Levodopa-resistant parkinsonism developing after ventriculoperitoneal shunting for obstructive hydrocephalus and improving after endoscopic third ventriculostomy, with specific consideration of brainstem morphology: illustrative case.

BACKGROUND: Parkinsonism has been reported in patients with obstructive hydrocephalus (OH) following ventriculoperitoneal shunting (VPS). While levodopa works well, some cases are drug resistant. A few case series have reported that endoscopic third ventriculostomy (ETV) is beneficial, though its mechanism remains unclear. The use of a pathophysiology-reflected marker can aid in the diagnosis and treatment strategy. The authors report a case of parkinsonism due to OH after VPS that improved after ETV in a patient taking levodopa, which was subsequently discontinued. OBSERVATIONS: A 52-year-old man who had undergone VPS for OH caused by aqueductal stenosis with a tectal tumor presented with severe consciousness disturbance due to acute hydrocephalus and levodopa-refractory parkinsonism after multiple episodes of shunt malfunction. Magnetic resonance imaging showed an elevation of the floor of the third ventricle. ETV was performed to stabilize the pressure imbalance across the stenosis, and his parkinsonism symptoms improved after long-term rehabilitation, resulting in levodopa discontinuation. His pontomesencephalic angle, the angle between the anterior surface of the midbrain and upper surface of the pons in the midline of the sagittal plane, was significantly decreased. LESSONS: The focus in such cases should be on the essence of the pathophysiology for improving the symptoms rather than on easy-to-understand indicators such as ventricle size. https://thejns.org/doi/10.3171/CASE2429.

Low-intensity pulsed ultrasound therapy promotes recovery from stroke by enhancing angio-neurogenesis in mice in vivo.

Since the treatment window of thrombolytic therapy for stroke is limited, new therapy remains to be developed. We have recently developed low-intensity pulsed ultrasound (LIPUS) therapy to improve cognitive dysfunction in mouse models of vascular dementia and Alzheimer's disease. Here, we further aimed to examine whether our LIPUS therapy improves neurological recovery from ischemic stroke, and if so, to elucidate the mechanisms involved. In a mouse model of middle cerebral artery occlusion (MCAO), we applied LIPUS (32 cycles, 193 mW/cm2) to the whole brain 3 times in the first week (days 1, 3, and 5) after MCAO. We evaluated neurological functions using behavioral tests and performed histological analyses. Furthermore, to elucidate how LIPUS works within the injured brain, we also tested the effects of LIPUS in endothelial nitric oxide synthase (eNOS)-deficient (eNOS-/-) mice. In wild-type mice, the LIPUS therapy markedly improved neurological functions in the tightrope and rotarod tests at 28 days after MCAO. Histological analyses showed that the LIPUS therapy significantly increased the numbers of CD31-positive blood vessels in the perifocal lesion and doublecortin (DCX)-positive neurons in the ischemic striatum, indicating the angio-neurogenesis effects of the therapy. Importantly, these beneficial effects of the LIPUS therapy were totally absent in eNOS-/- mice. No adverse effects of the LIPUS therapy were noted. These results indicate that the LIPUS therapy improves neurological functions after stroke through enhanced neuro-angiogenesis in mice in vivo in an eNOS-dependent manner, suggesting that it could a novel and non-invasive therapeutic option for stroke.