e know that headaches arecommon in the general popu-lation, but they are particularly

common among patients with psychiatricproblems. According to one review,(Pompili M et al., J Headache Pain 2009;10(4):283-290) patients with depressionhave a 46% lifetime prevalence ofmigraine, while bipolar patients have a51% prevalence. Patients with migraineshave triple the risk of developing depres-sion than patients without migraines.

In this article, we’ll review how tohandle patients with headaches in a psy-chiatric practice. How do we distinguishmigraine headaches from tensionheadaches from more dangerous second-ary headaches that may be caused by atumor or by hypertension? When shouldwe refer headache patients to a neurolo-gist? How should we treat these patients,both pharmacologically and psychothera-peutically?

DiagnosisTextbooks will tell you that head-

aches come in essentially two varieties:primary (migraine, tension-type, andcluster) and secondary (caused by anunderlying intracranial problem).

While tension-type headaches (46%prevalence) are more common thanmigraines (25% prevalence), migrainesare more likely to drive patients to seekmedical attention, because they are usu-ally more severe and debilitating.Migraine headaches are different fromtension-type headaches in several ways.They are often unilateral rather than

bilateral; they usually cause a throbbing,rather than a static pain; one third areassociated with a prodromal aura; theyoften are accompanied by nausea andvomiting (so-called “sick headaches”);and patients often complain of photo-phobia, meaning that bright light makesthe headache worse.

In one study a simple three questionscreen was remarkably predictive ofmigraine. These three questions are:

1. Are you nauseated or sick to yourstomach when you have a headache?

2. Have the headaches limited youractivities for a day or more in the lastthree months?

3. Does light bother you when youhave a headache?

When two of these questions areanswered “yes,” the positive predictivevalue for migraine was 93%; when allthree were answered positively, the pre-dictive value was 98% (Lipton RB et al.,Neurology 2003;61:375-382).

There’s a tendency among non-specialists to view tension-typeheadaches as being a waste-basket cate-gory for anything that is not a migraine,but in reality these headaches have fairlyspecific diagnostic criteria. According tothe International Headache Society, ten-sion-type headaches must meet at leasttwo of the following criteria: 1. Pressingor tightening (nonpulsating) quality; 2.Mild to moderate intensity (meaning notso severe as to prohibit any normal activi-ties); 3. Bilateral location; and 4. Noaggravation from walking on stairs orsimilar activities. Furthermore, tension-

IN THIS ISSUE

• Treating Headaches inPsychiatry• Evaluating and Treating Tremor• Research Updates• Expert Q & A:Bruce Price, MDThinking like a Neurologist

Focus of the Month:Topics in

Neuropsychiatry

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Treating Headaches in Psychiatry

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VOLUME 7, NUMBER 9 WWWWWW..TTHHEECCAARRLLAATTRREEPPOORRTT..CCOOMM SEPTEMBER 2009

The Carlat Psychiatry ReportThe Carlat Psychiatry ReportAN UNBIASED MONTHLY COVERING ALL THINGS PSYCHIATRIC

EDITORIAL INFORMATIONPublisher and Editor-in-Chief: Daniel J. Carlat, MD, is associate clinicalprofessor of psychiatry at Tufts UniversitySchool of Medicine and maintains a pri-vate practice in Newburyport, MAAssociate Editor:Marcia L. Zuckerman, MD,is the psychiatrist for a PACT team (commu-nity outreach program) in Lawrence, MAEditorial Board: Ronald C. Albucher, MD, director of counseling and psychological services, clinical assistant professor of psychiatry,Stanford University, Palo Alto, CARichard Gardiner, MD, psychiatrist in private practice in Ukiah, CAIvan Goldberg, MD, creator, DepressionCentral Web Site, psychopharmacologist inprivate practice, New York City, NYAlan D. Lyman, MD, child and adolescentpsychiatrist in private practice, New YorkCity, NYRobert L. Mick, MD, medical director,DePaul Addiction Services, Rochester, NYMichael Posternak, MD, psychiatrist inprivate practice, Boston, MAGlen Spielmans, PhD, assistant professorof psychology, Metropolitan StateUniversity, St. Paul, MNDr. Carlat, with editorial assistance by Dr.Zuckerman, is the author (unless otherauthorship is specified) of all articles andinterviews for The Carlat PsychiatryReport. All editorial content is peerreviewed by the editorial board. Dr.Albucher, Dr. Carlat, Dr. Gardiner, Dr.Goldberg, Dr. Lyman, Dr. Mick, Dr.Posternak, Dr. Spielmans and Dr.Zuckerman have disclosed that they haveno relevant financial or other interests inany commercial companies pertaining tothis educational activity.

