Abstract. Patients with rickettsial infection may present with encephalitis or meningitis but neurologic involvement is rare in murine typhus. Here, we report two patients with Rickettsia typhi meningitis who presented with cranial neuropathy, presumably caused by two distinct disease processes. Recognition of the disease manifestations is important because rickettsial infections are potentially associated with significant morbidity. Simple effective treatments are available.

Orbital apex syndrome (OAS) is an uncommon disorder characterized by visual loss, ophthalmoplegia, ptosis and hypoaesthesia of the forehead[1]. OAS may result from a variety of inflammatory, infectious, neoplastic and vascular conditions that cause damage to the superior orbital fissure (with resultant oculomotor (III), trochlear (IV), abducens (VI) and ophthalmic branch of the trigeminal nerve (V1) palsies) and to the optic canal leading to optic nerve (II) dysfunction. This case report describes the clinical development of OAS in a patient with bacterial sphenoid sinusitis.LEARNING POINTSOrbital apex syndrome (OAS) is an uncommon manifestation of a wide range of disease entities, with management ranging from antibiotic therapy to immunosuppression and surgery.OAS can be life-threatening if there is disease invasion through ophthalmic vessels or bone fissures, leading to intra-cranial involvement.Without adequate knowledge and clinical suspicion, OAS can be easily missed or misdiagnosed, resulting in delayed treatment and devastating loss of function or even death.

BACKGROUND Compared to patients with hypertension only (HTN), those with hypertension and diabetes (HTN/DM) have worse prognosis. We aimed to characterize morphological differences between HTN and HTN/DM using cardiovascular magnetic resonance (CMR); and compare differentially expressed proteins associated with myocardial fibrosis using high throughput multiplex assays. METHODS Asymptomatic patients underwent CMR: 438 patients with HTN (60+/-8 years; 59% males) and 167 age- and sex-matched patients with HTN/DM (60+/-10 years; 64% males). Replacement myocardial fibrosis was defined as non-ischemic late gadolinium enhancement on CMR. Extracellular volume (ECV) fraction was used as a marker of diffuse myocardial fibrosis. A total of 184 serum proteins (Olink Target CVD II and III panels) were measured to identify unique signatures associated with myocardial fibrosis in all patients. RESULTS Despite similar left ventricular (LV) mass (P=0.344) and systolic blood pressure (P=0.086), patients with HTN/DM had increased concentricity and worse multi-directional strain (P<0.001 for comparison of all strain measures) compared to HTN only. Replacement myocardial fibrosis was present in 28% of patients with HTN/DM compared 16% of those with HTN (P<0.001). NT-proBNP was the only protein differentially upregulated in HTN patients with replacement myocardial fibrosis and independently associated with ECV. In patients with HTN/DM, GDF-15 was independently associated with replacement myocardial fibrosis and ECV. Ingenuity Pathway Analysis demonstrated a strong association between increased inflammatory response/immune cell trafficking and myocardial fibrosis in patients with HTN/DM. CONCLUSIONS Adverse cardiac remodeling was observed in patients with HTN/DM. The novel proteomic signatures and associated biological activities of increased immune and inflammatory response may partly explain these observations.

Meralgia paresthetica (MP) is a condition characterised by abnormal sensations on the anterolateral aspect of the thigh due to the dysfunction of the lateral femoral cutaneous nerve. Here, I present a case of a 64-year-old female cook who attended the General Medicine clinic with 2 months of persistent numbness and ‘burning’ sensation over the right anterolateral thigh. Subsequent physical examination revealed the diagnosis of meralgia paresthetica. The significance of good history taking and thorough physical examination in reaching the diagnosis of meralgia paresthetica cannot be overemphasized. In most typical presentations, advanced imaging and neurodiagnostic testing do not add value to confirm the diagnosis. If the clinical diagnosis is doubtful, nerve conduction study and magnetic resonance imaging may still be performed to exclude other mimicking pathologies. Increasing awareness of MP among doctors unfamiliar with this condition will prevent the ordering of excessive investigations.

Neuronal intranuclear inclusion disease is a rare genetic condition, previously diagnosed only at postmortem, but its characteristic radiological features now allow its diagnosis in life. The clinical presentation is variable and we hope this case report will raise awareness of this condition.