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Retrospective Posttraumatic

Amnesia in Traumatic BrainInjury

To the Editor: Clinicians may needto determine the severity of a trau-matic brain injury (TBI) thatoccurred many years ago. This can

be challenging when there is nodirect information about the remoteTBI. One method of retrospectiveassessment is the duration of post-

traumatic amnesia, the periodduring which a person is disori-ented and unable to lay down newmemories after a head injury.1,2

Few modern investigators havestudied retrospective posttraumaticamnesia.3 Our study investigatesthe value of retrospective assess-ment of posttraumatic amnesia in astratified sample of post-TBIpatients using the Rivermead Post-traumatic Amnesia Protocol.4

MethodsWe evaluated post-TBI (mostlymotor vehicle) patients who pre-sented for residual cognitiveimpairment. They underwent aMini-Mental State Examination(MMSE) and tests of attention(digit span), verbal fluency (ani-mals/minute), verbal memory (10-item verbal learning task), and theFrontal Assessment Battery (FAB)

for executive functions.5

No indi-vidual participants were identified,and the information was codedanonymously.

All participants were men (U.S.veterans) with medical records ontheir prior TBI. Inclusion criteriaincluded absence of prior cognitiverehabilitation, litigation, substanceabuse, psychoactive medications,and other neurological or psychiat-

ric disorder that might affect cogni-tion. Participants were divided intoa recent TBI group (23 patients 25years post-TBI) and a remote TBIgroup (23 patients 615 years post-TBI). Group members were pair-wise matched on medical recorddocumentation of loss of conscious-ness (mild 60 minutes, moderate124 hours, severe 24 hours), age(within 3 years), and education(within 3 years). The RivermeadPosttraumatic Amnesia Protocol,which consists of five questions,

established the duration of post-traumatic amnesia to the nearesthour.4

ResultsThe recent and remote groups werecomparable in current age(37.067.02 years versus 38.1113.01), of age at the time of TBI(34.177.10 years versus 27.6613.78), and years of education(13.722.27 years versus

12.853.01). The posttraumaticamnesia duration (hours) did notdiffer between the recent andremote groups (21.8929.83 hoursversus 20.7628.29). Within therecent TBI group, the retrospectiveposttraumatic amnesia negativelycorrelated with four out of the fivevariables (MMSE: r0.79,F19.60, df1, 22, p0.01; atten-tion: r0.53, F5.02, df1, 22,p0.03; verbal fluency: r0.61,

F8.45, df1, 22, p0.01; verbalmemory: r0.66, F8.55, df1,22, p0.01). Within the remote TBIgroup, there were no significantposttraumatic amnesia-cognitivecorrelations.

DiscussionClinicians often assess whetherpatients have cognitive deficitsfrom an old traumatic brain injury.

Without direct access to medicalrecords about an old head injury,the retrospective posttraumaticamnesia is a potential indicator ofresidual cognitive deficits from TBI.Our preliminary study found thatthe retrospective posttraumaticamnesia duration correlated withcognitive impairments up to 5years post-TBI. After 5 years, how-ever, the retrospective posttrau-matic amnesia did not correlatewith cognitive deficits.

Investigators previously tested

the Rivermead PosttraumaticAmnesia Protocol for retrospectiveposttraumatic amnesia durationamong patients who were within 2years of injury, but not in thosewith more remote head injuries.4

This study suggests that retrospec-tively obtained posttraumaticamnesia is useful up to 5 yearspost-TBI, but becomes unreliableafter that. Despite limitations, suchas the small number of male partic-

ipants, the findings recommendfurther investigation exploring ret-rospective posttraumatic amnesiain larger populations and in com-parisons with prospective measuresof TBI.

Paul M. Ashla

Aaron M. McMurtray, M.D.

Eliot Licht, M.D.

Mario F. Mendez, M.D., Ph.D.

Departments of Neurology andPsychiatry & Biobehavioral

Sciences, David Geffen Schoolof Medicine, University of Cal-ifornia at Los Angeles; TheV.A. Greater Los AngelesHealth Care System

References

1. Trzepacz PT, Kennedy RE: Delirium andposttraumatic amnesia, in Textbook ofTraumatic Brain Injury. Edited by Silver

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467J Neuropsychiatry Clin Neurosci 21:4, Fall 2009 http://neuro.psychiatryonline.org 467

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JM, McAllister TW, Yudofsky SC. Arling-ton, Va, American Psychiatric Publishing,2005, pp 175200

2. Frey KL, Rojas DC, Anderson CA, et al:Comparison of O-Log and GOAT asmeasures of posttraumatic amnesia.Brain Inj 2007; 21:513520

3. McMillan TM, Jongen EL, GreenwoodRJ: Assessment of post-traumatic amne-sia after severe closed head injury: retro-spective or prospective? J Neurol Neuro-surg Psychiatry 1996; 60:422427