Learning objectives for this issue: 1. Describe common causes and treatments of headache. 2.Describe how different causes of tremor are diagnosed and treated. 3. Describe elements of theneuropsychiatric assessment. 4. Understand the most current findings in the literature regardingpsychiatric treatment. This CME/CE activity is intended for psychiatrists, psychiatric nurses, psy-chologists and other health care professionals with an interest in the diagnosis and treatmentof psychiatric disorders.

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type headaches must mean both of thefollowing: 1. No nausea or vomiting; and2. Only one of the following can be pres-ent: photophobia or phonophobia.Tension-type headaches typically lastfrom 30 minutes to seven days. Patientswill describe a “band of pain” extendingfrom the forehead around both templesto the back of the head.

Cluster headaches are rare and aredescribed as an excruciating “boring”pain, often over one eye, lasting from 15minutes to several hours. They mayoccur several times per day or night. Ihave a patient, a man in his early 30swith depression and OCD, who gets clus-ter headaches about once a year, and heis rendered completely out of commis-sion for several weeks. The condition hasplayed havoc with his ongoing efforts tocomplete a technical degree, and tomove out of his parent’s house problemsthat, in turn, have complicated his psy-chiatric treatment.

When should we refer to a neurolo-gist? The short answer: almost always.Anybody who has severe or chronicheadaches might have a secondary cause,and neurologists are experts at rulingthis out. The workup will include adetailed neurologic exam, with anemphasis on the fundoscopic exam, andmay or may not include a brain MRI,depending on the results of the examand the neurologist’s judgment or phi-losophy.

Medication TreatmentTension-type headaches. Once a

secondary cause of a headache has beenruled out by a neurologist, psychiatristsare generally qualified to treat headachedisorders, largely because of the greatoverlap between psychiatric drugs andheadache drugs.

For an episode of tension-typeheadaches, aspirin (500-1000 mg) andibuprofen (400 mg) work well, and bet-ter than acetaminophen (1000 mg) (seeLoder E and Rizzoli P, Brit Med J 2008;336:88-92 for a good review of tension-type headache management). Whenthese over-the-counter meds don’t work,you can move on to bigger guns such as

Fioricet, which is a combination of aceta-minophen (325 mg), butalbital (50 mg),and caffeine (40 mg). Why is this triad ofdrugs so effective? Well, acetaminophenis a standard analgesic, butalbital is a bar-biturate that relaxes the scalp’s musclecontractions, and caffeine relaxes bloodvessels, improving blood flow to scalpmuscles. Fioricet works for both tensionand migraine headaches, but it is addic-tive and can cause intermittent head-aches to convert to chronic headaches.

Generally, when headaches becomechronic, neurologists try to switch from“abortive” drugs (those that stop theheadache in its tracks) to prophylacticdrugs. The best prophylactic drug forchronic tension headaches is amitripty-line, usually dosed from 10 mg up to 75mg one or two hours before bedtime;nortriptyline may be as effective, withfewer side effects. While the newer anti-depressants such as the SSRIs and SNRIsare somewhat effective as well, they arenot as effective as amitriptyline.

Migraine headaches. Migrainescome in many varieties, ranging frommild and rare to severe and frequent. Ihave had two migraines in my life. Eachwas triggered by looking briefly at thesun, and each began with a strange visualaura like hundreds of translucent over-lapping gears spinning frenetically. Theaura lasted about 15 minutes, followedby the onset of a pulsing left-sidedheadache. On each occasion, I took 600mg of ibuprofen, and felt the need to liedown in a dark room. Within two hoursor so, I recovered.

