Systematic review of benign thyroid enlargement as a rare cause of arterial compression: clinical presentations and outcomes

Abstract

The objective of this study is to systematically characterize the presentation, management, and outcomes of arterial complications secondary to benign thyroid enlargement, thereby improving clinical recognition and management of this rare entity. A systematic review was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines across PubMed, Web of Science, Embase, and Scopus for studies published from January 1990 to February 2026. This review was registered with PROSPERO CRD420251156228. Studies describing arterial compression, displacement, stenosis, or occlusion attributable to benign thyroid pathology were included. Ten studies met the inclusion criteria, comprising 10 patients with a median age of 66 years, of whom 80% were female. Six patients presented with acute neurologic symptoms, including limb-shaking episodes and lateralized weakness, while the remainder exhibited subacute or chronic compressive complaints. Computed tomography with or without angiography was the primary diagnostic modality. The common carotid artery was involved in nine patients, including bilateral compression in two patients. Multinodular goiter was the most common pathology, with goiter sizes reaching up to 15 cm. Surgical management via thyroidectomy was performed in five patients, while the others were managed conservatively. Follow-up was documented in only five of the ten patients; in each of these, symptoms resolved without reported recurrence, while the remaining five reports contained no post-treatment follow-up data. In conclusion, benign thyroid enlargement is a rare but clinically significant cause of cervical arterial compression that can precipitate neurologic symptoms mimicking cerebrovascular disease. Cross-sectional imaging is essential for diagnosis, and both surgical decompression and conservative strategies were followed by symptom resolution in the cases with documented follow-up. Because the evidence base comprises ten single-patient reports with incomplete follow-up, no objective outcome measures, and no comparative data, certainty of evidence is very low, and these findings should be regarded as hypothesis-generating rather than as guidance for management.

Introduction

Thyroid enlargement is a common clinical finding, particularly among older adults and women, with multinodular goiter representing the most frequent benign etiology worldwide (1, 2). The prevalence of thyroid nodules increases with age and is substantially higher in women, with population-based studies demonstrating nodular disease in up to 50–60% of older adults on imaging or ultrasonography (1, 2, 3). Although many nodules remain clinically silent, progressive enlargement may result in clinically apparent goiter, especially in regions with historical iodine deficiency or in aging populations. Multinodular goiter is therefore a frequent diagnosis in endocrine and surgical practice. Benign goiters are a well-recognized cause of compressive symptoms, particularly in the trachea, esophagus, and venous structures. Venous complications, including jugular vein compression and superior vena cava–like syndromes, have been previously described and are established sequelae of large goiters (4, 5, 6). In contrast, arterial complications associated with thyroid enlargement are rarely reported and remain poorly characterized.

Vascular involvement of cervical arteries is more frequently discussed in the context of thyroid malignancy. Invasive thyroid cancers are known to encase, invade, or compress adjacent vascular structures, including the carotid arteries, often contributing to complex surgical decision-making and increased morbidity (7, 8). However, reports describing arterial complications arising from benign thyroid pathology are rare. As a result, arterial compression secondary to benign thyroid enlargement may be underrecognized or underreported.

Although isolated case reports have documented carotid artery compression, displacement, and hemodynamically significant stenosis due to benign thyroid growth, the clinical significance and patterns of presentation remain unclear (9, 10, 11). These cases are particularly important because symptoms may mimic transient ischemic attack, stroke, or other neurologic disorders, potentially leading to diagnostic uncertainty and delays in appropriate management.

Given the limited synthesis of existing evidence, this systematic review aims to characterize reported cases of arterial complications associated with benign thyroid enlargement, with emphasis on clinical presentation, imaging findings, management strategies, and outcomes.

Methods

This systematic review was reported in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines (12). This review was registered with PROSPERO CRD420251156228. A systematic search was conducted by a trained medical librarian. The literature was searched through the citation databases: PubMed for MEDLINE, Web of Science, Scopus, and Embase. Databases were searched for both keywords and controlled vocabulary (MeSH, etc.) when available, around the topics of thyroid enlargement and vascular complications. Limiters for English language, the exclusion of conference abstracts, and publication date restrictions were applied where available. As executed, the database searches were limited to records published from 2010 onward through September 2025 (see Supplementary Item 1 in Supplementary materials). Eligible reports published before 2010 were identified through backward citation searching of the reference lists of included articles and relevant narrative reviews. The eligibility window for this review was therefore January 1990 to February 2026, while the date limiter applied within the databases themselves was 2010 to February 2026.

