Hospital Noise and Post-Stroke Sleep Disorders: A Review of Mechanisms and Management Strategies

Abstract

Hospital noise is a pervasive environmental stressor that may adversely affect sleep quality and neurological recovery of post-stroke patients. Although the World Health Organization has established recommended limits for hospital noise levels, real-world conditions frequently exceed these limits, with the issue being particularly pronounced in stroke wards due to noise generated by medical equipment and staff activity. The incidence of post-stroke sleep disorders is notably high. Noise disrupts sleep architecture through pathophysiological mechanisms, including activation of the auditory pathway and cortical arousal, induction of stress responses and neuroendocrine dysregulation, and increased cardiovascular burden. These detrimental effects are further amplified by the heightened vulnerability resulting from post-stroke brain injury. Clinical evidence indicates a dose–response relationship between hospital noise levels and impaired subjective sleep quality and sleep efficiency. Furthermore, noise has been associated with delayed motor and cognitive functions and exacerbates mood disorders. Effective management strategies require systematic, multifaceted interventions, encompassing engineering and administrative modifications at the noise source, along with patient-centered protective measures and sound-masking therapies. However, challenges such as the complexity of hospital noise, individual patient differences, and implementation compliance persist, and high-quality research in this area remains insufficient. Future efforts should focus on developing intelligent monitoring systems, conducting research on personalized clinical pathways, and integrating noise management throughout the stroke rehabilitation process to establish an optimal acoustic environment conducive to neurological recovery.

KEY MESSAGES

• (1)Hospital noise exacerbates post-stroke sleep disorders through multiple pathophysiological mechanisms, with stroke patients exhibiting special vulnerability due to brain-injury-induced deficits in auditory filtering and sleep–wake regulation.
• (2)A significant dose–response relationship exists between hospital noise levels and sleep quality in stroke patients; noise-induced sleep fragmentation directly impairs motor, cognitive, and emotional recovery.
• (3)Systematic, multi-faceted hospital noise management strategies—including engineering, administrative, and patient-centered interventions—can effectively reduce ward noise and improve sleep quality in stroke patients.

INTRODUCTION

Environmental noise pollution has become a prevalent issue in healthcare facilities worldwide, exerting substantial negative impacts on patient recovery. The World Health Organization (WHO) recommends that background noise levels in hospital wards should not exceed 30 dB(A) at night and 35 dB(A) during the day, with nighttime peaks no higher than 40 dB(A) during the day. However, real-world conditions frequently surpass these standards.[1] Zhou et al.[2] reported that noise levels across various hospital departments generally exceeded recommended limits. Notably, noise in intensive care units (ICUs) can even exceed 100 dB(A), equivalent to the intensity of high-volume headphone music, far surpassing internationally recommended limits.[3] General ICU noise research can serve as a basis for noise management in stroke wards, and the noise control measures shown to be effective in ICUs can be optimized and applied to stroke wards according to the particular vulnerability of patients with stroke.[4] Noise pollution not only disrupts patient rest but also may also contribute to a series of physiological and psychological issues, emerging as a critical environmental factor affecting healthcare quality.

Post-stroke sleep disorders are highly prevalent. Research indicates that the incidence of sleep disorders is approximately 73% in patients with intracerebral hemorrhage and around 63% in those with cerebral infarction.[5] These sleep disturbances manifest in various forms, including difficulty initiating sleep, difficulty maintaining sleep, early awakening, or excessive daytime sleepiness, which may adversely affect the process of neurological rehabilitation. High-quality sleep supports brain remodeling and the formation of new neural synapses, thereby promoting motor function recovery in post-stroke patients.[6]

As a remarkable environmental stressor, noise may exacerbate sleep disturbances in patients with stroke through multiple mechanisms. A review by Basner et al.[7] showed that when noise exceeds 35 dB(A), the duration of deep sleep can be reduced by 50%; noise levels above 70 dB(A) may lead to the complete disappearance of deep sleep. Stroke survivors, due to impaired sleep–wake regulation mechanisms resulting from brain injury, exhibit increased sensitivity to noise stimuli. Sudden noises in the hospital environment, such as equipment alarms, staff conversations, and trolley movement, not only disrupt sleep architecture but may also activate the sympathetic nervous system, leading to elevated blood pressure and altered heart rate variability, thereby further hindering neurological recovery.[8]

Current research on the relationship between noise and post-stroke sleep disorders remains insufficient, and the effectiveness of noise management interventions has not been comprehensively synthesized. While most hospital noise control measures focus on equipment modification and workflow optimization, personalized management strategies tailored to vulnerable populations, such as stroke survivors, require further development. This review aims to elucidate the mechanisms by which noise affects post-stroke sleep disorders, summarize effective hospital noise management strategies, and provide evidence-based insights and practical guidance for improving the rehabilitation environment for post-stroke patients.

