Retrospective Posttraumatic Amnesia in Traumatic Brain Injury

LETTERS

Retrospective Posttraumatic Amnesia in Traumatic Brain Injury

To the Editor: Clinicians may need to determine the severity of a traumatic brain injury (TBI) that occurred many years ago. This can be challenging when there is no direct information about the remote TBI. One method of retrospective assessment is the duration of posttraumatic amnesia, the period during which a person is disoriented and unable to lay down new memories after a head injury.1,2 Few modern investigators have studied retrospective posttraumatic amnesia.3 Our study investigates the value of retrospective assessment of posttraumatic amnesia in a stratified sample of post-TBI patients using the Rivermead Posttraumatic Amnesia Protocol.4 Methods We evaluated post-TBI (mostly motor vehicle) patients who presented for residual cognitive impairment. They underwent a Mini-Mental State Examination (MMSE) and tests of attention (digit span), verbal fluency (animals/minute), verbal memory (10item verbal learning task), and the Frontal Assessment Battery (FAB) for executive functions.5 No individual participants were identified, and the information was coded anonymously. All participants were men (U.S. veterans) with medical records on their prior TBI. Inclusion criteria included absence of prior cognitive rehabilitation, litigation, substance abuse, psychoactive medications, and other neurological or psychiat-

ric disorder that might affect cognition. Participants were divided into a recent TBI group (23 patients 2–5 years post-TBI) and a remote TBI group (23 patients 6 –15 years postTBI). Group members were pairwise matched on medical record documentation of loss of consciousness (mild ⬍60 minutes, moderate 1–24 hours, severe ⬎24 hours), age (within 3 years), and education (within 3 years). The Rivermead Posttraumatic Amnesia Protocol, which consists of five questions, established the duration of posttraumatic amnesia to the nearest hour.4 Results The recent and remote groups were comparable in current age (37.06⫾7.02 years versus 38.11⫾ 13.01), of age at the time of TBI (34.17⫾7.10 years versus 27.66⫾ 13.78), and years of education (13.72⫾2.27 years versus 12.85⫾3.01). The posttraumatic amnesia duration (hours) did not differ between the recent and remote groups (21.89⫾29.83 hours versus 20.76⫾28.29). Within the recent TBI group, the retrospective posttraumatic amnesia negatively correlated with four out of the five variables (MMSE: r⫽⫺0.79, F⫽19.60, df⫽1, 22, p⬍0.01; attention: r⫽⫺0.53, F⫽5.02, df⫽1, 22, p⫽0.03; verbal fluency: r⫽⫺0.61, F⫽8.45, df⫽1, 22, p⫽0.01; verbal memory: r⫽⫺0.66, F⫽8.55, df⫽1, 22, p⫽0.01). Within the remote TBI group, there were no significant posttraumatic amnesia-cognitive correlations. Discussion Clinicians often assess whether patients have cognitive deficits from an old traumatic brain injury.

J Neuropsychiatry Clin Neurosci 21:4, Fall 2009

Without direct access to medical records about an old head injury, the retrospective posttraumatic amnesia is a potential indicator of residual cognitive deficits from TBI. Our preliminary study found that the retrospective posttraumatic amnesia duration correlated with cognitive impairments up to 5 years post-TBI. After 5 years, however, the retrospective posttraumatic amnesia did not correlate with cognitive deficits. Investigators previously tested the Rivermead Posttraumatic Amnesia Protocol for retrospective posttraumatic amnesia duration among patients who were within 2 years of injury, but not in those with more remote head injuries.4 This study suggests that retrospectively obtained posttraumatic amnesia is useful up to 5 years post-TBI, but becomes unreliable after that. Despite limitations, such as the small number of male participants, the findings recommend further investigation exploring retrospective posttraumatic amnesia in larger populations and in comparisons with prospective measures of TBI. Paul M. Ashla Aaron M. McMurtray, M.D. Eliot Licht, M.D. Mario F. Mendez, M.D., Ph.D. Departments of Neurology and Psychiatry & Biobehavioral Sciences, David Geffen School of Medicine, University of California at Los Angeles; The V.A. Greater Los Angeles Health Care System

References 1. Trzepacz PT, Kennedy RE: Delirium and posttraumatic amnesia, in Textbook of Traumatic Brain Injury. Edited by Silver

