Observations placeholder

Dusunen Adam The Journal of Psychiatry and Neurological Sciences 2016;29:79-84
DOI: 10.5350/DAJPN2016290109
Address reprint requests to / Yazışma adresi:
Erhan Akinci,
Buca Seyfi Demirsoy State Hospital, 
Departrment of Psychiatry, Ozmen Caddesi, 
No: 145, Buca Merkez/Izmir, Turkey
Phone / Telefon: +90-232-444-3508 
E-mail address / Elektronik posta adresi:
turcica@hotmail.com 
Date of receipt / Geliş tarihi:
February 24, 2015 / 24 Şubat 2015
Date of the first revision letter /
İlk düzeltme öneri tarihi:
April 10, 2015 / 10 Nisan 2015
Date of acceptance / Kabul tarihi:
June 28, 2015 / 28 Haziran 2015
INTRODUCTION
Nowadays, after cardiac diseases and cancer, stroke is the third largest cause for mortality. Despite a reduction of its incidence and mortality thanks to risk control over the last years, stroke is still one of the most important reasons for death (1). After stroke, a 
number of psychiatric conditions can be seen, such as depression, most of all, but also anxiety disorders, behavioral disorders, apathy, mania, and psychosis (2-4). Compared to other psychiatric presentations, mania and psychosis occur more rarely (4,5) (Table 1). 
Psychiatric complications developing after stroke affect not only the patient’s social life negatively, but impact on their entire quality of life and the rehabilitation process (6,7).  The relation between a cerebrovascular event and secondary psychosis was first described by Westphal in 1879. A 42-year-old male patient, developing left hemiplegia and left homonymous hemianopsia before his death, reported the sight of bright colors and hallucinations of a sword hanging above his head that might come down at any moment. Westphal described the aspect of the patient in that moment as “fixing his eyes on the ceiling as if he was seeing something 
scary”. At autopsy, brain atrophy and an involvement  of the posterior section of the right hemisphere were observed (8).
Physical and psychiatric symptoms developing after stroke show correlations with the affected brain regions (9,10). Anatomically, it has been established that stroke lesions in the temporoparietal/temporoparietooccipital 80 section, and particularly in the right rather than the left hemisphere, have a higher probability to lead to the development of secondary psychosis (11-13). In addition, psychosis cases with effects from the deep subcortical structures can be found in the literature (14-16). After stroke, a number of psychiatric disorders can develop, but psychosis is relatively rarely seen (9,16). Case reports about the development of psychosis 
after stroke are quite rare in the literature, and data about psychotic disorders related to stroke are limited (17).Aim of this report is to present a case of acutely developing tactile hallucinations, interpreted as delusional, after an infarction of the right middle cerebral 
artery (MCA) border region, and to discuss psychiatric presentations that may occur in relation to stroke in the 
light of information from the relevant literature.

CASE
H.O., a 61-year-old right-handed man, was 
admitted to the emergency room with complaints of 
forgetfulness and unusual behavior. After examination, 
the patient was admitted with a diagnosis of acute 
right MCA infarction. The patient provided written 
informed consent during his inpatient treatment.
Around 3 months earlier, the patient had suffered a 
transitory episode of dysmnesia while talking to his 
daughter on the phone, not remembering who she 
was. He described a moment of short-term confusion 
experienced the day before presenting to the hospital, 
while praying in the mosque: “I was praying in the 
mosque, and everyone was prostrating, but I was 
standing up; I was confused…”
It was learned that the following morning he had 
started to search for someone who had pushed him by 
his neck, trying to make him fall down, later pushing 
him on the stairwell in his own house. As the patient 
said: “That morning, it was as if someone put his hands 
on the back of my neck. I grabbed with my hand, as if I 
was holding his finger. I asked my wife ‘is there 
anyone?’” His family reported that the patient had 
opened the door of his house and was searching for 
someone on the staircase, angrily shouting “Someone 
pushed me from the bed to the ground”.
The patient was known to have suffered from 
hypertension for 10 years; he was regularly using 
irbesartan 300mg/day and hydrochlorothiazide 
12.5mg/day. No other disease was found, and the 
patient used neither alcohol nor any other psychoactive 
substance.
The patient was examined psychiatrically and 
neurologically. In the psychiatric examination, he 
appeared appropriate for his age, with sufficient selfcare and anxious affect. He showed full cooperation 
and orientation, speed and amount of speaking were 
normal, associations were linear and goal-directed. 
