Pituitary apoplexy mimicking meningitis.

Pituitary apoplexy is a rare but life-threatening disorder. Clinical presentation of this condition includes severe headaches, impaired consciousness, fever, visual disturbance, and variable ocular paresis. The clinical presentation of meningeal irritation is very rare. Nonetheless, if present and associated with fever, pituitary apoplexy may be misdiagnosed as a meningitis. We experienced a case of pituitary apoplexy masquerading as a meningitis. A 42-year-old man presented with meningitis associated symptoms and initial imaging studies did not show evidence of intra-lesional hemorrhage in the pituitary mass. However, a follow-up imaging after neurological deterioration revealed pituitary apoplexy. Hereby, we report our case with a review of literatures.

Reconstructive stent-buttressed coil embolization of a traumatic pseudoaneurysm of the supraclinoid internal carotid artery.

It is critical that traumatic intracranial pseudoaneurysms should be removed completely from the parent artery because there is a possibility of significant morbidity and mortality from the high risk of rebleeding from any remnants of the pseudoaneurysm. However, the deconstruction of the parent artery has the risk of ischemic damage to the distal to the trapped artery. We describe a case of a successful reconstructive stent-buttressed coil embolization in a patient with a traumatic pseudoaneurysm of the intracranial internal carotid artery. A 30-year-old man with a stuporous mentality was admitted to our institution after a traffic accident. The initial computed tomography scan showed a diffuse subarachnoid hemorrhage and a pseudoaneurysm of the left supraclinoid internal carotid artery. A reconstructive endovascular treatment using stent-assisted coil embolization with a stent-within-a-stent technique was conducted in order to save carotid blood flow. The pseudoaneurysm was completely obliterated and the patient recovered without any neurological deficit. We suggest that multiple stent placements with coiling may be considered as a treatment option for intracranial traumatic pseudoaneurysms as a reconstructive treatment.

Thromboxane A2 synthetase inhibitor plus low dose aspirin : can it be a salvage treatment in acute stroke beyond thrombolytic time window.

OBJECTIVE: There is no proven regimen to reduce the severity of stroke in patients with acute cerebral infarction presenting beyond the thrombolytic time window. Ozagrel sodium, a selective thromboxane A2 synthetase inhibitor, has been known to suppress the development of infarction. The antiplatelet effect is improved when aspirin is used together with a thromboxane synthetase inhibitor. METHODS: Patients with non-cardiogenic acute ischemic stroke who were not eligible for thrombolysis were randomly assigned to two groups; one group received ozagrel sodium plus 100 mg of aspirin (group 1, n=43) and the other 100 mg of aspirin alone (group 2, n=43). Demographic data, cardiovascular risk factors, initial stroke severity [National Institute of Health Stroke Scale (NIHSS) and motor strength scale] and stroke subtypes were analyzed in each group. Clinical outcomes were analyzed by NIHSS and motor strength scale at 14 days after the onset of stroke. RESULTS: There were no significant differences in the mean age, gender proportion, the prevalence of cardiovascular risk factors, stroke subtypes, and baseline neurological severity between the two groups. However, the clinical outcome for group 1 was much better at 14 days after the onset of stroke compared to group 2 (NIHSS score, p=0.007, Motor strength scale score, p<0.001). There was one case of hemorrhagic transformation in group 1, but there was no statistically significant difference in bleeding tendency between two groups. CONCLUSION: In this preliminary study, thromboxane A2 synthetase inhibitor plus a low dose of aspirin seems to be safe and has a favorable outcome compared to aspirin alone in patients with acute ischemic stroke who presented beyond the thrombolytic time window.

New understanding of the role of cerebrospinal fluid: offsetting of arterial and brain pulsation and self-dissipation of cerebrospinal fluid pulsatile flow energy.

Many theories have been postulated to date regarding the mechanisms involved in the absorption of the intracranial arterial blood flow energy in the intracranial space, but it is as yet nor clearly defined. The blood flow energy that is transmitted from the heart formulates the cerebrospinal fluid (CSF) pulsatile flow, and is known to constitute the major energy of the CSF flow, while the bulk flow carries only small energy. The intracranial space that is enclosed in a solid cranium and is an isolate system as in the Monroe-Kellie doctrine, and the authors propose to re-analyze the Monroe-Kellie doctrine concept in terms of energy transfer and dissipation of the Windkessel effect. We propose that the large blood flow energy that initiates in the heart is transferred in order of precedence to the arteries, arterioles, brain parenchyma, and finally to CSF within the cranium, in which the energy is confined and unable to be transferred, so that the final transfer of energy to the CSF pulsatile flow is self-dissipated in terms of direction and chronology in CSF pulsatile flow. In order for the CSF pulsatile flow that is transferred from arterial blood flow energy to be dissipated in the intracranial space, this cannot be explained with bulk flow energy in any perspective, since the pulsatile flow kinetic energy is greater than the bulk flow kinetic energy by at least a 100-fold. The pulsatile flow energy within the closed intracranial space cannot be transferred and is confined, as postulated by the Monroe-Kellie doctrine, and therefore the authors propound that the pulsatile flow dissipates by itself. The dissipation of the CSF pulsatile flow kinetic energy will be in all directions in a diffuse and random manner, and is offset by the CSF flow energy vector due to the CSF mixing process. Such energy dissipation will lead to maintenance of low CSF flow energy, which will result in maintaining low intracranial pressure (ICP), and sufficient brain perfusion. It is our opinion that our hypothesis will be able to explain the decreasing offsetting effect of arterial pulsation in chronic obstructive hydrocephalus, and the mechanisms for the ventricular dilatation in communicating hydrocephalus without changes in the mean ICP, and therefore highly justifying our hypothesis.