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rologic involvement Cranial CT scans are abnormal even in the hepatic stage and are invariably so when the neurologic disorder supervenes The lateral ventricles and often the third ventricle are slightly enlarged, the cerebral and cerebellar sulci are widened, the brainstem appears shrunken, and the posterior parts of the lenticular nuclei, red nuclei, and dentate nuclei become hypodense (Ropper et al) With treatment, these radiologic changes become less marked (Williams and Walshe) MRI is an even more sensitive means of visualizing the structural changes, particularly those in the subcortical white matter, midbrain, pons, and cerebellum (Starosta-Rubinstein et al) In the MRI survey by Saatci and colleagues, the putamen was involved most frequently (though not invariably), showing a symmetrical T2 signal change in a laminar pattern; there was also an increase in T1 signal throughout the basal ganglia, particularly in the pallidum Signal changes are almost universally found in the claustrum and also in the midbrain (pars compacta of the substantia nigra), dentate nucleus of the cerebellum, pons, and thalami We have been impressed with a glassy diffuse and con uent signal abnormality on T2-weighted and FLAIR images in the hemispheral white matter in some cases ndings that were mistaken for multiple sclerosis Neuropathologic Changes These vary with the rate of progress of the disease Exceptionally, in the rapidly advancing and fatal form, there is frank cavitation in the lenticular (putaminal and pallidal) nuclei, as observed in Wilson s original cases In the more chronic form there is only shrinkage and a light-brown discoloration of these structures Nerve cell loss and some degree of degeneration of myelinated bers in lenticular nuclei, substantia nigra, and dentate nuclei are usually apparent Subcortical myelin degeneration is found in some cases More striking, however, is a marked hyperplasia of protoplasmic astrocytes (Alzheimer type II cells) in the cerebral cortex, basal ganglia, brainstem nuclei, and cerebellum, almost certainly a reaction to liver failure and hyperammonemia Treatment Ideally treatment should be started before the appearance of neurologic signs; if this can be effected, neurologic deterioration can be prevented to a large extent Treatment consists of (1) reduction of dietary copper to less than 1 mg/day, which can usually be accomplished by avoidance of copper-rich foods (liver, mushrooms, cocoa, chocolate, nuts, and shell sh), and (2) administration of the copper chelating agent D-penicillamine (1 to 3 g/day) by mouth, in divided doses Pyridoxine 25 mg/day should be added in order to prevent anemia The use of D-penicillamine is associated with a number of problems Sensitivity reactions to the drug (rash, arthralgia, fever, leukopenia) develop in 20 percent of patients and require a temporary reduction of dosage or a course of prednisone to bring them under control Reinstitution of drug therapy should then be undertaken, using low dosages (250 mg daily) and, later, small, widely spaced increases If the patient is still sensitive to D-penicillamine or if severe reactions (lupus-like or nephrotic syndromes) occur, the drug should be discontinued and another chelating agent, triethylene tetramine (trientene) or ammonium tetrathiomolybdate may be substituted Zinc, which blocks the intestinal absorption of copper, is also a suitable treatment, but ineffective alone It is given as zinc acetate, 100 to 150 mg daily in three to four divided doses at least 1 h before meals (Hoogenraad et al) The appropriate drug must then be continued for the patient s lifetime Some women report improvement in neurologic symptoms during pregnancy, although there is no apparent change in copper metabolism during this time In most patients, neurologic signs improve in response to decoppering agents The Kayser-
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Fleischer rings disappear and liver function tests may return to normal, although the abnormalities of copper metabolism remain unchanged In moderately severe and advanced cases, clinical improvement may not begin for several months despite full doses of D-penicillamine, and it is important to resist discontinuing the drug during this latent period One of our patients had a complete remission of severe neurologic symptoms with penicillamine treatment and has remained symptom-free for 30 years It is also well known that the institution of treatment with penicillamine may induce an abrupt worsening of neurologic signs, and we have witnessed several such instances, including one that culminated fatally from a cardiac arrhythmia Furthermore, in many of these patients, the lost function is never retrieved Presumably this deterioration may be due to the rapid mobilization of copper from the liver and its redistribution to the brain The slow introduction of penicillamine may avoid this complication The additional use of zinc or one of the newer agents mentioned above should be instituted as soon as neurologic deterioration becomes evident In at least one reported case, new lesions of Wilson disease (shown by MRI) developed while the patient was receiving full doses of D-penicillamine and excellent decoppering of the liver had occurred (Brewer et al) In the few patients who develop epilepsy, the seizures may become apparent soon after therapy is begun Many wilsonian patients with advanced liver disease have been subjected to liver transplantation, which is curative for the underlying metabolic defect The degree of neurologic improvement varies; in some it has been remarkable and sustained, con rming that the hepatic defect is primary and that the brain is involved secondarily According to Schilsky and coworkers, the main indication for transplantation is severe and progressive liver damage, but the operation has been used successfully in some patients with intractable neurologic deterioration and only mild signs of liver disease An important aspect of treatment is the screening of potentially affected relatives for abnormalities of serum copper and ceruloplasmin; if any relative is found to have the disease, penicillamine should be given inde nitely to prevent the emergence of neurologic symptoms A full explanation of the dangers of ceasing the medication must be given, and compliance may have to be monitored Hereditary De ciency of Ceruloplasmin This is a rare illness, quite similar to Wilson disease, occurring in patients with a recessively inherited de ciency of ceruloplasmin; it is not simply a heterozygous form of Wilson disease (the mutation involves a different gene) Cirrhosis and Kayser-Fleischer rings are not features of the disease, but diabetes is common and extrapyramidal signs may or may not arise Rather than copper, iron is deposited in the brain and liver (see discussion by Logan) Those few cases that have been well studied, mainly Japanese, show mainly an ataxic disorder (Miyajima et al) Also noted here is a rare and poorly characterized progressive myelopathy that closely simulates subacute combined degeneration of B12 de ciency; it recently has been associated with low serum copper levels (page 1078) Hallervorden-Spatz Disease This disease is also known as pigmentary degeneration of the globus pallidus, substantia nigra, and red nucleus It is inherited as an autosomal recessive trait and is due, in all classic cases, to a defect in the gene encoding pantothenate kinase 2 (PANK2) usually in the form of a missense mutation The onset of symptoms is in late childhood or early adoles-
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