Studies were eligible for inclusion if they reported arterial involvement, including compression, displacement, stenosis, or occlusion, attributable to benign thyroid pathology. For the purposes of this study, benign thyroid enlargement was defined as a nonmalignant expansion of the gland (e.g., multinodular goiter or benign cysts) confirmed by histopathology or cytology. Arterial compression was specifically categorized as an objective reduction in vessel lumen diameter or significant anatomical deviation of the cervical vasculature as visualized on cross-sectional imaging. Reports involving malignant thyroid disease, isolated venous complications, nonthyroid etiologies, or insufficient clinical data were excluded. Full-text articles were subsequently reviewed to confirm eligibility, and discrepancies in study selection were resolved through consensus among the reviewers.

Search scope and anticipated constraints

The search strategies were anchored on terms for thyroid enlargement combined with vascular terms (vascular, carotid) and with complication or cerebrovascular terms (complication, compression, stroke, transient ischemic attack, cerebrovascular accident, CVA, TIA). Two consequences of this structure were recognized. First, because the vascular anchor emphasizes the carotid circulation and its neurologic sequelae, reports describing arterial displacement or kinking, vertebral artery compression, brachiocephalic or subclavian involvement, or hemodynamically significant stenosis unaccompanied by neurologic symptoms may have been captured inconsistently, particularly where such findings were incidental and were not reflected in the title, abstract, or indexing terms of the source article. While specific arterial outcomes were not searched individually, arterial outcomes were searched generally using broad vascular keywords to maximize the likelihood of capturing all relevant outcomes in this area; the addition of individual artery terms during strategy development did not return additional relevant records. Second, each database strategy excluded any record in which the words cancer, carcinoma, or neoplasm appeared in the title or abstract. This exclusion was deliberately restricted to the title and abstract fields rather than applied to any occurrence of these terms in the record, in the databases where field limitation was available, so that only reports focused on a cancer diagnosis would be removed. Although intended to enrich the yield for benign disease, this exclusion would also have removed reports in which malignancy was initially suspected or in which malignancy was discussed as part of the differential diagnosis, but in which benign thyroid pathology was ultimately confirmed on histopathology or cytology. Backward citation searching of the reference lists of included articles was undertaken in part to offset these effects, but the search cannot be regarded as exhaustive, and the likely impact of both constraints on the completeness of this review is addressed in the limitations.

Data extraction

Two reviewers independently extracted and analyzed data using a standardized data collection form, and disagreements were resolved through discussion with a third reviewer. Study characteristics and patient-level variables extracted included age, sex, comorbidities, thyroid pathology and size, presenting symptoms, symptom duration, imaging modalities used, arteries involved, management strategy, and clinical outcomes. The primary outcome was resolution of symptoms following management; secondary outcomes included type of vascular involvement, imaging patterns, and duration of follow-up. Outcomes were evaluated relative to the intervention described in each report. Symptoms or vascular findings occurring prior to diagnosis were recorded descriptively but were not incorporated into outcome comparisons because of inconsistent reporting across studies. Imaging modalities recorded included radiography, ultrasound, computed tomography (CT) with or without angiography, and magnetic resonance imaging (MRI) with or without angiography. Management strategies included thyroidectomy, medical management, and observation. No comparative hypotheses or pooled effect measures were tested or measured because of the small sample size and heterogeneity of reporting; instead, descriptive synthesis was used to characterize patterns of presentation, vascular involvement, and clinical outcomes. Formal statistical heterogeneity was not applicable because meta-analysis was not performed; instead, clinical and methodological heterogeneity was assessed qualitatively. Additionally, sensitivity analyses were not performed because the available evidence was exclusively composed of case reports with notable clinical heterogeneity. Formal statistical assessment of publication bias, for example, by funnel plot asymmetry or Egger test, was not possible because these methods require multiple comparative studies reporting effect estimates; publication bias was therefore appraised qualitatively and is discussed in the limitations. Certainty of evidence was likewise not graded using the formal GRADE framework, which is not constructed for bodies of evidence composed exclusively of single-patient reports. Instead, certainty was appraised narratively against GRADE-informed domains, namely, study design, risk of bias, inconsistency, indirectness, imprecision, and publication bias, and is reported together with the risk-of-bias synthesis in the section titled Results.

