Published online Nov 19, 2026. doi: 10.5498/wjp.125243
Revised: July 22, 2026
Accepted: August 10, 2026
Published online: November 19, 2026
Processing time: 118 Days and 0.2 Hours
Depression and anxiety after stroke are common neuropsychiatric disorders that disrupt participation in rehabilitation programs, quality of life, and functional outcomes. These symptoms rarely occur in isolation, and are often accompanied by sleep disturbances, fatigue, reduced daytime activity, and circadian dysregulation. Sleep disorders after stroke, including insomnia, poor sleep quality, disordered breathing, and excessive sleepiness during the daytime. These sy
Core Tip: This article synthesizes evidence on the clinical interplay between post-stroke depression/anxiety, sleep disturbance, and circadian dysregulation, highlighting shared inflammatory mechanisms. It proposes a comprehensive framework integrating mood monitoring, sleep-circadian evaluation, biomarker assessment, and phenotype-based interventions to address these interconnected contributors to poor functional recovery and rehabilitation outcomes.
- Citation: Liu XA, Liu J, Xu D, Zhao X. Inflammation, sleep-circadian disruption, and neuropsychiatric recovery after stroke: Mechanisms and integrated interventions for post-stroke depression and anxiety. World J Psychiatry 2026; 16(11): 125243
- URL: https://www.wjgnet.com/2220-3206/full/v16/i11/125243.htm
- DOI: https://dx.doi.org/10.5498/wjp.125243
Among stroke survivors, neuropsychiatric symptoms such as post-stroke depression and anxiety are common, and may adversely affect quality of life during recovery. According to previous studies, post-stroke depression is a frequent comp
Depression, anxiety, and sleep disorders rarely occur in isolation after stroke in clinical practice. Many patients experience difficulty sleeping, excessive daytime sleepiness, and fragmented sleep during hospitalization and rehabilitation. A recent systematic review and meta-analysis reported an association between post-stroke depression and post-stroke sleep disorders, suggesting that sleep disturbance is not merely a secondary complaint in patients with post-stroke emotional symptoms[5]. Post-stroke insomnia is also common, although prevalence estimates vary because of differences in sleep assessment tools, stroke stage, and the definition of insomnia across studies[6]. Beyond insomnia, sleep-disordered breathing, excessive daytime sleepiness, restless legs symptoms, and altered sleep architecture can also hinder neurological recovery and emotional adjustment in the post-stroke period[7].
Besides sleep disturbances, circadian rhythm dysregulation has increasingly been recognized as an important factor in post-stroke recovery. For instance, the circadian rhythm regulates sleep-wake timing, hormonal release, autonomic func
Inflammation links stroke injury, sleep-circadian disruption, and mood symptoms. Ischemic and hemorrhagic brain injury may trigger neuroinflammatory and peripheral immune responses, including microglial activation, blood-brain barrier dysfunction, and altered neuroendocrine regulation[9]. These processes may influence neurotransmitter metabolism and hypothalamic-pituitary-adrenal (HPA) axis activity, thereby increasing the vulnerability to depressive and anxiety symptoms in some patients[9]. Among the various inflammatory biomarkers, interleukin-6 (IL-6) has attracted particular attention, and peripheral IL-6 levels during the acute stage of stroke may predict the subsequent development of post-stroke depression[10]. However, inflammatory biomarkers should not be viewed as deterministic causes of mood disorders, because they may also reflect stroke severity, infection, comorbid metabolic disease, medication exposure, or other clinical conditions.
Sleep and circadian disturbances may also influence this inflammatory network. A recent narrative review suggested that sleep disruption may activate inflammatory pathways and contribute to depressive symptoms through immune and neuroendocrine mechanisms[11]. In stroke survivors, this relationship may be even more pronounced because sleep fragmentation and circadian misalignment are frequently accompanied by neurological impairment and emotional distress. Sleep disruption post-stroke is better conceptualized as a multifaceted condition encompassing psychological components, inflammatory processes, and environmental factors rather than as a single sleep disturbance[12].
Collectively, current evidence suggests that post-stroke depression and anxiety may be conceptualized within a broa
This narrative review was based on PubMed, Web of Science, and Google Scholar from database inception to 18 July 2026. Reference lists of relevant publications were also screened. Search terms combined stroke-related terms with terms related to depression, anxiety, sleep disturbance, circadian rhythm, inflammation, biomarkers, rehabilitation, and intervention.
