Horner Syndrome (HS), first described in 1869 by Swiss ophthalmologist Johann Friedrich Horner (1), is a clinical condition resulting from paralysis of the oculosympathetic pathway (OSP). Its characteristic triad of symptoms includes ptosis, miosis, and anhidrosis. Primary etiologies of HS encompass head and neck tumors, trauma, brainstem hemorrhage, infarction, myelitis, carotid artery dissection, infections, iatrogenic causes (e.g., surgical procedures), and other factors (2).

As early as 1915, Kaelin (3) reported two cases of HS following thyroid surgery (TS), which were documented but not published by Kappeler between 1865 and 1870. Both patients developed postoperative wound infections, leading Kaelin to hypothesize that infection irritated the cervical sympathetic nerve, resulting in HS. In 1965, Smith (4) documented seven additional cases of HS after TS; notably, these patients had no complications, including infection or hematoma. Based on these findings, Smith proposed that HS primarily resulted from surgical damage to the cervical sympathetic chain (CSC).

However, for over two decades, no further reports of HS as a postoperative complication of TS were published. Not until 1990, when Buhr (5) described three cases of HS following medullary thyroid carcinoma surgery, did this complication begin to garner attention in the surgical community. In the past decade, the number of reports of HS after TS has increased significantly. This article presents a case of HS after TS and provides a comprehensive analysis of its incidence, histopathology of associated tumors, surgical techniques and extent of resection, clinical manifestations, onset time, and recovery time, based on a review of literature published from 2000 to 2025. The aim of this study is to enhance surgeons’ awareness of this potential complication.

Of the 308 articles retrieved, 50 were selected for inclusion in this study, comprising 14 case series and 36 case reports. Among these, 18 articles (including 14 case series and 4 case reports) provided data on the incidence of HS (6–23) ( Table 1 ). Additionally, a total of 40 cases (including one from our own institution) were documented with detailed records in 36 case reports (7, 18, 20, 24–56) ( Table 2 ). No cases of transoral endoscopic thyroidectomy vestibular approach (TOETVA) were retrieved in the search.

According to the JBI quality assessment criteria for case reports, only six of the 36 included case reports met all eight criteria. For the majority of case reports, the treatment modalities implemented after the onset of Horner’s syndrome were not recorded; it is also possible that observation alone constituted the treatment strategy. Based on the JBI criteria for case series, only two of the 14 included case series met all ten criteria. Nevertheless, all studies fundamentally met the inclusion criteria and were deemed methodologically suitable for descriptive analysis. Figure 3 presents the risk of bias assessment for each included study using the Cochrane risk of bias tool.

HS refers to a group of clinical syndromes characterized by damage to the CSC (a nerve bundle located on the OSP), leading to nerve paralysis. Common etiologies include inflammation, trauma, surgical procedures, tumors, and thrombus formation. As a rare complication of TS, HS had an incidence of 0.25% in this study. Specifically, the incidence was higher in open - surgery cases compared to endoscopic - surgery cases (0.41% vs. 0.15%).

The mechanisms underlying the development of HS after TS mainly involve direct injury to the CSC, which is attributed to anatomical factors (57). Based on the reviewed literature, the mechanisms of injury can be summarized as follows: 1. Physical damage to the CSC; 2. Ischemia and edema of the CSC resulting from excessive traction and dissection of the carotid sheath; 3. Local compression of the CSC due to the elastic recoil of the carotid sheath; 4. Injury to the middle cervical ganglion (MCG) or its supplying blood vessels during manipulation of the inferior thyroid artery; 5. Excessive traction causing injury to the superior cervical ganglion (SCG) during manipulation of the superior thyroid artery; 6. Injury to the communicating branches between the CSC and the recurrent laryngeal nerve; 7. Thermal injury from energy devices; 8. Compression or infection may occur resulting from postoperative fluid accumulation or hematoma. The occurrence of HS immediately after surgery is related to direct CSC damage, such as excessive traction, thermal injury, or direct transection, while the delayed onset of HS may be due to tissue edema, inflammatory reactions, hematoma compression, or delayed nerve injury. In the case we presented, the patient developed Horner syndrome on POD 3, and the symptoms had not completely resolved even after 2 years. We suspect that this is related to the heat from the ultrasonic scalpel being conducted to the CSC, resulting in irreversible damage.

Understanding the anatomical basis of the OSP and CSC can further deepen our comprehension of HS. The OSP, composed of a pathway with three types of neurons, originates from the central nervous system, traverses the CSC, and ultimately reaches the eye (58). The second - order neurons, within which the CSC is located, are closely associated with iatrogenic injuries. The CSC is located posterior to the carotid sheath, anterior to the longus muscles, inferior to the prevertebral fascia, and is linked to the superior, middle, and inferior cervical ganglia. Excessive traction, dissection, extensive surgical procedures, or complex thyroid surgeries can cause CSC damage, which increases HS risk (59).

