Post stroke mania

Post stroke mania DEFAULT

Post Stroke Mood Disorders

close up of a crying woman

Although stroke effects are unpredictable, mood disorders such as depression, anxiety and pseudo-bulbar affect are all too common. Studies suggest that simply having a stroke increases the risk of anxiety, depression or both. Research indicates that PBA is more common in survivors of brainstem stroke, but it can occur with other types of strokes too. Depression affects between one- and two-thirds of stroke survivors. It's characterized by feelings of overarching sadness, lack of pleasure in old activities or changes in eating and sleeping patterns. Anxiety occurs when a survivor focuses on worries and concerns. Anxiety affects about 20 percent of survivors. PBA is characterized by a mismatch between feelings and expression, like laughing at a funeral or crying at a joke.

It's not uncommon for survivors to experience all three mood disorders. The good news is that treatment is available. For depression and anxiety, one of the best treatments is counseling or therapy with a licensed mental health practitioner. Caregivers should encourage their loved ones to get assessed. If they're reluctant to see a mental health professional, they might be willing to see a pastor, priest or rabbi.

Here is a short breakdown of possible therapeutic approaches:

Solution Focused Therapy

SFT is future-focused and goal-directed, and centers on solutions instead of the problems that bring people to therapy. It’s also called Solution Focused Brief Therapy and Solution Building Practice Therapy.

Problem Solving Therapy

PST is a brief psychological intervention or “talking therapy” that’s typically four to eight sessions. Problems are identified through collaboration, and the therapist teaches the person a structured approach to solving them.

Cognitive Behavioral Therapy

CBT focuses on examining the relationships between thoughts, feelings and behavior. By exploring thought patterns that lead to self-destructive actions and the beliefs that direct them. The therapist and individual actively work together toward recovery.

Attitude and Commitment Therapy

ACT (also known as Acceptance and Commitment Therapy) teaches people to "just notice," accept and embrace their thoughts, feelings, sensations, memories and other private events (especially unwanted ones) instead of trying to better control them.

Interpersonal Therapy

IT focuses on interpersonal relationships by improving the way the depressed person communicates and relates. Techniques help the person identify emotions and their sources, express emotions in a healthy way and deal with emotional baggage from past relationships.

Mindfulness Therapy

MT (also called Mindfulness-Based Cognitive Therapy)  helps those who suffer repeated bouts of depression and chronic unhappiness. It combines the ideas of cognitive therapy with meditative practices and attitudes based on cultivating mindfulness. The goal is to become acquainted with the mental states that often characterize mood disorders while learning to develop a new relationship to them.

Sours: https://www.stroke.org/en/about-stroke/effects-of-stroke/emotional-effects-of-stroke/post-stroke-mood-disorders

Journal of Geriatric Medicine and Gerontology






Department of Family Medicine, University of New England College of Osteopathic Medicine, USA


*Corresponding author: Dr. Mehl-Madrona, Associate Professor, Department of Family Medicine, Eastern Maine Medical Center, Acadia Hospital, Coyote Institute, University of New England College of Osteopathic Medicine, USA, Tel: 808-772-1099, E-mail: [email protected]
J Geriatr Med Gerontol, JGMG-2-015, (Volume 2, Issue 2), Case Series; ISSN: 2469-5858
Received: May 02, 2016 | Accepted: September 10, 2016 | Published: September 12, 2016
Citation: Mehl-Madrona L (2016) Post-Sroke Mania: A Case Series in a Rural, Community Hospital. J Geriatr Med Gerontol 2:015. 10.23937/2469-5858/1510015
Copyright: © 2016 Mehl-Madrona L, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Abstract

Background and purpose: Post-stroke mania is thought to be rare, and has been described after lesions in the territory of the left medial cerebral artery, biparietal cortex, and the left putamen.

Methods: Case-study methodology was used to identify similarities and difference among six cases of post-stroke mania in a rural, community hospital over 1 year.

Results: All patients had pre-existing moderate levels of small vessel occlusive disease and two had confirmed lacunar infarcts in the basal ganglia, while one had a small left sided fronto-parietal infarct consistent with the dysarthria-clumsy hand syndrome. Stroke was not initially recognized among these patients due to the absence of acute CT findings. Patients without pre-existing psychiatric diagnoses responded to low dose quetiapine. Two patients with pre-existing diagnoses of depression and anxiety, required higher doses.

Conclusions: Post-stroke mania may be under-appreciated due to the subtle neurological findings inherent to basal ganglia and/or lacunar infarcts in other locations. Acute CT is not reliable enough to confirm the diagnosis of stroke which may allow many of these cases to be missed.


Keywords

Post-stroke mania, Small vessel disease, Cerebrovascular disease


Introduction

Mania rarely occurs for the first time in late life [1]. A systematic review found only 74 reported cases of adult stroke patients with mania symptoms in the last 50 years, suggesting that mania is a rare consequence of stroke [2]. When it does occur, it often presents atypically with a mixture of manic, dysphoric, and cognitive symptoms and less euphoria than is seen in younger, more typical cases [3]. Increased cerebral vulnerability due to stroke or head trauma play a stronger role than life events in precipitating late-onset mania among the elderly [3,4]. The most relevant findings on imaging in late onset mania are silent cerebral infarctions and subcortical lesions [5]. Secondary mania has been documented in 17 to 43% of manic cases in the elderly and has been associated with a higher prevalence of cerebral organic disorders [6] especially cerebrovascular disease [7], dementia [8], space occupying lesions, infections, and head injuries. Post-stroke depression is the most common psychiatric disorder following stroke, but mania has been reported [9].


Materials and Methods

We reviewed 6 cases of mania in elderly patients followed cerebrovascular events from our geriatric medicine consultation service over the course of 1 year. We summarize the similarities and differences among these cases and with others reported in the literature using the case report methodology of Kratochwill and Levin [10].


