Apraxia and neglect are two of the most distinctive higher cortical syndromes in clinical neurology — both reflect disorders of the integration of action, perception, and attention rather than primary motor or sensory deficits. Apraxia is the inability to perform learned skilled movements despite intact strength, sensation, and comprehension. Neglect is failure to attend to or recognize a side of space, body, or stimulus. Both syndromes provide remarkably specific localizing information when recognized at the bedside. This page covers the major types of apraxia and neglect, their substrates, and the tests that distinguish them.

Apraxia

Apraxia is the loss of the ability to perform purposeful, learned movements despite preserved elementary motor function, sensation, comprehension, and motivation. It reflects damage to the cortical motor planning systems — predominantly in the dominant hemisphere — that translate intention into action.

Categories of Apraxia

Ideomotor Apraxia

Inability to perform a single learned motor act on command (pantomime tool use), despite being able to perform spontaneously.
Examples: “Show me how you would brush your teeth”; “Wave goodbye”; “Show me how to use a hammer.”
Often performs better with the actual object present.
Substrate: dominant inferior parietal lobule and connections to dominant premotor cortex. The “praxis” representations live in the left hemisphere parietal-premotor system.
Often accompanied by aphasia, Gerstmann syndrome, hemiparesis.

Ideational Apraxia

Inability to perform a multi-step sequence of learned acts to achieve a goal.
Examples: “Make a sandwich”; “Light a candle with these materials.”
The patient may perform individual steps but cannot sequence or plan.
Substrate: bilateral parietal damage, often with broader cognitive impairment (early dementia, especially Alzheimer disease).

Limb-Kinetic Apraxia

Loss of fine finger dexterity and skilled limb movement.
The clumsy, unrefined movement with preserved basic strength.
Substrate: contralateral premotor cortex or corticospinal involvement.

Constructional Apraxia

Inability to draw, copy, or construct figures or block designs.
Substrate: usually right (non-dominant) parietal; sometimes left.
Tested with clock drawing, copying figures (intersecting pentagons, cube), block design.
Right parietal patients tend to neglect the left side of the figure; left parietal patients produce poor but symmetric reproductions.

Dressing Apraxia

Inability to dress oneself appropriately despite intact strength and sensation.
Patient may put both feet through one pant leg or shirt on backward.
Substrate: right (non-dominant) parietal; often accompanies neglect.

Buccofacial / Orofacial Apraxia

Inability to perform learned face/mouth movements on command (blow out a match, blow a kiss, lick lips).
Substrate: dominant frontal opercular region; often accompanies Broca aphasia.

Gait Apraxia

Inability to walk despite intact strength, sensation, and motor control of individual limbs.
“Magnetic gait” — feet seem stuck to the floor.
Substrate: bilateral medial frontal disease (anterior cerebral artery territory or normal-pressure hydrocephalus).

Apraxia of Speech

Distinct from aphasia; deficit in motor programming of speech sounds.
Effortful, halting, with phonetic errors and inconsistent articulation.
Substrate: dominant frontal opercular cortex, anterior insula.
Common in primary progressive nonfluent aphasia.

Callosal Apraxia (Left-Hand Apraxia)

Apraxia of the LEFT hand only (in right-handed patient).
Substrate: anterior corpus callosum. The left hemisphere praxis system can no longer command the right motor cortex (which controls left hand).
Classic disconnection syndrome.

Testing for Apraxia

Pantomime to command: “Show me how you would…” — comb hair, brush teeth, use a key, salute, wave goodbye, etc.
Imitate the examiner: examiner demonstrates and asks the patient to copy.
Use of actual object: hand the patient a hammer or comb and ask them to use it.
Multi-step task: “Show me how to make a peanut butter sandwich (or some appropriate task).”
Sequence tasks (Luria three-step hand sequence): fist, edge, palm in a repeating sequence.
Constructional: draw a clock, copy intersecting pentagons or a 3D cube.
Dressing: observe; provide a garment with one sleeve inside out.
Gait: observe walking.

