She is 34 years old and pregnant. She had a seizure and trouble speaking clearly. She was sent right away for a head MRI scan. The scan showed a pattern doctors call the “Medusa head.” This means the veins in her brain are arranged in an unusual way that she was born with. There is a small blood clot at the outer part of this vein pattern. The blood is also moving slowly closer to the main vein.


A 77-year-old woman with haematemesis presented in shock (heart rate 100 beats/min, blood pressure 79/56 mmHg) with anaemia (haemoglobin 9.6 g/dL), consistent with upper gastrointestinal bleeding. Because of renal dysfunction, non-contrast CT was obtained and demonstrated the third portion of the duodenum flexed steeply on the right side of the aorta and coursing caudally without crossing anterior to the aorta. The duodenojejunal (DJ) junction and the jejunum were in the right hemi-abdomen. The second portion of the duodenum and the stomach were dilated, and high-density gastric contents suggested haematoma. Esophagogastroduodenoscopy showed a mucosal laceration at the gastric cardia, consistent with Mallory–Weiss syndrome; in this case, steep flexion with luminal narrowing of the third portion likely caused transient obstruction and repeated vomiting precipitating the tear. Seven days later, repeat CT showed spontaneous resolution of the malpositioned jejunum. Months later she re-presented with haematemesis; dynamic CT on admission demonstrated contrast extravasation in a dilated stomach and again showed the third portion of the duodenum flexed on the right of the aorta with the DJ junction and jejunum in the right hemi-abdomen. Endoscopy again revealed a cardia laceration. Two months after the second haematemesis, she presented with nausea; non-contrast CT showed normal duodenal positioning but oedematous wall thickening in the second portion. Over four CT examinations spanning five months, the third and fourth portions of the duodenum and the jejunum repeatedly deviated to the right and then spontaneously returned to normal position, a pattern incompatible with fixed intestinal malrotation. Dysplasia (incomplete fixation) of the ligament of Treitz was diagnosed. Laparotomy found no intestinal malrotation: the ligament of Treitz was formed, but fixation in the upper jejunum was incomplete (attached only to the duodenum); the DJ junction was not fixed to the retroperitoneum, and the jejunum folded readily with the ligament as a fulcrum. CT also indicated a loosely fixed, mobile anterior pararenal space. These anatomic factors likely permitted intermittent right-sided deviation of the small intestine. Surgically, the upper jejunum was fixed with four sutures to the left retroperitoneum; the postoperative course was uneventful, and she remained symptom-free.


A 28-year-old man had two red patches with small blisters and shallow sores on the inner part of his right arm and forearm for 2 days. The spots burned and itched. He had been on vacation on the coast of Ecuador when this started. The doctor took a small piece of skin to test. The diagnosis was a type of skin irritation called Paederus dermatitis. He was treated with allergy pills, a steroid cream, and cold packs. After 8 days, the rash went away. It left dark marks on the skin.


We retrospectively reviewed medical records from a pediatric neurology consultation at a third‑level hospital (2015–2020) for patients with congenital myotonia. Inclusion criteria comprised a clinical diagnosis (myotonia, warm‑up phenomenon, characteristic electromyographic pattern and/or family history) and/or a molecular diagnosis (CLCN1 mutation). For each patient we abstracted demographics (age, sex), disease course (age of onset, symptoms and signs, time to diagnosis, clinical evolution), family history, and treatment response, along with complementary testing and genotypes. Five cases with a clinical diagnosis of congenital myotonia were identified: three with Becker’s disease (recessive phenotype) and two with Thomsen’s disease (dominant phenotype). Incidence relative to births was estimated at 1:15,000 for Becker phenotypes and 1:21,000 for Thomsen phenotypes. Most patients were female; the single male was the only child with onset before age six. Initial presentation included myotonia in the lower limbs in four of five patients and in the upper limbs in all but one. Age at onset ranged from 22 months to 12 years (median 6 years). Genetic diagnosis was pursued approximately two years after onset; one family declined testing. All patients reported worsening with cold; the warming phenomenon was noted only in those with the Becker phenotype. Patients with recessive congenital myotonia showed some progression. Family history included: patients 2 and 3 were sisters with unaffected parents; the mother of patient 1 had mild, cold‑provoked, doubtful clinical signs; the patient who declined genetic testing had a maternal‑line history of myotonia. Serum creatine kinase was not elevated in any case. The electromyogram was abnormal in all patients except the first one at 2.8/12 years of age (not repeated). Initial therapy most often used was oxcarbazepine in the recessive form, with generally good response; in case 2 it lost efficacy and mexiletine was initiated. Case 4 trialed several drugs without success due to loss of efficacy or adverse effects. Case 5 declined treatment given mild symptoms. Patient 1 harbored a previously undescribed, likely pathogenic variant, CLCN1: c.824T>C, maternally inherited. Cases 1–3 (Becker phenotype) carried composite heterozygosity mutations; cases 4–5 had the Thomsen phenotype, and case 5 declined genetic testing.


