Pseudoulnar palsy with concurrent wrist drop: case report.

Introduction and importance: Pseudoulnar palsy, characterized by weakness in the fourth and fifth digits, is a condition typically attributed to infarction of the medial aspect of the precentral gyrus's "hand knob." This anatomical site is located in the primary motor cortex of the brain, in the posterior lobe of the frontal cortex. This report presents a novel case of pseudoulnar nerve palsy in conjunction with wrist drop stemming from an infarction of the hand knob gyrus. Case presentation: A 78-year-old female with hypertension and hyperlipidemia experienced sudden right wrist weakness and impaired mobility in her fourth and fifth digits. Clinical examinations, including neuroimaging, supported the diagnosis of an infarction in the medial precentral gyrus. Brain MRI confirmed the diagnosis of an acute infarction in the medial precentral gyrus. The patient was treated with enoxaparin, aspirin, and dexamethasone, and was discharged after symptom improvement. Clinical discussion: Unlike the classical presentations, this case highlights the co-occurrence of ulnar and radial deficits following a unique infarction pattern. The distinct presentation of right pseudoulnar palsy with wrist drop was caused by an infarction at the level of the medial aspect of the hand knob. Conclusion: This case underscores the importance of considering the central causes of peripheral-like deficits, especially in older individuals with vascular risk factors, emphasizing the significance of early intervention in mitigating potential long-term consequences. This report contributes to the evolving understanding of central neurological presentations, and serves as a reminder of the need for a comprehensive diagnostic approach.

A recombinant herpes virus expressing influenza hemagglutinin confers protection and induces antibody-dependent cellular cytotoxicity.

Despite widespread yearly vaccination, influenza leads to significant morbidity and mortality across the globe. To make a more broadly protective influenza vaccine, it may be necessary to elicit antibodies that can activate effector functions in immune cells, such as antibody-dependent cellular cytotoxicity (ADCC). There is growing evidence supporting the necessity for ADCC in protection against influenza and herpes simplex virus (HSV), among other infectious diseases. An HSV-2 strain lacking the essential glycoprotein D (gD), was used to create ΔgD-2, which is a highly protective vaccine against lethal HSV-1 and HSV-2 infection in mice. It also elicits high levels of IgG2c antibodies that bind FcγRIV, a receptor that activates ADCC. To make an ADCC-eliciting influenza vaccine, we cloned the hemagglutinin (HA) gene from an H1N1 influenza A strain into the ΔgD-2 HSV vector. Vaccination with ΔgD-2::HAPR8 was protective against homologous influenza challenge and elicited an antibody response against HA that inhibits hemagglutination (HAI+), is predominantly IgG2c, strongly activates FcγRIV, and protects against influenza challenge following passive immunization of naïve mice. Prior exposure of mice to HSV-1, HSV-2, or a replication-defective HSV-2 vaccine (dl5-29) does not reduce protection against influenza by ΔgD-2::HAPR8 This vaccine also continues to elicit protection against both HSV-1 and HSV-2, including high levels of IgG2c antibodies against HSV-2. Mice lacking the interferon-α/ß receptor and mice lacking the interferon-γ receptor were also protected against influenza challenge by ΔgD-2::HAPR8 Our results suggest that ΔgD-2 can be used as a vaccine vector against other pathogens, while also eliciting protective anti-HSV immunity.