Archives of Gerontology and Geriatrics 43 (2006) 223–232
www.elsevier.com/locate/archger

Secondary mania of vascular origin in elderly
patients: A report of two clinical cases
Nages Nagaratnam *, Ka-Kit Wong, Ilesh Patel
Department of Medicine, Aged Care and Rehabilitation Services, Blacktown-Mount Druitt Health,
Blacktown, NSW 2148, Australia
Received 18 May 2005; received in revised form 30 September 2005; accepted 18 October 2005
Available online 7 December 2005

Abstract
The concept of secondary mania continues to be debated together with unresolved or partially
resolved issues such as lateralization, localization, age of onset, disinhibition syndromes, and others.
We have described two patients with secondary mania following a stroke. One had a large left
hemisphere cerebral infarction and the symptoms arose about 2.5 years later, possibly triggered by a
transient ischemic attack involving the right hemisphere. The other had an infarction in the right
posterior artery territory extending to the thalamus and internal capsule together with infarctions in
the deep border zones of both hemispheres at the level of the centrum semiovale with the manic
symptoms concomitant with the onset of the event. The clinical and neuro-anatomic mechanisms that
underlie the diverse locations of secondary mania are discussed. The cerebral components of
secondary mania and disinhibition syndromes are very similar and it is proposed that disinhibition
syndromes, secondary hypomania and secondary mania with and without psychotic symptoms are
simply a continuum of severity of mood disorder and secondary mania with psychotic symptoms may
be an extreme form. The concept of secondary mania in the elderly is not likely to disappear although
several unresolved issues remain. For the neurophysician, geriatrician, and the psychiatrist there is
much to be attained by simplifying the issues and accepting the view that secondary mania is a
discrete entity.
# 2005 Elsevier Ireland Ltd. All rights reserved.
Keywords: Mania in old age; Secondary mania; Frontal-subcortical circuitry; Limbic system; Disinhibition
syndromes; Lateralization

* Corresponding author at: 20, Panaview Crescent, North Rocks, NSW, Australia. Tel.: +61 2 9872 1997;
fax: +61 2 9872 1997.
E-mail address: nage@mail2me.com.au (N. Nagaratnam).
0167-4943/$ – see front matter # 2005 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.archger.2005.10.009

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1. Introduction
Mania in old age has been comprehensively reviewed (Krauthammer and Klerman,
1978; Starkstein et al., 1988; Fujikawa et al., 1995; Shulman and Herrmann, 1999) but
despite difficulties in the diagnosis and classification (Shulman, 2004) interest in it
continues to grow. There remain unresolved issues such as whether ‘‘secondary’’ mania is a
definite entity, the age of onset, lateralization (Liu et al., 1996; Fenn and George, 1999),
localization, and mania subtypes amongst others. The term ‘‘manic syndromes’’ in old age
has its critics because of the high occurrence of medical and neurological conditions in old
people compared with the overall low incidence of late-onset mania. There were only three
cases of post-stroke mania among 700 stroke patients (Starkstein et al., 1988). Establishing
a causal relationship between manic symptoms and a specific medical condition can be
difficult as to whether it is the cause or merely a precipitant. Neurological lesions are
commonly associated with symptoms that may be diagnosed or labeled as psychiatric.
Most of the early cases of secondary mania were associated with a lesion in the nondominant hemisphere (Robinson et al., 1988). There had been, however, an increasing
number of reports of secondary mania where the dominant left hemisphere in right-handed
people is involved (Liu et al., 1996; Fenn and George, 1999).
We report two patients with secondary mania following cerebral vascular lesions, which
highlight some of the issues in question. This succinct review emphasizes the conceptual
shifts and information that have guided our contemporary view of mania in old age.
2. Subjects and methods
This is a retrospective study of two patients with secondary mania following stroke.
Both were referred to the geriatrician because of their behavior. Both patients fulfilled the
DSM-III-R criteria for mania (American Psychiatric Association, 1987) as determined by a
clinical review. This broadly includes elevated mood, flight of ideas, rapid pressured
speech, impaired judgment, and decreased sleep amongst others. The inclusion criteria for
secondary mania were the satisfaction of the criteria of Krauthammer and Klerman (1978),
namely, the presence of elevated or irritable mood together with at least two of the
symptoms in the diagnosis of mania; symptoms duration of at least 1 week and no history
of affective disorder and confusion. Mania was subdivided into manic episode, hypomania,
mania with psychotic symptoms (hallucinations or delusions both mood congruent), and
hypomania causing marked functional impairment but with no psychotic symptoms
(Treatment Proctocol Project, 1997). Bipolar disorder was characterized by episodes of
mania and depression that can last from days to months. Routine laboratory investigations
with a computed tomography (CT) scan of the brain had been done in both cases.
3. Results
3.1. Illustrative cases
A 72-year-old right-handed housewife presented with symptoms of elevated mood
and disinhibition with a past history of an embolic cerebral artery infarction in the