Results

Case 1

A 79-year-old female was calling 911 repeatedly from her hospital room, multiple local police departments with requests for action on their part, and multiple family members all night long. This was new behavior. The hospital operator had turned off her extension to prevent further calling. She had been treated for depression and anxiety, but never for bipolar disorder. She had known arteriosclerotic cardiovascular disease, hypertension, and hypercholesterolemia. She met DSM-5 criteria for mania. She was highly irritable with pressured speech. She had difficulty listening and launched into a new topic before her prior topic could be addressed. She was angry that family members were avoiding her, and that her rights had been violated by the operators' turning off her telephone. She thought a conspiracy was preventing the police from doing her bidding. On physical examination, she had subtle weakness of her right hand. She could not resist pressure to bring her outstretched fingers together. She had mild asymmetry of her mouth and nasolabial fold and was slightly dysarthric, which became more apparent the more rapidly she spoke. Balance on the right leg was unsteady compared to the left. Tandem gait was mildly unstable. She demonstrated increased nystagmus on lateral gaze. FLAIR MRI showed diffuse and extensive per ventricular small vessel occlusive disease with a recent lacunar infarct in the left basal ganglia (in our rural setting, we did not have access to DWI MRI studies). Her findings were consistent with the dysarthria-clumsy hand syndrome. Two months prior to the hospital admission, she had experienced increased difficulty with balance and speech, followed seven weeks later (one week prior to admission) by the acute onset of manic symptoms. Believing that we had encountered a post-stroke mania, we started 25 mg of quetiapine b.i.d., progressively increasing it to 100 mg b.i.d., at which point she no longer wanted to call police departments, family members at odd hours of the night, or to make excessive demands of the nursing staff. She was discharged on a once daily dose of 200 mg. She went to an assisted living facility, at which the staff physician stopped her quetiapine (reason undocumented), and her problematic behavior resumed. She was brought to see us as an outpatient by her family, who believed the quetiapine had greatly helped her and wanted her middle of the night calls to stop again. We resumed the quetiapine at the 200 mg dose and within one week, the problem behaviors had resolved. One year later, she continues on the same dose of quetiapine without the return of these behaviors.


Case 2

An 85-year-old retired nurse was admitted to the hospital after a fall. She was talking rapidly and continually, and not sleeping. She was incoherent. She had been diagnosed with minor neurocognitive disorder (mild cognitive impairment) using the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) three years previously, and had managed in her own home on her own with a daughter who lived nearby and checked on her at least every other day. Her daughter helped in managing finances and shopping. She had arteriosclerotic cardiovascular disease, hypertension, and hypercholesterolemia. A head CT from one year previous revealed moderate small vessel occlusive disease in per ventricular areas. No MRI scan was done at that time. Physical examination on admission revealed right-sided hand weakness (weakness in extension of fingers, weak pincer grip, and weak grasp) and mild drooping of the nasolabial fold with some stuttering and dysarthria, also consistent with the dysarthria-clumsy hand syndrome. She was unable to hold a cup with her hand or to write or draw. The patient was mildly delirious and appeared to have some difficulty communicating. Because of her nighttime agitation and manic symptoms, we started quetiapine 25 mg P.O. at 6 pm. By the next day, her speech was less pressured, and she had slept four hours during the night. She was no longer talking continually. Two days later, all her neurological findings had disappeared and her delirium was much improved. Her speech was coherent and she was fully oriented. Her speech was now normal rate and delivery. We continued the quetiapine and she was discharged 6 days after admission to a Skilled Nursing Facility (SNF) for acute rehabilitation. At the SNF, the quetiapine was stopped (reason undocumented) and her pressured, continuous speech returned, along with not sleeping at night. We were consulted again and recommended restarting the quetiapine, after which these problems resolved. An MRI scan just prior to hospital discharge revealed a new lacunar infarct in the area of the head of the caudate and the putamen. This patient had no previous psychiatric history. This patient had a major CVA six months later and died.


Case 3

A 76-year-old woman was admitted to the hospital after a second fall. Two months previously, she had fallen at home in Florida. Since the first fall, her behavior had been erratic. She gave a distant great-niece, whom she had never seen, $80,000 from the proceeds of the sale of her home. She bought a new Cadillac. She impetuously and impulsively moved back to Maine, where her brother and his wife lived. Just before her second fall, she was preparing to give her distant great-niece another $40,000; to give the Komen Breast Cancer Fund, $10,000; and to give our hospital's cancer center, $25,000. Her brother had learned of these pending transactions and had blocked them using his power of attorney two days before her second fall and admission.

On admission, she was agitated and angry. On arrival to her room, we met an angry woman who couldn't stop talking about her brother violating her rights and preventing her from using her money as she saw fit. She was grandiose and pressured. She was irritable. She had no idea how much money she had and was unable to do arithmetic. Her neurological exam was positive only for increased lateral nystagmus and difficulty balancing on one leg, in tandem, on heels, or on tiptoes. Her sternal nudge was positive. Neuropsychological testing with the RBANS and subtests of the Wcchsler Adult Intelligence Scale (WAIS) revealed minor neurocognitive disorder. Her MRI scan revealed moderate periventricular small vessel disease. A new (in the past two months), small lacunar infarct was noted in the area of the basal ganglia using FLAIR MRI. Minimal brain atrophy was present. Her past medical history was positive for coronary artery disease, hypertension, diabetes, and hypercholesterolemia. She had no prior diagnosis of bipolar disorder, but had treated for years for anxiety disorder, mostly with benzodiazepines. We agreed that she lacked capacity to manage her finances. The great-niece stopped visiting and would not return our telephone calls. We reported the situation to the Agency on Elder Abuse. Due to her high levels of agitation in the evening, we started quetiapine 25 mg PO bid. This was enough to eliminate her agitation and irritation. She stilled wished to give away her money and believed she had the right to do so, but was not having tantrums about her brother preventing her from doing so. She was discharged to an assisted living facility for further acute rehabilitation. The physician in acute rehabilitation stopped her quetiapine (reason undocumented) and her irritability and pressured speech returned. We were consulted again on an outpatient basis, recommended restarting the quetiapine, and eventually titrated it to a dose of 50 mg PO twice daily, which produced less sedation than 100 mg PO at bedtime. This dose kept her from being irritable, pressured, and demanding of her rights to give away her money. She continued to do well on this dose over the next 8 months.


Case 4

Through 6 are summarized in table 1. Evidence of clinical stroke existed in each of these cases on FLAIR MRI scans. In all three cases, mania came after a definitive neurological event. These six cases emerged from 262 inpatient geriatric consultations, which suggest a more common prevalence than previously appreciated.



