A Systematic Review Assessing the Impact of Surgery on Sleep Disturbances in Craniopharyngioma

INTRODUCTION

Craniopharyngiomas (CP) are embryonic malformations affecting the sellar/para sellar regions of the brain.¹ These rare, benign tumors develop in around 0.5–2 million people each year and have a bimodal age distribution, with 30–50% of all cases presenting during childhood and adolescence.¹ Clinical manifestations of CP are most often non-specific symptoms of raised intracranial pressure, e.g., nausea and headache, followed by visual impairments and endocrine disorders.² Despite their low-grade histological classification, the morbidity of CP is often high, due to the proximity of the tumor to important structures in the brain, such as the hypothalamus.¹ Damage to the hypothalamus can occur directly due to tumor growth, causing specific symptoms at diagnosis, or due to treatment of the tumor, causing long-term consequences.³

Treatment-induced hypothalamic injury is often the result of surgical resection of the tumor.³ There is debate regarding the optimal surgical strategy, with the choice between gross total resection (GTR) and subtotal resection (STR) usually being made on a case-by-case basis. GTR is associated with higher postoperative morbidity due to damage to structures such as the hypothalamus but carries a lower recurrence risk compared with STR. Because of this, STR is seldom used alone and is often combined with radiotherapy to reduce recurrence rates similar to those for GTR.⁴ Irrespective of radiotherapy use, surgery remains a pivotal component of CP treatment, but the risk of surgery-induced injury can significantly impair the quality of life of survivors.^4,5 Alternatively, surgery can bring about favorable outcomes by helping to alleviate symptoms due to the mass effect of the tumor.⁶ For example, studies show that symptoms such as impaired vision can be improved following surgery.^7,8

The hypothalamus is a structure that sits in the ventral brain and works in conjunction with the pituitary gland to secrete hormones as part of the hypothalamic-pituitary axis.⁹ As well as its endocrine role, the hypothalamus is key in regulating vital bodily functions such as appetite, thirst, and body temperature.⁹ Damage to the hypothalamus can manifest as disturbances in homeostatic functions and/or endocrine abnormalities, such as growth impairment and amenorrhea.^9,10

Another important, yet often overlooked, symptom of hypothalamic damage in CP is sleep disturbance, possibly due to damage of the suprachiasmatic nucleus of the hypothalamus.¹¹ This structure is termed the master circadian pacemaker as it regulates most circadian rhythms in the body including sleep-wake cycles. It receives input from the photosensitive ganglion cells in the retina and projects to structures such as the pineal gland to regulate melatonin production, mediating sleep and wakefulness.¹² Sleep is fundamental for almost every part of physical and mental health, with sleep disturbances having negative impacts on cardiovascular, immune, and metabolic health, contributing to overall morbidity and mortality.¹³ It is therefore important to identify and treat CP patients with sleep problems to improve clinical outcomes for these patients.

Sleep disturbances such as somnolence, narcolepsy, and sleep-disordered breathing have been reported throughout the literature as negative consequences of CP both before and after treatment. However, it is not clear to what extent these are due to a mass effect caused by the tumor or due to surgical management. A recent systematic review analyzed sleep disturbances in the pediatric CP population and found a high prevalence of disturbances, mainly postsurgery.¹⁴ For example, they found that excessive daytime sleepiness (EDS) occurs at rates between 14 and 35% post-treatment.¹⁴ These authors suggested that research aimed at examining sleep before and after treatment would be beneficial to compare types and severity of sleep disturbances, to better clarify the underlying pathogenic mechanisms of sleep disturbance.¹⁴ The present systematic review aims to assess sleep disturbances in CP patients pre- and postsurgery, to examine the potential role of surgery-induced injury or postsurgical improvement on sleep in these populations. This information may help guide surgical decision-making, helping to improve health outcomes and quality of life for CP patients.