Risk of bias

Risk of bias was assessed independently by two reviewers (A.M.H. and K.N.) using the Joanna Briggs Institute 2020 Critical Appraisal Checklist for Case Reports, as all included studies were single-patient case reports. Disagreements concerning bias were resolved by consensus with a third reviewer (N.B.). Items were rated as yes, no, or unclear. No study was excluded solely based on risk-of-bias rating, and assessments were considered qualitatively when interpreting the evidence (Supplementary Item 2). Item-level ratings were tabulated across all included reports (Supplementary Item 2), and the frequency of unmet items was summarized descriptively in order to characterize the methodological limitations of the evidence base as a whole rather than those of any individual report. Particular attention was directed to the completeness of follow-up reporting, the presence of objective as opposed to purely narrative outcome measures, and whether post-treatment imaging was performed to confirm that vascular compromise had resolved.

Results

Patient characteristics and presentation

The initial database search identified 581 records. After removal of duplicates and screening, 35 full-text articles were assessed for eligibility. Ten studies met the inclusion criteria (9, 10, 13, 14, 15, 16, 17, 18, 19, 20), comprising 10 patients with arterial complications attributable to benign thyroid enlargement (Fig. 1). Overall study quality was limited because of the inherent limitations of case reports and case series. Included studies adequately described patient presentation, imaging, interventions, and outcomes. However, incomplete follow-up was common. No studies were excluded based on risk-of-bias assessment. Because no comparative studies were identified, outcomes are reported descriptively without pooled effect estimates or inferential statistical analysis. There was considerable clinical heterogeneity with respect to reports of thyroid pathology, severity of arterial compression, presenting symptoms, imaging modalities, management strategies, and duration of follow-up, precluding quantitative synthesis.

Figure 1.

PRISMA flow diagram outlining the study selection process for the systematic review.

The median age was 66 years (interquartile range [IQR], 55–76), and eight of ten patients (80%) were female. Documented comorbidities included coronary artery disease, diabetes mellitus, bradycardia, and prior cervical spine surgery; however, comorbidity reporting was inconsistent. A subset of patients had known multinodular goiters with varying chronicity, including one case of steady enlargement for 6 months prior to admission. Patient demographics and clinical details are summarized in Table 1.

Table 1.

Concise case summary of thyroid arterial compression.

Study	Age/Sex	Symptom Duration	Pathology	Size	Presentation	Core Imaging Findings	Arteries Affected	Management	Outcome	F-U	VN on F-U imaging
Aykan et al. (13)	76/F	NR	Retrosternal goiter	NR	Dizziness	CT: Displaced & kinked CCAs	Internal carotid and common carotid	NR	NR	NR	NR
Baba et al. (14)	67/F	1 week	Thyroid abscess	15 cm	Neck swelling, pain	CT/US: Enlarged R lobe, displacement	R CCA	R thyroid lobectomy	Resolved	NR	NR
Braakman et al. (10)	93/M	NR	Cystic nodule	4.5 cm	Dizziness, limb-shaking	MRA: R cyst displacing carotid	R CCA	NR	NR	NR	NR
Camacho et al. (9)	90/F	<1 day	Massive goiter	15 cm	Stroke-like symptoms	CT: L CCA narrowing: MRI: Infarct	Bilat. CCAs	Total thyroidectomy	Resolved	2 months	NR
Evans & Timm (15)	33/F	2 months	Multinodular goiter	NR	Ear pain, headaches	MRA: R lobe displacing vessels	R CCA, and R proximal vertebral, Innom	R thyroidectomy	Resolved	NR	NR
Fernandes et al. (16)	55/F	Acute onset	Multinodular goiter	NR	L-sided weakness	MRI/MRA: Nodule displacing carotid	R. ICA, R. CCA, Innom	Conservative	NR	NR	NR
Milder et al. (17)	37/F	6 months	Multinodular goiter	R: 8.3 cm. L: 10 cm	Dyspnea, vision issues	MR: 5.5 cm mass compressing vessels	Bilat. CCAs	Thyroidectomy	Resolved	2 days	NR
Sahin et al. (18)	64/M	Acute onset	Hemorrhagic nodule	7x5 cm	Syncope, neck swelling	US: Hemorrhage displacing L lobe	L CCA, IJV, Vagus	Conservative	Resolved	Documented; duration NR	NR
Silvestri et al. (19)	72/F	Acute onset	Large goiter	NR	L paresis, weakness	US: Goiter with vascular changes	R subclavian and Innom	Thyroidectomy	NR	NR	NR
Smit et al. (20)	63/F	7 day	L-sided goiter	NR (Large)	Headaches, Horner’s	MRI: Compressed L CCA	L CCA	Medical	NR	NR	NR

