Parietal white matter

Table 65.4 Brain MRS findings obtained from frontal white matter, parietal white matter and the thalamus in neonates with hypothyroidism and healthy neonates (mean SD) ...

Notes Neonates with hypothyroidism had significantiy iower thalamic and parietal white matter NAA/Cr ratios than age-matched healthy neonates. After 8 weeks of thyroxine therapy, NAA/Cr ratios were normalized. Cerebral Cho/Cr ratios were not significantly affected in hypothyroidism (Cho ohoiine Cr creatine FWM frontai white matter NAA N-acetyl aspartate NS nonsignificant [p> 0.05] PWM ... 

Figure 6 A H MRS spectrum from normal human brain at 7T. An 8 ml VOI was localized in the parietal white matter using STEAM with effective TE 6 ms, repetition time 5 s, TM 32 ms, and the collection of 160 averaged echoes. Outer volume suppression, employing SECH pulses, was used and FASTMAP was used to shim the VOI. Peaks undefined in the main text are myoinositol - myo-lns taurine - Tau glutathione - GSH aspartate -ASP A/-acetylaspartylglutamate - NAAG macromolecule - MM. (Reprinted with permission from Tkac I, Anderson P, Adriany G, et at. (2001) In vivo NMR spectroscopy of the human brain at 7 Tesla. Magnetic Resonance in Medicine 46 451-456 Wiley-Liss, a subsidiary of Wiley.)...

Cross-sections clearly show that the increase in brain size is entirely due to swelling of the white matter which has a particular mucoid texture and appears confluent with the cerebral grey which is firmer than normal. Located within the white matter are irregularly outlined, edematous areas of cystic degeneration measuring up to 1 cm in diameter and occurring particularly in the deep layers of the frontal and parietal white matter (Aronson and Volk 1962). With duration of the disease over two years the discrepancy becomes more marked... 

Gazdzinski et al, (2005) 31 36 5.5 26 Chronic smoking in alcohol-dependent individuals and in light drinkers was associated with less parietal and temporal gray matter, and more temporal white matter than in non-smokers. 

Acute cerebral ischemia affects neurons first and the more resistant glia and blood vessels in later stages. Deep cortical layers such as layer III of the cerebral cortex are especially vulnerable, mainly in the parietal and occipital regions and less in the frontal and temporal areas. The more vulnerable neurons are those of the caudate and putamen, the pyramidal cells of Sommer s area and the Purkinje cells in the cerebellum. The thalamus and brainstem are more resistant to hypoxia and ischemia. White matter is generally considered to be more resistant than grey matter. 

You can activate the brain in sleep in whatever way you like, but you will not produce the psychological experience of dreaming without activating the parietal cortex or deep frontal white matter. Why not Are these restricted and discrete brain regions the brain s seats of dreaming Probably not. More likely they constitute connections allowing other brain regions to communicate with one another in such a way as to sustain dream consciousness. 

Kirkpatrick B, Conley RR, Kakoyannis A, Reep RL, Roberts RC. 1999. The interstitial cells of the white matter in the inferior parietal cortex in schizophrenia An unbiased cell-counting study. Synapse 34 95-102. 

Hypoperfusion in frontal, parietal, and temporal regions is a common finding in AD. White matter hyperintensities correlate... 

T2- and FLAIR-weighted sequences typically demonstrate bilateral, symmetric hyperintensity, and swelling in subcortical white matter and overlying cortex in the occipital, parietal, and posterior temporal lobes as well as the posterior fossa. The posterior circulation predominance is thought to result from the fact that there is less sympathetic innervation (which supplies vasoconstrictive protection to the brain in the setting of acute hypertension) in the posterior compared with the anterior circulation. However, anterior circulation lesions are not uncommon and are frequently in a border-zone distribution. 

In that study, NAA, Cho and Cr were measured in frontal white matter (FWM), parietal white mater (PWM) and the thalamus of the eight full-term neonates with hypothyroidism. They were 5-7 days of age, and were born to mothers living in iodine-deficient areas. Their mothers had not received iodine supplementation in the pregestational or gestational period. A repeat MRS examination was performed after 8 weeks of thyroxine therapy. Metabolite levels of these patients were compared to levels obtained from eight full-term age-matched healthy neonates of mothers who had been using iodine-supplemented salt since the pregestational period. 

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