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systems; (2) mild to moderate mental deterioration with behavioral disturbance in some but not all cases; (3) decreased or absent tendon re exes and evidence of chronic axonal neuropathy and denervation atrophy of muscles; (4) atrophy and gliosis of the caudate nuclei and putamens but no neuronal loss in the cerebral cortex or other parts of the brain; (5) the de ning element, acanthocytosis (thorny or spiky appearance of erythrocytes); and (6) an autosomal recessive inheritance pattern The acanthocytosis, according to Sakai and coworkers, is due to an abnormal composition of covalently (tightly) bound fatty acids in erythrocyte membrane proteins (palmitic and docosahexanoic acids increased and stearic acid decreased) Although the inheritance is usually autosomal recessive, at least one family with the dominantly transmitted trait has been described The acanthocytosis may be overlooked when it is mild but can be detected by scanning electron microscopy In the series of 19 cases reported by Hardie and colleagues, the manifestations included dystonia, tics, vocalizations, rigidity, and lip and tongue biting; more than half had cognitive impairment or psychiatric features The average age of onset was 32 years; 7 of the 19 cases were sporadic The disease has been linked in almost all families to chromosome 9q, where there is a mutation in the gene encoding a large (3100 amino acid) protein designated chorein that is thought to be involved in cellular protein sorting and traf cking (Rampoldi) Some of the families with dominantly inherited neuroacanthocytosis have mutations in the chorein gene McLeod s disease, another choreiform disorder with acanthocytosis and the gradual development of chorea in middle to late life, is characterized by degeneration of the caudate and putamen and a myopathy (elevated serum CPK) These individuals have fewer facial tics and orofacial features than those with neuroacanthocytosis McLeod s syndrome arises from mutations in a gene on the X chromosome that encodes the KX protein, which binds to surface Kell antigens on red cells In addition to the primary KX gene mutations, these individuals show diminished Kell antigen expression on the red-cell surface.

Included in this category are a somewhat heterogeneous group of degenerative diseases in which the symptoms of parkinsonism and corticospinal degeneration present in various combinations Some of the diseases that make up this group have not been sharply delineated and are dif cult to separate from one another (see also page 928) Variants of this category of disease continue to appear The authors have observed several patients in whom extreme rigidity, corticospinal signs, but no dementia have developed over a period of several years In the later stages of the disease, the patient, while alert, is totally helpless unable to speak, swallow, or move the limbs Only eye movements are retained, and even these are hampered by supranuclear gaze palsies in advanced cases Intellectual functioning appears to be better preserved than movement but is dif cult to assess Other bodily functions are intact The course is slowly progressive and ends fatally in 5 to 10 years There is no family history of similar disease, and there are no clues as to causation Gilbert and colleagues have described similar cases with signs of Parkinson disease, motor neuron disease, and dementia; in their cases, there were no senile plaques or Lewy bodies The concurrence of typical motor neuron disease and Parkinson disease may be coincidental, but Qureshi and colleagues described 13 patients in whom both clinical phenomena began within a short time

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A few reports of a slowly progressive, familial chorea and dementia in association with an abnormality of erythrocytes have appeared in English, American, and Japanese journals The disease has the following characteristics: (1) onset in adolescence or early adult life of generalized involuntary movements (described as chorea but including dystonia and tics), usually beginning as an orofacial dyskinesia and spreading to other parts of the body and to other neural

IPCONFIGEXE is a command-line version of the IP Configuration utility and is used in Windows 9x and Windows NT/2000/XP systems This command only works if the TCP/IP protocol stack is installed To use IPCONFIGEXE, enter IPCONFIG at a command prompt The IP address, subnet mask, and default gateway of each network adapter in the system will be listed (see Figure 11-11) To release an IP address, enter the command IPCONFIG /RELEASE To renew an IP address, enter IPCONFIG / RENEW

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October 2009 42U 7866 inches (1988 mm) H 2362 inches (600 mm) W 4724 inches (1,200 mm) D 2,119 lbs (9632 kg) 140 kW (143 kVA) 47,800 BTU/ hour

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