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Emotional Disturbances after Stroke



Impairment after stroke may have acute and long-lasting psychological implications. Additionally, organic brain dysfunction also appears to play an important role in poststroke affective modifications. Emotional state is multidetermined and can be specifically modified by alteration of some brain networks. This article illustrates a certain number of acute and more chronic emotional disturbances after stroke, such as mood disorders, emotional dyscontrol, and modification of emotional experiences. Some neural mechanisms implicated in these modifications are discussed. The main modifications described are depression anxiety, psychosis, modification of emotional experience, and fatigue.
Clinical and Experimental Hypertension, 28:243–249, 2006
Copyright © Taylor & Francis Group, LLC
ISSN: 1064-1963 print / 1525-6006 online
DOI: 10.1080/10641960600549173
LCEH1064-19631525-6006Clinical and Experimental Hypertension, Vol. 28, No. 03, February 2006: pp. 0–0Clinical and Experimental Hypertension
Emotional Disturbances after Stroke
Emotional DisturbancesJ.-M. Annoni et al. JEAN-MARIE ANNONI,1,2 FABIENNE STAUB,1
1Department of Neurology, University Hospital, Lausanne, Switzerland
2Department of Neurology, University Hospital, Geneva, Switzerland
Impairment after stroke may have acute and long-lasting psychological implications.
Additionally, organic brain dysfunction also appears to play an important role in
poststroke affective modifications. Emotional state is multidetermined and can be
specifically modified by alteration of some brain networks. This article illustrates a
certain number of acute and more chronic emotional disturbances after stroke, such as
mood disorders, emotional dyscontrol, and modification of emotional experiences.
Some neural mechanisms implicated in these modifications are discussed. The main
modifications described are depression anxiety, psychosis, modification of emotional
experience, and fatigue.
From the neurological point, emotion is a multicomponential process in response to exter-
nal and internal stimuli, which implicates perceptive (fear, joy, disgust), motivational
(arousal), autonomic (sympathetic reaction), motor response, and cognitive evaluation (1).
Emotional changes can affect short-lasting processing like emotional reaction or long-
standing states like mood. After stroke, emotional disturbances include mood disorders,
emotional dyscontrol, and alteration of emotional reactions. They are of utmost impor-
tance and certainly unrecognized by clinicians, not only in the acute phase, but also in the
chronic stage, when behavioral changes are noted. It has been recognized that emotional
state is not only an important part of the feeling of well-being but also it has high influence
on patients’ behavior. Behavior, which refers to the manner in which a person acts in a
given situation, is influenced by a multitude of cognitive and emotional lexicons, like
information from our semantic memory—including moral knowledge—our pattern of
preferences, our emotional states, and our pattern of reactivity (impulsivity or apathy).
A simple example of a classic emotional disturbance in the acute phase of stroke is
the anosognosia for the disease, that although exemplified in the Anton-Babinski
syndrome, reflects a typical tendency of the brain to neglect perceptual loss (2). Such
tendency partly explains why stroke patients take much longer time to arrive at the
Address correspondence to Jean-Marie Annoni, MD, Department of Neurology, University
Hospital, CH-1011 Lausanne, Switzerland; E-mail:
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244 J.-M. Annoni et al.
emergency department, while it takes less than 2 hr for a cardiac infarct. Another mecha-
nism that can explain defective cognitive-emotional integration is what can be called
“acute memory or acute remembering impairment” in patients with acute stroke (3).
According to these, up to 33% of stroke patients have no, or only a poor, memory of
what actually happened during the acute phase. The interesting aspect is that this usually
occurs without specific damage to the classic anatomical structures known to be involved
in learning. Whether this is an acute phenomenon, perhaps linked to some kind of “sider-
ation” of brain function or to the natural brain difficulty to recognize a neurological
impairment, is not always clear. We often call this anosognosia, although this term lumps
together quite different conditions, that can include the patient being convinced that he or
she is not ill, does not have motor impairment, does not have a potentially severe medical
condition, or does not have a brain problem. The particularity of these impairments during
acute phase can explain why immediate poststroke emotional changes are different from
the more chronic stages.
Acute Stage
One problem in looking at the literature is that descriptions combine the acute and chronic
consequences of stroke. For instance, mania and mania-like states may really be acute
phase problems, as is catastrophic reaction, seen in some patients very early in the course
of stroke, whereas depression, by definition, is a chronic manifestation. One of the main
issues is that in contrast to the plethora of studies on poststroke depression several weeks,
months, or years after stroke, emotion and behavior during the acute stroke phase have
received very little attention.
