A novel case of Horner syndrome as the presenting sign of craniosynostosis.

Craniosynostosis, the premature fusion of cranial sutures, can lead to distortion of skull shape and neurological dysfunction. We present a novel case of Horner syndrome as the presenting sign of craniosynostosis associated with elevated intracranial pressure. A 10-year-old boy presenting for strabismus follow-up was noted to have new-onset anisocoria, greater in the dark, and mild right upper eyelid ptosis. Apraclonidine testing was concerning for Horner syndrome. Neuroimaging demonstrated previously undiagnosed sagittal craniosynostosis with tortuous optic nerves and large cerebrospinal fluid spaces around both optic nerves. The patient was referred to neurosurgery and underwent a lumbar puncture with an opening pressure of 44 cm H2O. He underwent surgical cranial expansion. By six months postoperatively, his anisocoria had resolved.

Eighth Cervical Nerve Root Block During Interscalene Brachial Plexus Block Decreases Pain Caused by Posterior Portal Placement but Increases Horner Syndrome in Patients Undergoing Arthroscopic Shoulder Surgery: A Randomized Controlled Trial.

PURPOSE: To compare the intensity of pain on posterior portal placement between a C5-C7 root block (conventional interscalene brachial plexus block [ISBPB]) and a C5-C8 root block in patients undergoing arthroscopic shoulder surgery. METHODS: In this prospective, single-blinded, parallel-group randomized controlled trial, patients were randomized to receive either a C5-C7 root block (C5-C7 group, n = 37) or a C5-C8 root block (C5-C8 group, n = 36) with 25 mL of 0.75% ropivacaine. The primary outcome was the pain intensity on posterior portal placement, which was graded as 0 (no pain), 1 (mild pain), or 2 (severe pain). The secondary outcomes were the bilateral pupil diameters measured 30 minutes after ISBPB placement; the incidence of Horner syndrome, defined as a difference in pupil diameter (ipsilateral - contralateral) of less than -0.5 mm; the onset of postoperative pain; and the postoperative numerical rating pain score, where 0 and 10 represent no pain and the worst pain imaginable, respectively. RESULTS: Fewer patients reported mild or severe pain on posterior portal placement in the C5-C8 group than in the C5-C7 group (9 of 36 [25.0%] vs 24 of 37 [64.9%], P = .003). Less pain on posterior portal placement was reported in the C5-C8 group than in the C5-C7 group (median [interquartile range], 0 [0-0.75] vs 1 [0-1]; median difference [95% confidence interval], 1 [0-1]; P = .001). The incidence of Horner syndrome was higher in the C5-C8 group than in the C5-C7 group (33 of 36 [91.7%] vs 22 of 37 [59.5%], P = .001). No significant differences in postoperative numerical rating pain scores and onset of postoperative pain were found between the 2 groups. CONCLUSIONS: A C5-C8 root block during an ISBPB reduces the pain intensity on posterior portal placement. However, it increases the incidence of Horner syndrome with no improvement in postoperative pain compared with the conventional ISBPB (C5-C7 root block). LEVEL OF EVIDENCE: Level I, randomized controlled trial.

Efficacy of HIFU for the treatment of benign thyroid nodules: a systematic review and meta-analysis.

OBJECTIVE: Thyroid nodules are common and sometimes associated with cosmetic issues. Surgical treatment has several disadvantages, including visible scarring. High-intensity focused ultrasound (HIFU) is a recent noninvasive treatment for thyroid nodules. The present study aims to evaluate the effectiveness and safety of HIFU for the treatment of benign thyroid nodules. METHODS: We searched PubMed, Embase, and Cochrane Library for studies evaluating the outcomes of HIFU for patients with benign thyroid nodules. We conducted a meta-analysis by using a random effects model and evaluated the volume reduction ratio, treatment success rate, and incidence of treatment-related complications. RESULTS: Thirty-two studies were included in the systematic review. Only 14 studies were used in the meta-analysis because the other 18 involved data collected during overlapping periods. The average volume reduction ratios at 3, 6, and 12 months after treatment were 39.02% (95% CI: 27.57 to 50.47%, I2: 97.9%), 48.55% (95% CI: 35.53 to 61.57%, I2: 98.2%), and 55.02% (95% CI: 41.55 to 68.48%, I2: 99%), respectively. Regarding complications, the incidences of vocal cord paresis and Horner's syndrome after HIFU were 2.1% (95% CI: 0.2 to 4.1%, I2: 14.6%) and 0.7% (95% CI: 0 to 1.9%, I2: 0%), respectively. CONCLUSIONS: HIFU is an effective and safe treatment option for patients with benign thyroid nodules. However, the effects of HIFU on nodules of large sizes and with different properties require further investigation. Additional studies, particularly randomized controlled trials involving long-term follow-up, are warranted. CLINICAL RELEVANCE STATEMENT: Surgical treatment for thyroid nodules often results in permanent visible scars and is associated with a risk of bleeding, nerve injury, and hypothyroidism. High-intensity focused ultrasound may be an alternative for patients with benign thyroid nodules. KEY POINTS: • The success rate of HIFU treatment for thyroid nodules is 75.8% at 6 months. Average volume reduction ratios are 48.55% and 55.02% at 6 and 12 months. • The incidence of complications such as vocal fold paresis, Horner's syndrome, recurrent laryngeal nerve palsy, hypothyroidism, and skin redness is low. • HIFU is both effective and safe as a treatment for benign thyroid nodules.