Eligible publications included studies involving adult stroke survivors, systematic reviews, meta-analyses, clinical guidelines, and mechanistic studies directly relevant to the proposed network. Pediatric studies, isolated case reports, non-peer-reviewed publications, and studies without relevant mood, sleep, circadian, inflammatory, or rehabilitation outcomes were excluded. When direct stroke-specific evidence was unavailable, evidence from non-stroke populations was used only to support biological plausibility and was explicitly described as indirect evidence. Meanwhile, evidence was interpreted hierarchically. Clinical guidelines and systematic reviews or meta-analyses were given the greatest weight, followed by individual clinical studies.
Depression and anxiety after stroke share several clinical features, including poor sleep, fatigue, and decreased participation in rehabilitation. However, they do not represent a single syndrome. Depression following stroke is typically characterized by depressed mood, reduced interest, and decreased motivation. By contrast, anxiety following stroke is characterized by excessive worry, fear of recurrence, and somatic hypervigilance.
Sleep disturbance may further contribute to this clinical convergence. Recent studies have shown that sleep duration and sleep disorders are associated with post-stroke depression, suggesting that sleep disturbance may serve as a useful clinical indicator for identifying patients with emotional disorders after stroke[13]. Fatigue may also complicate clinical interpretation because it may be associated with mood disorders, central nervous system injury, or physical deconditioning[14]. Therefore, patients who report low energy or poor motivation should be assessed for mood symptoms, sleep quality, and circadian rhythm disruption.
Sleep disorders after stroke are clinically heterogeneous. For instance, insomnia, sleep-disordered breathing, and exce
This clinical heterogeneity has important implications for practice. For instance, difficulty initiating sleep may be asso
Circadian rhythm disruption is commonly associated with sleep disturbance; however, the two conditions are not identical. Circadian rhythm disruption primarily refers to alterations in the timing, regularity, and amplitude of daily biological rhythms. Clinically, it may present as irregular sleep-wake patterns, decreased daytime activity, or excessive daytime napping. Post-stroke, circadian rhythm may be disrupted by limited mobility, insufficient daytime light exposure, and prolonged bed rest. Environmental disturbances, such as noise at night time, can also reduce the distinction between day and night.
Circadian rhythm has increasingly been recognized as a clinically meaningful aspect of stroke recovery. From a clinician’s perspective, circadian rhythm may have important implications for sleep, vascular regulation, and rehabilitation participation[16]. Objective studies have also indicated that rest-activity rhythm disturbances can be detected during stroke rehabilitation, highlighting the value of evaluating daily rhythms beyond subjective sleep complaints[17]. Together, these studies suggest that circadian rhythm disruption may be a quantifiable and potentially targetable component of post-stroke recovery.
Taken together, depression, anxiety, sleep complaints, and circadian dysregulation may represent a coexisting clinical cluster after stroke. If emotional symptoms are treated without evaluating sleep and daily rhythms, important and treatable contributing factors may be overlooked. Conversely, treating sleep complaints without considering affective symptoms and circadian dysfunction may represent an incomplete approach. This clinical overlap provides the rationale for a more holistic approach to post-stroke neuropsychiatric evaluation and management.
Inflammation is a potential biological mechanism linking stroke injury, sleep-circadian disruption, and post-stroke mood symptoms. However, it should not be regarded as a single linear cause of post-stroke depression or anxiety. Inflammation contributes to both injury and repair, and the inflammatory milieu may fluctuate throughout different phases of recovery. A network-based view is therefore more appropriate because inflammatory activity may interact with neuroendocrine stress, sleep regulation, and participation in rehabilitation.
Both central and systemic inflammatory reactions may be triggered by stroke. Ischemic or hemorrhagic brain injury can activate glial cells, disrupt the blood-brain barrier, and induce oxidative stress. Stroke may also affect immune cell function and systemic immune responses in the periphery. These reactions are not static and can vary across the acute, subacute, and chronic phases of recovery[18].
Microglia and macrophages may promote tissue remodeling and clearance of cellular debris; however, sustained pro-inflammatory responses may interfere with synaptic repair and potentially amplify emotional vulnerability. A review of the literature on microglial and macrophage phenotypes suggests that neuroinflammation can contribute to post-stroke depression, possibly through cytokine signaling, tryptophan metabolism, and plasticity-related mechanisms[19].
Therefore, the key question is not whether inflammation is beneficial or detrimental. Rather, the clinical issue is whether inflammatory processes are adequately regulated and resolved. Prolonged systemic inflammation, infection, metabolic disease, or sleep disruption may promote a biological milieu that predisposes patients to mood symptoms.
Inflammation may contribute to depressive symptoms after stroke through several mechanisms. For instance, pro-inflammatory cytokines may influence monoamine metabolism and the HPA axis, both of which are involved in emotional regulation and cognitive function. An individual prospective clinical study reported associations between inflammatory cytokines and post-stroke depression, although the findings may have been influenced by differences in stroke characteristics, depression assessment, and adjustment for confounding factors[20].
