Cognitive impairment in idiopathic intracranial hypertension: A conceptual framework and therapeutic implications

Abstract

Background:

Cognitive impairment is an increasingly recognized but poorly understood manifestation of idiopathic intracranial hypertension (IIH). Although deficits in attention, executive functioning, memory, processing speed, and reaction time have been reported, the characteristics, trajectory, and underlying mechanisms of cognitive dysfunction remain incompletely defined. Interpretation of the literature is limited by heterogeneity in study design, variability in neurocognitive assessment methods, and the absence of standardized cognitive outcome measures. Consequently, cognitive morbidity is overlooked in clinical practice and is not incorporated into treatment decision-making, which remains centered around visual outcomes and papilledema.

Methods:

In this narrative review, we synthesize evidence from IIH studies and related disease models to examine the putative mechanisms underlying cognitive dysfunction and propose a conceptual framework for its pathogenesis.

Results:

Cognitive dysfunction in IIH may arise through interactions between elevated intracranial pressure, cerebral venous hypertension, symptom-related amplifiers including chronic headache, sleep disturbance, pulsatile tinnitus, and psychiatric comorbidity, and broader biological and socioeconomic modifiers influencing cognitive vulnerability and recovery. This framework integrates current evidence and identifies potential pathways linking IIH to cognitive impairment.

Conclusion:

Improved understanding of the cognitive effects of IIH may help improve recognition of cognitive dysfunction in clinical care. Recognition of cognition as a clinically meaningful and potentially treatment-responsive outcome may help inform future studies evaluating whether cognition has a role in treatment selection, particularly in patients without papilledema, in whom disease burden may currently be underestimated.

INTRODUCTION

Idiopathic intracranial hypertension (IIH) is a debilitating neurological disorder traditionally defined by elevated intracranial pressure (ICP) without an identifiable cause.[29,137] Increasing evidence, including recent work from our institution, suggests that hemodynamically significant venous hypertension secondary to venous sinus stenosis plays a central role in disease pathophysiology and is present in the vast majority of patients with IIH undergoing venous manometry. In one unselected (“all-comers”) cohort, over 80% of patients demonstrated a trans-stenotic pressure gradient of at least 4 mmHg.[40,41,125,129] IIH disproportionately affects young women and is strongly associated with obesity.[16,121] Consequently, its prevalence is projected to rise in parallel with the global obesity pandemic.[88,121] While the classical presentation includes headache, visual impairment, and pulsatile tinnitus (PT),[55,141] increasing evidence suggests that cognitive and psychological impairment may represent an important but under-recognized component of the disease process.[2,38,55,141,155,157]

Given that most patients are of working age, such deficits likely impose substantial socioeconomic burden and adversely affect quality of life.[33,76,81,100] In routine practice, however, cognitive and psychological symptoms may be overlooked and attributed to the overall symptomatic burden of IIH rather than considered intrinsic manifestations of the disorder. This is reflected in current treatment paradigms, where invasive interventions are reserved for refractory symptoms or threatened vision, while cognitive symptoms do not inform therapeutic decision-making.[91]

Although further research is required to clarify the relationship between IIH and cognitive dysfunction, exploration of potential mechanisms is warranted. A clearer mechanistic understanding would help reframe IIH as a multifaceted neurological condition, ensure cognitive morbidity is not overlooked in clinical care, and provide a biological rationale for future interventional studies evaluating cognitive outcomes. Ultimately, these insights could inform future therapeutic strategies in IIH and guide future studies evaluating whether cognition should be considered alongside established clinical and hemodynamic factors, such as elevated venous pressure gradients,[85] when selecting patients for intervention, particularly in those with IIH without papilledema (IIHWOP).

In this narrative review, we synthesize evidence from IIH studies and related disease models to propose a conceptual framework in which cognitive impairment arises from the interaction between primary disease mechanisms, secondary amplifiers, and biological and socioeconomic modifiers.