Table 1: Summary of the time course of events of the six patients with post-stroke mania. View Table 1


Similarities: All six patients had moderately severe small vessel occlusive disease in the periventricular white matter. Four had or developed lacunar infarcts in the area of the basal ganglia. Two had temporal lobe infarcts. None of the patients had a previous diagnosis of bipolar disorder. Four presented with problems with gait and balance. Subtle neurological findings existed on physical examination, which were not appreciated by the ED physician or the admitting hospitalist. The possibility of stroke contributing to these patient's psychiatric symptoms was minimized or denied by their hospitalists in relation to the absence of acute findings on the CT scan. Fall was a common sentinel event that brought these patients to the Emergency Department. While two of the patients had pre-existing minor neurocognitive disorder, none had major neurocognitive disorder.

Differences: Two of the patients had a pre-existing psychiatric history (depression and anxiety diagnoses) and required higher doses of quetiapine to manage their mania than the others who had no pre-existing psychiatric history.


Discussion

Our findings suggest that post-stroke mania may be more common than the current literature would suggest. Over one year in a rural 192-bed hospital, we encountered six cases (almost 2% of our geriatric consultations), and no cases of new-onset geriatric mania without a preceding neurological event. The neurological antecedents appear to be under-appreciated due to contemporary reliance on CT scanning to diagnose stroke versus clinical examination. We also noticed a tendency on the part of the hospitalists to not carefully assess gait and balance. The neurological findings may be subtle and transient and represent basal ganglia and/or lacunar infarcts in other locations. Our 6 patients convincingly demonstrated mania occurring after small cerebrovascular events.

Cognitive impairment, dementia, personality change, psychosis, apathy and anxiety all occur after stroke [11]. Lesions in the cerebral hemisphere and limbic structures may produce symptoms suggestive of mania. Right-sided cerebrovascular lesions involving regions connected to the limbic cortex have been implicated in late-onset mania [12]. In addition, secondary mania in right-handed people with dominant left hemisphere involvement is increasingly being recognized [13]. Removal of inhibitory tracks from the pre-frontal cortex to the limbic brain and ventral striatum may unmask mania that was previously kept in check. More attention should be directed to the basal ganglia and to small vessel occlusive disease in explaining new onset, geriatric psychiatric syndromes, and especially the role of basal ganglia lesions in post-stroke mania. The existence and sequelae of cerebral small vessel disease is only now becoming appreciated [ref], especially because the neurological findings are often transient and it may require diffusion tensor imaging to find the lesions to fiber tracts, a technology that most hospitals do not have.

The likelihood of developing a stroke is greater among patients with bipolar disorder than controls, and the all-cause mortality rate is higher among patients with bipolar disorder than controls [14]. Compared with schizophrenia patients, those with bipolar disorder were 19% more likely to have diabetes, 44% more likely to have coronary artery disease, and 18% more likely to have dyslipidemia, after adjustment for other factors [15].

Pathological generosity, as existed in one of our patients, has been described following a left lenticulocapsular stroke with hypoperfusion of several anatomically intact cortical areas [16]. A 49-year-old man developed excessive and persistent generosity as he recovered from a left lenticulocapsular hematoma. His symptoms resembled an impulse control disorder. (99m) Tc-HMPAO SPECT demonstrated hypoperfusion, mostly in the ipsilateral striatum, dorsolateral, and orbit frontal cortex. This case study adds pathological generosity to the range of behavioral changes that may result from discrete unilateral lesions of the lenticular nucleus and nearby pathways.

In another case report of post-stroke mania, SPECT scan performed during the manic state demonstrated hypoperfusion in the right temporal and frontal regions due to right putaminal hemorrhage [17], the site of lesion for one of our patients. It also showed hyperperfusion in the inferior lateral prefrontal lobe, the temporal lobe, and the medial and lateral parts of the parietal lobe in the left hemisphere. A second SPECT scan performed during the euthymic state demonstrated moderate improvement in the hypoperfusion in the right fronto-temporal regions. The focal hyperperfusion in the anterior insular cortex, inferior lateral prefrontal lobes, and superior-middle temporal gyrus in the left hemisphere had vanished.

Treatment of mania with even small doses of antipsychotic medication resolved the symptoms. The differentiation between neurological and psychiatric causation may not affect treatment, but it matters to families and to the care they receive. At least in our region, patients with psychiatric diagnoses are less likely to be accepted by assisted living facilities and skilled nursing facilities and are stigmatized more than patients with neurological diagnoses. Families also appear to be more comfortable with neurological explanations than that of late-onset bipolar disorder. The other lessons from this case series is the importance of a careful neurological examination after a fall, especially an assessment of gait and balance, and the avoidance of over-reliance on imaging to rule out small strokes in the presence of significant, albeit transient neurological findings.


Disclosures

None.


References
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  11. Paranthaman R, Baldwin RC (2006) Treatment of psychiatric syndromes due to cerebrovascular disease. Int Rev Psychiatry 18: 453-470.

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  14. HC W, Chou FH, Tsai KY, Su CY, Shen SP, et al. (2013) The incidence and relative risk of stroke among patients with bipolar disorder: a seven-year follow-up study. PLoS One 30.

  15. Kilbourne AM, Brar JS, Drayer RA, Xu X, Post EP (2007) Cardiovascular disease and metabolic risk factors in male patients with schizophrenia, schizoaffective disorder, and bipolar disorder. Psychosomatics 48: 412-417.

  16. Ferreira-Garcia R, Fontenelle L, Moll J, de Oliveira-Souza R (2014) Pathological generosity: an atypical impulse control disorder after a left subcortical stroke. Neurocase 20: 496-500.

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Sours: https://clinmedjournals.org/articles/jgmg/journal-of-geriatric-medicine-and-gerontology-jgmg-2-015.php?jid=jgmg
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Increased left anterior insular and inferior prefrontal activity in post-stroke mania

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Abstract

Background

Post-stroke mania is an infrequent complication after stroke, and the mechanisms underlying this disorder remain unclear. Although a contralesional release phenomenon has been implicated in post-stroke mania, empirical findings are lacking.