Selfie-Induced Diagnostic Challenge in Horner Syndrome.

This case report describes an 18-year-old woman with neurofibromatosis type 1 and prior right brachial plexus neurofibroma resection who reported intermittent, unilateral facial flushing after exertion.

Multifocal neuropathy and Horner's syndrome due to disseminated pyomyositis in an intravenous drug user.

BACKGROUND: The formation of abscesses with necrosis within large, striated muscles leads to pyomyositis, a condition relatively rarely encountered outside the tropics. Intravenous drug users and other immunocompromised individuals are predisposed toward this infection, which may occur due to local or haematogenous spread of infection to skeletal muscles previously damaged by trauma, exercise, or rhabdomyolysis. METHODS: We report a young male intravenous drug user with rhabdomyolysis due to use of a synthetic opioid, in whom disseminated pyomyositis was detected following evaluation for sciatic and radial neuropathies and Horner's syndrome and review available reports of peripheral nerve dysfunction in the setting of this uncommon infection. We searched online databases to identify all published reports on adult patients with pyomyositis complicated by peripheral nerve dysfunction. CONCLUSIONS: Peripheral nerve dysfunction may rarely occur via local spread of infection or compression from abscesses.

Harlequin syndrome.

A 56-year-old man presented to the clinic with episodic headaches for several years which had been worsening over a few months prior to the presentation. He described headache as sharp, stabbing pain around the left eye associated with nausea, vomiting, photophobia, and phonophobia lasting for hours associated with flushing on the left side of the face. The picture of his face during these episodes showed flushing of the left side of the face, ptosis of the right eyelid, and miosis (panel A). Flushing in his face would resolve with the abortion of the headache. At the time of presentation to the clinic, his neurological exam was only significant for mild left eye ptosis and miosis (panels B and C). Extensive workup including MRI brain, cervical spine, thoracic spine, lumbar spine, CTA head and neck, and CT maxillofacial was unremarkable. He had tried several medications in the past including valproic acid, nortriptyline, and verapamil without significant benefit. He was started on erenumab for migraine prophylaxis and was given sumatriptan for abortive therapy following which his headaches improved. The patient was diagnosed with idiopathic left Horner's syndrome and his migraines with autonomic dysfunction would present with unilateral flushing opposite to the site of Horner's presenting as Harlequin syndrome [1, 2].

Lessons of the month: Giant cell arteritis with Horner's syndrome and vertebral dissection.

We present a case of an 82-year-old woman presenting with left-sided Horner's syndrome and stroke. She also had a 6-week history of intermittent dizziness, reduced appetite, lethargy, muscle stiffness and weight loss. Examination revealed left temporal artery and left posterior auricular artery tenderness. Her ESR showed 62 mm/hr and imaging showed left vertebral artery dissection. Temporal artery biopsy was positive.The case highlights a rare presentation of giant cell arteritis with Horner's syndrome and left vertebral artery dissection. High clinical suspicion is required to prevent delay in diagnosis and treatment.

Cortico-hypothalamic pathway of Horner syndrome derived from isolated lenticulostriate stroke.

BACKGROUNDS: Horner syndrome presents with ipsilateral ptosis, miosis, and anhidrosis due to interruption of the oculosympathetic pathway. Patients with acute ischemic stroke may present with Horner syndrome, which may help locate the lesion. However, the underlying pathways involved in Horner syndrome caused by isolated lenticulostriate ischemic stroke remain unclear. METHODS: We screened consecutive patients with acute ischemic stroke admitted to the Second Affiliated Hospital of Guangzhou Medical University from 1 January 2020 to 31 December 2021, and searched for cases of isolated lenticulostriate strokes presenting with Horner syndrome. Strokes involving the brainstem or hypothalamus, or those caused by carotid dissection or carotid cavernous fistula were excluded based on neuroimaging and cerebrovascular examination. RESULTS: Among the 1706 acute stroke patients, three patients developed temporary or long-term Horner syndrome due to an ipsilateral lenticulostriate ischemic lesion. Diffusion-tensor imaging revealed disruption of an uncrossed pathway from Brodmann areas 3, 1, and 2 through the basal ganglia to the ipsilateral hypothalamus. CONCLUSION: These findings suggest that Horner syndrome may be due to a disruption of an uncrossed cortico-basal ganglia-hypothalamic sympathetic pathway.

