Horner's syndrome is a rare complication of thyroid surgery and is most commonly reported as a complication associated with lateral neck dissection. We present the case of a 46-year-old woman who developed a partial Horner's syndrome following hemithyroidectomy and central neck dissection, without lateral neck dissection. The patient underwent right hemithyroidectomy and central neck dissection for a TIRADS-5 nodule and developed right sided facial anhidrosis and absence of right-sided facial erythema on exertion 6 weeks post-operatively. No ocular involvement was detected. Neurologist review confirmed partial Horner's syndrome, which eventually resolved. The literature regarding development of Horner's syndrome as a complication of thyroid surgery without lateral neck dissection was reviewed via PubMed. All English language publications of adult patients developing features of Horner's syndrome after open thyroid surgery (hemithyroidectomy or thyroidectomy, +/- central neck dissection) were included. Twenty one cases of Horner's syndrome following thyroid surgery without lateral neck dissection were identified. Interestingly, only four of these cases featured anhidrosis, and no case reported asymmetrical facial erythema. Four possible mechanisms of cervical sympathetic chain dysfunction resulting in Horner's syndrome post-thyroidectomy have been proposed: neuropraxia from retraction; mass effect from post-operative haematoma; ischaemia-induced nerve damage; damage to communicating fibres during repeated inspection of the recurrent laryngeal nerve. To our knowledge, this is the only reported case of a post-thyroidectomy partial Horner's syndrome with associated asymmetrical flushing.

The term “ptosis” is derived from the Greek word falling and refers to drooping of a body part. Blepharoptosis is upper eyelid drooping with the eyes in the primary position of gaze. The shape of one's eyes along with the position of the eyelids, shape, and position of the eyebrow determines one's identity. Hence, drooping of the eyelids may produce a functional or a cosmetic deficit. Ptosis can occur in all age groups and is the result of various factors. One must remember that when a patient presents with complaints of drooping, it is a mere symptom and not the diagnosis. A thorough evaluation is of utmost importance to determine the cause. Ptosis can classify as true ptosis or pseudoptosis. True ptosis is further classified based on the age of presentation into congenital ptosis and acquired ptosis.[1] Acquired adult ptosis is further classified based upon the etiological factors as: 1. Aponeurotic ptosis. 2. Neurogenic ptosis. 3. Myogenic ptosis. 4. Mechanical ptosis. 5. Traumatic ptosis. Aponeurotic ptosis Aponeurotic ptosis is the most prevalent form of adult ptosis and usually presents in the 5th or 6th decade of life. It is also known as involutional ptosis. However, it can occur in young individuals following trauma, recent eyelid swelling, ocular surgery or prolonged use of contact lenses. The pathogenesis of aponeurotic ptosis is most often due to dehiscence or disinsertion of the levator aponeurosis.[2] In involutional cases, true dehiscence is sometimes absent, and ptosis occurs due to stretching or thinning of the aponeurosis. Rarely the levator muscle shows fatty infiltration. Characteristic features of this type of ptosis are that patients have a good levator function with a high lid crease, affected eyelid appears lower on down gaze and a thin upper eyelid with redundant skin. Neurogenic ptosis Neurogenic ptosis results from any condition which disrupts the innervation of either the levator muscle or muller’s muscle. The varieties most commonly encountered by an ophthalmologist are 3rd cranial nerve palsy and Horner syndrome. Third cranial nerve palsy Lesions along the oculomotor nerve present with ptosis and restriction of adduction, elevation and depression movements of the eyeball. Pupillary involvement may or may not be present. Bell's phenomenon is usually poor. Pupil-involving third nerve palsy is considered a neurological as it is most often due to a posterior communicating artery aneurysm compressing the nerve. Pupil-sparing third nerve palsy is most often due to an ischemic vascular cause and usually resolves spontaneously in 3 months. Other causes include inflammation, trauma or tumors along the course of the nerve. Lesions of the superior orbital fissure, orbital apex, or cavernous sinus, present in combination with other cranial nerve palsies. Treatment is challenging as the patients have a poor or absent Bell’s phenomenon placing them at high risk of developing exposure keratopathy post-surgery. Ideally, strabismus surgery is done first to correct the deviation followed by ptosis correction via the frontalis sling technique with planned under-correction. Horner syndrome (Oculosympathetic paresis) Horner syndrome consists of mild ptosis, pupillary miosis, apparent enophthalmos, and anhidrosis. It occurs due to interruption of the sympathetic nerve supply to the muller’s muscle and dilator pupillae muscle. Pupillary anisocoria can be well demonstrated in dim illumination. Patients with Horner’s syndrome occurring during childhood also have iris heterochromia due to decreased melanin production in melanocytes which is controlled by the sympathetic pathway. The diagnosis of Horner syndrome is often made clinically. Pharmacological tests using 4% cocaine, 1% hydroxyamphetamine or 2.5% phenylephrine help confirm the diagnosis. Myogenic ptosis Myogenic ptosis arises due to an abnormality in the levator muscle itself. These patients usually present with reduced levator action along with restricted extraocular motility and facial expression. Myasthenia gravis Myasthenia gravis is an autoimmune disorder characterized by the presence of antibodies to acetylcholine receptors located at the neuromuscular endplates of voluntary muscles.