Case presentation

We present a case report of post stroke mania. Single photon emission tomography (SPECT) was performed twice, during the manic state and during the remitted euthymic state. The first SPECT study performed during the manic state demonstrated hypoperfusion in the right temporal and frontal regions due to right putaminal hemorrhage. It also showed hyperperfusion in the inferior lateral prefrontal lobe, the temporal lobe, and the medial and lateral parts of the parietal lobe in the left hemisphere. The second SPECT study performed during the euthymic state demonstrated moderate improvement in the hypoperfusion in the right fronto-temporal regions. Furthermore, compared to the findings on the first SPECT study, the second study showed that the focal hyperperfusion in the anterior insular cortex, inferior lateral prefrontal lobes, and superior-middle temporal gyrus in the left hemisphere had vanished.

Conclusion

Increased left inferior prefrontal and anterior insular activity and reduced extensive right fronto-temporal lobe activity are involved in the development of post-stroke mania.

Peer Review reports

Background

Depression is a common neuropsychiatric consequence of stroke. In contrast, post-stroke mania is less common after stroke, and the mechanisms of this disorder remain unclear [1]. Findings from previous neuroimaging studies demonstrated that post-stroke mania is more often associated with lesions in the right hemisphere than in the left hemisphere [2–4]. One single photon emission tomography (SPECT) study showed that a patient with post-stroke mania had a unique pattern of left orbito-frontal hyperperfusion with extensive right frontal hypoperfusion [5]. This finding indicated that manic symptoms after stroke could be caused by a contralesional release phenomenon. In other words, the interruption of inter-hemispheric inhibition could give rise to increased activation of the left hemisphere after right hemisphere damage. However, few neuroimaging studies have directly investigated the relationship between changes in regional cerebral blood flow and the clinical course of post-stroke mania. In the present study, to investigate mechanisms of post-stroke mania, changes in regional cerebral blood flow were examined using SPECT studies during both the manic state and the remitted euthymic state on separate days in a patient with post-stroke mania following a right putaminal hemorrhage. We hypothesized that the regional cerebral blood flow in the manic state demonstrates right fronto-temporal lobe hypoperfusion due to the brain hemorrhage itself and hyperperfusion in the left orbito-fronto-temporo-parietal regions resulting from contralesional release phenomenon, and that this increased activity of the left hemisphere would resolve into the normal state after recovery from post-stroke mania.

Case presentation

The patient was a 68-year-old, right-handed male office worker who had retired at the age of 62 years. He had a past history of hypertension, hyperlipidemia, and gout. He had no prior psychiatric history, and no family history of psychiatric disorders. His medication at the time was digoxin, atenolol, candesartan, and atorvastatin.

His premorbid personality before the stroke was taciturn, serious, and not cyclothymic. In January 2009, he suffered a right putaminal hemorrhage [Figure 1], which led to left hemi paralysis. He was admitted to our hospital for treatment and then transferred to another hospital for rehabilitation. After rehabilitation, his left hemi paralysis improved without any motor complications. Six weeks after the stroke, however, he developed severe manic symptoms and was referred to our clinic.

Right putaminal hemorrhage in a patient with post-stroke mania.

Full size image

He presented with elevated mood, irritability, motor excitement, and pressure of speech with racing thoughts. He was euphoric and always smiling. Since he talked too fast and his conversational content fluctuated, it was difficult to understand what he said. He got angry over trivial events and often threw a newspaper at his wife. He also had psychomotor agitation and frequently tried to see estranged friends without a specific reason. He could not stop talking even when ordered to do so. Moreover, he also displayed less need for sleep. He believed that he could get along just fine on a few hours of sleep at night. These symptoms met the clinical criteria for a manic episode according to the DSM-IV-TR criteria [6]. His Young Mania Rating Scale (YMRS) [7] was 42 points, which indicated a severe manic state.

His consciousness level was clear. The findings on his electroencephalogram were normal. Clinical neuropsychological tests were performed during the manic state. The patient’s full-scale intelligence quotient (FIQ) on the Wechsler Adult Intelligence Scale III was 102 (verbal IQ 113, performance IQ 88). The Wechsler Memory Scale-Revised (WMS-R) revealed that he had mild memory deficits (general memory index 91, visual memory index 97, verbal memory index 90, delayed memory index 75). On executive function testing, his performances were normal on the Wisconsin Card Sorting Test, Modified Stroop Test, and the Word Fluency Test. Taken together, the neuropsychological assessments demonstrated a mild memory disorder with a slightly low PIQ and intact executive function.

The patient was treated at our hospital as an outpatient. He was started on sodium valproate, and the dose was gradually increased to 600 mg/day. Olanzapine 7.5 mg/day was also introduced. After 2 months, he showed considerable improvement, and the YMRS score dropped from 42 to 8. His manic symptoms diminished 2 years after stroke onset, and the YMRS score decreased to 0 points. During the course of post-stroke emotional impairment, he did not have a depressive state.

Single photon emission tomography (SPECT) was performed twice on separate days: during the manic state (YMRS 42 points) before treatment, and during the remitted state (YMRS 0 points) after treatment, with an interval of 2 years. At the time of first SPECT scan, he took sodium valproate 600 mg/day and olanzapine 5 mg/day, and at the time of second SPECT scan, he continued to take sodium valproate 600 mg/day and did not take any antipsychotic drug.

Projection data were acquired 30 minutes after an i.v. bolus injection of 740 MBq of 99mTc-ECD using a 3-headed rotating gamma camera (Toshiba GCA-9300A/DI; Toshiba Corporation, Tokyo, Japan) equipped with an ultra high-resolution fan beam collimator, and a medical image processor (GMS5500U/DI; Toshiba Corporation, Tokyo, Japan) was used image processing. The energy window for acquisition was set at 140 keV, with a width of 20%. The gamma camera was rotated continuously for 16 minutes, and SPECT data were arranged into 90 projection angles over 360 degrees. Images were reconstructed in a 128 x 128 matrix using a ramp filter after the data were processed with a Butterworth filter (order 8, 0.12 cycles/pixel). SPECT images were spatially normalized to standardized stereotactic space, smoothed using a 12-mm FWHM isotropic Gaussian kernel, and analyzed using the Easy Z-Score Imaging System (eZIS) [8]. Each SPECT image was compared with the mean and SD of SPECT images of 20 age-matched healthy male controls using voxel-by-voxel Z-score analysis after normalization to global mean voxel values; Z-score = ([control mean]_ [individual value])/(control SD). The Z-score maps were displayed by projection with an averaged Z-score of 14-m thickness to a surface rendering of the anatomically standardized MRI template with a two-tailed view of a hot color scale (hyper perfusion, Z-score level >2.0) and a cold color scale (hypo perfusion, Z-score level >2.0). The extent threshold of the cluster size was set at z300 voxels.