PATHOPHYSIOLOGICAL MECHANISMS OF NOISE IMPACT ON SLEEP

Activation of Auditory Pathways and Cortical Arousal

Environmental noise primarily affects the central nervous system through the auditory pathway. Auditory signals are converted into neural impulses by the cochlea, which are then transmitted via brainstem auditory nuclei to the medial geniculate nucleus of the thalamus, ultimately projecting to the primary auditory cortex for information processing.[9] During sleep, this continuous input of auditory information may activate arousal-related neural networks, particularly the ascending reticular activating system of the brainstem reticular formation, thereby inducing desynchronization of cortical electrical activity and leading to transitions between sleep and wake states.[10]

Patients with stroke exhibit significant deficits in auditory information filtering due to post-stroke brain injury. Three pathophysiological mechanisms have been proposed to explain this heightened vulnerability. First, impaired prefrontal cortical after stroke may weaken the sensory gating mechanism that inhibits cortical responses to irrelevant auditory stimuli during sleep in the healthy brain. Functional magnetic resonance imaging (fMRI) studies have suggested that upon exposure to noise stimuli, patients with stroke exhibit a two- to three-fold greater activation intensity in the primary auditory cortex compared with healthy individuals, and signal diffusion extends to the limbic and paralimbic systems, indicating central sensitization.[11] Second, stroke-induced blood-brain barrier disruption increases the permeability of cerebral microvessels, and noise stimulation may further promote neuroinflammatory responses in the auditory cortex and brainstem, with elevated levels of pro-inflammatory factors such as tumor necrosis factor-alpha and interleukin-6, which may contribute to cortical arousal and sleep fragmentation.[12] Third, post-stroke neuroinflammation in the brainstem reticular formation may impair the regulation of sleep–wake cycles and increase the responsiveness of the ascending activating system to auditory signals.

The temporal association cortex plays a crucial role in sound-induced arousal. Research has found that calcium/calmodulin-dependent protein kinase II alpha (CaMKIIα)-positive neurons in this region can encode sound intensity and may regulate the arousal threshold during non-rapid eye movement (NREM) sleep via glutamatergic pathways projecting to the basolateral amygdala.[13] When noise levels exceed 40 dB(A), even in the absence of complete awakening, a cortical microarousal phenomenon manifests as a reduction in delta wave activity and an increase in high-frequency beta waves, which directly disrupts sleep continuity.[14]

The pontine central grey matter plays a key role in mediating rapid arousal. Following the reception of auditory signals, glutamatergic neurons in this area can facilitate rapid transition from sleep to wakefulness within 100–200 ms through polysynaptic transmission to the medial dorsal thalamic nucleus, lateral hypothalamus, and ventral tegmental area.[15] This evolutionarily conserved defensive mechanism is particularly sensitive to sudden noises in post-stroke patients; persistent hospital noises, such as equipment alarms and staff activity, may repeatedly trigger this mechanism in such patients, leading to exacerbated sleep fragmentation due to their impaired sleep–wake regulation mechanisms.[16]

Stress Response and Neuroendocrine Effects

Noise, as an environmental stressor, can activate the hypothalamic–pituitary–adrenal (HPA) axis stress response system. While the auditory pathway transmits signals to the auditory cortex, it also sends collateral projections to limbic system structures such as the amygdala, initiating a neuroendocrine cascade. Yelden et al.[17] found that nocturnal exposure to noise above 50 dB(A) can increase plasma cortisol levels by 30%–45%, a change that not only prolongs sleep latency but also largely reduces the duration of deep sleep.

Post-stroke neuroplastic changes and neuroinflammation further amplify the neuroendocrine and stress damage caused by noise. Brain-derived neurotrophic factor (BDNF) in the hippocampal region is downregulated following cerebral ischemia, and BDNF is a key factor for post-stroke brain remodeling and synaptic plasticity. Reduced BDNF expression may increase neuronal vulnerability to metabolic stress induced by noise, and the combined effect of the two inhibits the formation of new synapses in patients with stroke, potentially hindering brain remodeling and delaying the recovery of motor and cognitive functions.[18] Concurrently, abnormal hyperexcitability of glutamatergic neurons in peri-infarct regions allows noise stimuli to trigger peri-infarct depolarizations via N-methyl-D-aspartate (NMDA) receptor-mediated mechanisms, which expands the ischemic penumbra and damages the impaired but potentially salvageable neurons in the penumbra, thus impeding the repair and functional recovery of the ischemic penumbra.[19] In addition, post-stroke blood-brain barrier disruption allows peripheral inflammatory factors to enter the central nervous system, and noise-induced HPA axis activation further upregulates inflammatory factor expression, forming a vicious cycle of stress and neuroinflammation, which may contribute to neuroendocrine dysregulation.

