Acquired hepatocerebral degeneration is an underdiagnosed neurologic syndrome
characterized by parkinsonism, ataxia or other movement disorders and by
neuropsychiatric and cognitive symptoms. It occurs in patients with chronic
liver disease, especially those who develop portosystemic shunting and is often
unrecognized as a cause of cognitive decline. Recently, its pathogenesis has
been associated with manganese accumulation in basal ganglia and some treatments
proposed. The aim of this article was to report a case and discuss some
discoveries in connection with the disease.
Infection of the human central nervous system (CNS) by the larvae of
Taenia solium, termed neurocysticercosis (NCC), is endemic
in most developing countries, where it is a major cause of acquired seizures and
other neurological morbidity, including neuropsychiatric symptoms. However,
despite its frequent manifestation, some findings, such as cognitive impairment
and dementia, remain poorly understood. Less commonly, NCC may affect the
ventricular system and subarachnoid spaces and this form is known as
extraparenchymal neurocysticercosis. A particular presentation of the
subarachnoid form is called racemose cysticercosis, which has a progressive
pattern, frequently leads to hydrocephalus and can be life-threatening. Here we
review a case of the racemose variety of cysticercosis, complicated by
hydrocephalus and reversible dementia, with remission of symptoms after
derivation and that remained stable with use of dexchlorpheniramine. We discuss
the challenges in diagnosis, imaging findings, treatment and follow-up of this
disease.
A 35-year-old, previously healthy man presented psychiatric symptoms lasting four
years, receiving treatment with neuroleptics. One year later he evolved with
gait disequilibrium. After a further six months, cognitive symptoms were
characterized with rapid evolution to a profound demented state. MRI showed
signal changes in cerebral white matter and very long-chain fatty acids were
detected in blood.
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