than for depression (J. Am. Acad. Child Adolesc. Psychiatry 2003;42:415-23).

But because anxiety disorders are transient in most children and the effect of SSRIs on developing brains is unknown, children "deserve a trial off medication" after a year of treatment, he said.

There’s also "very good evidence" that cognitive-behavioral therapy (CBT) helps anxiety, too, though it might be a bit slower than SSRIs. Combining the two also is a possibility. In one 12-week study (N. Engl. J. Med. 2008;359:2753-66), it was clear that combination treatment was the best, Dr. Pine said.

Despite the value of treating anxiety with SSRIs, it is important to remain vigilant of the increased risk of suicidal ideations and attempts that accompany use of these medications in children and adolescents. "You really are obliged to spend a fair amount of time reviewing with parents the nature of that risk," he said.

Dr. Pine said that he had no financial disclosures.

[email protected]

WASHINGTON – The DSM-5’s inclusion of separate criteria for posttraumatic stress disorder in preschool children probably will lead to more young children getting the diagnosis, which will be a positive development because PTSD is under-recognized in this population, Dr. Michael S. Scheeringa contended.

The preschool criteria are child friendly. Intrusive recollections, for instance, don’t have to be distressing, as in the adult criteria, because sometimes such recollections do not seem to bother very young kids. "They’ll bring up their intrusive recollections to the cashier at the supermarket and seem eager to talk about them, rather than distressed," he said.

Similarly, detachment and estrangement criteria have been "reworded to say ‘socially withdrawn,’ because children can’t verbalize that they feel detached, but it can be observed that they are socially withdrawn," said Dr. Scheeringa, a pediatric PTSD researcher who also serves as an associate professor of psychiatry and neurology at Tulane University in New Orleans.

Perhaps the biggest change is that preschool children – those below the age of 7 years – will need to show just one avoidance and numbing symptom instead of the three required by the DSM-IV. Three is "too high for young children because they can’t show or express a lot of those internalized avoidance and numbing symptoms. It’s just developmentally impossible, like the sense of a foreshortened future – a child’s sense of future when they are 3 or 4 is tomorrow," he said at a psychopharmacology update sponsored by the American Academy of Child and Adolescent Psychiatry.

The increase in the number of young children likely to get the PTSD diagnosis under the new criteria is significant, because the illness historically has been underdiagnosed and missed in children, said Dr. Scheeringa, whose research contributed to the changes.

The DSM-IV requirement for irritability and anger outbursts also has been tweaked for preschoolers to include extreme temper tantrums, and the requirement for diminished interest in significant activities has been broadened to include restrictions in play and social interactions. "Young children don’t have jobs; they don’t have school; they don’t have hobbies. What they do is play and interact with other people; that’s where their interests would be diminished," he said.

"A skeptic might say, ‘Aren’t you just diagnosing mildly symptomatic kids? Aren’t you just lowering the bar?’ " but that doesn’t seem to be the case – the DSM-IV was simply missing small children with PTSD, he said.

In one of Dr. Scheeringa’s studies, DSM-IV criteria diagnosed PTSD in 13% of 284 trauma-exposed children aged 3-6 years; the DSM-5 criteria did so in about half, and those children had at least six symptoms (J. Trauma Stress 2012;25:359-67).

"Usually in treatment studies, they require five symptoms, so [these children] were really symptomatic. We’re not just diagnosing mildly symptomatic kids with" the new approach, Dr. Scheeringa said.

In general, psychotherapy – trauma-focused cognitive-behavioral therapy (CBT) in particular – is the first-line treatment for PTSD in both children and adults. "I would consider [psychiatric drugs] a distant second," he said. If needed, prazosin is likely to help with nightmares, benzodiazepines can take the edge off situational anxiety, and sleeping pills can calm fitful sleep. SSRIs might help with overall anxiety, he said.

Comorbid depression and other problems get better as PTSD resolves, "so I would suggest, based on the evidence, to focus on the PTSD first and then see what’s left over," Dr. Scheeringa said.

Attention-deficit/hyperactivity disorder (ADHD) is the exception; patients will do better in CBT if their ADHD is under control, he said.

Dr. Scheeringa said that he had no financial disclosures.

[email protected]

WASHINGTON – The DSM-5’s inclusion of separate criteria for posttraumatic stress disorder in preschool children probably will lead to more young children getting the diagnosis, which will be a positive development because PTSD is under-recognized in this population, Dr. Michael S. Scheeringa contended.

The preschool criteria are child friendly. Intrusive recollections, for instance, don’t have to be distressing, as in the adult criteria, because sometimes such recollections do not seem to bother very young kids. "They’ll bring up their intrusive recollections to the cashier at the supermarket and seem eager to talk about them, rather than distressed," he said.

Similarly, detachment and estrangement criteria have been "reworded to say ‘socially withdrawn,’ because children can’t verbalize that they feel detached, but it can be observed that they are socially withdrawn," said Dr. Scheeringa, a pediatric PTSD researcher who also serves as an associate professor of psychiatry and neurology at Tulane University in New Orleans.

Perhaps the biggest change is that preschool children – those below the age of 7 years – will need to show just one avoidance and numbing symptom instead of the three required by the DSM-IV. Three is "too high for young children because they can’t show or express a lot of those internalized avoidance and numbing symptoms. It’s just developmentally impossible, like the sense of a foreshortened future – a child’s sense of future when they are 3 or 4 is tomorrow," he said at a psychopharmacology update sponsored by the American Academy of Child and Adolescent Psychiatry.

The increase in the number of young children likely to get the PTSD diagnosis under the new criteria is significant, because the illness historically has been underdiagnosed and missed in children, said Dr. Scheeringa, whose research contributed to the changes.

