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 25
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
124 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
(37.067.02 years versus 38.11
13.01), of age at the time of TBI
(34.177.10 years versus 27.66
13.78), and years of education
(13.722.27 years versus
12.853.01). The posttraumatic
amnesia duration (hours) did not
differ between the recent and
remote groups (21.8929.83 hours
versus 20.7628.29). Within the
recent TBI group, the retrospective
posttraumatic amnesia negatively
correlated with four out of the five
variables (MMSE: r0.79,
F19.60, df1, 22, p0.01; attention: r0.53, F5.02, df1, 22,
p0.03; verbal fluency: r0.61,
F8.45, df1, 22, p0.01; verbal
memory: r0.66, F8.55, df1,
22, p0.01). 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

http://neuro.psychiatryonline.org

467

LETTERS
JM, McAllister TW, Yudofsky SC. Arlington, Va, American Psychiatric Publishing,
2005, pp 175200
2. Frey KL, Rojas DC, Anderson CA, et al:
Comparison of O-Log and GOAT as
measures of posttraumatic amnesia.
Brain Inj 2007; 21:513520
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; 55:16211626

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

468

http://neuro.psychiatryonline.org

Case Report
We report a case of a 66-year-old
male who was diagnosed with Parkinsons 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
Parkinsons 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 patients 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; 4:895903
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;
22:17221728
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