The sympathetic–adrenal–medullary system also plays an important role in noise-induced stress. Sudden noise stimuli can cause adrenaline and noradrenaline levels to peak within 15 s, leading to accelerated heart rate and elevated blood pressure. Such physiological activation may interfere with the parasympathetic dominance required for sleep.[20] Chronic exposure to a noisy hospital environment may lead to autonomic nervous system dysfunction, characterized by reduced heart rate variability and diminished baroreflex sensitivity, further impairing sleep quality. For post-stroke patients, this noise-induced autonomic nervous system dysfunction is superimposed on the autonomic dysfunction caused by brain injury itself. The combined effects may contribute to a more severe disruption of neuroendocrine regulation and a greater reduction in the pulsatile secretion of growth hormone-releasing hormone (GHRH), which exacerbates the impairment of neurorepair processes in patients with stroke.

Neuroendocrine dysregulation also affects the secretion of key sleep-regulating hormones. Noise-induced disruption of the cortisol rhythm may interfere with melatonin synthesis by the pineal gland. As an endogenous sleep inducer, impaired melatonin secretion directly leads to disturbances in the sleep–wake cycle.[21] Concurrently, noise stress reduces the pulsatile GHRH secretion, affecting growth hormone release during slow-wave sleep. This is particularly detrimental to the neurorepair and recovery processes after stroke.

Impact on the Cardiovascular System

The acute effects of nocturnal noise on the cardiovascular system are primarily manifested as transient fluctuations in blood pressure and heart rate. A laboratory study reported that even brief exposure to sudden noise lasting only 0.5–2 s can increase systolic blood pressure by 10–15 mmHg and diastolic blood pressure by 5–8 mmHg.[22] This hemodynamic response is particularly pronounced during NREM sleep. The underlying mechanism involves the activation of sympathetic outflow via the amygdala–hypothalamic pathway by noise, leading to peripheral vasoconstriction and increased cardiac output.

Patients with stroke have a substantially higher cardiovascular burden due to brain injury, and the noise-induced acute cardiovascular response is more intense in such patients; frequent awakenings induced by noise can lead to a more obvious elevation of left ventricular end-diastolic pressure and a greater increase in myocardial oxygen consumption in patients after stroke.[23] For post-stroke patients comorbid with coronary artery disease, these alterations are more likely to trigger silent myocardial ischemia, and the noise-related reductions in heart rate variability and impaired baroreflex sensitivity, combined with post-stroke autonomic nervous system damage, become more severe independent risk factors for sudden cardiac death following stroke.

A clear association exists between chronic noise exposure and long-term cardiovascular damage. Epidemiological investigations indicate that individuals chronically exposed to nighttime traffic noise levels exceeding 55 dB(A) have a 27% increased risk of developing hypertension.[24] Noise-induced oxidative stress promotes vascular endothelial dysfunction, characterized by reduced flow-mediated vasodilation and decreased nitric oxide bioavailability. These pathological changes not only elevate the risk of atherosclerosis but may also exacerbate ischemic brain injury in patients with stroke by impairing cerebral autoregulation of blood flow. This chronic cardiovascular damage caused by noise further impairs the cerebral blood supply after stroke, hindering the recovery of ischemic brain tissue and reducing the efficiency of neurological rehabilitation.

Increased cardiovascular burden during sleep poses a particular hazard for patients with stroke. Research has demonstrated that frequent awakenings induced by noise can lead to elevated left ventricular end-diastolic pressure and increased myocardial oxygen consumption.[25] For post-stroke patients with comorbid coronary artery disease, these alterations may trigger silent myocardial ischemia. Furthermore, noise-related reductions in heart rate variability and impaired baroreflex sensitivity are independent risk factors for sudden cardiac death following stroke.