During the patient interview, occasional blocks in his 
speech were observed. Other than the acute tactile 
hallucination during the seizure and the subsequent 
delusional state, no further active psychotic signs were 
found in the patient. Abstract thinking was preserved 
and reasoning in the test complete.
In the neurological examination, the patient’s eyes 
were spontaneously open and aligned to the center 
Table 1: Neuropsychiatric presentations accompanying stroke (4,5)
Syndrome Prevalence Clinical signs
Depression 35% Depressive mood, reduced appetite, weight loss, insomnia, anergy, anhedonia, social withdrawal
Anxiety Disorder 25% Increased anxiety, unease, physical signs like palpitation, sweating, difficulties to concentrate or to fall asleep
Mania Rare Raised mood, reduced need to sleep, flight of ideas, increased speed and amount of speaking, grandiosity
Psychosis Rare Hallucinations and delusions
Apathy 20% Indifference and negligence (independent from depression)
Pathologic affect 20% Inappropriate laughing and crying attacks
Catastrophic reaction 20% Anxiety attacks developing in states of physical and cognitive inadequacy, crying, aggressive behavior, 
swearing, rejection and compensatory self-praise
Anosognosia 24% Denial of post-stroke deficits without concern 
81
Akinci E, Oncu F, Topcular B
Düşünen Adam The Journal of Psychiatry and Neurological Sciences, Volume 29, Number 1, March 2016
line. Other than a frust paresis in the right upper 
extremity, there were no motor deficits. Plantar 
responses were bilaterally flexor.
The patient’s laboratory tests (hemogram, 
biochemical tests and sedimentation) were normal.
In the diffusion brain MRI, a cortico-subcortical 
diffusion restriction at the level of the temporooccipital 
lobe in the upper section was observed, showing partly 
continuity towards the parietal lobe, consistent with 
acute infarction. The result was consistent with a 
border zone infarction (Figure 1).
Bilateral carotid and vertebral artery Doppler USG 
examination found multiple millimeter-thick local 
parietal fibrocalcific plaque formations in the carotid and 
its branches, which did not cause hemodynamic changes. 
With a diagnosis of acute ischemic cerebrovascular 
disease, the patient was started on antiaggregant and 
anticoagulant therapy. The antihypertensive treatment 
for the patient’s hypertension was continued. During 
monitoring, vital signs and clinical state appeared stable. 
At discharge, the patient’s self-care was assessed as 
good, his affect adequate, cooperation and orientation 
complete, association goal-directed, perception normal. 
The patient showed residual signs of an acute psychotic 
presentation developed secondarily to an ischemic 
attack; he still stated that the state experienced during 
the attack was real. Other than that, no active psychotic 
signs were found. Abstract thinking and test reasoning 
were evaluated as complete. Insight was partly present. 
DISCUSSION
While after stroke a number of neuropsychiatric 
disorders can be seen, especially depression, reports 
about acute psychotic attacks are quite rare in the 
literature (4,9).
While the risk of developing psychosis is higher in 
temporoparietooccipital lesions, secondary psychosis 
has also been reported with focal lesions in other brain 
regions. Depending on the localization of these lesions, 
differences in the psychotic presentation can be 
observed (9,11,18) (Table 2). Kumral et al. (19) did a 
study with 15 patients, reporting that the great majority 
of persecutory and jealousy-type delusions developing 
after stroke were related to the right posterior 
temporoparietooccipital region. 
In right hemisphere lesions, secondary psychosis is 
more likely to develop than in hemisphere lesions. This 
has been identified as a risk factor for secondary 
psychosis (13,25,26). Some sources, however, state 
that both right and left hemisphere lesions can result in 
psychotic symptoms (27,28).
Generally, a strong correlation is found between the 
lateralization of the lesion and the related 
neuropsychiatric clinical presentations. Cases of mania 
and alexithymia almost always have right hemisphere 
lesions. Anxiety, sexual behavior disorder, dissociative 
state and palinopsia cases are reported to show isolated 
right hemisphere or bilateral rather than isolated left 
Figure 1: Cranial MRI consistent with border zone infarction
82 Düşünen Adam The Journal of Psychiatry and Neurological Sciences, Volume 29, Number 1, March 2016
Tactile hallucination and delusion following acute stroke: a case report
hemisphere lesions. Visual hallucinations and 
psychosis cases have been reported equally for both 
hemispheres (18). Cutting (25) proposed the hypothesis 
that there are similarities between right hemisphere 
lesions and psychosis, and that schizophrenia might 
primarily be a right-brain dysfunction. However, some 
researchers assert that in schizophrenia, a dysfunction 
is evident in the left hemisphere or in both, rather than 
on the right side (29,30).