I describe this case to illustrate thespectrum of migraines and their treat-ment. Anybody who presents themselvesto a specialist will have had migraines farmore severe and more frequent. Whileover-the-counter analgesics are effectivefor milder cases, often you need to rampup treatment to drugs such as Fioricet,codeine, and various narcotics, all ofwhich are considered acceptable treat-ments for the occasional migraine. Butfor more severe and frequent migraines,the preferred abortive treatments aretriptans (such as sumitriptan and rizatrip-tan) which have replaced the ergots as

the treatment of choice. There are nowseven different triptans to choose fromand each company will brandish studiesto convince you theirs is best. Because ofthis complexity, neurologists are usuallythe better specialists to initiate treatmentwith a triptan.

More important is for psychiatrists toknow something about the controversysurrounding the safety of combining trip-tans with SSRIs. In 2006, the FDA issuedan alert that combining triptans witheither SSRIs or SNRIs can cause sero-tonin syndrome. The agency said this wasbased on 27 cases gathered over fiveyears. The announcement was met wide-ly with skepticism, because millions ofpatients had been combining triptanswith SSRIs over the years and serotoninsyndrome had rarely, if ever, beenreported in the literature. Despiterequests, the FDA has not made details ofthese 27 cases of supposed serotoninsyndrome public, and a recent reviewconcluded that “withholding these med-ications due to fears of serotonin syn-drome is difficult to justify” (Wenzel R etal., Ann Pharmacother 2008;42(11):1692 -1696).

Most of the drugs effective as pro-phylactics against migraines (as opposedto abortive drugs) are well-known to psy-chiatrists, including amitriptyline, nor-triptyline, Depakote (divalproex sodium),Neurontin (gabapentin), and Topamax(topiramate). Effective non-psychiatricprophylactic agents include the betablockers propranolol and atenolol, andthe ACE inhibitor verapamil. This is agood list to keep in mind for those “two-fer” opportunities, such as when you arechoosing something for a depressedpatient with migraines (go with the tri-cyclics) or for a migraine patient withbipolar disorder (the obvious choicewould be Depakote).

Non-pharmacological ApproachesWhile few psychiatrists will be invest-

ing in a biofeedback machine, this treat-ment may be the most effective non-pharmacological approach for headaches,especially tension-type headaches. Onerecent meta-analysis found that biofeed-

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back was more effective than headachemonitoring, placebo, and relaxation ther-apies (Nestoriuc Y et al., J Consult ClinPsychol 2008;76:(3):379–396.)

Headache clinics often have psychol-ogists and psychiatrists on staff and theyhave developed techniques that you canincorporate into your practice forpatients with comorbid depression oranxiety and migraine headaches. Called“behavioral medicine,” these are typicallyversions of cognitive behavioral therapy.

The usual strategy is to determine howmuch the patient is allowing headache tolimit activities, and to encourage them to“get back out there”, on the theory thatthey are inadvertently reinforcing theirdepressed mood through passivity. Helpthe patient make a list of enjoyable activi-ties and come up with a graded schedulefor re-engaging in life. Such techniqueshave been shown helpful in decreasingheadache severity in some studies(Smitherman TA et al., Headache

2007;48(1):45-50). Other techniques that have some

empirical support for relief of chronicheadaches include standard progressivemuscle relaxation exercises andacupuncture.

hile tremor is traditionallythought of as a neurologicalissue, the symptom pops up

often in psychiatric practice, and somebasic knowledge of its diagnosis andtreatment comes in handy.

Case vignette: A 67-year-old womanwhom I’ll call “Paula” came to see me fordepression and anxiety. She ascribed herdepression to her belief that neighborswere coming into her apartment andstealing things—which her daughterassured me was implausible. Her memo-ry and cognitive processing were normalotherwise, and her PCP had alreadyobtained an array of labs and a head CTto rule out a contributing medical illness.I provisionally diagnosed her withdepression with psychotic features, and Itreated her with a combination of Celexa(citalopram) and low dose Risperdal(risperidone), with Ativan (lorazepam)on an as needed basis. On Paula’s nextvisit, she held out her hands in front ofme and said, “Doctor, I’ve gotten evenshakier.” I did notice a fine tremor, butfurther questioning revealed that herdepression and paranoia had improvedmarkedly. Nonetheless, she interpretedher “shakiness” to mean that she wasworse.

