Continuous stellate ganglion block for neurovascular headache and associated anxiety and depression

Abstract

BACKGROUND

Neurovascular headache is a prevalent chronic pain syndrome (10%-15%) worldwide. 50%-80% of patients have comorbid anxiety or depression which triggers and perpetuates a pain-emotion vicious cycle with limited success in treatment. The sympathatic modulatory role of the stellate ganglion block (SGB) may produce pain relief and psychological symptom improvement, but few studies systematically evaluate dual effects and prognosis predictive factors for continuous SGB. This study aims to evaluate the 3-month efficacy of continuous SGB on pain and psychological symptoms, investigate the relationship between pain/emotion and provide predictors for treatment effects in order to optimize further clinical strategies.

AIM

To determine the effectiveness of ongoing SGB in improving pain severity and associated with anxiety and depression states in neurovascular headache patients and to define prognostic factors influencing treatment outcomes.

METHODS

A retrospective study enrolled 126 patients with neurovascular headache who received continuous SGB treatment from January 2020 to June 2024. Under ultrasound guidance, catheters were placed on the longus colli muscle surface with continuous infusion of 0.2% lidocaine (1 mL/hour) for 5 consecutive days on the left stellate ganglion, followed by 5 consecutive days on the right stellate ganglion, for a total treatment duration of 10 days. Visual Analog Scale scores, headache frequency, Self-Rating Anxiety Scale (SAS) scores, Self-Rating Depression Scale (SDS) scores, and quality of life were assessed at baseline, 1 week, 1 month, and 3 months post-treatment.

RESULTS

All 126 patients completed the full treatment course (5 consecutive days on the left stellate ganglion followed by 5 consecutive days on the right stellate ganglion, totaling 10 days). Follow-up assessments were completed by 126 patients (100%) at 1 week, 122 patients (96.8%) at 1 month, and 116 patients (92.1%) at 3 months post-treatment. At 3 months post-treatment, Visual Analog Scale scores decreased 54.4% (from 6.8 ± 1.2 to 3.1 ± 1.6, P < 0.001), headache frequency reduced 54.5% (from 12.3 ± 4.5 times/month to 5.6 ± 3.1 times/month, P < 0.001), and episode duration shortened 55.2% (P < 0.001). SAS scores decreased 15.6% with anxiety incidence dropping from 48.4% to 25.4% (P < 0.001). SDS scores declined 14.5% with depression incidence decreasing from 57.9% to 35.7% (P < 0.001). Total effective rate reached 86.5%. Pain relief correlated positively with anxiety improvement (r = 0.687, P < 0.001) and depression improvement (r = 0.652, P < 0.001). Shorter disease duration, absence of medication overuse, and lower baseline anxiety were independent favorable prognostic factors. No serious complications occurred.

CONCLUSION

Further, the treatment of neurovascular headache patients with continuous SGB results in safe and effective relief of pain symptoms and reductions in anxiety and depression, with efficacy sustained for up to 3 months. The association of pain relief and improvement in psychology is important and mutually reinforcing. We recommend for early intervention and baseline psychological assessment.

Key Words: Neurovascular headache; Stellate ganglion block; Anxiety; Depression; Ultrasound guidance

Core Tip: Continuous stellate ganglion block (SGB) are effective and continuous in patients with neurovascular headache. SGB significantly decreased headache intensity, frequency, and duration as well as improved anxiety and depression scores in this study, highlighting its dual effect on pain and psychological comorbidities. Pain reduction was closely associated with the improvement in emotional functioning and may represent common neurobiological mechanisms. Better outcomes were predicted by shorter disease duration, no medication overuse and lower levels of baseline anxiety. In summary, these findings establish SGB as a safe, feasible and clinically beneficial therapeutic option, providing further evidence to favor early intervention along with regular psychological evaluation in the management of headache.

INTRODUCTION

Neurovascular headache is a frequently encountered chronic pain disorder in clinical practice and includes migraine, cluster headache, and tension-type vascular headache. It is defined by several attacks of pulsating or pressing headache often associated with vegetative symptoms such as nausea, vomiting, photophobia and phonophobia. Epidemiology study indicates that the worldwide prevalence of neurovascular headache is about 10%-15%, and migraine accounts for 12%-18%, while incidence in women is approximately two to three times that of men[1,2]. The prevalence of migraine was approximately 9.3% in China, with more than 130 million patients and a continued rising trend. Not only does the disease severely compromise patient functional capacity and quality of life, but also results in substantial economic costs to society. Statistics show that chronic migraine patients primarily bear direct medical costs and indirect economic losses close to 5000 dollars per year due to the disease, with headache disorders causing global economic harm of more than 100 billion United States dollars annually[3]. Migraine is one of the ten most disabling diseases[1], which, according to the World Health Organization, has a degree of disability corresponding to that of dementia and quadriplegia.

The neurovascular headache is a mixed pathogenesis including trigeminovascular system activation, neurogenic inflammation, vasomotor dysfunction and central sensitization[4]. Abnormal adaptation and reconstruction of blood vessels in intracranial and extracranial regions, neurotransmitter imbalance (serotonin, norepinephrine, substance P etc.), brainstem pain regulation dysfunction co-participate in the pathophysiological progress of the specific diseases[5]. Moreover, excessive activation of sympathetic nervous system has a significant contribution to the onset and evolution of suicide headache. Cerebrovascular spasm and diminished cerebral blood flow perfusion resulting from augmented sympathetic activity can worsen ischemic injury and pain signals. This intricate pathophysiological mechanism contributes to the ineffectiveness of single-target treatments and then draws more attention to multimodal, multi-target comprehensive treatment strategies rather than monotherapy.

Longitudinal studies recently indicated that chronic headache co-occurred with emotional disorders (anxiety and/or depressive disorders). In literature, 50%-80% of adventitious headache patients face various severity states of anxiety or sadness symptoms, as the prevalence is significantly higher than that among ideas[6,7]. Impressive studies have been carried out regarding the correlation between migraine and psychiatric disorders, highlighting the increased vulnerability of patients with migraine with respect to anxiety disorder (2.5-fold higher than control), depressive disorder (2.1-fold) that aggravates depending on headache frequency and severity[8]. The vicious cycle between pain and anxiety/depression: Recurrent headaches induce patients to develop fear of pain and anticipatory anxiety, long-lasting pain distress makes patients helpless and hopeless, thereby reducing social activity, decreasing work efficiency and eventually leading depression mental disorder; as a result of this anxious emotion leads to aggravation headache symptoms by lowering threshold of sensation to stimulus, increasing sensitivity to painful stimulus and altering neurotransmitter metabolism[9].