NR, not reported; CCA, common carotid artery; ICA, internal carotid artery; Innom, innominate/brachiocephalic; Bilat, bilateral; F-U, whether post-treatment clinical follow-up was reported in the source article; VN on F-U imaging, vascular normalization: whether repeat imaging after treatment documented vascular normalization (restoration of arterial caliber or of flow).

Clinical presentations were heterogeneous and largely dictated by symptom acuity. Six patients (60%) presented with acute neurologic deficits, including limb-shaking, stroke-like symptoms, and lateralized weakness, occurring over hours to days. These patients frequently underwent urgent neurovascular imaging and were more likely to proceed to surgical intervention. In contrast, the remaining patients presented with subacute or chronic compressive symptoms, such as neck swelling, dysphagia, dyspnea, and progressive goiter enlargement. These individuals were typically evaluated in nonemergent settings and demonstrated a lower rate of immediate surgical management.

Imaging and vascular findings

Cross-sectional imaging was central to diagnosis in all cases. CT, frequently combined with angiography, was the most common modality. MRI and MRA were used particularly in patients presenting with neurologic symptoms.

Arterial involvement most frequently affected the common carotid artery, which was involved in nine patients (90%). This included bilateral involvement in two cases (20%). The internal carotid artery was also involved in two patients (20%). Furthermore, multivessel involvement was observed in several cases, including additional compromise of the innominate (30%), proximal vertebral (10%), and subclavian (10%) arteries.

Patterns of vascular compromise included extrinsic compression, luminal narrowing, arterial deviation, and kinking. In cases presenting with neurologic deficits, imaging more frequently demonstrated internal carotid artery involvement or luminal stenosis. In contrast, patients with predominantly chronic compressive symptoms more commonly demonstrated arterial displacement without clear hemodynamic quantification.

Larger goiters, particularly those measuring up to 15 cm or demonstrating retrosternal extension, were more frequently associated with multistructure compression, including tracheal deviation and bilateral vascular effects.

Thyroid pathology included multinodular goiter, retrosternal goiter, cystic nodules, acute suppurative thyroiditis progressing to thyroid abscess, and large solitary nodules. Reported thyroid size ranged from 4.5 to 15 cm.

Nature and severity of arterial involvement

Because the term arterial compression encompasses a spectrum of imaging findings of potentially differing clinical significance, the nature of vascular involvement was examined separately for each case using the descriptors reported by the original authors. Formal severity grading was not possible. No included report quantified the degree of stenosis against accepted criteria; none reported peak systolic velocities or other hemodynamic measurements, and none performed positional or dynamic imaging. Cases were therefore grouped only according to the vascular abnormality explicitly described in the source report.

Displacement or deviation of an otherwise patent vessel, with or without kinking, was the abnormality described in six of ten reports. Extrinsic compression with luminal narrowing was described in three reports, one of which was accompanied by radiographically confirmed cerebral infarction. In the remaining report, the vascular abnormality was described only as unspecified vascular change on ultrasonography and could not be classified.