Special Vulnerability of Post-Stroke Patients

Post-stroke brain injury can lead to deficits in auditory information filtering. While the healthy brain possesses sensory gating mechanisms during sleep that inhibit cortical responses to irrelevant auditory stimuli, post-stroke impairment of prefrontal cortical inhibitory function may weaken this filtering capacity. An fMRI study has revealed that upon exposure to noise stimuli, post-stroke patients exhibit a two- to three-fold greater activation intensity in the primary auditory cortex compared with healthy individuals. Furthermore, signal diffusion extends to the limbic and paralimbic systems, indicating the presence of central sensitization.[26]

Post-stroke neuroplastic changes may amplify the adverse neurological effects of noise. An animal model study suggests that reduced BDNF expression in the hippocampal region following cerebral ischemia may increase neuronal susceptibility to metabolic stress induced by noise.[27] Concurrently, abnormal hyperexcitability of glutamatergic neurons in peri-infarct regions may allow noise stimuli, via NMDA receptor-mediated mechanisms, to trigger peri-infarct depolarizations, potentially expanding the ischemic penumbra.

Structural damage to sleep–wake cycle regulatory systems may contribute to the increased susceptibility of patients with stroke to noise. Stroke can affect key sleep-regulatory areas, including the preoptic area and the tuberomammillary nucleus of the hypothalamus, thereby impairing the regulation of sleep homeostasis.[28] Clinical observations have found that stroke patients with lesions involving the brainstem reticular formation are more prone to noise-related sleep disturbances, with a positive correlation noted between reduced sleep efficiency and the degree of autonomic dysfunction.[29] Collectively, these pathological alterations constitute the neurobiological basis for noise sensitivity following stroke and highlight the need for personalized environmental intervention strategies.

CLINICAL EVIDENCE OF HOSPITAL NOISE AFFECTING SLEEP IN POST-STROKE PATIENTS

Association between Noise Levels and Sleep Quality

A clear dose–response relationship exists between noise levels in the hospital environment and poor subjective sleep quality as well as reduced sleep efficiency. A study reported that the average nighttime noise level in ICUs can reach 67.1 dB(A), with peak values even attaining 99.7 dB(A), equivalent to the noise intensity of a speeding motorcycle.[30] General ICU noise data provide a comparative reference for stroke ward noise assessment, and the dose–response relationship between noise and sleep quality verified in ICUs is consistent with the characteristics of post-stroke patients, and the sleep damage caused by the same noise intensity is more obvious in patients with stroke due to their special vulnerability.[31] A systematic review and dose–response meta-analysis by Fu et al.[32] showed a significant association between long-term environmental noise exposure and increased risk of stroke incidence and mortality, further emphasizing the potential threat of noise to the overall health of patients with stroke, including its effects through mechanisms such as sleep disruption.

The disruptive impact of noise on sleep depends not only on its intensity but also on its characteristics and source. Alarm sounds from medical equipment are more disruptive to sleep than conversational noise. Even brief exposure to sudden noise can disrupt sleep continuity, and such sleep disturbances are particularly noteworthy in patients with stroke as sleep plays a crucial role in motor learning and physical rehabilitation after stroke.[33] A large-scale prospective cohort study from Denmark further revealed the association between environmental noise and stroke risk: long-term exposure to traffic noise increases the risk of stroke. Although these findings were derived from community-based environmental noise exposure, they provide important epidemiological background support for the potential negative effects of hospital noise on sleep and overall recovery of post-stroke patients.[34] Polysomnographic studies have shown that noise exposure leads to decreased sleep efficiency, reduced total sleep time, increased wake time after sleep onset, a higher proportion of light sleep, and diminished deep sleep in patients with stroke.[14,30]

Specific Characteristics of Noise in Stroke Wards

Clinical exclusive noise baseline monitoring data for stroke wards show that the average daytime noise value is 45.3–49.7 dB(A), the average nighttime noise value is 38.6–42.9 dB(A), and both values are higher than the WHO recommended standards. In stroke wards, the mean equivalent continuous noise level for 24 hours significantly exceeds WHO recommendations. Czempik et al.[35] identified that sources of sound producing peak sound levels above 57.9 dB may lead to shorter sleep and should be eliminated from the ICU environment. The sound levels had no effect on sleep quality.