A 59-year-old woman with a 12-year history of secondary progressive multiple sclerosis presented with several weeks of bilateral blurred vision. Past ophthalmic history was unremarkable; there was no family history of corneal pathology, and prior examinations showed no signs of Fuchs' endothelial corneal dystrophy. She had been on amantadine 100 mg twice daily for 7 years and was started on levetiracetam 250 mg twice daily as an add-on agent after a breakthrough seizure; visual deterioration occurred shortly after levetiracetam initiation. On examination, BCVA was 0.5 logMAR OU. Slit-lamp examination revealed bilateral corneal edema without uveitis; IOPs were 16 mmHg OD and 18 mmHg OS. Corneal topography confirmed significant bilateral corneal thickening with CCT 936 μm OD and 1134 μm OS; the remainder of the ocular examination was normal. Because amantadine is a known cause of corneal edema, it was switched to lamotrigine while levetiracetam was continued, but there was no improvement after two months. Amantadine was then reintroduced and levetiracetam was tapered; visual improvement was noted within days of levetiracetam dose reduction. Levetiracetam was subsequently discontinued, and the patient remained on amantadine and lamotrigine. A provisional diagnosis of levetiracetam-induced corneal edema was made. Six months after stopping levetiracetam, BCVA improved to 0.2 logMAR OU; corneal topography showed CCT 567 μm OD and 573 μm OS, and slit-lamp confirmed clear corneas without guttata. At 13 months after initial presentation, medications were unchanged, vision remained stable at 0.2 logMAR OU, and repeat corneal topography was unchanged. The clinical course is consistent with a drug-induced, reversible corneal endothelial dysfunction temporally related to levetiracetam exposure, with no response to amantadine withdrawal.


A 42-year-old woman had a hard-to-treat headache condition. Headache pills made her feel sick, so she could not take them. She came to the clinic with very strong pain, 9 out of 10. We took her to a small operating room. We used ultrasound, like a live picture, to guide a numbing shot to a nerve at the back of her head. The numbing medicine made her pain drop to 2 out of 10 within minutes. We repeated the same shot once a week for four weeks. After two months, her headaches happened less often and hurt less. She had no side effects.


Female patient, 16 years old, with a depressed gray plaque measuring 10.5 × 8.0 cm, interspersed with hypochromic areas on the lower lateral left thigh. Telangiectatic vessels overlap the lesion peripherally, with visible veins adjacent to it. The plaque has been present since birth, initially violaceous, and evolved over the years with lightening and progressive depression. No discrepancy in lower limb length. Angioresonance demonstrated vascular malformations confined to the skin and subcutaneous tissue, supplied by intermuscular branches of the popliteal artery. There is early venous filling in both the region and the malformations, suggesting early venous shunting. Dilated draining veins were not documented, except for a superficial draining vein coursing along the subcutaneous cellular tissue of the anterior thigh. There is thinning of the subcutaneous tissue at the site of the vascular alteration, without intramuscular or bone extension.