[3] This leads to decreased action of acetylcholine which results in muscle weakness and fatigue. Myasthenia may be generalized or localized to the eye (ocular myasthenia). The most common presenting feature is variable ptosis associated with diplopia. Symptoms may be unilateral or bilateral. Patients with myasthenia initially have a good levator function. Prolonged upgaze will cause a worsening of ptosis in these patients due to muscle fatigue. Cogan lid twitch sign: Rapid saccadic eye movements from downgaze to primary position results in rapid upshoot of the lid followed by a gradual drop to the primary position. Other tests which help confirm the diagnosis include ice test, serum acetylcholine receptor antibody assay, single fiber electromyography, and repetitive nerve stimulation test. Treatment of such patients involves administration of acetylcholinesterase drugs, oral steroids or immunosuppressants. In patients with severe ptosis, ptosis correction with planned under-correction may be an option. Myotonic dystrophy Myotonic dystrophy is an autosomal dominant disorder which presents with gradually progressing ptosis and external ophthalmoplegia. The pathologic process is a failure of muscle to relax after contraction. It also involves muscles of facial expression, neck, and limbs. Ocular examination in these patients also shows pupillary light-near dissociation, chromatic cataracts (Christmas tree cataract), and retinal pigmentary degeneration. Males develop a frontal pattern of balding and testicular atrophy. Chronic progressive external ophthalmoplegia (CPEO) CPEO is a mitochondrial myopathy causing bilateral symmetrical involvement of the extraocular muscles. Manifestations begin in childhood or adolescent age and progress slowly during adulthood. Bilateral symmetrical involvement is the first symptom followed by bilateral ophthalmoplegia. Due to the symmetric involvement of extraocular muscles, patients often do not complain of diplopia. As the muscles of facial expression are involved, patients develop an expressionless face (Hutchinson's face) Diagnosis is confirmed by muscle biopsy which shows ragged red fibers due to enlarged mitochondria. Kearns-Sayre syndrome: A variant of CPEO which shows retinal pigmentary degeneration, cardiac conduction defects, complete heart block, ataxia, neuropathy, endocrine dysfunction, and occurs in young adults. There is no treatment to date for CPEO. Ptosis surgery to clear the visual axis can be done in severe cases keeping in mind the high risk of exposure keratopathy. Oculopharyngeal muscular dystrophy This autosomal dominant disorder manifests in the 4 to 5 decade of life with bilateral ptosis, progressive external ophthalmoplegia, dysphagia, dysarthria, facial muscle weakness, and proximal limb weakness. Mechanical ptosis Ptosis secondary to any tumor producing an increased weight on the lids, cicatrization or scarring of the conjunctiva, and blepharochalasis. Traumatic ptosis Ptosis occurs due to direct or indirect trauma to the levator muscle. Penetrating injuries involving the levator can be repaired immediately. However, ptosis secondary to blunt trauma may resolve spontaneously over time. Ptosis which does not improve after 6 months can have surgical repair. Pseudoptosis It is not true ptosis but apparent ptosis due to abnormalities in structures other than the levator muscle. Causes include dermatochalasis, brow ptosis, hypotropia, microphthalmos, anophthalmos, phthisis bulbi, and contralateral eyelid retraction. It is very important to distinguish true ptosis from a pseudoptosis before embarking upon any surgical correction for drooping. Clinical presentation Patients usually complain of: 1. Drooping of eyelids. 2. Feeling of heaviness in the eyes. 3. Visual obscuration due to drooping. 