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territory of the left middle cerebral artery 3 years earlier. The family had noticed a gradual
change in her mental state and was having difficulties coping with her disruptive behavior.
She had no previous history of mental illness and prior to the stroke she had been in good
health apart from hypertension and dyslipidemia.
Three years ago she had presented with isolated global dysphasia without
hemiparesis. She was unable to understand and could not answer simple questions. A
CT of the brain at the time revealed a hypodense area in the left insular region and
parietal lobe consistent with recent infarction in the middle cerebral artery territory.
As she was in atrial fibrillation, this incident was presumed to be cardio-embolic in
origin and she was anticoagulated. The echocardiography demonstrated normal left
ventricular size and function with no evidence of mural thrombus. The carotid Doppler
revealed no significant disease. She had markedly elevated serum cholesterol.
She recovered over the next 10 days and was discharged with mild reduction in her
speech fluency. Although her comprehension appeared normal, difficulties still
existed with word-finding as well as in writing both spontaneous and in response to
dictation.
She was next seen about 2.5 years later after the initial event complaining of fatigue
and discomfort in her left arm. She had been reasonably well but for an episode 4
months earlier when it was noticed that she was pale, vague and complained of a
feeling of numbness of her left arm. CT scan of the brain had shown no new changes
and neurological examination had revealed neither focal nor lateralizing signs
and she recovered within a day. It was about this time that her family first began to
notice subtle changes in her behavior. During this visit it was reported that she had
fluctuations in her mood ranging from apathy to elation. She had been sleeping poorly
and occasionally exhibited irritability, which was not a feature of her premorbid
personality. Pressured speech was noted with normal comprehension. Cognitive testing
using Mini-Mental State Examination (MMSE) (Folstein et al., 1975) revealed a score
of 25/30.
A year later her condition had worsened and the main problems appeared to be related to
changes in her behavior and mood. She was able to perform all activities of daily living but
was found to be impulsive and stubborn with pressured speech sand incoherency as well as
aimless wandering with annoying behavior and resistant to suggestions. Her mood
fluctuated from low flat to one of elation. Neurological examination was unremarkable.
Her symptoms were suggestive of hypomania.
Four months later her condition continued to worsen with deterioration in her ability to
care for herself. She was found to be unkempt and untidy with reports of wearing the same
soiled clothes repeatedly and poor personal hygiene. She was often agitated and verbally
aggressive at times. When seen for review she was found to be extremely cheerful to the
point of euphoria with overtalkativeness and pressured speech. Her stream of thought was
rapid with flight of ideas. The MMSE once again revealed a score of 25/30 part of which
may have been due to residual language difficulties following her initial stroke. Repeated
CT scan of the brain showed the same hypodense area in the left frontoparietal area with
negative mass effect and ex-vacuo dilatation of the ventricular system (Fig. 1a and b). She
was commenced on an atypical antipsychotic olanzapine and subsequently referred to a
psychiatrist.

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Fig. 1. (a) CT scan of the brain showing an infarction in the territory of the left middle cerebral artery involving
the frontal insula cortex and parietal regions. (b) CT scan showing ex-vacuo dilatation of the ventricles in the left
hemisphere secondary to long standing infarction.