Meta-analyses also support an association between acute inflammatory activation and subsequent depressive symptoms in patients with stroke. One meta-analysis showed that pro-inflammatory cytokines were associated with an increased risk of post-stroke depression during the acute phase of stroke[21]. These findings support the biological plausibility of inflammation-related depressive vulnerability; however, this association should not be overinterpreted. Elevated inflammatory markers may also reflect stroke severity or other systemic diseases.
Mechanistic and exploratory evidence suggest that the kynurenine pathway may provide another link between inflammation and depressive symptoms. Inflammatory activation may facilitate tryptophan catabolism through the kynurenine pathway, potentially affecting serotonin availability, glutamatergic activity, oxidative stress, and neurotoxicity. In acute ischemic stroke, tryptophan catabolism through the kynurenine pathway has been studied as a component of the immunometabolic response to brain injury[22]. Kynurenine-related biomarkers have also been evaluated in relation to depressive symptoms; however, the available evidence suggests that the relationship is not straightforward[23]. Thus, the kynurenine pathway should be considered a potential mechanistic pathway, although its precise role in post-stroke mood disturbance has not yet been clearly established.
The inflammatory basis of post-stroke anxiety is less well understood than that of post-stroke depression. However, this does not imply that inflammation is unrelated to anxiety. Rather, the available evidence is more limited and less conclu
Preliminary evidence from an individual clinical study suggests that immune markers may be associated with post-stroke anxiety. For example, reduced levels of serum IL-10 have been associated with post-stroke anxiety and cognitive dysfunction in patients with acute stroke, suggesting that anti-inflammatory signaling may play a role in neuropsychiatric outcomes[24]. However, this field is still emerging, and evidence supporting a causal role for inflammation in post-stroke anxiety remains limited. A more cautious interpretation is that inflammatory dysregulation may increase physiological vulnerability to subsequent psychological stress or sleep disturbance.
This distinction is critical for this review. Depression and anxiety may coexist following stroke, but they are not necessarily driven by the same inflammatory mechanisms. Depressive features may be more closely associated with sickness behavior and reduced motivation, whereas anxiety may be more closely associated with threat detection, anticipation, and autonomic activation. Therefore, future research should treat post-stroke depression and anxiety as distinct emotional outcomes.
Sleep disturbances may potentiate inflammatory signaling, thereby contributing to post-stroke mood symptoms. Indirect evidence from experimental and non-stroke clinical research indicates that sleep deprivation can promote inflammatory responses and impair adaptive immune regulation[25]. In stroke survivors, this pathway remains biologically plausible but requires more direct longitudinal validation.
In addition, poor sleep may contribute to fatigue and limit daytime activity and participation in rehabilitation. These behavioral sequelae may, in turn, maintain depressive withdrawal and anxiety-related avoidance. Conversely, inflammation-induced signaling can disrupt sleep and lead to fatigue, creating a bidirectional cycle. Hence, sleep disturbance may not only be a symptom of post-stroke depression or anxiety but also a contributing factor that sustains the biological and behavioral milieu associated with impaired emotional recovery.
This is not to suggest that treating sleep disturbances alone would prevent post-stroke depression or anxiety. Instead, sleep disturbance may be one treatable factor within the broader recovery process. Identifying specific sleep phenotypes, such as insomnia, sleep fragmentation, sleep-disordered breathing, or circadian dysregulation, may facilitate more targeted interventions and potentially lessen the inflammatory and stress-related burden that contributes to mood symptoms.
The circadian rhythm acts as a temporal organizer of sleep, activity, hormonal secretion, autonomic tone, metabolism, and immune function. Circadian disruption may result from the desynchronization of internal rhythms with environmental or behavioral time cues, such as light-dark cycles, sleep-wake schedules, meal patterns, and physical activity. Broader human evidence outside the stroke field indicates that circadian disruption is associated with adverse neurological, psychiatric, and metabolic outcomes[26].
Post-stroke circadian organization may be impaired by brain injury, decreased daytime activity, limited exposure to natural light, noise, sleep interruption, prolonged bed rest, fatigue, and irregular rehabilitation schedules. Such altera
Circadian disruption may, therefore, have important implications for mood symptoms. Reviews examining circadian rhythms and mood disorders indicate that disturbances in biological timing, rhythm amplitude, light exposure, and sleep-wake stability may contribute to depressive and anxiety-related symptoms[27]. In stroke survivors, direct evidence that post-stroke circadian immune misalignment contributes to depression and anxiety remains limited, highlighting an important area for future research.