A 19-year-old woman came to the emergency room with headache, nausea, vomiting and fever and was found to have very high blood pressure and a fast heart rate. Imaging incidentally showed a large mass on her left adrenal gland, and blood and 24-hour urine tests showed markedly raised catecholamines and their metabolites, confirming a diagnosis of pheochromocytoma. Despite the size of the tumor and receiving high‑dose glucocorticoid treatment early in her stay, she did not develop a hypertensive crisis. She had a past episode a year earlier diagnosed as myocarditis and a family history of sudden unexplained death. Genetic testing identified a pathogenic RET gene mutation (c.1900T>C, p.Cys634Arg) consistent with multiple endocrine neoplasia type 2A (MEN2A), so the thyroid and parathyroid glands were evaluated. Thyroid ultrasound found a small nodule and blood tests showed mildly raised calcitonin, while initial electrolytes and parathyroid hormone (PTH) were within the normal range. Three months later she underwent removal of the left adrenal tumor; pathology confirmed pheochromocytoma, and she recovered without recurrence of symptoms. Over 15 months of follow-up she continued to have mildly elevated calcitonin with a stable thyroid nodule, but PTH and serum calcium levels rose progressively. A 99mTc‑MIBI parathyroid scan did not show a parathyroid adenoma.


A 27-year-old woman with uncontrolled asthma and recent mild SARS-CoV-2 infection presented in March 2021 with left hemifacial pain and trismus 48 hours after completing phenoxymethylpenicillin 1,000,000 IU orally once daily for five days for a peritonsillar/oropharyngeal infection. She was hemodynamically stable, without oxygen requirement. Examination showed tender ipsilateral cervical lymphadenopathy and trismus. Admission labs demonstrated leukocytosis, thrombocytopenia, and elevated acute phase reactants; other parameters were within normal limits. Head and neck CT angiography identified a large thrombus within the internal jugular vein. Initial Doppler assessment of neck vessels did not add further actionable findings. Chest CT demonstrated bilateral septic pulmonary emboli. Management included immediate intravenous broad-spectrum antibiotics (ceftriaxone 1 g every 12 hours plus clindamycin 300 mg every 6 hours initially) and therapeutic anticoagulation with enoxaparin 60 mg subcutaneously every 12 hours, dose-adjusted to body weight and renal function. At 72 hours, she developed fever to 38.5 °C with rising leukocytosis; transthoracic echocardiography showed no valvular vegetations. Blood cultures remained negative and a pharyngeal exudate culture was obtained. Antibiotics were escalated to piperacillin–tazobactam 4.5 g IV every 6 hours, with subsequent clinical improvement and no organisms isolated. After 14 days of the revised regimen, follow-up chest CT showed resolution of pulmonary lesions. She was transitioned to oral clindamycin 300 mg every 6 hours and oral anticoagulation with acenocoumarol (dose-adjusted to body weight) and discharged. The presentation and imaging were consistent with internal jugular vein thrombosis complicated by septic pulmonary emboli.


A 51-year-old male presented with acute, painful visual loss of the left eye (LE) for 3 days. Best-corrected distance visual acuity (BCDVA) was 20/20 OD and hand motion (HM) OS. Ocular motility and anterior segment were unremarkable OU. Fundus OS showed optic nerve head (ONH) swelling, choroidal bulging, multiple patches of subretinal fluid (SRF), and retinal pigment epithelial (RPE) corrugations; OD fundus was unremarkable.

Multimodal imaging was obtained: OCT (OptoVue, Inc., Fremont, CA, USA; software version 2018.0.0.18) demonstrated mild RPE and choroidal bulging, RPE hyper-reflectivity with back shadowing, subretinal and intraretinal fluid, and mild retinal thickening. Indocyanine green angiography (ICGA) showed a geographic macular hypocyanescent area OS. Blue-autofluorescence (BAF) revealed a geographic macular area with speckled autofluorescence. B-scan ultrasonography showed optic nerve enlargement. Fluorescein angiography (FA) demonstrated vascular leakage at the ONH (hot disc) and a geographic patchy hypofluorescent area with speckled hyperfluorescent margins measuring approximately three disc diameters. Orbital and brain MRI with gadolinium revealed a retrobulbar nodular enhancing mass at the optic nerve–sclera junction. Oncology consultation was unremarkable.