A right-handed 80-year-old man was seen because of his behavior. His background
included hypertension and ischemic heart disease (triple vessel disease with normal
ventricular function) over 10 years culminating in coronary artery bypass grafting. Perioperatively he had suffered a cerebrovascular accident.
He was a lifelong non-smoker and a non-drinker. He had no allergies and was not a
diabetic and had normal blood cholesterol levels. He had no history of mental illness or
earlier stroke. Family history was positive for heart disease but negative for psychiatric or
dementing illnesses.
He had a left-sided weakness, a left homonymous hemianopia, and significant left-sided
neglect. His moods ranged from one of amiability to frank hostility. He struck out at the
nurses. He had visual hallucinations (seeing spiders and skinned chickens hanging on
the wall). He screamed loudly day and night and slept poorly and was demanding. His
memory for recent and past events was normal. He displayed verbal hyperactivity
and pressured speech. He was agitated, verbally aggressive and had no insight into his
behavior. He was impulsive and demonstrated emotional lability. Subsequently, he had
post-stroke central pain and post-stroke seizures. He had been treated with antidepressants,
antipsychotics, anti-epileptics, and benzodiazepines and the medications included
risperidone, haloperidol, thioridazine, clonazepam, temazepam, diazepam, and phenytoin
with varying effect.
CT scan of the brain showed a large infarction in the right posterior cerebral artery
territory extending from the occipital lobe to the thalamus and the genu of the internal
capsule (Fig. 2a). There were other cerebral infarcts (i) in the anterior deep border zone in
the right hemisphere and (ii) a small hypodense area in the anterior deep border zone in
the left hemisphere both at the level of the centrum semiovale (Fig. 2b), both due to
hemodynamic compromise during surgery.

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Fig. 2. (a) CT scan of the brain showing a large infarction in the territory of the right posterior cerebral artery
involving the right occipital lobe and extending to the thalamus and genu of the internal capsule. (b) CT scan of the
brain showing deep border zone infarcts in the right hemisphere and a smaller one in the left.

4. Discussion
Shulman and Herrmann (1999) indicated three broad groups of manic syndromes in old
age, namely (i) middle-age-onset depressives who after a latency of several years convert to
bipolarity; (ii) mixed-aged bipolar patients; and (iii) late-onset mania (LOM) in association
with a heterogenous group of neurological disorders. Both patients in this study satisfied
the criteria for secondary mania after Krauthammer and Klerman (1978). Several
neurological conditions have been correlated with secondary mania. There is now a
growing awareness of the influence of vascular-based LOM lending support to LOM as a
distinct vascular subtype. The ‘‘vascular syndromes’’ are the most distinctive and can be
caused by cerebral infarction (including silent cerebral infarction (SCI)), transient
ischemic attack (TIA), and small vessel disease. In general 30–50% of stroke patients
develop major and minor depressive disorders (Starkstein and Robinson, 1989). Fujikawa
et al. (1993) studied the incidence of SCI in patients with major depression and found
half the cases of late-onset mania to be secondary mania related to SCI and often
associated with larger areas of brain damage as compared with late-onset depression
(Fujikawa et al., 1995).
Cassidy and Carroll (2002) have recently focused on vascular factors in secondary
mania and published a retrospective review of 366 bipolar patients, in particular
looking at the age of onset and histories of vascular disease and risks including
cholesterol levels. They noted a bipolar distribution in first age of onset for mania with
an intermode of age 47. Using this age as a cut-off early onset mania comprised of
93.7% of the group whereas LOM (age > 47 years) made up 6.3%. This cut-off age also
agreed with that proposed by Krishnan et al. (1997) for late mania with onset age >50
years. This bimodal distribution provides further evidence that secondary mania is a
distinct clinical entity.