At Lausanne, we have developed the Emotional Behavioural Index, that can be com-
pleted by nurses in continuous care units. Its advantage is that it provides a description,
rather than an interpretation, of behavior in acute stroke patients (4). In principle, depres-
sion already is a diagnosis, i.e., it is already an interpretation of the facts rather than a
simple description that the patient looks sad or is crying. The measurement of behavior
may be much closer to reality, especially in patients with communications problems, e.g.,
aphasics, who are usually systematically excluded from studies because of their communi-
cation problems. The Emotional Behavioural Index bypasses the need for language
communication (5).
In our experience in over 300 acute patients, overt sadness is the most common
manifestation (72%), followed by disinhibition (56%), lack of adaptation (44%), envi-
ronmental withdrawal (40%), crying (27%), anosognosia (24%), passivity (24%), and
aggressiveness (11%). Overt sadness is more frequently associated with left (86%) rather
than right (61%) hemisphere lesions (p < 0.05), and the association is even greater in
the case of crying (50% versus 20% for left and right hemisphere lesions, respectively;
p= 0.02). With right-side lesions, anosognosia is clearly associated with neglect (95%
versus 34% for neglect versus nonneglect, respectively; p = 0.01). However, with right
hemisphere lesions, both sadness and indifference also are more frequent in anosognosic
patients. It is interesting to see that even in right hemisphere stroke, sadness is not absent
by any means.
Moreover, anosognosia may coexist with severe sadness, that at first sight may seem
paradoxical. However, it is obvious that sadness, even leading to depression in some
cases, actually can develop in patients who are not really aware of their own condition (6).
A particular emotional modification in the acute phase is the catastrophic reaction (CR) in
acute stroke (7). The prevalence is as low as 3% (n = 12 among 326 patients with
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Emotional Disturbances 245
first-ever stroke), but the very strong correlation with the presence of aphasia (100%
patients were aphasics) and with left insular location suggests that it is an emotional
behavior that is induced by specific network damage. It also has been interpreted as
“reflex” or “avoidance” behavior more than a psychological reaction. Interestingly, 66%
of patients with CR developed depression in the chronic stage.
Acute phase emotional changes also can present psychosis. Acute psychosis has been
described rarely but in a precise way after acute stroke. In the case of Low, an 82-year-old
man was admitted very restless, agitated, and noisy and was shouting and screaming
incessantly, after a left posterior cerebral artery infarct (8).
Chronic Phase
Poststroke depression (PSD) is not rare, occurring in 40% of stroke victims, with minor
and major poststroke depression occurring in equal proportions. Data from different studies
have found prevalence rates for major depression of 19.3% among hospitalized patients
and 23.3% among outpatient samples (9). Although in our group the proportion of PSD
patients remains similar at 12 months than at 3 months (35% in both groups), the late
depression are different patients than the early depressed (10).
The cause of PSD has been associated with left anterior lesion location in numerous
independent studies. Although a meta-analysis (11) of PSD and lesion location failed to
find a significant association, it seems that during the first 2 months after an acute stroke,
left frontal and left basal ganglia lesions were significantly more frequent among patients
with major depression compared with any other lesion location (9).
Furthermore, another meta-analysis of the literature examining the correlation
between severity of depression and proximity of the lesion to the left frontal pole found a
significant correlation (pooled correlation coefficient: r = .53 fixed model, r = .59
random model) for patients who were less than 6 months poststroke (12). Interestingly,
some findings suggest that left stroke could be a predictor of treatment resistance to selec-
tive serotonin reuptake inhibitors (13). These results fit with the ones obtained in control
subjects on the role of left frontal areas on positive thinking.
The chronic PSD and anxiety also are more frequent in patients with subcortical
(white matter, thalamus, basal ganglia) or brain stem lesion. One recent finding in biolog-
ical psychiatry is the fact that silent brain infarcts and cerebral white matter lesions on
magnetic resonance imaging (MRI) were found to be more frequent in the depressed
elderly than in controls. Cerebral small vessel disease has been rediscovered as a potential
cause of depression (14).