4. King NS, Crawford S, Wenden FJ, et al:Measurement of post-traumatic amnesia:how reliable is it? J Neurol NeurosurgPsychiatry 1997; 62:3842

5. Dubois B, Slachevsky A, Litvan I, et al:The FAB: a frontal assessment battery at

bedside. Neurology 2000; 55:16211626

Acute Depression and

Suicidal Attempt Following

Lowering the Frequency of

Deep Brain Stimulation

To the Editor: Deep brain stimula-tion (DBS) is a neurosurgical inter-vention that enables deep brain

structures to be stimulated electri-cally by an implanted pacemaker.1

The method was initially devel-oped for movement disorders inseveral target areas such as thethalamus, pallidum, and subtha-lamic nucleus.2 It has now also

been extended to other neuropsy-chiatric conditions and has shownsome promising results in patientssuffering from profound depres-sion.3

In depression, dysfunction of thelimbic-cortico-striatal-pallidal-tha-lamic pathways has been pro-posed.46 Although the exact mech-anism of action of DBS remainselusive, stimulation of selectedareas implicated in mood regula-tion may have therapeutic potentialor lead to adverse consequencesdue to modulation of circuitsrelated to depression.5

Case ReportWe report a case of a 66-year-oldmale who was diagnosed with Par-kinsons disease 20 years ago andwas implanted with a subthalamicdeep brain stimulation treatmentsystem bilaterally for the last 8years. He continued taking oralParkinsons disease medication.Subsequently, his dyskinesia andmovements markedly improved.There were no psychiatric adverseevents experienced following DBSimplantation. Four years later, hedeveloped a major depressive epi-sode after his retirement andresponded well to an adequate trialof bupropion. He did not report

prior history of suicidal thoughtsor attempts and followed up regu-larly with a psychiatrist.

Reportedly, for the last 5 yearshis neurologist had been changingthe frequency of the brain stimula-tion through the implanted devicesto negate the patients changingdyskinetic symptoms and diseaseprogression. The frequency of thestimulation was lowered from 185Hz to 60 Hz. Within 24 hours of

lowering the frequency, the patientdeveloped acute depression andmade a serious suicide attempt byoverdosing on sleeping pills. Hewas admitted to an intensive careunit and transferred to a psychiat-ric facility. His neurologist report-edly increased the frequency whilethe patient was in the hospital, andaccordingly, his depressive feelingsimproved considerably over thenext few days with complete remis-

sion of his suicidal thoughts.

DiscussionSeveral case reports have beenpublished showing the potential ofdeep brain stimulation in the treat-ment of depression.7 Our casedemonstrates the risk of suicidewhen lowering the frequency of thestimulation. Patients undergoing anadjustment to the stimulation

parameters according to theirchanging motor symptoms should

be prescreened and assessed thor-oughly for suicide risk prior to thechanges.7 Additionally, patients

should be monitored closely forsuicidal behavior after the chang-es.7 Patients at high risk for suicideshould be excluded from deep

brain stimulation surgery.8

Nahla A. Mahgoub, M.D.

Nabil Kotbi, M.D.

Department of Psychiatry,Weill Medical College of Cor-nell University, White Plains,

NY

References

1. Pereira EA, Green AL, Nandi D, et al:

Deep brain stimulation: indications and

evidence. Expert Rev Med Devices 2007;

4:591603

2. Benabid AL: What the future holds for

deep brain stimulation. Expert Rev Med

Devices 2007; 4:895903

3. Schlaepfer TE, Cohen MX, Frick C, et al:

Deep brain stimulation to reward cir-

cuitry alleviates anhedonia in refractory

major depression. Neuropsychopharma-cology 2008; 33:368377

4. Kopell BH, Greenberg BD: Anatomy and

physiology of the basal ganglia: implica-

tions for DBS in psychiatry. Neurosci

Biobehav Rev 2008; 32:408422

5. Kosel M, Sturm V, Frick C, et al: Mood

improvement after deep brain stimula-

tion of the internal globus pallidus for

tardive dyskinesia in a patient suffering

from major depression. J Psychiatr Res

2007; 41:801803

6. Kopell BH, Greenberg B, Rezai AR:

Deep brain stimulation for psychiatric

disorders. J Clin Neurophysiol 2004;

21:5167

7. Appleby BS, Duggan PS, Regenberg A,

et al: Psychiatric and neuropsychiatric

adverse events associated with deep

brain stimulation: a meta-analysis of ten

years experience. Mov Disord 2007;

22:17221728

8. Burkhard PR, Vingerhoets FJ, Berney A,

et al: Suicide after successful deep brain

stimulation for movement disorders.

Neurology 2004; 63:21702172

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468468 http://neuro.psychiatryonline.org J Neuropsychiatry Clin Neurosci 21:4, Fall 2009