Assessment of the changes in cardiac sympathetic nervous activity using the pupil size changes measured in seated patients whose stellate ganglion is blocked by interscalene brachial plexus block.

BACKGROUND: As a side effect of interscalene brachial plexus block (ISBPB), stellate ganglion block (SGB) causes reductions in pupil size (Horner's syndrome) and cardiac sympathetic nervous activity (CSNA). Reduced CSNA is associated with hemodynamic instability when patients are seated. Therefore, instantaneous measurements of CSNA are important in seated patients presenting with Horner's syndrome. However, there are no effective tools to measure real-time CSNA intraoperatively. To evaluate the usefulness of pupillometry in measuring CSNA, we investigated the relationship between pupil size and CSNA. METHODS: Forty-two patients undergoing right arthroscopic shoulder surgery under ISBPB were analyzed. Pupil diameters were measured at 30 Hz for 2 s using a portable pupillometer. Bilateral pupil diameters and CSNA (natural-log-transformed low-frequency power [0.04-0.15 Hz] of heart rate variability [lnLF]) were measured before ISBPB (pre-ISBPB) and 15 min after transition to the sitting position following ISBPB (post-sitting). Changes in the pupil diameter ([right pupil diameter for post-sitting - left pupil diameter for post-sitting] - [right pupil diameter for pre-ISBPB - left pupil diameter for pre-ISBPB]) and CSNA (lnLF for post-sitting - lnLF for pre-ISBPB) were calculated. RESULTS: Forty-one patients (97.6%) developed Horner's syndrome. Right pupil diameter and lnLF significantly decreased upon transition to sitting after ISBPB. In the linear regression model (R2 =0.242, P=0.001), a one-unit decrease (1 mm) in the extent of changes in the pupil diameter reduced the extent of changes in lnLF by 0.659 ln(ms2/Hz) (95% CI [0.090, 1.228]). CONCLUSIONS: Pupillometry is a useful tool to measure changes in CSNA after the transition to sitting following ISBPB.

Horner Syndrome subsequent to ultrasound-guided cervical lymph node fine-needle aspiration - A case report and literature review.

Horner Syndrome (HS) is characterized by symptoms of ipsilateral miosis, ptosis, enophthalmos, and facial anhidrosis, which is caused by the damaged oculosympathetic pathway. HS is rarely reported as postoperative complications of fine-needle aspiration (FNA). We report a case of HS triggered by Ultrasound-guided FNA during thyroid cancer management and conducted the literature review. A 31-year-old male with differentiated thyroid cancer underwent total thyroidectomy and regional lymph node dissection as well as radioactive iodine ablation, presented with persistently elevated tumor marker of thyroglobulin and suspicious left level IV and V cervical lymph nodes by neck ultrasound. Ultrasound-guided left cervical lymph nodes FNA for cellular diagnosis was performed, and typical manifestations of HS appeared immediately after the procedure. Subsequent ultrasound evaluation of the same area demonstrated a subtle strip of the hypo-echogenic area in the superior pole of the suspected level IV structure, suggesting sympathetic ganglia with the visible originating nerve fiber on the superior pole. All of the patient's symptoms of HS were resolved 2 months after the incidence. Cervical sympathetic ganglia can be similar in size, shape, and ultrasound characteristics to a malignant lymph node. Thorough ultrasound examination by directly comparing the potential ganglia with a typical malignant lymph node, and paying attention to any potential root fibers on the target is key to avoiding ganglia injury before the neck invasive procedures.

Horner syndrome after thyroid-related surgery: a review.