So what was causing Paula’s tremor?Anxiety? Celexa? Risperdal? A neurologi-cal condition such as Parkinson’s disease?Or was this “essential tremor”?

By far, the most common cause oftremor is essential tremor, also called

“benign familial tremor.” (See Smaga S,Am Fam Physician 2003;68:1545-1552,for a helpful review of the differentialdiagnosis of tremor). It generally beginsin the 50s, is familial in up to 60% ofcases, and usually presents as a symmet-rical fast, fine tremor of the wrist mostvisible when the patient stretches thearms in front of you. It is gradually pro-gressive, and sometimes affects the head,causing either yes-yes or no-no headmovements. Essential tremor is typicallya constant tremor, but may wax andwane, and famously improves transientlywith alcohol ingestion.

Upon careful questioning, it turnedout that Paula’s father had a tremor formuch of his life, and in fact Paula saidshe had a tremor for many years. Studieshave shown that essential tremor oftengoes unrecognized because it can be verymild—in fact, about 50% of people withessential tremor are unaware of it (EibleRJ, Mov Disord 1998;13:457-464).

Drug-induced tremor is also com-mon and often looks just like essentialtremor. Psychiatric drugs that can causetremor include the SSRIs, the tricyclicantidepressants, lithium, and Depakote(divalproex sodium). (For a recentreview of tremor in psychiatric practice,see Arbaizar B et al., Psych Clin Neurosc2008;62:638-645.) Antipsychotics, espe-cially the first generation antipsychotics,also can cause tremor, but this tremor isdistinct from other tremors in that itmimics the tremor of Parkinson’s dis-

ease: it is worse at rest, and it is a slow-er, “coarse” tremor. Tremors are oftentechnically described in terms of “fre-quency” (the speed of the tremor) and“amplitude” (the breadth of the tremor).Thus, essential tremor and most drug-induced tremors are of high frequencyand low amplitude, while a Parkinsoniantremor is of lower frequency and higheramplitude.

Differentiating essential tremor fromdrug-induced tremor is not easy. Did itclearly begin after the patient started tak-ing the drug? Did it go away when thepatient had a gap in compliance? Is thetremor more prominent an hour or soafter ingesting the drug (often seen inlithium-induced tremor)? “Yes” answerssupport a drug-induced tremor.

While my patient Paula did, indeed,have a history of essential tremor, it wasalso clear that her tremor had worsenedsince she began Celexa and Risperdal. Inaddition to her fine postural tremor(consistent with essential tremor), I not-iced that she had a coarse resting tremorof her wrists, typical of a neuroleptic-induced tremor.

My solution was to discontinue theRisperdal, with the intention of replacingit with Seroquel if her paranoia returned.Her tremor improved back to her base-line, and luckily the combination of theCelexa and lorazepam kept her psychi-atric symptoms at bay.

Another kind of tremor-relatedsymptom deserves special mention: anti-

Evaluating and Treating Tremor

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depressant-induced jitteriness. In 1990,an influential case series of six patientswho developed intense suicidal ideationafter treatment with Prozac (fluoxetine)brought this issue to our attention(Teicher MH, et al., Am J Psychiatry1990;147:207-210). Since then, case stud-ies have been published associating SSRIsand other antidepressants with what hasvariously been termed: jitteriness, akath-isia, shakiness, activation, and agitation.

