Case report

Bipolar disorder following a stroke involving
the left hemisphere
Chia-Yih Liu, Shuu-Jiun Wang, Jong-Ling Fuh, Yong-Yi Yang, Hsiu-Chih Liu

Objective: Post-stroke mania has rarely been noted and researched, and
reported cases have mostly involved the non-dominant hemisphere. In this
paper, we report a case of bipolar disorder secondary to a stroke over the dominant hemisphere.
Clinical picture: A 48-year-old, right-handed man had a cerebral infarct over the
left temporal region. He became depressed after the stroke, and 4 months later
developed a manic episode.
Treatment: The patient was treated with haloperidol and lorazepam.
Outcome: The symptoms subsided within 2 months after treatment.
Conclusions: It is premature to consider mania to be a syndrome of the right,
or non-dominant, hemisphere. We suggest that further study focusing on specific anatomical regions, rather than laterality, will help to elucidate the interrelationship between mood and brain function.
Australian and New Zeaiand Journal of Psychiatry 1996; 30:688-691
Secondary mania refers to the occurrence of symptoms which meet the diagnostic criteria for mania
produced by neurological, metabolic or toxic disorder [ 11. Focal brain lesions, including haemorrhage
and infarction, have been associated with secondary
mania [2,3]. The frequent occurrences of depression
after a stroke have been documented in the literature
[4]. In contrast. mania after stroke has rarely been
noted [2,5].
Dunne rt nl. [6] identified only three cases of poststroke mania among 661 stroke patients. Starkstein et
al. [7] also identified three cases in a series of 700

Department of Psychiatry, Chang-Gung Medical College and
Chang-Gung Memorial Hospital, Taoyuan, Taiwan, ROC
Chia-Yih Liu MD, Lecturer and Inpatient Unit Chief
Yong-Yi Yang MD, Associate Professor and Department Head

Neurological Institute, Veterans' General Hospital-Taipei and
National Yang-Ming University School of Medicine, Taipei,
Taiwan, ROC
Shuu-Jiun Wang MD, Lecturer
Jong-Ling Fuh MD. Lecturer
Hsiu-Chih Liu MD, Associate Professor and Section Chief

consecutive stroke patients. Most cases reported had
a lesion in the non-dominant hemisphere [2,3]. Only
four cases of post-stroke mania with left hemisphere
lesion have been reported [7-101. Among them, two
cases presented both depressive and manic episodes
1101.
We report another case of bipolar disorder secondary to a stroke involving the left hemisphere.

Case report
A 48-year-old, right-handed, previously healthy man
had a sudden onset of speech difficulty in June 1993.
Sensory aphasia was discovered by neurological
examination, and a computerised tomography scan of
the brain showed a suspicious low density lesion over
the left posterior temporal region. A magnetic resonance image of the brain 4 days later showed a low
signal on T1-weighted (Fig. la) and a high signal on
T2-weighted (Fig. lb) images over the left temporal
region, consistent with a recent infarction.
An electroencephalogram revealed continuous
polymorphic delta activity over the left temporal

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C.-Y. LIU, S.-J. WANG. J.-L. FUH. Y.-Y. YANG. H.-C. LILT

6x9

Figure 1. Magnetic resoiimce image of the patient:y brairi shocring a low sigiiril oii ( a ) TI-weighted and high
sigiial lesion aiid (b) T2-weighted inluges in the leji teniporal region, compatible with recent ii!farction.

region. The patient became depressed after the
stroke. Clinical features included depressed mood.
sleep disturbance, inappropriate guilt, poor appetite
and the idea of death. Benzodiazepines, such as
lorazepam and estazolam, were the only drugs prescribed by neurologists. The depressive symptoms
subsided within 3 months. Sensory aphasia also gradually improved. There were no major neurological
sequelae except mild impairment of abstract thinking
and comprehension. The patient was able to do
domestic work and returned to his job as an office
worker with fair proficiency.
Four months later, the patient experienced diminished sleep, became increasingly irritable, hyperactive, hypertalkative and elated with grandiose
ideation. Sent to our emergency room, he was given
a physical examination which yielded essentially
unremarkable results, except an extensor plantar
response on the right side. His blood pressure was
150/90 mmHg with a regular heart rate 88 bpm. He
had neither a personal nor a familial history of psy-

chiatric illness, nor a history of symptoms suggesting
recurrent depression; and neither a history of episodic change of energy. nor that of unusual periods of
expansive, erratic or provocative behaviour. He had a
history of hypertension for 12 years and non-insulin
dependent diabetes mellitus for 4 years. Both were
under regular treatment.
Throughout his mental status examination, the
patient was fully alert and well-oriented. His
thoughts, with grandiose and religious content,
flowed rapidly from idea to idea. His mood was
euphoric and elated. He exhibited loud, abusive and
pressured speech. His digit span was seven forward
and four backward. He performed calculation normally and could recall three objects after 3 minutes
without difficulty. No hallucination or delusion could
be detected.
Laboratory data, including complete blood count,
urinalysis and biochemical screening, all were within
normal limits, except fasting blood sugar (147 mg%).
Computerised tomography scan of the brain showed

