Which of the following complementary and alternative medicine (CAM) therapies may have beneficial effects on symptoms of mild cognitive impairment (MCI) and Alzheimer disease (AD)? Integrative psychiatry specialist, James Lake, MD, answers this question and discusses the latest research in this Q&A. Take the quiz and test your knowledge.



For the answer and discussion, please click here



The above-mentioned CAM therapies may reduce symptoms of MCI and AD.

Select CAM therapies may lessen symptoms of cognitive impairment related to AD, stroke, traumatic brain injury (TBI), and normal aging.

Dietary changes that are correlated with a reduced risk of AD include restricted intake of saturated fats and moderate wine consumption. Regular aerobic exercise may also reduce the risk of any kind of dementia. There is evidence that Ginkgo biloba is an effective treatment of moderate cognitive impairment in early AD and vascular dementia.

 Phosphatidylserine and huperzine A are other natural products that will probably play increasingly important roles as adjunctive agents or stand-alone treatments in early or moderate AD, MCI, and age-related cognitive decline.

In addition, cytidinediphosphocholine (CDP-choline) holds promise as a treatment of cognitive impairment following stroke or TBI. The essential oils of lemon balm and common sage reduce agitation and nighttime anxiety (eg, “sundowning”) in individuals with dementia when applied to the arms and face.

Regular music therapy may yield transient improvements in agitated behavior and cognitive functioning in patients with AD. Research findings suggest that regular Healing Touch

 may have beneficial calming effects and improve global functioning in AD.

Articles

Which of the following complementary and alternative medicine (CAM) therapies may have beneficial effects on symptoms of mild cognitive impairment (MCI) and Alzheimer disease (AD)?

Benefits of CAM Therapies for Dementia

Quick . . . name a class of prescription medications that, by most evidence, appears to be overprescribed and abused and the use of which has resulted in an increasing number of emergency department visits.

If you said “opioids,” you would be right. This is probably the answer most health care professionals would give. However, there is another response that is given much less frequently but would be equally true: benzodiazepines.

I wish I could say that this inattention to benzodiazepines is something new, but my personal experience indicates it is not. Twenty years ago, I coauthored one of the first papers that examined the use of benzodiazepines by patients with chronic pain and found that these agents were overprescribed.

 With rare exception since that time, the lectures I have attended on overprescription of medications have focused on opioids. When I have raised the issue of overuse of benzodiazepines, the speakers have either responded that they were unaware of any problem or offered the odd response that the audiences were interested in opioids, not benzodiazepines.

Two reports from the CDC indicate the scope of the problem with benzodiazepines. From 2004 to 2008, there was a 111% increase (going from 144,600 to 305,900) in the estimated number of emergency department visits involving nonmedical use of opioid analgesics.

 For the same period, there was an 89% increase (from 143,500 to 271,700) in such visits for benzodiazepines. Data from the National Vital Statistics System multiple cause-of-death file from 2010 show that opioid analgesics were involved in 75% of pharmaceutical overdose deaths; benzodiazepines were in second place, with involvement in 29% of such deaths.

 Benzodiazepines were also involved in 30% of opioid-related deaths-far more than any other class of drugs. This indicates that combining benzodiazepines and opioids may be especially dangerous.

Of course, patients who use prescription drugs for nonmedical purposes may be purchasing drugs illicitly, so it is difficult to determine how many of those in the CDC studies may have had prescriptions written for them by physicians. However, 2 studies on opioid prescriptions in the Department of Veterans Affairs health care system indicate that benzodiazepines continue to be frequently prescribed for patients with chronic pain.

In the first study, the authors found that 32% of patients taking what they defined as high doses of opioid analgesics for chronic noncancer pain and 25% of those taking what was considered a traditional dose of opioids for the pain were also taking a benzodiazepine.

In contrast, only 10% of patients who were not receiving an opioid were given a prescription for a benzodiazepine.

The second study involved patients receiving methadone or a long-acting form of morphine for chronic pain. In this study, at least 28 days of a benzodiazepine had also been prescribed for 26% of the patients at the same time as they were taking the opioid.

Concerns about benzodiazepine use by patients with chronic pain

 the use of benzodiazepines by patients with chronic pain was generally contraindicated. Since that time, additional studies have only strengthened this premise-most notably research indicating that benzodiazepines reduce the analgesic effects of opioids and that their long-term use can result in hyperalgesia, thereby exacerbating the pain by lowering the pain threshhold.

There are the additional problems well known to psychiatrists. Benzodiazepines can be addictive. In fact, from my experience, it is often more difficult to discontinue benzodiazepines than opioids. Many times after patients have told me that they are willing to do anything to reduce their pain and I have recommended trying to discontinue benzodiazepine use, they have modified their responses to “anything but that!”

