Prefrontal cortical thickness in motor neuron disease

Abstract

Objective

To examine whether the distribution of prefrontal cortical thickness in patients with motor neuron disease is normal or bimodal and how it compares to the normal population.

Methods

158 patients with motor neuron disease (MND) and 86 healthy controls (HC) were enrolled in a prospective, two-center study with a common structural MRI protocol. Cortical thickness measures were extracted for the prefrontal cortex, premotor cortex, motor cortex, and occipital cortex using FreeSurfer, adjusted for age and sex, and tested for normality of distribution.

Results

Cortical thickness measures of the bilateral prefrontal, premotor, motor, and occipital cortex were normally distributed in patients and healthy controls. MND-related cortical thinning was observed in the right motor cortex ( p = 0.002), reflected in a significantly higher proportion of MND cases being worse than −1 standard deviation of the healthy control mean: 29.1% in the right motor cortex ( p = 0.002). Cortical thinning of the left motor cortex was a function of clinical phenotype and physical disability. Left prefrontal cortical thickness was reduced in patients with additional cognitive and/or behavioural deficits compared to MND patients without cognitive deficits. Prefrontal, premotor, motor, and occipital cortical thickness was related to patients' general cognitive abilities.

Conclusion

The study shows that prefrontal cortical thickness in MND is normally distributed but shifted towards thinner cortex in MND patients with cognitive and/or behavioural impairment. The distribution of thickness values did not indicate the assumption of a bimodal distribution although patients with comorbid cognitive deficits are more likely to suffer from prefrontal cortical thinning.

Highlights

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  There is an increased prevalence of prefrontal cortical thinning in MND patients with cognitive and/or behavioural impairment.

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  Distribution of thickness values among different MND subgroups appear unimodal.

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  Thinning is dependent of clinical phenotype, disease severity, and cognitive impairment.