Posterior Frontal White Matter Research Articles

A CASE OF RELAPSING-REMITTING TUMEFACTIVE MULTIPLE SCLEROSIS

A 23-year-old left-handed female developed progressive right arm weakness and expressive dysphasia. She had papilloedema and right-sided UMN facial palsy, arm weakness and positive Babinski reflex. MRI brain demonstrated a...

Longitudinal Assessment of Gray and White Matter in Chronic Schizophrenia: A Combined Diffusion-Tensor and Structural Magnetic Resonance Imaging Study

Previous studies have reported continued focal gray matter loss after the clinical onset of schizophrenia. Longitudinal assessments in chronic illness, of white matter in particular, have been less conclusive.We used diffusion-tensor and structural magnetic resonance imaging in 16 healthy subjects and 49 chronic schizophrenia patients, subdivided into good-outcome (n=23) and poor-outcome (n=26) groups, scanned twice 4 years apart. Fractional anisotropy, gray matter and white matter volumes were parcellated into the Brodmann’s areas and entered into multiway ANCOVAs.At baseline, schizophrenia patients had 1) lower anisotropy in frontoparietal white matter, 2) larger posterior frontal white matter volumes, and 3) smaller frontal, temporal, and parietal gray matter volumes. On follow-up, healthy subjects showed a more pronounced 1) decline in anisotropy, 2) expansion of regional white matter volumes, and 3) reduction in regional gray matter volumes than schizophrenia patients. Good-outcome patients showed a more pronounced decline in white matter anisotropy and a less pronounced increase in white matter volumes than poor-outcome patients. Poor-outcome patients displayed a greater gray matter loss throughout the brain than good-outcome patients.In the chronic phase of the illness, longitudinal changes in both gray and white matter are in the direction of an effacement of between-group differences among schizophrenia patients and healthy subjects. Similarly, preexisting white matter differences between good-outcome and poor-outcome patients diminish over time. In contrast, gray matter volumes in poor-outcome patients continue to decline more rapidly than in patients with good outcome. These patterns are consistent with earlier onset of aging-associated changes in schizophrenia.

From Cavern-Dwellers to Cavernoma Science

See related article, pages 3222–3230. Since the introduction of noninvasive imaging tools roughly 30 years ago, vascular malformations of the brain have attracted increasing interest. Among them, cerebral cavernous malformations (CCM) appear to be the most frequently diagnosed entity with current prevalence estimates ranging from 100 to 500 cases per 100000 in the general population.1 They may come to clinical attention after epileptic seizures, progressive neurological syndromes, or symptomatic hemorrhage, but overall, asymptomatic lesions seem to be most frequently encountered since the introduction of highly sensitive gradient echo (T2*) weighted sequences in routine MR imaging protocols.2 Despite increasing detection rates and growing insight into underlying molecular and genetic mechanisms, many practical issues remain as yet unsolved, particularly when it comes to actual patient care and counseling: First, no standardized imaging protocols exist. Brain MRI with the aforementioned T2*-weighted images are now considered the diagnostic standard, but the absence of contrast-enhanced T1 sequences may miss an associated developmental venous anomaly and vice versa, which may for example impact on the strategy of any neurosurgical intervention (Figure 1). Figure 1. Brain MRI study of a 37-year-old woman presenting with left internuclear ophtalmoplegia, ataxia, and a dissociated sensory deficit attributable to a left posterior pontine hematoma on FLAIR-weighted images (left plane). Three-month follow-up …

Tumefactive demyelinating lesion

A previously healthy 31-year-old woman presented with a 2-week history of progressive left hemiparesis. MRI (figure) demonstrated a 3 cm enhancing mass in the right posterior frontal white matter with several smaller lesions in …

Brain Metabolic Alterations in Patients with Type 1 Diabetes–Hyperglycemia-Induced Injury

Microangiopathic end-organ injury is common in type 1 diabetes. However, the pathophysiology of diabetic encephalopathy is poorly understood. The authors studied 10 normotensive patients with type 1 diabetes with retinopathy, autonomic neuropathy, but without nephropathy, and 10 healthy subjects. Proton magnetic resonance spectroscopy was performed at 1.5 T in the frontal cortex, thalamus, and posterior frontal white matter. There was no change in N-acetyl-containing compounds (NA), but choline-containing compounds (Cho) were increased in the white matter and in the thalamus; myo-inositol was increased in the white matter, glucose excess was found in all brain, and water intensity was increased in the cortical voxel in the patients. Calculated lifetime glycemic exposure correlated inversely with Cho and NA in white matter and with Cho in thalamus. Concentrations of soluble intercellular adhesion molecules and vascular cell adhesion molecules were increased in the patients. In conclusion, in patients with type 1 diabetes, the increase in adhesion molecules and an association between altered brain metabolites and glycemic exposure suggest the presence of a vascularly mediated, progressive metabolic disturbance in the brain.

Quantitative apparent diffusion coefficient measurements in term neonates for early detection of hypoxic-ischemic brain injury: initial experience.

To determine the utility of using quantitative apparent diffusion coefficient (ADC) values as an objective means of early detection of brain injury caused by hypoxic-ischemic encephalopathy (HIE) in term neonates. Conventional images, diffusion-weighted images, ADC maps, and clinical charts from 13 term neonates clinically suspected of having HIE were retrospectively reviewed. Four term neonates without HIE served as control subjects. ADC values were calculated in predefined regions in patients and compared with those in control subjects. A Student t test was performed for each region to compare patients and control subjects. Abnormalities were more easily detected on diffusion-weighted images and ADC maps, compared with conventional images. ADC values in patients with HIE were significantly different from those of control subjects in the posterior limb of the internal capsule, corona radiata, posterior frontal white matter, and parietal white matter bilaterally. Evaluation of ADC maps can improve conspicuity of hypoxic-ischemic injury in the acute and/or subacute setting (within 12 days of insult), and calculation of ADC values can provide an objective measure of hypoxic-ischemic injury.