Although benzodiazepines can be effective for the treatment of anxiety for short periods, they are, with rare exceptions, not generally indicated for chronic anxiety in the absence of a diagnosable anxiety disorder. However, few of the patients with chronic pain that I have seen during my career have had a diagnosis of an anxiety disorder at any time while receiving these medications. Furthermore, many of those who have anxiety also have associated depression, which may be exacerbated by the benzodiazepines. Obviously, treatment with an antidepressant would be a far better choice for these patients-especially in light of the fact that SNRIs can provide marked analgesia in addition to their antidepressant and anxiolytic benefits. Even for medication management of brief periods of anxiety, buspirone may be a better choice.

Benzodiazepines have been and continue to be frequently used for the treatment of insomnia. In fact, this was the most common reason why the patients in my study were taking benzodiazepines.

 Studies of patients with chronic pain who had difficulty in sleeping show that benzodiazepines interfere with the same stages of sleep most likely to be problematic. The patients I studied found that the benzodiazepines provided little benefit for improving sleep. With the availability of the non-benzodiazepine sedative hypnotics, including zolpidem, zaleplon, and eszopiclone, there is now little rea-son for benzodiazepines to be used to aid sleep.

Benzodiazepines are also frequently employed as muscle relaxants, but there is limited literature to support this. Whether they provide much direct muscle relaxation or whether their benefits are primarily related to their sedating effects is open to question. There are better choices if a muscle relaxant is indicated, such as cyclobenzaprine and tizanidine, which do not carry the potential problems that are associated with benzodiazepines.

Although there has been a growing focus on the abuse of opioid analgesics, with the development of tamper-resistant formulations and the requirement that physicians take risk evaluation and mitigation strategy (REMS) programs to prescribe certain opioids, benzodiazepines have not received similar attention.

There is no doubt that abuse of opioid analagesics is a major problem that needs to be addressed. But ignoring problems associated with benzodiazepine use is injurious to the nation’s public health.

 Governale L. Outpatient prescription opioid utilization in the US, years 2000-2009. July 22, 2010. http://
www.fda.gov/downloads/AdvisoryCommitteesMeetingMaterials/Drugs/AnestheticandLifeSupportDrugsAdvisoryCommittee/ucm220950.pdf. Accessed May 20, 2013.

 Centers for Disease Control and Prevention. Primary Care and Public Health Initiative. Balancing pain management and prescription opioid abuse: educational module. October 24, 2012. http://www.cdc.gov/primarycare/materials/opioidabuse. Accessed May 20, 2013.

 Centers for Disease Control and Prevention. Suicide among adults aged 35-64-United States, 1999-2010. 

 Bair MJ, Robinson RL, Katon W, Kroenke K. Depression and pain comorbidity: a literature review. 

 Ilgen MA, Zivin K, Austin KL, et al. Severe pain predicts greater likelihood of subsequent suicide. 

 Pereira A, Gitlin MJ, Gross RA, et al. Suicidality associated with antiepileptic drugs: implications for the treatment of neuropathic pain and fibromyalgia. 

Quick . . . name a class of prescription medications that, by most evidence, appears to be overprescribed and abused and the use of which has resulted in an increasing number of emergency department visits. If you said "opioids," you would be right.

Benzodiazepines and Pain

How often are you confronted with an ethical dilemma in your clinical practice? How comfortable-and how prepared-are you to deal with these issues? Have the ethical dilemmas you face become more difficult in recent years?

Those are just a few of the questions posed in the Psychiatric Times Ethics Survey-a survey that turned out to be the largest ever of its kind: 708 psychiatrists took time to respond along with other health professionals, including nurses, psychologists, and students-for a grand total of 1400 responses. Another ethics survey is planned for later this year.

The charts you see here are randomly culled from that ethics survey. The survey included 19 questions that touched on end-of-life issues, boundary issues, confidentiality, and third-party influence.



How often are you confronted with an ethical dilemma in your clinical practice? How comfortable-and how prepared-are you to deal with these issues? Those are just a few of the questions posed in the Psychiatric Times Ethics Survey-a survey that turned out to be the largest ever of its kind.

The Moral Struggles of Practicing Psychiatrists

-acetylcysteine and bipolar-specific psychotherapies is on the horizon for this bipolar series. But with DSM-5 about to arrive, one more examination of bipolar diagnosis is warranted. After all, if a diagnosis is inaccurate, treatment efforts, however well-intentioned, may misfire.

The formal changes in DSM-5 will not be official or public until this month. But the bipolar disorder workgroup proposed 4 changes on the 

 (since removed in anticipation of publication).

 Two of the proposed changes will tighten bipolar diagnostic requirements, and two will loosen them.