Noise sources in stroke wards have characteristics typical of the healthcare environment, primarily categorized into medical equipment noise and human activity noise, and these noises exert unique adverse effects on post-stroke patients due to their increased vulnerability to environmental noise following stroke. Medical equipment is a major source of ward noise, with alarms from devices such as electrocardiogram (ECG) monitors, infusion pumps, and ventilators accounting for a large proportion of all noise sources. Stroke survivors often require multiple monitoring and support devices resulting in frequent alarms from several monitoring parameters. Persistent exposure to such noise may disrupt sleep and has also been associated with increased motor variability, which impairs the accuracy of reaching movements in post-stroke patients.[36] Occupational noise exposure in healthcare settings has been linked to an elevated risk of stroke.[37] This research conclusion provides additional evidence that chronic noise exposure may have adverse neurological and cardiovascular consequences, which also provides a mechanistic basis for explaining why post-stroke patients are more susceptible to noise-induced neurological dysfunction in the noisy ward environment.

Noise generated by human activities is concentrated during medical operation periods, such as nursing shift changes, nighttime rounds, and rehabilitation procedures, creating obvious noise peaks. Due to mobility impairments and restricted movement during hospitalization, post-stroke patients exhibit heightened sensitivity to ambient noise; sounds from other patients (e.g., moaning, snoring, or coughing) and caregivers or visitors (e.g., conversations and movement) further exacerbate sleep disturbances. Moreover, post-stroke patients often have deficits in working memory and attentional control, and ward noise can substantially impair their speech comprehension, affecting communication and rehabilitation outcomes.[38] In addition, the design of stroke wards also influences the propagation of noise and patient perception. A qualitative study using virtual reality technology found that reasonable ward design can alleviate noise-induced negative emotions and improve patients’ activity levels and social connections, while unreasonable design may amplify the adverse effects of noise.[39]

The combination of diverse noise sources, the unique vulnerability of post-stroke patients, and the influence of ward design renders stroke wards—one of the most acoustically complex areas within hospitals. These noise characteristics not only disrupt patients’ sleep and rest but also interfere with their cognitive and motor function recovery, highlighting the necessity of implementing targeted noise control measures tailored to the characteristics of stroke wards and the special needs of patients with stroke.

Impact of Noise on Stroke Rehabilitation Outcomes

Noise-induced sleep disturbances exert multifaceted negative effects on stroke rehabilitation outcomes. First, sleep deprivation leads to exacerbated daytime fatigue and reduced alertness, diminishing patients’ motivation to participate in rehabilitation. Studies have shown that stroke patients with comorbid sleep disorders are more prone to impaired motor coordination and attentional deficits, which may hinder motor function recovery.[40]

The process of cognitive recovery is substantially hindered by sleep fragmentation. High-quality sleep facilitates memory consolidation and the formation of new neural synapses, which are crucial for the relearning of motor skills post-stroke. Noise disrupts NREM sleep, particularly slow-wave sleep, impairing offline memory consolidation and negatively affecting the recovery of executive function and information processing speed. Sleep disturbances are also closely associated with mood disorders, with 86.7% of patients reporting negative emotions such as unease, tension, and fear in response to ward noise.[41] Prolonged sleep insufficiency can induce anxiety and depression, with an incidence exceeding 30%, thereby creating a vicious psychophysiological cycle.

Overall quality of life may be adversely affected by noise-related sleep problems. Reduced sleep efficiency not only aggravates the degree of neurological deficit but also, through activation of the sympathetic nervous system, leads to elevated blood pressure and altered heart rate variability, increasing the risk of cardiovascular events. Research indicates that patients with post-stroke hypersomnia are more likely to require institutional care and demonstrate poorer functional independence.[42] Effectively controlling ward noise has thus become a crucial aspect of improving stroke prognosis and enhancing patients’ quality of life, highlighting the need for high priority and systematic noise management strategies in clinical practice.

HOSPITAL NOISE MANAGEMENT STRATEGIES FOR STROKE PATIENTS

Engineering and Administrative Interventions (Targeting the Noise Source)

Engineering and administrative interventions targeting the sources of hospital noise form the foundation of environmental noise control. Engineering modifications primarily target the acoustic properties of the physical environment. Soundproof ceilings and sound-absorbing wall materials used in ward renovations have been shown to be effective in sound transmission and reverberation. Installing silent door closers or buffers on ward doors can reduce the impact noise generated by door opening and closing, which can transiently exceed 70 dB(A). The installation of real-time decibel monitors in public areas such as nursing stations and corridors enables the visualization of noise levels. When noise levels exceed a preset threshold (e.g., 60 dB[A], alerts are triggered, prompting healthcare staff to actively reduce noise levels.[43]

Regarding medical equipment, routine maintenance of treatment cart wheels by logistics departments, including replacement with silent shock-absorbing wheels and addition of cushioning pads to the cart bodies, may help reduce clattering noises during movement. Concurrently, equipment management departments may optimize the alarm systems of monitors and infusion pumps. While ensuring patient safety, alarm volumes are generally reduced by 30%, and alarm priority levels are optimized to minimize interference from non-critical alerts.