The DSM-IV requirement for irritability and anger outbursts also has been tweaked for preschoolers to include extreme temper tantrums, and the requirement for diminished interest in significant activities has been broadened to include restrictions in play and social interactions. "Young children don’t have jobs; they don’t have school; they don’t have hobbies. What they do is play and interact with other people; that’s where their interests would be diminished," he said.

"A skeptic might say, ‘Aren’t you just diagnosing mildly symptomatic kids? Aren’t you just lowering the bar?’ " but that doesn’t seem to be the case – the DSM-IV was simply missing small children with PTSD, he said.

In one of Dr. Scheeringa’s studies, DSM-IV criteria diagnosed PTSD in 13% of 284 trauma-exposed children aged 3-6 years; the DSM-5 criteria did so in about half, and those children had at least six symptoms (J. Trauma Stress 2012;25:359-67).

"Usually in treatment studies, they require five symptoms, so [these children] were really symptomatic. We’re not just diagnosing mildly symptomatic kids with" the new approach, Dr. Scheeringa said.

In general, psychotherapy – trauma-focused cognitive-behavioral therapy (CBT) in particular – is the first-line treatment for PTSD in both children and adults. "I would consider [psychiatric drugs] a distant second," he said. If needed, prazosin is likely to help with nightmares, benzodiazepines can take the edge off situational anxiety, and sleeping pills can calm fitful sleep. SSRIs might help with overall anxiety, he said.

Comorbid depression and other problems get better as PTSD resolves, "so I would suggest, based on the evidence, to focus on the PTSD first and then see what’s left over," Dr. Scheeringa said.

Attention-deficit/hyperactivity disorder (ADHD) is the exception; patients will do better in CBT if their ADHD is under control, he said.

Dr. Scheeringa said that he had no financial disclosures.

[email protected]

WASHINGTON – The DSM-5’s inclusion of separate criteria for posttraumatic stress disorder in preschool children probably will lead to more young children getting the diagnosis, which will be a positive development because PTSD is under-recognized in this population, Dr. Michael S. Scheeringa contended.

The preschool criteria are child friendly. Intrusive recollections, for instance, don’t have to be distressing, as in the adult criteria, because sometimes such recollections do not seem to bother very young kids. "They’ll bring up their intrusive recollections to the cashier at the supermarket and seem eager to talk about them, rather than distressed," he said.

Similarly, detachment and estrangement criteria have been "reworded to say ‘socially withdrawn,’ because children can’t verbalize that they feel detached, but it can be observed that they are socially withdrawn," said Dr. Scheeringa, a pediatric PTSD researcher who also serves as an associate professor of psychiatry and neurology at Tulane University in New Orleans.

Perhaps the biggest change is that preschool children – those below the age of 7 years – will need to show just one avoidance and numbing symptom instead of the three required by the DSM-IV. Three is "too high for young children because they can’t show or express a lot of those internalized avoidance and numbing symptoms. It’s just developmentally impossible, like the sense of a foreshortened future – a child’s sense of future when they are 3 or 4 is tomorrow," he said at a psychopharmacology update sponsored by the American Academy of Child and Adolescent Psychiatry.

The increase in the number of young children likely to get the PTSD diagnosis under the new criteria is significant, because the illness historically has been underdiagnosed and missed in children, said Dr. Scheeringa, whose research contributed to the changes.

The DSM-IV requirement for irritability and anger outbursts also has been tweaked for preschoolers to include extreme temper tantrums, and the requirement for diminished interest in significant activities has been broadened to include restrictions in play and social interactions. "Young children don’t have jobs; they don’t have school; they don’t have hobbies. What they do is play and interact with other people; that’s where their interests would be diminished," he said.

"A skeptic might say, ‘Aren’t you just diagnosing mildly symptomatic kids? Aren’t you just lowering the bar?’ " but that doesn’t seem to be the case – the DSM-IV was simply missing small children with PTSD, he said.

In one of Dr. Scheeringa’s studies, DSM-IV criteria diagnosed PTSD in 13% of 284 trauma-exposed children aged 3-6 years; the DSM-5 criteria did so in about half, and those children had at least six symptoms (J. Trauma Stress 2012;25:359-67).

"Usually in treatment studies, they require five symptoms, so [these children] were really symptomatic. We’re not just diagnosing mildly symptomatic kids with" the new approach, Dr. Scheeringa said.

In general, psychotherapy – trauma-focused cognitive-behavioral therapy (CBT) in particular – is the first-line treatment for PTSD in both children and adults. "I would consider [psychiatric drugs] a distant second," he said. If needed, prazosin is likely to help with nightmares, benzodiazepines can take the edge off situational anxiety, and sleeping pills can calm fitful sleep. SSRIs might help with overall anxiety, he said.

Comorbid depression and other problems get better as PTSD resolves, "so I would suggest, based on the evidence, to focus on the PTSD first and then see what’s left over," Dr. Scheeringa said.

Attention-deficit/hyperactivity disorder (ADHD) is the exception; patients will do better in CBT if their ADHD is under control, he said.

Dr. Scheeringa said that he had no financial disclosures.

[email protected]

About a third of children are already in diabetic ketoacidosis by the time they are diagnosed with type 1 diabetes, which means that earlier signs of the disease were missed, according to researchers from the Pediatric Diabetes Consortium.

Among 805 children in the group’s database, 34% presented in diabetic ketoacidosis (DKA), half of whom had moderate or severe DKA (pH less than 7.2). The risk of DKA was 54% in children under 3 years old and 33% in older children (P = .006). The findings were consistent with previous studies.

"Unfortunately, there has been no apparent change in the rate of DKA at presentation of T1D [type 1 diabetes] in children over the past 25 years; the incidence of DKA in children at the onset of T1D remains high. Effective techniques for increasing awareness of the early symptoms of T1D in both the general public and primary care providers are needed to decrease the incidence of this life-threatening complication," the investigators wrote (J. Pediatr. 2013;162:330-4).

