Bipolar disorder after traumatic brain injury

Abstract

Objective. We report the case of a 47-year-old man with no psychiatric antecedents who developed manic and depressive symptoms after traumatic brain injury (TBI). Methods and results. Findings on neurobehavioral examination, neuropsy-chological test battery, electrophysiological and imaging exams suggested the presence of a diffuse cerebral injury with a predominance of left fronto-temporal findings. Conclusions. This case demonstrates that TBI may cause vulnerability to psychiatric disorders, with long latency periods, and that its course may be independent of cognitive impairment and recovery.

Full text

CASE REPORT
Bipolar disorder after traumatic brain injury
SOFIA BRISSOS
1
& VASCO VIDEIRA DIAS
2
1
Department of Psychiatry, Santare
´m District Hospital, Santare
´m, Portugal, and
2
Department of Psychology and Sociology,
Autonomous University of Lisbon (UAL), Portugal
Abstract
Objective. We report the case of a 47-year-old man with no psychiatric antecedents who developed manic and depressive
symptoms after traumatic brain injury (TBI). Methods and results. Findings on neurobehavioral examination, neuropsy-
chological test battery, electrophysiological and imaging exams suggested the presence of a diffuse cerebral injury with a
predominance of left fronto-temporal findings. Conclusions. This case demonstrates that TBI may cause vulnerability to
psychiatric disorders, with long latency periods, and that its course may be independent of cognitive impairment and
recovery.
Key Words: Bipolar disorder, cognitive dysfunction, traumatic brain injury
Introduction
Traumatic brain injury (TBI) can result in a variety
of neuropsychiatric disturbances, ranging from
subtle to severe intellectual and emotional distur-
bances, and may cause vulnerability to psychiatric
disorders, with latency periods of over 10 years [1].
These include problems with attention and arou-
sal, concentration, executive function, intellectual
changes, memory impairment, personality changes,
affective and anxiety disorders, psychosis, sleep
disorders, aggression and irritability [2].
Despite the emphasis placed on physical deficits
shortly after severe brain injury, it is cognitive and
behavioural deficits that give rise to the major
morbidity that most impairs the capacity to return
to work and maintain social activities [3], contribut-
ing to long-term disability [4] and compromising the
quality of life [5].
TBI is the result of mechanical forces on the skull
and transmitted to the brain leading to focal and/or
diffuse brain damage, as well as secondary effects
(cerebral oedema, hydrocephalus, increased intra-
cranial pressure, infection, hypoxia, neurotoxicity,
and others) [2]. The differential motion of the brain
within the skull also causes shearing and stretching
of the axons [6], with injuries ranging from brief
physiological disruption to widespread axonal tear-
ing, called diffuse axonal injury [7]. Delayed
effects include the release of excitatory amino
acids, oxidative free-radical production, the release
of arachidonic acid metabolites, and disruption of
neurotransmitters like monoamines and serotonin
[8/10].
Mood disorders are more frequent in patients with
sustained TBIs than in patients with similar back-
ground characteristics who underwent similar levels
of stress but without sustaining brain injury [11],
which would suggest that neuropathological pro-
cesses associated with TBI constitute an important
contributing factor to the development of mood
disorders [12].
Major depression is the most common psychiatric
disorder after TBI, with rates varying from 14 to
77% [1,4,13,14]. Mania after TBI is less common
than depression, but occurs more frequently than in
the general population, and can be seen in about 9%
of patients [15]. Positive family history of affective
disorder and subcortical atrophy prior to TBI are
also considered risk factors [16]. Rates for post-TBI
bipolar disorder have ranged from 1.7 to 17%
[1,17], some authors stating that post-TBI bipolar
disorder appears only in individuals with a previous
history of axis I psychopathology, usually remaining
chronic [17], but such data have come primarily
from case reports.
We describe the case of a 47-year-old patient who
presented with behavioural and mood symptoms
after a severe head injury, and discuss the issues
Correspondence: Sofia Brissos, Rua Ilha dos Amores, Lote 4.12.01 Bloco C 18esq, 1990 /122 Lisbon, Portugal. Tel: /351 934203521. Fax: /351
218163379. E-mail: sofiabrissos@netcabo.pt
International Jour nal of Psychiatry in Clinical Practice, 2005; 9(4): 292 /295
(Received 2 February 2005; accepted 3 May 2005)
ISSN 1365-1501 print/ISSN 1471-1788 online #2005 Taylor & Francis
DOI: 10.1080/13651500510029219