The evidence reviewed above supports a bidirectional network model rather than a single-cause model. Within this framework, stroke injury initiates neuroinflammatory and systemic immune responses. These responses may affect neurotransmitter metabolism, neuroplasticity, HPA axis activity, autonomic regulation, fatigue, and emotional processing. Simultaneously, sleep disruption and circadian disruption may promote inflammation and impair behavioral recovery. These interacting pathways are illustrated in the proposed bidirectional inflammatory network shown in Figure 1.
This model contributes to our understanding of why post-stroke depression and anxiety commonly occur alongside sleep disturbance, fatigue, and reduced participation in rehabilitation. In an insomnia-dominant phenotype, poor sleep may exacerbate fatigue and emotional lability, potentially hindering engagement in rehabilitation. Reduced activity and limited daylight exposure may, in turn, contribute to further circadian disruption. In an anxiety-dominant hyperarousal phenotype, fear of recurrence and hypervigilance to bodily sensations may lead to more frequent nighttime awakenings, sustained autonomic arousal, and further sleep disruption. These profiles may share overlapping inflammatory and neuroendocrine mechanisms while exhibiting distinct dominant clinical phenotypes.
The model also stresses that inflammation is context-dependent. Elevated cytokine or inflammatory marker levels may reflect immune activation, but they may also reflect stroke severity, infection, obesity, diabetes, vascular disease, medication exposure, or poor sleep. Likewise, sleep and circadian disruption may also result from brain injury, emotional distress, environmental influences, or coexisting sleep disorders. Thus, no single marker or symptom should be regarded as sufficient to explain post-stroke mood symptoms.
Current evidence does not support the existence of a single universal driver of post-stroke mood disturbance. Instead, the relative importance of each component is likely to vary according to the stage of recovery and the dominant clinical phenotype. Stroke injury and neurological impairment represent upstream initiating factors. In selected patients, however, persistent insomnia or untreated sleep-disordered breathing may become proximal and modifiable drivers of fatigue, emotional distress, and reduced rehabilitation participation.
Inflammation is more appropriately viewed as a biological mediator and marker of vulnerability than as a standalone cause of post-stroke depression or anxiety. Although meta-analytic evidence supports an association between acute inflammatory activation and subsequent depression, inflammatory markers remain nonspecific and may also reflect stroke severity or medical comorbidity. Circadian disruption may act primarily as an amplifier, linking weak light and activity cues to sleep instability and reduced rehabilitation engagement. However, direct evidence establishing circadian immune misalignment as an independent cause of post-stroke mood symptoms remains limited.
Fatigue and reduced participation in rehabilitation are generally downstream consequences of these processes. Never
One actionable aspect of this model is the need for a phenotype-based evaluation. Some patients may present with an insomnia-predominant phenotype; others may exhibit anxious hyperarousal, circadian misalignment, inflammatory-risk phenotypes, sleep-disordered breathing, or fatigue-dominant recovery patterns. These patterns may help move post-stroke neuropsychiatric care beyond symptomatic treatment alone. Rather than treating depression, anxiety, sleep disturbance, and fatigue as discrete problems, clinicians and researchers should consider how these domains interact within the same recovery network.
Overall, this network model provides a balanced framework by recognizing that inflammation, sleep disturbance, and circadian dysregulation may have different roles across patients and recovery stages. It also provides the conceptual basis for the phenotype-based assessment framework described below.
A comprehensive evaluation framework is required because post-stroke depression, anxiety, sleep disturbance, circadian disruption, and inflammatory activity may coexist while remaining distinct clinical entities. This does not imply that mood symptoms can be attributed to a single cause. Instead, the evaluation should assist clinicians in identifying treatable contributing factors and determining the predominant clinical phenotype. The relevant assessment domains, recommended tools, their clinical value, and key considerations are summarized in Table 1.