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With post-stroke mania the strongest association is with lesions in the right hemisphere.
Major depression is said to be more frequent with left anterior lesions (frontal or basal
ganglia), whereas minor depression occurs with either right or left parietal-occipital lesions
(Starkstein and Robinson, 1989). Post-stroke mania, however, is associated with right
hemispheric lesions, which have connections with the frontal lobes (Starkstein and
Robinson, 1989). But others (House et al., 1990; De Haan et al., 1995) found no difference
between right and left hemispheric stroke in the association between mood symptoms and
lesion location. There are also a growing number of reports of secondary mania following
left hemispheric stroke (Herlihy and Herlihy, 1979; Jampala and Abrams, 1983; Starkstein
et al., 1988; Turecki et al., 1993; Lui et al., 1996; Fenn and George, 1999). Case 1 in this
study demonstrated mania following a dominant hemispheric infarct as evidenced by the
global dysphasia she displayed at the time of her stroke.
Among reported cases mania may occur concomitantly with the stroke as in Case 2
or may be delayed for up to 2 years (Starkstein et al., 1988) or even up to 3–5 years or
more (Oyewumi and Lapierre, 1981; Shukla et al., 1987). In Case 1 there appeared to be
an interval of at least 2.5 years after the initial insult, but it is possible that the
symptoms of mania emerged after the possible transient ischemic attack. It is known
that patients with clinically silent unilateral subcortical lesions may develop
neurobehavioral deficits after suffering a new, often contralateral lesion (Gold et al.,
1997). A lesion may not be able to produce secondary mania by itself but may
predispose to activation of secondary mania after a second lesion, or a stressful life
event. Thus, it is possible that both hemispheres contributed to the emergence of mania
in Case 1. Case 2 had bihemispheric lesions but the one on the right involving the
territory of the posterior cerebral artery was the largest.
Case 2 had visual hallucinations and also a left-sided hemianopia and very often in
patients a causal relationship between visual hallucinations and visual field defects had
been recognized. The right hemisphere is said to have a certain degree of predominance in
this occurrence (Lhermitte, 1983). Kolmel (1985), however, did not find any predilection of
one hemisphere for patients with complex visual hallucinations experienced in the
hemianopic field. Peduncular hallucinosis characterized by visual hallucinations of
brightly colored objects arising from posterior cerebral artery occlusion but the exact
location of the lesion remains unclear. The former seem to be a more likely explanation and
it is unlikely that it is related to the mania.
The lesions in secondary mania following stroke are in the limbic or limbic-connected
areas (orbito-frontal, basotemporal cortex, head of caudate and thalamus), but secondary
mania has been reported after ventral pontine infarction in two patients involving the left
side in one and the right in the other (Drake et al., 1990). Cummings (1985) reviewed
reported cases and noted that mania was similar to orbito-frontal syndrome and could be
caused by lesions in the thalamus or orbito-frontal regions. Starkstein et al. (1991) found
that the main areas involved were the limbic or limbic-related areas, right orbito-frontal,
basotemporal, and basal ganglia regions all of which have frontal connections.
Bogousslavasky et al. (1988) suggested that a manic-like syndrome could be produced
by a thalamic lesion causing an ipsilateral frontal dysfunction via deafferentation. This
dysfunction manifested as hypoperfusion of the frontal lobe imaged by cerebral SPECT.
Case 2 in this study had involvement of the thalamus and the genu of the internal capsule

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resulting from a posterior cerebral artery territory infarct. The polar region and the
paramedian territory are massively connected to the frontal structures. A capsular genu
infarct could interrupt the inferior and anterior thalamic peduncles resulting in functional
deactivation of the ipsilateral frontal cortex (Tatemichi et al., 1992). All the lesions were
located in the right hemisphere.
The lesions that have been described with mania following left hemispheric stroke were
in the fronto-temporal, frontal, temporal, and basal ganglia regions (Turecki et al., 1993).
Starkstein et al. (1991) indicated that patients with right subcortical lesions tend to develop
bipolar disorder whilst right cortical lesions tend to develop unipolar mania. Turecki et al.
(1993) described a patient with bipolar disorder following a left basal ganglia infarction
and Liu et al. (1996) a left temporal infarction. It is well known that the left medial
thalamus and paramedian territory (Sandson et al., 1991; Nagaratnam et al., 1999) and left
polar thalamic regions (Clarke et al., 1994) are massively connected to the frontal
structures and that their damage may result in frontal lobe dysfunction.
Attention has been drawn to the clear resemblance of mania to the disinhibition syndrome
(Shulman, 2004). Lesions in specific brain areas could give rise to disinhibition syndromes
ranging from inappropriate social behavior or full blown mania and a significant association
between disinhibition syndromes and dysfunction of the orbito-frontal and basotemporal
cortices of the right hemisphere had been demonstrated (Starkstein and Robinson, 1997).
Nearly all lesions producing disinhibition syndromes and secondary mania have involved the
right hemisphere (Steffens and Krishnan, 1998). In two studies of five and six patients,
respectively, with sexually-related behaviors (Nagaratnam et al., 1998a; Nagaratnam and
Gayagay, 2002) following stroke, all had two or more of the core features of mania, namely,
elated mood, aggression, irritability and hostility, decreased sleep, impulsive behavior,
overtalkativeness, restlessness, and increased activity, increased sexual activity, and activity
with poor attention. Their ages ranged from 54 to 91 years with a mean of 73 years. All were
males but one. The lesions were located in the left putamen (2), right parieto-temporal (2),
right parietal (1); right thalamus (1), left orbito-frontal (2), left dorso-lateral (1), left
mesencephalo-thalamic (1), and bilateral lesions in one, with right posterior cerebral artery
territory infarction and left middle cerebral artery infarction. The cerebral components of
secondary mania and disinhibition syndromes are, thus, very similar.
Alexander et al. (1986) proposed five segregated circuits and each circuit linked the
striatum, globus pallidus, substantia nigra, and the thalamus with topographically organized
divisions of the frontal cortex. Involvement of the orbitofrontal circuit gives rise to
tactlessness, disinhibition, and impulsivity. A relationship between basal ganglia and the
frontal cortical areas was proposed by De Long and Georgepolous (1979) through a concept of
‘‘motor’’ and ‘‘complex’’ loops. Several functions mediated by both hemispheres interact with
the limbic system. The limbic system has dense projections to the basal ganglia creating an
integrated limbic-cortical system that mediates mood, motivation, and motion (Nauta, 1982).
The limbic system particularly the amygdala, hypothalamus, septum, and mesencephalon
together with the reticular formation with frontal cortical interaction control a person’s
emotional behavior (Nauta, 1982). It is well accepted that the limbic system and the temporal
lobe are closely related to a number of psychological syndromes. Secondary mania occurs
with lesions affecting the orbitofrontal-subcortical circuit (Cummings and Mendez, 1984;
Starkstein et al., 1987). Lesions of the temporobasal regions including the amygdala and