METHODS

The protocol was registered with the International Prospective Register of Systematic Reviews (PROSPERO CRD42023469112). This systematic literature review was undertaken in accordance with the preferred reporting items for systematic reviews and meta-analyses (PRISMA) statement.¹⁵

RESULTS

The systematic search identified 1095 publications, of which 11 were included in the review (Fig. 1).¹⁵ Critical appraisal of the included publications is shown in Table 1 (case-control) and Table 2 (cohort). In studies where only presurgical data were extracted, questions 3, 6a, and 6b were marked “not applicable (N/A)” as exposure to surgery and follow-up were irrelevant. Overall, the risk of bias across all studies included in this review is high. The main reasons for this across all studies included insufficient information regarding the method of cohort recruitment, exposure (surgery) inadequately described, subjective outcome measures, insufficient follow-up, confounding factors, a lack of statistical analysis, and small sample sizes. Table 3 reports the main characteristics of the studies included in this review.

Fig. 1: PRISMA flow diagram of search results

All included articles assessed sleep in adult and/or pediatric CP patients presurgery, postsurgery, or both.^20,22 Dates of publication ranged from 1998 to 2023. Study designs included case-control and cohort studies. Five studies included pediatric CP only^23,27 and three studies included adult CP only. Three studies included both adult and pediatric CP patients,^25,26 of which two studies did not differentiate results between ages;^3,25 therefore, it was not possible to differentiate results of this review by age group. Pituitary hormone dysfunction (PHD) was found in variable frequency. GTR had a relatively high prevalence of PHD compared to STR. Most of the patients had hormone replacement therapy at the time of sleep analysis.

As radiotherapy was an exclusion criterion in this systematic review, only the presurgical information was used from Guo et al.³ as, in the postsurgical group, patients received radiotherapy alongside surgical intervention. Similarly, Larijani et al.²⁵ looked at two postsurgical groups but only the group without adjuvant radiotherapy was included in this review.

There was a discrepancy in the number of patients who experienced somnolence in Pascual et al.²⁶ The authors reported the clinical symptoms at diagnosis for each patient individually in Table 1 of their study. From this table, we identified 92 patients with pathologically verified CP and out of these, 41 patients (44.6%) had a clinical symptom of somnolence. However, when the data are summarized in Table 2, it was reported that 43 patients (46.7%) had a clinical symptom of somnolence. We have used the reported figure of 46.7% in the analysis.

The corresponding author from Foschi et al.¹⁹ was consulted via email regarding queries and discrepancies in their data (see Appendix 1 for details).

DISCUSSION

The aim of this review was to evaluate sleep disturbances in CP patients pre- and postsurgery. Only four studies in this review made this comparison, so studies that assessed sleep only pre- and only postsurgery were also included, but these provide weaker evidence due to the lack of control/comparison groups. No significant difference between the weighted prevalence of sleep disturbances in CP patients pre- vs postsurgery was found. This may suggest that surgery does not consistently cause hypothalamic damage leading to sleep disturbances, or that if the CP tumor extends into the hypothalamus presurgery, then surgery does not improve sleep outcomes. However, the strength of this conclusion is severely limited by several factors. Firstly, the analysis relies on comparisons made between cohorts who may not be representative of one another due to a variety of confounding factors. These include the presence of hypothalamic injury, BMI, time of measurement before/after surgery, age, and histological subtype. Also, most studies in this review assessed sleep as a secondary outcome and used subjective measures that rely on self-report, which might not report sleep as accurately as objective measures and are more prone to bias.

The combined findings of the four individual studies that compared sleep pre- and postsurgery displayed no clear patterns in terms of sleep disturbances. Some studies reported improvement in sleep postsurgery, while others reported the opposite or no effect, which supports our statistical analysis of no overall difference pre- to postsurgery. However, these studies all display strengths and weaknesses which must be taken into consideration. Guo et al.²³ was the highest-weighted study in this group, with 185 participants compared to a total of 88 participants across the other three studies. Guo et al.²³ found no statistical difference between sleep disturbances pre- and postsurgery, which supports the comparison of weighted prevalence in this review. However, sleep was measured subjectively (ESS) by Guo et al.²³ Conversely, Foschi et al¹⁹ was the only study in this cohort to measure sleep objectively and found improvement in sleep efficiency postsurgery but worsening of daytime drowsiness. However, these authors had a very small sample size and performed no statistical analysis. Small sample sizes used in many of the studies make results more susceptible to confounding by other variables and lack of statistical analysis prevents the drawing of solid conclusions.

