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Approximately 85% of cases of HNPP are caused by an inverse of the mutation that is responsible for most cases of CMT1A19,47,62 While CMT1A is usually associated with a 15-MB duplication in chromosome 17p112, an extra copy of PMP-22 gene, HNPP is caused by inheritance of the chromosome with the corresponding 15-MB deletion of this segment and thus have only one copy of the PMP-22 gene (Fig 9 5) De novo deletions are usually paternally inherited and arise due to unequal crossingover during meiosis, while rare de novo mutations are of female origin and the result of intrachromosomal rearrangements28 In addition, as with CMT1A, mutations within the PMP-22 gene itself can cause HNPP63 Why some point mutations in the PMP-22 gene result in a CMT1A clinical phenotype and other are associated with a HNPP phenotype is not known It is speculated that mutations causing CMT1A produce a gain of function of the PMP-22 protein, while mutations causing HNPP cause a loss of function of the PMP-22 Nerve biopsies demonstrate an underexpression of PMP-22

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keyword represents three different objects Make sure you understand which object the this keyword represents in each context and why

myInt = (( myInt + 1 ) * ( myInt + 1 ));

Nerve biopsies demonstrate focal globular thickening of the myelin sheath, which is best appreciated on teased

mRNA and the protein31,33 that inversely correlate with the mean diameter of the axons and clinical severity64 Normal expression of PMP-22 appears important for proper axonal development

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CMT DISEASE TYPE 2 (CMT2)

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If the syntax to communicate to a particular movie clip ever seems confusing, you can use the Insert Target Path button in the Actions panel to have Flash write the path for you The Insert Target Path button will give you the path to any object with an instance name in your Flash file This is a very quick and effective way to communicate from one object to another, without requiring you to remember each object s instance name

which is not what we wanted. The multiplication that gets performed by this statement is 1 * myInt, because the * operator has a higher precedence than the + operator. Be sure you pay strict attention to your use of white space in your #define macros. For example, there s a world of difference between this macro

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CMT2 refers to the axonal hereditary motor and sensory neuropathies Most of these are associated with autosomal-dominant inheritance The prevalence of CMT2 is about half that of CMT1 There are several well-de ned subtypes based on the clinical features and genetic localization (Table 9 1)9,21 23,65,66 70 CMT2A2 caused by mitofusin-2 mutations is the most common subtype accounting for approximately onethird of CMT2 cases overall70 72 The different subtypes can be dif cult to distinguish from one another and even from CMT1; however, there are clinical features that may be helpful CMT2 tends to present later in life compared to CMT1 Individuals who are affected usually become symptomatic in the second decade but some remain asymptomatic into late adult life while others present in the rst decade of life69,74 People with CMT2 tend to have less severe involvement of the intrinsic hand muscles than that appreciated in CMT1 In contrast, CMT2 is associated with more profound atrophy and weakness of both the anterior compartments (peroneal and anterior tibial) and the posterior compartments (gastrocnemius and soleus) of the distal legs compared to CMT1 Generalized are exia is rare in CMT2, while it is rather common in CMT1 Ankle re exes are usually absent in both types of diseases Individuals with CMT2 are less likely to have a tremor (Roussy Levy syndrome) than people with CMT1 Although patients generally do not complain of sensory loss or paresthesia, 50 70% of those with CMT2 have signi cant reductions in light touch, pain, joint position, and vibration sense While pes cavus and hammertoe deformities may be seen in CMT2, these are less frequent than in CMT1 There are some features that also help distinguish the different subtypes of CMT2 For example, optic atrophy, hearing loss, pyramidal tract, and subcortical white matter abnormalities on brain magnetic resonance imaging ndings are sometimes seen in CMT2A2, which was previously reported as hereditary motor and sensory neuropathy type 6 (HMSN VI)75,76 Severe mutilating neuropathic ulcerations similar to those typically seen in HSAN type 1 (HSAN1) sometimes complicate CMT2B77,78 80 CMT2B1 caused by homozygous mutations involving lamin A/C is allelic to limb-girdle muscular dystrophy 1B81 84 Most of the reported cases have been from North.

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