4. Cosmetic complaints. Assessment A thorough history taking and clinical examination help determine the etiology of ptosis and plan appropriate treatment. History History taking should include the age of onset of ptosis, progression, duration, and any aggravating or relieving factors. Any associated symptoms such as diplopia, diurnal variation, pain, lid swelling, dysphagia or muscle weakness help provide a provisional diagnosis. Predisposing factors such as trauma, ocular or eyelid surgery, contact lens use, and botulinum toxin injection should be carefully ruled out. A family history of ptosis should be looked for to rule out hereditary disorders. In patients where the history is inconclusive, assessment of old photographs gives an idea about the time of onset. Any systemic illness, mental health issues, and medication history require documentation. Patients on blood thinners such as aspirin should be advised to stop medications 1 week before surgery. Clinical examination Clinical examination starts from the moment the patient walks into the doctor's clinic. It is essential to look for any facial asymmetry, frontalis overaction, chin up or head tilt posture. Ocular examination : 1. Visual acuity and refraction. 2. Cover test to look for any hypotropia and rule out any component of pseudoptosis. 3. Extraocular motility disturbance and any aberrant eyelid movements. 4. Pupillary examination to look for Horner syndrome or 3rd cranial nerve palsy. 5. Examination to look for any giant papillary conjunctivitis or symblepharon. 6. Corneal sensation and dry eye evaluation as they can predispose to post-operative keratopathy. 7. Fundus examination for features of retinal pigmentary degeneration. Specific examination of ptosis  Lid measurements should be done positioning the face in the frontal plane, negating the action of frontalis muscle with the thumb, and eyes in the primary position of gaze. The examiner should be seated at the eye level of the patient to avoid parallax error.  1. Palpebral fissure height (PFH): It is the vertical palpebral aperture height between the upper and lower eyelid margin in the pupillary plane with eyes in the primary position of gaze. Average PFH is around 10mm.  2. Marginal reflex distance 1 (MRD 1): MRD 1 is the distance between the upper lid margin and the corneal light reflex. Normal MRD 1 is 4-5mm. The difference in MRD 1 between the two eyes helps classify ptosis as mild, moderate or severe in patients presenting with unilateral ptosis. The difference in MRD 1 between two eyes: 2mm – Mild ptosis. 3mm – Moderate ptosis. 4mm – Severe ptosis  3. Marginal reflex distance 2 (MRD 2): MRD 2 is the distance between the corneal light reflex and lower eyelid margin. Normally MRD 1 + MRD 2 = PFH.  4. Levator action: It is the amount of excursion measured with a millimeter scale when the eyelid moves from extreme downgaze to extreme upgaze with frontalis action negated. Normal levator action is greater than 15mm. It is the single most important measurement in a patient with ptosis as its value determines the choice of surgical procedure. Grading of levator action[4]: Less than 4 mm – Poor. 5 to 9 mm – Fair. 9 to 11 mm – Good. Greater than 12 mm – Excellent. In patients with poor levator action (less than 4mm), frontalis sling surgery is the preferred procedure.  5. Margin crease distance (MCD): It is the distance between the lid margin and skin crease in downgaze. Normal MCD is 7 to 8mm in men and 8 to 10 mm in women. In congenital ptosis, MCD is usually absent or faint, whereas in aponeurotic ptosis MCD is higher than normal. During surgery, it is very important to reform the crease identical to the contralateral eye to maintain symmetry and achieve good cosmesis.  6. Bell’s phenomenon: This is another very important factor to be considered before ptosis correction. The patient is asked to close the eyes gently, and an attempt is made to open them. In patients with poor bell’s, ptosis correction should be avoided or undercorrected to avoid the risk of post-operative exposure keratopathy.  7. Assess presence of lagophthalmos and lid lag on downgaze which if present will worsen post-surgery.  8. Any brow ptosis or dermatochalasis if present should be documented. In involutional ptosis, blepharoplasty procedure is often combined with ptosis repair.  9. Hering test: In patients with unilateral ptosis, the ptotic lid is gently elevated manually, and the contralateral eyelid observed. Due to Hering's law of equal innervation, the contralateral eyelid may drop (See-saw effect). It is important to demonstrate this to the patient preoperatively and warn them about the possibility of requiring ptosis surgery in the contralateral eye. In such cases, a planned under-correction may be the treatment.  10. Phenylephrine test: It is a useful test in patients with mild ptosis or ptosis due to Horner syndrome; instill 2.5% phenylephrine drops in the superior fornix. Ptosis measurements are repeated after 10 minutes. Patients in whom the ptotic lid elevates due to stimulation of Muller's muscle are ideal candidates for posterior approach ptosis correction (conjunctival – mullerectomy surgery).  11. Tests to rule out myasthenia gravis: Fatigue test: The patient maintains fixation in upgaze for 30 seconds. In patients with myasthenia, the eyelid gradually drops down due to muscle fatigue. Ice test: An ice pack is placed over the closed ptotic eyelid for 2 minutes. Ptotic measurements are repeated after 2 minutes. Improvement in PFH by 2mm or more is considered positive for myasthenia. This is because cooling improves neuromuscular transmission.  12. Hertel exophthalmometry: A Hertel reading helps rule out any proptosis or enophthalmos and thus excludes pseudoptosis.