Symptom severity did not correspond closely with the described extent of vascular involvement. The only patient with documented cerebral infarction presented with stroke-like symptoms, as would be expected. However, focal neurologic deficits were not confined to cases with luminal narrowing: two patients in whom imaging described displacement of a patent vessel without narrowing presented with limb-shaking episodes and with lateralized weakness, respectively, and the patient whose imaging could not be classified presented with paresis. Conversely, the two patients with described luminal narrowing but without infarction presented with mechanical or local symptoms – namely, dyspnea and visual disturbance in one and headache with Horner syndrome in the other – rather than with ischemic deficits. Because the imaging descriptors available were narrative rather than quantitative, and because symptoms attributable to hypoperfusion are likely to depend on collateral circulation, cerebrovascular reserve, and head position at least as much as on the static appearance of the vessel on a single study, no relationship between the extent of vascular compromise and symptom severity can be established from these data.

Management and outcomes

Surgical intervention was performed in five patients (50%), consisting of four thyroidectomies and one thyroid lobectomy. Operative management was typically selected in patients with acute neurologic symptoms, imaging demonstrating hemodynamically significant arterial compression or stenosis, or progressive compressive complaints.

Nonsurgical strategies were employed in the other half of patients (50%) and included conservative monitoring, medical management, and observation. Conservative approaches were generally selected in patients with milder symptoms, absence of progressive neurologic deficits, or elevated surgical risk. Delayed improvement was more commonly reported in this group, with symptom resolution occurring over weeks to months. In one case, medical therapy with carbamazepine reduced limb-shaking episodes attributed to transient cerebral hypoperfusion. Other conservatively managed patients demonstrated stabilization or gradual improvement without operative intervention.

Postoperative outcomes were favorable in every report in which they were described. Immediate improvement was frequently described following surgical decompression, particularly in patients presenting with neurologic manifestations. Several reports noted rapid resolution of limb-shaking episodes, focal deficits, or dizziness occurring within hours to days after thyroidectomy. Improvement in mechanical compressive symptoms, including dyspnea and dysphagia, was similarly observed early in the postoperative course. Objective post-treatment vascular imaging was, however, reported inconsistently. Repeat cross-sectional imaging documenting restoration of vessel caliber or normalization of flow dynamics was described in only a minority of reports, and in most cases, the resolution of vascular compromise was inferred from symptomatic improvement alone (Table 1). Among the five patients with documented follow-up data across both treatment groups, all cases demonstrated complete symptom resolution with no recurrences or persistent neurologic deficits documented. The remaining five reports (50%) contained no post-treatment follow-up data of any kind, so outcomes are known for only half of the cohort, and the apparent resolution rate of 100% applies only to the reported subset.

Risk of bias and certainty of evidence

All ten included publications were single-patient case reports, and each was appraised with the Joanna Briggs Institute 2020 Critical Appraisal Checklist for Case Reports (Supplementary Item 2). Patient demographics, diagnostic assessment methods, adverse events, and takeaway lessons were adequately described in 10 of 10 reports (100%). Clinical history presented as a clear timeline was absent in 1 of 10 reports (10%), the clinical condition of the patient at presentation was incompletely described in 1 of 10 (10%), and the intervention or treatment procedure was not clearly described in 2 of 10 (20%).

The most consistent methodological deficiency, however, concerned outcome ascertainment. Post-treatment clinical status was reported for only 5 of 10 patients (50%), with the remaining five reports concluding without any documented follow-up. No report specified a follow-up interval in a manner permitting comparison across cases, and no report employed an objective outcome instrument such as a standardized neurologic score, formal measurement of cerebral perfusion, or quantitative duplex velocity criteria. Post-treatment cross-sectional imaging confirming restoration of arterial caliber or flow was documented in only a minority of cases, so that in most patients, resolution of vascular compromise was inferred from symptomatic improvement alone. Comorbidity reporting was similarly incomplete, and thyroid dimensions were unreported or reported only qualitatively in 5 of 10 cases (50%), which limits any assessment of the relationship between gland size and vascular compromise.