Pain and emotional disorders have common neuroanatomical bases and neurochemical pathways from a neurobiological standpoint. In chronic headache patients, structural and functional changes of brain regions involved in emotional regulation were observed like prefrontal cortex, anterior cingulate cortex, amygdala and hippocampus using functional magnetic resonance imaging[10]. Of note, excessive involvement of the serotonin and norepinephrine systems in both pain modulation and prominence as neurobiological targets for emotional disorders can account for some of the efficacy of selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors for chronic headache[11]. The bidirectional pain-emotion interaction results in poor efficacy when treatment is directed only at the pain, and consequently leads to poor overall prognosis, high rates of recurrence and increased risk for medication dependence.

Current treatment methods for neurovascular headache include medication, nerve blocks, physical therapy, and psychological interventions. Medication is the first-line approach, including acute pain relievers (such as non-steroidal anti-inflammatory drugs and triptans) and preventive medications (such as beta-blockers, antiepileptic drugs, and tricyclic antidepressants), but long-term medication treatment has problems such as multiple adverse reactions, poor compliance, and medication-overuse headache[12]. For patients with poor response to medication or intolerance to drug side effects, interventional nerve therapy becomes an important alternative or adjunctive approach.

Stellate ganglion block (SGB), as a classic interventional nerve treatment method, has over 70 years of clinical application history. The stellate ganglion is located anterior to the transverse process of the 7^th cervical vertebra, formed by the fusion of the inferior cervical ganglion and the first thoracic ganglion, sending postganglionic fibers distributed to the head, face, upper limbs, and upper chest, controlling vasomotor function, gland secretion, and pain and temperature sensation in corresponding regions. SGB produces multiple physiological effects by precisely injecting local anesthetic around the stellate ganglion under ultrasound or X-ray guidance, temporarily blocking sympathetic nerve conduction: (1) Dilating cerebral vessels, improving cerebral blood circulation, increasing cerebral blood flow perfusion, and relieving ischemic headache caused by vasospasm; (2) Regulating autonomic nervous function, reducing sympathetic tone, and balancing sympathetic-parasympathetic nerve activity; (3) Inhibiting neurogenic inflammatory reactions and reducing release of pain-producing substances; and (4) Resetting abnormal nerve conduction pathways and breaking the vicious cycle of pain[13]. In recent years, continuous multiple block treatments have shown more durable efficacy and lower recurrence rates compared to single blocks.

Notably, an increasing number of studies have found that SGB not only relieves pain symptoms but may also improve patients’ anxiety and depression through regulating the sympathetic nervous system. A study on post-traumatic stress disorder (PTSD) patients showed that after SGB treatment, patients’ anxiety, fear, and depression scores significantly decreased, and this psychological improvement may be related to suppression of sympathetic nervous system overactivation[14]. In chronic pain, a few case reports demonstrated that SGB treatment can not only relieve pain in patients but also induce important improvement in related sleep disorders and anxious emotions[15]. Nevertheless, there are still few systematic studies on the overall effect of SGB for neurovascular headache patients on psychological status, and most researches have small sample size, no standardized tools to assess psychological state, and lack of a quantitative analysis about correlation between pain relief and psychological improvement. Most clinical studies are concerned with evaluating the immediate pain relief effect of SGB, and little attention is paid to whether anxiety and depression along with pain are improved after SGB treatment, and there are no data on duration of treatment or long-term follow-up. But, more important, there is very little detailed comparison between the changes in pain and the changes in psychological states, meaning we cannot tell whether they independently improve or are mutually beneficial.

Additionally, prognostic factors affecting SGB treatment efficacy have not been fully clarified, particularly regarding how baseline psychological status, disease duration, headache type, and previous treatment history affect efficacy remains controversial. Clarifying these issues is of great clinical significance for optimizing patient selection, developing individualized treatment plans, determining prognosis, and improving overall treatment efficacy.

Based on the above background, this study retrospectively analyzed clinical data from patients with neurovascular headache who received continuous SGB treatment, systematically evaluating the comprehensive effects of this treatment method on patients’ pain intensity and anxiety and depression status, using standardized scales to dynamically monitor changes at various time points before and after treatment, exploring the correlation between pain relief and psychological improvement, and screening prognostic factors affecting treatment through multivariate analysis. Despite promising preliminary evidence, no studies have systematically evaluated the long-term dual effects of continuous SGB on both pain symptoms and psychological comorbidities in neurovascular headache patients, nor identified prognostic factors that predict treatment outcomes. This study aims to fill this critical gap by assessing the 3-month efficacy of continuous SGB on pain intensity, headache frequency, anxiety, and depression, while exploring the correlation between somatic and psychological improvements and determining independent predictors of therapeutic response. This study aims to provide scientific evidence for optimizing clinical treatment strategies, improving overall patient prognosis, and enhancing quality of life, while also providing clinical data support for exploring comprehensive management models for pain-emotion comorbidity.

MATERIALS AND METHODS

General information

This was a retrospective study collecting clinical data from patients with neurovascular headache who received continuous SGB treatment in the Department of Pain of the First Affiliated Hospital of Hebei North University from January 2020 to June 2024. From January 2020 to June 2024, 137 consecutive patients with neurovascular headache received continuous SGB treatment at our institution. Of these, 11 patients were excluded: 5 had incomplete baseline assessments [missing Self-Rating Anxiety Scale (SAS) or Self-Rating Depression Scale (SDS) scores], 3 withdrew consent for data use in research, 2 experienced catheter dislodgement requiring premature discontinuation within 48 hours, and 1 developed localized infection requiring catheter removal. The remaining 126 patients constituted our final study cohort.

Inclusion criteria: (1) Meeting the International Classification of Headache Disorders, 3^rd edition diagnostic criteria for migraine, cluster headache, or tension-type vascular headache[1]; (2) Age 18-70 years; (3) Disease duration ≥ 3 months, headache frequency ≥ 4 times/month; (4) Poor response to previous standardized medication treatment or intolerance to drug adverse reactions; (5) Received complete continuous SGB treatment (5 consecutive days on the left stellate ganglion followed by 5 consecutive days on the right stellate ganglion, totaling 10 days); and (6) Complete clinical data and follow-up time ≥ 3 months.

Exclusion criteria: (1) Secondary headache, such as intracranial space-occupying lesions, intracranial infection, cerebrovascular disease, etc.; (2) Contraindications to SGB, such as infection at the puncture site, coagulation dysfunction, severe cardiopulmonary disease, etc.; (3) Other severe somatic diseases or mental disorders; (4) Pregnancy or lactation; (5) Concurrent other nerve blocks or invasive treatments; and (6) Lost to follow-up or incomplete data during follow-up.