raised regarding the physiopathological mechanisms,
and the treatment implications for his illness.
Case report
JPF is a 47-year-old divorced, right-handed, male
patient who was educated up to 6th grade and who
had previously worked in security. He had antece-
dents of operated mitral cardiopathy, auricular
fibrillation and HTA, and a history of tobacco use
and alcohol abuse. According to the patient and his
ex-wife, there were no personal or family histories of
psychiatric disorders. He suffered a traffic road
accident, with polytraumatisms and TBI, after which
he remained in a coma for 4 days. Subdural
haematoma drainage was carried out and he was
medicated with phenytoin and corticoids. Routine
laboratory tests including thyroid hormones and
thyroid-stimulating hormone were within normal
range. The first cranial computed tomography
(CT) scan revealed left temporo-parietal craniot-
omy, and haematoma substitution by hypodensity in
the left cortico-parietal area of the left cerebral
hemisphere. Five months later the CT scan revealed
no anomalies. The EEG revealed incidence of slow
waves (theta and delta) over the left fronto-temporal
region. Short latency auditory evoked potentials
showed no significant changes and the cognitive
evoked potentials (P300 wave) were compatible with
cognitive dysfunction.
Neuropsychological evaluation 5 months post-
TBI revealed attentional deficit (sustained, divided
and selected), mental tracking deficit, slowing of
information processing speed, verbal fluency deficit
(semantic subtype), anomic specking and dysarthria,
impaired repetition, reading and writing deficits
(semantic alexia and phonological alexia), secondary
dyscalculia, ideokinetic apraxia, melokinetic apraxia,
ideomotor apraxia, writing apraxia and construc-
tional dyspraxia, memory deficits in learning, short-
and long-term memory; problem-solving deficits,
planning deficit, and flexibility capacity impairment.
Although he started neuropsychological rehabilita-
tion, he has not been able to return to work.
A year and a half after the accident he was referred
for inpatient psychiatric treatment because of beha-
vioural symptoms, namely, disinhibition, pressure of
speech, aggressive behaviour and irritability, but
with no psychotic symptoms. Corticoids were slowly
withdrawn and he was discharged a week later
with the diagnosis of post-TBI organic personality
disorder and was medicated with gabapentin
(1600 mg/day), haloperidol (2 mg/day), quetiapine
(200 mg/day), propanolol, digoxin, lisinopril, spir-
onolactone, furosemide and citicoline.
The following month he started complaining of
depressive symptomatology, with sadness, apathy,
abulia, anedonia and suicidal ideation, being medi-
cated with escitalopram (20 mg/day) and lamotrigine
(100 mg/day). A month later he became dysphoric,
with pressured speech, coprolalia, excessive spend-
ing and psychotic symptoms (delusions of persecu-
tion and jealousy), but without hallucinations or
significant changes in sleep patterns. Escitalopram
was suspended, and haloperidol was titrated to
10 mg/day. His symptoms abated after 2/3 weeks,
but by the fourth week he started complaining again
of depressive symptoms; escitalopram was re-pre-
scribed, and a dose of 1200 mg/day of carbamaze-
pine was added. A week later he was again
disinhibited and slightly euphoric, with no psychotic
symptoms.
The alternation of manic and depressive symp-
toms led to the diagnosis of post-TBI bipolar
disorder; however, the patient has attended psychia-
try consultation only sporadically, with irregular
treatment adherence.
Discussion
The patient can be considered to have suffered
severe TBI, even though some medical notes were
unavailable for scrutiny, such as his initial score on
the GCS (Glasgow Coma Scale), and the length of
PTA (posttraumatic amnesia) which created diffi-
culty in assessing the severity of the injury. The long
latency period might have caused some of the
uncertainty around whether the bipolar disorder
was due to TBI, although longer latency periods
have been reported in the literature [1,18].
Although some authors consider that post-TBI
bipolar disorder appears only in individuals with
previous personal [17] or family [16] history of axis I
psychopathology [17], in contrast to the findings of
other researchers, besides alcohol abuse we found no
evidence of other personal or family histories of
psychiatric disorders [19,20].
Lishman [21] hypothesises that psychiatric symp-
toms following a head injury are precipitated initially
by organic factors, but in some patients are main-
tained by socioeconomic and psychosocial factors
that can predict cognitive dysfunction after TBI
[22]. It is well documented that patients with TBI
are often young men who come from lower socio-
economic backgrounds, who tend to misuse alcohol
and drugs, and possess certain premorbid person-
ality traits. However, some authors have not found
enough evidence to suggest that persons who sustain
mild TBI show substantially different premorbid
personality to that of their peers [23]. Even though
it was not possible to adequately assess the level of
our patient’s premorbid personality, emotional pro-
blems are usually exacerbated after injury [2].
Alcohol consumption is considered a predisposing
factor to head injury [4], and may continue after-
wards, delaying the reparative process within the
central nervous system [21].
Bipolar disorder after traumatic brain injury 293