Considered together with the absence of any comparative or controlled design, the exclusive reliance on single-patient reports, the marked clinical heterogeneity across cases, the very small sample, and the high likelihood of selective reporting of unusual or dramatic presentations, the certainty of evidence for every outcome examined in this review is very low. No proportion reported here – including the frequency of common carotid involvement, the apparent complete symptom resolution among patients with follow-up, and the relative distribution of operative and conservative management – should be interpreted as a reliable estimate of effect or prevalence. These figures characterize the published literature and do not characterize the underlying population of patients with benign thyroid enlargement.

Discussion

Although benign thyroid enlargement is frequently encountered in clinical practice, arterial compression remains an uncommon but clinically meaningful complication. The findings of this systematic review raise the possibility that vascular involvement is underrecognized rather than truly rare, although ten published cases spanning three decades cannot distinguish between these explanations. Most reported patients were older women with multinodular goiter, reflecting the established epidemiology of benign thyroid disease (1, 2). The predominance of carotid artery involvement is anatomically intuitive, given the close spatial relationship between the thyroid gland and the carotid sheath. Unlike other neck masses known to involve the carotid vasculature, such as carotid body tumors or metastatic lymphadenopathy, thyroid enlargement typically produces extrinsic displacement or compression of adjacent vessels rather than intrinsic vascular invasion or hypervascular encasement. As a result, the vascular findings in thyroid-related compression tend to reflect mechanical narrowing or deviation rather than tumor-related infiltration, which may influence both imaging interpretation and management decisions.

The clinical presentations observed across cases were heterogeneous, ranging from chronic compressive symptoms to acute neurologic deficits. Notably, six of the ten patients (60%) presented with acute neurologic symptoms, most commonly limb-shaking episodes, lateralized weakness, or stroke-like presentations. These presentations are particularly important because they may mimic embolic transient ischemic attack (TIA) or cerebrovascular accident, potentially leading to misdiagnosis or delays in definitive management. Limb-shaking TIAs, described in several reports, are classically associated with cerebral hypoperfusion rather than embolic disease (21, 22). In the context of thyroid enlargement, external carotid compression may produce transient reductions in cerebral blood flow, especially with positional changes, thereby generating neurologic symptoms.

Taken together, these cases suggest a recognizable clinical trigger pattern. Patients with large or longstanding thyroid enlargement who develop new neurologic symptoms, unexplained dizziness, limb-shaking episodes, or stroke-like presentations in the absence of clear embolic sources may warrant evaluation for mechanical vascular compression. Similarly, patients with significant goiter and progressive compressive symptoms may develop vascular compromise as the gland enlarges or extends retrosternally. Awareness of this pattern may help clinicians identify cases in which vascular imaging should be pursued earlier.

Cross-sectional imaging played a critical role in diagnosis. CT/CTA was the most frequently utilized modality. CT provides rapid characterization of thyroid morphology, substernal extension, and the spatial relationship between the gland and adjacent vascular structures (23). MRI/MRA were useful adjuncts in select cases, particularly when further evaluation of cerebral perfusion or vascular integrity was warranted. Importantly, the imaging findings across reports demonstrated consistent patterns of arterial deviation, focal narrowing, or kinking adjacent to enlarged thyroid tissue, supporting a mechanical compressive mechanism rather than primary vascular disease. In clinical practice, these observations suggest that CTA of the neck may be an appropriate early diagnostic study when neurologic symptoms coexist with visible thyroid enlargement, as it simultaneously evaluates thyroid anatomy and vascular patency.