| Domain | Suggested assessments | Clinical value | Important cautions |
| Mood symptoms | PHQ-9, HDRS, HADS, GAD-7, clinical interview | Identify depression, anxiety, comorbidity, and symptom severity | Somatic items may overlap with fatigue, aphasia, cognitive impairment, and neurological deficits |
| Sleep disturbance | PSQI, ISI, ESS, sleep diary, snoring/apnea screening | Identify insomnia, daytime sleepiness, sleep-disordered breathing, and fragmented sleep | Subjective sleep complaints may be influenced by mood and cognition |
| Circadian rhythm | Sleep timing, nap pattern, light exposure, activity rhythm, actigraphy | Identify irregular sleep-wake rhythm, low daytime activity, and weak day-night contrast | Actigraphy is useful but not always available in routine care |
| Inflammatory status | CRP, IL-6, TNF-α, IL-1β, NLR | Characterize inflammatory risk and biological vulnerability | Markers are nonspecific and affected by infection, stroke severity, metabolic disease, and medications |
| Rehabilitation context | Activity level, therapy participation, ward environment, pain, nocturia | Identify modifiable barriers to recovery | Requires multidisciplinary observation and repeated assessment |
Assessment of mood after stroke should encompass both depression and anxiety using the Patient Health Questionnaire-9, the Hamilton Depression Rating Scale, and the Hospital Anxiety and Depression Scale. Emerging evidence suggests that the Patient Health Questionnaire-9 and Hamilton Depression Rating Scale are valid for assessing post-stroke depression. The choice of scale, however, should be based on the patient's neurological status, communication ability, and cognitive function[28]. For anxiety, the Generalized Anxiety Disorder-7 or the Hospital Anxiety and Depression Scale anxiety subscale can be administered; however, the results should be interpreted in conjunction with the clinical interview and the patient's functional status.
Total scores should not be used in isolation to evaluate mood. Symptoms such as poor sleep, fatigue, and reduced concentration may reflect mood disturbance, neurological impairment, or post-stroke fatigue. Clinician-rated assessments and caregiver input may also be necessary for patients with aphasia or cognitive impairment. Repeated evaluation is also important because patients' emotional states may fluctuate during the transition from acute hospitalization to rehabilitation and subsequent community reintegration.
Sleep evaluation should focus on identifying the specific sleep phenotype rather than simply determining whether the patient reports poor sleep. Routine screening should include questions regarding symptoms of insomnia, daytime sleepiness, and signs of sleep-disordered breathing. Clinicians should also assess pain, nocturia, and medication burden because these factors may contribute to post-stroke sleep complaints. Subjective sleep assessment tools, such as the Pittsburgh Sleep Quality Index, Insomnia Severity Index, and Epworth Sleepiness Scale, can be used to quantify sleep quality and associated daytime impairment.
Objective evaluation may be warranted if symptoms are ambiguous or if sleep-disordered breathing, an irregular sleep-wake rhythm, or chronic fatigue is suspected. Actigraphy may be used to collect data over multiple days on sleep timing, sleep continuity, and rest-activity cycles in the patient’s natural environment[29]. Polysomnography should be considered when sleep apnea or other complex sleep disorders are suspected. In stroke survivors, sleep evaluation should also consider the care environment because nighttime nursing care and rehabilitation schedules may affect sleep quality.
Circadian evaluation should focus on assessing the phase and stability of daily rhythms. Clinically, the assessment can begin with simple questions about sleep-wake timing, daytime napping, and exposure to morning light. Sleep logs and caregiver reports may be useful for determining whether the primary issue is insomnia, a circadian rhythm disorder, or excessive daytime sleepiness.
Actigraphy offers a more objective assessment of rest-activity rhythms. It provides information beyond sleep measurement by helping determine whether patients maintain a regular day-night rhythm and engage in sufficient daytime activity. In community-dwelling stroke survivors, rest-activity rhythm parameters have been associated with mood and cognitive complaints, indicating that rhythm evaluation may have clinical implications in this population beyond sleep duration alone[30]. More complex measures, such as melatonin or cortisol rhythm assessments, may be used for research purposes, but they are not routine clinical tools.
Inflammatory markers may aid in identifying biological susceptibility, but they should not be interpreted in isolation as diagnostic tools for post-stroke depression or anxiety. Markers, including C-reactive protein and IL-6, may be valuable in research and risk stratification, particularly when assessed serially and interpreted in conjunction with clinical data[31]. Their principal use is to provide a biological context rather than replace clinical assessment.
Several cautions should be considered. Inflammatory markers may reflect stroke severity, infection, or comorbid illness rather than mood symptoms. It is also important to appropriately time blood collection, as acute and chronic inflammation may have different clinical implications. Thus, biomarker evaluation should be interpreted in conjunction with assessments of mood, sleep, circadian rhythm, and functional status rather than be performed independently.
A combined treatment approach for emotional symptoms, sleep disruption, and circadian misalignment is warranted. The intent is not to supplant evidence-based treatment for post-stroke depression or anxiety but rather to expand care beyond single-symptom management by incorporating a network-based approach to recovery. In practice, interventions should be tailored to the degree of neurological impairment, communication ability, and functional capacity.
Sleep and circadian health should be incorporated into evaluation and treatment beginning in the stroke unit and continuing throughout rehabilitation. Stroke rehabilitation recommendations and clinical guidelines emphasize early assessment, participation in rehabilitation, and multidisciplinary care[32,33]. In this context, sleep and circadian care can be integrated into routine clinical practice without placing an undue burden on healthcare providers.
