A 65-year-old woman presented to a tertiary care center with a classical clinical scenario-3 months of persistent, right-sided frontal headache. Over the course of 20 days, a right-sided frontal headache developed into ptosis of the right upper eyelid. The headache was associated with throbbing pain in front of her skull along with periocular pain but without any systemic or neurological red flags. She had longstanding total blindness in the right eye which was diagnosed by complete absence of Perception of Light (PL). On examination, she was awake and afebrile, with unilateral right-sided ptosis and periocular tenderness. Diagnostic workup, including complete blood count, revealed no significant abnormalities, but MRI characterized by non-specific white matter hyperintensities with post-contrast enhancement of the cavernous sinus, indicative of THS. The patient showed a dramatic response to methylprednisolone, with significant ptosis improvement within 48 h, suggesting an underlying inflammatory etiology. This case highlights the importance of early diagnosis by clinical features, radiological evidence & utility of steroid trials in atypical neuro-ophthalmological presentations with inflammatory markers.

Invasive skull base of rhino-orbital-cerebral mucormycosis is rare, rapidly progressive, and potentially life-threatening disease, and it usually occurs in immunocompromised patients. We are witnessing an unprecedented peak of rhino-cerebral mucormycosis since the second wave of the Coronavirus Disease-2019 pandemic. A 31-year-old man experienced a sudden onset of decreased visual acuity associated with right exophthalmos and paroxysmal headache that had been ongoing for 2 months before his presentation. On examination, he presented a frontal syndrome with preserved eye movement, with vision impairment, and with bilateral stage 3 papilledema. In addition, the patient is feverish, and the general examination showed no lesion of the nose or skin. All biological investigations were done and were negative, even a COVID-19 test. Brain magnetic resonance imaging revealed a right extra-axial temporal lesion that was isointense on T1-weighted imaging, hypointense on T2-weighted imaging, and well enhancing with gadolinium. The lesion extended into the orbit, cavernous sinus (involving the optic nerve and internal carotid artery), and the infratemporal fossa, suggestive of a sphenoidal meningioma. The patient underwent subtotal resection. Postoperatively, the patient remained feverish, and his condition was worsening. He died 6 days after the surgery. A brain infection was impossible to diagnose until after his death. The anatomopathological examination confirmed mucormycosis. The findings from the present case indicate that a large intracranial mass is an uncommon clinical characteristic of cerebral mucormycosis in an immunocompetent patient. It can manifest with the classic symptoms of large temporal spheno-orbital invasive meningiomas. To the best of our knowledge, very few studies are reported depicting the patterns of skull base involvement and associated neurological implications of patients with skull base involvement of rhino-orbital-cerebral mucormycosis along with its clinical, radiological, intraoperative, and post-operative correlates.

The objective of this study is to describe a rare case of orbital compartment syndrome (OCS) following complicated frontoethmoidal mucopyoceles. This report involves a 72-year-old woman with prior functional endoscopic sinus surgery who presented with acute painful proptosis, tense eyelid swelling, and ophthalmoplegia in her left eye. Imaging revealed infected mucoceles (mucopyoceles) in the left frontal and ethmoidal sinuses with intraorbital extension. Based on clinical and radiological findings, OCS was diagnosed. Emergency management included immediate lateral canthotomy and cantholysis, followed by urgent endonasal drainage of the mucopurulent material. The patient made a full recovery, with only transient eyelid numbness. This case underscores the importance of prompt recognition and timely coordinated intervention in OCS to prevent irreversible visual loss and intracranial extension. Enophthalmos is defined as the posterior displacement of the globe within the anteroposterior plane of the orbit, producing the clinical impression of a sunken eye (see Image. Orbit, Anterior View). The condition represents a descriptive clinical finding rather than a diagnosis, indicating an