Akinetic mutism following prefrontal injury by an electrical grinder a case report: A diffusion tensor tractography study.

RATIONALE: A 72-year-old male had suffered from head trauma resulting from injury to his frontal area by an electrical grinder while working at his home. PATIENT CONCERNS: He lost consciousness for approximately 10 minutes and experienced continuous post-traumatic amnesia. DIAGNOSES: He was diagnosed as traumatic intracerebral hemorrhage in both frontal lobes, intraventricular hemorrhage, and subarachnoid hemorrhage, and underwent decompressive craniectomy and hematoma removal.
INTERVENTIONS: The patient's Glasgow Coma Scale score was 5. At 2 months after onset, when starting rehabilitation, he showed no spontaneous movement or speech; he remained in a lying position all day with no spontaneous activity. OUTCOMES: On 2-month diffusion tensor tractography, decreased neural connectivity of the caudate nucleus to the medial prefrontal cortex (PFC, Broadmann area [BA]: 10 and 12) and orbitofrontal cortex (BA 11 and 13) was observed in both hemispheres. LESSONS: Akinetic mutism following prefrontal injury.

Introduction

A 72-year-old man had suffered from head trauma resulting from injury to his frontal area by an electrical grinder while working at his home. He was diagnosed as traumatic intracerebral hemorrhage in both frontal lobes, intraventricular hemorrhage, and subarachnoid hemorrhage, and underwent decompressive craniectomy and hematoma removal (Fig. 1A). He lost consciousness for approximately 10 minutes and experienced continuous posttraumatic amnesia. The patient's Glasgow Coma Scale score was 5. At 2 months after onset, when starting rehabilitation, he showed no spontaneous movement or speech; he remained in a lying position all day with no spontaneous activity. Brain magnetic resonance imaging at 2 months after onset showed leukomalactic lesions in both frontal lobes (Fig. 1B). The patient's wife provided signed, informed consent, and our institutional review board approved the study protocol.

Figure 1

(A) Brain computed tomography images at onset show traumatic intracerebral hemorrhage in both frontal lobes and intraventricular hemorrhage. (B) T2-weighted brain MR images at 2 months after onset show leukomalactic lesions in both frontal lobes. (C) On 2-month diffusion tensor tractography, the neural connectivity of the caudate nucleus to the medial prefrontal cortex (PFC, Broadmann area [BA]: 10 and 12) and orbitofrontal cortex (BA 11 and 13) is decreased (arrows) in both hemispheres.

Diffusion tensor imaging data were acquired at 2 months after onset using a 6-channel head coil on a 1.5T Philips Gyroscan Intera (Philips, Ltd., Best, the Netherlands) with 32 diffusion gradients by single-shot echo-planar imaging. Imaging parameters were as follows: acquisition matrix = 96 × 96; reconstructed to matrix = 192 × 192; field of view = 240 × 240 mm2; repetition time = 10,398 ms; echo time = 72 ms; parallel imaging reduction factor = 2; echo-planar imaging factor = 59; b = 1000 s/mm2; and a slice thickness of 2.5 mm. Head motion effect and image distortion due to eddy current were corrected by affine multiscale two-dimensional registration. Fiber tracking was performed using probabilistic tractography, and applied in the default tractography option in the Oxford Centre for Functional Magnetic Resonance Imaging of the Brain (FMRIB) Diffusion Software (5000 streamline samples, 0.5 mm step lengths, curvature thresholds = 0.2). For reconstruction of the connectivity of the caudate nucleus (CN), the seed region of interest: the CN which was isolated by adjacent structures—the lateral ventricle (medial boundary), the anterior limb of the interal capsule (lateral boundary).[ The threshold of 10 streamlines was applied for the results of fiber tracking.

On 2-month diffusion tensor tractography (DTT), decreased neural connectivity of the CN to the medial prefrontal cortex (PFC, Broadmann area [BA]: 10 and 12) and orbitofrontal cortex (BA 11 and 13) was observed in both hemispheres (Fig. 1C).

In this study, the patient lost the majority of both medial and orbitofrontal prefrontal cortex by an electrical grinder injury. The PFC is involved in various cognitive functions including working memory, attention, decision-making, execution, behavior inhibition, and motivation.[ The PFC consists of 4 subregions, each of which is known to have specific roles in cognition: dorsolateral prefrontal cortex attention, planning, working memory and mood control, ventrolateral prefrontal cortex—deliberation of decision-making, behavior regulation, trial-and-error learning, and goal-directed behavior, orbitofrontal cortex—emotional control and inhibitory control of behavior, and the medial PFC—motivation and initiation of activity.[ The PFC receives afferent fibers from the thalamic mediodorsal nucleus through the prefronto-thalamic tract and the CN through the prefronto-caudate tract.[ In this patient, the neural connectivity from the CN to the medial and orbitofrontal prefrontal cortices was decreased in both hemispheres. This result indicated severe injury of both prefronto-caudate tracts. Akinetic mutism (AM) is characterized by a complete absence of spontaneous behavior and speech.[ Bilateral disruption of the fronto-subcortical circuit has been suggested as a pathogenetic mechanism of AM.[ In particular, the neural tract connected to the medial PFC is associated with motivation among the neural tracts in the fronto-subcortical circuit.[ Thus, the patient's AM appeared to be ascribed, at least in part, to injury of the prefronto-caudate tract in both hemispheres.

In conclusion, using DTT, injuries of the prefronto-caudate tract were demonstrated in a patient who developed AM following severe traumatic brain injury. We believe that injury of the prefronto-caudate tract might be a pathogenetic mechanism of AM in patients with brain injury. However, because this study was conducted retrospectively and the patient showed severe mutism, we could not perform other neuropsychological tests. Therefore, our results suggest the necessity of evaluation of the fronto-subcortical circuit in patients who develop AM after brain injury.