Hemispatial Neglect

Neglect is failure to attend to, perceive, or respond to stimuli on one side of space, the body, or external objects — despite intact primary sensory function. It is most commonly seen from right (non-dominant) parietal lesions, producing left-sided neglect. The asymmetry reflects the right hemisphere’s dominance for spatial attention to both sides of space, while the left hemisphere preferentially attends to the right side only.

Components and Types of Neglect

Personal Neglect

Failure to attend to one side of the body.

Patient may shave only one side of the face, fail to dress the affected side, eat with one hand while neglecting the other.
Patient may not recognize the affected limb as their own.

Peripersonal (Extrapersonal) Neglect

Failure to attend to one side of immediate surrounding space.

Patient may eat only food on one side of the plate.
May bump into objects on the affected side.
When drawing a clock, all numbers may be on the right side.

Representational Neglect

Failure to attend to one side of imagined or remembered scenes.

When asked to imagine a familiar scene (Bisiach’s famous Milan plaza experiment), patient describes only the side that would be on the right from their imagined viewpoint.

Motor Neglect

Reduced spontaneous movement of the contralesional limb despite preserved strength.

Visual Extinction

When two stimuli are presented simultaneously, only the ipsilesional stimulus is perceived; each stimulus alone is perceived. Tested with bilateral simultaneous finger wiggles.

Tactile Extinction

Same principle for touch: bilateral simultaneous touch, the contralesional side is not perceived.

Associated Phenomena

Anosognosia

Denial or unawareness of the deficit. Severe left hemiparesis denied: “I’m fine, there’s nothing wrong.” Right parietal damage.

Anosodiaphoria

Indifference to the deficit; patient acknowledges the weakness but is unconcerned.

Asomatognosia

Denial that the affected limb belongs to the patient. “This is not my hand; whose hand is this?”

Allesthesia

Stimulus on the affected side perceived on the unaffected side.

Somatoparaphrenia

Bizarre beliefs about the affected limb (e.g., that it belongs to a relative).

Testing for Neglect

Line bisection: ask the patient to mark the midpoint of a horizontal line. Right parietal patients mark to the right of true center.
Cancellation tests: cross out all the As (or similar) scattered across a page. Patient misses the contralesional side.
Drawing tests: clock drawing (numbers all on one side), copying figures (left half omitted or distorted).
Sensory extinction: double simultaneous touch.
Visual extinction: double simultaneous visual stimulation.
Reading: may omit the left side of words or sentences.
Bedside observation: notice if patient ignores the left side of the bed, food, or examiner.
Personal care: does the patient groom, wash, dress only one side?

Localization

Neglect is most strongly associated with right parietal damage, particularly the inferior parietal lobule (including the temporoparietal junction). The right superior temporal gyrus has also been implicated. The right hemisphere appears to be specialized for spatial attention to both sides — when damaged, the left hemisphere can only direct attention to the right side, producing left-sided neglect. Left parietal damage rarely produces neglect because the right hemisphere compensates.

Some neglect can also arise from frontal lesions (premotor, anterior cingulate), thalamus (pulvinar), and basal ganglia.

Causes of Apraxia and Neglect

Stroke: most common. MCA territory for both apraxia (dominant) and neglect (non-dominant).
Tumor: glioma, meningioma, metastasis in parietal regions.
Demyelinating: MS plaques in parietal white matter.
Trauma: parietal contusion.
Neurodegenerative:
- Alzheimer disease: progressive apraxia, sometimes neglect (especially in posterior cortical atrophy variant).
- Corticobasal degeneration: asymmetric apraxia + alien limb + cortical sensory loss + parkinsonism.
- Posterior cortical atrophy: Balint syndrome features + simultanagnosia + alexia.
Watershed infarct: bilateral parieto-occipital (Balint syndrome features).

Clinical Significance and Treatment

Apraxia

Affects daily activities even when patients have preserved strength.
Speech-language and occupational therapy focus on training compensation.
Often improves over months following stroke; persists in degenerative disorders.