The tightening criteria are (1) diagnosis of hypomania or mania will now require a finding of increased energy along with the rest of the unchanged criteria and (2) bipolar not otherwise specified (BP NOS) becomes bipolar not elsewhere classified (BP NEC), with tighter definitions of subthreshold bipolar variations. The loosening criteria are (1) mixed states will encompass a spectrum of admixtures of manic and depressive symptoms, down to specific minimums and (2) antidepressant-induced hypomania or mania will now qualify a patient for a diagnosis of bipolar disorder.

Will the tighter criteria help address the reported overdiagnosis problem?

 Take the fictional case of 31-year-old Ms Alvarez, who, since age 18, has had many clearly recognizable episodes of depression that last a week or more. When asked, she endorses phases of increased activity and remarkable productivity; increased social interaction; and a confident, positive outlook that is otherwise unusual for her-all on about 4 to 5 hours of sleep. She does not endorse increased energy during these phases, however.

Does she have bipolar II? According to DSM-IV, she might qualify (barring other diagnoses that trump bipolar disorder, such as a mood disorder due to a general medical condition). But because she does not endorse increased energy phases, she does not quite reach a diagnosis of bipolar II according to DSM-5. Will this tighter requirement increase diagnostic accuracy?

Intuitively, the answer seems obvious: surely the harder it is for a patient to meet all the diagnostic requirements, the harder it should be to award a diagnosis of bipolar disorder. Yet surprisingly, if we look at the statistical determinants of diagnostic accuracy, tighter criteria will have little impact. The reward for working through the following review of these statistical determinants is the understanding that the greatest impact of diagnostic accuracy comes from clinicians, not from tightening criteria.

Diagnostic accuracy: positive predictive value

When a clinician tells a patient “you have bipolar disorder,” how likely is it that the diagnosis is correct? In a widely cited study of overdiagnosis, Zimmerman and colleagues

 found that the answer is “less than 50% of the time.” My essay “

Overdiagnosis: Examine the Assumptions, Anticipate New Bipolar Criteria

 questions the broad assumptions that underlie that conclusion. Zimmerman and colleagues derived the 50% diagnostic accuracy figure by calculating a positive predictive value (PPV): in patients said to have bipolar disorder by local clinicians, how many will be found positive by the gold standard (in this case, a structured clinical interview)? In their study, a structured interview did not support the diagnosis in 56% of patients who had been told they had bipolar disorder.

Two key factors determine PPV, and thus determine why in this study the PPV was so low (only 46%). First is the specificity of the test in question, which in this case is the DSM criteria set as applied by the local clinicians. The other determinant of PPV is prevalence-how likely is the illness before the clinician starts trying to diagnose it?

Another related concept needs to be introduced to show that clinicians have more impact on accuracy than the DSM criteria, namely: prevalence is but one form of prior probability. Clinicians can increase prior probability, ie, the likelihood that the patient has bipolar disorder, by assessing other markers of bipolar disorder that are not in DSM.

Compare tightening diagnostic criteria (eg, adding an increased-energy criterion to the required symptoms of hypomania to increase specificity) with increasing prior probability (eg, by asking the patient for additional information not in the DSM criteria: family history, age of onset, course of illness, and response to treatment). As a starting point for this comparison, 

 (first row) presents the results from the Zimmerman study, with the very low PPV of 46%.

In the second row, using the same starting point, prevalence is held constant while specificity is increased. This reflects the intent of tightening changes in DSM-5 to make it harder to confirm the diagnosis. Although the increase in specificity is small, from 86% to 90%, this is likely in the range of what tightening criteria could produce. Note that with this change in specificity, PPV increases from 46% to 55%. (Greater increases in specificity are clinically very difficult to achieve, but even if specificity were somehow to be increased to 95%, the conclusions presented here still hold.


Increasing positive predictive value (PPV) increases diagnostic accuracy of bipolar disorder

In the third row, specificity is held constant at the same 86% value found in the Zimmerman study, while prior probability is increased to 30%. This is what happens when a clinician has a hunch (eg, by inquiring about family history and response to prior treatment attempts) that the likelihood of bipolar disorder underlying Ms Alvarez’s depression is higher than population prevalence (eg, about 1 chance in 3). Note that now PPV increases to 68%: a better than two-thirds chance of accuracy, up from less than 50% as found by Zimmerman and colleagues, and well above the increase associated with a moderate improvement in specificity shown in the second row.


Markers of bipolar disorder not found in DSM-5

Finally, the fourth row shows what happens when a clinician narrows the possibility that the patient has bipolar disorder to a 50/50 chance, before applying DSM criteria. For example, imagine that Ms Alvarez, presenting with depression, had multiple features of bipolar disorder: a first-degree relative with a firm diagnosis; onset of her first depression at age 18; postpartum depression; multiple, brief episodes; a strong adverse reaction to an antidepressant; and no sustained benefit in 4 well-conducted antidepressant trials. With all this, the likelihood that her depression is a bipolar depression is at least 50% (a conservative estimate

). With a 50/50 prior probability, use of DSM criteria with a specificity of 86% achieves a PPV of 83%. This is much higher than can be achieved by tightening DSM criteria to a specificity of 90%, or even 95%.