Clinically, this shows important differences from what psychiatrists call endogenous
depression. Even severe cases of PSD are not identical to endogenous depression, as they
have much more reactive diurnal mood variation and emotionalism, show an absence of
guilt, and are rarely suicidal. Among 142 patients with 2-year follow-up, the psychologi-
cal symptoms that were not significantly more frequent in the depressed compared with
the nondepressed group were suicide plans, simple ideas of reference, pathologic guilt
irritability, and self-depreciation (15). Gainotti (16) comparing patients with poststroke
major depression with 30 patients found that patients with endogenous depression (i.e., no
associated brain injury) had higher scores on anhedonia and suicide, and patients with
PSD had higher scores on hyperemotionalism, catastrophic reactions, and diurnal mood
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246 J.-M. Annoni et al.
Anxiety Disorders
Anxiety disorders are frequent ( 25%) after strokes (17). Furthermore, heavy cognitive def-
icits increase difficulty in recognizing anxiety, supporting the need for more studies in minor
strokes. In a prospective study including 90 patients assessed 6 months after a minor stroke,
isolated significant anxious scores were present in 26/90 patients (29%) Hospital Anxiety
and Depression Scale, anxiety > or = to 8). In particular, symptoms consistent with posttrau-
matic stress disorder (PTSD) can occur after stroke as a consequence of the sudden occur-
rence of a life-threatening event. One year after stroke, posttraumatic-like symptoms were
present in 15 of the 49 patients (31%) who completed the impact event scale (IES; > or = to
30). PTSD-like syndrome was independent of neurological impairment, physical disability,
and nosognosia during hospitalization and peristroke amnesia, but it was more frequent in
patients who felt concerned about death in the acute phase. Concerning lesion localization,
no specific lesion localization was associated with PTSD symptoms. Nevertheless, intrusive
symptoms were increased after lesions involving basal ganglia strokes, suggesting that re-
experiencing phenomena may be modulated by frontal-subcortical pathways (18, 19).
Mania and Bipolar Disorders
Mania seems to be related more strongly to right hemispheric lesions. One study found
that of 9 patients with mania following stroke, 8 had right hemisphere lesions, while in
major depression in which only 7 of 31 patients had right hemisphere strokes (20). While
major depression during the acute stroke period was associated with left frontal and left
basal ganglia lesions, mania was associated with right orbital frontal, basotemporal, basal
ganglia (21), or thalamic lesions (22). In addition, when poststroke patients with mania
were compared with poststroke patients matched for lesion size and location, the mania
patients had significantly greater subcortical atrophy (23–25).
Psychosis is quite rare after stroke. Among 157 patients following their first stroke, the
frequency of all depressive disorders was 17.2%, but no cases of mania or psychosis were
found (26). Some other clinical pictures take the form of “delusional misidentification
syndromes” (DMS), that include “reduplicative paramnesia” (RP) for places, reduplica-
tion of people, events, objects, and roles; Capgras’ syndrome where an impostor is thought
by the patient replaces the real person, and numerous variations such as Fregoli syndrome,
intermetamorphosis syndrome, the “reverse” syndromes.
Some observations suggest that DMS is a functional disconnection between past mne-
sic information and the ability to integrate them with actual experiences (28). Although
most of the DMS are related to diffuse brain dysfunction, some can be induced by stroke.
Some isolated case reports suggest that left perilimbic lesions may play a role in the devel-
opment of psychotic symptoms (29, 30). Susceptibility to develop schizophreniform ill-
ness after stroke includes pre-existing subcortical, atrophy, and right hemisphere lesion
location of the stroke (31).
Emotional Hyperactivity and Flattening
Mood swing and emotional hyperactivity are well known after bilateral cerebrovascular
lesion and in vascular dementia. Some of them are associated with emotional disinhibition
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Emotional Disturbances 247
with outburst and loss of emotional control, as in basal ganglia and frontal degenerative
pathologies (32, 33).
Emotional flattening is the frequent consequence of amygdala or medioventral frontal
cortex damage (34) and can be associated with impaired autonomic reactivity. However,
blunting of affect or disinhibited and inappropriate behaviors can be observed—together
with executive and other cognitive dysfunction—in patients with lesions involving the
posterior lobe of the cerebellum and the vermis (35). This type of emotional flattening
seems to be associated with an impaired autonomic system response to the emotional
valence of stimuli (36).