The problem is that those early T1D symptoms – often an abrupt increase in thirst and urination – are "not infrequently" overlooked by parents unfamiliar with the disease and sometimes even by clinicians, especially in very young children, said coinvestigator Dr. William Tamborlane, deputy director for clinical research at Yale University, New Haven, Conn., and chair of the diabetes consortium, a research collaboration between university pediatric diabetes centers.

The classic signs of diabetes in children have a variety of harmless possible explanations. Excess thirst might be chalked up to hot weather or a growth spurt. Polyuria might be mistaken for a urinary tract infection. Weight loss, particularly in an obese child, might be attributed to dieting. It’s also hard to tell the difference between normal and abnormal thirst and urination in children less than 1 or 2 years old, and they’re unlikely to be able to voice any complaints, he said in an interview.

Indeed, younger age (P = .002) proved to be an independent predictor of DKA at diagnosis, as did lack of private health insurance (P less than .001), African American race (P = .01), and no family history of T1D (P = .001).

Children in the study were under 19 years old and positive for at least one diabetes-associated autoantibody. Their average age was 9 years, half were girls, and 63% were non-Hispanic whites.

Almost all of the DKA kids (91%) were admitted to the hospital; 58% required ICU treatment and 3% had cerebral edema, but none died. Their mean hospital stay was 3 days. DKA was defined in the study as a venous pH below 7.3 and/or a serum bicarbonate below 15 mEq/L.

Commenting on the study, Dr. Alan Rogol, a Journal of Pediatrics editorial board member, wrote, "It is incumbent upon us as pediatricians and health care professionals to consider the diagnosis of T1D to prevent, or at least minimize, the severity of the acute metabolic disturbance and to enter into a long-term treatment plan."

Dr. Tamborlane noted that, like juvenile diabetes, DKA can be missed too, especially when its associated nausea and vomiting mimic a viral infection. "When a child presents with a flulike illness, it’s worth getting a simple urine dipstick to make sure there’s no sugar or ketones in the urine," he said.

The investigators said that they had no disclosures.

About a third of children are already in diabetic ketoacidosis by the time they are diagnosed with type 1 diabetes, which means that earlier signs of the disease were missed, according to researchers from the Pediatric Diabetes Consortium.

Among 805 children in the group’s database, 34% presented in diabetic ketoacidosis (DKA), half of whom had moderate or severe DKA (pH less than 7.2). The risk of DKA was 54% in children under 3 years old and 33% in older children (P = .006). The findings were consistent with previous studies.

"Unfortunately, there has been no apparent change in the rate of DKA at presentation of T1D [type 1 diabetes] in children over the past 25 years; the incidence of DKA in children at the onset of T1D remains high. Effective techniques for increasing awareness of the early symptoms of T1D in both the general public and primary care providers are needed to decrease the incidence of this life-threatening complication," the investigators wrote (J. Pediatr. 2013;162:330-4).

The problem is that those early T1D symptoms – often an abrupt increase in thirst and urination – are "not infrequently" overlooked by parents unfamiliar with the disease and sometimes even by clinicians, especially in very young children, said coinvestigator Dr. William Tamborlane, deputy director for clinical research at Yale University, New Haven, Conn., and chair of the diabetes consortium, a research collaboration between university pediatric diabetes centers.

The classic signs of diabetes in children have a variety of harmless possible explanations. Excess thirst might be chalked up to hot weather or a growth spurt. Polyuria might be mistaken for a urinary tract infection. Weight loss, particularly in an obese child, might be attributed to dieting. It’s also hard to tell the difference between normal and abnormal thirst and urination in children less than 1 or 2 years old, and they’re unlikely to be able to voice any complaints, he said in an interview.

Indeed, younger age (P = .002) proved to be an independent predictor of DKA at diagnosis, as did lack of private health insurance (P less than .001), African American race (P = .01), and no family history of T1D (P = .001).

Children in the study were under 19 years old and positive for at least one diabetes-associated autoantibody. Their average age was 9 years, half were girls, and 63% were non-Hispanic whites.

Almost all of the DKA kids (91%) were admitted to the hospital; 58% required ICU treatment and 3% had cerebral edema, but none died. Their mean hospital stay was 3 days. DKA was defined in the study as a venous pH below 7.3 and/or a serum bicarbonate below 15 mEq/L.

Commenting on the study, Dr. Alan Rogol, a Journal of Pediatrics editorial board member, wrote, "It is incumbent upon us as pediatricians and health care professionals to consider the diagnosis of T1D to prevent, or at least minimize, the severity of the acute metabolic disturbance and to enter into a long-term treatment plan."

Dr. Tamborlane noted that, like juvenile diabetes, DKA can be missed too, especially when its associated nausea and vomiting mimic a viral infection. "When a child presents with a flulike illness, it’s worth getting a simple urine dipstick to make sure there’s no sugar or ketones in the urine," he said.

The investigators said that they had no disclosures.

About a third of children are already in diabetic ketoacidosis by the time they are diagnosed with type 1 diabetes, which means that earlier signs of the disease were missed, according to researchers from the Pediatric Diabetes Consortium.

Among 805 children in the group’s database, 34% presented in diabetic ketoacidosis (DKA), half of whom had moderate or severe DKA (pH less than 7.2). The risk of DKA was 54% in children under 3 years old and 33% in older children (P = .006). The findings were consistent with previous studies.

"Unfortunately, there has been no apparent change in the rate of DKA at presentation of T1D [type 1 diabetes] in children over the past 25 years; the incidence of DKA in children at the onset of T1D remains high. Effective techniques for increasing awareness of the early symptoms of T1D in both the general public and primary care providers are needed to decrease the incidence of this life-threatening complication," the investigators wrote (J. Pediatr. 2013;162:330-4).