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temporal stem also produce mania. It could be asked how similar neuroanatomical
changes could give rise to syndromes whose features are not uniform. According to
Cummings (1985), the occurrence of different psychological syndromes could be influenced
by several factors such as genetic constitution, age of onset, personality characteristics, early
life experiences, and exact location and extent of the lesion amongst others. Subcortical
lesions involving the thalamus and the caudate tend to produce a bipolar type of mood disorder
whereas lesions of the cortex produce mania and are not followed by a cyclic mood disorder
(Starkstein et al., 1991).
Several transmitters and modulators are involved in the fronto-subcortical circuits. It has
been postulated that the mechanism by which these lesions give rise to an affective disorder
is due to functional excess of neurotransmitters including dopamine and noradrenaline
rather than the direct anatomical damage caused by the lesions. It is well known that several
transmitters contribute to the efficiency of a specific brain area and it seems that there may
be more than one transmitter involved with many cases of secondary mania. This may be
the reason why there is no single effective therapeutic agent.
Overall the character of the symptoms is better defined by the location rather than the
particular neurotransmitter. For instance, left anterior lesions (frontal, basal ganglia) give
rise to major depression whereas minor depression occurs with right or left parietooccipital lesions (Fenn and George, 1999), obsessive-compulsive behaviors with bilateral
basal ganglia (Laplane et al., 1989), and pathological crying and laughing with bihemispheric or other lesions (Nagaratnam et al., 1998b). In secondary mania there is a
strong association with orbitofrontal (Cummings, 1985; Starkstein et al., 1991) basal
ganglia (Fenn and George, 1999), thalamus (Bogousslavasky et al., 1988), frontotemporal,
and temporal lesions (Liu et al., 1996).
In conclusion, there is substantial evidence to emphasize that secondary mania is a
distinct clinical entity. The current state of our knowledge has created a certain stability on
the consensus that the concept of secondary mania is well founded. Although nearly all
lesions producing secondary mania and disinhibition syndromes involved the right cerebral
hemisphere they can also be produced by left hemispheric lesions. The cerebral
components of secondary mania and disinhibition syndromes are very similar and it is
proposed that disinhibition syndromes, secondary hypomania, and secondary mania with
psychotic symptoms are simply a continuum of severity of mood disorder and secondary
mania may be an extreme form. Lesion location appears to play a critical role in the
development of secondary mania and disinhibition syndromes.