Poststroke Fatigue
In our study, we have defined fatigue as a reversible decrease or loss of abilities associated with
a heightened sensation of physical or mental strain, even without conspicuous effort. This con-
dition is due to an overwhelming feeling of exhaustion, that leads to an inability to sustain, or a
difficulty in sustaining, even routine activities. Preliminary data show that patients with fatigue
can be depressed, but that a large cohort (20% to 50%) of patients are not (37). The important
aspect is that patients with poststroke fatigue do not show either severe neurological distur-
bance or functional impairment. Our preliminary findings emphasize that patients with so-
called primary poststroke fatigue may have mainly brain stem lesions (38). At 1 year, there was
a significant association of fatigue with young age, neurological impairment, and anxiety lev-
els (for cortical and subcortical lesions), and with attentional performances for cortical lesions.
There was no significant association with laboratory workup (cortisol, thyroxine, Thyrotropin
Releasing Hormone, adeno-corticotropic hormone).
We speculate that many cases of poststroke fatigue may correspond to subtle attentional
dysfunction, although neuropsychological assessment shows no cognitive-executive distur-
bance. Some researchers noted that the patients with a postpolio fatigue syndrome had spe-
cific neuropsychological disorders with attentional difficulties and slowing of information
processing speed. A cognitive profile was compatible with an impairment of basal ganglia
and reticular activating system. The neuroanatomical studies (autopsic Magnetic Resonance
Imaging and studies) indeed revealed constant and severe lesions in the reticular formation,
hypothalamic and thalamic nuclei, and basal ganglia, thus showing that the poliovirus dam-
ages cerebral areas responsible for cortical activation. Finally, the authors found a significant
negative correlation between fatigue and level of plasmatic adrenocorticotropic hormone
suggesting a hypofunctionning of the hypothalamic-pituitary-adrenal axis (39).
This work was supported by the Swiss National Science Foundation grant number
3151AO-102271 to J.-M. Annoni and 3200–061342.00 to J. Bogousslavsky. We thank
Cephalon very much for his contribution in the present study. A short study about the
effect of modafinil on fatigue after stroke is in progress.
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... Following a stroke, which happens when blood flow to a region of the brain is cut off or reduced, emotional alterations are typical (4,5). Because the damage alters the brain, which determines behavior and reactions, stroke survivors frequently experience more negative emotional states than they did originally (4,5). ...
... Following a stroke, which happens when blood flow to a region of the brain is cut off or reduced, emotional alterations are typical (4,5). Because the damage alters the brain, which determines behavior and reactions, stroke survivors frequently experience more negative emotional states than they did originally (4,5). Indeed, the American Stroke Association associates post-stroke patients' conditions with irritability, perplexity, anger, and depression (6). ...
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Background: Stroke is a leading cause of disability and death worldwide. There are numerous debates regarding the relationship between depression, anxiety, insomnia, perceived stress, and ischemic stroke. Moreover, no research on the efficacy of emotion regulation, which is critical for various components of healthy affective and social adaptability, is being conducted. To the best of our knowledge, this is the first study in the MENA region to shed light on the relationship between these conditions and stroke risk, aiming to determine whether depression, anxiety, insomnia, stress, and the way of coping with emotions may be risk factors for ischemic stroke occurrence and to further investigate the ability of two specific types of emotion regulation (cognitive reappraisal and expressive suppression) as possible moderators of the relationship between these psychological diseases and ischemic stroke risk. As a secondary objective, we sought to determine how these pre-existing conditions affect stroke severity levels. Methods: This is a case–control survey study involving 113 Lebanese inpatients with a clinical diagnosis of ischemic stroke admitted in hospitals and rehabilitation centers in Beirut and Mount Lebanon, and 451 gender-matched volunteers without clinical signs of stroke as controls recruited from the same hospitals as the cases or attending outpatient clinics for illnesses or treatments unconnected to stroke or transient ischemic attack, as well as visitors or relatives of inpatients (April 2020–April 2021). Data was collected by filling out an anonymous paperbased questionnaire. Results: According to the outcomes of the regression model, depression (aOR: 1.232, 95%CI: 1.008–1.506), perceived stress (aOR: 1.690, 95%CI: 1.413–2.022), a lower educational level (aOR: 0.335, 95%CI: 0.011–10.579), and being married (aOR: 3.862, 95%CI: 1.509–9.888) were associated with an increased risk of ischemic stroke. The moderation analysis revealed that expressive suppression had a significant moderating effect on the relationship between depression, anxiety, perceived stress, insomnia, and ischemic stroke risk, resulting in an increased risk of stroke incidence. In contrast, cognitive reappraisal significantly reduced the risk of ischemic stroke by moderating the association between ischemic stroke risk and the following independent variables: perceived stress and insomnia. On the other hand, our multinomial regression model revealed that the odds of moderate to severe/severe stroke were significantly higher in people with pre-stroke depression (aOR: 1.088, 95% CI: 0.747–1.586) and perceived stress (aOR: 2.564, 95% CI: 1.604–4.100) compared to people who had never had a stroke. Conclusion: Despite several limitations, the findings of our study suggest that people who are depressed or stressed are more likely to have an ischemic stroke. Consequently, additional research into the causes and effects of depression and perceived stress may provide new directions for preventive strategies that can help reduce the risk of stroke. Since pre-stroke depression and perceived stress were also found to be strongly correlated with stroke severity, future studies should evaluate the association between pre-stroke depression, perceived stress, and stroke severity to gain a deeper understanding of the complex interaction between these variables. Lastly, the study shed new light on the role of emotion regulation in the relationship between depression, anxiety, perceived stress, insomnia, and ischemic stroke.