COGNITIVE IMPAIRMENT IN IIH

Nature

Often described as “brain fog” by patients, cognitive impairment in IIH was first formally examined in 1986, where IIH patients were reported to exhibit general intellectual impairment on neuropsychological examination.[124] Since then, multiple studies have reported multidomain cognitive deficits in IIH across a range of neurocognitive batteries. Impairments have been described in executive functioning,[55,56] sustained and complex attention,[38,55,108] working and long-term memory,[2,38,56] reaction time,[154] processing speed,[56,108,154] language,[2] and visuo-spatial skills.[38,157] While the association between IIH and cognitive impairment is increasingly recognized, interpretation of the literature is limited by heterogeneity in study design, variability in neurocognitive batteries employed, and the absence of IIH-specific cognitive screening tools.[65,108]

Characteristics

Neurocognitive deficits in IIH may be long-lasting, with studies demonstrating sustained deficits at 3–12 months, although cognition has not been systematically evaluated beyond 1 year.[55,140,154] Evidence regarding reversibility of deficits is conflicted. ICP lowering treatments appear pivotal in instigating improvement.[7,55,56,124,154] Chronic ICP reduction has been shown to improve executive function, sustained attention, and verbal short-term memory at 12 months,[55] and acute ICP reduction has been reported to improve sustained attention and word fluency, but not long-term verbal memory, following lumbar puncture.[55,132] Conversely, persistent deficits in executive functioning, working memory, processing speed, and reaction time have also been observed despite ICP normalization at 3 months.[154] Collectively, these findings suggest that cognitive dysfunction in IIH may not be uniformly reversible and that certain domains are more responsive to ICP reduction and may also be influenced by the rate of ICP reduction.

CONTRIBUTORS

Two pathophysiological processes existing in IIH have been implicated in cognitive impairment: raised ICP (intracranial hypertension) and cerebral venous congestion (CVC) secondary to venous sinus stenosis.[2,6,55,56,65] However, establishing an independent relationship between cognitive dysfunction and these disease processes is challenging due to several confounding variables, which may themselves lie on the causal pathway with cognitive impairment.[108] These variables include IIH symptom burden and related medical and psychiatric co-morbidities such as obstructive sleep apnea (OSA), anxiety and depression,[38,47,55] use of ICP lowering medications,[38] socioeconomic status,[39,124] and metabolic abnormalities.[55] A structured exploration of the contribution of these variables to cognitive impairment in IIH, and their interrelationships, is therefore warranted.

PRIMARY DISEASE MECHANISMS

IIH has traditionally been regarded as a disorder driven by elevated ICP.[90] However, venous sinus stenosis is now recognized to be highly prevalent in IIH, suggesting that venous pathology may play an important role in disease pathogenesis.[95] Whether venous hypertension precedes intracranial hypertension, or vice versa, remains debated, but the two processes appear closely intertwined.[43,81,109] Nevertheless, each may directly influence cognition through its own biological mechanisms.

Effects of elevated ICP on cognition

In IIH, sustained elevation of ICP may cause a reduction in cerebral perfusion pressure, resulting in impaired microvascular flow and potentially resulting in chronic, low-grade cerebral hypoxia. In turn, this may result in neuronal dysfunction and cause cognitive impairment. Although cerebral hypoxia has not been demonstrated in IIH, mechanistic insight can be drawn from conditions characterized by chronic reduction in oxygen delivery or perfusion.

Chronic hypoxia has been associated with cognitive impairment across several conditions, including chronic obstructive pulmonary disorder,[123,139] OSA,[142] anemia, and prolonged high-altitude exposure.[156] These conditions are linked to deficits in executive function, memory, attention, and processing speed. Similar cognitive profiles have also been described in cerebral small vessel disease, where regional hypoperfusion affects vulnerable subcortical structures. Although it remains unclear whether perfusion abnormalities in IIH are global or region-specific, altered cerebral oxygen delivery represents a biologically plausible mechanism underlying cognitive dysfunction.

Chronic cerebral hypoxia may contribute to neuronal dysfunction through oxidative stress, neuroinflammation, impaired neuroplasticity, and altered neurotransmission.[49,97] Metabolically active regions such as the hippocampus, neocortex, and striatum may be particularly susceptible to sustained perfusion abnormalities,[141] providing a possible framework for the multidomain cognitive deficits observed in IIH. However, direct evidence of hypoxia-mediated structural or metabolic injury in IIH remains limited, and further studies investigating biomarkers and neuroimaging markers of cerebral hypoxia in IIH are warranted.

