Apraxia can be defined as a higher order motor disorder of skilled and/or learned movements [
1]. The motor control deficit in apraxia may be specific for particular movements or body parts: amongst these, apraxia of limb movements is most often described, however apraxias of the cranial musculature (orofacial apraxia: [
2]) and apraxia of the finely coordinated movements of articulation (apraxia of speech, AOS: [
3]) are also well recognised. The nature and brain basis for these specific disorders of voluntary action have not been fully defined, and apraxia remains an issue of considerable neurobiological as well as clinical interest. Anatomical evidence, chiefly from patients with stroke, has implicated distributed cerebral circuitry in the voluntary control of orofacial and limb movements and the production of apraxias [
4,
5]: for orofacial apraxia, prefrontal areas and their subcortical projections are particularly implicated whilst for limb apraxia more posterior areas, particularly the parietal lobe and its connections appear to be most commonly involved [
4,
5]. Aphasia (and in particular, impaired speech production) has often been documented in association with apraxia [
5], and frontoparietal circuits in the dominant hemisphere have also been implicated in the programming of speech sounds and in association with AOS, with particular emphasis on the insula and posterior left inferior frontal gyrus (‘Broca’s area’) [
6‐
9]. However, the relations between these different forms of apraxia and their precise anatomical substrates remain contentious.
Progressive nonfluent aphasia (PNFA) is a neurodegenerative disorder considered to be one of the primary progressive aphasias (PPA) and falling within the frontotemporal lobar degeneration (FTLD) spectrum [
10,
11]. Although the term PNFA was originally considered to include all patients with progressively “nonfluent” speech of any cause [
5], some recent studies have limited PNFA to include only those patients with motor speech impairment and/or expressive agrammatism [
12,
13]. In particular, these studies have stressed the importance of apraxia of speech (AOS) as a defining feature of this group of patients [
14]: AOS is a motor speech disorder with the features of hesitancy, effortfulness with articulatory groping, phonetic errors and dysprosody [
3,
15]. PNFA may be associated clinically with parkinsonian syndromes, in particular either a corticobasal degeneration syndrome (CBS) or a progressive supranuclear palsy (PSP) syndrome. At post mortem, abnormal tau inclusions are often seen in PNFA, with the 4-repeat tauopathies of corticobasal degeneration or PSP common underlying pathologies [
16,
17]. Limb apraxia is a well-known feature of CBS [
18] and can also occur with PSP syndromes [
19,
20]. Although less well studied, orofacial apraxia may also develop in CBS [
21,
22]. The clinico-pathological overlap of CBS and PSP with PNFA, coupled with the central role of AOS in the PNFA syndrome, suggests that apraxia of different kinds may be clinically relevant in PNFA. Both orofacial (or buccofacial) apraxia [
23‐
27] and limb apraxia [
28] have been reported in PNFA, however these associations have not been studied systematically. Furthermore, although AOS has been associated with atrophy in the left frontal lobe and insula [
14,
16], the neuroanatomical correlates of the apraxias accompanying focal dementia syndromes have not been established. In this study, we assessed speech, orofacial and limb praxis in a cohort of patients with PNFA and assessed neuroanatomical correlates of the corresponding apraxis using the semi-automated and unbiased technique of voxel-based morphometry (VBM).