Abstract

Apraxia, traditionally defined as a disorder of skilled action despite preserved strength, sensation, and comprehension, has been described since Liepmann's early 20th-century work as ideomotor, ideational, and limb-kinetic subtypes. Contemporary lesion-symptom mapping and network neuroscience extend this view: praxis failures arise when networks that translate intention into execution are disrupted, whether the effector is limb, face, eyes, speech, or visuospatial construction. We review the clinical phenomenology and examinations that distinguish apraxias at the bedside, map their likely cortical territories relative to the motor/sensory homunculus, and integrate historical and modern evidence for a unifying, network-level account—including sensory, executive, and social analogs.

Introduction

Apraxia is a clinicoradiologic construct: a reproducible pattern of "how" failures (praxis) that cannot be explained by elementary deficits. Liepmann formalized the taxonomy (ideomotor, ideational, limb-kinetic) and emphasized left-hemisphere dominance; Geschwind reframed many apraxias as disconnection syndromes, anticipating modern network analyses. Current evidence situates limb praxis in a left-lateralized parietal-premotor system with temporal semantic inputs and long-range association tracts; ocular, speech, gait, and constructional variants recruit adjacent dorsal, ventral, and fronto-subcortical circuits.

Historical Background

From Jackson and Liepmann to De Renzi and Goldenberg, the literature moved from gyrus-centric localization toward systems that store tool knowledge, configure gestures, and sequence actions. The disconnection perspective—revived by tractography and lesion-network mapping—now anchors praxis as a network failure rather than a single "apraxia center."

A Homuncular Scaffold for Clinical Localization

At the central sulcus, primary motor (M1) and somatosensory (S1) cortices host classic homuncular maps; just anterior lie premotor and supplementary motor areas (execution/selection), and posterior lie inferior/superior parietal regions (body schema, visuomotor transformations, tool concepts). Precision fMRI suggests M1 is interrupted by inter-effector "somato-cognitive action" zones, consistent with praxis as a distributed, integrative function. This scaffold helps place each apraxia subtype "in front of," "on," or "behind" the strip.

Clinical Taxonomy, Examination Anchors, and Networks

Ideomotor Apraxia (IMA)

• Clinical definition: On command or imitation, gestures are spatially/temporally incorrect (mis-posturing, body-part-as-object), with relative sparing in automatic contexts.
• Bedside discrimination: Test transitive pantomimes (e.g., "use a key/hammer") and imitation of meaningless hand shapes; configuration and timing errors with intact power favor IMA.
• Localization & network: Left inferior parietal lobule (angular/supramarginal) with premotor coupling via the superior longitudinal fasciculus; temporal inputs subserve tool semantics. Behind S1/M1 (parietal) with spill anterior to premotor in severe cases.
• Associated conditions: Left MCA stroke; corticobasal syndrome; posterior cortical variants with tool-knowledge load.

Ideational Apraxia

• Clinical definition: Breakdown of multi-step action plans (order, selection, object misuse) despite intact single steps.
• Bedside discrimination: Have the patient "make tea" or "mail a letter"; look for sequencing, selection, and utensil errors.
• Localization & network: Left temporo-parietal conceptual systems with frontal sequencing controllers. Posterior (TPJ/IPL) extending anteriorly with complexity.
• Associated conditions: Alzheimer's disease; large left-hemisphere infarcts.

Limb-Kinetic Apraxia (LKA)

• Clinical definition: Loss of deftness/individuation (coin rotation, pegboard, piano-like sequences) despite normal strength and comprehension; automaticity does not normalize.
• Bedside discrimination: Dexterity tasks (rapid finger alternation, coin rotation) degrade; pantomime may be relatively better than in IMA.
• Localization & network: Lateral premotor and caudal M1 (area 4p)—on/just anterior to the M1 hand zone; corticospinal timing pathways.
• Associated conditions: Corticobasal degeneration; PSP; frontal strokes; post-MCA lesions.

Buccofacial (Orofacial) Apraxia

• Clinical definition: Failure to perform non-speech oral/facial actions on command (blow, pucker, puff) with preserved spontaneous movements.
• Localization & network: Frontal operculum, anterior insula, and inferior frontal gyrus (ventral to the face homunculus).
• Associated conditions: Large left MCA strokes; Broca-zone lesions; insular degenerations.

Apraxia of Speech (AOS) & Primary Progressive AOS (PPAOS)

• Clinical definition: Effortful, halting speech with trial-and-error "groping," inconsistent phoneme errors, and length/complexity effects; distinct from dysarthria (execution) and aphasia (linguistics).
• Localization & network: Lesion studies identified the left anterior insula/superior precentral gyrus of the insula as a critical node; progressive forms implicate superior premotor/SMA and broader speech-salience networks.
• Associated conditions: Left MCA stroke; PPAOS (often a 4R-tauopathy—PSP/CBD spectrum).

Constructional Apraxia

• Clinical definition: Impaired copying/assembly/drawing with spatial disorganization, omissions, fragmentation (e.g., Rey-Osterrieth figure, interlocking pentagons).
• Localization & network: Bilateral parietal with right-hemisphere bias (SPL/IPL, parieto-occipital junction); frontal co-lesions add perseveration. Prominent in posterior cortical atrophy (PCA).
• Associated conditions: Right parietal stroke; Alzheimer's disease; PCA.

Dressing Apraxia

• Clinical definition: Misorientation of clothing relative to body schema; often coexists with neglect but can be isolated.
• Localization & network: Right parietal body-schema network behind S1; conceptual status debated (neglect vs discrete deficit).
• Associated conditions: Right MCA stroke; PCA spectrum.

