The cofactors potentially affecting exercise performance after COVID-19 are still incompletely investigated. The contribution of several clinical and demographic variables to the exercise capacity measured with the 6-min walk test was assessed in multivariable analyses that used the absolute distance walked in 6 min (6MWD) and an impaired performance (6MWD < 60% of the predicted value) as study outcomes. The variables considered were age, sex, preexisting comorbidities, COVID-19 severity, pandemic phase, treatments administered in acute phase, SARS-CoV-2 vaccination, reinfection, time from acute infection, and presence of 30 persisting symptoms. The mean 6MWD recorded among 686 patients at a mean interval of 184 days from COVID-19 was 474 m, with 8.3% of them presenting values below 60% of the predicted value. 6MWD was affected by sex, comorbidities, COVID-19 severity, and some persisting symptoms. The estimated effect sizes were -29.9 m for severe/critical acute disease, between -26 and -87 m for six comorbidities (atrial fibrillation, renal failure, chronic liver disease, chronic pulmonary disease, ischemic heart disease, diabetes) and between -21 and -99 m for four persisting symptoms (nausea/vomiting, paresthesia, depressed mood, dyspnea). The 6MWD increased by 2.6 m per month elapsed from acute infection. A 6MWD < 60% was associated with female sex, more intensive respiratory support, four comorbidities (atrial fibrillation, renal failure, chronic pulmonary disease and ischemic heart disease), and two persisting symptoms (nausea/vomiting and palpitations/tachycardia). Exercise performance after COVID-19 is affected by multiple factors, with estimated effect sizes that are clinically relevant. The results also suggest some spontaneous improvement over time.

The inferior alveolar nerve (IAN) is a sensory branch of the mandibular nerve that supplies sensation to teeth, the chin, and the lower lip. IAN injuries often result from trauma or iatrogenic causes, leading to the development of symptoms like difficulty in eating, smiling, pain, and paraesthesia. IAN regeneration is limited because of the confinement of the nerve within the mandibular canal. Current pharmacological and surgical interventions offer only partial recovery. Therefore, alternative approaches to enhance nerve repair and regeneration are required. To address this limitation, we developed a 3D-bioprinted scaffold composed of alginate, methylcellulose, and Schwann cell-derived acellular matrix (Alg/MC/ACM) for IAN regeneration. The Alg/MC hydrogel showed good mechanical stability and printability, and ACM provides biological cues for nerve regeneration. Proteomics analysis showed that there were 904 common proteins present when the Schwann cell lysate was compared with ACM. The rheological analysis demonstrated shear-thinning and viscoelastic properties of the Alg/MC/ACM hydrogel. In vitro cytocompatibility tests, such as MTT and Live/Dead assays using rat Schwann (RSC96) cells and neuronal (PC12) cells, demonstrated that Alg/MC/ACM2 significantly enhanced cell proliferation and viability when compared to Alg/MC and Alg/MC/ACM1 scaffolds. In vivo study in SD rat IAN crush injury model demonstrated that implantation of Alg/MC/ACM2 scaffolds improved the behavioral response when compared with injury control. Alg/MC/ACM2 scaffolds also promoted cellular infiltration, axonal organization, and remyelination, as observed in hematoxylin and eosin and Luxol fast blue staining. Overall, the incorporation of Schwann-cell-derived ACM within Alg/MC scaffolds provided a bioactive microenvironment that supported neural regeneration. This study presents the first evidence demonstrating the potential of Alg/MC/ACM bioprinted scaffolds as promising therapeutic strategies for IAN repair.

Severe hypokalemia is a common electrolyte disorder with a broad spectrum of etiologies. We report the case of a 44-year-old woman admitted to the emergency department with nausea, vomiting, chills, and chronic diffuse paresthesia. On admission, the patient was hypertensive. Laboratory evaluation revealed profound hypokalemia (2.3 mmol/L), severe hypophosphatemia, metabolic alkalosis, and electrocardiographic abnormalities, including U waves and a prolonged corrected QT interval, a key marker of severity associated with a high risk of life-threatening arrhythmias. Further investigations demonstrated inappropriate renal potassium wasting in the setting of suppressed plasma renin and aldosterone levels. A detailed dietary history uncovered the excessive consumption of licorice tea, approximately 2 L daily over a year, leading to the diagnosis of licorice-induced pseudo-hyperaldosteronism. In this context, associated electrolyte disturbances, including hypophosphatemia and hypomagnesemia, are likely secondary to mineralocorticoid receptor activation and renal tubular losses rather than a direct effect of licorice. The patient required admission to the intensive care unit for aggressive potassium repletion and antihypertensive therapy. Following cessation of licorice intake, electrolyte abnormalities and blood pressure gradually normalized. This case highlights the critical importance of obtaining a thorough dietary history in patients with unexplained severe hypokalemia. Although uncommon, licorice intoxication represents a reversible cause that can be rapidly corrected with appropriate recognition and management. It also underscores the prognostic significance of QTc prolongation in severe electrolyte disturbances and the need for prompt cardiac monitoring.

Guillain-Barré syndrome (GBS) is an acute immune-mediated polyneuropathy marked by rapidly progressive, symmetrical paralysis, paresthesia, and hypo-/areflexia. Early recognition and management are crucial as the condition can rapidly become life-threatening. We report a healthy 51-year-old man who presented to a physician in Reyðarfjörður, eastern Iceland, with symmetrical hand weakness and paresthesia. Within 24 hours, weakness progressed to all four limbs. The patient was transferred by air ambulance to Akureyri where GBS was clinically diagnosed and intravenous immunoglobulin therapy was initiated. Nerve conduction study confirmed acute motor axonal neuropathy, a GBS variant. Treatment halted progression, and the patient is undergoing rehabilitation.