underlying imbalance among orbital structures. Under normal conditions, the globe occupies a stable position within the orbital cavity, maintained by equilibrium among the bony orbital walls, orbital fat, extraocular muscles, connective tissue septae, and vascular components. Disruption of this anatomical harmony—whether from trauma, inflammation, infection, congenital anomalies, or degenerative processes—can result in globe displacement. Recognition of enophthalmos provides a significant clinical clue to local and systemic pathologies affecting the orbit. Differentiation from pseudo-enophthalmos, which reflects an apparent posterior position of the globe due to structural asymmetry or ocular abnormalities, is essential. Common causes of pseudo-enophthalmos include microphthalmos, phthisis bulbi, and anophthalmic socket, in which a small or absent globe produces a deceptive impression of posterior displacement. Globe malpositions, such as hyperglobus, hypoglobus, esoglobus, or exoglobus, as well as contralateral proptosis, can also simulate enophthalmos. Accurate distinction between true and pseudo-enophthalmos is critical for appropriate diagnosis and management. Clinically, enophthalmos manifests as a posteriorly displaced globe, often accompanied by a deep superior sulcus (superior sulcus deformity) and a hollowed periorbital contour. Eyelid position may be variably affected, including ptosis, retraction, or lagophthalmos, and severe cases can result in functional disturbances such as diplopia, restricted ocular motility, or impaired eyelid closure. The opposite clinical finding is proptosis (exophthalmos), defined by anterior displacement of the globe. While proptosis is often more overt due to its cosmetic prominence, enophthalmos typically develops gradually and may remain unnoticed until functional or aesthetic complications arise. From an anatomical perspective, the orbit is a pyramidal cavity formed by the frontal, zygomatic, maxillary, ethmoid, lacrimal, sphenoid, and palatine bones. The orbital cavity contains the globe, extraocular muscles, adipose tissue, neurovascular structures, and fascial septae, which collectively cushion and stabilize the eyeball. Approximately 40% of the orbital volume consists of fat, a critical determinant of globe position. The integrity of the orbital walls and the volume of soft tissue together define ocular projection. The pathophysiology of enophthalmos can be classified into 3 principal mechanisms: loss or atrophy of orbital fat, structural expansion of the bony orbit, and fibrosis or scarring of orbital soft tissues that retract the globe posteriorly. Posttraumatic enophthalmos is one of the most common acquired forms, typically resulting from blowout fractures of the orbital floor or medial wall. Herniation of orbital fat into adjacent sinuses increases the effective orbital volume, displacing the globe posteriorly. Chronic maxillary sinusitis, also referred to as “silent sinus syndrome,” can similarly produce progressive inward bowing of the orbital floor, resulting in spontaneous enophthalmos in the absence of overt trauma. Inflammatory and infectious processes can also alter orbital anatomy. Chronic granulomatous disease, orbital pseudotumor, and postinflammatory fibrosis may lead to contracture of periorbital tissues and scarring, tethering the globe. Iatrogenic causes include radiotherapy-induced fat atrophy and fibrosis, often observed after orbital irradiation for malignancies such as retinoblastoma or nasopharyngeal carcinoma. Progressive hemifacial atrophy (Parry-Romberg syndrome) and scleroderma can produce localized orbital tissue loss, contributing to unilateral enophthalmos. Congenital and developmental anomalies also contribute to enophthalmos. Microphthalmos and craniofacial malformations, such as Crouzon or Apert syndromes, may result in asymmetric globe positioning. In these cases, the apparent enophthalmos arises from dysmorphic orbital bones or reduced globe size rather than true posterior displacement. Postsurgical and postenucleation socket contracture can similarly simulate enophthalmos due to inadequate prosthetic support or soft tissue scarring. The natural history of enophthalmos is largely determined by its underlying etiology. Traumatic cases may become apparent weeks to months after the initial injury, as edema resolves and tissue remodeling occurs. Inflammatory or degenerative causes typically progress gradually, with slow orbital fat loss or fibrosis