Administrative interventions primarily focus on standardizing personnel activities and optimizing workflow processes. Hospitals establish and strictly enforce visitation and accompanying policies, clearly defining visitation times, number of visitors, and duration. Responsible nurses conduct regular rounds to promptly remind family members to maintain a quiet environment. Training for medical staff emphasizes the “Four Quiet” principle—speaking quietly, walking quietly, operating quietly, and opening/closing doors and windows quietly. Staff are also instructed to set mobile phones to vibration mode and avoid making or receiving loud calls in patient care areas. Practices from Beijing Ditan Hospital have demonstrated that replacing traditional loud intercom methods with in-ear wireless headsets effectively reduces communication-related noise. Workflow optimization is equally critical. By implementing measures such as a primary nurse responsibility system, increasing rounding frequency, pre-preparation of materials, and grouping tasks, the nursing service model can shift nursing care from reactive to proactive care. This has been shown to reduce the frequency of patient call bell usage and decrease associated noise disturbances in wards.[44]

Patient-Centered Interventions (Targeting Transmission Pathways and Recipients)

For populations with increased vulnerability to noise, such as post-stroke patients, individualized interventions targeting both noise transmission pathways and patient-level susceptibility are especially important. Hospital noise exerts both direct and indirect impacts on sleep quality in patients with stroke. Direct acoustic stimulation disrupts sleep architecture, while persistent noise exposure may induce or aggravate sensorineural hearing loss, tinnitus and vertigo—common complications in stroke patients with auditory pathway or vestibular nucleus lesions. These otological symptoms further trigger anxiety, irritability and hypervigilance in patients, forming a vicious cycle between otological discomfort, negative psychological state, and further sleep disturbance.[45] Personal protective equipment represents the most direct and feasible measure, and interventions should be customized according to the presence of hearing loss, tinnitus, and vertigo in patients with stroke. For patients with mild-to-moderate hearing loss, provide noise-cancelling earplugs with adjustable sound attenuation levels to avoid over-blocking of environmental sounds. For patients with tinnitus, select sound masking devices that integrate tinnitus masking tones and white noise to simultaneously alleviate tinnitus and mask environmental noise. For patients with vertigo, avoid using high-frequency sound masking stimuli and adopt low-frequency, gentle natural sounds (e.g., slow flowing water) to reduce vestibular system stimulation.[46] Nurses educate patients and families on the impact of noise on sleep and rehabilitation and provide the above personalized protective devices to patients in need, creating a personalized quiet environment. These tools are particularly beneficial for patients requiring early rehabilitation who are easily awakened by medical equipment alarms from roommates, as they help maintain continuous sleep.

Active sound intervention strategies leverage the principle of sound masking to improve patients’ auditory experience. Stratified sound masking therapy may be considered based on the clinical characteristics of patients with stroke. For patients with stroke without otological complications, exposure to steady, soothing background sounds such as white noise or rainfall sounds may help mask environmental noise.[47] For those with tinnitus, sound masking may be combined with tinnitus retraining therapy. For those with vestibular disorders/vertigo, a low-intensity and stable auditory environment with low-decibel, monaural sound stimulation may be preferable, with the avoidance of sudden sound changes in the ward.[48] For patients with comorbid anxiety, playing soft instrumental music or mindfulness music tailored to patient preference can not only cover environmental noise but also modulate mood, potentially facilitating parasympathetic nervous system activity and creating favorable conditions for sleep.

Non-pharmacological therapies focus on enhancing patients’ own psychological coping mechanisms for noise-induced stress. For patients with stroke who experience tinnitus, hearing loss, or vertigo, integrate otological symptom intervention with psychological support strategies. Interventions may incorporate tinnitus relaxation training and vertigo postural training on the basis of simple meditation, mindful breathing, or progressive muscle relaxation techniques, and guide patients to reduce attention to otological discomfort and noise stimuli. When environmental noise is unavoidable, these methods help patients shift their attention from external stimuli to internal bodily sensations, alleviating the irritation and tension caused by noise, lowering cortical arousal levels, and thereby mitigating the disruption of sleep architecture.[49] Combining sound intervention with non-pharmacological therapies can construct a psychoacoustic barrier for patients with stroke, attenuating the negative impact of noise.

Based on the above targeted interventions, a stratified management system may be considered for patients with stroke according to their noise-related clinical characteristics.