The first SPECT study performed during the manic state demonstrated that the patient had hypoperfusion in the right temporal and frontal regions due to right putaminal hemorrhage [Figure 2]. It also revealed hyperperfusion in the inferior lateral prefrontal lobes, the temporal lobe, and the medial and lateral parts of the parietal lobes in the left hemisphere. The second SPECT study performed during the euthymic state demonstrated moderate improvement of the hypoperfusion in the right fronto-temporal regions. Furthermore, compared to the findings on the first SPECT study, the second study showed that the focal hyperperfusion had vanished in the anterior insular cortex, inferior lateral prefrontal lobes, and superior-middle temporal gyrus in the left hemisphere.

SPECT images obtained during a) the manic state and b) the euthymic state, and c) Comparison of regional cerebral blood flow of the left anterior insula between the manic state and the euthymic state.

Full size image

Informed consent was obtained from this patient.

Discussion and conclusions

To the best of our knowledge, this is the first case report to demonstrate the relationship between the contralesional release phenomenon and the clinical symptoms of post-stroke mania with direct comparison of regional cerebral blood flow during the manic state with that during the remitted euthymic state.

Before we discuss the possible implication of our findings, several diagnostic issues should be considered. The present patient clearly suffered from post-stroke mania, and his symptoms met the clinical criteria for a manic episode according to DSM-IV-TR criteria [6]. His symptoms were not a disinhibition syndrome after stroke, because he had a distinct elevated mood without a dysphoric state, and neuropsychological examination revealed that he had normal executive function. Normal findings on his electroencephalogram provided evidence that epilepsy was not involved in his manic symptoms. Furthermore, the development of the manic state could not be explained by his positive psychological state due to recovery of neurological symptoms or as a manic defence to the experience of stroke, because his distinct elevated mood and other manic symptoms were too long continued and at a pathological level. Therefore, we concluded that he suffered from post-stroke mania with brain dysfunction.

The first SPECT study demonstrated a unique pattern of left fronto-temporo-parietal hyperperfusion with extensive right fronto-temporal hypoperfusion during manic symptoms. This pattern was consistent with that due to a contralesional release phenomenon after brain lesions, and it was similar to a past case report [5]. Interestingly, this imbalance in the regional cerebral blood flow improved after recovery of his manic symptoms. In particular, the increased brain activity in the inferior lateral prefrontal lobes, anterior insular cortex, and superior-middle temporal gyrus in the left hemisphere disappeared in the remitted euthymic state.

Results of SPECT studies in the present case were consistent with previous findings from functional neuroimaging studies of primary mania. For example, Blumberg et al. demonstrated decreased right prefrontal cortex activation and increased left prefrontal cortex activation in patients with primary mania using PET [9, 10]. They proposed that primary mania is associated with an imbalance in prefrontal activity, with right less than left, and ventral less than dorsal [10]. Similarly, other researchers showed a pattern of greater left than right regional cerebral blood flow in the inferior prefrontal cortex in acute mania [11], and they suggested that manic symptoms are related to relatively increased left frontal activity [12]. It has also been reported that greater left than right frontal cortical activity is associated with positive affect and approach motivation, which can generate a manic state [13]. Thus, it is plausible that the imbalance in brain perfusion, reduced right fronto-temporal activity, and increased left inferior prefrontal activity may have contributed to the development of manic symptoms in the present patient.

In the present case, the hyperperfusion in the left anterior insular cortex vanished after recovery from mania. Hyperperfusion in the left anterior insular cortex was shown in a previous case report [5]. The anterior insular cortex may be implicated in emotional awareness [14]. Several neuroimaging studies of emotional awareness reported joint activation of the anterior insular cortex and the anterior cingulate cortex in the subjective experience of emotional feelings, including happiness, sexual arousal, and empathy. Furthermore, activation of the left anterior insular cortex was reported in subjects hearing pleasant music, seeing a smile, and experiencing joy [14]. Clinical neurophysiologic studies demonstrated that intensive positive feelings in ecstatic seizures can originate from the left anterior insula, a region that has been suggested to engender self-awareness associated with positive feelings [15, 16]. In addition, it has been proposed that the right anterior insular cortex is closely associated with negative emotion, while the left anterior insular cortex is associated with positive emotion [14]. Therefore, in the present patient, the hyperactivation in the left anterior insular cortex may have led to the patient’s pathologically elevated mood, which is the core symptom of mania. Moreover, the hypoactivation in the right anterior insular cortex in this patient might have prevented him from having negative emotions, which exacerbated his manic symptoms.

In the present study, we observed the treatment effect of sodium valproate and olanzapine in improving the manic symptoms. Therefore, effect of drugs on the regional cerebral blood flow should be considered. This patient took olanzapine at the time of first SPECT scan, and sodium valproate at the time of both SPECT scans. It was reported that olanzapine does not affect regional cerebral blood flow [17]. Furthermore, it was also shown that sodium valproate diminishes global cerebral blood flow in wide areas of the brain [18]. Based on these findings, it is difficult to determine whether there is any kind of treatment effect or not. It is still unclear whether these regional changes are related to the cessation of olanzapine or to a possible effect of sodium valproate. In order to evaluate this, there is need for another study design including the pre and post treatment effect of both drugs (olanzapine and sodium valproate), although there are restricted studies in this topic.”

In conclusion, the present case showed that increased left inferior prefrontal and anterior insular activity and reduced right fronto-temporal lobe activity was involved in the development of post-stroke mania, possibly due to an interhemispheric prefrontal and insular imbalance with a contralesional release phenomenon.

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  1. Department of Neuropsychiatry, Ashikaga Red Cross Hospital, Tochigi, Japan

    Akihiro Koreki

  2. Department of Neuropsychiatry, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan

    Akihiro Koreki, Keisuke Takahata, Hajime Tabuchi & Motoichiro Kato

  3. Molecular Neuroimaging Program, Molecular Imaging Center, National Institute of Radiological Sciences, Chiba, Japan

    Keisuke Takahata

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Correspondence to Motoichiro Kato.

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Authors’ contributions

MK and HT cared for the patient, and participated in the design of the case report and neuroimaging research. AK, KT, HT and MK analyzed SPECT data and wrote the paper. All authors read and approved the final manuscript.

