ABSTRACT
Objectives: Akinetic mutism (AM) is characterized by a complete absence of spontaneous behaviour and speech. We report on a patient with AM associated with injury of the prefronto-caudate tract and prefronto-thalamic tract following mild traumatic brain injury (TBI), diffusion tensor tractography (DTT).
Case presentation: A 20-year-old man suffered from TBI resulting from a pedestrian car accident. Following the TBI, he developed abulia (decreased activity and speech) that worsened over approximately a year. His typical features of AM that remained stable from one year until two years after the TBI are: he showed no spontaneous movement or speech and remained recumbent with no spontaneous activity.
Results: On one-month DTT, the neural connectivity of the caudate nucleus to the medial prefrontal cortex was low in both hemispheres, and this neural connectivity was lower on two-year DTT. The orbitofrontal-thalamic tract was thin in the left hemisphere on one-month DTT, whereas this tract became thinner in both hemispheres on two-year DTT.
Conclusions: Using serial DTTs, injuries of the prefronto-caudate tract and orbitofrontal-thalamic tract and degeneration of these injured neural tracts concurrent with aggravation of abulia to AM were demonstrated in a patient with mild TBI.
ABBREVIATIONS AM akinetic mutism; BA Brodmann areas; CN caudate nucleus; CST corticospinal tract; CRT corticoreticulospinal tract; DTT diffusion tensor tractography; FAC Functional Ambulation Category; PFC prefrontal cortex; MMSE Mini-Mental State Examination; ROI region of interest; TBI traumatic brain injury
Declaration of Interest
The authors report no conflicts of interest. This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korean government (MSIP) (NRF-2015R1A2A2A01004073).