Recently, a group of psychiatristsconducted a systematic review of all 107articles they could locate describing anti-depressant-induced jitteriness/anxiety(Sinclair LI et al., Br J Psychiatry 2009;194:483-490). Since there is no agreed-upon definition of AD-induced jitteri-ness, the published incidence rates areall over the map, ranging from 4% to65%. The two antidepressants most likelyto cause jitteriness were Prozac andimipramine (perhaps merely becausethey were the most studied in relation tojitteriness), although it has beendescribed for other tricyclics and otherSSRIs including Zoloft and Paxil. The syn-drome is particularly likely in patientswith panic disorder, and somewhat lessso in depression. It generally beginswithin the first two weeks of treatment.Trying to distinguish jitteriness fromakathisia has proven very difficult, andthese reviewers concluded that they may

be one and the same entities. Regardingthe risk of suicide, an FDA-commissionedanalysis of antidepressant clinical trials inchildren and adolescents found an ele-vated risk of suicidal behaviors amongyouth who experienced symptoms of“activation” (Hammed T www.fda.gov/ohrms/dockets /ac/04/slides/2004-4065S1_08_FDA-Hammad.ppt). InPfizer’s clinical trials of sertraline fordepression in children, aggression, agita-tion, and akathisia led to study discontin-uation in eight of 189 patients takingsertraline compared to 0 of 184 patientstaking placebo, a statistically significantdifference (Wagner KD et al., JAMA 2003;290:1033-1041).

Management of TremorThe management of tremor and jit-

teriness depends on the cause. When it isclearly caused by a drug, discontinuingthe offending agent is the best solution,but often a drug works so well that thepatient prefers to stay on it. Antidotes totremor include the following (for refer-ences, see the review article Arbaizar B etal., Psych Clin Neurosc 2008;62:638-645).

Beta-blockers. Propranolol(Inderal) is usually used, starting at 10mg BID or TID; some patients require upto 40 mg TID. You can also try theextended release version, Inderal LA,which has the advantage of once-a-day

dosing; the beginning dose is 60 mg QD.Warn patients about the common beta-blocker side effects of fatigue and postur-al light-headedness.

Benzodiazepines. Both alprazolamand clonazepam have been shown to behelpful for tremor, and are also helpful(as are all the other benzos) for AD-induced jitteriness.

Primidone (Mysoline). Primidoneis an anti-seizure drug that it also effec-tive for essential tremor. Its mechanismof action is unknown. Start at 12.5-25 mgQHS, and increase gradually as needed.Effective doses range from 50-250 mgQD, usually given at bedtime because ofthe side effect of sedation.

Topiramate (Topamax). Topiramatehas been shown to be more effectivethan placebo for essential tremor. Thestarting dose is 25 mg/day, which mayneed to be increased up to 200-400mg/day.

Gabapentin (Neurontin).Somewhatless effective than the options alreadydescribed, gabapentin sometimes easesboth tremor and anxiety, but the effectivedose varies widely, with a suggestedmaintenance dose of 1200-3600 mg/day.

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Section editor, Glen Spielmans, PhDGlen Speilmans, PhD has disclosed that he has no relevant financial or other interests in any commercial companies pertaining to thisarticle.

Role of Depression “Risk Gene”Questioned

It has long been thought that one’sgenetic makeup combines with stressorsto cause depression, but for many yearsthere was little data to support thishypothesis. This changed in a 2003 paperby Caspi and colleagues, which strongly

supported the idea that variation in theserotonin transporter gene, when com-bined with stressors, drastically influ-ences the rate of depression (Caspi A etal., Science 2003;301:386-389). By itself,this variation did not predispose partici-pants to depression. But people with oneshort allele of “serotonin transporterlinked polymorphic region” (5-HTTLPR)were more likely to become depressed in

the face of stressful life events, and peo-ple with two short alleles were evenmore so. These results supported thepopular serotonin theory of depression,since short alleles decrease the produc-tion of the serotonin transporter, lead-ing, presumably, to faulty regulation ofserotonin in the synapses. Intrigued bysuch findings, other scientists attemptedto replicate them. A new meta-analysis

DEPRESSION

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examined the results of 14 such studies,and found that the short allele result wasapparently a chance finding. In fact, onlyfour studies supported the link betweenthe short allele and depressive responseto life events, whereas two found oppo-site results (long allele was linked todepressive response to life events), withothers finding no consistent linkbetween 5-HTTLPR and depressiveresponse to stress. When the studieswere combined, there was no linkbetween the 5-HTTLPR genotype andresponding to stressors with depression.(Risch et al., JAMA 2009;301:2462-2471).

