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This is an autosomal recessive disease without ethnic predilection, rst described by Krabbe, a Danish neurologist, in 1916 The onset is usually before the sixth month and often before the third month (10 percent after 1 year) Early manifestations are generalized rigidity, loss of head control, diminished alertness, frequent vomiting, irritability and bouts of inexplicable crying, and spasms induced by stimulation With increasing muscular tone, opisthotonic recurvation of the neck and trunk develops Later signs are adduction and extension of the legs, exion of the arms, clenching of the sts, hyperactive tendon re exes, and Babinski signs Later still, the tendon re exes are depressed or lost but Babinski signs remain, an indication that neuropathy is added to corticospinal damage This nding, shared with some of the other leukodystrophies, is of diagnostic value Blindness and optic atrophy supervene Convulsions occur but are rare and dif cult to distinguish from tonic spasms Myoclonus in response to auditory stimuli is present in some cases The head size is normal or, rarely, slightly increased In the last stage of the disease, which may occur from one to several months after the onset, the child is blind and usually deaf, opisthotonic, irritable, and cachectic Most patients die by the end of the rst year and survival beyond 2 years is unusual, although a considerable number of cases of later onset have been reported (see below) The EEG shows nonspeci c slowing without spikes, and the CSF protein is usually elevated (70 to 450 mg/dL) CT scanning and MRI reveal symmetrical nonenhancing areas of increased density in the internal capsules and basal ganglia As the disease advances, more of the cerebral white matter and brainstem become involved (Fig 37-2) Neuropathy is a feature in most cases, but clinical signs may be dif cult to detect except for a decrease or loss of tendon re exes; however, there is electromyographic (EMG) evidence of denervation and slowed motor and sensory nerve conduction velocities, re ecting a demyelinating type of polyneuropathy The de cient lysosomal enzyme in Krabbe disease is galactocerebrosidase (also called galactosylceramide -galactosidase, or GALC); it normally degrades galactocerebroside to ceramide and galactose The de ciency results in the accumulation of galactocerebroside; a toxic metabolite, psychosine, leads to the early destruction of oligodendrocytes and depletion of lipids in the cerebral white matter The globoid cell reaction, however, indicates that impaired catabolism of galactosylceramide is also important Gross examination of the brain discloses a marked reduction in the cerebral white matter, which feels rm and rubbery Microscopically, there is widespread myelin degeneration, absence of oligodendrocytes, and astrocytic gliosis in the cerebrum, brainstem, spinal cord, and nerves The characteristic globoid cells are large histiocytes containing the accumulated metabolite Schwann cells have tubular or crystalloid inclusions under electron microscopy.

Every OS problem can be resolved Whether it involves replacing a missing file or reinstalling the entire OS, you can get the system up and running again The more familiar you are with the normal function and processes of the OS, the easier it will be to determine the source of a problem and repair it You must also be familiar with the procedures described so far in this chapter and the troubleshooting techniques and tools described in this and previous chapters However, you can save some time troubleshooting Windows OS problems by familiarizing yourself with some of the most common problems and their resolutions

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Figure 37-2 Krabbe disease T2-weighted MRI in the axial plane demonstrating an abnormal high signal in the periventricular white matter Arcuate bers are spared The patient was a 14-month-old boy with severe generalized rigidity Diagnosis was proved postmortem (4 months after the MRI) (Reproduced by permission from Lee SH, Rao K, Zimmerman RA: Cranial MRI and CT, 3rd ed New York, McGraw-Hill, 1992)

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