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Koreki, A., Takahata, K., Tabuchi, H. et al. Increased left anterior insular and inferior prefrontal activity in post-stroke mania. BMC Neurol12, 68 (2012). https://doi.org/10.1186/1471-2377-12-68

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Keywords

  • Contralesional release phenomenon
  • Insula
  • Mania
  • SPECT
  • Stroke
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Poststroke Pain: What It Is, What Causes It, How to Treat It

Post-Stroke Psychiatric Syndromes: Diagnosis and Pharmacologic Intervention

The post-stroke patient is at significant risk for various psychiatric syndromes. The most commonly reported of these in the literature are post-stroke depression (PSD) and post-stroke dementia (PSDem), which may present simultaneously with overlapping mood and cognitive symptoms. In this article, we offer a review of current literature on post-stroke psychiatric syndromes and an integrated clinical approach to screening, diagnosis, and pharmacologic intervention.The importance of psychiatric illness complicating the post-stroke period is well established.1 Integrating assessment for psychiatric symptoms into the care of post-stroke patients is especially critical in the first 6 months following a stroke, a period of high risk for psychiatric complications. Psychiatric and substance abuse history, past treatment with psychopharmacologic agents, family psychiatric history, and personal and family history of suicidal behavior are important items to assess.Evaluation of the patient's living situation, level of social support, and cultural variables is also critical. Careful attention to caregivers' and family members' behavioral observations is necessary, especially in patients with cognitive impairment or other neurologic barriers to communication, such as residual aphasia. Social support for caregivers and patients may decrease the risk of PSD.1,2 Considering psychiatric referral at a low threshold is advisable in these patients, particularly those with more than 1 post-stroke psychiatric disorder.Post-Stroke DepressionDepression that is attributable to a medical disorder, such as stroke, is referred to as "secondary" depression in the psychiatric literature, as opposed to "primary" or "endogenous" depression.1 PSD is thus classified as "mood disorder due to a general medical condition" (code 293.83) in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR).3 It is advisable to apply DSM-IV-TR criteria inclusively in cases of apparent PSD, rather than to attribute mood symptoms to other, less specific causes, such as "stress" or the challenges of coping with neurologic impairment.4 Attribution of mood symptoms to nonspecific stressors can lead to delayed or deficient clinical intervention for PSD.A higher risk of PSD has been linked to left-sided cortical and basal ganglia lesions and to lesions closer to the frontal lobe than to left posterior or right frontal lesions.5-9 This hemispheric localization of PSD risk may be most robust in the first month following stroke.2,4,9 Large reviews have found the risk of PSD to be between 20% and 79%.10-13 For up to 18 months post-stroke, the risk of major depression is nearly twice that in persons who have not suffered stroke.2,14,15 Although patients with PSD may recover spontaneously within 12 months, untreated patients are at risk for chronic illness (even beyond 2 years).12,16Risk factors for PSD include female sex, age less than 60 years, being divorced, alcoholism, nonfluent aphasia, major motor deficit, cognitive deficits, and nursing home residence.17,18 PSD is associated with delayed functional recovery, decreased social function, and greater mortality.12,16,19-24 Suicidal ideation in PSD has been reported up to 24 months after stroke.25PSD may involve a spectrum of mood disorders, including major and minor depression, "vascular depression," and dementia-related depression. Vascular depression (predating stroke) is associated with anhedonia and psychomotor retardation as well as with older age at onset, fewer feelings of guilt, and higher degrees of cognitive impairment than that seen in "primary" major depression.16,26,27 Vascular depression may predict subsequent stroke, myocardial infarction, and greater mortality, although this relationship is complex.21,26,28,29 In addition, primary major depression may present with prominent cognitive symptoms, a condition referred to as depressive pseudodementia, which may itself be a prodromal state for later Alzheimer disease (AD).30 Because these relationships between depression and dementia are imprecise at present, the physician is advised to offer treatment of PSD early in the post-stroke period to maximize mood and cognitive function.24,31-35A helpful screening mnemonic for depression is SIGECAPS: Sleep, Interest level, Guilt, Energy level, Concentration, Appetite, Psychomotor activity level, and Suicidal thoughts can be quickly examined with use of this mnemonic device. The presence of 5 or more of these symptoms (one of which must be depressed mood or decreased interest level) for 2 weeks is the threshold for a diagnosis of major depression. Sub-threshold cases involving clinically significant impairment may also be considered for psychopharmacologic therapy. Other depressive symptoms include tearfulness, pessimism, hopelessness, and nihilism.Depression inventories such as the self-administered Beck Depression Inventory (BDI) and clinician-administered Hamilton Rating Scale for Depression (HDS) can be used to quantify depressive symptoms.36,37 The clinician-administered Post-Stroke Depression Rating Scale (PSDRS) addresses the "major" and "minor" forms of PSD.38 Alternative self-administered scales for PSD and post-stroke anxiety disorders include the Geriatric Depression Scale (GDS) and General Health Questionnaire (GHQ).39 Generally, patients can complete either the BDI, GDS, or GHQ; however, if a patient has significant cognitive deficits, he or she may not be able to report mood symptoms reliably, and clinician evaluation by the HDS or PSDRS may be more helpful.Evaluation for PSD must include an assessment of suicidality, with an urgent psychiatry referral to assess need for psychiatric hospitalization in actively suicid-al patients. As part of the systemic workup for PSD, one should check thyroid-stimulating hormone (TSH) levels, since mild hypothyroidism may mimic depression.40-43 Other systemic factors in PSD include various medications, such as opioids and corticosteroids, and electrolyte abnormalities, which can alter mood and/or cognition.Evidence-based psychopharmacologic treatments for PSD include tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), and psychostimulants (eg, methylphenidate). No controlled trials have been conducted on other classes of antidepressants (eg, bupropion, venlafaxine, and mirtazapine) for post-stroke treatment, although they are commonly used in clinical practice. Dosing information for antidepressants and augmenting agents in PSD is included in the Table.In the acute phase of PSD, it is advised that SSRIs be used as first-line treatments, since they cause fewer serious side effects, such as delirium and sedation, than do TCAs.44 Case reports of SSRI-related stroke suggest that these medications may increase bleeding risk in some patients because of their effects on platelet function, although a