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 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 inpatinet 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 self-care 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 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 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.

Conflict of Interest: Authors declared no conflict of Interest.

Financial Disclosure: Authors declared no financial support.

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