TCPR’s Take: Several studies wereexcluded from the meta-analysis becausetheir measurements were not directlycomparable to the original Caspi et al.paper; this could have biased the find-ings somewhat. However, such exclu-sions happen in most meta-analyses andare unlikely to have altered the resultssignificantly. Given the complexity of ourgenetic makeup and the frequent failureto replicate psychiatric genetics findings,it is likely wise to wait for consistentreplication when a “risk gene” is identified.

Restricting Drug Samples MayReduce Costs

Drug samples are a staple of pharma-ceutical marketing. The drug industryargues, quite logically, that samples areuseful to treat patients who lack thefunds to purchase medications. Yet somereformers have called for drug samples to be banned, an idea that hasreceived a decidedly mixed reception. Asmall body of research has investigatedthe topic of drug samples, including arecent study that examined changes inprescriptions when samples of brand-name statins, levothyroxine, and SSRIswere removed from an internal medicineclinic in Iowa. Over the 180-day periodin which samples were removed, generic

prescriptions increased by 23% forstatins, 10% for SSRIs, and 3% forlevothyroxine (Miesner AR et al., ArchIntern Med 2009;169:1241-1242). Inanother study, a university-based internalmedicine clinic moved, leaving its samplecloset inaccessible for nine months.During this time, the rate of generic pre-scribing for uninsured patients increasedfrom 12% to 30%, though there was nochange in generic prescribing forMedicaid patients (Miller DP et al., SouthMed J 2008;101:888-893).

Surprisingly, drug samples are moreoften given to insured Americans than tothe uninsured or poor (Cutrona SL et al.,Am J Public Health 2008;98:284-289). Inthat case, drug samples also tend toincrease costs for patients who receivethem (Alexander GC et al., Med Care;46:394-402); when patients receive asample, they often remain on that moreexpensive drug once the sample expiresrather than switching to a less expensivegeneric drug. Samples probably produceoverall cost savings only if they will begiven indefinitely to patients who haveno coverage for prescriptions and cannotafford to pay out of pocket for genericdrugs.

TCPR’s Take: The combined resultsof these studies suggest that cliniciansshould be wary of drug samples and con-sider carefully whether they are actuallyhelping to reduce costs for patients.

N-Acetylcysteine Effective ForTrichotillomania

Trichotillomania (TTM) is animpulse control disorder in whichpatients feel that they can relieve tensionby pulling out hair from different parts oftheir bodies. While sharing some featureswith obsessive compulsive disorder,DSM-IV-TR does not officially classify it asa type of OCD. The pharmacologicaltreatment of trichotillomania has often

frustrated patients and clinicians alike.Clomipramine has outperformed place-bo, but its benefits appear to diminishsubstantially after discontinuation andSSRIs have failed to beat placebo acrossfour trials (Bloch MH et al., BiolPsychiatry 2007;62:839-846). A recentstudy compared an amino acid (N-acetyl-cysteine, or NAC) to placebo. Why NAC?Because NAC is converted to cysteine,which reduces synaptic release of gluta-mate. Some research has implied thatrepetitive behaviors like TTM my becaused by excessive glutamate, providinga biochemical rationale for a trial of NACfor TTM. Of the 50 enrolled patients,most had at least one comorbid condi-tion, including depression (28%), an anx-iety disorder (28%), or another impulsecontrol disorder such as compulsive skinpicking (36%). About half were takingother psychotropic medications, andmaintained their dose of these drugs dur-ing the study. Participants took 1200mg/day of NAC for six weeks (or match-ing placebo), then increased dosage to2400 mg daily for the remaining sixweeks. Patients on NAC outperformedplacebo patients on all trichotillomaniameasures by a quite large effect size. 44%of NAC patients experienced a 50% orgreater drop in trichotillomania symptomrating scores compared to zero patientson placebo. NAC did not improvedepression or anxiety scores more thanplacebo. Remarkably, no patients on NACreported any side effects (Grant JE et al.,Arch Gen Psychiatry 2009;66:756-763),though NAC may worsen asthma.