Somnolence, hypersomnolence, and EDS were the most frequently reported sleep disturbances in both pre- and postsurgical CP patients.²⁷ While these terms all have slightly different definitions, they all share symptoms of excessive tiredness, particularly during waking hours.²⁸ Somnolence was measured subjectively in many of the studies and often was the only sleep outcome reported. This may provide some explanation on why it was reported most commonly, as it may be more easily detected or reported compared with other sleep disturbances that need objective measurements for diagnosis. Somnolence was described in 4/6 of the studies that assessed sleep presurgery. However, the amount of patients experiencing this differed between studies, with an apparent relationship with age. The studies in this review may suggest that adults are more likely to present with somnolence at diagnosis than children. Pediatric cohorts reported a lower prevalence of somnolence presurgery (3.7%,²⁷ 0.05%²³) than adults (70%).¹⁹ A potential reason for this difference may be that children present more frequently with the adamantinomatous (ACP) CP subtype, while the papillary (PCP) form occurs more often in adults.²⁹ Hypothalamic dysfunction is higher in patients with PCP than ACP,³ indicating a higher risk of sleep disturbance, possibly because PCP originates mainly in the suprasellar region, where the hypothalamus resides, while ACP originates in the sellar region.³

Somnolence/EDS was also the most frequently reported sleep disturbance in studies looking at postsurgical CP patients (reported in 2/6 studies), alongside OSA, which is a potential cause of somnolence. OSA was reported in 2/6 studies postsurgery and 1/6 studies presurgery. However, only one of these papers compared sleep both before and after surgery and only reported OSA presurgery, despite a mean increase in BMI after surgery. Obesity is a well-known risk factor for OSA in the general population,³⁰ but O’Gorman et al.²² found that OSA was significantly more frequent in CP patients with hypothalamic obesity (HO) postsurgery than BMI-matched controls.²² These findings are consistent with other studies suggesting patients with HO have a higher risk of OSA than those with obesity due to other etiology.^31,32 This indicates a direct role of hypothalamic damage in the development of OSA in CP patients, which does not appear to be different depending on whether due to mass effect from the tumor or surgical injury. For OSA, other causes for somnolence may include poor/insufficient sleep and disorders of the sleep-wake cycle such as narcolepsy,³³ the latter of which was reported in patients postsurgery by Muller et al.²⁰ Secondary narcolepsy occurs due to damage to hypothalamic neurons producing/transmitting orexin, a neuropeptide important in regulating sleep and wakefulness,³⁴ so the findings from this study may suggest a specific role of surgery in inducing this damage. However, this study was limited by having only 10 participants, 1 unmatched control, and no comparison to presurgical data, so it is not possible to confidently make this conclusion.

Other sleep problems were also reported in the studies included in this review, some of which have been previously mentioned in the literature as consequences of CP or its treatment.^14,35 These included sleep rhythm disturbances, with no significant difference found in frequency between pre- and postsurgery.²³ Problems with sleep quality were also seen postsurgery in one study²¹ and sleep scores NHP seemed to improve postsurgery in another study.¹⁸ However, two other sleep disturbances were mentioned that are not as commonly reported; PLMD and insomnia. PLMD was seen presurgery in two patients in Foschi et al.¹⁹ PLMD appears to be related to restless leg syndrome (RLS) and previous research found that if the A11 nucleus of the posterior hypothalamus, a major source of dopamine for the spinal cord, is lesioned then the development of an RLS-like phenotype can occur in mice.^36–38 Considering 50% of the patients in Foschi et al.¹⁹ had posterior hypothalamic involvement of the tumor, this may provide an explanation for why PLMD was seen in this study. However, this disturbance was not reported postsurgery and it is unlikely that surgery would have reversed any hypothalamic damage. Therefore, this brings into question possible confounding factors such as physical inactivity, smoking, or obesity, which all increase the risk of PLMD.³⁹ Similarly, insomnia was only reported in one study postsurgery.²⁵ Insomnia has been reported in survivors of other childhood brain tumors, potentially due to disruption of the ventrolateral preoptic nucleus located in the hypothalamus.³⁴ Hence, it is possible that surgery-induced hypothalamic injury could explain this finding. However, this is less likely considering that surgical management was STR, which is associated with a lower risk of damage.⁵ It was also reported as a “late postsurgical complication,” and sleep disturbances frequently occur in patients postoperatively, irrespective of type of surgery.^40,41 Therefore, it is difficult to determine to what extent the results are confounded by the act of surgery itself rather than specifically the iatrogenic hypothalamic damage done by the surgery. The same may be true for other studies in this review, particularly those where measurements were only taken days/months presurgery^19,23 and postsurgery.^18,23

