Review article (meta-analysis)
Specific Brain Lesions Impair Explicit Motor Imagery Ability: A Systematic Review of the Evidence

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Abstract

Objective

To determine which neurologic disorders/lesions impair or restrict motor imagery (MI) ability.

Data Sources

CINAHL, Cochrane, Embase, MEDLINE, Web of Science, PsychINFO, Physiotherapy Evidence Database, and Grey Literature were searched between May 8 and May 14, 2014. Keywords and Medical Subject Headings from 2 concepts (MI and lesion) were exploded to include related search terms (eg, mental practice/mental imagery, neurologic damage/lesion).

Study Selection

Two independent reviewers assessed the 3861 studies that resulted from the database search. The studies were assessed for relevancy using the following inclusion criteria: use of explicit kinesthetic MI; neurologic lesion location identified; and use of an MI ability assessment tool.

Data Extraction

Twenty-three studies encompassing 196 participants were included. The 23 studies used 8 different methods for assessing MI ability. MI assessment scores were then normalized to facilitate comparison across studies.

Data Synthesis

Lesion locations comprised many brain areas, including cortical (eg, parietal and frontal lobes), subcortical (eg, basal ganglia, thalamus), and cerebellum. Lesion etiology primarily was comprised of stroke and Parkinson disease. Several participants presented with lesions resulting from other pathologies. Subjects with parietal lobe damage were most impaired on their ability to perform MI. Subjects with frontal lobe and basal ganglia damage also consistently showed impairment in MI ability.

Conclusions

Subjects with damage to specific brain structures, including the parietal and frontal lobes, showed impaired MI ability. As such, MI-based neurorehabilitation may not be efficacious in all patient populations. Therefore, decisions related to the use of MI in neurorehabilitation should, in part, be based on the patient's underlying pathophysiology.

Section snippets

Study selection criteria

The literature search was conducted between May 8 and May 14, 2014, by a reference librarian. Seven electronic databases were searched, including CINAHL, Cochrane, Embase, MEDLINE, Web of Science, PsychINFO, Physiotherapy Evidence Database, and the Grey Literature (eg, Canadian Public Policy Collection, Cochrane Central Register of Controlled Trials) from inception to present. The search was limited to adult (≥18y) participants. Keywords and Medical Subject Headings from 2 concepts (MI and

Study selection

Figure 2 summarizes how studies were selected for inclusion in this systematic review. The 23 studies comprised 196 participants, including 97 patients poststroke, 75 patients with PD, 7 surgical patients, 1 patient with herpes encephalitis, 1 patient with degenerative pyramidal syndrome, and 15 healthy subjects in whom temporary lesions were created using transcranial magnetic stimulation (see table 2). The 23 studies included 8 different methods for assessing MI ability, including subjective

Discussion

In keeping with our aim to investigate the impact of brain damage on MI ability, we identified 3 structures that when damaged impair MI ability: the parietal lobe, frontal lobe, and basal ganglia. Specifically, we show MI ability is greatly impacted by parietal lobe damage and moderately impacted by frontal lobe damage, albeit outside the posterior region (see fig 3). Furthermore, we show that damage to the basal ganglia, specifically the putamen, impairs MI ability in patients with

Conclusions

Although previous reviews have explored which regions of the brain are involved in MI,5, 27 we have shown which regions, when damaged, impair or prevent MI performance. Our results suggest that parietal lobe damage prevents MI ability, whereas frontal lobe and basal ganglia damage impair MI ability. Although the patients with PD and cerebellar damage in our study show unimpaired MI ability, this finding should be interpreted in the context of methodologic limitations. The aforementioned

Acknowledgments

We thank Carl Helmick, MSc, and the Brain Imaging Laboratory in the Department of Psychiatry, Dalhousie University for assistance in generating figure 2.

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  • Cited by (0)

    Supported by a Summer Studentship from the Canadian Stroke Network and an Early Career Research Award from the Heart and Stroke Foundation of Canada.

    Disclosures: none.

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