resulting in increasing asymmetry. Early recognition and intervention are critical, as chronic enophthalmos can lead to secondary changes, including fibrosis of the extraocular muscles, restrictive strabismus, and orbital volume distortion, which complicate reconstructive efforts. Clinical assessment requires careful inspection of facial symmetry in multiple gaze positions and measurement using exophthalmometry. A difference greater than 2 mm between both eyes is generally considered significant. Palpation of orbital rims may reveal step deformities in posttraumatic cases, while ocular motility assessment evaluates extraocular muscle involvement. Imaging, particularly high-resolution computed tomography (CT), provides detailed information regarding orbital wall integrity, fat distribution, and muscle morphology. Magnetic resonance imaging (MRI) offers superior soft-tissue resolution, facilitating differentiation between fat atrophy, fibrosis, and infiltrative lesions. A detailed understanding of orbital anatomy is essential for correlating clinical findings with radiologic evidence. The inferior orbital wall, thin and adjacent to the maxillary sinus, is the most common site of trauma-induced defects. The medial wall, composed of the lamina papyracea of the ethmoid bone, is also susceptible. Expanding these walls increases the volume of the orbital cavity, and even minor volumetric changes can substantially alter the globe's position due to the confined orbital space. Conversely, reduction of retrobulbar soft tissue volume, particularly adipose tissue, produces posterior displacement of the globe without skeletal alteration. Orbital pathology influencing enophthalmos varies widely. Inflammatory and infectious processes may extend from adjacent sinuses, particularly the maxillary and ethmoidal sinuses, causing osteolysis and remodeling of the orbital walls. Malignant lesions, such as metastatic carcinoma or orbital lymphoma, may induce bone resorption and fibrosis, indirectly contributing to enophthalmos. Infiltrative processes that primarily expand orbital tissues, such as thyroid-associated orbitopathy, typically cause proptosis but may also produce secondary enophthalmos during the fibrotic phase. Enophthalmos has substantial functional and aesthetic consequences. The sunken appearance of the eye, combined with asymmetrical eyelid contour, can lead to psychological distress and self-consciousness. Functionally, altered globe position impairs binocular vision, restricts ocular motility, and disrupts tear film dynamics, predisposing to exposure keratopathy. Lagophthalmos and incomplete lid closure exacerbate ocular surface compromise, particularly when associated with facial nerve dysfunction or cicatricial lid changes.

Cerebral venous sinus thrombosis (CVST) is a rare but potentially life-threatening form of stroke. It may present with nonspecific neurological symptoms, including headache, seizures, or focal deficits. One of the rare but important underlying causes is antiphospholipid syndrome (APS), an autoimmune prothrombotic condition associated with persistent antiphospholipid antibodies: lupus anticoagulant (LA), anticardiolipin (aCL), or anti-β2 glycoprotein I (anti-β2GPI). APS-related CVST is typically seen in young women, often with systemic autoimmune disease such as systemic lupus erythematosus. We present a rare and atypical case of a 55-year-old man with no prior autoimmune history who developed new-onset seizures and right-sided weakness while visiting the UK. Imaging revealed a haemorrhagic infarct in the left frontal lobe secondary to superior sagittal sinus thrombosis. Initial thrombophilia screening identified an isolated positive lupus anticoagulant, with confirmatory repeat testing at 12 weeks fulfilling the revised Sapporo criteria for APS. The patient was managed with anticoagulation, antiepileptics, and specialist follow-up. This case is unusual due to several factors: the patient's demographic (middle-aged male), the absence of systemic autoimmune disease, presentation with seizures and intracerebral haemorrhage, and the isolated lupus anticoagulant positivity without triple antibody presence. It highlights the importance of considering APS in unprovoked CVST even in the absence of classic risk factors. Early diagnosis, appropriate imaging, and timely anticoagulation can improve outcomes. This case reinforces the need for autoimmune and thrombophilia screening in atypical stroke presentations.