The heterogeneity of the vascular findings themselves also deserves emphasis because collecting them under the heading of arterial compression implies a uniformity that the data do not support. Displacement of a patent vessel by an enlarging gland is a common and frequently incidental finding on cervical imaging, and in isolation, it carries no established risk of cerebral ischemia. Kinking or tortuosity introduced by mass effect may be more relevant hemodynamically, but its significance depends on whether the resulting geometry is flow-limiting, which none of the included reports assessed. Extrinsic compression producing measurable luminal narrowing is a more plausible substrate for hypoperfusion, and hemodynamically significant stenosis with documented infarction represents a categorically different clinical problem. In the present cohort, symptom severity did not track cleanly with the extent of vascular involvement described. Focal neurologic deficits occurred in patients whose imaging described displacement alone, whereas both patients with documented luminal narrowing but no infarction presented with mechanical rather than ischemic symptoms. This dissociation argues against inferring clinical risk from the imaging descriptor alone. It also argues for the prospective use of standardized criteria, including quantified degree of stenosis, positional or dynamic imaging, and, where feasible, direct assessment of cerebral perfusion or cerebrovascular reserve, before mass effect on a cervical artery is accepted as the cause of a patient’s neurologic symptoms.

Management strategies varied across cases and appeared to be guided by symptom acuity, severity of arterial compromise, presence of neurologic deficits, and patient-specific factors such as comorbidities, surgical candidacy, and concurrent airway or esophageal compression. Thyroidectomy was the most common intervention and was associated with symptom resolution in every case in which follow-up was reported. This outcome aligns with prior studies demonstrating that surgical decompression effectively alleviates airway, esophageal, and venous compression in large goiters (6, 24). The present review suggests that similar benefits extend to arterial compression. The cases included in this review also suggest a practical decision framework. Patients presenting with acute neurologic deficits, imaging-confirmed arterial compression, or progressive compressive symptoms were more likely to undergo operative management, often with rapid improvement following decompression. In contrast, conservative management was generally reserved for patients with milder symptoms, transient neurologic episodes, or elevated surgical risk. Differences between treatment groups were primarily related to the time course of symptom resolution rather than ultimate outcome. Surgically treated patients more often experienced rapid and definitive improvement, especially when neurologic symptoms were present. Conservatively managed patients also demonstrated favorable outcomes, although improvement was typically less immediate and dependent on clinical stability. Conservative management was also associated with improvement in select patients, indicating that observation may be reasonable in carefully selected cases with mild or transient symptoms.

However, it is important that clinical improvement among conservatively managed patients be interpreted with caution. These patients with nonoperative management exhibited milder symptoms and, in some cases, were poor surgical candidates, introducing substantial selection bias. In addition, spontaneous resolution of edema or hemorrhage may have contributed to symptomatic improvement. Given the small number of cases and inconsistent follow-up, no definitive conclusion should be made regarding the effectiveness of operative versus conservative management.

Despite the rarity of reported cases, the potential consequences of carotid compression are significant. Unrecognized arterial involvement may expose patients to ongoing cerebral hypoperfusion, recurrent neurologic events, or unnecessary anticoagulation if symptoms are misattributed to embolic disease. Increased awareness among otolaryngologists, endocrinologists, neurologists, and radiologists is therefore essential.

From a clinical standpoint, thyroid-related vascular compression should be considered when three features coexist: (1) substantial thyroid enlargement, (2) unexplained neurologic or cerebrovascular symptoms, and (3) absence of alternative vascular pathology on standard evaluation. In such situations, targeted vascular imaging of the neck may help identify mechanical compression and guide management decisions. Consideration of thyroid-related vascular compression should therefore be incorporated into the differential diagnosis of unexplained cerebrovascular symptoms, particularly in patients with visible or known thyroid enlargement.

A final interpretive caution concerns the quality of the underlying evidence. Every conclusion in this review rests on ten single-patient reports, half of which contain no post-treatment follow-up, none of which used objective outcome instruments, and few of which documented imaging confirmation that vascular compromise had resolved. Case reports are selected for publication precisely because they are unusual or instructive, so cases with dramatic presentations and favorable responses to treatment are systematically more likely to reach the literature than cases that were asymptomatic, were managed without incident, or failed to improve. The uniformly favorable outcomes observed here are therefore better understood as a property of the publication process than as an estimate of prognosis. Applying GRADE-informed reasoning across the domains of study design, risk of bias, inconsistency, indirectness, imprecision, and publication bias, certainty of evidence is very low for all outcomes. The observations offered above should accordingly be read as prompts for pattern recognition by clinicians rather than as evidence-based management guidance.