BACKGROUND: Horner syndrome (HS) is caused by damage to the cervical sympathetic nerve. HS is a rare complication after thyroidectomy. The main manifestations of HS include miosis and ptosis of the eyelids, which seriously affect esthetics and quality of life. At present, there is a lack of research on HS after thyroidectomy, and its etiology is not completely clear. This review aimed to evaluate how to reduce the incidence of HS and promote the recovery from HS as well as to provide a reference for the protection of cervical sympathetic nerves during surgery. RESULTS: HS caused by thyroid surgery is not particularly common, but it is still worthy of our attention. After searching with "Horner Syndrome," "Thyroid" as keywords, a total of 22 related cases were screened in PubMed. The results showed that open surgery, endoscopy, microwave ablation, and other surgical methods may have HS after operation. In addition, the statistics of 1213 thyroid surgeries in our hospital showed that the incidence of HS after endoscopic surgery (0.39%) was slightly higher than that after open surgery (0.29%). Further, this review analyzed potential causes of HS after thyroidectomy, so as to provide a theoretical basis for reducing its incidence. CONCLUSION: Preventing HS during thyroidectomy is a difficult problem. The close and highly variable anatomical relationship between the thyroid and cervical sympathetic nerves increases the risk of sympathetic nerve damage during thyroidectomy. Surgery and the use of energy equipment are also closely related to the occurrence of HS.

Transposition of anomalous left vertebral to carotid artery during the management of thoracic aortic dissections and aneurysms.

OBJECTIVES: Preservation of antegrade flow to the left vertebral artery (LVA) is often achieved by transposition or bypass to the left subclavian artery during zone 2 thoracic endovascular aortic repair. An anomalous LVA (aLVA) originating directly from the aortic arch is a common arch variant with a reported incidence of 4% to 6%. In addition, 6% to 10% of vertebral arteries terminate in a posterior inferior cerebellar artery, increasing the risk of stroke if not revascularized. Few series of aLVA to carotid transposition have been reported. The aim of this study was to evaluate the outcomes of patients who underwent aLVA to carotid transposition for the management of aortic disease. METHODS: A retrospective review of all aLVA-carotid transpositions performed for the management of thoracic aortic dissection or aneurysm at a single center from 2018 to 2021 was performed. The primary outcomes were postoperative stroke and patency of the transposed aLVA. Secondary outcomes were spinal cord ischemia, postoperative cranial nerve injury, and Horner's syndrome. RESULTS: Seventeen patients underwent aLVA to carotid transposition as an adjunct to management of aortic disease during the study period. Most were men (n = 14) and the mean age was 54 ± 16 years. The primary indication for aortic repair was dissection in 10, aneurysm in 6, and Kommerell diverticulum in 1. Nine patients underwent zone 2 thoracic endovascular aortic repair, seven received open total arch repair, and there was one attempted total endovascular arch repair that was aborted owing to unfavorable anatomy. Twelve transpositions were performed before or concomitant with planned aortic repair owing to high-risk cerebrovascular anatomy (three posterior inferior cerebellar artery termination, six dominant aLVA, four intracranial LVA stenosis), and two were performed postoperatively for treatment of type II endoleak. LVA diameter ranged from 2 to 6 mm (mean, 3.3 mm). The mean operative time for transposition was 178 ± 38 minutes, inclusive of left subclavian artery revascularization, and the mean estimated blood loss was 169 ± 188 mL. No patients experienced 30-day postoperative spinal cord ischemia, stroke, or mortality. There were two cases of postoperative hoarseness, presumably owing to recurrent laryngeal nerve palsy, both of which resolved within 4 months. There were no cases of Horner's syndrome. At follow-up (mean, 306 days; range, 6-714 days), all transpositions were patent. CONCLUSIONS: Vertebral-carotid transposition is a safe and effective adjunct in the management of aortic disease with anomalous origin of the LVA.

Acute Horner syndrome secondary to glandular fever due to Epstein Barr virus infection.

We present a clinical situation where a 47-year old female patient consulted with left partial ptosis and miosis that started, two weeks before, with an episode of glandular fever secondary to Epstein-Barr infection. Apraclonidine 0.5% and Phenylephrine 1% drop testing was performed with results consistent with suspected left Horner Syndrome (HS), with a probable postganglionic location. Magnetic Resonance Angiography (MRA) at the moment of the acute presentation did not show any image suggesting carotid arterial dissection but showed irregular narrowing of the left internal carotid artery on its paravertebral extracranial way, consistent to enlarged intra-carotid sheath lymphoid tissue. A week later, a Doppler ultrasound was performed, showing bilateral images compatible with internal carotid arterial dissection. When Postganglionar HS is suspected, the first aetiology to rule out is a carotid arterial dissection because of its potentially fatal outcome and for being a more described entity as postganglionic HS aetiology. However, it is also evidenced that a certain diagnose is not always possible. Furthermore, we describe the enlarged internal carotid artery sheath lymphoid tissue as a possible cause of sympathetic nerve disruption causing a Postganglionar HS, although not common.