... Patients were classified into "no anger" group if they scored 0 in all the selected items and into "anger" group, if not. Other rating tools used were the Emotional Behavior Index 15 and Emotional and Social Dysfunction Questionnaire. 16 ...
... In the acute stage of stroke (i.e., when patients are admitted to a hospital), PSA or aggressive behaviors occurred in 11% to 35% of the patients. [9][10][11]15 In the subacute stage (3 to 12 months after stroke onset), the prevalence was 19% to 32%. 2,7 Thus, despite the different study settings and diagnostic tools used, PSA appears to be relatively common during both the acute and subacute stages of stroke. ...
Post-stroke mood and emotional disturbances are frequent and diverse in their manifestations. Among them, post-stroke depression is the best known. Although post-stroke anger (PSA) has been studied relatively less, it can be as frequent as depression. Manifestations of PSA range from overt aggressive behaviors (including hitting or hurting others) to becoming irritable, impulsive, hostile, and less tolerable to family members. The possible pathophysiological mechanisms of PSA include neurochemical dysfunction due to brain injury, frustration associated with neurological deficits or unfavorable environments, and genetic predisposition. PSA causes distress in both patients and their caregivers, negatively influences the patient’s quality of life, and increases the burden on caregivers. It can be treated or prevented using various methods, including pharmacological therapies. In addition, anger or hostility may also be a risk or triggering factor for stroke. The hazardous effects of anger may be mediated by other risk factors, including hypertension or diabetes mellitus. The identification of anger as a result or cause of stroke is important because strategic management of anger may help improve the patient’s quality of life or prevent stroke occurrence. In this narrative review, we describe the phenomenology, prevalence, factors or predictors, relevant lesion locations, and pharmacological treatment of PSA. We further describe the current evidence on anger as a risk or triggering factor for stroke.
... Stroke's most common symptoms include speech/language problems, tiredness, fatigue, and pain. The effect of Stroke also causes emotional disturbance issues, cognitive impairment, and other neurological disorders [8]. Among the different types of effects, the emotional disturbance is most common in all patients who suffered from Stroke, and it is caused due to the dysfunction of the emotion-processing network in brain hemispheres [9][10][11]. ...
... Compared to the spectral feature extraction method based on FFT, time-frequency analysis based on Wavelet Transform (WT) has been broadly used in emotion classification using EEG signals. DWT features extracted from three frequency bands such as alpha (8)(9)(10)(11)(12)(13), beta (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30), and gamma (30-49 Hz) using different mother wavelet functions are used to classify five basic emotions using KNN and LDA classifiers [40]. Nasehi and Pourghassem utilized the DWT-based features to classify the emotions and achieved a maximum mean accuracy of 59.99% [41]. ...