Limitations

Several limitations should be acknowledged. First, the available evidence is limited to case reports and small case series, which restricts the strength of conclusions. Such studies are subject to publication bias because unusual or dramatic presentations are more likely to be reported than asymptomatic or conservatively managed cases. Consequently, the true incidence of arterial compression secondary to benign thyroid enlargement remains unknown, and overall certainty of evidence is very low in the absence of comparative studies. Second, heterogeneity among included studies limited quantitative synthesis. Variations in imaging modalities, definitions of vascular involvement, symptoms reported, and follow-up duration precluded meta-analysis. The descriptive nature of this review therefore limits the ability to establish causality or identify predictive factors. Third, follow-up durations were relatively short. While all patients with documented follow-up experienced symptom resolution, long-term recurrence risk or delayed vascular consequences cannot be reliably assessed. Additionally, imaging-based confirmation of hemodynamic normalization was inconsistently reported. Finally, selection bias is unavoidable. Patients with mild or nonspecific symptoms may not undergo vascular imaging, potentially resulting in underdiagnosis. Conversely, incidental vascular displacement without clinical significance may be overlooked or unreported. Future comparative and prospective studies are needed to better characterize prevalence, risk factors, and long-term outcomes.

Several further limitations warrant explicit acknowledgment. Formal statistical assessment of publication bias was not feasible given the study designs available, so publication bias could be addressed only narratively, even though in this literature it is likely to be substantial. The search strategy imposed further constraints: the vascular anchor terms were centered on carotid and cerebrovascular concepts, so reports of vertebral, brachiocephalic, or subclavian involvement, of arterial displacement or kinking described incidentally, and of hemodynamically significant stenosis unaccompanied by neurologic symptoms may have been captured incompletely. In addition, the exclusion of any record mentioning cancer, carcinoma, or neoplasm in the title or abstract is likely to have removed some reports in which malignancy was initially suspected but benign pathology was ultimately confirmed, a scenario of direct relevance to the population of interest, although restricting this exclusion to the title and abstract fields rather than to any occurrence of these terms in the record limited the number of such reports removed. The database date limiter of 2010 onward means that pre-2010 reports entered this review only through citation searching and were therefore identified less systematically than more recent reports. A final consideration is that aggregating displacement, kinking, luminal narrowing, and hemodynamically significant stenosis under the heading of arterial compression groups entities of probably differing clinical importance. The nature of vascular involvement described in each report has been set out separately in the section titled Results, but the source reports offered narrative imaging descriptions rather than standardized measurements, so no reliable inference about the relationship between degree of vascular compromise and clinical risk can be drawn from ten patients. Taken together, these considerations place the overall certainty of evidence at a very low level.

Conclusion

Benign thyroid enlargement may be an underrecognized cause of cervical artery compromise, which appears to most frequently affect the carotid artery. While goiters typically involve the airway or venous structures, they can precipitate acute neurologic deficits, such as limb-shaking or stroke-like symptoms, that mimic embolic events. Recognizing this mechanical extrinsic compression is vital to avoid diagnostic delays or inappropriate vascular interventions. CT/CTA was the most frequently reported and most informative modality for characterizing the relationship between the thyroid gland and the carotid sheath. Thyroidectomy was the most frequently reported definitive intervention and was followed by symptom resolution in every case in which follow-up was documented, while selected patients with mild or transient symptoms improved without operation. Given ten single-patient reports, follow-up in only half of them, and no comparative data, certainty of evidence is very low, and no recommendation can be made regarding the relative merits of operative and conservative management. Clinicians should maintain a high index of suspicion for thyroid-related vascular compromise in patients with significant goiter and unexplained cerebrovascular symptoms.

Declaration of interest

The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.

Funding

This research did not receive any specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Author contribution statement

Ammar Matthew Hudefi, Noah Bogart, and Kenny Nguyen contributed to data collection, data analysis, and writing the abstract. Lindsay Blake contributed to the database search strategy and writing of the section titled Methods. Alexa Robbins and Anvesh Kompelli contributed to the conception of the study, data analysis, and review of the final abstract for submission.

Ethical approval

Exempt by UAMS Institutional Review Board #299472.