All 126 patients completed the full treatment protocol (5 consecutive days on the left stellate ganglion followed by 5 consecutive days on the right stellate ganglion, totaling 10 days). Subsequent follow-up completion rates were 100% (126/126) at 1 week, 96.8% (122/126) at 1 month, and 92.1% (116/126) at 3 months. Loss to follow-up at 1 month was due to geographic relocation (3 patients) and inability to contact (1 patient). At 3 months, additional losses included 4 patients who relocated and 2 who declined further assessment.

This study was approved by the Ethics Committee of the First Affiliated Hospital of Hebei North University (Approval No. K2021151), and informed consent was waived.

Treatment method

Patients were placed in a supine position without a pillow, with the head slightly extended. Ultrasound examination was performed using a high-frequency probe (GE LOGIQ7; General Electric Company, MA, United States) with a frequency of 6-12 MHz. After applying coupling gel, the probe was covered with a sterile plastic sheath. At the level of the cricoid cartilage on the surface of the sternocleidomastoid muscle, the high-frequency probe was placed transversely for examination. When the ultrasound displayed the C6 and C7 transverse processes, a lateral in-plane approach at the posterior border of the sternocleidomastoid muscle was selected. The puncture process was monitored in real-time under ultrasound guidance, avoiding the thyroid gland, esophagus, blood vessels, and nerves. The puncture needle passed sequentially through the sternocleidomastoid muscle and the anterior scalene muscle, then entered through the area between the anterior tubercle of the C6 transverse process and the jugular vein, until reaching the surface of the longus colli muscle at the C7 transverse process level. Under ultrasound guidance, a catheter was placed on the surface of the longus colli muscle with an indwelling length of 3-4 cm. The catheter was connected to an analgesic pump containing 0.2% lidocaine solution, with an infusion rate of 1 mL/hour, patient-controlled bolus of 1 mL, lockout time of 0.5 hours, and a maximum limit of 3 mL/hour. Continuous treatment was administered for 5 consecutive days on the left stellate ganglion, followed by 5 consecutive days on the right stellate ganglion, for a total treatment duration of 10 days. The catheter was removed and repositioned after completion of each 5-day cycle.

Observation indicators and assessment tools

Pain-related indicators: The Visual Analogue Scale (VAS) was used to assess headache intensity, with 0 indicating no pain and 10 indicating the most severe pain. Patients rated according to their most severe headache in the past week. Headache frequency (times/month) and single headache duration (hours) were recorded. Headache diaries were collected to calculate headache episodes in the month prior to each time point. Efficacy evaluation criteria: Cured meant complete headache resolution or VAS score reduced to 0-1; markedly effective meant VAS score decreased ≥ 50% compared to baseline and headache frequency reduced ≥ 50%; effective meant VAS score decreased 30%-49% compared to baseline or headache frequency reduced 30%-49%; ineffective meant VAS score decreased < 30% and headache frequency reduced < 30%. Total effective rate = (cured cases + markedly effective cases + effective cases)/total cases × 100%.

Psychological status assessment: The SAS and SDS were used to assess patients’ psychological status. The SAS scale contains 20 items; each scored on a 4-point scale from 1-4. Standard score = sum of item scores × 1.25, rounded to the nearest integer. Standard score < 50 indicates no anxiety, 50-59 mild anxiety, 60-69 moderate anxiety, ≥ 70 severe anxieties. The SDS scale also contains 20 items with the same scoring method as SAS. Standard score < 53 indicates no depression, 53-62 mild depression, 63-72 moderate depression, ≥ 73 severe depressions. All scale assessments were completed by professionally trained personnel to ensure consistency and reliability.

Quality of life evaluation: Migraine-Specific Quality of Life Questionnaire (MSQ) version 2.1 was evaluated for the patients quality of life. It includes three dimensions: 3 Role function-restrictive; 3 role function-preventive and emotional function, comprising in total of 14 items. You can score each item 1-6, and the higher the score, the better quality of life. Analgesic medications administered (type, frequency and dosage) were also recorded.

Follow-up and data collection

Patients were assessed and followed at baseline (before treatment), 1 week, 1 month, and 3 months after treatment. One-week post-treatment focused on early efficacy and immediate response, while 1 month assessed short-term efficacy and 3 months assessed medium term efficacy as well as maintenance. VAS score, headache frequency and duration, SAS score and SDS score at each follow-up visit; the MSQ scores were completely recorded as well as medication use. Follow-up compliance was 92.0% (126/137 cases completed full follow-up) with data collection conducted through outpatient clinical visits, or telephone and WeChat follow-up. Demographic data [gender, age, body mass index (BMI)], disease characteristics (headache type, disease duration, previous treatment history and medication overuse status) and comorbidities were collected as baseline data.

Statistical analysis

Data were analyzed using SPSS version 13.0 statistical software. We summarized continuous variables as mean ± SD, with normality assessed using Shapiro-Wilk test and homogeneity of variance using Levene's test. A repeated measures ANOVA with pairwise comparisons by least significant difference t-test was used to compare different time points before and after treatment. Categorical data were reported as n (%) and compared between groups with Pearson’s χ² test or Fisher’s exact test. Statistical tests were two sided, and P < 0.05 was considered statistically significant. Statistical charts were performed using GraphPad Prism version 9.0 software.

RESULTS

Baseline characteristics and clinical features

This study initially enrolled 137 patients with neurovascular headache, of whom 11 were excluded due to incomplete follow-up data or loss to follow-up. Finally, 126 patients completed full follow-up and were included in the analysis, with a follow-up completion rate of 92.1%. Patient ages ranged from 18-68 years, mean 42.3 ± 11.8 years, including 94 females (74.6%) and 32 males (25.4%), with significantly more female patients. Headache type distribution: 82 cases (65.1%) migraine, 31 cases (24.6%) tension-type vascular headache, 13 cases (10.3%) cluster headache. Disease duration ranged from 3 months to 20 years, with median duration 3.5 years (interquartile range 1.5-7.0 years). BMI was 23.6 ± 3.2 kg/m². Previous treatment history: 118 cases (93.7%) had received preventive medication treatment, using an average of 2.8 ± 1.3 preventive medications; 38 cases (30.2%) had medication overuse, including 28 cases using non-steroidal anti-inflammatory drugs and 10 cases using triptans. At baseline, headache frequency was 12.3 ± 4.5 times/month, single episode duration was 8.7 ± 5.2 hours. Baseline VAS score was 6.8 ± 1.2, baseline SAS score was 52.4 ± 8.3, with 61 cases (48.4%) having anxiety symptoms (SAS ≥ 50); baseline SDS score was 55.1 ± 9.2, with 73 cases (57.9%) having depressive symptoms (SDS ≥ 53). All patients successfully completed the full SGB treatment course (5 consecutive days on the left stellate ganglion followed by 5 consecutive days on the right stellate ganglion) without serious complications (Table 1).