Level 1 (noise sensitivity without otological complications): basic noise reduction protection and conventional sound masking.

Level 2 (noise sensitivity with a single otological complication, such as tinnitus/hearing loss/vertigo): personalized protective devices, phenotype-specific sound masking, and targeted symptom intervention;

Level 3 (noise sensitivity with multiple otological complications): multidisciplinary collaboration involving neurology, otolaryngology, rehabilitation and medicine, combined with individualized comprehensive intervention plan and real-time acoustic environment monitoring.[50,51]

To facilitate rapid clinical bedside assessment of noise-related vulnerability in patients with stroke, a brief screening tool could be developed in future research, such as a “Stroke Patient Noise Sensitivity Rapid Screening Scale.” Such a tool might include: (1) a whispered voice test at 30 cm for preliminary hearing loss screening (inability to repeat ≥3 of 6 bisyllabic words indicating possible hearing impairment); (2) two single-item screening questions for tinnitus (“Do you currently experience ringing in the ears?”) and vertigo (“When changing position, do you experience a spinning sensation or dizziness?”); and (3) the assignment of patients to the corresponding management level based on the presence or absence of each otological symptom. The validity, reliability, and clinical feasibility of such a tool would need to be established through prospective validation studies.

Effectiveness of Comprehensive Noise Management Strategies

Multiple clinical studies have suggested that the comprehensive noise management strategies, which integrate engineering control (such as sound insulation materials and equipment noise reduction), administrative management (such as operating standards and personnel training), and patient education (such as personal protection and psychological adjustment), are more effective than single component interventions.[52] Although most of this evidence comes from ICUs or mixed wards, the systematic and multi-level intervention approaches can be adapted to stroke wards according to the special vulnerability of patients with stroke (e.g., placing greater emphasis on patient-centered personalized interventions), and the implementation framework may offer valuable guidance for stroke wards with complex noise environments.[53] The ultimate benefit of the comprehensive strategy is reflected in the improvement of patient rehabilitation outcomes. For patients with stroke, effective noise control is directly related to improved sleep quality. Research has shown that reducing environmental noise can prolong patients’ total sleep time, reduce nighttime awakenings, and improve sleep efficiency.[54] The improvement of sleep quality has a positive impact on daytime function. Adequate rest at night reduces daytime fatigue, increases willingness and tolerance to participate in rehabilitation training, accelerates cognitive recovery, stabilizes emotional states, and reduces the incidence of depression and anxiety. Therefore, establishing a patient-centered, multi-party collaborative, and end-to-end hospital noise comprehensive management system is a key link in optimizing the neurological rehabilitation environment and improving long-term prognosis. Table 1 summarizes the multi-level noise management framework for stroke wards.

Table 1.

Multi-level Hospital Noise Management Framework for Stroke Wards

Intervention level	Core measures	Targets	Key efficacy indicators for stroke patients
Noise source	Equipment noise reduction, alarm priority optimization, standardized personnel operation	Medical equipment/human activity	Reduce ward average noise by ≥5 dB(A); reduce non-critical alarms by ≥40%
Transmission path	Sound insulation materials, silent ward facilities, reasonable ward layout	Sound propagation	Reduce sound reflection in wards by ≥30%; isolate inter-bed noise
Recipient (stroke patients)	Noise-cancelling equipment, sound masking therapy, non-pharmacological stress relief	Patient sensory/cognitive response	Increase sleep efficiency by ≥15%; reduce nighttime awakenings by ≥20%

CHALLENGES, LIMITATIONS, AND FUTURE PERSPECTIVES

Differential effects of noise on patients with stroke may vary according to noise characteristics, the balance between medical alarms and sleep protection, and lesion location. Intermittent high-frequency noise (e.g., equipment alarms; 2000–4000Hz) is more likely to trigger cortical micro‑arousal, whereas continuous low-frequency noise (<500Hz) may cause sustained sympathetic activation. Medical alarms represent one of the major sources of peak noise source, and a conflict exists between alarm necessity and sleep protection. However, personalized alarm strategies based on lesion location and neurological status remain underdeveloped. Furthermore, available evidence suggests that patients with brainstem/thalamus lesions may have the highest noise sensitivity, those with cortical lesions show moderate sensitivity, and those with subcortical white matter lesions may have relatively low sensitivity. Future studies are needed to define noise-exposure thresholds for different noise types and to develop lesion-specific management strategies.