The analysis above suggests that the tightening of DSM criteria will have only a small effect on diagnostic accuracy. A far greater effect can be achieved if clinicians adopt a practice of routinely assessing the non-DSM markers of bipolar disorder shown in 

 Their presence does not make the diagnosis. Rather, their presence increases the probability that a depression is a bipolar depression.



This is not a novel approach. Routine assessment of these bipolar markers has been part of the assessment of patients at the Harvard-associated mood disorder clinic for 10 years, as part of a 

 suggested that routine assessment of these bipolar markers is “what good clinicians already do.”

Unfortunately, more than half of all mental health care in the US is delivered in primary care settings, where assessment of non-DSM bipolar markers is not “what good clinicians already do.” How can psychiatrists and psychologists improve diagnostic accuracy there? At minimum, they should help primary care colleagues screen as effectively as possible for bipolar disorder.

Screening questionnaires are far from ideal. Their results are too often interpreted as a diagnosis. But they can be used to identify patients who should not receive an antidepressant before further assessment by a mental health specialist. Because the 

 (BSDS) has been found to be more sensitive for bipolar II, it is preferable for use in primary care, where bipolar II is more likely to be missed than bipolar I.

 that assesses all of the factors shown in 

 This version of the BSDS does not require further validation, because the additional questions merely gather data for interpretation by a clinician.

Good clinicians will not only routinely assess non-DSM bipolar markers, they will also encourage their primary care colleagues to do the same, using a screening tool developed for this purpose. These steps will do more for improving diagnostic accuracy across the entire mental health care delivery system than using the new DSM criteria.

 American Psychiatric Association. DSM-5 Development. 

Mitchell PB. Bipolar disorder: the shift to overdiagnosis. 

Zimmerman M, Ruggero CJ, Chelminski I, Young D. Is bipolar disorder overdiagnosed? 

Phelps J, Ghaemi SN. The mistaken claim of bipolar ‘overdiagnosis’: solving the false positives problem for DSM-5/ICD-11. 

 Mitchell PB, Frankland A, Hadzi-Pavlovic D, et al. Comparison of depressive episodes in bipolar disorder and in major depressive disorder within bipolar disorder pedigrees. 

 Ghaemi SN, Ko JY, Goodwin FK. “Cade’s disease” and beyond: misdiagnosis, antidepressant use, and a proposed definition for bipolar spectrum disorder. 

 Mitchell PB, Goodwin GM, Johnson GF, Hirschfeld RM. Diagnostic guidelines for bipolar depression: a probabilistic approach. 

http://www.psycheducation.org/depression/STEPBipolarityIndex.htm

 Ketter TA, Citrome L. Addressing challenges in bipolar diagnosis: what do good clinicians already do? 

 Zaratiegui RM, VÃ¡zquez GH, Lorenzo LS, et al. Sensitivity and specificity of the mood disorder questionnaire and the bipolar spectrum diagnostic scale in Argentinean patients with mood disorders. 

http://www.psycheducation.org/PCP/launch/downloadMoodCheck.htm

With DSM-5, one more examination of bipolar diagnosis is warranted. After all, if a diagnosis is inaccurate, treatment efforts, however well-intentioned, may misfire.

DSM-5 Won’t Solve the Overdiagnosis Problem-But Clinicians Can

Come next year, psychiatrists will start seeing patients who have purchased new individual and small-group health plans on the state exchanges mandated by the Affordable Care Act. But mental health benefits will differ from state to state, and it is hard to know whether they will meet the requirements of the Mental Health Parity and Addiction Equity Act of 2008 (MHPAEA). Moreover, important issues such as network adequacy as far as psychiatrist coverage is concerned and physician payment rates are also up in the air.

Julie Clements, JD, MPP, Deputy Director of Regulatory Affairs at the American Psychiatric Association, recently conducted a webinar for psychiatrists. She told 

, “A lot of them don’t yet realize how big an issue this is. They are just beginning to understand that the state exchanges will offer private plans and subsidies for individuals of up to 400% of the poverty rate. So this could mean 60 million to 70 million people impacted.”

The Department of Health and Human Services (HHS) issued a final rule on February 25, 2013, that outlines the essential health benefits (EHBs) that all qualified health plans (QHPs) on each state exchange must cover. Those EHBs fall into 10 categories. Two are of prime importance to psychiatric patients: mental health and substance use disorder services, including behavioral health treatment, and prescription drugs.