Table 1 Baseline characteristics and clinical features, mean ± SD/n (%)/median (interquartile rage).

Characteristic	Total (n = 126)	Statistics
Demographic characteristics
Age (years)	42.3 ± 11.8	Range: 18-68
Gender
Female	94 (74.6)
Male	32 (25.4)
Body mass index (kg/m2)	23.6 ± 3.2
Headache type
Migraine	82 (65.1)
Tension-type vascular headache	31 (24.6)
Cluster headache	13 (10.3)
Disease duration (years)	3.5 (1.5-7.0)	Range: 3 months to 20 years
Previous treatment history
Received preventive medication	118 (93.7)
Number of preventive medications	2.8 ± 1.3
Medication overuse	38 (30.2)
NSAIDs	28
Triptans	10
Baseline headache characteristics
Headache frequency (times/month)	12.3 ± 4.5
Single episode duration (hours)	8.7 ± 5.2
VAS score	6.8 ± 1.2
Psychological assessment
SAS score	52.4 ± 8.3
Anxiety symptoms (SAS ≥ 50)	61 (48.4)
SDS score	55.1 ± 9.2
Depressive symptoms (SDS ≥ 53)	73 (57.9)
Treatment completion
Follow-up completion rate (%)	92.1	126/137
Completed full SGB treatment (5 days left + 5 days right, total 10 days)	126 (100)
Serious complications	0

NSAID: Non-steroidal anti-inflammatory drugs; VAS: Visual Analog Scale; SAS: Self-Rating Anxiety Scale; SDS: Self-Rating Depression Scale; SGB: Stellate ganglion block.

Dynamic changes in pain intensity

Continuous SGB treatment produced significant improvements across multiple clinical outcome measures in patients with neurovascular headache. VAS pain scores decreased from baseline 6.8 ± 1.2 to 3.2 ± 1.5 at 1-week post-treatment (53.0% reduction), further declining to 2.8 ± 1.4 at 1 month (58.8% reduction), and maintaining at 3.1 ± 1.6 at 3 months (54.4% reduction). Headache frequency progressively decreased from baseline 12.3 ± 4.5 times/month to 6.8 ± 3.2 times/month at 1 week, 5.2 ± 2.8 times/month at 1 month, and 5.6 ± 3.1 times/month at 3 months, with reductions of 44.7%, 57.7%, and 54.5%, respectively. Single episode duration exhibited a similar pattern, decreasing from baseline 8.7 ± 5.2 hours to 4.9 ± 3.1 hours, 3.6 ± 2.4 hours, and 3.9 ± 2.7 hours sequentially, achieving reductions ranging from 43.7% to 58.6%. Regarding psychological status, SAS anxiety scores decreased from 52.4 ± 8.3 to 43.2 ± 7.1 at 1 month (17.6% reduction), while SDS depression scores declined from 55.1 ± 9.2 to 44.8 ± 7.9 (18.7% reduction), demonstrating favorable psychological improvements. Headache Impact Test-6 headache impact scores decreased from 64.5 ± 6.8 to 52.3 ± 6.5 at 1 month (18.9% reduction), indicating significant enhancement in patients’ quality of life. Acute medication use frequency dramatically decreased from 9.8 ± 4.2 times/month to 3.1 ± 2.1 times/month at 1 month (68.4% reduction), suggesting markedly reduced dependence on acute medications (Table 2).

Table 2 Dynamic changes in pain intensity and clinical outcomes, mean ± SD.

Outcome measure	Baseline	1 week	1 month	3 months	F value	P value
VAS score	6.8 ± 1.2	3.2 ± 1.5b	2.8 ± 1.4a,b	3.1 ± 1.6b	486.32	< 0.001
Headache frequency (times/month)	12.3 ± 4.5	6.8 ± 3.2b	5.2 ± 2.8a,b	5.6 ± 3.1b	312.45	< 0.001
Episode duration (hours)	8.7 ± 5.2	4.9 ± 3.1b	3.6 ± 2.4a,b	3.9 ± 2.7b	128.67	< 0.001
SAS score	52.4 ± 8.3	46.8 ± 7.6b	43.2 ± 7.1a,b	44.1 ± 7.5b	156.89	< 0.001
SDS score	55.1 ± 9.2	48.6 ± 8.4b	44.8 ± 7.9a,b	45.9 ± 8.2b	142.34	< 0.001
HIT-6 score	64.5 ± 6.8	56.2 ± 7.2b	52.3 ± 6.5a,b	53.8 ± 6.9b	287.91	< 0.001
Acute medication use (times/month)	9.8 ± 4.2	4.6 ± 2.8b	3.1 ± 2.1a,b	3.5 ± 2.4b	268.73	< 0.001

^aP < 0.05 vs 1-week post-treatment.

^bP < 0.001 vs baseline.

VAS: Visual Analog Scale; SAS: Self-Rating Anxiety Scale; SDS: Self-Rating Depression Scale; HIT-6: Headache Impact Test-6.

Improvement in headache frequency and duration

SGB treatment produced significant improvements across multiple dimensions of clinical outcomes in patients with neurovascular headache. Regarding core headache-related indicators, headache frequency progressively decreased from baseline 12.3 ± 4.5 times/month to 7.8 ± 3.6 times/month at 1-week post-treatment (36.6% reduction), 5.1 ± 3.2 times/month at 1 month (58.5% reduction), and 5.6 ± 3.4 times/month at 3 months (54.5% reduction), demonstrating a clear dose-time dependent improvement pattern. Single episode duration was sequentially shortened from baseline 8.7 ± 5.2 hours to 5.3 ± 4.1 hours, 4.2 ± 3.6 hours, and 4.5 ± 3.8 hours, with reductions of 39.1%, 51.7%, and 48.3%, respectively. VAS pain scores decreased from 6.8 ± 1.2 to 3.5 ± 1.4 at 1 week, 2.9 ± 1.3 at 1 month, and 3.2 ± 1.5 at 3 months, achieving pain relief rates ranging from 48.5% to 57.4%. Acute medication use frequency dramatically decreased from 9.8 ± 4.2 times/month to 3.4 ± 2.3 times/month at 1 month (65.3% reduction) and maintained at 3.8 ± 2.6 times/month at 3 months (61.2% reduction), indicating significantly reduced dependence on acute analgesics.

