Aging brain

Among these changes are alterations of the white matter. They may be seen in the deep and subcortical white matter or in a periventricular location. With advancing age, the periventricular and subcortical white matter becomes susceptible to a heterogeneous assortment of tissue alterations that cannot be easily categorized in terms of traditionally defined neuropathological disease. These alterations appear radiolucent on CT and hyperintense on T2-weighted imaging and they are more common in patients with chronic hypertension and perhaps other microvascular atherosclerotic risk factors. In clinically asymptomatic individuals the reported prevalence ranges from 20-60% for deep and subcortical white matter hyperintensities and from 15-94% for periventricular changes, after 60 years of age.The clinical significance of these findings is uncertain. Punctate lesions in the deep and subcortical white matter correspond to minor perivascular reduction in myelin content, possibly because of a lower permeability of thickened arteriolar walls. Larger patchy and confluent hyperintensities, however, appear to indicate more extensive ischaemic damage consistent with advanced microangiopathy. Another frequently observed microscopic change includes dilated perivascular spaces. They are also defined as perivascular spaces of Virchow-Robin. These are an extension of the subarachnoid space that accompanies penetrating vessels into the brain to the level of capillaries. CT studies can demonstrate large dilated perivascular spaces while MR imaging permits the visualization of normal perivascular spaces due to greater resolution and contrast. On MR they appear as small foci which remain isointense to cerebrospinal fluid on all pulse sequences and conform to the path of penetrating arteries. They lack mass effect, and are round, oval, or curvilinear with well-defined smooth margins. Small perivascular spaces (less than 2 mm) are found in all age groups and represent a normal finding. With advancing age they are found with increasing frequency and size. On MR it may be difficult to distinguish a lacunar infarct from a prominent perivascular space. It can be useful to remember that lacunar infarcts occur in the upper two thirds of the putamina, are not isointense to CSF on all pulse sequences unless they have undergone cystic changes and are usually larger (5mm or more). Perivascular spaces are typically smaller, bilateral and often symmetrical, and are in the inferior one third of the putamen.

Aging also causes an enlargement of both cerebral sulci and ventricles, indicating a process of mixed central and cortical volume loss. Histologically, these changes are attributed to neuronal loss and they are greater and evolve more rapidly in Alzheimers disease. Moreover the hippocampal formation is heavily involved in the pathology of Alzheimer's disease and considerably less affected in normal aging. Consequently, focal, symmetrical or asymmetrical enlargement of the temporal horns and sylvian fissures may be useful in discriminating between Alzheimer's patients and the normal elderly.

Another change that may occur in elderly individuals without neurological deficits is a progressive prominence of hypointensity on T2-weighted images of the putamen, almost equal to that of the globus pallidus. The cause of this age-related MR observation is most likely iron deposition. Iron is an essential element for cellular metabolism and regularly accumulates in certain brain areas such as the extrapyramidal nuclei, thalami and deep white matter. During the first 10 years of life the extrapyramidal nuclei are isointense to cortical grey matter at MR imaging. In most patients by the age of 25, the globus pallidus, followed by the red nucleus and pars reticulata of the substantia nigra, becomes hypointense relative to cortical grey matter and to white matter on the long TR/TE sequence. With further aging, hypointensity in the caudate and putamen progresses and may equal that in the globus pallidus in individuals in their eighth decade.
 
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