Rabins et al. (26) report temporoparietal lesions in 
five cases with post-stroke atypical psychosis, 
accompanied by subcortical atrophy. Subcortical 
atrophy and right hemisphere lesions have been 
reported as risk factors for psychosis. Some sources 
have claimed that only the anatomical localization of 
the lesion alone may not be sufficient to explain the 
psychosis and that lesion-related seizures might 
increase the probability for the development of 
psychosis. Levine and Finklestein (32) reported that in 
seven out of eight cases with right temporoparietal 
stroke or traumatic injury psychosis occurred together 
with a seizure. As a hypothesis, it may be thought that 
the lesion region causes continuous electrical activity, 
thus constituting the organic substrate for the 
psychotic phenomenon (16). The association between 
post-lesion seizure and acute psychosis is important 
for the diagnosis and the therapeutic process of the 
disease.
It is still not precisely known how focal lesions in 
which regions constitute what kind of psychotic 
presentations. In our case, it can be assumed that an 
ischemic lesion in the right MCA border irrigation area 
involving the right temporoparietooccipital region 
triggered the patient’s acute psychotic presentation.
The inadequacy of today’s approaches to 
psychiatric diagnostic systems shows that we still need 
a better understanding of the pathophysiology of 
psychiatric diseases. A broader collaboration between 
neurology and psychiatry may point a way towards an 
understanding of a number of neuropsychopathologies 
still waiting for an explanation (33). In conclusion;
1. After a stroke, a number of psychiatric 
presentations can develop, first of all depression. 
Depending on localization, different clinical 
presentations can be seen.
2. Psychotic symptoms are rarely seen after stroke. 
The likelihood of psychotic symptoms is higher with 
right hemisphere temporoparietooccipital lesions. 
However, with other localizations, especially in deep 
subcortical structures, psychosis can also be seen.
3. A good understanding of the psychiatric signs 
accompanying focal brain lesions can provide 
important hints for an understanding of the organic 
reasons for psychiatric diseases.
4. After stroke, seizures can be seen and related 
neuropsychiatric presentations can occur. This 
condition may affect diagnosis and treatment process 
of the disease.
Table 2: Cases of cerebrovascular lesions and accompanying psychotic presentations
Author Psychotic Presentations Localization of Lesion
Kumral and Ozturk, 2004 (19) Jealousy or persecutory or somatic delusions Mostly lenticular, thalamic, and medullar lesions in the right
posterior temporoparietooccipital cortex
Nagaratnam and O’Neile, 2000 (20) Tactile hallucinations and bizarre delusions Left temporoparietooccipital ischemic stroke
Beniczky et al., 2002 (21) Complex visual and tactile hallucinations Right temporoparietooccipital ischemic stroke
Narumoto et al., 2005 (22) Persecutory delusions Bilateral caudate ischemic infarction (caput caudatum lesion)
Nye and Arendts, 2002 (23) Episodic olfactory hallucinations Hemorrhagic left uncus lesion
Berthier and Starkstein, 1987 (24) Sporadic auditory and sensory hallucinations 
accompanied by complex visual hallucinations
Reduplicative paramnesia
Wide right frontotemporoparietal ischemic infarction
Barboza et al., 2013 (17) Delayed persecutory-type delusion Right frontotemporoparietal lesion
Peroutka et al., 1982 (31) Complex hallucinations and delusions Right temporoparietooccipital lesion
Levine and Finklestein, 1982 (32) Delayed psychosis: Hallucinations and in some
cases delusions and agitation
Right temporoparietooccipital lesion
83
Akinci E, Oncu F, Topcular B
Düşünen Adam The Journal of Psychiatry and Neurological Sciences, Volume 29, Number 1, March 2016
Conflict of Interest: Authors declared no conflict of Interest.
Financial Disclosure: Authors declared no financial support.
REFERENCES
1. Broderick JP, Phillips SJ, Whisnant JP, O’Fallon WM, Bergstralh 
EJ. Incidence rates of stroke in the eighties: the end of the decline 
in stroke? Stroke 1989; 20:577-582. [CrossRef]
2. Carota A, Staub F, Bogousslavsky J. Emotions, behaviours and 
mood changes in stroke. Curr Opin Neurol 2002; 15:57-69. 