Effects of venous hypertension on cognition

Venous hypertension, or CVC, occurs when normal intracranial venous outflow is disrupted. In IIH, this commonly results from venous sinus stenosis.[64,73] Venous hypertension may contribute to cognitive impairment through several mechanisms, including cerebral hypoperfusion, blood–brain barrier (BBB) dysfunction, neuroinflammation, and impaired metabolic clearance.

Across a range of other neurological conditions that feature venous hypertension, cognitive impairment is uniformly present, including cerebral dural arteriovenous fistulas (dAVF), arteriovenous malformations (AVM), and cerebral venous sinus thrombosis (CVST). In cerebral dAVF, venous hypertension results from abnormal shunting between dural arteries and venous sinuses or cortical veins without an intervening capillary bed.[107] Cognitive deficits involving attention, memory, learning, and executive function[62,67] have been reported and may improve following treatment. Indeed, dAVFs are increasingly recognized as a reversible cause of dementia in the elderly.[12,61,134] Multi-domain cognitive impairment has also been observed in CVST and AVMs,[17,18,32,100,115] where venous hypertension arises from acute venous outflow obstruction and high-flow shunting through a parenchymal nidus, respectively. In AVMs, however, cognitive dysfunction may also reflect an “arterial steal” phenomenon, whereby blood is diverted away from surrounding adjacent brain tissue due to the presence of a low-resistance shunt. As this mechanism is not present in IIH, the pathophysiology of cognitive impairment in IIH may be more comparable to other venous hypertensive states.[12] Cognitive symptoms may also arise when venous outflow is obstructed extracranially;[104] in mice, ligation of the jugular veins has been shown to impair cognition, spatial learning, and memory.[74]

Venous hypertension is known to cause end-organ dysfunction in other organ systems. For example, portal hypertension in cirrhosis contributes to portal hypertensive gastropathy,[89,127] while chronic venous hypertension in the lower limbs leads to pain, edema, pigmentation, and ulceration.[4,19,110,122] Similarly, venous compression syndromes such as nutcracker syndrome can result in renal venous hypertension, leading to hematuria, flank pain, and in severe cases, progressive renal dysfunction.[75] It is therefore plausible that brain parenchyma is similarly vulnerable to the deleterious effects of sustained venous hypertension.

Cerebral perfusion depends on an arteriovenous pressure gradient driving microvascular flow through a capillary bed. In IIH, elevated cerebral venous pressures secondary to a hemodynamically significant venous stenosis may reduce this gradient, thereby impairing capillary perfusion and tissue oxygen delivery. At the same time, retrograde transmission of venous pressure can increase capillary hydrostatic pressure, promoting vasogenic edema, BBB dysfunction, and cerebral swelling.[42,116,129]

In humans, venous dysfunction has been linked to structural brain changes associated with cognitive decline. Population-based imaging and pathological studies have established relationships between venous abnormalities, white matter hyperintensities, and cognitive impairment during ageing.[93] In addition, clearance of metabolic by-products in the brain depends on the glymphatic system and dural lymphatic vessels, which are closely coupled with the cerebral venous system. Venous stasis may impair this clearance pathway, disrupting glymphatic outflow and promoting the accumulation of neurotoxic metabolites within the central nervous system.[50,78,147] Supporting this concept, several imaging studies have demonstrated impaired glymphatic clearance in patients with IIH, particularly in those with more severe venous sinus stenosis.[36,69,118]

These observations support biologically plausible mechanisms by which venous outflow abnormalities may affect brain function. Future research should focus on clarifying the effects of CVC on cortical perfusion and network function, whether alterations are seen after venous sinus stenting, and if there is a correlation between these parameters and cognitive performance.

SECONDARY MECHANISMS AMPLIFYING COGNITIVE IMPAIRMENT

Symptomatic burden in IIH may amplify underlying cognitive dysfunction caused by primary disease mechanisms through direct and indirect mechanisms. Symptoms which may impact on cognition include chronic headache, PT, sleep disturbances, visual impairments, and psychiatric symptoms.

