A neural basis of rational inattention models: consistency of cognitive cost with the mutual information criterion.

The rational inattention model has recently attracted much attention as a promising candidate to model bounded rationality in the research field of decision-making and game theory. However, in contrast to this energetic promotion of the theoretical works, empirical verification of the validity of the RI model has not progressed much. Furthermore, to our knowledge, the central assumption of the RI model, that the amount of mutual information obtained from signals adequately represents the cognitive cost of information, has not been tested from a neuroscientific perspective. The purpose of the present study was to test whether the amount of mutual information adequately represents the cognitive cost of information from a neuroscientific perspective. We proposed a sequential investment task, in which the two main models of RI can be treated simultaneously in a more realistic experimental environment. We used a model-fitting approach to analyze the subjective information cost, and compared the model parameters representing the information cost with the concentration of oxidized hemoglobin in the brain blood. Our results showed that the cost parameter λ of the stochastic choice type model, which fits the behavioral data of the present experiment better than the Kalman filter type model, was significantly positively correlated with the activation status of the rostral prefrontal cortex and dorsolateral prefrontal cortex. The cognitive cost represented by the amount of mutual information employed in the RI model is consistent with the activation of brain regions associated with cognitive cost, and, thus, indirectly supports the assumption of the RI model.

Repeated cerebellar infarction in the affected nondominant vertebral artery distribution with reversible vertebral artery occlusion elicited by head tilt: illustrative case.

BACKGROUND: Bow hunter's syndrome or stroke (BHS) is characterized by rotational vertebrobasilar insufficiency elicited by rotation of the neck. It is caused by dynamic and reversible occlusion of the vertebral artery (VA). Reversible symptoms of rotational vertebrobasilar insufficiency are described as bow hunter's syndrome, although brain infarction is rarely reported as bow hunter's stroke. OBSERVATIONS: A 70-year-old man experienced repeated cerebellar infarctions three times in the posterior inferior cerebellar artery (PICA) distribution of the nondominant right VA connecting the basilar artery. The onset of symptoms indicating cerebellar infarcts and the patient's head position changes were unrelated. Dynamic digital angiography (DA) revealed that the nondominant right VA was occluded by an osteophyte from the C4 vertebral body, and the right PICA branches were shown to be passing through the distal right VA from the left VA. These findings were observed when the patient's head was tilted to the right. An arterio-arterial embolic mechanism was suggested as the cause of repeated cerebellar infarctions. LESSONS: Transient nondominant VA occlusion has been rarely reported as a cause of BHS when the head is tilted. To confirm the diagnosis of BHS, additional head tilt is recommended when performing dynamic DA in patients with a cervical osteophyte.

Fluid structure interaction analysis reveals facial nerve palsy caused by vertebral-posterior inferior cerebellar artery aneurysm.

Cranial nerve palsy caused by aneurysmal compression has not been fully evaluated. The main causes of symptoms are considered to be direct mechanical compression and aneurysm pulsations. Recent studies indicate that nerve dysfunction is mainly induced by pulsation rather than by direct compression, and successful cases of endovascular surgery have been reported. We describe a patient with an unruptured vertebral artery-posterior inferior cerebellar artery (VA-PICA) aneurysm compressing the facial nerve at the root exit zone (REZ). The patient presented with peripheral facial nerve palsy but not hemifacial spasm and was successfully treated by coil embolization. To investigate the mechanisms underlying peripheral facial nerve palsy, fluid structure interaction (FSI) analysis can approximate displacement and the magnitude of aneurysmal wall motion due to hemodynamic forces. In our case, maximum mesh displacement was observed at the aneurysmal wall attached to the facial nerve inside the pons rather than the REZ, which explains the clinical manifestation of facial nerve palsy in the absence of hemifacial spasm. This preliminary report demonstrates the utility of FSI analysis for investigating cranial nerve neuropathy.

Myxoid chondrosarcoma in the pineal region.

The authors report a case of a myxoid chondrosarcoma of the pineal region in a 37-year-old woman who presented with an intratumoral hemorrhage. Partial removal of the tumor in an initial surgery resulted in failure to establish a definitive diagnosis. The residual tumor enlarged after a second intratumoral hemorrhage 14 months after the onset of the first symptoms, and gross-total resection of the tumor was achieved in a second surgery. Histological and immunohistochemical findings after the second surgery were consistent with a diagnosis of myxoid chondrosarcoma. Radical excision of a tumor was considered to play an important role in the management of intracranial myxoid chondrosarcoma.

Unusual giant cerebral venous varix associated with brain abscess: variant of hereditary hemorrhagic telangiectasia--case report.

A 35-year-old man suffered secondary generalized tonic-clonic convulsions due to a large brain abscess. Neuroimaging incidentally revealed another tumor-like lesion. Cerebral angiography confirmed that the lesion was an unusual giant venous varix associated with a high-flow pial arteriovenous fistula (AVF) and showed one more small arteriovenous malformation (AVM). Pulmonary AVF, which can cause brain abscess, was also detected. Surgical ligation of the AVF and removal of the small AVM via individual craniotomies resulted in successful extirpation of the cerebrovascular malformations. Although the typical mucocutaneous symptoms were absent in this patient, the combination of arteriovenous anomalies was highly suggestive of hereditary hemorrhagic telangiectasia.