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for a period of 35 to 200 ms By interlocking EMG and electroencephalographic (EEG) recordings, Ugawa et al found that a sharp wave, probably generated in the motor cortex, immediately precedes the period of EMG silence This con rmed that asterixis differs physiologically from both tremor and myoclonus, with which it was formerly confused; it has incorrectly been referred to as a negative tremor Asterixis is most readily evoked by asking the patient to hold his arms outstretched with hands dorsi exed or to dorsi ex the hands and extend the ngers while resting the forearms on the bed or the arms of a chair Flexion movements of the hands may then occur once or several times a minute The lapses in sustained muscle contraction and the corresponding lapses in EMG activity can be provoked by the persistent contraction of any muscle group including, for example, the protruded tongue, the closed eyelids, or the trunk muscles If small nger muscles are affected, an EMG may be required to separate asterixis from tremor and myoclonus This sign was rst observed in patients with hepatic encephalopathy but was later noted in those with hypercapnia, uremia, and other metabolic and toxic encephalopathies However, lapses of this type may sometimes appear in the neck and arms of a normal person during a period of drowsiness They may also be evoked by phenytoin and other anticonvulsants, then indicating that these drugs are present in excessive concentrations Unilateral asterixis has been noted in an arm and leg on the side opposite an anterior thalamic infarction or small hemorrhage, stereotaxic thalamotomy, and with an upper midbrain lesion, usually as a transient phenomenon after stroke A few cases have reportedly followed an infarction in the territory of the anterior cerebral artery, but our experience is limited to those arising from thalamic lesions Montalban and colleagues observed unilateral asterixis in 45 patients without metabolic or toxic abnormalities In more than half of these patients, there were lesions in the contralateral thalamus; in the remainder, there was an abnormality in the pons or a cerebral hemisphere Anticonvulsants exaggerate the sign, which, in one of our patients who had a small hemorrhage in the anterior thalamus, appeared only when the drug was administered.

10:

Unavoidably, one must refer here to certain inherited metabolic diseases already described that permit survival into late childhood

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and adolescence as well as to diseases that begin in adolescence or adult life after a normal childhood There is a tendency for them to be less severe and less rapidly progressive, an attribute shared by many diseases with a dominant mode of inheritance Nonetheless, there are diseases, such as Wilson disease, in which the onset of neurologic symptoms occurs after the 10th year and in rare instances after the 30th year, and the mode of inheritance is recessive in type However, in the latter instance, the basic abnormality has existed since early childhood in the form of a ceruloplasmin de ciency with early cirrhosis and splenomegaly; only the neurologic disorder is of late onset This brings us to another principle that the pathogenesis of the cerebral lesion may involve a factor or factors once removed from the underlying biologic abnormality Genetic heterogeneity poses another problem with respect to both the clinical and biochemical ndings It is well established that a single clinical phenotype such as the one seen in Hurler disease can be the expression of a number of different alleles of a given gene mutation Conversely, a number of different clinical phenotypes may be based on different degrees of the same enzyme de ciency One must, therefore, not rely solely on clinical appearances for diagnosis but always combine them with biochemical tests and molecular genetic studies for con rmation No one of these lines of data, including genomics, is suf cient for classi cation of disease The diseases in this category are probably of greater interest to neurologists than the preceding ones, for they more consistently cause familiar neurologic abnormalities such as epilepsy, polymyoclonus, dementia, cerebellar ataxia, choreoathetosis, dystonia, tremor, spastic-ataxic paraparesis, blindness, deafness, and stroke These manifestations appear much the same in late childhood and adolescence as they do in adult life, and the neurologist whose experience has been mainly with adult patients feels quite comfortable with them Diseases in this age period have a diversity of manifestations, yet each disease tends to have a certain characteristic pattern of neurologic expression, as though the pathogenetic mechanism were acting more selectively on particular systems of neurons Such af nities between the disease process and certain anatomic structures raise the question of pathoclisis, ie, speci c vulnerability of particular neuronal systems to certain morbid agents Stated another way, for each disease there is a common and relatively stereotyped clinical syndrome and a small number of variants; conversely, certain other symptoms and syndromes are rarely observed with a given disease At the same time, however, it is clear that more than one disease may cause the same syndrome In deference to these principles, the diseases in this section are grouped according to their most common mode of clinical expression, as follows: 1 2 3 4 5 6 7 8 The progressive cerebellar ataxias of childhood and adolescence The familial polymyoclonias and epilepsies Extrapyramidal syndromes of parkinsonian type The syndrome of dystonia and generalized choreoathetosis The syndrome of bilateral hemiplegia, cerebral blindness and deafness, and other manifestations of focal cerebral disorder Strokes in association with inherited metabolic diseases Metabolic polyneuropathies Personality changes and behavioral disturbances as manifestations of inherited metabolic diseases.

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