In the studied cases, malignant surgeries outweighed benign ones (67.5% vs. 32.5%), with 60% (24/40) undergoing lymph node dissection. HS incidence was high after specific surgeries, such as 27.3% (3/11) in medullary thyroid carcinoma cases involving TT+ CLND+LLND (5). Another study, encompassing 45 patients who underwent LLND, the incidence of HS was 4.4% (2/45) (11). When the tumor is intimately associated with the carotid sheath, surgical dissection of this structure significantly contributes to CSC damage (27, 30). Close adhesions between metastatic lymph nodes and the carotid sheath can lead to misidentification and inadvertent removal of ganglia. Therefore, it is evident that extensive cervical lymph node metastasis with subsequent LLCD is a significant factor contributing to postoperative HS. Additionally, McCrory (43) reported a case in which a cervical ganglioneuroma was mistakenly identified as an ectopic parathyroid adenoma and subsequently removed, ultimately resulting in HS.

Communicating branches between the recurrent laryngeal nerve and the CSC are present in some individuals (60). During the dissection and identification process of the recurrent laryngeal nerve, there exists a potential risk of damaging these communicating branches. In this study, five patients developed HS along with ipsilateral vocal fold paralysis, which underscores the close relationship between these two conditions.

The MCG, representing the smallest ganglion within the CSC, is located in close proximity to the inferior thyroid artery and may receive its blood supply from this artery (57). Consequently, during the dissection of the inferior thyroid artery, there exists a risk of directly damaging the MCG. Moreover, ligation of these vessels may result in ischemic injury to the MCG, thereby triggering the onset of HS (8).

The parapharyngeal space is another anatomical site that warrants particular attention. At the C1 - C4 levels, the SCG, which constitutes the largest ganglion within the CSC, is situated posterior to the carotid sheath and is anatomically contiguous with the parapharyngeal space. Excision of parapharyngeal metastatic lymph nodes (14), ectopic thyroid tissue (39), and excessive dissection of the upper pole during ETS (55) can result in HS, and all these cases may be associated with SCG injury.

A study indicates that although the incidence of HS after endoscopic surgery is lower than that after open TS, the incidence of HS remains relatively high during the initial phase of implementing endoscopic surgery (61). However, the results of this review cannot effectively support this conclusion. When performing endoscopic surgery to manage the superior pole of the thyroid, it is often necessary to retract the carotid sheath within the confined surgical space to adequately expose the operative field (55). Using a retractor to retract the carotid sheath carries the risk of exposing or injuring the SCG.

Energy - based devices, especially ultrasonic instruments that provide the dual benefits of cutting and coagulation, have been extensively employed in a variety of surgical procedures and play a pivotal role in endoscopic surgery. During surgical operations, thermal injury resulting from ultrasonic instruments represents another potential etiological factor for nerve damage, particularly in patients with anatomical variations of the CSC. In a rat model study, Carlander (62) reported that the local thermal energy effects generated by ultrasonic instruments can induce neurological dysfunction, and the severity of nerve damage is contingent upon the duration of thermal exposure. Furthermore, other studies have demonstrated that the incidence of temporary recurrent laryngeal nerve paralysis is elevated following the use of ultrasonic instruments compared to traditional techniques (63). Similarly, thermal ablation employs thermal energy to induce coagulative necrosis of tumor tissues, which may potentially cause thermal injury to the CSC (64).

Carsote (51) documented a case of chylous leakage following TS. Insufficient drainage resulted in the development of a lymphatic cyst, which subsequently exerted compression on the CSC and led to HS. After undergoing repeated needle aspiration for fluid drainage, the patient’s symptoms resolved completely. This indicates that postoperative fluid accumulation, lymphatic cysts, or hematomas that compress the CSC can also serve as a causative factor for HS.

Although the classical manifestations of HS encompass ptosis, miosis, and anhidrosis, the findings from the aforementioned literature indicate that ptosis and miosis are more prevalent than anhidrosis. Ptosis arises from the loss of sympathetic tone in Müller’s muscle (which is capable of elevating the upper eyelid by approximately 1–2 millimeters), leading to a narrowed palpebral fissure (65). There exists a muscle with a comparable function in the lower eyelid; consequently, in HS, the lower eyelid may be slightly elevated (occasionally termed ‘upside - down ptosis’) (66). It is noteworthy that, despite ptosis being mentioned in all these records, one study revealed that 12% of patients did not manifest symptoms of ptosis (67). When the symptoms are mild, the lower eyelid may also close more tightly. This condition imparts a sunken appearance to the eyes even in the absence of actual enophthalmos; true enophthalmos is relatively rare (68). The sympathetic cholinergic fibers within the OSP govern the function of facial sweat glands, and disruption of this pathway can result in anhidrosis. In specific cases, OSP dysfunction can induce facial flushing, conjunctival congestion, lacrimation, and nasal congestion due to vasodilation in the innervated regions (51).

When HS manifests subsequent to TS, a differential diagnosis should be carried out in collaboration with departments including neurology and ophthalmology. This is to rule out potential etiologies, such as intracranial lesions, cervical spinal cord lesions, cervicothoracic tumors, infections, immunologic diseases, or carotid artery lesions, prior to considering HS as a complication of TS.

