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In 1892, Arnold Pick of Prague rst described a special form of cerebral degeneration in which the atrophy is circumscribed (most often in the frontal and/or temporal lobes), with involvement of both gray and white matter hence the term lobar rather than cortical sclerosis In 1911, Alzheimer presented the rst careful study of the microscopic changes The most complete analyses of the pathologic changes until recently have been those of Spatz, van Mansvelt, Morris and coworkers, and Tissot and associates The nosology of the lobar atrophies has become extremely confusing over the past decade It has become clear that the pathologic change associated with neuronal loss in this category of disease may be any one of several types: lobar atrophy with Pick inclusion bodies, with neuro brillary tangles, with other inclusions, or no characteristic changes Furthermore, gliosis and mild spongiform changes in the super cial layers of cortex, and even typical Alzheimer plaque and tangle pathology, have all been associated with syndromes and gross pathologic atrophy of the frontal and/or temporal lobes Confusion has arisen because these illnesses have been denominated either by the clinical syndrome that derives from a particular region of atrophy or by the pathologic change Several terms have been applied to various forms of lobar atrophy, frontotemporal dementia being the most common (see below) Nonetheless, among these, fairly distinct clinicopathologic syndromes of Pick disease and of frontotemporal dementia are recognizable Since the recognition of Pick disease rests more on pathologic than on clinical criteria, this is described rst In contrast to Alzheimer disease, in which the atrophy is relatively mild and diffuse, the pathologic change in lobar atrophy is more circumscribed and sometimes asymmetrical The atrophy may extend to the island of Reil and the amygdaloid-hippocampal structures The parietal lobes are involved less frequently than the frontal and temporal lobes The affected gyri become paper-thin, resembling the kernel of a dried walnut The cut surface reveals not only a marked narrowing of the cortical ribbon but a grayish appearance and reduced volume of the underlying white matter The corpus callosum and anterior commissure share in the atrophy The overlying pia-arachnoid is thickened, and the ventricles are enlarged The pre- and postcentral, superior temporal, and occipital convolutions are relatively unaffected and stand out in striking contrast to the wasted parts Pick insisted that the disease essentially involves the association areas of Flechsig, but this is not always so In some instances, atrophy of the caudate nuclei has been pronounced, almost to the degree seen in Huntington chorea The thalamus, subthalamic nucleus, substantia nigra, and globus pallidus may also be affected, but only to a slight degree The salient histologic feature of Pick disease is a loss of neurons, most marked in the rst three cortical layers Surviving neurons are often swollen, and some contain argentophilic (Pick) bodies within the cytoplasm Ultrastructurally, the Pick bodies are made up of straight brils, thus differing from the paired helical laments that characterize Alzheimer disease These bodies predominate in the medial parts of the temporal lobes, especially in the atrophic hippocampi Ballooning of cortical neurons is found.

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1 Remove the power supply and ribbon cables from the back of the hard drive Ensure that you grasp the plastic connector, not the wires themselves If the connector doesn t come out easily, try gently rocking it lengthwise from side to side (never front to back) while you pull it out 2 Remove the restraining screws that attach the hard drive to the drive bay (these are usually located on the sides of the drive) 3 Slide the drive out of the computer To install a hard drive, the procedure is reversed, with a few important notes The top of the drive is typically smooth and includes a manufacturer s label The circuit board is on the bottom of the drive Never install a hard drive upside down

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