Pain

Chronic headache is the most frequently reported symptom in IIH,[45] affecting over 68% of patients and often presenting as migraines and tension-type headaches.[48] Chronic pain has been associated with impairments in memory, disorientation, reduced attention, impaired emotional decision-making, and executive dysfunction.[24,55,84,85,149,155] Pain and cognition share overlapping neural pathways. Persistent nociceptive signaling may compete with attentional and cognitive processing resources, possibly contributing to reduced cognitive performance.[94] Neuroimaging in chronic pain populations demonstrates altered activity in regions involved in cognitive control and emotional processing,[94] including the anterior cingulate cortex, insula, and prefrontal cortex. Dysregulation of these networks, for example through neurotransmitter imbalances, may impair attention, working memory, and executive function.[124]

Differing thoughts exist regarding headache burden and cognitive function. While one study revealed cognitive impairment in IIH patients which correlated with headache burden,[47] others argue cognitive dysfunction did not.[2,140] Hence, rather than acting as a primary driver of cognitive impairment, chronic pain may serve as a secondary amplifier.

PT

PT is a common symptom of IIH reported in a substantial proportion of patients.[15,63,117,133] PT can impair cognitive abilities by acting as a persistent auditory distraction. This is reflected in studies demonstrating deficits in key domains such as concentration, orientation, short-term memory, abstraction, judgment, and language abilities among those affected by PT.[143] Reduced performance on tasks requiring sustained auditory and executive attention has also been found.[79] In addition, PT may contribute to cognitive impairment through its associations with psychiatric disorders including anxiety and depression, poor sleep, and hearing loss, all of which commonly co-exist in IIH and worsen preexisting cognitive dysfunction.[60,113,151]

Sleep

Driven by a combination of chronic headache, PT, and a higher prevalence of OSA, sleep disturbance is common in patients with IIH.[26,34,59,120,148] Poor sleep is well known to impair cognitive performance,[55] particularly attention, memory consolidation, and executive function.[55] Sleep deprivation disrupts memory consolidation during long-term potentiation in the hippocampus, where N-methyl-Daspartate receptors are affected by changes in surface and receptor subunit composition.[70]

In IIH, sleep deprivation can heighten pain perception and reduce the effectiveness of analgesic pathways, creating a cycle in which headache and poor sleep reinforce one another. Poor sleep can also promote weight gain, which may worsen intracranial hypertension and perpetuate a cycle of disease progression and cognitive impairment [Figure 1].

Figure 1:

A conceptual framework incorporating the primary disease mechanisms, symptom-driven amplifiers, and biological and socioeconomic modifiers and how they relate to cognitive dysfunction.

Loss of vision

Visual impairment is common in IIH, with moderate to severe vision loss reported in over 50% of patients and approximately 1–2% of cases progressing to blindness annually.[13,66] Visual impairments are correlated with cognitive deficits in patients with IIH, particularly in visuospatial processing, attention, and executive functioning.[37,72] Increased retinal nerve fiber layer thickness is linked to a higher antisaccade error rate,[140] and severe papilledema and diplopia are associated with worse performance across several cognitive domains.[38] Visual impairment may contribute to cognitive dysfunction by increasing cognitive load and reducing processing efficiency, thereby limiting the resources available for higher-order cognitive tasks.[135]

Psychiatric comorbidities

Studies demonstrate higher prevalence of anxiety and depression in IIH patients compared to the general population.[31,92,99] The prevalence of these conditions is comparable to that observed in women with migraines matched for age and BMI, suggesting chronic headaches may be a key contributor.[92] This is further supported by findings that IIH patients with psychiatric comorbidities report greater headache severity and fatigue than IIH patients without psychiatric disorders.[105] Anxiety is known to cause impairments in memory,[52] verbal fluency,[52] spatial attention,[136] and executive function,[136] whereas depression may produce persistent deficits in domains including concentration, memory, and processing speed.[86,102] Similar patterns of cognitive impairment are observed in IIH.

Psychiatric disorders are associated with structural and functional brain alterations. Anxiety has been shown to disrupt connectivity within the amygdala-prefrontal and amygdala-hippocampal circuits, weakening top-down emotional regulation and impacting memory and cognitive control, respectively.[35] Depression has been linked to reductions in gray matter intensity in the striatum,[68] a core component of the extrapyramidal system involved in reward-oriented behavior and cognitive function. Increased cortical thickness of the parietal lobe,[68] a region involved in the Default Mode Network and self-focus, along with increased amygdala thickness and hyperactivity,[77] may contribute to heightened emotional reactivity and negative affect. In the presence of elevated ICP and venous hypertension, the brain’s capacity to compensate for these additional structural alterations may be further limited.

