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the Lysosomal Enzyme Laboratory of the E K Shriver Center Four types have been identi ed: Santavuori-Haltia Finnish infantile type, Jansky-Bielschowsky early-childhood type, Vogt-Spielmeyer juvenile type, and Kufs adult type All except a few adult cases are autosomal recessive The storage material in neuronal cytoplasm consists of two pigmented lipids, presumably ceroid and lipofuscin, which are cross-linked polymers of polyunsaturated fatty acids and have the property of auto uorescence Mole has published a useful review of the genetics of these diseases and points out that at least eight gene loci are implicated, for six of which the mutation has been identi ed All the infantile forms and one juvenile form of the disease are due to mutations affecting the lysosomal enzyme palmitoyl-protein thioesterase Other lysosomal enzymes are abnormal in the remaining juvenile and in the adult forms In the Finnish form of the disease, infants from 3 to 18 months of age, after a normal period of development, undergo psychomotor regression with ataxia, hypotonia, and widespread myoclonus There are retinal changes with extinction of the electroretinogram, slowing of the EEG with spike and slow-wave discharges, and eventually an isoelectric record Within a few years these patients become blind, develop spastic quadriplegia and microcephaly, and succumb In the Jansky-Bielschowsky type, the onset of symptoms is between 2 and 4 years, after normal or slightly retarded earlier development, with survival to 4 to 8 years of age Usually the rst neurologic manifestations are seizures (petit mal or grand mal) and myoclonic jerks evoked by proprioceptive and other sensory stimuli, including voluntary movement and emotional excitement Incoordination, tremor, ataxia, and spastic weakness with lively tendon re exes and Babinski signs, deterioration of mental faculties, and dysarthria proceed to dementia and eventually to mutism In patients with relatively late onset, a progressive dementia is the carTable 37-7 Classi cation of the mucopolysaccharidoses.

FIGURE 1-17

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dinal manifestation Visual failure may occur early in some cases because of retinal degeneration (of rods and cones) with pigmentary deposits, but in others vision is normal The electroretinogram becomes isoelectric if vision is affected Abnormal inclusions (translucent vacuoles) are seen in 10 to 30 percent of circulating lymphocytes, and azurophilic granules in neutrophils High-voltage EEG spikes are induced by photic stimuli Only in early-onset cases is there microcephaly Pathologic examination shows neuronal loss in the cerebral and cerebellar cortices (granule and Purkinje cells), and curvilinear storage particles and osmophilic granules are visible in the remaining neurons Inclusions are also observed in cutaneous nerve twigs and endothelial cells of blood vessels, ndings which permit diagnosis during life by electron microscopy of skin, conjunctival, or rectal mucosal biopsies In many patients with lipofuscinoses, diagnosis can be con rmed by demonstrating the presence of one of several recently identi ed gene mutations There are no de nite markers for the group in blood or urine, but in some patients a structural component of mitochondria is excreted in excess (the socalled C-fragment) In the differential diagnosis, one must consider late infantile GM1 gangliosidosis, idiopathic epilepsy, Alpers disease, and other forms of neuronal ceroid-lipofuscinosis The lipofuscinoses of later onset the Vogt-Spielmeyer (juvenile) type and the Kufs (adult) type are discussed further on There is no treatment for the basic disease process, but approaches involving gene therapy are being explored

Mucopolysaccharidoses (Table 37-7)

This is a group of diseases in which the storage of lipid in neurons is combined with that of polysaccharides in connective tissues As a consequence there is a conjunction of neurologic and skeletal

FIGURE 3-8

Serial communications are most notably distinguished by the fact that they transfer data one bit at a time (in series) Serial communications implement Recommended Standard-232 (RS-232), which defines the connection methods for serial devices For this reason, serial ports are sometimes referred to as RS-232 ports Serial communications can be either synchronous, in which data is sent in a continuous stream, or asynchronous, in which data is sent in intermittent bursts In synchronous serial communications, the stream of data never stops When there is no real data to send, the devices send dummy bits to remain synchronized with one another This constant activity keeps the devices ready to receive real data Asynchronous data is intermittent, so it is accompanied by start and stop bits that indicate the beginning and end of a data stream This system helps the receiving device distinguish real data from line noise Most serial devices, such as serial mice and modems, use asynchronous communications Synchronous communications are usually driven by a clock or other timing signal that controls communications The PCI computer bus is an example of a synchronous environment Each of the controllers that are attached to the bus synchronizes to the other device on the bus Even though the controller may communicate or control an external device such as a mouse, network, or asynchronous bus, the controllers communicate with each other using the clock speed of the bus A clearly defined protocol and communications method is established to allow high-speed communications to occur in an orderly manner

Corneal clouding, severe skeletal changes and MR,b organomegaly, heart disease Dysostosis, normal corneas, MR, joint stiffness, hydrocephalus, short stature, organomegaly MR, mild or absent somatic changes, hyperactivity, hepatosplenomegaly Distinctive skeletal abnormalities, slight corneal clouding, odontoid hypoplasia, normal intelligence, hepatomegaly

No longer used Maroteaux-Lamy Dysostosis, corneal clouding, normal intelligence, spinal cord compression, organomegaly Sly Dysostosis, hepatosplenomegaly, wide range of severity, corneal clouding

Less severe phenotypes are known as Scheie or Hurler-Scheie syndromes MR mental retardation SOURCE: Modi ed by permission from Neufeld and Muenzer

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