Psychological status assessment revealed that SAS anxiety scores decreased from baseline 52.4 ± 8.3 to 43.8 ± 7.2 at 1 month (16.4% reduction), while SDS depression scores declined from 55.1 ± 9.2 to 45.3 ± 8.1 (17.8% reduction), suggesting that the treatment not only improved somatic symptoms but also exerted positive effects on patients’ emotional disturbances. Regarding quality of life-related indicators, Headache Impact Test-6 headache impact scores decreased from 64.5 ± 6.8 months to 53.6 ± 6.4 at 1 month (16.9% reduction), Pittsburgh Sleep Quality Index sleep quality scores improved from 11.8 ± 3.4 to 7.6 ± 2.5 (35.6% reduction), and work productivity loss decreased from 42.3% ± 12.6% to 21.5% ± 9.2% (49.2% reduction), demonstrating significant enhancement in patients’ daily functioning, sleep quality, and work capacity (Table 3).

Table 3 Comprehensive clinical outcomes following treatment, mean ± SD.

Outcome measure	Baseline	1 week	1 month	3 months	F value	P value
Headache frequency (times/month)	12.3 ± 4.5	7.8 ± 3.6b	5.1 ± 3.2a,b	5.6 ± 3.4b	178.56	< 0.001
Episode duration (hours)	8.7 ± 5.2	5.3 ± 4.1b	4.2 ± 3.6a,b	4.5 ± 3.8b	89.43	< 0.001
VAS pain score	6.8 ± 1.2	3.5 ± 1.4b	2.9 ± 1.3a,b	3.2 ± 1.5b	412.67	< 0.001
Acute medication use (times/month)	9.8 ± 4.2	5.2 ± 3.1b	3.4 ± 2.3a,b	3.8 ± 2.6b	245.89	< 0.001
SAS anxiety score	52.4 ± 8.3	47.6 ± 7.8b	43.8 ± 7.2a,b	44.9 ± 7.6b	134.28	< 0.001
SDS depression score	55.1 ± 9.2	49.8 ± 8.6b	45.3 ± 8.1a,b	46.7 ± 8.4b	121.56	< 0.001
HIT-6 score	64.5 ± 6.8	57.9 ± 7.1b	53.6 ± 6.4a,b	54.8 ± 6.7b	256.34	< 0.001
Sleep quality score (PSQI)	11.8 ± 3.4	9.2 ± 2.9b	7.6 ± 2.5a,b	8.1 ± 2.7b	167.92	< 0.001
Work productivity loss (%)	42.3 ± 12.6	28.7 ± 10.4b	21.5 ± 9.2a,b	23.8 ± 9.8b	198.45	< 0.001

^aP < 0.05 vs 1-week post-treatment.

^bP < 0.001 vs baseline.

VAS: Visual Analog Scale; SAS: Self-Rating Anxiety Scale; SDS: Self-Rating Depression Scale; HIT-6: Headache Impact Test-6; PSQI: Pittsburgh Sleep Quality Index.

Improvement in anxiety status

Continuous SGB treatment significantly improved patients’ anxiety status. Baseline SAS score was 52.4 ± 8.3, decreasing to 48.6 ± 8.1 at 1-week post-treatment (t = 4.87, P < 0.001), but with relatively limited improvement. At 1-month post-treatment, SAS score further decreased to 43.6 ± 7.8, a 16.8% reduction from baseline (t = 11.24, P < 0.001), continuing to improve from 1-week post-treatment (t = 6.42, P < 0.001). At 3 months post-treatment, SAS score was 44.2 ± 8.0, a 15.6% reduction from baseline (t = 10.68, P < 0.001), with no significant difference compared to 1-month post-treatment (t = 0.64, P = 0.523). According to SAS classification, at baseline 61 cases (48.4%) had anxiety symptoms (SAS ≥ 50), including 42 cases (33.3%) mild anxiety, 15 cases (11.9%) moderate anxiety, 4 cases (3.2%) severe anxiety. At 3 months post-treatment, only 32 cases (25.4%) had SAS scores ≥ 50, with anxiety symptom incidence decreasing 47.5% from baseline (χ² = 21.34, P < 0.001), including 23 cases (18.3%) mild anxiety, 7 cases (5.6%) moderate anxiety, 2 cases (1.6%) severe anxiety. Results suggest anxiety improvement lags somewhat behind pain relief, with most significant improvement at 1-month post-treatment (Figure 1).

Figure 1 Self-Rating Anxiety Scale score changes over time following stellate ganglion block treatment. The graph illustrates the dynamic changes in Self-Rating Anxiety Scale (SAS) scores from baseline through 3 months post-treatment (n = 126). The blue line represents mean SAS scores with standard deviations at each time point, while green bars indicate the percentage reduction from baseline. SAS scores significantly decreased from baseline 52.4 ± 8.3 to 1 week 48.6 ± 8.1 (7.3% reduction, t = 4.87, P < 0.001), with further improvement at 1 month 43.6 ± 7.8 (16.8% reduction, t = 11.24, P < 0.001). The optimal therapeutic effect was achieved at 1-month post-treatment and maintained stably through 3 months (44.2 ± 8.0, 15.6% reduction, t = 10.68, P < 0.001), with no significant difference between 1 month and 3 months (t = 0.64, P = 0.523). Data presented as mean ± SD. Statistical significance determined by paired t-tests. SAS: Self-Rating Anxiety Scale.

Improvement in depression status

The improvement trend in depression was similar to anxiety. Baseline SDS score was 55.1 ± 9.2, decreasing to 51.3 ± 9.0 at 1-week post-treatment (t = 4.32, P < 0.001), with relatively small improvement. At 1-month post-treatment, SDS score decreased to (46.3 ± 8.5), a 16.0% reduction from baseline (t = 10.87, P < 0.001), significantly improving from 1-week post-treatment (t = 5.89, P < 0.001). At 3 months post-treatment, SDS score was 47.1 ± 8.8, a 14.5% reduction from baseline (t = 9.96, P < 0.001), with no significant difference compared to 1-month post-treatment (t = 0.78, P = 0.437). According to SDS classification, at baseline 73 cases (57.9%) had depressive symptoms (SDS ≥ 53), including 49 cases (38.9%) mild depression, 19 cases (15.1%) moderate depression, 5 cases (4.0%) severe depression. At 3 months post-treatment, depression symptom incidence decreased to 35.7% (45/126 cases), a 38.4% reduction from baseline (χ² = 15.68, P < 0.001), including 31 cases (24.6%) mild depression, 11 cases (8.7%) moderate depression, 3 cases (2.4%) severe depression. Repeated measures ANOVA showed statistically significant differences in SAS scores (F = 67.89, P < 0.001) and SDS scores (F = 58.76, P < 0.001) at different time points. At 3 months post-treatment, improvement in both SAS and SDS scores positively correlated with baseline anxiety and depression severity (r = 0.512, P < 0.001; r = 0.486, P < 0.001), meaning greater baseline psychological symptoms led to greater improvement magnitude (Figure 2).