Stroke is a cerebrovascular disorder, and one of the most common effects of stroke is emotional disturbances. This present work classifies six emotions (anger, sadness, happiness, fear, disgust, and surprise) of two types of stroke (left brain damage and right brain-damage) using electroencephalogram (EEG) signals. EEG signals are collected from 19 each subject of LBD, RBD, and normal control (NC) at a sampling rate of 128 Hz. The IIR Bandpass filter and amplitude thresholding methods are used to reduce noise and artifacts' effects, respectively. Discrete Wavelet Packet Transform is used to extract five EEG frequency bands (alpha, beta, gamma, alpha to gamma, and beta to gamma). A set of nonlinear features are extracted from five different EEG frequency ranges using recurrent quantification analysis. Finally, the extracted features are mapped to six corresponding emotions using three nonlinear classifiers (K nearest neighbor, probabilistic neural network, and random forest). The experimental results indicate that LBD subjects have severe emotional impairment than RBD. The mean of diagonal line length (< L >), recurrence rate, and maximum mean diagonal length (Lmax) feature give maximum classification rate of 85.24% NC, 79.54%, and 79.09% using RF classifier compared to other features. The alpha to gamma (13–49 Hz) band helps identify Stroke emotional state changes compared to other frequency bands.
... Strengthening the eye movements seems thus important. Research on ocular motor problems following brain injuries (Wilhelmsen, 2000) and ocular motor deficits among pupils (Gallaway & Boas, 2007) show that structured exercises can reduce the amplitude of unsteady fixation, strengthen the binocular vision, improve VA through better accommodation and lead to improved reading skills. Accommodative ability in particular is poor in learners with albinism (Karlén & Milestad, 2019). ...
... For pupils' development there ought to be competent vision teachers who can follow up Barraga's (1964) work and develop individual suitable methods in an educational setting. A lot of research show that a specter of vision exercises has a positive influence on ocular motor disorders and leads to better functional vision for a range of vision problems connected to different diagnoses (Examples: Amani & Poustinch, 2019;Coats, 2012;Sterner et al., 2001;Wilhelmsen, 2000;Wilhelmsen et al., 2015). Given the significant problems of children with albinism in reading and due to their low reading speed, it is time for further investigations on stimulating vision methods in education. ...
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Albinism is a huge challenge both socially and educationally in Tanzania and many other countries. Pupils with albinism are normally encouraged to read with a fixed gaze due to their nystagmus, and there are doubts about whether refraction improves their reading. The aim is to get more knowledge about their functional vision as a fundament for educating pupils with albinism. The article presents a case study with three pupils from a primary school in Tanzania who went through a functional assessment of vision using standardized methods and a new eye-tracker software measuring smooth pursuits. The assessment reveals large individual differences not only in visual acuity but also in ocular motor functions. There is a need for better understanding of the vision challenges these pupils face so that professionals can develop more suitable methods in school for securing their education.
... The participants in this study expressed a variety of feelings, emotions, and mental health concerns, including feelings of hopelessness, embarrassment, shame, shock, fear, anxiety, anger, sadness, grief, and depression. These findings are consistent with Annoni et al. (2006), who highlighted the wide variety of acute and chronic feelings and emotional disturbances that commonly occur after a stroke. Moreover, consistent with Miller et al. (2010) and Towfighi et al. (2017), who revealed that the emotional and psychological ramifications of having a stroke are often underdiagnosed and untreated, the majority of the participants in this study felt as though their health care providers typically avoided the emotional and psychological ramifications of having a stroke. ...
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Background: Depression and anxiety can negatively impact one’s recovery, outcomes, and quality of life. Even though therapists consider the mental health needs of their clients to be a priority, they are dissatisfied with their ability to completely address these needs. The purpose of this study was to examine the client’s perspective regarding the extent to which health care professionals addressed their psychosocial needs after a stroke. Method: A phenomenological research design was used to collect data from six participants. Interviews and focus group were audiotaped, transcribed verbatim, and thematically analyzed. Member checks, peer-review, multiple coders, triangulation, and expert examination were used to increase trustworthiness of findings. Results: Five themes emerged. People with strokes: (a) experience an array of emotions, (b) are not likely to initiate disclosure of their state of mental health, (c) feel their psychosocial needs are not being addressed by health care professionals, (d) grieve the loss of prior roles post stroke and work hard to establish a new normal routine and purpose in life, and (e) have suggestions for improved care. Conclusion: These findings reinforce the importance of addressing the mental health needs of individuals post stroke and the importance of identifying methods to enhance the ability to effectively address the psychosocial needs of clients post stroke.