The problem is that those early T1D symptoms – often an abrupt increase in thirst and urination – are "not infrequently" overlooked by parents unfamiliar with the disease and sometimes even by clinicians, especially in very young children, said coinvestigator Dr. William Tamborlane, deputy director for clinical research at Yale University, New Haven, Conn., and chair of the diabetes consortium, a research collaboration between university pediatric diabetes centers.

The classic signs of diabetes in children have a variety of harmless possible explanations. Excess thirst might be chalked up to hot weather or a growth spurt. Polyuria might be mistaken for a urinary tract infection. Weight loss, particularly in an obese child, might be attributed to dieting. It’s also hard to tell the difference between normal and abnormal thirst and urination in children less than 1 or 2 years old, and they’re unlikely to be able to voice any complaints, he said in an interview.

Indeed, younger age (P = .002) proved to be an independent predictor of DKA at diagnosis, as did lack of private health insurance (P less than .001), African American race (P = .01), and no family history of T1D (P = .001).

Children in the study were under 19 years old and positive for at least one diabetes-associated autoantibody. Their average age was 9 years, half were girls, and 63% were non-Hispanic whites.

Almost all of the DKA kids (91%) were admitted to the hospital; 58% required ICU treatment and 3% had cerebral edema, but none died. Their mean hospital stay was 3 days. DKA was defined in the study as a venous pH below 7.3 and/or a serum bicarbonate below 15 mEq/L.

Commenting on the study, Dr. Alan Rogol, a Journal of Pediatrics editorial board member, wrote, "It is incumbent upon us as pediatricians and health care professionals to consider the diagnosis of T1D to prevent, or at least minimize, the severity of the acute metabolic disturbance and to enter into a long-term treatment plan."

Dr. Tamborlane noted that, like juvenile diabetes, DKA can be missed too, especially when its associated nausea and vomiting mimic a viral infection. "When a child presents with a flulike illness, it’s worth getting a simple urine dipstick to make sure there’s no sugar or ketones in the urine," he said.

The investigators said that they had no disclosures.

When resurfacing the skin with nonablative, midinfrared fractional lasers, "don’t think you’re just going to set these devices to the highest [density] setting, and get the best results," Dr. Mathew Avram said at the SDEF Las Vegas Dermatology Seminar.

The percentage of skin in the treatment area that receives microscopic thermal wounds doesn’t necessarily translate to better results, said Dr. Avram, director of the dermatology laser and cosmetic center at Massachusetts General Hospital in Boston.

One study randomized 20 patients with hypertrophic scars to either 26% or 14% scar coverage with 40 mJ. Patients in the 14% group rated the results better at 3 months’ follow-up. "Low-density treatment is at least as effective as high-density treatment and [has] fewer side effects," the authors wrote (Lasers Surg. Med. 2011;43:265-72).

"If you did a lower-density [treatment]," Dr. Avram explained, "you got the same improvement as you did with a higher density, which is counterintuitive. You’d think the more damage you do the better, but basically all you get is more side effects" like pain, peeling, and inflammation. "Density is the key in terms of side effects and risk of hyperpigmentation."

Depth of treatment, which is determined by pulse energy, is another major consideration. "The pulse energy should reflect the pathology of the condition being treated," he said. With superficial pathology, photoaging, for instance,"you use a low pulse energy." With deeper pathology, such as deeper rhytides or traumatic scars, "you use higher pulse energy to penetrate more deeply. Adjust the depth of treatment and density for the pathology you are treating," Dr. Avram advised.

"You want to tell patients about procedural discomfort, side effects, and real expectations. It’s going to take multiple treatments, and these treatments will only partially improve fine to moderate wrinkles, pigmentation, and scars about 3 months after the time of treatment," he said.

Cold-air cooling is an option for anesthesia, as are topical lidocaine/tetracaine and locally injected anesthesia. The anesthetized area should be allowed to settle down a bit before the procedure to reduce the risk of ulceration, he said.

To prevent treatment-induced flares, Dr. Avram said he gives patients with histories of herpes labialis 500 mg of valacyclovir twice daily on the day before the procedure and continues this for about a week. Patients should also have been off isotretinoin for at least 6 months before treatment, he noted.

"I treat through skin type 6, but I’m very cautious doing it. I’m not so much worried about how deeply I’m treating, but I really dial back the density to avoid hyperpigmentation, and pretreat with hydroquinone, as well," he said.

For poikiloderma of Civatte, fractional lasers are more effective for pigment than erythema. Pulsed dye lasers are more effective for erythema. "You can do [the pulsed dye treatment] first, and then do the fractional resurfacing," he said.

Dr. Avram is a paid consultant to Zeltiq Aesthetics, Unilever, and Living Proof.

SDEF and this news organization are owned by Frontline Medical Communications.

When resurfacing the skin with nonablative, midinfrared fractional lasers, "don’t think you’re just going to set these devices to the highest [density] setting, and get the best results," Dr. Mathew Avram said at the SDEF Las Vegas Dermatology Seminar.

The percentage of skin in the treatment area that receives microscopic thermal wounds doesn’t necessarily translate to better results, said Dr. Avram, director of the dermatology laser and cosmetic center at Massachusetts General Hospital in Boston.

One study randomized 20 patients with hypertrophic scars to either 26% or 14% scar coverage with 40 mJ. Patients in the 14% group rated the results better at 3 months’ follow-up. "Low-density treatment is at least as effective as high-density treatment and [has] fewer side effects," the authors wrote (Lasers Surg. Med. 2011;43:265-72).

"If you did a lower-density [treatment]," Dr. Avram explained, "you got the same improvement as you did with a higher density, which is counterintuitive. You’d think the more damage you do the better, but basically all you get is more side effects" like pain, peeling, and inflammation. "Density is the key in terms of side effects and risk of hyperpigmentation."