Given concern for malignancy and the enhancing orbital nodule, the patient underwent transconjunctival lateral orbitotomy one week after presentation. Intraoperatively, a pink localized scleral nodule with edematous Tenon was identified. With a clinical diagnosis of nodular posterior scleritis, sub-Tenon triamcinolone acetonide was administered. The patient declined admission and intravenous corticosteroids; oral prednisolone 50 mg/Kg was initiated. Rheumatologic and infectious work-up, including PPD (tuberculosis), chest X-ray, serum ACE (sarcoidosis), and C-ANCA (Wegener granulomatosis), was unremarkable.

At the one-week postoperative follow-up, BCDVA was 20/20 OD and counting fingers at 2 meters OS. SRF had resolved, and the macula was atrophic. Oral prednisolone was tapered over three months.


A 25-year-old man went to the mouth clinic because he had painful canker sores on his lips. The outside of his lips had crusty scabs that hurt and bled easily. Inside his mouth, the inner parts of his upper and lower lips had red, sore, uneven patches. A blood test for the cold sore virus (HSV-1) was positive. The doctor said he had a condition called HAEM. His treatment included a steroid mouth paste (triamcinolone acetonide 0.1% in orabase), acyclovir pills, multivitamins, and salt-water (0.9% NaCl). He was also told to keep his mouth clean, avoid spicy and sour foods, and stop licking his lips.


A 27-year-old woman with familial adenomatous polyposis and multiple colorectal cancers underwent robot-assisted total proctocolectomy with complete lymph node dissection using the Hugo RAS system. The robotic work was organized into three steps: 1) in Trendelenburg position, ascending colon complete mesocolic excision up to the hepatic flexure; 2) descending colon complete mesocolic excision and total mesorectal excision with D3 lymph node dissection; and 3) in a flat position, central vessel ligation along the superior mesenteric artery. After undocking, the specimen was removed transanally. An ileal pouch was created through a small umbilical incision and then connected to the anus (ileal pouch–anal anastomosis). The operation lasted 632 minutes with minimal blood loss, and the postoperative course was uneventful.


A 59-year-old woman with secondary progressive multiple sclerosis developed a few weeks of blurry vision in both eyes shortly after starting levetiracetam for new seizures. Eye examination showed corneal edema in both eyes, confirmed by corneal topography. When the levetiracetam dose was reduced, her symptoms improved, and the drug was then stopped. On follow-up, both her vision and the corneal swelling returned to normal. She had no prior eye disease or family history of corneal problems, and changes to other medications did not help beforehand, supporting levetiracetam as the likely cause.


Who: A 27-year-old woman, 16 weeks pregnant. She has a blood problem called beta thalassemia major. She gets a blood transfusion every month. She stopped her iron-removing medicine because she is pregnant.

Main mouth problems: Her gums are swollen, red, soft, and bleed easily. She has bad breath. Her lips are very dry and peeling. There are deep spaces like pockets around her teeth that trap germs and cause pain all around her mouth. She had never seen a dentist before. Her blood test showed anemia and signs of an infection.

What the dentists called it: Swollen gums and long-term gum disease linked to pregnancy and her blood problem.

Care plan: Rinse the mouth with 3% hydrogen peroxide. Use a chlorine dioxide spray mouthwash. Take antibiotics. Get a professional teeth cleaning to remove hard buildup. Follow simple daily mouth-care steps at home. Keep getting monthly blood transfusions. Do not take the iron-removing medicine during pregnancy.

Result: After three months of care by a dental and medical team, her mouth got much better.


A 75-year-old woman in Western Ethiopia had a birth control loop in her womb for 40 years. She had lower belly pain after her periods had stopped. Doctors looked inside the vagina with a small tool. They saw part of the loop at the opening of the womb. They gently pulled it out with a soft clamp. She went home with pain medicine. She also took an antibiotic called doxycycline two times a day for 3 days.