... Many adult stroke patients suffer from generalized anxiety, major depressive disorder, phobias, and/or obsessive-compulsive disorder following a stroke in which the basal ganglia was involved. [1][2][3][4][5][6][7][8][9] However, there are few studies describing mood disorders after pediatric basal ganglia stroke, and little data on how mental health issues in children after stroke affect the whole family, or how long recovery takes. This report presents 2 children with mental health issues after basal ganglia stroke and reviews the literature on the effects of basal ganglia stroke on mental health in adults and children. ...
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Background The impact of basal ganglia stroke on mental health is better described in adults than in children. We report 2 children with significant mental health issues after basal ganglia stroke. Case Reports Patient 1, an 8-year-old boy, had mild anxiety before his left basal ganglia stroke. Post-stroke, he developed severe anxiety, obsessions, depression, and attention deficit hyperactivity disorder, in addition to a right hemiplegia and some mild chorea. He gradually improved over 3 years with psychiatric care and medication but continued to have residual symptoms. Patient 2, a 10-year-old boy, had no history of mental health issues before his right basal ganglia stroke. Post-stroke, he developed significant anxiety and mild depression, along with a left hemiplegia. He improved over 9 months and returned to his mental health baseline. Conclusions Mental health issues after basal ganglia stroke in children can be significant, and recovery can take months to years.
... A post-stroke depression has been found to be highly correlated with cognitive impairments, with a passive perception of quality of life and increased mortality. It has been shown that in patients who have had a stroke within 15 months of rehabilitation, patients with depression died 8 times more often than the patients without depression [12,13,14]. According to transcranial dopleography there is a decrease of the rate of cerebral blood flow in patients with poststroke depression [15]. ...
The article presents data aboutthe impactof the drug Melitor (agomelatine) on the psycho-emotional activity, cerebral hemodynamics, bioelectric activity ofthe brain and their intersystem connectionsinpatients with post-stroke depression. 30 patients with post-stroke depression have been takena dose of Melitor25 mg per day for 2 months. It has been established that Melitor has a positive effect on psycho-emotional activity, improves cerebral hemodynamics, harmonizes the structure of bioelectric activity of the braininpatients with post-stroke depression.Melitor has more strong effect on cerebral hemodynamics and bioelectric activity of the brain inpatients with right-sided stroke than among thepatients with left-sided stroke. Melitor's multimodal influencejustifies the use of the drug during the rehabilitationtreatment of post-stroke patients for the improvementboth functional and psycho-emotional state.
... [1,2] Such neurological disease can cause important organic, psychological and emotional disturbances, such as pseudobulbar affect (PBA) and emotional dysregulation. [3] PBA includes pathological laughing and crying, emotional liability, emotional dysregulation, involuntary emotional expression disorder, and emotional incontinence. Among these disorders, alexithymia should not be confused with PBA or pathological laughing and crying. ...
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Introduction: About 66% of stroke survivors present with cognitive or physical consequences, which are often complicated by emotional instability. Alexithymia is defined as "a difficulty in identifying and describing feelings", although there is no consensus on the exact diagnosis and treatment. Patient concerns: A 36-year-old right-handed man, affected by ischemic stroke (which occurred about 3 months before admission) involving the right hemisphere (ie, the fronto-parieto-temporal region) with left hemiparesis and behavioral abnormalities, came to our observation for intensive rehabilitation. He was treated unsuccessfully with a traditional and behavioral training. Diagnosis: Alexithymia due to ischemic stroke. Interventions: Then, a specific combined protocol using computerized emotional and virtual emotional training was applied in a semi-immersive virtual reality environment using the BTS-Nirvana device. Outcomes: At the end of this novel rehabilitation approach, the patient showed a significant improvement in emotional skills, cognitive performances, and coping strategies. Conclusions: Virtual reality, in addition to standard therapy, may be a valuable tool in improving emotional abnormalities due to brain lesions, such as alexithymia.
Post-stroke mood and emotional disturbances are frequent and diverse in their manifestations. Out of these, post-stroke depression is best known. Although post-stroke anger (PSA) has been relatively less studied, this is not less common than depression. Manifestations of PSA range from overt aggressive behaviors such as hitting or hurting others to becoming irritable, impulsive, hostile, and less tolerable to family members. The pathophysiological mechanism of PSA remains unclear, but the neurochemical dysfunction due to brain injury, frustration associated with neurological deficits or surrounding environment, or genetic predisposition have been considered. In general, PSA is distressing for both the patients and their caregivers, negatively influences the patient’s quality of life, and increases the burden of caregivers. Fortunately, PSA can be treated or prevented by various methods, including pharmacological therapy. To administer appropriate management, we have to properly diagnose PSA and understand its phenomenology, predicting factors and pathophysiology. Nevertheless, PSA has been understudied and under-recognized, and well-designed clinical trials are rare. This narrative review describes the phenomenology, prevalence, factors or predictors, relevant lesion locations, and pharmacological treatment for PSA.