The apraclonidine test represents the simplest and most reliable diagnostic modality for HS in adults, as it induces mydriasis of the affected pupil owing to the upregulation of α - 1 postsynaptic receptors (69). A potential limitation is that the test is contingent upon the presence of hypersensitivity, suggesting that OSP dysfunction must have persisted for a sufficient period to facilitate the upregulation of postsynaptic receptors (70). Consequently, the test exhibits limited diagnostic utility in the acute phase of HS but is generally deemed reliable two weeks after the onset of symptoms. Apraclonidine eyedrops are also capable of elevating the affected eyelid, offering temporary cosmetic amelioration for ptosis (71). Cocaine eyedrops serve as the preferred diagnostic agent for the diagnosis of HS (72). They inhibit the presynaptic uptake of norepinephrine, thereby elevating its concentration in the synaptic cleft and resulting in pupil dilation (73). A positive test outcome is indicative of HS when the mydriasis on the suspected side is significantly less than that on the healthy side (74).

HS typically does not result in functional impairment; however, alterations in appearance may lead to psychological distress. Short - term administration of steroids in conjunction with neurotrophic therapy can facilitate neuronal repair and aid in the alleviation of these symptoms. In the present study, 7.5% (3/40) of the cases presented with decreased visual acuity, and 2.5% (1/40) of the patients developed heterochromia. These findings suggest that patients with concurrent HS following TS necessitate close monitoring of ocular functional changes to enable timely intervention and prevent disease progression. Additionally, the results demonstrated that complete recovery occurred in all cases within one year, with the likelihood of complete recovery significantly diminishing after this time frame. It is noteworthy that, among the retrieved literature, no definition has been provided for the term “incomplete resolved.” Based on our case, during the two - year follow - up period, the patient’s ptosis and anhidrosis demonstrated improvement, whereas the degree of miosis remained unchanged. Another concern is that, for the group of patients categorized as ‘no improvement’ and ‘incomplete resolved,’ the assessment of HS outcomes may have been biased due to short follow-up durations or loss to follow-up. Therefore, we contend that the statistically reported HS outcomes in the article do not accurately reflect the true prognosis of this complication, as they omit the process of long-term follow-up and management.

Additionally, although IONM was employed in our case to ensure the normal function of the recurrent laryngeal nerve and the vagus nerve, HS still developed. This indicates that IONM may not be able to prevent CSC injury, which is consistent with previous reports (75). IONM primarily focuses on monitoring motor nerves, such as the recurrent laryngeal nerve and the vagus nerve; however, it does not provide feedback on autonomic nerve fibers, like those that constitute the CSC (76). Therefore, relying solely on IONM without direct visualization or anatomical knowledge of the CSC may give a false sense of security regarding nerve preservation during thyroid surgery. Surgeons should be aware of these limitations and integrate direct visualization and anatomical knowledge into their surgical techniques to minimize the risk of CSC injury.

This study has several limitations. The included literature is limited in both quality and quantity, with substantial heterogeneity present in research methodologies. This increases the difficulty of data extraction and comprehensive analysis. The studies are predominantly observational in nature, which makes it difficult to establish a definitive causal relationship between TS and HS, and mechanistic investigations remain speculative. There is insufficient data on pediatric patients and specific surgical techniques, impeding the assessment of their impact on specific patient subgroups and surgical modalities. Inconsistent follow-up durations and outcome assessment criteria reduce the comparability of results and the thorough evaluation of the long - term effects of HS.

Although this study conducted a systematic review following the PRISMA guidelines (77), its methodological rigor still did not fully meet the expected level of the Cochrane/Campbell standards. Future research endeavors ought to utilize multicenter prospective cohorts or randomized controlled trials (RCTs) to establish causality. Animal models, in conjunction with intraoperative neuromonitoring, can offer insights into the underlying mechanisms. Particular attention should be directed towards pediatric populations and minimally invasive surgical techniques, accompanied by long - term follow - up (≥5 years) to evaluate chronic outcomes. The establishment of a global registry and the development of multidisciplinary guidelines would further enhance the management of HS.

HS is a clinical manifestation that describes the impairment of the CSC, representing a rare and non-fatal complication following TS, which arises from multiple injury mechanisms. Although HS typically does not affect ocular function, it causes significant cosmetic and psychological distress to patients, particularly after endoscopic surgeries that are intended to enhance appearance. In rare cases, decreased vision and heterochromia may also occur. For acute symptoms of CSC injury following surgery, diagnosis can be made using the apraclonidine test and cocaine eyedrops. Once HS is diagnosed, short-term steroid and neurotrophic treatments can be administered. If complete recovery is not achieved within a year, the likelihood of complete recovery decreases significantly thereafter. Therefore, patients should be fully informed of this risk prior to surgery, and the area surrounding the CSC should be carefully assessed and operated on with precision to avoid damaging it. However, currently, substantial disparities exist in the evidence level and heterogeneity among the published literature. In the future, it is imperative to establish a comprehensive recording system to analyze the etiology and prognosis of such rare complications.