Injury of the cortico-ponto-cerebellar tract in a patient with mild traumatic brain injury: A case report.

RATIONALE: We report on a patient with injury of the cortico-ponto-cerebellar tract (CPCT) following mild traumatic brain injury (TBI), diagnosed by diffusion tensor tractography (DTT). PATIENT CONCERNS: A 53-year-old female patient was injured in a car crash. While under treatment at a local medical center for headache, mild motor weakness, and cognitive impairment that developed following the car crash, she fell, hitting her head on the ground, about six weeks after the car crash. DIAGNOSES: Approximately three months after the car crash, she began to show tremor on both hands and mild truncal ataxia. Twenty months after the car crash, when she underwent neurological evaluation at the rehabilitation department of a university hospital, she presented with mild resting and intentional tremor on both hands, and mild truncal ataxia.
INTERVENTIONS: N/A. OUTCOMES: On 20-month DTT, the left CPCT showed tearing at the level of the subcortical white matter and pons, and discontinuation at the cerebellar portion. However, the integrity of the DRTT was well-preserved in both hemispheres. LESSONS: Using DTT, injury of the CPCT was demonstrated in a patient with ataxia and tremor following mild TBI.

Introduction

The cerebellum, located in the posterior fossa of the brain, is important in coordinating movement by communicating with the cerebrum via cerebellar peduncles.[ The cortico-ponto-cerebellar tract (CPCT) and dentato-rubro-thalamic tract (DRTT) are major neural circuits on the cerebellum for movement coordination.[ The CPCT, a major afferent fiber in the middle cerebellar peduncle, and the DRTT, a major efferent fiber in the superior cerebellar peduncle, are involved in coordination of movement.[ Hence, injury of the CPCT and DRTT is usually accompanied by cerebellar symptoms including ataxia and tremor.[ Several studies have reported clinical features following injury of the CPCT or DRTT in stroke, neurodegenerative disease, and traumatic brain injury (TBI).[

Mild TBI, comprising 70% to 90% of all TBI, is defined as less than 30 minutes of loss of consciousness, less than 24 hours of post-traumatic amnesia, and an initial Glasgow Coma Scale (GCS) score of 13 to 15. At least 15% of patients with mild TBI present with disabling symptoms even though no abnormal lesion is observed in the brain computed tomography (CT) and magnetic resonance imaging (MRI).[ It is very difficult to find an abnormal lesion following mild TBI with conventional MRI.[ Recently developed diffusion tensor tractography (DTT), derived from diffusion tensor imaging (DTI), allows estimation and visualization of the microstructural integrity of white matter and has a unique advantage in detection of invisible neural injury in patients with mild TBI.[ A recent study using DTT demonstrated injury of the DRTT in a patient with mild TBI.[ However, no study on injury of the CPCT in patients with mild TBI has been reported.

In this study, we report a patient with injury of the CPCT following mild TBI, diagnosed by DTT.

Case report

A 53-year-old female patient was injured in a car crash. The patient was struck from behind by a mini-bus while stopped waiting for a signal at an intersection. Her head hit the wheel during head flexion. The patient lost consciousness for approximately 10 minutes and experienced post-traumatic amnesia for approximately 15 minutes after the head trauma. Her GCS score was 15. While under treatment at a local medical center for headache, mild motor weakness, and cognitive impairment that developed following the car crash, she fell, hitting her head on the ground, about 6 weeks after the car crash. She lost consciousness for approximately 10 minutes, without post-traumatic amnesia. However, her GCS score was 15. Approximately 3 months after the car crash, she began to show tremor on both hands and mild truncal ataxia. Twenty months after the car crash, when she underwent neurological evaluation at the rehabilitation department of a university hospital, she presented with mild resting and intentional tremor on both hands, and mild truncal ataxia (the Scale for the Assessment and Rating of Ataxia---8 points, full score: 40 points; higher points means more severe ataxia).[ No specific lesion was observed on conventional brain MRI (Fig. 1A). The patient provided written and informed consent. The study protocol was approved by the Yeungnam University Hospital Institutional Research Board.