References
Alexander, G.E., De, Long., Strick, P.L., 1986. Parallel organization of functionally segregated circuits linking
basal ganglia and cortex. J. Neurosci. 9, 357–381.
American Psychiatric Association, 1987. Diagnostic and Statistical Manual of Mental Disorders, third ed.
(revised). American Psychiatric Association, Washington, DC.
Bogousslavasky, J., Ferrazzini, M., Regli, F., Assal, G., Tanabe, H., Delaloye-Bischof, A.M., 1988. Manic
delirium and frontal-like syndrome with paramedian infarction of the right thalamus. J. Neurol. Neurosurg.
Psychiatry 51, 116–119.
Cassidy, F., Carroll, B.J., 2002. Vascular risk factors in late onset mania. Psychol. Med. 32, 359–362.

N. Nagaratnam et al. / Archives of Gerontology and Geriatrics 43 (2006) 223–232

231

Clarke, S., Assal, G., Bogousslavsky, J., Regli, F., Townsend, D.W., Leenders, K.L., Blecic, S., 1994. Pure amnesia
after unilateral left polar thalamic infarct. Topographic and sequential neurophysiological and metabolic
(PET) correlations. J. Neurol. Neurosurg. Psychiatry 57, 27–34.
Cummings, J.L., 1985. Organic delusions, phenomenology, anatomical evaluation and review. Br. J. Psychiatry
146, 184–197.
Cummings, J.L., Mendez, M.F., 1984. Secondary mania with focal cerebrovascular lesions. Am. J. Psychiatry 141,
1084–1087.
De Haan, R.J., Limburg, M., Van der Meulen, J.H.P., Jacobs, H.M., Aaronson, N.K., 1995. Quality of life after
stroke: impact of stroke type and lesion location. Stroke 26, 402–408.
De Long, H.R., Georgepolous, A.P., 1979. Motor functions of the basal ganglia as revealed by studies of single cell
activity in the behaving primate. Arch. Neurol. 24, 131–140.
Drake Jr., M.E., Pakalnis, A., Phillips, B., 1990. Secondary mania after ventral pontine infarction. J. Neuropsychiatry Clin. Neurosci. 2, 322–325.
Fenn, D., George, K., 1999. Post-stroke mania late in life involving the left hemisphere. Aust. N.Z. J. Psychiatry
33, 598–600.
Folstein, H.Y., Folstein, E.E., McHugh, P.P., 1975. Mini-Mental State: a practical method of grading the cognitive
state of patients for the clinician. J. Psychiatr. Res. 12, 189–198.
Fujikawa, T., Yamawaki, S., Touhouda, Y., 1993. Incidence of silent cerebral infarction in patients with major
depression. Stroke 24, 1631–1634.
Fujikawa, T., Yamawaki, S., Touhouda, Y., 1995. Silent cerebral infarctions in patients with late-onset mania.
Stroke 26, 946–949.
Gold, M., Nadeau, S.E., Jacobs, D.H., Adair, J.C., Rothi, L.J., Heilman, K.M., 1997. Adynamic aphasia: a
transcortical motor aphasia with defective semantic strategy formation. Brain Lang. 57, 374–393.
Herlihy Jr., C.E., Herlihy, C.E., 1979. Lithium and organic brain syndrome. J. Clin. Psychiatry 40, 455 (Letter to
the Editor).
House, A., Dennis, M., Warlow, C., Hawton, K., Molneux, A., 1990. Mood disorders after stroke and their relation
to lesion location: a CT scan study. Brain 113, 1113–1129.
Jampala, V.C., Abrams, R., 1983. Mania secondary to left and right hemispheric damage. Am. J. Psychiatry 140,
1197–1199.
Kolmel, H.W., 1985. Complex visual hallucinations in the hemianopic field. J. Neurol. Neurosurg. Psychiatry 48,
21–38.
Krauthammer, C., Klerman, G.L., 1978. Manic syndromes associated with antecedent physical illness or drugs.
Arch. Gen. Psychiatry 35, 1333–1339.
Krishnan, K.R.R., Hars, J.C., Blazer, D.G., 1997. MRI-defined vascular depression. Am. J. Psychiatry 154, 497–
501.
Laplane, D., Levasseur, M., Pillon, B., Dubois, B., Baulac, M., Mazoyer, B., Tran Dinh, S., Sette, G., Danze, F.,
Baron, J.C., 1989. Obsessive-compulsive and other behavioral changes with bilateral basal ganglia lesions. A
neuropsychological, magnetic resonance imaging and positron tomography study. Brain 112, 699–725.
Lhermitte, F., 1983. Utilization behavior and its relation to lesions of the frontal lobe. Brain 6, 237–255.
Liu, C.Y., Wang, S.J., Fuh, J.L., Yang, Y.Y., Liu, H.C., 1996. Bipolar disorder following a stroke involving the left
hemisphere. Aust. N.Z. J. Psychiatry 30, 688–691.
Nagaratnam, N., Gayagay, G., 2002. Hypersexuality in nursing care facilities—a descriptive study. Arch.
Gerontol. Geriatr. 35, 195–203.
Nagaratnam, N., Tse, A., Lim, R., Chowdhury, M., 1998a. Aberrant sexual behavior following stroke. Eur. J. Int.
Med. 9, 207–209.
Nagaratnam, N., Wong, V., Jeyaratnam, D., 1998b. Left anterior choroidal artery infarction and uncontrollable
crying. J. Stroke Cerebrovasc. Dis. 7, 263–264.
Nagaratnam, N., McNeill, C., Gilhotra, J.S., 1999. Akinetic mutism and mixed transcortical aphasia following
infarction of the left sided medial thalamus. J. Neurol. Sci. 163, 70–73.
Nauta, W.J.H., 1982. Limbic innervation of striatum. In: Friedhoff, A.J., Chase, T.N. (Eds.), Gilles de la Tourette
Syndrome. Raven Press, New York, pp. 41–48.
Oyewumi, I.K., Lapierre, Y.D., 1981. Efficacy of lithium in treating mood disorder occurring after brain stem
injury. Am. J. Psychiatry 138, 110–121.