The division of the mediastinum into specific compartments is essential for identifying, characterizing, and managing mediastinal abnormalities. The current international standard is the three-compartment model proposed by the International Thymic Malignancy Interest Group (ITMIG), which divides the mediastinum into prevascular (anterior), visceral (middle), and paravertebral (posterior) compartments. This model has replaced the traditional four-compartment system, which included the superior mediastinum, due to its simplicity, familiarity, and clearly defined boundaries. However, given the superior mediastinum's unique anatomy and distinct pathology, it remains clinically reasonable to consider it separately. Continued clinical use of the term "superior mediastinum" has produced numerous conflicting definitions, while the Japanese Association for Research on the Thymus (JART) has recently proposed a computed tomography (CT)-based four-compartment model. Disease distribution in the superior mediastinum is dominated by thyroid goiters and neurogenic tumors, while the incidence of thymic epithelial tumors (TETs) in this region varies among studies. Surgery in the superior mediastinum is challenging due to its narrow space and the presence of major blood vessels and nerves. Operative complications frequently include Horner's syndrome. Furthermore, studies suggest that superior mediastinal thymomas may demonstrate more aggressive behavior and lower survival rates than thymomas in other locations. Establishing a clear, standardized definition of the superior mediastinum would resolve current inconsistencies and facilitate the accumulation of detailed clinical data on superior mediastinal lesions. This article focuses on the superior mediastinum and discusses its classification, clinical features, surgical approaches, treatment outcomes, and future perspectives.

Neuroblastoma (NBL) constitutes the most common extracranial solid tumor in children that arises from the sympathetic ganglia. Its manifestations depend on the localization of the tumor and metastases. This research aimed to assess the incidence of ophthalmological symptoms and their correlations with different prognostic factors. We collected and analyzed retrospectively the data of 776 children with a clinical diagnosis of peripheral neuroblastic tumors reported between 2004 and 2022 from 14 Polish pediatric oncology centers. Ophthalmological symptoms occurred in 17.10% of the patients, and in 12.70% they were diagnosed at the time of the first presentation. The reported manifestations comprised opsoclonus-myoclonus syndrome (OMS), Horner syndrome (HS), exophthalmos, periorbital hemorrhages, with the highest incidence of OMS (4.74% of all the patients). Moreover, we described the cases with neurological manifestations of NBL like paraparesis and facial nerve paresis. The age correlated with the form of symptoms, and HS was observed in the youngest patients. Similarly, the time from the symptoms onset to NBL diagnosis differed significantly among the patients, therefore the diagnosis of HS was associated with the longest period. In conclusion, the ophthalmological manifestations of NBL represent an essential group of symptoms. Therefore, clinicians should consider them as possible signs of tumors, particularly HS, which may be most challenging in the diagnostic process.

