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Neuropsychiatric Manifestation in a Patient with Wilson’s Disease

Ming-Yih Lee, Siou-Mei Wang, Shi-Yi Lee

A 34-year-old male patient was admitted to
acute psychiatric ward under the impression as
R/O manic episode with psychotic feature.
Unexpectedly, acute delirium was developed days
after admission. He was diagnosed with acute hepatic
failure (amonia up to 257 g/dL, ASL: 122
U/L) and rhabdomyolysis (CPK up to 47,819
U/L). He was found to be HBs Ag-positive. The
result of abdominal sonogram revealed mild fatty
liver. The brain computerized tomography showed
negative fi ndings except mild brain atrophy. After
his medical condition was stabilized, he showed
persistent confusional features with ataxia, restlessness,
and intermittent agitation. He also had
prominant decline of language function. Under
the impression of R/O delirious mania, he had received
lorazepam, olanzapine, lithium, topiramate,
and even clozapine, but he had poor response
with all those mdications.

Tracing back his history, we did not fi nd that
the patient had developmental delay in his childhood.
Although he had poor academic performance
in school, his intellectual problem had not
found until his age of 18 years. He was not drafted
for military service then. Later, he kept a job for
4-5 years. At his age of 24 years, he was found to
show personality change, becoming quiet, passive,
and often dysphoric. At his age of 29 years,
his family found him to spend hours lying quietly
in bed. He then got lost even in a familiar place.
He had salient progressive decline of activities of
daily life function. His family brought him for
psychiatric help, and he was told to have moderate
mental retardation. Later, he stayed in a nursing
home to receive a two-year rehabilition program.
But in December 2014, he was found to become
restless, impulsive, and agitated. He was admitted
to acute psychiatric ward due to unstable mood
and aggressive behavior.

In summary, the patient’s diagnosis was
highly suspected to have a progressive neurodegenerative
disorder. Although the Kayser-
Fleischer ring was absent, the diagnosis of
Wilson’s disease (WD) was established because
of his high 24-hour urinary copper excretion
(206.1 μg/day; normal range < 60 μg/day) and low
ceruloplasmin (163.9 mg/L) level [1]. He began to
receive D-penicillamine, a chelating drug, and his
mood and behavior became stablized within days.
But he still had prominant impairment of cognitive
and language function as well as mild ataxia.
Key Word
Editorial Committe, Taiwanese Journal of Psychiatry
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