Leprosy or Hansen's disease is an infectious disease caused by the intracellular organism Mycobacterium leprae (M. leprae). The disease has a low prevalence in the United States and follows an indolent course with symptoms often manifesting several years after initial exposure. Reaching a diagnosis of Hansen's disease can often be challenging in a non-endemic setting. Additionally, reaching a diagnosis in the absence of skin symptoms is difficult, as the diagnostic method that provides the most clinical reliability is a skin biopsy or slit skin smear (SSS). Through this skin test, the acid-fast bacillus M. leprae is visualized. We present a case of a 55-year-old woman from California who initially presented with neuropathy and continued to suffer from three years of progressive sensory and motor neuropathies before the diagnosis of Hansen's disease. She lived in a non-endemic setting but was likely exposed through her work in medical tourism in Playa del Carmen, Mexico. A diagnosis was ultimately reached once she presented with skin lesions that allowed for a biopsy. This case also highlights the challenge in reaching a timely diagnosis of Hansen's disease, which, due to its low prevalence in North America, can often be overlooked in a differential diagnosis.

Here, we report the case of a 65-year-old man who presented to the emergency department with paresthesia, psychomotor retardation, and dysarthria. Contrast-enhanced brain MRI revealed a solitary, contrast-enhancing mass in the right head of the caudate nucleus with extensive perifocal edema, raising a primary differential diagnosis of glioblastoma versus metastasis, among other possibilities. Prior to surgical removal of the suspected glioblastoma, the patient underwent additional diffusion tensor imaging and research MRI, including multifrequency magnetic resonance elastography (MRE) to generate mechanical property maps of stiffness and tissue viscosity and to potentially differentiate between glioma, brain metastases, and benign masses based on tissue biomechanical properties. MRE revealed abnormally high values of stiffness and viscosity-a mechanical signature known to be associated with brain metastases or meningioma, but not glioblastoma, which typically exhibits soft tissue properties with reduced viscous dissipation. Histopathologic evaluation confirmed MRE by revealing a distant metastasis of squamous cell carcinoma, the primary tumor of which was detected by PET-CT within the right hilus of the lung. This case demonstrates the diagnostic value of the biomechanical properties of brain tumors and raises the prospect of applying MRE as an easy-to-use MRI contrast that can rule out glioma when the suspicious lesion exhibits stiff-viscous material properties.

The coexistence of Guillain-Barré syndrome with a spinal cord syrinx is extremely rare. This report presents the emergency admission of a 57-year-old female presenting with an abrupt and progressive loss of motor function and abnormal sensation in her lower extremities. MRI of the cervical spine revealed a syrinx extending from C2 to C7. Neurology referred the case to neurosurgery, who assessed the patient and recommended nonoperative and supportive treatment given the size of the syrinx and the patient's status as a poor surgical candidate. She was subsequently discharged to a local extended care facility (ECF) with a diagnosis of syringomyelia. Despite physical therapy and rehabilitation, her symptoms progressed to include loss of motor function in bilateral lower extremities, worsening paresthesia in bilateral upper and lower extremities, and progressive dyspnea. Nerve conduction studies performed during neurologic evaluation at the ECF demonstrated a sensorimotor demyelinating polyneuropathy, and she was urgently transferred to the emergency department, where Guillain-Barré syndrome was confirmed. The patient developed respiratory failure requiring mechanical ventilation and was treated with intravenous immunoglobulin. Although she experienced transient stabilization, her clinical course was complicated by progressive functional decline. This case highlights how a cervical syrinx may obscure the initial presentation of Guillain-Barré syndrome, contributing to delayed treatment, and demonstrates the importance of maintaining a broad differential diagnosis in patients with atypical or overlapping neurologic findings.

BACKGROUND Copper deficiency-an underrecognized cause of anemia, neutropenia, and neuropathy-can mimic myelodysplastic syndrome (MDS), particularly in patients with prior bariatric surgery or excess zinc exposure. Recognition is critical because hematologic and neurologic manifestations may resemble clonal bone marrow disorders but are potentially reversible with appropriate treatment. CASE REPORT A 58-year-old woman with prior Roux-en-Y gastric bypass displayed progressive fatigue, exertional dyspnea, and distal paresthesias. Laboratory evaluation revealed severe hypoproliferative anemia (hemoglobin 5.8 g/dL) and neutropenia (absolute neutrophil count 980/µL; nadir <500/µL). Peripheral smear showed anisopoikilocytosis and pseudo-Pelger-Huët-like changes, suggesting MDS. Subsequently, the patient developed febrile neutropenia and coronavirus disease 2019. Vitamin B12 (910 pg/mL) and folate (6.8 ng/mL) levels were normal. Hemolysis markers were not significantly elevated (lactate dehydrogenase 149 U/L, haptoglobin 205 mg/dL). Serum copper was below 10 µg/dL (reference, 77-206 µg/dL), ceruloplasmin was below 60 mg/L (reference, 200-600 mg/L), and serum zinc was elevated (130 µg/dL [reference, 60-106 µg/dL]). Bone marrow biopsy showed preserved trilineage hematopoiesis without increased blasts, supporting a nutritional etiology. Further assessment revealed nonadherence to recommended multivitamin and mineral supplementation, along with chronic excessive use of zinc-containing denture adhesive. The patient received intravenous followed by oral copper supplementation and underwent discontinuation of zinc exposure, resulting in rapid hematologic improvement and partial resolution of neurologic symptoms. CONCLUSIONS Copper deficiency should be considered in patients with unexplained cytopenias and neurologic symptoms, especially after bariatric surgery or under chronic zinc exposure. With early recognition, this condition is reversible; patients can avoid unnecessary evaluation, misdiagnosis, and complications.