232

N. Nagaratnam et al. / Archives of Gerontology and Geriatrics 43 (2006) 223–232

Robinson, R.G., Boston, J.D., Starkstein, S.E., Price, T.C., 1988. Comparison of mania and depression after brain
injury: casual factors. Am. J. Psychiatry 145, 172–178.
Sandson, T.A., Daffner, K.R., Carvalho, P.A., Mesulam, M., 1991. Frontal lobe dysfunction following infarction of
the left-sided medial thalamus. Arch. Neurol. 48, 1300–1303.
Shukla, S., Cook, B.L., Mukerjee, S., Goodwin, C., Miller, M.G., 1987. Mania following head trauma. Am. J.
Psychiatry 144, 93–96.
Shulman, K.I., 2004. Mania in old age: a neuropsychiatric syndrome. Geriatrics Aging 7, 34–37.
Shulman, K.L., Herrmann, N., 1999. The nature and management of mania in old age. Psychiatr. Clin. N. Am. 22,
649–663.
Starkstein, S.E., Robinson, E.R., 1989. Affective disorders in cerebrovascular disease. Br. J. Psychiatry 154,
170–182.
Starkstein, S.E., Robinson, R.G., 1997. Mechanism of disinhibition after brain lesions. J. Nerv. Ment. Dis. 185,
108–114.
Starkstein, S.E., Pearlson, G.B., Bosh, J., Robinson, R.G., 1987. Mania after brain injury: controlled study of
causative factors. Arch. Neurol. 44, 1064–1073.
Starkstein, S.E., Boston, J.D., Robinson, R.G., 1988. Mechanisms of mania after brain injury: 12 cases reports and
review of the literature. J. Nerv. Ment. Dis. 176, 87–100.
Starkstein, S.E., Fedoroff, P., Berthier, M.L., Robinson, R.G., 1991. Manic depressive and pure manic states after
brain lesions. Biol. Psychiatry 29, 149–158.
Steffens, D.C., Krishnan, K.R.R., 1998. Structural neuroimaging and mood disorders. Recent findings, implications for classification, and future directions. Biol. Psychiatry 43, 705–712.
Tatemichi, T.K., Desmond, D.W., Prohovnik, I., Cross, D.T., Gropen, T.I., Mohr, J.P., Stern, Y., 1992. Confusion
and memory loss from capsular genu infarction: a thalamocortical disconnection syndrome? Neurology 42,
1966–1979.
Treatment Proctocol Project, 1997. Management of Mental Disorders, vol. 1, second ed. Sydney, World Health
Organisation Collaborating Centre for Mental Health and Substance Abuse, pp. 193–207.
Turecki, G., De Mari, J., Porto, J.A.D., 1993. Bipolar disorder following a left basal ganglia stroke. Br. J.
Psychiatry 163, 690.