Depression in late life is a recognised public health problem. After establishing socio-demographic and psychological risk factors for depression, epidemiological research has focused on biological factors. This review summarises the evidence on the associations of cerebrovascular pathology, inflammation, and endocrine and nutritional status with depression in the elderly. The most consistent finding in biological psychiatry is the disturbance of the hypothalamic - pituary - adrenal axis in depressed persons. About half of the patients with severe depression have a disturbed glucocorticoid feedback mechanism and many exhibit hypercortisolism. Longitudinal studies show that this endocrine dysfunction increases the risk of relapse. More recently, silent brain infarcts and cerebral white matter lesions on MRI were found to be more frequent in the depressed elderly than in controls. Cerebral small vessel disease has been rediscovered as a potential cause of depression. Furthermore, there is evidence of immune activation in depressed persons. However, it remains unclear as to whether inflammation contributes to the pathological process as longitudinal studies are lacking. Clinical studies have also related many nutrients to psychological symptoms, but the evidence in elderly persons is consistent only for some vitamin deficiencies. In conclusion, despite a substantial body of literature on biological correlates of late life depression, little is known about causal relations. Prospective population-based studies are warranted.
Reduplicative paramnesia refers more often to places than to time or to persons. We report here the case of a 16-year-old student who, after a severe brain injury, presented the delusion of a double who was I year younger than himself and with no physical impairment. This patient presented a severe memory deficit, particularly in the verbal modality, uninhibited behaviour, decreased self awareness, difficulties in planning and impaired mental flexibility. There were no visuo-spatial or autotopognosic deficits. His delusion diminished over 2.5 years and, at the same time, learning and executive functions returned to normal. However, a retrograde amnesia of 1 year persisted. This observation is in line with Staton et al.'s(Cortex 1982; 18: 23-36) hypothesis about reduplicative paramnesia being a functional disconnection between past mnesic information and the ability to integrate it with actual experiences. Magnetic resonance imaging showed bilateral frontal contusions more severe on the left side, a small left anterior thalamic contusion, and a secondary atrophy of the left hippocampus and the left anterior temporal pole. The role of the left temporal paralimbic posttraumatic lesions in relation to reduplication of self is discussed.
This chapter explores the neural basis of emotional experience. Although emotional experience may be induced by conditioned stimuli, most emotional behavior and experiences are induced by complex stimuli that may be verbal or nonverbal, visual, auditory, or even tactile. The cerebral cortex of humans has complex modular systems that analyze these stimuli, develop precepts, and interpret meaning. The portions of the brain that process emotional stimuli depend upon the modality and mode of the stimulus. The determination of valence is based upon whether or not the stimulus is beneficial—positive—or detrimental—negative—to the well-being of the person or the person's family or society. The right frontal lobe appears to be important in the mediation of emotions with negative valence and the left frontal lobe in the mediation of emotions with positive valence. Depending upon the nature of the stimulus, some positive and some negative emotions are associated with high arousal and others with low arousal. The right parietal lobe appears to be important in mediating arousal response and the left appears to inhibit the arousal response. Similarly, some positive and negative emotions are associated with motor activation and others are not.
Reviews the role of lateralization and localization of dysfunction and proposes a neuroanatomic and neuropsychologic model for the delusion. In 570 cases, 252 reports of the delusion of substitution yielded 200 cases (aged 14–90 yrs) with an organic contributor to the occurrence of the delusion. In 79 cases, lateralization or localization could be determined, with lesions primarily in the left temporal or right frontal areas. A slight trend favored occurrences in the elderly, mood and schizophrenic disorders made up 30% of the population, and 82% had only 1 form of Capgras syndrome. Factors related to feature recognition, familiarity, and reduplication could be found and are discussed in relation to the neurobehavioral features of the symptom, including atrophy in the frontal, temporal, and parietal lobes. (PsycINFO Database Record (c) 2012 APA, all rights reserved)