Depth of treatment, which is determined by pulse energy, is another major consideration. "The pulse energy should reflect the pathology of the condition being treated," he said. With superficial pathology, photoaging, for instance,"you use a low pulse energy." With deeper pathology, such as deeper rhytides or traumatic scars, "you use higher pulse energy to penetrate more deeply. Adjust the depth of treatment and density for the pathology you are treating," Dr. Avram advised.

"You want to tell patients about procedural discomfort, side effects, and real expectations. It’s going to take multiple treatments, and these treatments will only partially improve fine to moderate wrinkles, pigmentation, and scars about 3 months after the time of treatment," he said.

Cold-air cooling is an option for anesthesia, as are topical lidocaine/tetracaine and locally injected anesthesia. The anesthetized area should be allowed to settle down a bit before the procedure to reduce the risk of ulceration, he said.

To prevent treatment-induced flares, Dr. Avram said he gives patients with histories of herpes labialis 500 mg of valacyclovir twice daily on the day before the procedure and continues this for about a week. Patients should also have been off isotretinoin for at least 6 months before treatment, he noted.

"I treat through skin type 6, but I’m very cautious doing it. I’m not so much worried about how deeply I’m treating, but I really dial back the density to avoid hyperpigmentation, and pretreat with hydroquinone, as well," he said.

For poikiloderma of Civatte, fractional lasers are more effective for pigment than erythema. Pulsed dye lasers are more effective for erythema. "You can do [the pulsed dye treatment] first, and then do the fractional resurfacing," he said.

Dr. Avram is a paid consultant to Zeltiq Aesthetics, Unilever, and Living Proof.

SDEF and this news organization are owned by Frontline Medical Communications.

When resurfacing the skin with nonablative, midinfrared fractional lasers, "don’t think you’re just going to set these devices to the highest [density] setting, and get the best results," Dr. Mathew Avram said at the SDEF Las Vegas Dermatology Seminar.

The percentage of skin in the treatment area that receives microscopic thermal wounds doesn’t necessarily translate to better results, said Dr. Avram, director of the dermatology laser and cosmetic center at Massachusetts General Hospital in Boston.

One study randomized 20 patients with hypertrophic scars to either 26% or 14% scar coverage with 40 mJ. Patients in the 14% group rated the results better at 3 months’ follow-up. "Low-density treatment is at least as effective as high-density treatment and [has] fewer side effects," the authors wrote (Lasers Surg. Med. 2011;43:265-72).

"If you did a lower-density [treatment]," Dr. Avram explained, "you got the same improvement as you did with a higher density, which is counterintuitive. You’d think the more damage you do the better, but basically all you get is more side effects" like pain, peeling, and inflammation. "Density is the key in terms of side effects and risk of hyperpigmentation."

Depth of treatment, which is determined by pulse energy, is another major consideration. "The pulse energy should reflect the pathology of the condition being treated," he said. With superficial pathology, photoaging, for instance,"you use a low pulse energy." With deeper pathology, such as deeper rhytides or traumatic scars, "you use higher pulse energy to penetrate more deeply. Adjust the depth of treatment and density for the pathology you are treating," Dr. Avram advised.

"You want to tell patients about procedural discomfort, side effects, and real expectations. It’s going to take multiple treatments, and these treatments will only partially improve fine to moderate wrinkles, pigmentation, and scars about 3 months after the time of treatment," he said.

Cold-air cooling is an option for anesthesia, as are topical lidocaine/tetracaine and locally injected anesthesia. The anesthetized area should be allowed to settle down a bit before the procedure to reduce the risk of ulceration, he said.

To prevent treatment-induced flares, Dr. Avram said he gives patients with histories of herpes labialis 500 mg of valacyclovir twice daily on the day before the procedure and continues this for about a week. Patients should also have been off isotretinoin for at least 6 months before treatment, he noted.

"I treat through skin type 6, but I’m very cautious doing it. I’m not so much worried about how deeply I’m treating, but I really dial back the density to avoid hyperpigmentation, and pretreat with hydroquinone, as well," he said.

For poikiloderma of Civatte, fractional lasers are more effective for pigment than erythema. Pulsed dye lasers are more effective for erythema. "You can do [the pulsed dye treatment] first, and then do the fractional resurfacing," he said.

Dr. Avram is a paid consultant to Zeltiq Aesthetics, Unilever, and Living Proof.

SDEF and this news organization are owned by Frontline Medical Communications.

WASHINGTON – Children diagnosed with pervasive developmental disorder not otherwise specified probably will not meet the criteria for an autism diagnosis under the DSM-5, according to Lawrence Scahill, Ph.D.

"I don’t think schools are going to rearrange labels, but down the road, children we call PDD-NOS [pervasive developmental disorder not otherwise specified] are going to be harder to fit into the new criteria" when the DSM-5 is published in May, said Dr. Scahill, a pediatrics professor at Emory University and the Marcus Autism Center, both in Atlanta.

For some children repetitive behaviors and language, and social delays, will not be "profound [enough]. [Instead,] maybe they’ll get some of what they need by a diagnosis of ADHD," Dr. Scahill said at a psychopharmacology update, sponsored by the American Academy of Child and Adolescent Psychiatry.

The DSM-5’s autism requirements are more restrictive than those of the DSM-IV. For example, in the new manual, autism, Asperger’s syndrome, and PDD-NOS will be lumped together under a single diagnosis of autism spectrum disorder, which is likely to require, among other things, early onset of social communication and interaction deficits, restricted interests, and repetitive behavior, plus an indication of severity level.

The idea is to make the diagnosis of autism more precise. Under the DSM-IV’s more subjective requirements, clinicians could have valid disagreements about where to slot a child, said Dr. Scahill, who formerly served as director of the Research Unit on Pediatric Psychopharmacology at the Yale Child Study Center, New Haven, Conn.