General Challenges and Limitations

Noise management in stroke care faces multiple challenge. Its complexity stems not only from noise intensity itself but is also closely linked to the deficits in auditory information processing following stroke and substantial inter-individual differences in subjective perception. Factors such as stroke type, lesion location, and patient age contribute to marked variability in individual noise sensitivity, necessitating highly personalized management strategies. Furthermore, an inherent conflict exists between essential clinical activities and the need for a quiet environment. Coupled with the difficulty in sustaining staff adherence to noise control measures due to heavy workloads, maintaining the long-term effectiveness of systematic interventions (e.g., the Plan–Do–Check–Act cycle) remains challenging.

Several important limitations remain in the current evidence base. High-quality studies focusing on noise interventions specifically in stroke units are still limited, with most evidence derived from general ICUs or mixed wards. Existing studies often emphasize short-term effects, lacking follow-up evidence on long-term neurological recovery and quality of life. Economic evaluations and cost–benefit analyses of noise management strategies remain scarce. In addition, the mechanisms by which different acoustic characteristics affect the injured brain after stroke remain incompletely understood, which may limit the development of targeted interventions.

Future Research Directions

Future research should focus on developing intelligent noise monitoring and intervention systems integrated with Internet of Things technology to enable dynamic management and personalized noise-management strategies. Patient- and family-engaged design studies warrant further investigation, utilizing technologies such as virtual reality to optimize the acoustic environmental experience of wards, combining architectural features such as single-room settings and sound-absorbing materials. Another important direction involves exploring evidence-based personalized clinical pathways. Large-scale, multi-center trials are needed to establish stratified management guidelines based on stroke lesion location and noise sensitivity. Moreover, noise management should be deeply integrated throughout the entire stroke rehabilitation process, ultimately forming a sustainable, high-quality standard of care. [Figure 1] summarizes the pathophysiological mechanisms of noise-induced sleep disorders in patients with stroke, including unique vulnerability factors.

Figure 1.

Pathophysiological mechanisms of noise-induced sleep disorders in patients with stroke (including unique vulnerability factors).

CONCLUSION

Hospital noise is an important and modifiable environmental factor that exacerbates sleep disturbances and delays neurological recovery in patients with stroke. Post-stroke sleep disorders are highly prevalent. As a prominent environmental stressor, noise disrupts sleep architecture not only by activating auditory pathways and stress-response systems but also imposes additional adverse effects due to the specific vulnerability of patients with brain injury. Available evidence suggests that systematic noise management strategies may improve patient sleep quality. For instance, bundled sleep nursing interventions have been associated with longer sleep duration and improved sleep efficiency, while initiatives like “Quiet Wards” have achieved substantial reductions in average ward noise levels and improved patient-reported sleep quality by up to 40%.

The implementation of systematic, multi-faceted noise management strategies holds important clinical importance for stroke care. A comprehensive management model that combines engineering interventions, behavioral modifications, and patient-centered personalized measures may reduce noise exposure across the source, transmission, and patient levels. These considerations highlight the importance of collaboration among healthcare professionals, hospital administrators, and researchers to optimize the acoustic environment in stroke wards, integrating noise control as an important component of comprehensive stroke care. Future research should focus on exploring evidence-based, personalized clinical pathways for noise management, strengthening the application of intelligent monitoring technologies, and constructing quiet clinical environments that support neurological recovery and rehabilitation outcomes in patients with stroke.

Availability of Data and Materials

This is a narrative review article and no original datasets were generated or analyzed during the research process. All relevant data referenced in this article are derived from the published literatures cited in the reference list.

Author Contributions

FangFang Xu designed the study, performed the literature search and synthesis, and drafted the manuscript.

LiPing Cao performed the literature search and synthesis, participated in manuscript drafting, and critically revised the manuscript.

Ting Wang and YuYu Dong participated in manuscript drafting and critical revision.

Qing Wang and ShiYing Cao contributed to critical revision of the manuscript for important intellectual content and literature synthesis.

ChaoJun Zou supervised the study, critically revised the manuscript, and gave final approval of the version to be published.

All authors participated fully in the work, took public responsibility for appropriate portions of the content, and agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or completeness of any part of the work are appropriately investigated and resolved.

Ethics Approval and Consent to Participate

This article is a narrative review based on published domestic and foreign literatures, and no human or animal subjects were involved in the research. Therefore, ethical approval and informed consent are not required.

Conflict of Interests

The authors declare that there are no conflicts of interest.

Funding Statement

This work was supported by Hangzhou Municipal Medical and Health Science and Technology Projects (Grant No. A20252201).