[CrossRef]
3. Dilbaz N. Neuropsychiatric and pathophysiological results of 
acute stroke. Klinik Psikiyatri Dergisi 2001; 4:166-174.
4. Chemerinski E, Robinson RG. The neuropsychiatry of stroke. 
Psychosomatics 2000; 41:5-14. [CrossRef]
5. Robinson RG, Starkstein SE. Cerebrovascular Disease. In 
Bourgeois JA, Hales RE, Young JS, Yudofsky SC (editors). 
The American Psychiatric Publishing Board Review Guide for 
Psychiatry. First Ed. Arlington: American Psychiatric Publishing 
Inc., 2009, 679-687.
6. King RB. Quality of life after stroke. Stroke 1996; 27:1467-1472. 
[CrossRef]
7. Clark MS, Smith DS. Abnormal illness behavior in rehabilitation 
from stroke. Clin Rehabil 1997; 11:162-170. [CrossRef]
8. Horrax G. Visual hallucinations as a cerebral localizing 
phenomenon: with especial reference to their occurrence in 
tumors of the temporal lobes. AMA Arch Neurol Psychiatry 
1923; 10:532-547. [CrossRef]
9. Almeida OP, Starkstein SE. Cerebrovascular Disease and 
Psychosis. In Sachdev SP, Keshavan MS (editors). Secondary 
Schizophrenia. Cambridge: Cambridge University Press, 2010, 
197-203. [CrossRef]
10. Birkett DP. The Psychiatry of Stroke. New York: The Haworth 
Press, 2008.
11. Starkstein SE, Robinson RG, Berthier ML. Post-stroke hallucinatory 
delusional syndromes. Neuropsychiatry Neuropsychol Behav 
Neurol 1992; 5:114-118.
12. Peroutka SJ, Sohmer BH, Kumar AJ, Folstein M, Robinson 
RG. Hallucinations and delusions following a right 
temporoparietooccipital infarction. Johns Hopkins Med J 1982; 
151:181-185.
13. Edwards-Lee T, Cummings JL. Focal Lesions and psychosis. 
Bogousslavsky J & Cummings JL (Ed), Behavior and mood 
disorders in focal brain lesions. Cambridge: Cambridge 
University Press 2000, 419-437.
14. Santos S, Alberti O, Corbalán T, Cortina MT. Stroke-psychosis. 
Description of two cases. Actas Esp Psiquiatr 2009; 37:240-242.
15. Kitabayashi Y, Narumoto J, Otakara C, Hyungin C, Fukui 
K, Yamada K. Schizophrenia-like psychosis following right 
putaminal infarction. J Neuropsychiatry Clin Neurosci 2006; 
18:561-562. [CrossRef]
16. Mishra NK, Hastak S. Poststroke hallucination delusion 
syndrome. J Neuropsychiatry Clin Neurosci 2008; 20:116. 
[CrossRef]
17. Barboza RB, De Freitas GR, Tovar-Moll F, Fontenelle LF. 
Delayed-onset post-stroke delusional disorder: a case report. 
Behav Neurol 2013; 27:287-291. [CrossRef]
18. Cummings JL. Neuropsychiatric manifestations of right 
hemisphere lesions. Brain Lang 1997; 57:22-37. [CrossRef]
19. Kumral E, Ozturk O. Delusional state following acute stroke. 
Neurology 2004; 62:110-113. [CrossRef]
20. Nagaratnam N, O’Neile L. Delusional parasitosis following 
occipito-temporal cerebral infarction. Gen Hosp Psychiatry 2000; 
22:129-132. [CrossRef]
21. Beniczky S, Kéri S, Vörös E, Ungureán A, Benedek G, Janka 
Z, Vécsei L. Complex hallucinations following occipital lobe 
damage. Eur J Neurol 2002; 9:175-176. [CrossRef]
22. Narumoto J, Matsushima N, Oka S, Shimizu H, Kooguchi Y, 
Kitabayashi Y, Kunizawa M, Ueda H, Fukui K. Neurobehavioral 
changes associated with bilateral caudate nucleus infarctions. 
Psychiatry Clin Neurosci 2005; 59:109-110. [CrossRef]
Contribution Categories Name of Author
Follow up of the case E.A., B.T.
Literature review E.A., F.O., B.T.
Manuscript writing E.A., F.O.
Manuscript review and revisation E.A., F.O., B.T.
84 Düşünen Adam The Journal of Psychiatry and Neurological Sciences, Volume 29, Number 1, March 201