Almost all 50 states and the District of Columbia have chosen “benchmark plans,” which set minimum levels of benefits for QHPs in each of the 10 EHB categories. The EHB rule is very general with regard to the mental health category and does not address how the MHPAEA affects those minimums.

Clements explains that most states have chosen the largest small-group plan in their state as their benchmark. These typically have less generous mental health benefits than private employer plans. California, for example, has chosen the Kaiser Small Group HMO 30 plan as its benchmark. “Many stakeholders in California have grave concerns over Kaiser’s minimal mental health services,” reports Jane Adcock, Executive Officer, California Mental Health Planning Council. “Recently, Kaiser was found to be out of compliance with access and availability rules and is in a corrective action plan mode.”

States do have the option of supplementing mental health or any other category of benefits within the benchmark plans. But they will not get federal financial assistance to do so, which decreases the likelihood that supplementation will occur, according to Clements. “NASMHPD is learning that states’ approaches to supplementing benefits or substitution are diverse,” explains, Joel E. Miller, Senior Director of Policy and Healthcare Reform, National Association of State Mental Health Program Directors (NASMHPD). “NASMHPD is concerned that this flexibility could affect mental health consumers’ ability to make apples-to-apples comparisons among plans and allow plans to use benefit design to cherry-pick healthier enrollees.”

Minimum mental health coverage in the mental health category theoretically should be affected once the HHS publishes a long-delayed final rule on the MHPAEA. That law-also known as the Wellstone-Domenici Mental Health Parity Act-says that all insurance plans must equalize access for patients with mental health issues with access for medical/surgical patients, and provide equal payment for all physicians billing the same codes (eg, evaluation and management codes).

In a letter to the HHS on March 13, 2013, the American Psychiatric Association voiced concern that states would judge network adequacy for psychiatrists included in QHP networks on the basis of the number of psychiatrists in a network, as opposed to the number of days it takes for a patient to get an appointment with a psychiatrist.

Patient access to medications is also an issue. The HHS declined to order formularies in QHPs to adhere to the Medicare Part D requirement that all drugs in 6 “protected” categories be available. Those 6 include antidepressants and antipsychotics. QHPs will have to offer at least 

• One drug in every United States Pharmacopeia category and class

• The same number of prescription drugs in each category and class as the state EHB benchmark plan

Patients who want an off-formulary drug will be able to file an appeal for it.

“It’s nice to say that people who need a drug that’s not on the formulary can appeal for it, but typically appeals are a lengthy and burdensome process, and this will be a difficult process for many mentally ill patients who seek a medically necessary but not covered drug,” responds Clements. “The drug benefit is still very limiting. Most very sick mental health patients need drugs from at least 3 different classes within the drug formulary.”

Come next year, psychiatrists will start seeing patients who have purchased new individual and small-group health plans on the state exchanges mandated by the Affordable Care Act.

Update on Mental Health Benefits and Substance Use Disorder Services Under the Affordable Care Act

CME credit for this article is now expired. It appears here for your reference.

The electroencephalogram (EEG) has a limited but definitive role in understanding and managing psychiatric conditions. When the presentation is unusual, a neurological workup that includes an EEG is essential. In conditions in which EEG abnormalities are demonstrably common, an EEG should be considered part of the essential workup. A simplified EEG can have substantial diagnostic usefulness, particularly in emergency department settings. The abbreviated EEG can be done in a matter of minutes using a 10- or 12-channel recording instrument.

The EEG is an extremely sensitive voltmeter. Typical signals range from approximately 30 to 80 Î¼V, but can be as low as 10 Î¼V in some tracings or as high as 150 or 200 Î¼V in some high-voltage “spike” epileptic discharges. Electrical potentials measured between any 2 EEG electrodes fluctuate or oscillate rapidly, usually many times per second. These EEG signals are the result of summated field potentials generated by excitatory and inhibitory postsynaptic potentials in vertically oriented pyramidal cells of the cortex.

The simultaneous recording of brain waves from many scalp locations is important because it:

• Allows direct comparisons between homologous cortical regions

• Permits recording arrays to locate focal or regional abnormal features more clearly

• Increases the ability to detect various artifacts (ie, waveforms of non-brain origin) that can contaminate the recording

The EEG of an awake and relaxed healthy adult is usually dominated by frequencies between 8 and 13 cycles/second (8 to 13 Hz alpha activity). Once the person focuses his or her attention or becomes stressed, the frequency increases to the beta range (above 13 Hz). When an adult begins to get drowsy, EEG rhythms slow to the theta (4 to 8 Hz) range and finally to the delta (below 4 Hz) range with sleep. The appearance of excessive theta or any delta during wakefulness is a definite abnormality. While excessive beta during wakefulness has been linked with anxiety disorders, it is not considered an EEG abnormality (by today’s standards) and cannot be used to diagnose anxiety states.