Although corticoid treatment has been considered
as one cause of the appearance of mood symptoms
[24], this does not explain our patient’s symptoms,
since they persisted even after corticoids were with-
drawn.
Patients with post-TBI bipolar disorder show
predominantly subcortical lesions (right head of
caudate and right thalamus), while patients with
post-TBI unipolar mania more often show cortical
involvement (mainly right orbitofrontal and baso-
temporal cortices) [15,16,25,26], suggesting that
subcortical and cortical right hemisphere lesions
may produce different neurochemical and/or remote
metabolic brain changes that may be the underlying
cause of either a bipolar disease or a unipolar mania.
Our patient’s CT scans and EEGs revealed a lesion
on the temporo-parietal area of the left cerebral
hemisphere. The neuropsychological evaluation re-
vealed deficits in the areas affected by the lesion, but
also changes suggesting dysfunction in other areas,
such as the left frontal dorsolateral, right parietal
cortex, the supplementary motor area, and in the
right frontal dorsolateral and orbito-frontal area.
The possible mechanisms involved in the dysfunc-
tions found in our patient, not exclusively explained
by the location of the lesion, are possibly due to
widespread axonal tearing and diffuse axonal injury
caused by acceleration /deceleration forces [7].
These forces commonly are the origins of certain
brain injury profiles including orbitofrontal, anterior
and inferior temporal contusions, with diffuse axonal
injury. The latter particularly affects the corpus
callosum, superior cerebellar peduncle, basal gang-
lia, and periventricular white matter [6]. Cognitive
impairment is often diffuse with more prominent
deficits in the rate of information processing, atten-
tion span, memory, cognitive flexibility, problem
solving, impulsiveness, affective instability, and dis-
inhibition. These symptoms are frequently observed
characterizing the ‘‘changes’’ in TBI patients as seen
in our patient.
However, some of the cognitive deficits might also
be due to, or aggravated by, the mood disorder itself,
since it has been reported that there may be a
subgroup of bipolar patients who develop cognitive
deficits due to the disease process, and which are
independent of the mood state [27].
The complex processes of cognition and mood are
not mediated by any specific brain region, but
require the coordinated activity of several areas; a
compromise of neural connectivity may result
in attenuation of the functions regulated by
these areas and result in clusters of signs and
symptoms currently recognised as psychiatric dis-
orders [28].
Another proposed mechanism is the ‘‘diaschisis
model’’, whereby the loss of function produced by
acute focal brain damage, even without axonal
shearing, may produce dysfunction in adjacent or
remote regions connected through fibre tracts [29].
The severity of the neuropsychiatric sequelae of
the brain injury is determined by multiple factors,
but, in general, prognosis is associated with the
severity of injury [2].
Since TBI can cause permanent vulnerability to
psychiatric disorders, contributing substantially
to long-term disability [4] and quality of life
[5], psychiatric evaluation and (long-term) monitor-
ing should be included in the routine follow-up
of TBI.
Treatment should include cognitive and physical
rehabilitation, family and personal support, and
psychopharmacological management of mood and
other behavioural syndromes [30]. Pope et al. [31]
described a case of bipolar disorder after TBI was
successfully treated with valproate and lithium, and
Monji et al. [19] reported a case where valproate was
effective in monotherapy. Although the exact me-
chanisms of action for valproate have not yet been
determined, postulated theories include an ‘‘anti-
kindling’’ effect in the limbic system on emotion,
cognition, and behaviour; an enhancement of
GABAergic-mediated inhibitory control; and
action as a general CNS stabiliser, making it a
primary pharmacological intervention for the treat-
ment of neuropsychiatric symptoms after brain
injury [19].
Future research should also focus on the efficacy
and timing of psychological interventions in combi-
nation with medications, in the treatment of post-
TBI Axis I disorders, to create standards of care, and
most importantly, enhance the quality of life of
individuals after TBI [17,32].
Key points
.Traumatic brain injury (TBI) may cause vul-
nerability to psychiatric disorders, with latency
periods of over 10 years.
.Bipolar disorder is a rare outcome after TBI,
major depression being the most common
disorder.
.The complex processes of cognitive and mood
requires the coordinated activity of several brain
areas, and lesions in one area may influence the
functioning of adjacent or remote ones.
.Treatment of bipolar disorder after brain injury
should include psychopharmacological man-
agement, namely valproate as the primary
pharmacological intervention, cognitive and
physical rehabilitation, and family and personal
support.
Acknowledgement
We thank Dr Eduard Vieta for his helpful advice.
294 S. Brissos & V. Videira Dias

Statement of interest
The author has no conflict of interest with any
commercial or other associations in connection with
the submitted article.
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