Psychiatric comorbidities may also indirectly worsen cognitive outcomes. Depression and anxiety are associated with poorer sleep quality, increased fatigue, and heightened pain perception, factors that are already prevalent in IIH and have been linked to reduced cognitive performance.[8] Together, these findings suggest that psychiatric comorbidities may act as important amplifiers of cognitive dysfunction in IIH.

BIOLOGICAL AND SOCIOECONOMIC MODIFIERS

Beyond disease-specific mechanisms and symptom-related amplification, biological and socioeconomic modifiers may influence susceptibility to, severity of, and recovery from cognitive dysfunction in IIH. Rather than acting as primary drivers, these factors shape individual vulnerability and contribute to the heterogeneity of cognitive outcomes.

Endocrine dysfunction

Concomitant endocrine abnormalities may reduce cognitive resilience and worsen cognitive impairment in IIH. Polycystic ovarian syndrome (PCOS), which is strongly associated with obesity, has been frequently reported in patients with IIH.[10,126] Elevated androgen levels have been proposed as a possible contributing factor toward the etiology of IIH, with some evidence suggesting increased cerebrospinal fluid (CSF) production and altered neuroendocrine signaling in affected patients.[82] Evidence also suggests that elevated testosterone in females decreases coupling of the amygdala with various cortical regions,[74] potentially affecting cognitive control.

Empty sella syndrome, a common radiological finding in IIH arising secondary to raised ICP,[22,106,111,119] may reflect pituitary dysfunction and dysregulation of multiple endocrine pathways including thyroid, growth hormone, and sex steroids. While partially empty sella is usually benign, the effect of complete effacement of the pituitary gland on its ability to function may not be.[7,23,30,51,53,58,80,150] Complete empty sella has been shown to be associated with dysregulation of thyroid hormones,[7,23,51,53,150] growth hormone,[23,51,53,150] ACTH,[23,30] prolactin,[30,53,58,80] and sex steroids.[23,30,52] Table 1 lists the hormone systems that may be associated with an empty sella, coupled with known cognitive effects of dysregulation in each system.

Table 1:

Hormones and their effects on cognition.

Diabetes and insulin resistance are common among IIH patients and have been associated with cognitive decline through mechanisms including vascular injury, white matter changes, and subtle brain atrophy.[14,93]

Endocrine abnormalities, including obesity, PCOS, and altered cortisol signaling, may promote systemic inflammation and dysregulate metabolism. In patients with IIH, these changes could predispose to cognitive dysfunction.[55]

Because pituitary function testing is not routinely performed in IIH, the true prevalence of endocrine dysfunction and the effect ICP lowering treatment may have in this population remain unclear, warranting further prospective investigation.

The role of IIH medications

Medication side effects remain a challenge in the management of IIH and may contribute to cognitive and psychological symptoms reported by patients. The cognitive side effects of commonly prescribed IIH medications may therefore confound the assessment of disease-related cognitive impairment and are listed in Table 2.

Table 2:

Commonly used medications in IIH along with their mechanisms and adverse effects.

Acetazolamide, the most commonly prescribed medication for IIH, reduces CSF production and improves papilledema and visual outcomes. Its effects on cognition however are less clear, with some studies showing improvement[130] while others showing impairment[138,152] in cognitive function.

Acetazolamide has been shown to enhance glymphatic clearance and, in one study, resulted in improvements in attention, sequencing, mental flexibility, visual search, and motor function.[130]

On the other hand, another study of subjects who received a 4-day treatment of acetazolamide before air travel and underwent neuropsychological assessments demonstrated impaired concentration, reaction time, cognitive processing speed, short-term memory, and working memory.[96] Thus, while its exact influence on cognitive function remains unclear, future work into cognitive outcomes in IIH should consider its confounding effects.[39]

Glucagon-like peptide (GLP)-1 agonists are increasingly used for chronic weight management and may therefore be prescribed to patients with IIH. Although these medications have demonstrated potential neuroprotective and cognitive benefits in some populations,[28] psychiatric side effects including anxiety and depression have also been reported.[25,112] This should again be considered in IIH, although early data does not suggest poorer cognitive function in those taking GLP-1 medications.[145]

Topiramate is also frequently prescribed for IIH patients to lower ICP and can cause cognitive deficits[1,20,87,131] in language, attention, and memory. One study showed withdrawal of topiramate led to improvements in verbal learning, digit span, and verbal fluency.[131]

Clinicians must therefore balance the benefits of controlling ICP and headaches with the potential side effects of these medications. Awareness of medication-related cognitive effects is important when evaluating cognitive symptoms in patients with IIH.

