Objective: To investigate intracranial cerebrospinal fluid (CSF) distribution in patients with a clinical diagnosis of idiopathic normal pressure hydrocephalus (INPH). Methods: 24 patients with a clinical diagnosis of INPH were studied. Control groups comprised 17 patients with secondary normal pressure hydrocephalus (SNPH), 21 patients with brain atrophy, and 18 healthy volunteers. Ventricular volume (VV) and intracranial CSF volume (ICV) were measured using a magnetic resonance based method and the VV/ICV ratio was calculated. Results: The SNPH group showed a marked increase in the VV/ICV ratio compared with the healthy volunteers (37.8% v 15.6%, p < 0.0001). The brain atrophy group showed a significant increase in ICV compared with the healthy volunteers (284.4 ml v 194.7 ml, p =0.0002). The INPH group showed an increase in ICV (281.2 ml, p = 0.0002) and an increase in the VV/ICV ratio (38.0%, p < 0.0001). Fifteen of 24 INPH patients underwent shunting; 11 improved and four did not. Conclusions:The results suggest that INPH patients have brain atrophy in addition to hydrocephalic features. This may help to explain the difficulties encountered in the diagnosis and the unpredictable response rate to shunt surgery in INPH patients.T he diagnosis and appropriate treatment of patients with cognitive decline, ataxia, and incontinence is not easy, as only a proportion will have idiopathic normal pressure hydrocephalus (INPH), 1-3 and many of these patients may also have early Alzheimer's disease or vascular dementia. Coexistent cerebrovascular disease or Alzheimer's disease is generally a predictor of poor outcome following CSF diversion. 5However, others have reported that despite vascular or Alzheimer changes in biopsy specimens from patients with clinically diagnosed INPH, some are still improved by shunting. 5 6 Indeed, several studies have suggested that vascular changes might play an important role in the pathophysiology of INPH in some patients. 7Secondary normal pressure hydrocephalus (SNPH), which is not uncommon after subarachnoid haemorrhage and other disorders, generally responds well to CSF diversion and may share some neuroradiological features with INPH.1 7 It would be very helpful, therefore, if we could explain the differences between INPH, SNPH, Alzheimer's disease, and vascular dementia in terms of quantitative diagnostic variables. We have reported that, using a magnetic resonance based cerebrospinal fluid (CSF) measurement method, an increase in the intracranial CSF volume is seen in patients with brain atrophy and a disproportionate increase in the ventricular CSF volume is seen in patients with hydrocephalus. 8 9 Our method is non-invasive and relatively easy to perform in elderly or uncooperative patients.Our aim in this study was to investigate intracranial CSF distribution in patients with suspected INPH in comparison with SNPH or brain atrophy. METHODS SubjectsWe studied 80 subjects, all of whom gave their informed consent. The INPH group included 24 of 41 patients with suspected INPH (11 ...

The fast inversion recovery (IR) technique was evaluated for the localization of gliomas. Fast IR imaging with real reconstruction and T 1 -weighted spin echo (SE) imaging before and after contrast administration were performed in 20 patients with gliomas. The tumor-to-white matter contrast ratio (TWCR), tumor-to-gray matter contrast ratio (TGCR), tumor-to-white matter contrast-to-noise ratio (TWCNR), and tumor-to-gray matter contrast-to-noise ratio (TGCNR) were calculated and compared. Fast IR imaging visualized tumors with significantly higher TWCR, TGCR, TWCNR, and TGCNR values (p º 0.01) than those for T 1 -weighted SE imaging. In particular, fast IR imaging clearly revealed seven nonenhanced tumors that were poorly visualized on T 1 -weighted SE imaging. Fast IR imaging showed a similar TGCR and significantly higher TWCR (p º 0.01) compared to T 1 -weighted SE imaging with contrast medium in 13 enhanced tumors. However, fast IR imaging showed similar TWCNR and lower TGCNR compared to T 1 -weighted SE imaging with contrast medium. The fast IR technique can discriminate tumors from normal cerebral tissues with high contrast and without the use of contrast medium. This technique is extremely useful for the localization of non-enhanced tumors.

These results suggest that patients with NPH have a unique intracranial CSF distribution, with an enlarged VV and a slightly increased ICV, resulting in a high VV/ICV ratio. Shunting led to dramatic improvement in our patients. It is likely that CSF measurement can provide valuable information in the management of patients with NPH.

Background: Intracranial hypotension is a disorder characterized by low cerebrospinal fluid (CSF) pressure typically caused by loss of CSF. Although some mechanisms account for the CSF leakage have been elucidated, spinal canal stenosis has never been reported as a pathological cause of intracranial hypotension. C1-C2 sign is a characteristic imaging feature, which indicates CSF collection between the spinous processes of C1 and C2, occasionally observed on magnetic resonance imaging (MRI) in patients with intracranial hypotension. Case presentation: A 58-year-old man was presented to our institute with complaints of posterior cervical pain persisting for 3 months, along with numbness and muscle weakness of extremities. A fat suppression T2-weighted image of MRI illustrated fluid collection in the retrospinal region at C1-C2 level, and an 111In-DTPA cisternoscintigram clearly revealed the presence of CSF leakage into the same region. The MRI also showed stenosis in spinal canal at C3/4 level, and a computed tomography (CT) myelogram suggested a blockage at the same level. We gave a diagnosis as intracranial hypotension due to the CSF leakage, which might be caused by the spinal canal stenosis at C3/4 level. Despite 72 h of conservative therapy, a brain CT showed the development of bilateral subdural hematomas. We, therefore, performed burr-hole drainage of the subdural hematoma, blood-patch therapy at C1/2 level, and laminoplasty at C3-4 at the same time. Improvement of symptoms and imaging features which suggested the CSF leak and subdural hematoma were obtained post-operatively. Conclusion: The present case suggested the mechanism where the CSF leakage was revealed as fluid collection in the retrospinal region at C1-C2 level. Increased intradural pressure due to the spinal canal stenosis resulted in dural tear. CSF leaked into the epidural space and subsequently to the retrospinal region at C1-C2 level, due to the presence of spinal canal stenosis caudally as well as the vulnerability of the tissue structure in the retrospinal region at C1-C2 level. Thus, our theory supports the mechanisms of previously reported CSF dynamics associated to C1-C2 sign, and also, we suggest spinal canal stenosis as a novel etiology of intracranial hypotension.

A method to visualize possible waste clearance pathway in the brain was proposed earlier. The method is based on an assumption that there exist water containing macromolecules along the clearance pathway, and this water can be visualized using T2 component analysis. Preliminary results of this method applied for Alzheimer patients, as well as healthy volunteers, are presented. Distinct differences between the patients and healthy volunteers were observed. It is expected that this method can be a powerful tool for understanding the patho-physiology of the Alzheimer disease.