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may also be some degree of rigidity, tremor, and bradykinesia, elements suggestive of Parkinson disease (the Westphal or rigid variant, which is more common with a childhood onset) Tendon re exes are exaggerated in one-third of patients, but only a few have Babinski signs Voluntary movements are initiated and executed more slowly than normal, but there is no weakness and no ataxia, although speech, which becomes dysarthric and explosive due to incoordination between tongue and diaphragm, may convey the impression of a cerebellar disorder There is poor control of the tongue and diaphragm In late-onset cases there may be an almost constant rapid movement of the tongue and mouth, simulating the tardive dyskinesia that follows the use of neuroleptic drugs DennyBrown pointed out that when the Huntington patient is suspended, the upper limbs assume a exed posture and the legs an extended one, a posture that he considered to be expressive of the striatal syndrome The disorder of movement that characterizes Huntington chorea has been described more fully in Chap 4 Oculomotor function is subtly affected in most patients (Leigh et al; Lasker et al) Particularly characteristic are impaired initiation and slowness of both pursuit and volitional saccadic movements and an inability to make a volitional saccade without movement of the head Excessive distractibility may be noticed during attempted ocular xation The patient feels compelled to glance at extraneous stimuli even when speci cally instructed to ignore them Upward gaze is often impaired As Wilson stated, the relation of the choreic to the mental symptoms abides by no general rule Most often the mental symptoms precede the chorea, but they may accompany or follow it, sometimes by many years In our own material, with several exceptions of late onset with rigidity rather than chorea, once the movement disorder was fully established, there was nearly always some degree, perhaps slight, of cognitive abnormality Exceptional cases have been reported in which the movement disorder existed for 10 to 30 years without mental changes in patients with the gene abnormality of Huntington disease (Britton et al) After 10 to 15 years, most patients deteriorate to a vegetative state, unable to stand or walk and eating little; in this late stage, a mild amyotrophy may appear Noteworthy is the high suicide rate in huntingtonians, as pointed out by Huntington himself (see also Schoenfeld et al) There is a higher than normal incidence of head trauma; therefore chronic subdural hematoma is another common nding at autopsy The rst signs of the disease may appear in childhood, before puberty (even under the age of 4), and several series of such earlyonset cases have been described (Farrer and Conneally; van Dijk et al) Mental deterioration at this early age is more often accompanied by cerebellar ataxia, behavior problems, seizures, bradykinesia, rigidity, and dystonia than by chorea (Byers et al) However, this rigid form of the disease (Westphal variant, as it is known) also occurs occasionally in adults, as mentioned above Functional decline is much faster in children than it is in adults (Young et al) At the gene locus in Huntington disease there are normally 11 to 34 (median 19) consecutive repetitions of the CAG triplet, each of which codes for glutamine Individuals with 35 to 39 triplets may eventually manifest the disease, but it tends to be late in onset and mild in degree or limited to the below-mentioned senile chorea, and those with more than 42 almost invariably acquire the signs of disease if they live long enough Earlier onset in successive generations (anticipation) is well described in the early writings on the subject and is now known to be attributable to increasing lengths of the CAG repeat sequence The dementia is generally more severe in cases of early onset (15
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to 40 years) than in those of later onset (55 to 60 years) In adult patients with early onset, the emotional disturbance tends to be more prominent initially and precedes the chorea and intellectual loss by years; with older age of onset, choreiform features are more often the initial components; in the middle years, dementia and chorea have their onset at nearly the same age At the other extreme of age, the rst features may become evident in the eighties, with orofacial or other dyskinesias that are mistakenly attributed to an exposure to neuroleptic drugs Pathology and Pathogenesis Gross atrophy of the head of the caudate nucleus and putamen bilaterally is the characteristic abnormality, usually accompanied by a moderate degree of gyral atrophy in the frontal and temporal regions The caudatal atrophy alters the con guration of the frontal horns of the lateral ventricles in that the inferolateral borders do not show the usual bulge formed by the head of the caudate nucleus In addition, the ventricles are diffusely enlarged (Fig 39-4); in CT scans, the bicaudate-cranial ratio is increased in the majority of patients, and this nding corroborates the clinical diagnosis in the moderately advanced case The early articles of Alzheimer and Dunlap and the more recent one of Vonsattel and DiFiglia contain the most authoritative descriptions of the microscopic changes The latter authors have graded the disease into early, moderately advanced, and far advanced stages In ve early but genetically veri ed cases, no striatal lesion was found, which suggests that the rst clinical manifestations are based on a biochemical disorder without visible structural change, at least by light microscopy This view is supported by the observation that Huntington patients studied with PET show a characteristic decrease in glucose metabolism in the caudate nuclei, which appears early in the disease and precedes the loss of tissue (Hayden et al) The striatal degeneration begins in the medial part of the caudate nucleus and spreads, tending to spare the nucleus accumbens Of the six cell types in the striatum (a differentiation based on size, dendritic arborizations, spines, and axon trajectories), the smaller neurons are affected before the larger ones Loss of dendrites of the small spiny neurons has been an early nding, while the large cells are relatively preserved and exhibit no special alterations The lost cells are replaced by brous astrocytes The anterior parts of the putamen and caudate are more affected than the posterior parts In our own cases we have not been impressed with changes in the globus pallidus, subthalamic nucleus, red nucleus, or cerebellum, but others have observed slight changes in these parts and in the pars reticulata of the substantia nigra In the cerebral cortex, there is said to be slight neuronal loss in layers 3, 5, and 6, with replacement gliosis Cases are reported with typical striatal lesions but normal cortices, in which only chorea had been present during late life In our early to moderately advanced cases, even quantitative analyses of the cortex have not disclosed a signi cant loss of neurons Several neuropathologists have observed marked cell loss and gliosis in the subthalamic nuclei in children or young adults with chorea and behavior disorders The biochemical defects in Huntington chorea are only beginning to be understood Impaired glucose metabolism in the caudate nucleus, preceding visible atrophy, has already been noted in some studies Since at least a partial explanation for L-dopa induced involuntary movements is an excess of dopamine (in contrast to Parkinson disease, in which there is a decrease in dopamine), it has been postulated that the abnormal movements of Huntington chorea represent a heightened sensitivity of striatal dopamine receptors There are disturbances in the metabolism of other putative
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