Peak Resembling N-acetylaspartate (NAA) on Magnetic Resonance Spectroscopy of Brain Metastases.

Background and Objectives: Differentiating between a high-grade glioma (HGG) and solitary cerebral metastasis presents a challenge when using standard magnetic resonance imaging (MRI) alone. Magnetic resonance spectroscopy (MRS), an advanced MRI technique, may assist in resolving this diagnostic dilemma. N-acetylaspartate (NAA), an amino acid found uniquely in the central nervous system and in high concentrations in neurons, typically suggests HGG over metastatic lesions in spectra from ring-enhancing lesions. This study investigates exceptions to this norm. Materials and Methods: We conducted an MRS study on 49 histologically confirmed and previously untreated patients with brain metastases, employing single-voxel (SVS) techniques with short and long echo times, as well as magnetic resonance spectroscopic imaging (MRSI). Results: In our cohort, 44 out of 49 (90%) patients demonstrated a typical MR spectroscopic profile consistent with secondary deposits: a Cho peak, very low or absent Cr, absence of NAA, and the presence of lipids. A peak at approximately 2 ppm, termed the "NAA-like peak", was present in spectra obtained with both short and long echo times. Among the MRS data from 49 individuals, we observed a peak at 2.0 ppm in five brain metastases from mucinous carcinoma of the breast, mucinous non-small-cell lung adenocarcinoma, two metastatic melanomas, and one metastatic non-small-cell lung cancer. Pathohistological verification of mucin in two of these five cases suggested this peak likely represents N-acetyl glycoproteins, indicative of mucin expression in cancer cells. Conclusions: The identification of a prominent peak at 2.0 ppm could be a valuable diagnostic marker for distinguishing single ring-enhancing lesions, potentially associated with mucin-expressing metastases, offering a new avenue for diagnostic specificity in challenging cases.

Evolution of acute "black hole" lesions in patients with relapsing-remitting multiple sclerosis.

OBJECTIVE: Gadolinium-enhanced T1-weighted lesions are a well-established marker of areas with acute inflammatory activity. A majority of these gadolinium-enhanced T1 lesions are isointense relative to the surrounding white matter, but 20-40% of such active lesions will evolve during one year into areas of low signal ("black hole"). This study sought to characterize evolution of "black hole" lesions in patients with relapsing-remitting multiple sclerosis (MS) using the magnetic resonance imaging (MRI), which measures active lesions via the count of new or enlarged T2 and gadolinium-enhanced T1-weighted lesions. MATERIALS AND METHODS: This was a prospective, observational case-series study which utilized pre- and post-gadolinium contrast T1-weighted and Proton density MRI scans. Twenty-nine patients (8 males and 21 females) with average age of 38.86 ± 6.58 years and disease duration of 5.75 ± 7.00 years were used to analyze 196 acute demyelinating plaques detected on MRI images during the 24-month follow-up of post-gadolinium signal intensity enhancement of MS plaques. RESULTS: Significant difference in black hole development was found between the shapes of acute and chronic "black holes". Ring-shaped and patchy plaques were 4.09 (1.87-8.91) times more likely and 1.49 (0.71-3.12) times less likely to develop an acute "black holes" than homogeneous plaques, respectively. Acute plaques with higher lesion-to-CSF SI ratio and larger surface area showed a greater tendency to develop into acute and chronic "black holes". CONCLUSIONS: The value of lesion-to-CSF SI ratio and surface area were found as the predictors of the "black hole" formation.

Clinical characteristics and outcome in the acute phase of ischemic locked-in syndrome: case series of twenty patients with ischemic LIS.

BACKGROUND: Locked-in syndrome (LIS) is a condition characterized by quadriplegia and anarthria. The most common cause is a ventral pontine lesion due to atherosclerotic basilar artery disease. METHODS: Cases with LIS were prospectively identified among the patients with acute ischemic stroke over 3 years, between 2009 and 2011. Clinical characteristics, topographic localization of lesions, and outcome were determined during the first 6 months from onset of LIS. RESULTS: Our case series consists of 20 patients (mean age 62 ± 10 years; range 46-82). Initially 16 patients had a reduced level of consciousness (mean 3 days; range 1-15). Respiratory disturbance, mainly as impairment of the breathing pattern, was noted in all cases. Five patients died within the first 10 days due to stroke progression or cardiac arrest. In the remaining cases the most frequent causes of death were pulmonary infections and sepsis. Overall mortality in the acute phase of LIS is 75%, and the median survival time is 42 days. There was a statistically significant association between the more extensive parenchymal brain stem lesions and observed mortality. CONCLUSIONS: Ischemic LIS is commonly caused by an acute complete occlusion of the basilar artery due to atherosclerotic lesions in intracranial vertebrobasilar vessels. Mortality remains high in the acute phase of the disease.