The prevalence of EEG abnormalities in psychiatric patients is significantly elevated and ranges from 20% to 68% higher than in healthy controls.

 EEG findings in psychiatric populations include generalized or focal slowing of cortical activity and a variety of focal or generalized paroxysmal EEG discharges. Part of the reason that these patients have such a wide range of EEG abnormalities may be because the EEG signal is quite sensitive to many variables (eg, metabolic, vascular, endocrinological) that affect CNS function.

Although EEG abnormalities may not have direct primary psychiatric diagnostic specificity, they suggest the presence of other, organic/medical/physiological variables that could contribute to the psychiatric presentation. Moreover, EEG discharges without overt seizures (ie, isolated epileptic discharges) may have behavioral consequences such as emotional lability, irritability, or temper dyscontrol that cut across broad diagnostic labels.


Indications for clinical EEGs in patients with psychiatric disorders

The EEG may reveal 1 of 2 classes of deviations: the slowing of normal rhythms and the appearance of abnormal paroxysmal (episodic) electrical activity suggestive of an epileptic process. Both kinds of abnormalities can be focal and suggestive of a localized pathological process, or generalized and more diffused, suggestive of a degenerative or metabolic process. If slowing is suspected, the patient must be awake while the EEG is recorded; if paroxysmal activity is suspected, the EEG needs to be done during both sleep and wake periods. The 

summarizes indications for which EEGs might prove useful for patients with psychiatric disorders.

There are few psychiatric conditions in which the prevalence of epileptic activity has been documented to be elevated, and which warrant consideration of an EEG on the basis of presenting symptoms. In general psychiatric practice, the leading indication for initiating some form of organic or neurological workup is an atypical presentation (


Summary of the types of abnormalities an EEG can detect

A major question is whether resistance to standard treatment interventions is an indication to obtain an EEG. For example, a number of case reports describe patients who received a diagnosis of borderline personality disorder (BPD) and who were subsequently found to have isolated epileptic discharges over one or both temporal regions.

 showed that patients with BPD have a significantly higher rate of both definitive and less definitive EEG abnormalities than persons with dysthymic disorder. Abnormalities (mainly cortical slowing) were most frequently bilateral and of frontal, temporal, or frontotemporal distribution.

BPD patients were found to exhibit a much higher prevalence of symptoms commonly seen in complex partial seizures or episodic dyscontrol than patients with unipolar depression.

 Similarly, in patients with BPD, there was a much higher prevalence of paroxysmal EEG activity, particularly in posterior sharp waves (suggestive of an epileptic-like profile).

 found that 6.3% of adolescents with BPD and 2.6% of patients with dysthymic disorder had bilateral spike and wave discharges. None of the subjects in a comparison group of other personality disorders had similar discharges. Thus, an EEG may enable identification of a brain abnormality that is responsible for treatment resistance.

 Epilepsy is common in children with autistic spectrum disorders (ASD). A significant proportion of children with ASD have abnormal EEGs, even those who have never had a seizure. EEG abnormalities can range from mild slow wave abnormalities to frank epileptiform discharges (epileptiform discharges may only be detected during sleep and at times may require prolonged monitoring).

 examined the EEGs (including sleep) of children with ASD. Epileptiform discharges were seen in 59% of epileptic children but in only 8% of non-epileptic children. The authors concluded that EEGs are not indicated in the absence of seizures. When historical clinical deterioration is evident, the rate of epileptiform EEG abnormalities is significantly higher (14%) than in children without obvious deterioration (6%). The average child who participated in this study was first evaluated neurologically 4 years after the onset of deterioration. This point highlights the need for studies conducted at a much earlier stage of the illness.

Whether treatments to eliminate EEG spikes have a therapeutic effect on the behavioral abnormalities in children with pervasive developmental disorders and autism remains an open and important question.

 Nevertheless, it may be most crucial to attempt treatment at the earliest indication of the illness rather than after many years of damaging spikes before the onset of the first seizure.

 described 5 patients with brief simple partial seizures that mimicked panic attacks. They concluded that the most common psychiatric disorder that must be differentiated from temporal lobe epilepsy is panic disorder. In their sample, seizures were briefer and more stereotyped than panic attacks. In addition, aphasia and dysmnesia accompanied seizure activity in some patients. This differentiation could be diagnostically challenging because patients with documented complex partial seizures of temporal lobe origin may have concomitant nonictal episodic emotional symptoms, including phobia, true panic attacks, and anxiety.

 compared the symptoms of panic disorder–agoraphobia with symptoms of complex partial seizures. Because of the similarities, they concluded that the two may have a common neurophysiological substrate. Whether the source and frequency of the isolated epileptic discharges may influence the responses to antiepileptic drugs and make treatment response difficult to predict also remain open and important questions.