Cervical ganglioneuroma is a relatively rare benign neurogenic tumor for which standardized evidence-based guideline is lacking. It is more common in women, adolescents, and children and presents as an asymptomatic neck mass. Preoperative imaging and needle biopsy are insufficient to confirm the diagnosis, making postoperative histopathological examination of a specimen the gold standard. Herein, we present the case of a middle-aged man with a giant ganglioneuroma of the neck, discussing the relevant diagnostic and therapeutic characteristics. The patient was a 43-year-old man who had been diagnosed with a left neck mass 6 years prior, without obvious symptoms, received no treatment. One year prior, the patient presented with aggravated speech with content sounds and was admitted at our hospital for relevant examinations and surgical treatment. The patient underwent transcervical tumor resection under general anesthesia. Symptoms such as Horner syndrome, left deviation of tongue protrusion, and dysphagia occurred after surgery. At follow-up 2 months after surgery, symptoms such as left deviation of tongue extension and dysphagia disappeared, and symptoms such as ptosis were alleviated to a certain extent. Surgical resection remains the primary treatment for cervical ganglioneuromas. For large tumors, the transcervical approach can not only completely resect the tumor but also contribute to postoperative recovery.

Pancoast or superior sulcus tumor consists of a wide range of tumors invading the apical chest wall and producing a characteristic syndrome named “Pancoast -Tobias syndrome.” The superior sulcus is an anatomical pleuro-pulmonary groove that is formed by the subclavian artery when it curves in front of the pleura and runs upward and lateral immediately below the apex.[1] Not all superior sulcus tumors are in this exact location, but this term signifies any tumor that presents in the apices of the lungs associated with clinical signs and symptoms that are the hallmark of Pancoast syndrome. The combination of severe shoulder/arm pain along with the distribution of the C8, T1, T2 nerve trunks, Horner syndrome (ipsilateral ptosis, miosis, and anhidrosis; caused due to interruption of sympathetic nerve chain running to the head) and atrophy of the intrinsic hand muscles is termed “Pancoast-Tobias syndrome.”[2] The overall prognosis of patients with this disease is poor, although recent advancements in the treatment regimen showed significant improvement. Treatment of Pancoast tumors involves interprofessional care coordinated among a thoracic surgeon, a radiation oncologist, and a medical oncologist.[2]

Neuroblastoma in neonates is a rare solid tumor. This report presents two rare cases of cervical neuroblastoma, both characterized by stridor and coughing during feeding due to tumor compression. The first case of neuroblastoma presented with an intact capsule, allowing for complete surgical resection with preservation of the cervical vasculature and nerves. In contrast, although preoperative MRI indicated an intact capsule in the second case, the intraoperative findings revealed no discernible capsule formation and involvement of both the internal and external carotid arteries. None of the two patients developed Horner's syndrome postoperatively, and no evidence of recurrence or metastasis has been observed during the 10-month follow-up period. These cases also underscore that surgical intervention remains the primary treatment option for cervical neuroblastoma, particularly in alleviating the respiratory and feeding difficulties caused by tumor compression.

Exercise in the heat often causes gastrointestinal (GI) disturbances, which can impair performance. Single amino acid supplementation can attenuate gut damage and enhance exercise tolerance; however, the effectiveness of innate amino acid blends from plant-based proteins remains underexplored. In this study, we investigated the effects of a novel fava bean-derived plant protein (ATURA) on thermoregulation, endurance performance and GI disturbances during exercise. Twelve healthy, non-heat-acclimatized participants completed an exercise trial (10 min walk, 40 min run, graded exercise test) in the heat (35°C; 40% relative humidity), before and after 8 days of ATURA (60 g/day) or placebo, in a double-blind, randomized, cross-over design. Whole-body sweat rate, local sweat rate, pulmonary gas exchange, skin and core temperature and perceptual responses were monitored, with pre- and post-trial blood samples. ATURA increased whole-body sweat rate (11%; P = 0.03) and back local sweat rate (11%; P < 0.001) and reduced core temperature (ATURA, 38.7°C ± 0.5°C; placebo, 38.8°C ± 0.5°C; P = 0.04) and thermal sensation (P = 0.05) in comparison to placebo. There were no differences for skin temperature, thermal comfort or graded exercise test time (P > 0.05). ATURA reduced postexercise intestinal fatty-acid binding protein (22%) compared with placebo (P = 0.05), with no difference for soluble CD14 or GI symptoms. Pre-to-post HSP70 was higher after ATURA (12%, P = 0.05), with no difference for interleukin-6 (P > 0.05). Pre-exercise fava bean protein reduced postexercise intestinal fatty-acid binding protein, indicating a potential protective effect on intestinal integrity, and was well tolerated, without increasing GI symptoms. Exploratory outcomes suggest possible thermoregulatory benefits, warranting further investigation.