In addition, "a large amount of genetic research from twin studies supports the idea of a spectrum disorder. [Often,] twin one has full autism and twin two has a pastel version, [especially] in monozygotic twins," he said.

The changes will probably decrease the prevalence of autism if people "are careful in their diagnoses," Dr. Scahill said. Many PDD-NOS children will better fit DSM-5’s new "social communication language disorder." The DSM-5s drafters were "trying to get kids with delayed language out of autism," he noted.

Asperger’s is going away, too, which has caused "a great hue and cry from [the Asperger’s] community. They say things like ‘it’s helped me understand myself’ and feel like they won’t have that explanation [anymore], but I don’t think that many kids with [true] Asperger’s will fail to meet the criteria for autism spectrum disorder. There are people who have been given an Asperger’s diagnosis who might not meet it; they might have been overdiagnosed. I don’t think [the change] is as harmful as some think," he said.

The DSM-5 also will allow patients with autistic disorder to be diagnosed with attention-deficit/hyperactivity disorder (ADHD); the DSM-IV specifies that such a dual diagnosis is not made.

In general, ADHD drugs are less effective in children with autism and more likely to cause side effects, Dr. Scahill said.

"Methylphenidate has small to medium effects. Tolerabilities are okay at conservative doses. Study results are mixed" on whether atomoxetine helps or not, but "I wouldn’t say don’t try it. We need more data on guanfacine." Small studies on clonidine suggest children with autistic disorder "are exquisitely sensitive to its sedative side effects," he said.

"When dealing with parents, be up-front and say, ‘We are looking for some help here, but we are not expecting big effects.’ If we can get some benefit at low and medium doses, we’re going to take the money and run," he said.

Dr. Scahill is a consultant for Biomarin and Roche. He also receives research funding from Pfizer, Roche, and Shire Pharmaceuticals.

WASHINGTON – Children diagnosed with pervasive developmental disorder not otherwise specified probably will not meet the criteria for an autism diagnosis under the DSM-5, according to Lawrence Scahill, Ph.D.

"I don’t think schools are going to rearrange labels, but down the road, children we call PDD-NOS [pervasive developmental disorder not otherwise specified] are going to be harder to fit into the new criteria" when the DSM-5 is published in May, said Dr. Scahill, a pediatrics professor at Emory University and the Marcus Autism Center, both in Atlanta.

For some children repetitive behaviors and language, and social delays, will not be "profound [enough]. [Instead,] maybe they’ll get some of what they need by a diagnosis of ADHD," Dr. Scahill said at a psychopharmacology update, sponsored by the American Academy of Child and Adolescent Psychiatry.

The DSM-5’s autism requirements are more restrictive than those of the DSM-IV. For example, in the new manual, autism, Asperger’s syndrome, and PDD-NOS will be lumped together under a single diagnosis of autism spectrum disorder, which is likely to require, among other things, early onset of social communication and interaction deficits, restricted interests, and repetitive behavior, plus an indication of severity level.

The idea is to make the diagnosis of autism more precise. Under the DSM-IV’s more subjective requirements, clinicians could have valid disagreements about where to slot a child, said Dr. Scahill, who formerly served as director of the Research Unit on Pediatric Psychopharmacology at the Yale Child Study Center, New Haven, Conn.

In addition, "a large amount of genetic research from twin studies supports the idea of a spectrum disorder. [Often,] twin one has full autism and twin two has a pastel version, [especially] in monozygotic twins," he said.

The changes will probably decrease the prevalence of autism if people "are careful in their diagnoses," Dr. Scahill said. Many PDD-NOS children will better fit DSM-5’s new "social communication language disorder." The DSM-5s drafters were "trying to get kids with delayed language out of autism," he noted.

Asperger’s is going away, too, which has caused "a great hue and cry from [the Asperger’s] community. They say things like ‘it’s helped me understand myself’ and feel like they won’t have that explanation [anymore], but I don’t think that many kids with [true] Asperger’s will fail to meet the criteria for autism spectrum disorder. There are people who have been given an Asperger’s diagnosis who might not meet it; they might have been overdiagnosed. I don’t think [the change] is as harmful as some think," he said.

The DSM-5 also will allow patients with autistic disorder to be diagnosed with attention-deficit/hyperactivity disorder (ADHD); the DSM-IV specifies that such a dual diagnosis is not made.

In general, ADHD drugs are less effective in children with autism and more likely to cause side effects, Dr. Scahill said.

"Methylphenidate has small to medium effects. Tolerabilities are okay at conservative doses. Study results are mixed" on whether atomoxetine helps or not, but "I wouldn’t say don’t try it. We need more data on guanfacine." Small studies on clonidine suggest children with autistic disorder "are exquisitely sensitive to its sedative side effects," he said.

"When dealing with parents, be up-front and say, ‘We are looking for some help here, but we are not expecting big effects.’ If we can get some benefit at low and medium doses, we’re going to take the money and run," he said.

Dr. Scahill is a consultant for Biomarin and Roche. He also receives research funding from Pfizer, Roche, and Shire Pharmaceuticals.

WASHINGTON – Children diagnosed with pervasive developmental disorder not otherwise specified probably will not meet the criteria for an autism diagnosis under the DSM-5, according to Lawrence Scahill, Ph.D.

"I don’t think schools are going to rearrange labels, but down the road, children we call PDD-NOS [pervasive developmental disorder not otherwise specified] are going to be harder to fit into the new criteria" when the DSM-5 is published in May, said Dr. Scahill, a pediatrics professor at Emory University and the Marcus Autism Center, both in Atlanta.

For some children repetitive behaviors and language, and social delays, will not be "profound [enough]. [Instead,] maybe they’ll get some of what they need by a diagnosis of ADHD," Dr. Scahill said at a psychopharmacology update, sponsored by the American Academy of Child and Adolescent Psychiatry.