Cognitive reserve and socioeconomic modifiers

Childhood cognitive ability and educational attainment contribute to cognitive reserve, influencing both baseline cognitive performance and the capacity to compensate for disease-related disruption. While unlikely to play a role in the development of IIH, these factors shape how cognitive deficits are expressed once the disease is present. Individuals with lower baseline cognitive ability or educational attainment appear more vulnerable to impairment across multiple domains, whereas higher cognitive reserve may mitigate the clinical impact of IIH, preserving function despite underlying pathology.[39] These effects are closely linked to socioeconomic context, as IIH disproportionately affects individuals from more deprived backgrounds, where reduced access to education, poorer health behaviors, and a higher burden of chronic health conditions may further compound cognitive vulnerability.[83,87] Notably, improvements in occupational and social circumstances have been associated with gains in cognitive function, suggesting that these influences are, in part, modifiable.[124] Together, these findings support the view that childhood IQ, education, and socioeconomic factors act as modifiers of cognitive dysfunction in IIH, influencing vulnerability and recovery rather than representing primary pathological mechanisms. Consideration of developmental history and socioeconomic context may therefore improve prediction of cognitive outcomes in IIH.

A conceptual whole-brain model illustrating the interaction between primary disease mechanisms, symptom-related amplifiers, and individual modifiers in contributing to cognitive dysfunction in IIH is demonstrated in Figure 1.

CLINICAL AND RESEARCH IMPLICATIONS

Clinical

Cognitive impairment in IIH is slowly gaining recognition in clinical practice, with growing evidence of its prevalence and impact. Cognitive symptoms may occur independently of other clinical features and may persist even after normalizing ICP, emphasizing the need for clinicians to routinely assess cognitive and psychological function when managing IIH patients.

Primary disease-related mechanisms, system-related amplifiers, and individual vulnerabilities likely contribute to cognitive dysfunction in a multifactorial manner and therefore require a multidisciplinary approach. Collaboration among neurosurgery, neurology, ophthalmology, psychology, and primary care may improve patient outcomes and reduce the risk of cognitive deficits.

These considerations also raise the possibility that, in carefully selected patients with hemodynamically significant cerebral venous outflow obstruction, cognitive function may represent an important outcome to evaluate following venous sinus stenting. Whether cognitive impairment should influence patient selection for venous sinus stenting remains unknown, and requires prospective study.

RESEARCH

Prospective studies should focus on directly assessing cognition in patients with IIH. With a lack of studies specifically designed to measure cognition in IIH, research should be conducted with standardized neuropsychological assessments with clearly defined cognitive measures. In addition, longitudinal studies would allow for clear characterization of cognitive trajectories over disease course and treatment.

Future research should also elucidate the effects of elevated ICP and cerebral venous hypertension on cognition. Evaluation of cognitive outcomes before and after venous sinus stenting could offer great insights into how venous pathology and cerebral dysfunction are related. These studies could help inform intervention timing, patient selection, and treatment goals.

CONCLUSION

Cognitive impairment in IIH is an underrecognized yet clinically significant feature of the disease, with important implications for quality of life. Although the nature and extent of impairment remain incompletely characterized, current evidence suggests that IIH is associated with multidomain cognitive dysfunction, likely reflecting disruption of subcortical networks. These deficits appear to arise from a combination of potentially reversible factors, including primary disease mechanisms, symptom-related amplification, and individual vulnerability. Improved understanding of how IIH affects brain function, particularly in relation to elevated ICP and cerebral venous hypertension, has the potential to influence the treatment offered and improve patient outcomes. Importantly, determining whether treatment improves cognitive function may help establish whether cognition has a role in future treatment selection, particularly in patients with IIHWOP, in whom disease burden may currently be underestimated.

Ethical approval:

Institutional Review Board approval is not required.

Declaration of patient consent:

Patient’s consent is not required as there are no patients in this study.

Financial support and sponsorship:

Nil.

Conflicts of interest:

There are no conflicts of interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation:

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

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