Hypothalamic damage is thought to be the most important factor in determining sleep disturbances in CP patients,¹¹ which may be due to the tumor or due to surgery. However, studies that demonstrated hypothalamic damage in patients found varying results in terms of sleep.^19,21,22

This may have been due to variation in other factors that affect sleep, or due to differences in the extent and/or location of hypothalamic damage. For example, in two studies where postsurgical hypothalamic damage was present, one study found that sleep outcomes were significantly worse in CP patients compared to controls,²² but the other study found no significant difference in sleep outcomes between CP patients and controls.²¹ The exact location of hypothalamic damage and extent of surgical resection is not clear in either paper, which may have provided insight into the precise mechanisms of sleep disturbances and reasons for conflicting results between papers. In contrast, Foschi et al.¹⁹ demonstrated that 50% of patients had tumors located at the posterior hypothalamus, the location of the suprachiasmatic nucleus which is critical for sleep,¹² and reported a high prevalence of sleep disorders presurgery. Additionally, there was an apparent worsening of overall sleep disorders postsurgery when a GTR method was used in the majority of patients, which has been predicted to cause further damage in patients with hypothalamic-invading tumors.⁵ Many studies did not report the extent of hypothalamic damage or the extent of surgical resection, which makes it difficult to assess the precise role of hypothalamic injury on sleep disturbances. It is possible that when predicting adverse outcomes, one needs to consider that preoperative grading to define the exact location of hypothalamic damage is more important than simply just the presence or absence of damage. This may suggest a need to refine the already existing grading system to improve clinical outcomes both pre- and postsurgery.⁴²

To conclude, this review suggests that surgery does not increase the risk of sleep disturbance in CP patients based on weighted prevalence calculations and a lack of clear differences in individual studies comparing sleep pre- and postsurgery. However, the quality of the literature is not strong enough to make any firm conclusions, with many limitations mentioned throughout. This highlights the need for more suitably designed studies, with adequate sample sizes that quantify sleep disturbances pre- vs postsurgery, with self-reported measurements supported by objective assessment of sleep quality, and measurements preferably taken at diagnosis/early stages in the disease followed by months-years postsurgery.^43,44 It would also be useful to assess the location of the tumor and the extent of hypothalamic damage pre- and postsurgery to improve knowledge of mechanisms contributing to sleep disturbances. Additionally, future research could focus on the effect of radiotherapy on sleep, as it is becoming more frequent in addition to surgery in CP treatment, and there is already a plethora of primary studies evaluating its use. Radiotherapy may carry its own consequences on sleep, hence it would be useful to examine sleep pre- and posttreatment in CP where radiotherapy is used and assess if there are any differences to the current review.

ACKNOWLEDGMENTS

The author would like to thank Joydeep Basu from the University of Warwick for assistance with statistical analysis and Dr Asad Ali, Respiratory and Sleep Medicine Consultant at University Hospitals Coventry and Warwickshire, for their feedback during manuscript preparation.

SUPPLEMENTARY MATERIALS

All the supplementary materials are available online on the website of www.ijsm.in/journalDetails/IJSM.

ORCID

Jacqueline G Nash https://orcid.org/0009-0003-3384-9350

Peter J Davies https://orcid.org/0009-0003-7440-9618

Pratibha Natesh https://orcid.org/0009-0008-3587-2059

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APPENDIX 1

The corresponding author from Foschi et al. was consulted via email regarding queries and discrepancies in their data. There were queries regarding a duplicate dataset with this paper and another paper identified during the screening process, and the number of males and females was reported differently in each paper. In this communication, the author confirmed that the two papers contained the same dataset and confirmed the correct number of females and males used for their study. The number of males and females is correctly reported in this systematic review (Table 3) as 4 and 6, respectively. The other paper was excluded for the reason of a duplicate dataset. The author was also consulted regarding discrepancies between results, e.g., the results state that all patients developed hypothyroidism and diabetes insipidus postsurgery yet Table 1 in their paper reported hypothyroidism and diabetes insipidus in 90 and 70%, respectively. The author did not respond so the values in Table 1 were extracted and used in this review.