This article aims to present and interpret two instances of Dyke-Davidoff-Masson syndrome (DDMS), with the main features of cerebral hemiatrophy and compensatory skull changes, focusing on the clinical spectrum, imaging features, and variations in timing of presentation. Two male patients with left cerebral hemisphere involvement were evaluated. The first case was an 8-year-old child presenting with intellectual disability, delayed milestones, right hemiparesis, abnormal jerky movements, and generalized seizures. The second case was a 22-year-old adult with hemiparesis and generalized seizures since birth. Both underwent detailed neurological examination and magnetic resonance imaging (MRI) on a 3T scanner, including time-of-flight (TOF) angiography to assess cerebral vasculature. MRI of the first patient demonstrated left cerebral hemiatrophy with dilatation of the ipsilateral lateral ventricle and sulcal prominence, mild falcine deviation toward the affected side, and compensatory hypertrophy of the left calvarial bones (temporal, parietal, frontal, occipital) with enlargement of the frontal sinus and mastoid air cells and elevation of the left petrous ridge. Mild attenuation of the left middle cerebral artery (MCA) segments was seen on TOF imaging. The second patient's MRI revealed left cerebral hemisphere atrophy with gliosis in the MCA territory, left ventricular dilatation, ipsilateral sulcal prominence, and a neuroglial cyst in the left insular cortex with similar bony changes as those of the previous patient. TOF angiography showed attenuation of the left MCA segments without filling defects. DDMS is associated with a certain specific set of clinical and radiological features. Early recognition through MRI and computed tomography is essential for appropriate management and improved outcomes. These cases illustrate the variability in presentation and emphasize the importance of considering DDMS in the differential diagnosis of unilateral cerebral atrophy with neurological deficits. Air leak (AL) is a clinical phenomenon associated with the leakage or escape of air from a cavity that contains air into spaces that usually, under normal circumstances, do not have air. The terminology air leak syndrome (ALS) is the presence of air leak with associated symptoms of respiratory distress. Air containing cavities include Upper Airway: Tracheobronchial tree. Sinuses . Ethmoid sinus. Frontal sinus. Maxillary sinus. Gastrointestinal Tract: Esophagus. Stomach. Small intestine. Large intestine. The escape of air from air containing cavity to non-air containing cavity can create a condition where some vital organs in the non-air containing cavity can be compressed, creating life-threatening conditions. These life-threatening conditions can be created as a result of compression of the lung or major blood vessels. When the lung or major blood vessels are flattening by the presence of air, gas exchange or blood flow can be severely compromised.  The presence of air in spaces that it is not "supposed" to be is prefixed with the word “pneumo.”: Pneumothorax - the presence of air in the pleural cavity. Pneumopericardium - the presence of air in the pericardial sac. Pneumoperitoneum – the presence of air in the peritoneal cavity. Subcutaneous emphysema – the presence of air in the subcutaneous tissue. The presence of air in the pleural cavity that is associated with the collapse of the lung (Pneumothorax) has clinical significance because of the risk of airway collapse. If the major blood vessels are compressed with the presence of air in the pleural cavity, a clinical condition call tension pneumothorax can ensue. This is a medical emergency that requires immediate medical attention.   Pneumothoraxes Classifications Spontaneous pneumothorax These occur without any precipitating event and is divided into two following groups: 1. Primary spontaneous pneumothorax occurs on healthy, non-diseased lungs. 2. Secondary spontaneous pneumothorax develops from lungs that are diseased with changes in the parenchymal structures. Traumatic pneumothorax  These pneumothoraxes occur from traumatic injury to the lung and pleura space. The traumatic injury may be direct or indirect. Iatrogenic In critically ill patients, iatrogenic pneumothorax causing an air leak can occur from the following conditions: Barotrauma and volutrauma – Aggressive use of high pressure or volume on patients placed on mechanical ventilation or high-frequency oscillatory ventilation, especially for patients with acute respiratory distress syndrome; respiratory distress syndrome can lead to the development of air leak or ALS. The placement of a subclavian central line - This can lead to the introduction of air into the pleural cavity creating pneumothoraxes and air leaks. Surgical interventions - When on the lung, heart, and mediastinal structures, these can create air leak syndrome. Determination of the Presence of an Air Leak To quantify the amount of air leak in a patient connected to a chest tube, the patient is asked to cough, and the water column and the water seal column in the chest tube drainage system are observed. If there are no air bubbles, the pleural cavity is devoid of air. The presence of air bubbles signifies the presence of air leaks. If the amount of air bubbles is the same in quantity, this might signify the presence of a significant leak or an active leak. On the contrary, a gradual reduction in the amount of the bubble is indicative of a small leak or a passive leak. After thoracic surgery, especially resection of the lung, warm sterile saline is instilled into the thoracic cavity. The resected lung is usually insufflated with air to a peak pressure of around 30 mmHg, and the resected section of the lung is then checked for the presence of air leak. Macchiarini et al. suggested a way to classify the air leak: 1. Grade 0 - No leak. 2. Grade I - Countable bubbles. 3. Grade II - Streams of bubbles. 4. Grade III - Coalesced bubbles. After lung resection, air leak that persists for more than five days postoperatively is defined as a prolonged air leak (PAL).