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Iron de ciency anemia and low ferritin levels have been associated with the syndrome in a few instances, as has thyroid disease, pregnancy, cigarette smoking, certain drugs such as antidepressants and antihistamines, and varicose veins Also, reduced levels of iron in the cerebrospinal uid (CSF) have been found with periodic limb movements of sleep The basis for this is not well de ned One hypothesis is that iron depletion in the basal ganglia contributes to a decrement in dopamine agonist binding by dopamine receptors and transporters, as has been reported in studies using PET and single-photon emission tomography (SPECT) scans A closely related if not identical disturbance and one that may result in sleep deprivation and daytime somnolence or in disturbance of a bed partner is periodic leg movements during sleep Originally described as nocturnal myoclonus, periodic leg movements are slower than myoclonic jerks.

10.2. SENSOR MODELS = = asin ( 2(b2 b4 + b1 b3 )) atan2 2(b2 b3 b1 b4 ), 1 2(b2 3 + b2 ) 4 .

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They consist of a series of repetitive movements of the feet and legs occurring every 20 to 90 s for several minutes to an hour; mainly the anterior tibialis is involved, with dorsi exion of the feet and big toes, sometimes followed by exion of the hip and knee The movements are similar to the triple exion (Babinski) response, which can be elicited in normal sleeping persons These movements produce frequent microarousals or, if severe and periodic, full arousals The patient, usually unaware of these sleep-related movements at the time they occur, is told of them by a bedmate or suspects their occurrence from the disarray of the bedclothes This type of periodic leg movement may be associated with restless legs as well as with narcolepsy, sleep apnea, the use of tricyclic and serotonin reuptake inhibiting antidepressants, L-dopa, and withdrawal from anticonvulsants and hypnotic-sedative drugs.

There are, in addition, a few patients who have true myoclonic jerks in the leg or trunk muscles, often associated with dyskinesias that are dif cult to characterize but may include walking-like movements and arrhythmic abduction-adduction of one or both.

versions f'hus,we havederived zero-order the version Eq. (4.14). of The higher-order Thefirst-order aremerely logical a exfension ol'thereasoning to derive (4.16). used Eq. version is

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these disorders will re ect differences in the patterns of expression of the affected proteins; ie, each is expressed in different subpopulations of neurons and at different stages in development This raises the possibility that the cascade of events that triggers neuronal degeneration is similar in each of the diseases with a CAG expansion and that a therapy might be discovered that is effective in all of them Table 39-5 summarizes the chromosomal loci, genetic terminology, related neural abnormalities, and clinical features of the CAG-dependent (and other) cerebellar atrophies The main types are summarized again here with some clinical comments: SCA 1: 6p; ophthalmoparesis, pyramidal and extrapyramidal signs; included in this group are most of the olivopontocerebellar atrophies SCA 2: 12q; slowed eye movements and saccades (Wadia type) Dentatorubropallidoluysian atrophy (DRPLA): 12p SCA 3:14q; the Machado-Joseph phenotype with several allelic variants.

SCA 4: 16q; sensory neuropathy and pyramidal signs SCA 7: 3p; retinal degeneration SCA 6: 19p; related to the alpha subunit of a voltage-dependent calcium channel; a different mutation at the same locus causes the acetazolamide-responsive episodic ataxia (EA-2) EA-1: (episodic ataxia) 12p; potassium channelopathy EA-2: (acetazolamide-responsive episodic ataxia) 19p; calcium channelopathy Differential Diagnosis of the Degenerative Ataxias (See Table 51, Page 78) Sporadic forms of cerebellar ataxia in adults are in some instances traceable to strokes involving cerebellar pathways (Safe et al) These are, of course, of acute onset Some cases of ataxia are alcoholic-nutritional in origin, and a few are related to abuse of drugs, especially anticonvulsants, which may in a few cases cause a slowly progressive and permanent ataxia; rarely, organic mercury induces subacute cerebellar degeneration, and adulterated heroin causes a more abrupt and severe ataxic syndrome.

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