The DSM-5’s autism requirements are more restrictive than those of the DSM-IV. For example, in the new manual, autism, Asperger’s syndrome, and PDD-NOS will be lumped together under a single diagnosis of autism spectrum disorder, which is likely to require, among other things, early onset of social communication and interaction deficits, restricted interests, and repetitive behavior, plus an indication of severity level.

The idea is to make the diagnosis of autism more precise. Under the DSM-IV’s more subjective requirements, clinicians could have valid disagreements about where to slot a child, said Dr. Scahill, who formerly served as director of the Research Unit on Pediatric Psychopharmacology at the Yale Child Study Center, New Haven, Conn.

In addition, "a large amount of genetic research from twin studies supports the idea of a spectrum disorder. [Often,] twin one has full autism and twin two has a pastel version, [especially] in monozygotic twins," he said.

The changes will probably decrease the prevalence of autism if people "are careful in their diagnoses," Dr. Scahill said. Many PDD-NOS children will better fit DSM-5’s new "social communication language disorder." The DSM-5s drafters were "trying to get kids with delayed language out of autism," he noted.

Asperger’s is going away, too, which has caused "a great hue and cry from [the Asperger’s] community. They say things like ‘it’s helped me understand myself’ and feel like they won’t have that explanation [anymore], but I don’t think that many kids with [true] Asperger’s will fail to meet the criteria for autism spectrum disorder. There are people who have been given an Asperger’s diagnosis who might not meet it; they might have been overdiagnosed. I don’t think [the change] is as harmful as some think," he said.

The DSM-5 also will allow patients with autistic disorder to be diagnosed with attention-deficit/hyperactivity disorder (ADHD); the DSM-IV specifies that such a dual diagnosis is not made.

In general, ADHD drugs are less effective in children with autism and more likely to cause side effects, Dr. Scahill said.

"Methylphenidate has small to medium effects. Tolerabilities are okay at conservative doses. Study results are mixed" on whether atomoxetine helps or not, but "I wouldn’t say don’t try it. We need more data on guanfacine." Small studies on clonidine suggest children with autistic disorder "are exquisitely sensitive to its sedative side effects," he said.

"When dealing with parents, be up-front and say, ‘We are looking for some help here, but we are not expecting big effects.’ If we can get some benefit at low and medium doses, we’re going to take the money and run," he said.

Dr. Scahill is a consultant for Biomarin and Roche. He also receives research funding from Pfizer, Roche, and Shire Pharmaceuticals.

The DSM-5’s new diagnosis of disruptive mood dysregulation disorder was made to address the overdiagnosis of bipolar disorder by creating a diagnostic home for children with explosive rages, but only some of those children will qualify for the diagnosis, according to Dr. Gabrielle A. Carlson.

It "will relieve [only] some of the stress" on bipolar disorder, but "it won’t solve all the problems of false diagnosis," she said at a psychopharmacology update, sponsored by the American Academy of Child and Adolescent Psychiatry.

When the DSM-5 is published in May, disruptive mood dysregulation disorder (DMDD) probably will require at least 12 months of very severe outbursts from trivial triggers that happen more than three times per week and are developmentally inappropriate; persistently irritable mood between outbursts most of the day every day; outbursts or negative mood in at least two separate settings; and onset before the age of 10, among other criteria.

"And there are a number of really important exclusionary criteria. You don’t see [DMDD] if there’s any hint of mania, if there’s major depressive disorder," or if there is dysthymia, psychosis, posttraumatic stress disorder (PTSD), pervasive developmental disorders, or separation anxiety, said Dr. Carlson, director of child and adolescent psychiatry at the State University of New York at Stony Brook.

"Here’s the problem: Many children with explosive outbursts have depression and dysthymia, or PTSD," or some other exclusionary problem, or don’t meet all of the DMDD requirements. "If we follow the rules," only about 25% of inpatient explosive children and a fifth of children on the outpatient side will have DMDD, she said, based on analyses of her own inpatient and outpatient services.

Having a diagnostic home and treatment focus for explosive children is probably a positive development, Dr. Carlson said, because rages are probably the "single most vexing problem we have in child psychiatry. On the other hand, [DMDD] is just as likely to be abused as bipolar disorder, because it doesn’t capture the vast majority of kids with explosive outbursts. In fact, it may well mask conditions we already know about and can treat. If you go rushing right to ‘whoa, explosive outbursts – DMDD,’ you’re not going to look for depression, you are not going to look for ADHD, you’re not going to look for stuff you can treat," Dr. Carlson said.

Remember that "kids [with explosive outbursts] are doing the best they can," she said. "They aren’t getting up in the morning saying, ‘I’m really going to try to anger my parents and teachers.’ "

It’s important to first "maximize treatment of the base condition, whether it’s ADHD, depression, or some other problem." If outbursts remain a symptom, consider adding an atypical or conventional antipsychotic or a mood stabilizer, she said. It might take a while to see benefit, so "keep a record of the frequency, duration, and intensity of outbursts" to show parents that progress is being made.

"Medication is for executive functioning and mood regulation. For language and social" problems, it’s about psychoeducation – trying to understand the rage triggers and how not to feed them. Parent training can help. In addition, "if a parent has a psychiatric disorder, get it treated." Parents will not be able to help their child – and follow through on treatment recommendations – if they don’t have their own issues under control.

Dr. Carlson disclosed research funding from Pfizer, GlaxoSmithKline, Schering-Plough, Bristol-Myers Squibb, and Otsuka.

The DSM-5’s new diagnosis of disruptive mood dysregulation disorder was made to address the overdiagnosis of bipolar disorder by creating a diagnostic home for children with explosive rages, but only some of those children will qualify for the diagnosis, according to Dr. Gabrielle A. Carlson.