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LETTERS JM, McAllister TW, Yudofsky SC. Arlington, Va, American Psychiatric Publishing, 2005, pp 175–200 2. Frey KL, Rojas DC, Anderson CA, et al: Comparison of O-Log and GOAT as measures of posttraumatic amnesia. Brain Inj 2007; 21:513–520 3. McMillan TM, Jongen EL, Greenwood RJ: Assessment of post-traumatic amnesia after severe closed head injury: retrospective or prospective? J Neurol Neurosurg Psychiatry 1996; 60:422– 427 4. King NS, Crawford S, Wenden FJ, et al: Measurement of post-traumatic amnesia: how reliable is it? J Neurol Neurosurg Psychiatry 1997; 62:38 – 42 5. Dubois B, Slachevsky A, Litvan I, et al: The FAB: a frontal assessment battery at bedside. Neurology 2000; 55:1621–1626

Acute Depression and Suicidal Attempt Following Lowering the Frequency of Deep Brain Stimulation

To the Editor: Deep brain stimulation (DBS) is a neurosurgical intervention that enables deep brain structures to be stimulated electrically by an implanted pacemaker.1 The method was initially developed for movement disorders in several target areas such as the thalamus, pallidum, and subthalamic nucleus.2 It has now also been extended to other neuropsychiatric conditions and has shown some promising results in patients suffering from profound depression.3 In depression, dysfunction of the limbic-cortico-striatal-pallidal-thalamic pathways has been proposed.4 –6 Although the exact mechanism of action of DBS remains elusive, stimulation of selected areas implicated in mood regulation may have therapeutic potential or lead to adverse consequences due to modulation of circuits related to depression.5

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Case Report We report a case of a 66-year-old male who was diagnosed with Parkinson’s disease 20 years ago and was implanted with a subthalamic deep brain stimulation treatment system bilaterally for the last 8 years. He continued taking oral Parkinson’s disease medication. Subsequently, his dyskinesia and movements markedly improved. There were no psychiatric adverse events experienced following DBS implantation. Four years later, he developed a major depressive episode after his retirement and responded well to an adequate trial of bupropion. He did not report prior history of suicidal thoughts or attempts and followed up regularly with a psychiatrist. Reportedly, for the last 5 years his neurologist had been changing the frequency of the brain stimulation through the implanted devices to negate the patient’s changing dyskinetic symptoms and disease progression. The frequency of the stimulation was lowered from 185 Hz to 60 Hz. Within 24 hours of lowering the frequency, the patient developed acute depression and made a serious suicide attempt by overdosing on sleeping pills. He was admitted to an intensive care unit and transferred to a psychiatric facility. His neurologist reportedly increased the frequency while the patient was in the hospital, and accordingly, his depressive feelings improved considerably over the next few days with complete remission of his suicidal thoughts. Discussion Several case reports have been published showing the potential of deep brain stimulation in the treatment of depression.7 Our case demonstrates the risk of suicide when lowering the frequency of the stimulation. Patients undergoing an adjustment to the stimulation

parameters according to their changing motor symptoms should be prescreened and assessed thoroughly for suicide risk prior to the changes.7 Additionally, patients should be monitored closely for suicidal behavior after the changes.7 Patients at high risk for suicide should be excluded from deep brain stimulation surgery.8 Nahla A. Mahgoub, M.D. Nabil Kotbi, M.D. Department of Psychiatry, Weill Medical College of Cornell 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; 4:591– 603 2. Benabid AL: What the future holds for deep brain stimulation. Expert Rev Med Devices 2007; 4:895–903 3. Schlaepfer TE, Cohen MX, Frick C, et al: Deep brain stimulation to reward circuitry alleviates anhedonia in refractory major depression. Neuropsychopharmacology 2008; 33:368 –377 4. Kopell BH, Greenberg BD: Anatomy and physiology of the basal ganglia: implications for DBS in psychiatry. Neurosci Biobehav Rev 2008; 32:408 – 422 5. Kosel M, Sturm V, Frick C, et al: Mood improvement after deep brain stimulation of the internal globus pallidus for tardive dyskinesia in a patient suffering from major depression. J Psychiatr Res 2007; 41:801– 803 6. Kopell BH, Greenberg B, Rezai AR: Deep brain stimulation for psychiatric disorders. J Clin Neurophysiol 2004; 21:51– 67 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; 22:1722–1728 8. Burkhard PR, Vingerhoets FJ, Berney A, et al: Suicide after successful deep brain stimulation for movement disorders. Neurology 2004; 63:2170 –2172

J Neuropsychiatry Clin Neurosci 21:4, Fall 2009