recent major review found no causal relationship between SSRIs and bleeding in post-stroke patients.45 Dosing should follow the aphorism of "start low and go slow," with cautious initial dosing and slower pace of dose increases to avoid significant side effects, but the usual full dose of antidepressant ultimately may be needed. Consider starting antidepressants at half the typical adult starting dose. In an extremely regressed patient, concurrent therapy with a psychostimulant and antidepressant may allow for an earlier response. In general, allow 1 to 2 weeks between dose increases for most antidepressants. It is best to conduct an adequate trial (dose and duration) of the antidepressant: minimally, a trial of 6 weeks' duration at the usual adult therapeutic dose. If the patient achieves clinical remission, continue treatment for up to 12 months at the full effective dose.If no clinical response is seen despite demonstrated adherence, or if the initial antidepressant is poorly tolerated, switch to a different antidepressant class and/or augment the therapy with a psychostimulant (eg, methylphenidate, dextroamphetamine). Consider psychiatric consultation after 2 failed monotherapy trials with different antidepressants or 1 failure with augmentation using a psychostimulant.Psychostimulants may be effective as monotherapy in the short term (1 to 14 days), are generally well tolerated, and may be combined with antidepressants. However, no information is available on long-term effectiveness, tolerability, or other risks. Follow up at least monthly until clinical remission is achieved, repeating the cognitive examination and depression inventory at each visit to monitor treatment response. Post-stroke patients at high risk for PSD-for example, those with prior episodes of depression, left-sided lesions, history of other psychiatric illness, or strong family history of psychiatric illness-may be considered for prophylactic treatment with an antidepressant.The use of psychostimulants for PSD and/or apathy states may be associated with a risk of seizure and/or cardiac side effects. There is little prospective research on the side effects of psychostimulants for PSD, but some studies have shown either no difference from placebo with regard to side effects46 or low incidence of treatment-emergent side effects.47 Concern for these risks must be balanced against undertreatment of PSD. In cases of premorbid cardiac disease, consultation with a cardiologist and careful dosing of psychostimulantsappear warranted. In a patient with post-cerebral vascular accident depression and a history of seizures, consideration of antiseizure medication, along with psychostimulants, appears reasonable.48,49In treatment-refractory cases leading to psychiatric referral, the psychiatrist will consider electroconvulsive therapy for depression-related emergencies, such as repeated suicide attempts and severe melancholic PSD; cases refractory to maximal medication management; or cases in which complex psychopharmacologic regimens cause intolerable side effects. Psychotherapeutic and psychosocial treatments may also be helpful in treatment-refractory cases.Post-Stroke DementiaPSDem, a type of vascular dementia (VaD), is another common psychiatric complication of stroke.50 VaD is coded in the DSM-IV-TR as 290.4X, the fifth digit of the code being "0" for uncomplicated, "1" with concurrent delirium, "2" with concurrent delusions, or "3" with concurrent depressed mood.3 PSDem is the subject of some semantic imprecision because of its overlap with multi-infarct dementia (MID), which results from a series of deep white matter infarcts.51 Some patients may have a mixed model of VaD: preexisting MID with subsequent further decline in cognitive status following a larger stroke.50Some cases of dementia diagnosed in the post-stroke period may represent previously unrecognized cases of AD. In addition, many patients have PSDem because of combined neuropathology, the most important "mixed dementia" being concurrent AD and VaD. Mixed dementia, coded as 290.1X, has multiple causes. The fifth digit of the code is "0" to signify lack of behavioral disturbances; "1" signifies presence of behavioral disturbances.3Dementia symptoms include amnesia, cognitive disorganization, paranoia, visual-spatial dysfunction, language deficits, apraxia, disinhibited and/or unsafe behavior, and poor social judgment. Clinical cognitive examinations such as the Folstein Mini-Mental State Examination or the cognitive portion of the Cambridge Examination for Mental Disorders of the Elderly should be used even in cognitively asymptomatic patients post-stroke and can be repeated serially to monitor progression and/or treatment response.52,53Any precipitous deterioration in cognition in a patient post-stroke should raise the index of suspicion that an additional stroke may be responsible. Structural abnormalities, such as hemorrhagic conversion of stroke or subdural hematoma, also should be considered and usually can be readily excluded with noncontrast CT.54Treatment for post-stroke dementia begins with a low threshold for psychiatry referral for agitated behavior, persistent confusion, or cognitive inability to participate in treatment. An additional workup (vitamin B12, folate, and TSH analysis; toxicology screening; and rapid plasma reagent and HIV testing) for reversible causes of dementia should also be accomplished.55,56The clinical similarities and overlap of VaD and AD should lead the physician to treat PSDem with antidementia pharmacotherapy, even though cholinesterase inhibitors and memantine have been FDA-approved only for AD. PSDem patients may benefit from pharmacotherapy for AD (cholinesterase inhibitors and memantine) and consideration of possibly neuroprotective agents such as antioxidants (vitamin E) and NSAIDs.55,56 Therapy with cholinesterase inhibitors has been shown to benefit AD patients with multiple vascular risk factors, many of whom may represent the mixed dementia described above.57 Some preliminary work with cholinesterase inhibitors for VaD has shown promising results.58,59Patients with PSDem should be followed up monthly, with reassessment of cognitive examination, repeated depression inventory, and screening for psychotic symptoms.-The dose of cholinesterase inhibitor can be increased at monthly intervals if needed to titrate dose to response.-Initiate atypical antipsychotics and/or antidepressants for agitated behavior in PSDem, with a low threshold for psychiatry referral for these symptoms.-Seek caregiver support through psychoeducation, the Alzheimer's Association (www.alz.org), and other community resources-and screen for caregiver distress and depression.-Assess safety of driving and other potentially hazardous activities, which need to be curtailed in patients with significant cognitive and/or psychotic symptoms.-Be sure that PSDem patients have matters of consent, legal competency, and durable power of attorney addressed early in the course of illness.-Facilitate respite care for caregivers through adult day-care centers, in-home caregivers, and outreach nursing intervention.