It "will relieve [only] some of the stress" on bipolar disorder, but "it won’t solve all the problems of false diagnosis," she said at a psychopharmacology update, sponsored by the American Academy of Child and Adolescent Psychiatry.

When the DSM-5 is published in May, disruptive mood dysregulation disorder (DMDD) probably will require at least 12 months of very severe outbursts from trivial triggers that happen more than three times per week and are developmentally inappropriate; persistently irritable mood between outbursts most of the day every day; outbursts or negative mood in at least two separate settings; and onset before the age of 10, among other criteria.

"And there are a number of really important exclusionary criteria. You don’t see [DMDD] if there’s any hint of mania, if there’s major depressive disorder," or if there is dysthymia, psychosis, posttraumatic stress disorder (PTSD), pervasive developmental disorders, or separation anxiety, said Dr. Carlson, director of child and adolescent psychiatry at the State University of New York at Stony Brook.

"Here’s the problem: Many children with explosive outbursts have depression and dysthymia, or PTSD," or some other exclusionary problem, or don’t meet all of the DMDD requirements. "If we follow the rules," only about 25% of inpatient explosive children and a fifth of children on the outpatient side will have DMDD, she said, based on analyses of her own inpatient and outpatient services.

Having a diagnostic home and treatment focus for explosive children is probably a positive development, Dr. Carlson said, because rages are probably the "single most vexing problem we have in child psychiatry. On the other hand, [DMDD] is just as likely to be abused as bipolar disorder, because it doesn’t capture the vast majority of kids with explosive outbursts. In fact, it may well mask conditions we already know about and can treat. If you go rushing right to ‘whoa, explosive outbursts – DMDD,’ you’re not going to look for depression, you are not going to look for ADHD, you’re not going to look for stuff you can treat," Dr. Carlson said.

Remember that "kids [with explosive outbursts] are doing the best they can," she said. "They aren’t getting up in the morning saying, ‘I’m really going to try to anger my parents and teachers.’ "

It’s important to first "maximize treatment of the base condition, whether it’s ADHD, depression, or some other problem." If outbursts remain a symptom, consider adding an atypical or conventional antipsychotic or a mood stabilizer, she said. It might take a while to see benefit, so "keep a record of the frequency, duration, and intensity of outbursts" to show parents that progress is being made.

"Medication is for executive functioning and mood regulation. For language and social" problems, it’s about psychoeducation – trying to understand the rage triggers and how not to feed them. Parent training can help. In addition, "if a parent has a psychiatric disorder, get it treated." Parents will not be able to help their child – and follow through on treatment recommendations – if they don’t have their own issues under control.

Dr. Carlson disclosed research funding from Pfizer, GlaxoSmithKline, Schering-Plough, Bristol-Myers Squibb, and Otsuka.

The DSM-5’s new diagnosis of disruptive mood dysregulation disorder was made to address the overdiagnosis of bipolar disorder by creating a diagnostic home for children with explosive rages, but only some of those children will qualify for the diagnosis, according to Dr. Gabrielle A. Carlson.

It "will relieve [only] some of the stress" on bipolar disorder, but "it won’t solve all the problems of false diagnosis," she said at a psychopharmacology update, sponsored by the American Academy of Child and Adolescent Psychiatry.

When the DSM-5 is published in May, disruptive mood dysregulation disorder (DMDD) probably will require at least 12 months of very severe outbursts from trivial triggers that happen more than three times per week and are developmentally inappropriate; persistently irritable mood between outbursts most of the day every day; outbursts or negative mood in at least two separate settings; and onset before the age of 10, among other criteria.

"And there are a number of really important exclusionary criteria. You don’t see [DMDD] if there’s any hint of mania, if there’s major depressive disorder," or if there is dysthymia, psychosis, posttraumatic stress disorder (PTSD), pervasive developmental disorders, or separation anxiety, said Dr. Carlson, director of child and adolescent psychiatry at the State University of New York at Stony Brook.

"Here’s the problem: Many children with explosive outbursts have depression and dysthymia, or PTSD," or some other exclusionary problem, or don’t meet all of the DMDD requirements. "If we follow the rules," only about 25% of inpatient explosive children and a fifth of children on the outpatient side will have DMDD, she said, based on analyses of her own inpatient and outpatient services.

Having a diagnostic home and treatment focus for explosive children is probably a positive development, Dr. Carlson said, because rages are probably the "single most vexing problem we have in child psychiatry. On the other hand, [DMDD] is just as likely to be abused as bipolar disorder, because it doesn’t capture the vast majority of kids with explosive outbursts. In fact, it may well mask conditions we already know about and can treat. If you go rushing right to ‘whoa, explosive outbursts – DMDD,’ you’re not going to look for depression, you are not going to look for ADHD, you’re not going to look for stuff you can treat," Dr. Carlson said.

Remember that "kids [with explosive outbursts] are doing the best they can," she said. "They aren’t getting up in the morning saying, ‘I’m really going to try to anger my parents and teachers.’ "

It’s important to first "maximize treatment of the base condition, whether it’s ADHD, depression, or some other problem." If outbursts remain a symptom, consider adding an atypical or conventional antipsychotic or a mood stabilizer, she said. It might take a while to see benefit, so "keep a record of the frequency, duration, and intensity of outbursts" to show parents that progress is being made.

"Medication is for executive functioning and mood regulation. For language and social" problems, it’s about psychoeducation – trying to understand the rage triggers and how not to feed them. Parent training can help. In addition, "if a parent has a psychiatric disorder, get it treated." Parents will not be able to help their child – and follow through on treatment recommendations – if they don’t have their own issues under control.

Dr. Carlson disclosed research funding from Pfizer, GlaxoSmithKline, Schering-Plough, Bristol-Myers Squibb, and Otsuka.