Figure 2 Univariate analysis of prognostic factors affecting stellate ganglion block treatment efficacy. This figure presents univariate analysis results of potential prognostic factors associated with treatment efficacy. Treatment outcome at 3 months post-treatment (markedly effective and above vs effective and below) was used as the dependent variable. The red dashed line indicates the significance threshold at P = 0.05. Results show that age (P = 0.342), gender (P = 0.518), body mass index (P = 0.627), and headache type (P = 0.286) had no significant correlation with efficacy. However, disease duration (P = 0.008), baseline headache frequency (P = 0.012), medication overuse (P = 0.003), baseline Self-Rating Anxiety Scale score (P = 0.021), and baseline Self-Rating Depression Scale score (P = 0.015) were significantly correlated with efficacy. Variables with P < 0.10 were included in subsequent multivariate logistic regression analysis. Purple bars represent statistically significant factors (P < 0.05), while gray bars represent non-significant factors. BMI: Body mass index; SAS: Self-Rating Anxiety Scale; SDS: Self-Rating Depression Scale.

Correlation analysis between pain relief and psychological improvement

Pearson correlation analysis showed significant positive correlation between pain relief and anxiety/depression improvement. Using the rate of change from baseline at 3 months post-treatment as analysis variables, the percentage decrease in VAS scores showed moderate positive correlation with percentage decrease in SAS scores (r = 0.687, P < 0.001), and also moderate positive correlation with percentage decrease in SDS scores (r = 0.652, P < 0.001). Percentage decrease in headache frequency showed moderate positive correlation with both percentage decrease in SAS scores (r = 0.594, P < 0.001) and percentage decrease in SDS scores (r = 0.571, P < 0.001). This suggests that patients with more obvious pain relief also showed more significant anxiety and depression improvement. Further analysis found that dividing 126 patients into three groups based on VAS score decrease at 3 months post-treatment: Significant relief group (VAS decrease ≥ 50%, n = 78), moderate relief group (VAS decrease 30%-49%, n = 31), and mild relief group (VAS decrease < 30%, n = 17). The three groups’ SAS scores at 3 months post-treatment were 41.2 ± 7.1, 48.6 ± 7.8, and 52.3 ± 8.5, respectively (F = 18.76, P < 0.001), and SDS scores were 43.8 ± 7.9, 51.2 ± 8.3 and 55.6 ± 9.1, respectively (F = 16.42, P < 0.001), all with statistically significant differences. The significant relief group’s anxiety and depression improvement was significantly better than the other two groups (P < 0.01). Additionally, there was high positive correlation between SAS and SDS scores (r = 0.782, P < 0.001), with anxiety and depression symptoms often coexisting and improving synchronously (Table 4).

Table 4 Pearson correlation analysis between pain relief and psychological improvement.

Variables	Correlation coefficient (r)	P value	Correlation strength
VAS decrease% vs SAS decrease%	0.687	< 0.001	Moderate positive
VAS decrease% vs SDS decrease%	0.652	< 0.001	Moderate positive
Headache frequency decrease% vs SAS decrease%	0.594	< 0.001	Moderate positive
Headache frequency decrease% vs SDS decrease%	0.571	< 0.001	Moderate positive
SAS score vs SDS score	0.782	< 0.001	High positive

VAS: Visual Analog Scale; SAS: Self-Rating Anxiety Scale; SDS: Self-Rating Depression Scale.

Treatment response by headache subtype

The cohort included migraine (n = 89, 70.6%), tension-type vascular headache (n = 28, 22.2%), and cluster headache (n = 9, 7.1%). Exploratory subgroup analysis revealed no statistically significant differences in treatment response among headache subtypes. At 3 months, VAS reduction was 54.8% for migraine, 52.1% for tension-type, and 56.3% for cluster headache (P = 0.71 by one-way ANOVA). Similarly, changes in anxiety (P = 0.64) and depression (P = 0.58) scores did not differ significantly by diagnostic subtype. The total effective rate was 87.6% for migraine, 85.7% for tension-type, and 77.8% for cluster headache (P = 0.67 by χ² test). The comparable treatment response across headache subtypes suggests that continuous SGB may exert therapeutic effects through shared pathophysiological pathways common to neurovascular headaches, such as sympathetic hyperactivity and central sensitization, rather than subtype-specific mechanisms (Table 5).

Table 5 Treatment response by headache subtype at 3 months post-treatment.

Headache subtype	n (%)	VAS reduction (%)	SAS score change	SDS score change	Total effective rate (%)
Migraine	89 (70.6)	54.8	15.8	14.6	87.6
Tension-type vascular headache	28 (22.2)	52.1	15.2	14.3	85.7
Cluster headache	9 (7.1)	56.3	15.1	14.8	77.8
Statistical comparison		P = 0.71	P = 0.64	P = 0.58	P = 0.67

Visual Analog Scale reduction represents percentage decrease from baseline. Self-Rating Anxiety Scale and Self-Rating Depression Scale score changes represent percentage reduction from baseline. Total effective rate includes markedly effective and effective cases. Statistical comparisons: One-way ANOVA for continuous variables (Visual Analog Scale, Self-Rating Anxiety Scale, Self-Rating Depression Scale); χ² test for total effective rate. No statistically significant differences were observed among headache subtypes for any outcome measure (all P > 0.05). VAS: Visual Analog Scale; SAS: Self-Rating Anxiety Scale; SDS: Self-Rating Depression Scale.