TCPR’s Take: NAC can be found atmany health food stores and is cheaperthan most prescription medications. Thevery promising safety and efficacy profiledemonstrated in this study providesmuch needed hope to patients and clini-cians alike, though replication is needed.Also keep in mind that habit reversaltherapy (a form of behavior therapy), has demonstrated efficacy for trichotillomania.

CLINICAL PRACTICE

TRICHOTILLOMANIA

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TCPR: Dr. Price, for most of your career, you’ve worked closely with psychiatrists in treating patients with neuropsychiatric disease. Ithought we might start by discussing how psychiatrists might bring more neurological thinking into their evaluations. When shouldpsychiatrists start thinking neurologically? Which patients should raise the red flag that something “organic” is going on?Dr. Price: When a patient has an atypical history that doesn’t quite fit the usual DSM definitions or that doesn’t fit your clinical experience. Forexample, when there is an unusual age of onset of a psychiatric symptom, like a late onset of mania or major depression, especially when it is outof the blue, with no psychosocial explanation. Also, if there is an unusually acute onset of a sudden change in behavior, or the absence of a familyhistory of a disorder that is usually familial, such as bipolar disorder. TCPR: So, basically, any patient whose history and symptom pattern don’t quite jibe with what we normally see. Dr. Price: Right. I also look at treatment history. If a patient has not responded to multiple psychiatric medications or therapies that are normallyeffective, you should wonder about an underlying neuropsychiatric problem. And then, of course, there are certain symptoms that are red flags.Patients who, in addition to typical psychiatric symptoms, also report things like new or worsening headache, somnolence, incontinence, focalweakness, sudden incoordination or gait difficulties, may have neurological illness. TCPR: Are there any other things that we should be focusing on in the history?Dr. Price: Yes, it is crucial to ask about a history of head injury. Traumatic brain injury can lead to syndromes that can appear “psychiatric,” likeimpulsivity, poor memory, anger, and the like. And when you ask about head injury, try to get the full story of what actually happened. Was therea loss of consciousness, and if so, how long did it last? And after the patient regained consciousness, how many hours or days did it take for himor her to regain normal memory functioning? Answers to these questions will give you a sense of how severe the head injury was, and how likelyit is that current symptoms might be due to the event. On the other hand, getting a detailed history might reveal that the head injury was lesssevere than you originally thought. Sometimes families will exaggerate the extent of the injury because of an understandable desire to find someexplanation for the patient’s psychiatric symptoms. TCPR: What are some of the typical psychiatric symptoms that can be caused by traumatic brain injury (TBI)?Dr. Price: There are many. The most common are cognitive impairment which gradually improves over the course of time, and a disinhibitedpersonality, which might present as being atypically quick to anger, or, conversely, as being unusually or inappropriately jovial. Two syndromesthat many psychiatrists are not aware of as possibly being worsened by TBI are borderline personality disorder and perpetration of domestic vio-lence. TBI can contribute to both of these by causing impulsivity and disinhibition. TCPR: We’ve heard a lot recently about post-concussive syndrome in athletes leading to depression. What is a concussion, exactly?Dr. Price: In the old days we used to think that it had to include loss of consciousness, but we now consider it to be any sudden impact of thehead that even temporarily and briefly alters your mental state. TCPR: Aside from a careful neuropsychiatric history, should psychiatrists be doing more of the actual neurological exam?Dr. Price: In my dream world, yes, psychiatrists would conduct an elementary neurologic exam on intake, especially for patients whose historyhints at a neuropsychiatric problem. TCPR: Before going into exactly what that exam ought to be, how should we introduce this to our patients? After all, a neurologicexam involves touching the patient, which is something that most patients are not expecting from a psychiatrist. Dr. Price: I would say something like, “The brain is so complex and we need to understand different angles to understand it. The neurologicexam offers one angle and we want to be sure we get the correct diagnosis.”TCPR: That sounds reasonable. So what should we include in our neurological exam?Dr. Price: Start by examining the visual field to make sure there is not a field cut. You have them look at your nose and you bring your hand outinto the four quadrants of their visual field and wiggle your fingers, asking if they can see it. Then examine their gait for stability and for a focalweakness on one side or the other. TCPR: My office is pretty small—how do we evaluate gait in a small space? Dr. Price: I have some small offices too, and I watch them walk for five steps towards the door and then come back five steps to the chair. And Iwould ask them to do a tandem gait, the heel-to-toe kind of test that cops use to check sobriety. You should tap the basic reflexes, including thebiceps, the patellar (just below the knees), and the ankle. And I would stroke the bottom of the foot to make sure the toe goes down. Finally, teststrength of the arms and legs, focusing on symmetry of strength.

