Sensitive Detection of Infratentorial and Upper Cervical Cord Lesions in Multiple Sclerosis with Combined 3D FLAIR and T2-Weighted (FLAIR3) Imaging.

BACKGROUND AND PURPOSE: Infratentorial and spinal cord lesions are important for diagnosing and monitoring multiple sclerosis, but they are difficult to detect on conventional MR imaging. We sought to improve the detection of infratentorial and upper cervical cord lesions using composite FLAIR3 images. MATERIALS AND METHODS: 3D T2-weighted FLAIR and 3D T2-weighted images were acquired in 30 patients with MS and combined using the FLAIR3 formula. FLAIR3 was assessed against 3D T2-FLAIR by comparing the number of infratentorial and upper cervical cord lesions per subject using the Wilcoxon signed rank test. Intrarater and interrater reliability was evaluated using the intraclass correlation coefficient. The number of patients with and without ≥1 visible infratentorial/spinal cord lesion on 3D T2-FLAIR versus FLAIR3 was calculated to assess the potential impact on the revised MS diagnostic criteria. RESULTS: Compared with 3D T2-FLAIR, FLAIR3 detected significantly more infratentorial (mean, 4.6 ± 3.6 versus 2.0 ± 1.8, P < .001) and cervical cord (mean, 1.58 ± 0.94 versus 0.46 ± 0.45, P < .001) lesions per subject. FLAIR3 demonstrated significantly improved interrater reliability (intraclass correlation coefficient = 0.77 [95% CI, 0.63-0.87] versus 0.60 [95% CI, 0.40-0.76] with 3D T2-FLAIR, P = .019) and a tendency toward a higher intrarater reliability (0.86 [95% CI, 0.73-0.93] versus 0.79 [95% CI, 0.61-0.89], P = .23). In our cohort, 20%-30% (47%-67%) of the subjects with MS had ≥ 1 infratentorial (cervical cord) lesion visible only on FLAIR3. CONCLUSIONS: FLAIR3 provides higher sensitivity than T2-FLAIR for the detection of MS lesions in infratentorial brain parenchyma and the upper cervical cord.

Indentation and Transverse Diameter of the Meckel Cave: Imaging Markers to Diagnose Idiopathic Intracranial Hypertension.

BACKGROUND AND PURPOSE: Clinical and imaging manifestations of idiopathic intracranial hypertension should prompt early diagnosis and treatment to avoid complications. Multiple diagnostic imaging criteria are reported to suggest the diagnosis of idiopathic intracranial hypertension with questionable sensitivity and/or specificity. Increased intracranial pressure results in dilation of the perineural cisternal spaces such as the optic nerve sheaths and the Meckel cave. It may also cause protrusion of cisternal structures of the Meckel cave through the skull base foramina, which could result in indentation or a bilobed appearance of the Meckel cave. We investigated the changes in the Meckel cave in patients with proved idiopathic intracranial hypertension versus healthy controls. MATERIALS AND METHODS: We studied 75 patients with a diagnosis of idiopathic intracranial hypertension and 75 age-and sex-matched healthy controls. The transverse diameter of Meckel cave was measured in the axial and coronal planes of T2-weighted MR imaging sequences, and comparison was made between the 2 groups. RESULTS: The mean diameters of the Meckel cave on the coronal T2 plane in patients with idiopathic intracranial hypertension were 5.21 ± 1.22 mm on the right side and 5.16 ± 0.90 mm on the left side, while in the control group, they measured 3.89 ± 0.62 mm and 4.09 ± 0.68 mm, respectively (P value < .001). Of 75 patients with an approved diagnosis of idiopathic intracranial hypertension, 57 (76%) showed an indented Meckel cave as opposed to 21 (28%) in the control group. CONCLUSIONS: Our results confirm for the first time that the shape and size of the Meckel cave can be used as sensitive and specific diagnostic imaging markers for the diagnosis of idiopathic intracranial hypertension.

Relationship of Physical Frailty to Phosphocreatine Recovery in Muscle after Mild Exercise Stress in the Oldest-Old Women.

BACKGROUND: Physical frailty is a clinical syndrome associated with aging and manifesting as slowness, weakness, reduced physical activity, weight loss, and/or exhaustion. Frail older adults often report that their major problem is "low energy", and there is indirect evidence to support the hypothesis that frailty is a syndrome of dysregulated energetics. We hypothesized that altered cellular energy production underlies compromised response to stressors in the frail. METHODS: We conducted a pilot study to assess muscle energetics in response to a mild isometric exercise challenge in women (n=30) ages 84-93 years. The frailty status was assessed by a validated physical frailty instrument. Localized phosphorus (P31) magnetic resonance spectroscopy with a 1.5T magnet was used to assess the kinetics of Phosphocreatine recovery in the tibialis anterior muscle following maximal isometric contraction for 30 seconds. RESULTS: Phosphocreatine recovery following exertion, age-adjusted, was slowest in the frail group (mean=189 sec; 95%CI: 150,228) compared to pre-frail (mean=152 sec; 95%CI: 107,197) and nonfrail subjects (mean=132 sec; 95%CI: 40,224). The pre-frail and frail groups had 20 sec (95%CI: -49,89) and 57 sec (95%CI: -31,147) slower phosphocreatine recovery, respectively, than the non-frail. This response was paralleled by dysregulation in glucose recovery in response to oral glucose tolerance test in women from the same study population. CONCLUSIONS: Impaired muscle energetics and energy metabolism might be implicated in the physical frailty syndrome.