-If the patient cannot safely live independently because of cognitive impairment, agitated behavior, or inability to care for self, assist in getting the patient placed in an appropriate facility (eg, skilled nursing facility expert in caring for patients with dementia).Post-Stroke Psychotic DisorderPost-stroke psychotic disorder, coded as 293.81 with delusions and 293.82 with hallucinations, may be difficult to clearly distinguish from PSD and PSDem.3 Psychotic symptoms include delusions, hallucinations (which may affect various sensory modalities; auditory and visual hallucinations are the most common), ideas of reference, thought disorganization, and regressed motor behavior. Psychotic symptoms may represent PSDem with associated psychosis. Post-stroke psychotic disorder has been reported to correlate with right-sided lesions and cortical/subcortical atrophy.4 Any history of premorbid psychotic illness should be explored. Because of the complexity of these overlapping diagnostic possibilities, and because of the risk of dangerous and disorganized behavior, persons with post-stroke psychosis should be referred for psychiatric care, with subsequent comanagement from the psychiatrist.Treatment includes an atypical antipsychotic, such as risperidone, 0.5 to 1 mg PO bid (use liquid risperidone as needed to facilitate administration), or olanzapine, 2.5 mg PO (tablet), or SL (orally disintegrating Zydis) qhs. Very rare minor strokes have been reported after the use of these medications, but the clinical significance of these events appears to be small.60 Close follow-up every 2 weeks and titration of antipsychotic dose to effect is recommended. Reassessment for reemergence of psychosis, repeated cognitive examination, and depression inventory at each visit are recommended.A patient with preestablished psychotic illness, such as schizophrenia, may decompensate into psychotic symptoms following a major stressor such as a stroke. The "cleanest" case of post-stroke psychosis would be a patient with no previous history of psychotic symptoms in whom psychosis develops only following stroke. It is not clear how previous psychiatric illness affects risk of post-stroke syndromes. Treatments would not differ because they are based on manifest symptoms.Post-Stroke ManiaPost-stroke mania is rare, although it may be associated with right-sided stroke.5,61,62 Manic symptoms include expansive and/or irritable mood, decreased need for sleep, increased goal-directed activity, recklessness, disregard for social constraints, talkativeness, racing thoughts, excessive laughter or giggling, and poor judgment. The clinician should carefully explore any history of premorbid bipolar disorder, personality disorder characterized by mood instability, and family history of bipolar disorder. In addition, cognitive disorders increase the risk of irritable and aggressive behavior.Because management of bipolar-spectrum disorders often requires complex psychopharmacologic regimens, persons with post-stroke mania should routinely be referred for psychiatric care. Thereafter, ongoing comanagement with a psychiatrist (as with post-stroke psychosis) can be facilitated. The typical psychopharmacologic regimen includes a mood stabilizer (lithium is problematic in patients with renal disease and other medically ill patients) and/or an atypical antipsychotic. Observation for downward cycling of mood into an episode of PSD, using mood screening questions and/or depression inventories and clinical observation, is necessary. Antidepressants may induce an elevated mood episode in patients at risk for mania, and treatment of depressed episodes in bipolar-spectrum patients may require an antidepressant and 1 or more mood stabilizers.Post-Stroke Anxiety DisordersPost-stroke anxiety disorders, coded as 293.84, may be comorbid with PSD and may be more common in cortical than subcortical stroke.3,4,8 Anxiety symptoms include discrete episodes of panic, tonic levels of increased anxiety, excessive sweating, worrying, and decreased sleep. Risks of 26% and 39% have been found for post-stroke anxiety disorders in men and women, respectively.17 A combination of anxiety and depression may be more common in left cortical stroke, while depression without anxiety may be more common in left subcortical stroke.4,63Treatment of post-stroke anxiety disorder includes assessment for comorbid PSD. Many anxiety syndromes respond well to antidepressants but may be exacerbated by psychostimulants.64 A trial of 1 or more antidepressants, as described above in the discussion of PSD treatment, is usually best as first treatment. Avoidance of benzodiazepines is important; these agents may cause cognitive decline, verging on PSDem.65 Follow-up should be done in 1 month to assess response. If symptoms are incompletely responsive to antidepressant(s), consider buspirone, either with an antidepressant or as monotherapy.66Other Post-Stroke Psychiatric SyndromesLess frequently seen post-stroke psychiatric symptoms include pathologic crying, pathologic laughter, apathy, and isolated fatigue. These are coded as 293.9: mental disorder due to a general medical condition not otherwise specified.3 Pathologic laughter and crying are sometimes grouped as pathologic emotions (PE) with sudden paroxysms of either laughter or crying, irrespective of the ambient mood state.4 PE can be triggered by nonspecific stimuli or by a low-threshold emotive stimulus. Curiously, the PE do not themselves induce a mood change other than during the affective display, and they are not under voluntary control.12,67 Some literature recommends the use of antidepressants for PE; lithium and anticonvulsants are alternatives.5,67-69Apathy in the absence of depression may be difficult to appreciate, but it presents with profound lack of initiative without tearfulness, sleep/appetite disturbance, hopelessness, or suicidality.5 Some literature supports the use of antidepressants and/or psychostimulants for post-stroke apathy.5 Post-stroke fatigue may be difficult to separate from apathy.70 Antidepressants and psychostimulants may be indicated, particularly those with effects on noradrenergic and/or dopaminergic activity (eg, bupropion, venlafaxine, and mirtazapine). Follow-up within 1 month is needed.ConclusionsPatients post-stroke are at risk for a range of specific psychiatric syndromes. Because these may impair function and/or safety, close follow-up, surveillance, and management should be integrated into the care of these patients. Appropriate use of pharmacotherapy and psychiatric referral may facilitate clinical management and optimize treatment and rehabilitative outcomes.James A. Bourgeois, OD, MD, is associate professor, Department of Psychiatry and Behavioral Sciences, and director, Psychiatry Consultation/Liaison Service, University of California, Davis Medical Center.Donald M. Hilty, MD, is associate professor, Department of Psychiatry and Behavioral Sciences, University of California, Davis Medical Center.Celia H. Chang, MD, is assistant professor, Department of Neurology, University of California, Davis Medical Center.Mark E. Servis, MD, is associate professor, Department of Psychiatry and Behavioral Sciences, University of California, Davis Medical Center.REFERENCES1. Bourgeois JA, Hilty DM, Chang CH, et al. 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Sours: https://www.psychiatrictimes.com/view/post-stroke-psychiatric-syndromes-diagnosis-and-pharmacologic-intervention

Stroke mania post

Assessment of poststroke mania and diagnosis

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Cognition Post-Stroke - Stephanie Orient

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