Figure 1

(A) T2-weighted brain MR images at 20 months after onset show no abnormality. (B) Results of diffusion tensor tractography for the cortico-ponto-cerebellar tract (CPCT). The left CPCT shows tearing (blue arrows) at the level of the subcortical white matter and pons, and discontinuation (purple arrows) at the cerebellar portion. However, the integrity of the dentato-rubro-thalamic tract is well preserved in both hemispheres.

Diffusion tensor tractography

DTI data were acquired at 20 months after the car crash using a 1.5T (Philips, Ltd, Best, The Netherlands) with 32 gradients. Imaging parameters were as follows: acquisition matrix = 96 × 96; reconstructed to matrix = 192 × 192; field of view = 240 × 240 mm2; echo time = 10,398 ms; repetition time = 72 ms; b = 1000 s/mm2; and a slice thickness of 2.5 mm. Before the fiber tracking, eddy current correction was applied to correct the head motion effect and image distortion using the Oxford Centre for Functional Magnetic Resonance Imaging of the Brain (FMRIB) Software Library.[ For fiber tracking, we used FMRIB Software Library based on probability tracking with a result threshold of 2 streamlines.[ For reconstruction of the CPCT, seed region of interest (ROI) was given at the primary sensorimotor cortex on the axial image and 2 target ROIs were placed at the anterior portion of pons on the axial image and the contralateral middle cerebellar peduncle on the coronal image.[ For the DRTT, seed ROI was placed on the dentate nucleus behind the floor of the fourth ventricle on the coronal image.[ Two target ROIs were given at the junction of the superior cerebellar peduncle between the upper pons and cerebellum on the coronal image and the contralateral red nucleus of the upper midbrain on the axial image.

On 20-month DTT, the left CPCT showed tearing at the level of the subcortical white matter and pons, and discontinuation at the cerebellar portion (Fig. 1B). However, the integrity of the DRTT was well preserved in both hemispheres.

Discussion

In this study, using DTT, we found injury (tearing and discontinuation) of the left CPCT with preservation of the DRTT in both hemispheres in a patient with ataxia and tremor following mild TBI. Thus, the ataxia and tremor in this patient can be partially ascribed to injury of the left CPCT. Because no definite brain lesion was detected on conventional brain MRI, traumatic axonal injury (TAI) was the most likely pathogenetic mechanism in this patient.[ However, we could not discern whether this injury resulted from the car crash or the later fall. The delayed onset (3 months after the car crash and 6 weeks after the fall) of ataxia and tremor suggests that the TAI was a secondary injury in which axons were not initially damaged, but injured by a sequential process of impaired axoplasmic transport, continued axonal swelling, and disconnection.[

Several studies using DTI have reported injury of the CPCT in patients following stroke and neurodegenerative disease.[ Kitamura et al[ reported that fractional anisotropy value of damaged CPCT was associated with ataxia severity in 18 patients with neurodegenerative disease. In 2012, Min et al[ described an abnormal portion of the CPCT in a patient with cerebellar ataxia following central pontine myelinolysis. In 2016, Jang et al[ reported that severe ataxia in a patient with bilateral tegmental pontine hemorrhage was attributed to thinning of the CPCTs in both hemispheres. The following year, Schulz et al[ reported that injury of the CPCT related with residual motor function in 26 patients with chronic ischemic stroke. To our best knowledge, this is the first study to demonstrate injury of the CPCT in a patient with mild TBI. However, this study is limited because it is based on a single case report. In addition, DTT can produce both false-positive and negative results due to multiple fiber directions in a voxel or partial volume effect throughout the white matter of the brain.[

In conclusion, using DTT, injury of the CPCT was diagnosed in a patient with ataxia and tremor following mild TBI. We believe that evaluation of the CPCT would be helpful in diagnosis of patients who show movement coordination problems such as ataxia and tremor following mild TBI.