RESUMEN
Background: The provision of healthcare services in Iraq has been negatively affected by a lack of resources, strained healthcare infrastructure, and low patient socioeconomic status. This paper describes a case of multiple intracranial aneurysms (MIAs) that highlight the challenges of practicing vascular neurosurgery in Iraq. Case Description: A 57-year-old female presented with sudden-onset severe headache, photophobia, and drowsiness and was diagnosed with subarachnoid hemorrhage in the basal cistern. Despite international guidelines recommending urgent treatment for suspected ruptured intracranial aneurysms, the patient's healthcare team in Babylon advised against a CT angiogram (CTA). The patient's family took responsibility for transferring her to a private facility for a CTA, which showed four aneurysms. Due to financial constraints, the family opted for open surgery, during which a ruptured aneurysm was found and successfully managed. The remaining two aneurysms were monitored with serial follow-up imaging. Conclusion: The case highlights the challenges of practicing vascular neurosurgery in Iraq and the impact of financial constraints on the management of MIA. It emphasizes the need for increased resources and expertise in the country's healthcare system to provide optimal care for patients with life-threatening conditions.
RESUMEN
Growing evidence has established that a subset of dopamine (DA) neurons co-release glutamate and express vesicular glutamate transporter 2 (VGLUT2). VGLUT2 expression in DA neurons plays a key role in selective vulnerability to DA neurodegeneration in Parkinson's disease (PD). In this review, we summarize recent findings on impacts of VGLUT2 expression and glutamate co-release from DA neurons on selective DA neuron vulnerability. We present evidence that DA neuron VGLUT2 expression may be neuroprotective, boosting DA neuron resilience in the context of ongoing neurodegenerative processes in PD. We highlight genetic and pesticide models of PD that have provided mechanistic insights into selective DA neuron vulnerability. Finally, we discuss potential neuroprotective mechanisms, focusing on roles of VGLUT2 and glutamate in promoting mitochondrial health and diminishing oxidative stress and excitotoxicity. Elucidating these mechanisms may ultimately lead to more effective treatments to boost DA neuron resilience that can slow or even prevent DA neurodegeneration.