A practical intervention is to reinforce the day-night cycle. During daytime care, adequate light exposure, appropriate activities, and regular rehabilitation programs should be encouraged. Unless clinically contraindicated, nighttime noise, light exposure, and unnecessary care interruptions should be minimized. Urinary symptoms, pain, and anxiety should also be managed because they frequently interfere with sleep. These foundational practices may be particularly beneficial in the hospital setting, where the natural distinction between day and night is often diminished.
Sleep-targeted interventions should be selected according to the predominant sleep phenotype. For insomnia-dominant presentations, cognitive behavioral therapy for insomnia (CBT-I) is the preferred first-line nonpharmacological treatment for adults with chronic insomnia[34]. Stroke survivors may require adapted treatment delivery, as cognitive impairment, aphasia, or fatigue can limit the implementation of standard CBT-I procedures. A pragmatic, stroke-tailored model could incorporate simplified elements of sleep education, behavioral guidance, and caregiver participation using a case-based approach.
When sleep-disordered breathing is suspected, screening and referral for a comprehensive sleep evaluation are warranted. Continuous positive airway pressure therapy can be used in patients with stroke and sleep apnea; however, adherence remains a major challenge[35]. Pharmacological treatment for sleep disorders may be considered in selected cases, but should be used with caution because sedation, falls, and cognitive adverse effects are among the most important concerns following stroke. Whenever feasible, medication should be supplemented with behavioral and environmental interventions rather than used as the sole treatment.
Interventions targeting the circadian system are designed to promote the restoration of a stable day-night pattern. Exposure to morning light, a consistent wake time, and structured daytime activity may help stabilize circadian rhythms. These strategies may be especially relevant for patients with excessive daytime napping, low daytime activity, or irregular sleep-wake patterns.
Bright light therapy is a promising circadian-targeted intervention. In a randomized, double-blind, placebo-controlled study of patients with mild-to-moderate stroke and post-stroke insomnia, morning bright light therapy improved sleep-related outcomes and was also associated with improved daytime functioning[36]. However, the evidence remains limited. The optimal timing, duration, and patient selection criteria require further investigation. Melatonin and other chronobiotic approaches may also be considered; however, their use after stroke should be individualized and undertaken with caution.
Inflammation- and neuroplasticity-targeted strategies should be considered within a broad clinical framework. Currently, there is insufficient evidence to support the use of anti-inflammatory drugs specifically for preventing or treating post-stroke depression or anxiety. However, established rehabilitation and neuropsychiatric interventions may have secondary effects on inflammatory activity through their positive effects on sleep, stress reduction, and physical rehabilitation.
Evidence-based treatment of post-stroke depression includes both pharmacological and nonpharmacological approaches. A Bayesian network meta-analysis indicated that several antidepressant and psychotherapeutic interventions may alleviate depressive symptoms, although the optimal treatment may vary among patients[37]. Repetitive transcranial magnetic stimulation has also recently demonstrated potential efficacy for post-stroke depression, although protocol heterogeneity remains a significant limitation[38]. Exercise interventions may help reduce depressive symptoms and promote functional recovery after stroke[39]. These interventions should therefore be considered part of an integrated care approach rather than standalone anti-inflammatory therapies.
Table 2 summarizes phenotype-based integrated intervention strategies to help clinicians identify the most prominent modifiable pathway in each patient and tailor care according to the predominant clinical phenotype. For example, patients with insomnia-dominant symptoms may require sleep-focused care, whereas those with circadian disruption may benefit more from daytime activity and light-based interventions. Patients with sleep-disordered breathing may require respiratory sleep assessment and continuous positive airway pressure therapy, when appropriate, whereas those with anxiety-dominant hyperarousal may benefit from psychoeducation, relaxation training, and sleep stabilization. When inflammatory-risk features are prominent, clinicians should also address infection, pain, and metabolic comorbidities.