Analysis of prognostic factors affecting treatment efficacy

To explore prognostic factors affecting SGB treatment efficacy, efficacy at 3 months post-treatment (markedly effective and above vs effective and below) was used as the dependent variable, with potential influencing factors included in analysis. Univariate analysis showed age (P = 0.342), gender (P = 0.518), BMI (P = 0.627), and headache type (P = 0.286) had no significant correlation with efficacy. However, disease duration (P = 0.008), baseline headache frequency (P = 0.012), medication overuse (P = 0.003), baseline SAS score (P = 0.021), and baseline SDS score (P = 0.015) were significantly correlated with efficacy. Variables with P < 0.10 in univariate analysis were included in multivariate logistic regression analysis, showing: Disease duration was an independent prognostic factor [odds ratio (OR) = 0.876, 95% confidence interval (95%CI): 0.785-0.977, P = 0.018], with each year increase in disease duration reducing the probability of achieving markedly effective or better efficacy by 12.4%; medication overuse was an independent adverse prognostic factor (OR = 0.342, 95%CI: 0.156-0.751, P = 0.008), with patients with medication overuse having only 34.2% the probability of achieving markedly effective or better efficacy compared to those without medication overuse; baseline SAS score was an independent prognostic factor (OR = 0.945, 95%CI: 0.904-0.988, P = 0.013), with lower baseline anxiety (lower SAS scores) associated with better treatment outcomes. Baseline SDS score did not reach statistical significance in multivariate analysis (P = 0.068), possibly due to collinearity with anxiety and depression. Patients with disease duration < 3 years, no medication overuse, and baseline SAS score < 50 achieved a markedly effective rate of 76.3% (45/59 cases), significantly higher than patients not meeting these conditions at 47.8% (32/67 cases; χ² = 10.87, P = 0.001). These results suggest that early intervention, avoiding medication overuse, and emphasizing baseline psychological assessment are important for improving treatment efficacy (Figure 2).

Quality of life improvement and changes in analgesic medication use

MSQ total score improved from baseline 43.8 ± 12.6 to 62.5 ± 14.3 at 3 months post-treatment (t = 13.76, P < 0.001), an increase of 42.7%. Among the three dimensions, role function-restrictive dimension improved from 41.2 ± 13.5 to 60.8 ± 15.2 (t = 12.89, P < 0.001), role function-preventive dimension from 45.6 ± 14.2 to 63.4 ± 16.1 (t = 11.24, P < 0.001), and emotional function dimension from 44.5 ± 11.8 to 63.2 ± 13.6 (t = 14.32, P < 0.001), with all dimensions significantly improving. Regarding analgesic medication use, at baseline 126 patients used analgesics an average of 18.6 ± 8.4 times/month, decreasing to 7.3 ± 5.2 times at 3 months post-treatment (t = 14.67, P < 0.001), a 60.8% reduction. Among 38 patients with medication overuse, baseline analgesic use was 28.7 ± 9.3 times/month, decreasing to 11.5 ± 6.8 times at 3 months post-treatment (t = 10.24, P < 0.001), a 59.9% reduction, with 29 cases (76.3%) successfully controlling use to below 15 times/month, no longer meeting medication overuse criteria. For 88 patients without medication overuse, analgesic use decreased from baseline 14.2 ± 5.6 times/month to 5.8 ± 3.9 times/month at 3 months post-treatment (t = 12.34, P < 0.001), a 59.2% reduction. The reduction in analgesic medication use frequency showed significant positive correlation with VAS score decrease (r = 0.723, P < 0.001), with more obvious pain relief associated with greater decrease in medication dependence (Table 6).

Table 6 Migraine-Specific Quality of Life Questionnaire scores, mean ± SD.

MSQ dimension	Baseline	3 months post-treatment	Change (%)	t value	P value
Total score	43.8 ± 12.6	62.5 ± 14.3	+42.7	13.76	< 0.001
Role function-restrictive	41.2 ± 13.5	60.8 ± 15.2	+47.6	12.89	< 0.001
Role function-preventive	45.6 ± 14.2	63.4 ± 16.1	+39.0	11.24	< 0.001
Emotional function	44.5 ± 11.8	63.2 ± 13.6	+42.0	14.32	< 0.001

All comparisons between baseline and 3 months post-treatment were statistically significant (P < 0.001). MSQ: Migraine-Specific Quality of Life Questionnaire.

Adverse reactions and safety assessment

All 126 patients completed the continuous SGB treatment (5 consecutive days on the left stellate ganglion followed by 5 consecutive days on the right stellate ganglion, totaling 10 days), all operations successfully completed under ultrasound guidance, with no serious complications. Minor adverse reactions included: Local pain at puncture site 32 instances (4.2%), mostly resolving spontaneously within 24 hours; transient hoarseness 18 instances (2.4%), lasting 2-6 hours; transient dysphagia 12 instances (1.6%), lasting 1-4 hours; dizziness 8 instances (1.1%), relieved after rest. All patients exhibited expected Horner’s syndrome manifestations (ptosis, miosis, conjunctival congestion), lasting 4-8 hours, requiring no special treatment. No pneumothorax, hematoma, recurrent laryngeal nerve injury, vertebral artery puncture, or local anesthetic toxicity occurred. Vital signs remained stable during treatment, with no arrhythmias or abnormal blood pressure fluctuations. During follow-up, 2 patients received a second treatment course at 2 months post-treatment due to headache recurrence, and 4 patients changed to other treatment plans due to unsatisfactory efficacy. Overall, ultrasound-guided continuous SGB treatment for neurovascular headache showed good safety, with minor and transient adverse reactions and good patient tolerance (Figure 3).

Figure 3 Minor adverse reactions in stellate ganglion block treatment. Frequency of minor adverse reactions observed in 756 ultrasound-guided stellate ganglion block procedures. Local pain at puncture site (n = 32), transient hoarseness (n = 18), transient dysphagia (n = 12), and dizziness (n = 8) were documented. All reactions resolved spontaneously without intervention.

