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Ewing sarcoma is a rare cancer that most often affects children and teenagers aged 10–20. It usually starts in the bone (about 87% of cases) and less commonly in nearby soft tissues such as muscle or cartilage. The most frequent locations are the pelvis, chest wall and long bones of the legs. In the United States, around 200 children and young adults are diagnosed each year. There are several related forms of Ewing sarcoma, including Askin tumor, extraosseous Ewing sarcoma and peripheral primitive neuroectodermal tumor (pPNET). These tumors share the same genetic origin and are treated as one disease group. At Sheba Medical Center, patients with Ewing sarcoma receive comprehensive, multidisciplinary care. As the largest medical center in the region, Sheba brings together internationally trained pediatric oncologists, orthopedic surgeons, radiologists and radiation oncologists to deliver personalized treatment plans. Each case is carefully evaluated to ensure accurate diagnosis, staging and the most effective therapy. Symptoms Persistent or intermittent bone pain Swelling, tenderness or a lump near the tumor Limping or reduced movement if a limb is affected Fever, fatigue, weight loss Unexplained fractures Advanced disease may cause shortness of breath or chest pain if the lungs are involved Diagnosis & Staging Diagnosis includes imaging (X-ray, MRI, CT, PET), biopsy, and molecular genetic testing to confirm the characteristic chromosomal changes. Disease is classified as localized, regional, metastatic or recurrent, which guides treatment decisions. Treatment Treatment typically combines chemotherapy, surgery and radiation therapy, with options such as targeted therapy, immunotherapy or bone marrow transplantation in selected cases. Sheba’s approach addresses both medical outcomes and quality of life. Prognosis When diagnosed early, outcomes are favorable. Localized Ewing sarcoma has a 5-year survival rate of up to 82%, while prognosis depends on stage, tumor size, location, age and response to therapy. Early expert care makes a critical difference in Ewing sarcoma outcomes.

What is Idiopathic Intracranial Hypertension (IIH)? Idiopathic intracranial hypertension (IIH) — also known as benign intracranial hypertension or pseudotumour cerebri — is a neurological condition in which pressure inside the skull (intracranial pressure) becomes abnormally high without a detectable cause, such as a brain tumour or infection. The increased pressure can compress the brain and cause swelling of the optic nerves (papilloedema). If IIH is not treated in time, it can lead to permanent vision loss, making early diagnosis and management essential. The term idiopathic means that the exact cause is unknown. Types of Idiopathic Intracranial Hypertension 1. Primary (Idiopathic) IIH The most common form No identifiable underlying cause Often affects women of childbearing age, particularly those who are overweight 2. Secondary IIH Occurs due to an underlying condition or trigger, such as: Certain medications Hormonal disorders Systemic medical conditions Symptoms of Idiopathic Intracranial Hypertension Symptoms may develop gradually or suddenly and often worsen over time: Persistent, severe headaches, often throbbing and worse with movement or straining Visual disturbances, including: Blurred vision Double vision (diplopia) Temporary vision loss or “blackouts” (visual obscurations) Papilloedema (optic nerve swelling seen on eye examination) Pulsatile tinnitus, described as a whooshing or heartbeat sound in the ears Nausea and vomiting, linked to raised pressure Neck and shoulder pain Balance and coordination difficulties ⚠️ Any visual symptoms should be assessed urgently. What Causes Idiopathic Intracranial Hypertension? Although the precise cause is unknown, several factors are strongly associated with IIH: Obesity, especially in women of reproductive age Hormonal influences, including: Pregnancy Menstrual irregularities Polycystic ovary syndrome (PCOS) Medications, such as: Tetracycline antibiotics Oral contraceptives Steroids (especially withdrawal) Excess vitamin A or retinoid-based treatments Associated medical conditions, including: Sleep apnoea Kidney disease Certain autoimmune disorders Complications of Idiopathic Intracranial Hypertension If IIH is not properly treated, it can lead to serious complications: Permanent vision loss due to optic nerve damage Chronic, disabling headaches that impair daily functioning Persistent papilloedema, causing progressive visual decline Reduced quality of life due to ongoing neurological symptoms How Can Idiopathic Intracranial Hypertension Be Prevented? There is no guaranteed way to prevent IIH, but risk can be reduced by: Maintaining a healthy weight, particularly for those at higher risk Reviewing medications with a healthcare provider to avoid known triggers Managing underlying conditions, such as sleep apnoea or hormonal disorders Regular medical and eye check-ups, especially if headaches or vision changes occur

Lacunar Syndromes – Clear Clinical Overview Lacunar syndromes are a group of distinct neurological presentations caused by small deep infarcts (lacunes) in the brain. These infarcts result from occlusion of small penetrating arteries, most commonly due to chronic hypertension, but also diabetes and smoking. Unlike large strokes, lacunar strokes do not involve the cerebral cortex, which explains their characteristic pattern of symptoms. The Five Classical Lacunar Syndromes 1. Pure Motor Stroke (Pure Motor Hemiparesis) Most common lacunar syndrome Weakness or paralysis of the face, arm, and leg on one side No sensory loss Common lesion sites: Posterior limb of the internal capsule Basis pontis 2. Pure Sensory Stroke Numbness, tingling, or altered sensation on one side of the body No motor weakness Typically involves the thalamus (especially the ventral posterolateral nucleus) 3. Ataxic Hemiparesis Combination of: Ipsilateral weakness Poor coordination (ataxia), especially affecting gait Often appears as “clumsy walking” Common lesion sites: Pons Internal capsule Corona radiata 4. Dysarthria–Clumsy Hand Syndrome Slurred speech (dysarthria) Clumsiness and poor fine motor control of the hand Facial weakness may be present Lesions usually located in: Pons Internal capsule 5. Mixed Sensorimotor Stroke Motor weakness and sensory loss on the same side of the body Often due to lesions involving both: Thalamus (sensory) Internal capsule (motor) Causes & Pathophysiology Lacunar strokes result from disease of small penetrating arteries: 🔹 Main mechanisms Occlusion of a single small artery Lipohyalinosis Vessel wall thickening and degeneration from chronic hypertension Microatheroma Small atherosclerotic plaque within the penetrating artery 🔹 Resulting lesion Lacune: A small, fluid-filled cavity in brain tissue Size: 3–15 mm Common Brain Locations Involved Internal capsule Thalamus Pons Basal ganglia Corona radiata These are deep brain structures, which explains the symptom pattern. Diagnosis & Key Clinical Characteristics Diagnosis Clinical syndrome recognition is essential MRI (especially DWI) confirms diagnosis by showing a small deep infarct Key distinguishing features ✅ Deficits confined to motor and/or sensory pathways ❌ No cortical signs, such as: Aphasia Neglect Visual field loss Seizures This absence of cortical features helps differentiate lacunar syndromes from larger territorial strokes. Clinical Importance Lacunar strokes often have better short-term survival, but: Recurrent lacunes can lead to vascular dementia Associated with chronic small vessel disease Strongly linked to long-standing uncontrolled hypertension