Neglect

Predicts poorer rehabilitation outcome.
Patient may not engage in therapy because they don’t perceive the affected side.
Anosognosia compounds the rehabilitation challenge.
Approaches: prism adaptation, vestibular stimulation, mirror therapy, visual scanning training.
Often improves over weeks to months but may persist.

🔍 Did You Know?

The classical Bisiach “Milan plaza” experiment (1978) demonstrated something remarkable about representational neglect. Researchers asked patients with right parietal damage and left-sided neglect to imagine standing in the Piazza del Duomo in Milan and describe what they could “see.” When asked to imagine standing at the cathedral facing the plaza, patients described only the buildings and landmarks on the right side of their imagined scene — the left side of the plaza was simply absent from their mental image. When asked to imagine standing at the opposite end facing the cathedral, they then described the buildings that previously had been on their imagined left (now on their imagined right) but neglected the buildings now on their imagined left. The experiment showed that neglect affects not just current perception but also the construction of mental images — the patient’s right hemisphere damage impaired their ability to represent the left side of remembered scenes from any viewpoint. The finding had profound implications: neglect is not a deficit of incoming sensory information but a deficit of spatial attention applied to representations, including those generated from memory. The right hemisphere appears to be specialized for representing the entire spatial layout of a scene — when damaged, the leftward half of any space cannot be attended to, whether the space is in the room, on the body, on the page, or in imagination. The Bisiach experiment helped establish that neglect is a disorder of representation and attention, not of basic perception — a conceptual breakthrough that shaped modern cognitive neuroscience.

Pitfalls and Pearls

Apraxia is not weakness. The patient cannot perform a learned act on command despite intact strength, sensation, comprehension.
Ideomotor apraxia: cannot pantomime tool use; dominant inferior parietal.
Ideational apraxia: cannot sequence multi-step acts; bilateral parietal, often with dementia.
Limb-kinetic apraxia: clumsy finger movement; premotor or corticospinal.
Constructional apraxia: cannot copy or construct; usually right parietal.
Dressing apraxia: usually right parietal, often with neglect.
Buccofacial apraxia: dominant frontal opercular; often with Broca aphasia.
Gait apraxia (magnetic gait): bilateral medial frontal; NPH classic.
Callosal apraxia: left-hand apraxia only; anterior corpus callosum.
Apraxia of speech: motor programming deficit; can coexist with aphasia. Common in nfvPPA.
Hemispatial neglect: failure to attend to left side from right parietal damage.
Anosognosia: denial of deficit. Predicts worse rehabilitation outcome.
Sensory and visual extinction: bilateral simultaneous stimulation reveals subtle neglect.
Line bisection and cancellation tests: bedside neglect screens.
Right parietal damage classically produces left neglect + anosognosia + dressing apraxia + constructional apraxia.
Left parietal damage classically produces ideomotor apraxia + Gerstmann syndrome + aphasia.
Corticobasal degeneration: asymmetric apraxia + alien limb + cortical sensory + parkinsonism. Tau pathology.
Posterior cortical atrophy: atypical AD with visuospatial features + Balint syndrome + alexia.

References

Brazis PW, Masdeu JC, Biller J. Localization in Clinical Neurology. 7th ed. Wolters Kluwer; 2017.
Mesulam MM. Principles of Behavioral and Cognitive Neurology. 2nd ed. Oxford University Press; 2000.
Heilman KM, Valenstein E, eds. Clinical Neuropsychology. 5th ed. Oxford University Press; 2012.
Bisiach E, Luzzatti C. Unilateral neglect of representational space. Cortex. 1978;14(1):129-133.
Goldenberg G. Apraxia: The Cognitive Side of Motor Control. Oxford University Press; 2013.
Ropper AH, Samuels MA, Klein JP, Prasad S. Adams and Victor’s Principles of Neurology. 11th ed. McGraw-Hill; 2019.