Background: Calvarial bone thinning is a rare clinical entity, with only several cases reported (including Gorham-Stout disease), but the cause is often unknown. Here, we report such a case of unilateral calvarial thinning with an unknown cause. Case Description: A 77-year-old woman undergoing imaging examination for unruptured cerebral aneurysms for the past several years noticed a progressive cranial deformity. Computed tomography revealed progressive thinning of the right parietal bone and cranial deformity but laboratory tests showed no causative findings. A cranioplasty was performed to protect the brain and confirm the pathology. Grossly, pigmentation and deformity were observed on the outer plate of the bone but the inner plate was intact. Pathological examination revealed preserved bone cells and no necrosis. In addition, there were no findings of vascular hyperplasia or malignancy. It appeared that localized osteoporosis had occurred, mainly in the outer plate of the bone, but the cause was unclear. Conclusion: Progressive focal calvarial thinning is rarely reported and the mechanism in this case was unknown. It is important to determine the cause of the bone thinning to evaluate the need for surgical intervention from the viewpoint of brain protection and prevention of cerebrospinal fluid leakage.

Background: Diseases presenting with only downward gaze palsy are extremely rare particular in cerebral hemorrhage. Case Description: A 63-year-old man with no medical history developed a downward-dominant vertical gaze paralysis with a convergence disorder. Computed tomography and magnetic resonance imaging showed a small hemorrhage of 13 mm in diameter in the right midbrain tegmental area. The patient was conservatively treated. His symptoms showed a gradual improvement from upward gaze paralysis and convergence disorder followed by downward gaze paralysis. All symptoms disappeared in 3 weeks after the onset. The center of vertical eye movement was thought to be the rostral interstitial nucleus of medial longitudinal fasciculus (riMLF) and posterior commissure (PC). Conclusion: In this case, bilateral riMLF and PC were impaired, resulting in bilateral vertical ocular motility disorder with upward gaze paralysis. Brainstem hemorrhage rarely presents with vertical gaze palsy. Most are cerebral infarctions, and few are due to cerebral hemorrhage. This case was important for better understanding the pathophysiology of an ocular motility disorder. We also summarized the characteristics of isolated vertical gaze palsy caused by cerebral hemorrhage.