 The prevalence of abnormal EEGs ranges widely, from 6.6% in patients with rage attacks and episodic violent behavior to 53% in patients with antisocial personality disorder.

 showed that anticonvulsants can block EEG epileptiform discharges and can lead to dramatic clinical improvement in individuals who exhibit aggressive behavior. Similarly, Neppe

 provided evidence on the clinical usefulness of adding carbamazepine to the treatment of violent schizophrenia patients with repeated aggressive episodes who also exhibit temporal lobe abnormalities on the EEG but who have no history of a seizure disorder.

In an earlier study, a reduction of aggressive episodes was seen when carbamazepine was added to the neuroleptic regimen of women with schizophrenia who also had EEG abnormalities.

 Other studies suggest that anticonvulsant therapy may have a beneficial effect on aggressive tendencies irrespective of the presence or absence of EEG abnormalities.

Until large, multicenter, double-blind efficacy studies are done, patients should be given the benefit of the doubt, and an anticonvulsant should be used when an EEG demonstrates isolated epileptic discharges.

 The majority of patients with ADHD respond favorably to psychostimulants. Therefore, an EEG may be useful only when there is no response to treatment. A number of studies found variable rates of EEG abnormalities in children with ADHD. Phillips and colleagues

 reported on EEG screening in children hospitalized over an 18-month period for behavioral problems; 9% had abnormalities with background electrocortical slowing or paroxysmal discharges. The authors concluded that EEG screening may be of limited value in children with behavioral problems who had no clinical evidence of a neurological disorder.

 reported significantly higher rates of abnormalities. In a sample of children with ADHD, 31% had abnormal routine EEGs. Of the children with abnormal EEGs, 84% had spikes or spike-wave discharges; the others had excessive background cortical slowing.

 reported an incidence of 7% of definite abnormalities suggestive of seizure disorder and an additional 19% moderately abnormal dysrhythmias not diagnostic of seizure disorder in children with ADHD. On the basis of their findings, they suggested these 6 indications for an ECG in a child presenting with ADHD:

• Personal or family history of seizures

• Inattentive episodes characterized by excessive daydreaming and/or periodic confused states

• Comorbid episodic, unprovoked temper or rage attacks

• A history of head trauma, encephalitis, or meningitis preceding the onset of ADHD

• Abnormalities on neurological examination

 Patients with rapid cycling bipolar disorder may exhibit isolated epileptic discharges on an EEG. Levy and associates

 compared the EEGs of patients with rapid cycling with those of non-rapid cycling patients. The EEGs of 3 of the 5 rapid cycling patients had isolated epileptic discharges, compared with none of the controls.

 The characteristics of what has been termed “subictal mood disorders” include brief euphorias, mixed bipolar episodes, brief severe depressive dips with impulsive suicide attempts, compulsive symptoms, irritability and hostile outbursts, and marked premenstrual worsening.

 Patients with subictal mood disorders may also have paradoxical reactions to mood-active drugs (lithium and antidepressants), with a better response to anticonvulsants.

Note that the EEG does not contribute to the diagnosis of schizophrenia or bipolar disorders except that it helps the clinician rule out a neurological cause for the symptoms when a patient presents with an atypical picture (eg, unusual age of onset).

Cortical slowing in psychiatric conditions

 Because patients with advanced dementia rarely have a normal EEG, a normal EEG can play an important role in diagnosing cases of pseudodementia (dementia secondary to depression or psychosis). When dementia and depression coexist, it becomes important to have some idea about the relative contribution of each disorder to the overall clinical presentation. Brenner and associates

 compared the EEGs of patients with depression, dementia, pseudodementia, and dementia plus depression with the EEGs of age-matched healthy controls. Their findings indicate that the more abnormal the EEG is, the less likely it is that a patient will respond favorably to an antidepressant. This is particularly important because aging increases the likelihood of experiencing adverse effects from antidepressants.

A 56-year-old woman with Alzheimer disease who has been in a nursing home for 4 years stopped eating and was admitted to the neuropsychiatry ward of a psychiatric hospital. In reviewing her history, a complete workup for possible reversible causes of dementia had never been done. A comprehensive evaluation was started that included blood work, a CT scan, and an EEG. There was nothing significantly abnormal on any test; the EEG was normal.

A normal EEG was incompatible with advanced stage Alzheimer disease. A trial of antidepressant therapy was therefore initiated. Nothing happened for 2 weeks. During the third week, the patient started speaking. Her speech was completely disorganized with severe psychotic content. Haloperidol was added, and the patient was ambulatory and able to leave the hospital within 2 weeks.