| Dominant phenotype | Clinical clues | Immediate clinical priority | Integrated management |
| Insomnia-dominant | Difficulty initiating or maintaining sleep, early awakening | Exclude pain, nocturia, medication effects, and major environmental disruption | Sleep hygiene, stroke-adapted CBT-I, pain/nocturia control, nighttime environment optimization |
| Sleep-disordered breathing phenotype | Snoring, witnessed apnea, daytime sleepiness, resistant fatigue | Confirm respiratory risk and arrange formal sleep evaluation | Sleep medicine referral, CPAP if appropriate, vascular risk management |
| Circadian-disruption phenotype | Excessive daytime napping, nighttime wakefulness, low daytime activity | Restore daytime light exposure and regular activity timing | Morning light exposure, regular wake time, structured rehabilitation schedule, reduce evening light |
| Anxiety-hyperarousal phenotype | Fear of recurrence, bodily vigilance, panic-like symptoms, nocturnal worry | Assess symptom severity and stabilize nocturnal hyperarousal | Psychoeducation, relaxation training, graded return to activity, sleep stabilization |
| Inflammatory-risk phenotype | High CRP/IL-6, infection, pain, obesity, diabetes, poor sleep | Identify infection or uncontrolled medical comorbidity | Treat infection/pain, metabolic control, activity promotion, mood and sleep treatment |
| Fatigue-dominant phenotype | Low energy, reduced participation, daytime sleepiness | Distinguish sleepiness, mood symptoms, and physical deconditioning | Activity pacing, rehabilitation adjustment, sleep/circadian care, mood management |
This phenotype-based model may help translate the proposed network framework into individualized post-stroke care. It encourages clinicians to consider how mood symptoms, sleep disturbance, circadian rhythms, and rehabilitation engagement interact within the same patient rather than treating each problem as a separate condition.
The target populations, main advantages, limitations, and current evidence and clinical status of the principal interventions discussed above are compared in Table 3.
| Intervention | Main target population or indication | Main advantages | Major limitations and implementation issues | Current evidence and clinical status |
| Basic sleep and circadian care | Stroke patients receiving acute or inpatient rehabilitation care, particularly those with environmental sleep disruption or a weakened day-night rhythm | Low risk, inexpensive, and feasible within routine multidisciplinary care | Effects on mood and functional recovery are difficult to isolate; implementation depends on ward organization and staff coordination | Routine supportive care consistent with rehabilitation guidelines, although direct intervention evidence for mood outcomes remains limited[32,33] |
| Stroke-adapted CBT-I | Medically stable patients with an insomnia-dominant phenotype; caregiver support may be required when communication or cognitive limitations are present | First-line nonpharmacological treatment for chronic insomnia; avoids sedative adverse effects and addresses behavioral factors that maintain insomnia | Requires trained personnel and adaptation for aphasia, cognitive impairment, or severe fatigue; treatment engagement may be difficult | Established for chronic insomnia in adults; clinically reasonable after stroke, but stroke-specific evidence remains limited[34] |
| Continuous positive airway pressure | Patients with confirmed sleep apnea, particularly those with snoring, witnessed apnea, or persistent daytime sleepiness | Directly treats airway obstruction and intermittent hypoxia; may support vascular and neurological recovery | Adherence and mask tolerance remain major barriers; cognitive or physical impairment may complicate treatment; direct effects on mood remain uncertain | Established treatment for confirmed sleep apnea; evidence for post-stroke recovery is supportive but heterogeneous[35] |
| Morning bright light and circadian scheduling | Patients with circadian disruption, excessive daytime napping, low daytime activity, or irregular sleep-wake timing | Low pharmacological burden and directly strengthens environmental timing cues; feasible during rehabilitation | Optimal light intensity, timing, and treatment duration remain uncertain; response may vary among patients | Promising but still exploratory as a stroke-specific intervention; evidence is based on a limited number of clinical trials[36] |
| Exercise and structured daytime activity | Medically stable patients with reduced activity, physical deconditioning, fatigue, or depressive symptoms | Already forms part of routine rehabilitation and may support mood, sleep, and functional recovery | Intensity must be adapted to neurological and cardiovascular status; intervention protocols remain heterogeneous | Routine rehabilitation component with supportive evidence for reducing depressive symptoms[39] |
| Antidepressant medication and structured psychotherapy | Patients with clinically significant or persistent post-stroke depression or anxiety | Directly targets emotional symptoms and can be integrated with rehabilitation and sleep-focused care | Medication adverse effects and interactions require monitoring; psychotherapy may be limited by aphasia, cognitive impairment, or access to trained professionals | Established components of post-stroke depression care; evidence is stronger for depression than for post-stroke anxiety[37] |
| Repetitive transcranial magnetic stimulation | Selected medically stable patients with persistent post-stroke depression, particularly when standard treatment is insufficient or poorly tolerated | Nonpharmacological neuromodulation with potential antidepressant effects | Requires specialized equipment and trained personnel; treatment protocols remain heterogeneous; accessibility and cost may limit use | Specialized adjunct rather than routine first-line treatment; supported by meta-analytic evidence but requiring further protocol standardization[38] |
| Anti-inflammatory pharmacotherapy | No established routine indication for post-stroke depression or anxiety; currently relevant mainly to research settings | Biologically plausible and may target pathways implicated in the proposed network | Clinical efficacy, appropriate patient selection, and safety remain uncertain; inflammatory biomarkers are nonspecific | Exploratory; anti-inflammatory medication cannot currently be recommended specifically for post-stroke depression or anxiety outside clinical research |
| Melatonin and other chronobiotic strategies | Selected patients with circadian misalignment or persistent sleep-timing disturbance | May support circadian timing with a relatively low treatment burden | Stroke-specific efficacy and optimal timing remain uncertain; medication interactions and individual tolerability require consideration | Exploratory in post-stroke care and not yet supported for routine phenotype-based use |
| Sedative or hypnotic medication | Selected patients with severe short-term sleep disturbance when nonpharmacological measures are insufficient | May provide short-term symptom relief | Sedation, falls, cognitive adverse effects, respiratory suppression, and daytime impairment are important concerns after stroke | Selective and cautious use only; not preferred as the sole or first-line long-term strategy |
Clinical priorities should change across the stages of stroke recovery. During the acute stage, the first priority is to identify conditions that require immediate medical management, such as respiratory compromise, infection, delirium, uncontrolled pain, or medication-related sedation. Basic sleep-circadian care and brief mood screening can be initiated at this stage, but intensive behavioral treatment may not yet be feasible.