Gait ("Frontal") Apraxia

• Clinical definition: Initiation failure with short-stepped, broad-based gait; legs move normally supine.
• Localization & network: Medial frontal (SMA/cingulate) and fronto-subcortical loops; classic in idiopathic normal-pressure hydrocephalus (iNPH).
• Associated conditions: iNPH; bilateral frontal vascular disease.

Oculomotor Apraxia (OMA)

• Clinical definition: Inability to initiate voluntary saccades (often horizontal) with compensatory head thrusts; reflexive saccades may be preserved.
• Localization & network: Frontal eye fields and parietal eye fields within dorsal attention/visuomotor networks; bilateral involvement is typical.
• Associated conditions: Bálint syndrome; genetic AOA1/2; acquired bifrontal/biparietal lesions.

Optic Ataxia (Visuomotor Apraxia)

• Clinical definition: Misreaching and grip-orientation errors when vision must guide the reach (especially to peripheral targets), with intact strength/fields.
• Localization & network: Superior parietal lobule and occipito-parietal dorsal stream (parietal reach region)—posterior to the hand area of S1/M1.
• Associated conditions: Bálint syndrome; bilateral parieto-occipital strokes; PCA.

Apraxia of Eyelid Opening (AEO)

• Clinical definition: Nonparalytic inability to voluntarily open eyelids after closure; levator strength and cranial nerve function otherwise intact.
• Localization & network: Frontal-basal ganglia-brainstem circuits; lesion-network mapping and DBS series implicate fronto-subcortical control of levator inhibition/disinhibition.
• Associated conditions: Parkinson's disease and PSP; rare after stroke or STN-DBS.

Callosal (Disconnection) Apraxia

• Clinical definition: Left-hand apraxia on command with preserved right hand; often with left-hand agraphia/tactile anomia.
• Localization & network: Corpus callosum body/anterior trunk interrupting transfer from the language-dominant praxis network to the right motor cortex.
• Associated conditions: Callosal infarct, surgical callosotomy, agenesis.

Networks, Tracts, and the "Where" of Praxis Failure

Structural and lesion-network mapping converge on a praxis connectome: inferior parietal (conceptual/tool/body schemas) ↔ premotor/SMA (selection, sequencing) via SLF; temporal conceptual hubs route through ILF/IFOF; dorsal stream PPC supports vision-for-action; fronto-subcortical circuits handle initiation/inhibition (gait, eyelid). Disconnections between temporal conceptual stores and parietal-premotor "how" systems predict limb apraxia severity and error type.

Sensory, Executive, and Social Analogs

Optic ataxia shows that apraxia-like failures can be sensory-guided: vision is intact, movement is intact, but vision-for-action mapping is broken (parietal reach region). By analogy, failures of touch-guided manipulation, auditory-to-vocal reproduction, or vestibular-guided action are plausible praxis analogs; frontal network injury can yield "social/executive apraxias" (goal neglect, utilization behavior) where intention fails to become context-appropriate action. These expand the construct without diluting its core: a network translation failure between representation and realization.

Differential Diagnosis and Exam Strategy (Practical "Five-Minute" Flow)

1. Exclude elementary confounds (weakness, sensory loss, visual fields, neglect, aphasia, dysarthria).
2. Gesture tasks (pantomime + meaningless imitation) → configuration/timing errors = IMA.
3. Dexterity tasks (coin rotation, rapid finger sequences) → fluent vs clumsy: clumsiness regardless of context = LKA.
4. Copy/build (Rey figure, blocks) → spatial disorganization/fragmentation = constructional apraxia.
5. Ocular (commanded vs reflexive saccades) → initiation failure with blink/head "unlock" = OMA.
6. Visuomotor reach (peripheral targets, crossed hand/field) → field- and hand-specific misreaching = optic ataxia. Localize "anterior/on/posterior" to the strip and consider tract-level disconnection.

Where This Leaves the Homunculus

The modern motor map is not a simple ribbon but a mosaic alternating effector territories with inter-effector, higher-order zones. This aligns with apraxia as a systems disorder: lesions behind the strip (parietal/dorsal stream) mis-specify space, tools, and sequences; lesions on/just in front of the strip (M1/premotor/SMA) degrade execution and initiation; ventral frontal/insular systems program speech and orofacial praxis; eye fields and their parietal partners govern the ocular analog.

Conclusions

A century after Liepmann, apraxia reads best as a family of network disconnection phenotypes anchored to the homunculus: each bedside error pattern implies a tract-supported circuit between what (concept) and how (program). Using disciplined examination, clinicians can differentiate subtypes (IMA vs LKA; optic ataxia vs cerebellar ataxia; OMA vs supranuclear palsy), localize to cortex and connections, and anticipate associated syndromes (stroke patterns, PCA, PSP/CBD, iNPH). This reframing unifies classical taxonomy with modern systems neuroscience and makes apraxia a practical tool for bedside localization.

References

1. Liepmann H: historical syntheses.
2. Geschwind N: disconnection syndromes.
3. Goldenberg G; Buxbaum LJ: parietal-premotor praxis network.
4. Rosenzopf H et al.: structural network in apraxia.
5. Rounis E et al.: limb apraxias and higher-order perceptual/body-schema influences.
6. Andersen RA et al.: optic ataxia and parietal reach region.
7. Dronkers NF; Josephs KA; Duffy JR: apraxia of speech and PPAOS.
8. Russell C et al.; Crutch SJ et al.: constructional apraxia and PCA.
9. StatPearls/Brain Communications/DBS series: apraxia of eyelid opening.
10. iNPH gait/apraxia.