 Patients with a history of head injury or an early brain insult during infancy or childhood may have developed behavior that helps them compensate for the deficit resulting from the injury. Such behavior could be deemed aberrant. An EEG may detect focal slowing (most commonly frontal or temporal), which indicates a disordered brain region. Knowledge of the focal deficit followed by detailed neuropsychological evaluation could shed much light on the particular case and help guide treatment and rehabilitation efforts.

 The differential diagnosis of acutely disorganized and disoriented patients often includes delirium. In acutely agitated delirious patients, the EEG often helps determine the cause of altered consciousness: a diffuse encephalopathic process, a focal brain lesion, or continuous epileptic activity without motor manifestations (ambulatory nonconvulsive status epilepticus). Most often, patients with delirium have a toxic-metabolic encephalopathy.

In general, as encephalopathy progresses, there is diffuse slowing of the background rhythms, including alpha (8 to 13 Hz) to theta (4 to 7.5 Hz) activity. Delta (less than 3.5 Hz) activity usually does not become prominent until the patient approaches nonresponsiveness. The major exception to the above rule is seen during withdrawal from alcohol and during delirium tremens (DTs). Excessive fast activity (rather than slowing) dominates the EEG (beta activity: 13 to 30 Hz) in patients with alcohol withdrawal delirium.

A 44-year-old man with a long history of alcohol dependence presented to the emergency department with a blood alcohol level of 0.42%. He was admitted for detoxification. As his alcohol level started coming down, he became progressively more confused. The benzodiazepine dosage was increased. He progressively became agitated and was placed in 4-point restraints. A neurology consultation was called. The consultant diagnosed DTs and suggested increasing the benzodiazepine dose. Symptoms continued to escalate despite increasing doses of the benzodiazepine. Later that day, the patient had a medical consultation. It was suggested that the patient was in iatrogenic delirium and that all medications should be stopped. An abbreviated (8 leads) EEG was obtained and revealed a moderate degree of diffuse slowing, consistent with encephalopathy and not the fast low-voltage picture expected with DTs. Medications were rapidly tapered and the patient recovered.

Electroencephalography is burdened by several constraints that place limitations on the information provided. These constraints have been extensively discussed elsewhere

• The scalp: recorded activity reflects mainly cortical activity with minimal to no reflection of subcortical or deeper neural processes

• Skin, skull, dura, and brain tissue impose varying degrees of impedance between the source of the electrical discharge and the scalp electrodes

• Time sampling (many important EEG abnormalities are paroxysmal, or “episodic,” and may require prolonged recording time)

• Non-specificity of results (the brain’s electrical activity can only respond to stimuli or insult by becoming faster or slower in frequency or higher or lower in voltage, or a combination of these two responses)

A number of problems make detection of isolated epileptic discharges in nonepileptic psychiatric patients difficult and likely an expensive process. Standard neurological training in EEG interpretation strongly emphasizes under-interpretation to avoid stigmatizing the patient with the diagnosis of seizure disorder. In psychiatric EEGs, abnormalities, when present, tend to be infrequent in the record and require full vigilance on the part of the interpreter. The chance of a false negative can be lessened by repeating the EEG or by doing the EEG testing for extended periods (eg, 1 to 3 days), which increases the chances of recording the EEG signal when the patient is actually in a panic attack or a rage episode.

Additional problems may arise because the patient does not understand the special needs associated with obtaining an accurate recording-eg, staying still, activating procedures such as hyperventilating or staying up all night before the procedure (sleep deprivation improves the detection of isolated epileptic discharges), or relaxing and falling asleep during the test. Furthermore, a patient may behave inappropriately during the test. These factors necessitate that the laboratory be placed in a psychiatrically oriented space with psychiatrically trained technicians who can help the patient (particularly children) relax and cooperate.

The contents presented herein are largely derived from the textbook Standard Electroencephalography in Clinical Psychiatry: A Practical Handbook.

Note: This article was originally published as a CME in the May 2013 issue of 

 Portions of it may have since been updated.

Nash Boutros, MD, has no disclosures to report.

Natalia Jaworska, PhD, MSc (peer/content reviewer), has no disclosures to report.

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The electroencephalogram (EEG) has a limited but definitive role in understanding and managing psychiatric conditions. When the presentation is unusual, a neurological workup that includes an EEG is essential.

Psychiatric Times Vol 30 No 5

Benefits of CAM Therapies for Dementia

Benzodiazepines and Pain

The Moral Struggles of Practicing Psychiatrists

DSM-5 Won’t Solve the Overdiagnosis Problem-But Clinicians Can

Update on Mental Health Benefits and Substance Use Disorder Services Under the Affordable Care Act

The Electroencephalogram in the Management of Psychiatric Conditions

An Update on ADHD

Trauma Associated With Living in Violent Neighborhoods

Sweet Tea and Mental Health Transformation

Prayer