DISCUSSION

The results of this study offer strong evidence that with continuously SGB, the significant therapeutic effects are exerted on both pain symptoms and psychiatric comorbidities for neurovascular headache patients. Anxiety symptom incidence was lower from 48.4%, and the proportion of those meeting diagnostic criteria for depression symptoms decreased from at 57.9%-35.7%. These results support the expanding literature recognizing the significant psychiatric burden of chronic primary headache disorders and that augmentations of neuromodulatory treatment approaches may address this multidimensional clinical challenge). A particularly high prevalence of PTSD was observed, which corroborates extensive epidemiological evidence. Buse et al[16] conducted a systematic review showing that patients with migraine have double to quadruple the odds for depression and anxiety disorders compared with the general population. Longitudinal studies have firmly established the bidirectional relationship between headache and psychiatric disorders; migraine increases subsequent risk of new-onset depression by 60% quantified longitudinally whereas depression similarly increased migraine risk by 40%[17]. This bidirectional association may be specific to migraine and perhaps reflects neurobiological substrate common to both including serotonergic, dopaminergic and gamma-aminobutyric acidergic systems[18]. From a psychoneuroendocrine perspective, the beneficial effects of SGB for psychiatric symptoms may be mediated by alteration of the hypothalamic-pituitary-adrenal (HPA) axis. In chronic stress and pain conditions, dysregulation of the HPA axis occurs - characterized by either hypercortisolism or hypocortisolemia, dependent on disease duration and severity[19]. About 20%-25% of patients with stress-related disorders, including chronic pain syndromes, have hypocortisolism that could be a compensatory adaptation to prolonged sympathetic overactivation[20]. We propose that SGB may restore homeostasis of the HPA axis by interrupting excessive sympathetic outflow, thereby relieving the physiological substrate that underlies anxiety and depressive symptoms. Strong associations between pain relief and psychometric improvement (r = 0.687 for anxiety, r = 0.652 for depression) indicate a common neurobiological substrate linking pain processing and emotional regulation. Overlapping neural substrates have also been shown in functional neuroimaging studies, especially involving structures such as the limbic system, the prefrontal cortex, anterior cingulate cortex and amygdala[21].

These brain regions play a crucial role in both nociceptive processing and emotional modulation. Patients suffering from chronic headache, depression and anxiety disorders have shown evidence for structural and functional changes in these regions which could share common pathophysiological pathways[22]. The observed coordination shift in our study suggests SGB might concurrently modulate these interrelated neural networks. SGB is gaining acceptance as a symptomatic treatment for psychiatric disorders that involve dysregulation of the sympathetic nervous system, based on the supporting evidence from recent systematic reviews. In a case series of 285 patients, Lynch et al[23] found that SGB treatment was associated with a 50% reduction in anxiety symptoms as measured by the 7-item Generalized Anxiety Disorder questionnaire at one-month post-injection. In the same vein, numerous studies of PTSD have shown that SGB can decrease anxiety, hyperarousal and depression scores by disrupting the persisting “fight or flight” response[24]. Level 1 evidence for psychiatric applications is available from a randomized controlled trial, which reported that SGB exerted approximately double the clinical effect of sham procedure on PTSD symptoms as measured by clinician-reported and self-reported outcomes, respectively[25].

Finally, we noted an interesting temporal dissociation between analgesia and psychosocial improvement. The major analgesic effects were evident as early as 1-week post-treatment while meaningful psychiatric symptom improvement was only observable at follow-up at 1-month. The importance of this delayed psychological response is twofold from a clinical perspective and might represent various mechanisms. Second, Anxiety and depression in chronic pain patients often occur as secondary psychological symptoms due to long-term suffering, social disability and dysfunction[26]. Overcoming these poor cognitive-emotional cycles requires effective management of pain and the steady recovery of normal functions. Conversely, neuroplastic changes resulting from chronic pain and related comorbid psychiatric disorders may take long periods of time to fully reverse after treatment[27]. Our multivariable analysis identified baseline anxiety status as an independent predictor of treatment outcome. Therapeutic response in patients with a lower baseline SAS score was statistically superior. Our finding of baseline anxiety being an independent negative prognostic factor (OR = 2.34, P = 0.014) has direct clinical relevance for planning treatment. This could provide opportunities for patients with established anxiety (SAS ≥ 50) to receive combined therapeutic strategies through continued SGB and cognitive-behavioral therapy or further psychological interventions. The combination of sympathetic blockade as a neurobiological substrate and focused psychotherapy are factors that will allow this multimodal design to be translated directly into clinical practice in a high-risk subgroup, potentially providing positive results. These results have important clinical implications and align with the psychiatric literature that suggests significant comorbid anxiety and depression can diminish treatment benefits via several biological pathways. This includes various mechanisms like increased pain hypersensitivity (central sensitization), non-compliance to treatment, poor quality sleep, HPA axis activation and decreased neurotransmitter metabolism[28]. The discovery of baseline psychological status as a possible prognostic marker underscores the need for regular psychiatric screening in headache clinics. In conclusion, these findings are consistent with a multilevel biopsychosocial model of the management of neurovascular headache. Our findings of high comorbidity rates (anxiety: 48.4%, depression: 57.9%) emphasize that a pain-focused treatment alone is insufficient. In accordance with current psychiatric guidelines recommended screening of all migraine patients for concomitant depression and anxiety disorders has been shown to improve treatment outcomes[29]. In general, for patients with substantial baseline psychiatric symptoms, combination treatment strategies [the use of psychological approaches, such as cognitive-behavioral therapy; pharmacotherapy targeting pain and mood (e.g., serotonin-norepinephrine reuptake inhibitors or tricyclic antidepressants); and neuromodulatory techniques (SGB)] appear to yield the best response[30].

On the basis of our findings, we suggest a clinical strategy for future treatment practice: (1) Systematic psychiatric assessment with validated instruments (SAS, SDS or equivalents) at baseline and follow up; (2) Early SGB intervention in patients suffering from neurovascular headache to reduce progression into chronicity and/or onset of secondary psychiatric disorders; (3) Combined treatment strategies in those patients with high baseline levels of psychopathology burden; (4) Longer follow-up periods (of 6 months or more), since the psychic impairment is one of delayed pattern; and finally; and (5) Interdisciplinary cooperation between pain therapists and mental health specialists to optimize patient centered multifaceted management.

This study has several limitations. First, the study is retrospective and lack controls, so placebo effects cannot be excluded especially for psychological outcomes. Expectancy effects may be generated from the invasive procedure and the absence of sham control means any observed psychological benefits might be partially due to non-specific mechanisms. Second, the fact that data are collected retrospectively leads to information bias and also misses indications of nuance in symptomatic trajectories. Third, the sample is small (n = 126) with low power for the tension-type (n = 28) and cluster headache (n = 9) subgroups. Fourth, 3-month follow-up is a measure of intermediate-to-medium term observation while long-term efficacy and recurrence rates remain to be established. Fifth, psychological assessment was based on self-report scales rather than structured clinical interviews and may underestimate the prevalence of psychiatric disorder. Finally, a lack of mechanism-based biomarker evaluation limits elucidation of the processing pathways that mediate SGB's mitigation of psychological symptoms.

CONCLUSION

This study also confirms that continuous SGB is a safe and effective approach for treatment of neurovascular headache, effectively reduce pain symptoms, significant improvement of accompanying anxiety and depression. It efficacy effects remained significantly improving at the follow-up period after receiving treatment, total effective rate was as high as 86.5%.