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mediately adjacent to the site of the mutation for Charcot-MarieTooth disease type 1B (Table 46-6) During childhood, one of the patients of Swanson et al had high fever when the environmental temperature was raised, and the other possibly had orthostatic hypotension One of the patients died in his twelfth year and was found to have an absence of small neurons in the dorsal root ganglia, an absence of Lissauer s tracts, and a decrease in size of the descending spinal tracts of the trigeminal nerves Sweat glands were present in the skin but were not innervated Other Forms of Inherited Sensory Neuropathy Included here are the neuropathy of Friedreich ataxia, which is discussed in Chap 39; the Riley-Day syndrome, which is discussed further on in this chapter; neuropathy with cerebellar degeneration; and the neuropathies in which there are recognized metabolic abnormalities, including familial amyloidosis We regularly see unclassi able examples of an almost pure sensory or sensorimotor type Some years ago a young man and woman with universal anesthesia affecting head, neck, trunk, and limbs came to our attention (Adams et al); all forms of sensation were absent The patients were are exic but retained nearly full motor power; their movements were ataxic Autonomic functions were impaired but not abolished In a sural nerve biopsy, nearly all bers large and small, myelinated and unmyelinated had disappeared Surprisingly, there were no trophic changes of any kind Donaghy and others have described a unique variant of the recessively inherited form of sensory neuropathy in which there was an associated neurotrophic keratitis and a selective loss of small myelinated bers in sural nerve biopsies We continue to observe variant and unclassi able cases such as these every year Hereditary Are exic Dystasia (Roussy-Levy Syndrome, CMT3) In 1926 Roussy and Levy reported 7 cases of a domi nantly inherited ataxic and neuropathic malady that had not previously been described Its close relation to Friedreich ataxia and the amyotrophy of Charcot-Marie-Tooth disease was recognized For many years thereafter the existence of this entity was disputed and, only recently, on the basis of molecular genetic testing, have these relationships been clari ed The condition in question is a sensory ataxia (dystasia) with pes cavus and are exia, affecting mainly the lower legs and progressing later to involve the hands Some degree of sensory loss, mainly of vibratory and position sense, has been described in all cases Atrophy of the muscles of the legs and postural tremor eventually become prominent The patients do not have evidence of cerebellar disease (dysarthria, tremor, nystagmus, etc) Kyphoscoliosis, a feature typical of Friedreich disease, has been described in several cases Although the feet may be cold or slightly discolored, no autonomic defects are documented and the nerves are not palpably enlarged Electrocardiographic abnormalities similar to those of Friedreich ataxia have been noted in one family but are not usual The onset in many patients is during infancy, possibly dating from birth, and the course is relatively benign; all descendants of the original Roussy-Levy family were still able to walk during their seventh decade of life On clinical and pathologic grounds, Dyck et al placed the Roussy-Levy kinships within the category of the demyelinating type of Charcot-Marie-Tooth disease (CMT1) The mode of inheritance of the two syndromes, their benign course, pattern of neurologic signs, slow nerve conduction, and biopsy features (demyelination of nerve bers with onion bulb formation) are much the
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same This view has been reinforced by the genetic ndings reported by Plante-Bordeneuve et al In affected members of the orig inal Roussy-Levy family, these investigators identi ed a point mu tation in the domain of the myelin protein gene PO, the same gene that is implicated in Dejerine-Sottas disease Based on limited pathologic study, there is no cerebellar degeneration; nevertheless, the shared clinical features with Friedreich ataxia are unmistakable Polyneuropathy with Cerebellar Degeneration (See page 934) Several such cases of adult onset have come to our attention over the years Unlike Friedreich disease, the ataxia is mild, and there is no kyphoscoliosis but pes cavus or hammer-toe deformities are found, attesting to the early onset of the neuropathy The lower legs become atrophic and ndings characteristic of CMT such as absent ankle re exes and mild to moderate loss of distal deep sensibility are present There is no Romberg sign and no Babinski signs The outstanding feature is a profound atrophy of the cerebellar hemispheres, and to some extent of the vermis, on MRI Although the illness is slowly progressive, our patients, like those with RoussyLevy disease, have remained highly functional into late age, having dif culty mostly with maintaining balance when dancing or wearing high-heeled shoes The EMG is consistent with CMT2 The electrocardiogram has been normal Several, but not all, such patients have had a family history of a similar process but the available genetic testing has failed to reveal the site of a mutation Polyneuropathy with Spastic Paraplegia From time to time we have observed children and young adults with unmistakable progressive spastic paraplegia superimposed on a sensorimotor polyneuropathy of extremely chronic evolution Sural nerve biopsy in two of our cases disclosed a typical hypertrophic polyneuropathy In another case only loss of nerve bers was found Cavanaugh and colleagues and Harding and Thomas have reported similar patients Our patients were severely disabled, being barely able to stand on their atrophic legs The disease is slowly progressive The patients described by Cavanaugh and coworkers had mainly sensory de cits and were not disabled A more ambiguous form of disease has been described by Vucic and colleagues in which there is typical CMT but with brisk re exes There were Babinski signs in half the patients and spastic dysphonia in a few others The mutation is not known While few in number, some cases of chronic polyneuropathy are combined with optic atrophy, with or without deafness or retinitis pigmentosa, and Dyck has classed these in a separate group Jaradeh and Dyck have also described a hereditary motor-sensory polyneuropathy with the later development of a parkinsonian or a choreic-dystonic syndrome that responded to L-dopa Most cases of this type have had an autosomal recessive inheritance Hereditary Recurrent Brachial Plexopathy (Hereditary Neuralgic Amyotrophy, HNA) This entity, mentioned earlier in relation to hereditary neuropathy with pressure palsies because of the implication of a similar genetic locus, is discussed in a later section of the chapter under Brachial Neuritis
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