QAWith

the Expert

This Month’s Expert:Thinking like a NeurologistBruce Price, MDChief, Department of Neurology, Mclean Hospital Assistant Professor of Neurology, Harvard Medical School

Dr. Price has disclosed that he has no relevant relationships or financial interestsin any commercial company pertaining to this educational activity.

&

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PAGE 7September 2009

The Carlat Psychiatry ReportThe Carlat Psychiatry Report

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Please identify your answer by placing a check mark or an X in the box accompanying the appropriate letter. Note: learning objectivesare listed on page 1.

1. The most effective prophylactic drugs for tension-type headaches are: (Learning Objective #1)[ ] a. Tricyclic antidepressants.[ ] b. Serotonin reuptake inhibitors. [ ] c. Divalproex sodium (Depakote).[ ] d. Ibuprofen and aspirin.

2. The most common cause of tremor is: (L.O. #2)[ ] a. Parkinsonian tremor.[ ] b. Essential tremor.[ ] c. Drug-induced tremor.[ ] d. Anxiety-induced tremor.

3. A recent meta-analysis found that the short allele of a serononin transporter gene is correlated with high risk of depression.(L.O. #4)

[ ] a. True [ ] b. False

4. A recent study of N-Acetylcysteine (NAC) in Trichotillomania found: (L.O. #4)[ ] a. NAC is effective only at low doses of 25-50 mg/day.[ ] b. NAC was effective, but no more effective than placebo. [ ] c. NAC worsened skin-picking symptoms.[ ] d. NAC was more effective than placebo at 1200-2400 mg/day.

5. According to Dr. Price, traumatic brain injury can lead to syndromes that can appear “psychiatric,” like impulsivity, poor mem-ory, and anger. (L.O. #3)

[ ] a. True [ ] b. False

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The Carlat Psychiatry ReportThe Carlat Psychiatry ReportClearview Publishing, LLCP.O. Box 626Newburyport, MA 01950

This Month’s Focus:Topics in

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The Carlat Psychiatry Report

TCPR: How long should this exam typically take? Dr. Price: This is a five-minute neurologic exam. If it’s normal, docu-ment that so you have that as a baseline, and any abnormalities wouldprompt a referral to a neurologist. TCPR: I know that lately you have been interested in the comorbid-ity of depression and major neurological diseases. Is there any-thing in particular psychiatrists should know about?Dr. Price: Yes, depression is highly comorbid in some very commonneurological diseases, such as Alzheimer’s disease, traumatic brain injury,multiple sclerosis, Parkinson’s disease, stroke, and epilepsy. Between30%-50% of patients with these diseases will develop depression at somepoint, and there is increasing evidence that the pathogenesis of neuro-logic diseases and depression may have common mechanisms. TCPR: How might this information be particularly relevant in apsychiatric practice?Dr. Price: For example, patients who present with late-onset depression(defined as 65 years old or after) have a 2 to 4 times higher incidence ofAlzheimer’s disease and Parkinson’s disease than people with no depres-sion. Thus, late-onset depression may be an independent risk factor forthe development of Parkinson’s and Alzheimer’s.TCPR: If I have a late-onset depression patient, should I automati-cally refer them to a neurologist saying, “Look Ms. Smith, there isdata that you are 2 to 4 times more likely to develop a neurologiccondition because of what is going on with you; I would like youto see Dr. Price.”Dr. Price: Let’s put it this way. It would certainly heighten my aware-ness as a psychiatrist that there may be an accompanying neurodegenera-tive disease, and it would lower my threshold for neurologic referral.TCPR: Thank you very much Dr. Price.

Continued from Page 6Q & A With the Expert

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