During inpatient rehabilitation, assessment should focus on identifying the dominant sleep-mood-circadian phenotype. A patient with snoring, witnessed apnea, and persistent daytime sleepiness should be prioritized for respiratory sleep evaluation before insomnia-focused treatment. By contrast, a medically stable patient with persistent sleep-onset difficulty and anxiety-related hyperarousal may benefit from stroke-adapted CBT-I, psychoeducation, and structured daytime activity. Patients with marked daytime inactivity and irregular sleep timing may require greater emphasis on morning light exposure and rehabilitation scheduling.
During long-term community recovery, persistent depression or anxiety should prompt structured psychiatric or psychological treatment. Sleep treatment, exercise, and circadian stabilization should continue when relevant, while repetitive transcranial magnetic stimulation may be considered as a specialized adjunct in selected patients with persistent post-stroke depression.
Implementation requires multidisciplinary collaboration. Neurologists should evaluate stroke-related and other medical contributors; rehabilitation professionals should optimize activity and treatment schedules; sleep specialists should assess suspected sleep-disordered breathing; and mental health professionals should manage persistent mood symptoms and provide behavioral sleep interventions. The rehabilitation team should integrate these recommendations into a shared and periodically updated care plan.
Several important gaps remain in this field. Many existing studies are cross-sectional, making it difficult to determine whether inflammation, sleep disturbance, or mood symptoms occur first. Longitudinal studies with repeated assessments are needed to clarify temporal relationships and identify patients at greater risk at specific stages of the recovery process. Furthermore, post-stroke anxiety has been studied less extensively than post-stroke depression. Future research should assess depression and anxiety as distinct outcomes while also accounting for their frequent comorbidity.
Assessment procedures also require further refinement. Sleep assessment continues to rely primarily on subjective questionnaires, which are susceptible to biases related to mood, cognition, and communication difficulties. Future rese
Greater methodological rigor is needed when studying inflammatory biomarkers. Biomarker levels may be influenced by stroke severity, infection, comorbidities, or medication use. Repeated biomarker assessments and standardized samp
Intervention studies should also move beyond single-domain treatment. Integrated interventions incorporating mood management, sleep care, circadian regulation, and rehabilitative engagement may be more appropriate for evaluating the network model proposed in this review. Future models of care should become more phenotype-informed. By integrating clinical symptoms, daily activity, and biomarker data, clinicians may be better able to identify predominant recovery-limiting phenotypes and personalize intervention strategies.
Emerging digital technologies may support more dynamic and individualized assessment of post-stroke neuropsychiatric recovery. Machine-learning models could integrate clinical, biomarker, and neuroimaging data to identify patien
Post-stroke depression and anxiety should not be considered merely psychological responses to, or isolated psychiatric sequelae of, the physical consequences of stroke. Instead, they may arise from complex interactions among brain injury, inflammation, sleep disturbance, and circadian dysregulation. Sleep and circadian disruption may be particularly important because they are prevalent, clinically observable, and potentially modifiable throughout stroke recovery.
A network-based framework does not suggest that any single pathway fully explains post-stroke mood symptoms. Instead, it emphasizes that inflammation, sleep disruption, circadian instability, and rehabilitation engagement may interact throughout different stages of recovery. Integrated assessment and phenotype-based interventions may therefore provide a more practical approach than treating mood symptoms, sleep disturbance, fatigue, and rehabilitation participation as separate problems. Future longitudinal and interventional studies are needed to determine whether targeting sleep-circadian regulation and inflammatory risk can improve emotional recovery after stroke.
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