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POST-STROKE BIPOLAR DISORDER

690

an old infarction over the left posterior temporal area.
No additional lesion was noted.
During hospitalisation, the patient was intrusive,
hyperactive and disinhibited. He felt full of energy,
wandered around and talked to others all day long,
and stayed awake all the night. Occasional abortive
episodes of tearfulness were also noted. He was
treated with haloperidol 8 mg per day, trihexyphenidyl 1 mg t.i.d., lorazepam 0.5 mg t.i.d., and
estazolam 2 mg before sleep. All symptoms gradually improved. He was discharged 2 weeks later.
Psychotropics were discontinued 2 months after discharge.

Discussion
This patient met the DSM-111-R criteria for organic
mood disorder [ 1 I] and Krauthammer and Klerman’s
criteria for secondary mania [I]. Although Krauthammer and Klerman [ 11 and Stasiek and Zetin [ 121
considered ‘secondary mania’ should be reserved for
cases without personal or family history, some other
authors suggested prior vulnerability may predispose
to organic mood disorders [ 131. In this case, the onset
followed a stroke without a personal or familial
history of mood disorder. It is certainly suggestive of
a causal relationship.
Among the reported cases, mania may occur
immediately after stroke or may be delayed for up to
2 years [7]. In some cases, recurrent episodes of
depression and mania were quite similar to an idiopathic bipolar disorder [ 10,12-15]. Starkstein et al.
[ 161 indicated that patients with right subcortical
lesions tend to develop bipolar disorder; whereas
patients with right cortical lesions tend to develop
unipolar mania. Pappata et al. [ 171 suggested that

subcortical lesions may produce hypometabolic
effect in both ipsilateral and contralateral brain areas,
which may lead to bipolar mood changes. But in the
present case, no subcortical lesion was noted.
A conventional hypothesis says that the organisation of mood in individuals may be lateralised to the
right or non-dominant hemisphere [7, I3,18-20]. Our
case is an example of the less common findings. Not
only was the patient right-handed, but he also had
transient post-stroke aphasia. This is the fifth case
reported in the literature in which secondary mania
followed a stroke in the dominant hemisphere
[7-101, and it is the third case in which both depressive and manic episodes occurred (Table I).
Cummings [3] reviewed the reported cases and
concluded that most lesions associated with secondary mania involved the diencephalonic region.
Robinson et al. [2] indicated that the patients with
secondary mania had lesions involving mainly the
right orbitofrontal, basotemporal cortex or areas
related to the limbic system. Bogousslavsky et al.
[2 I ] suggested that an ipsilateral frontal dysfunction
caused by deafferentiation due to a right thalamus
lesion may produce a manic-like disinhibition syndrome. Other than laterality, they pointed out some
specific regions which may be responsible for the
illness.
In a review article on post-stroke depression,
Starkstein and Robinson [5] contended that the lateralised effect of post-stroke depression was restricted
to left-sided basal ganglia and left frontal lesions. It
is probable that the lateralised effect of post-stroke
mania is also restricted to right-sided diencephalonand limbic-associated lesions.
The authors suggest that it is premature to consider mania to be a syndrome of the right, or non-domi-

Table I . Reported cnses of mania following left hemisphere stroke
Authors

Handed

Type of lesion

Location

Herlihy and Herlihy [8]
Jampala and Abrams [9]
Starkstein eta/. [7]*
Tureki eta/. [lo]*
Present case*

Unknown
Right
Right
Right
Right

Haemorrhage
Haemorrhage
Infarction
Unknown
Infarction

Left frontotemporal
Left frontotemporal
Left frontal
Left basal ganglia
Left temporal

*Presenting both depressive and manic episodes

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C:Y.

LIU, S.-J. WANG, J:L.

nant, hemisphere. Further study focusing on specific
anatomical regions, rather than laterality, will help to
elucidate the inter-relationship between mood and
brain function.

Acknowledgement
This study was supported in part by a National
Science Council grant (NSC 83-0412-B-010-045).

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