PubMed · 14091507
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J MULAREK. [AKINETIC MUTISM].. https://pubmed.ncbi.nlm.nih.gov/14091507/
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BACKGROUND: It is common knowledge that the frontal lobes mediate complex human behavior and that damage to these regions can cause executive dysfunction, apathy, disinhibition and personality changes. However, it is less well known that subcortical structures such as the caudate and thalamus are part of functionally segregated fronto-subcortical circuits, that can also alter behavior after injury. CASE PRESENTATION We present a 57 year old woman who suffered penetrating brain injury during endoscopic sinus surgery causing right basal ganglia injury which resulted in an abulic syndrome. CONCLUSION: Abulia does not result solely from cortical injury but can occur after disruption anywhere in the anterior cingulate circuit--in the case of our patient, most prominently at the right caudate.
INTRODUCTION: When patients present with a characteristic clinical picture of Creutzfeldt-Jakob disease (CJD) associated with positive 14-3-3 assay, periodic sharp wave complexes, high-signal of the striatum on magnetic resonance imaging, and homozygosis methionine (M) in codon 129, the median survival is 4 to 6 months. CLINICAL CASE: We report a 58-year-old woman with these typical features who survived 21 months, 19 of them in an akinetic mutism state. The autopsy confirmed the diagnosis of the most common CJD phenotype (MM1), usually associated with a shorter survival, and demyleinitation of the white matter (panencephalopathic form). CONCLUSIONS: The MM1 variant of CJD, with a rapidly progressive course leading into an akinetic mutism shortly after disease onset can be followed by a long akinetic mutism state. This profile is suggestive of panencephalopathic form and should be taken into account when counselling about survival.
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