Praxis and Related Cortical Movement Abnormalities

Clinicians have applied the term “praxis,” and its disorder, “apraxia,” to a wide number of conditions involving impaired motor performance. A strict and specific use of the term “apraxia” (or “dyspraxia”), however, is limited to disturbances in learned skilled movements due to a cognitive defect in motor programming, such as errors in pantomiming brushing one’s teeth or gesturing “good-bye.” Patients with apraxia have normal basic motor and sensory functions but cannot perform movements because of disturbances at a cognitive command and control level. The term “apraxia” is misapplied to visuospatial deficits, such as “constructional apraxia,” “dressing apraxia,” and “oculomotor apraxia” (see Chapter 10 ); the unique “apraxia of speech,” or disorder of motor planning of speech sounds, is discussed in Chapter 8. This chapter primarily discusses the examination of apraxias of the upper extremities, with some discussion of orobuccal-facial, whole body, and gait apraxia and related cortical movement abnormalities.

Apraxia

Apraxia is not rare. It may occur in over half of patients with acute left hemisphere lesions. Causes of apraxia include strokes, tumors, multiple sclerosis, corticobasal syndrome, Alzheimer disease, Creutzfeldt-Jakob disease, Lewy body dementias, and others. In addition, apraxias cause significant dysfunction, particularly when there is difficulty with critical upper extremity and hand movements. Despite the importance of apraxia, clinicians often fail to recognize or evaluate for apraxia, particularly in the presumably spared extremity contralateral to a hemiparetic limb from stroke or other focal lesion.

The model for praxis representation in the brain is analogous to kinesthetic software programs (“praxicons”) for automatized movements, which are usually localized in a left parietal hub ( Fig. 11.1 ). This model originates with Hugo Liepmann from the early 1900s and, with elaboration, continues to be the basis for the neuroanatomy of limb praxis. These left parietal praxicons are essentially spatiotemporal movement formulas associated with the meaning of the actions (action semantics). Despite the left hemisphere lateralization, it takes both parietal lobes for automatizing effortful, unfamiliar movements, with the right parietal region contributing to spatial orientation and positioning. Through ventral and dorsal streams, the praxicons connect to the left supplementary motor area for translation into motor programs, which output to primary motor cortex for control of the contralateral limb. Finally, the motor program information traverses the corpus callosum in the frontal region for control of the ipsilateral limb. There are additional influences on praxis from frontal-subcortical motor loops in the basal ganglia, the thalami, and their white matter connections. Left-handed patients may have right parietal praxicons and apraxia from right hemisphere lesions; however, hand preference can be dissociable from the laterality of the movement formulas.

Based on this model, a useful clinical classification of the apraxias includes ideomotor (parietal or disconnection), dissociation, ideational, conceptual, limb-kinetic, and callosal types ( Table 11.1 ). Ideomotor apraxia is the prototypical apraxia syndrome with spatiotemporal errors in performing learned motor acts from problems executing the spatiotemporal movement formulas for these acts, either from left inferior parietal disorders or from disconnection along the pathways from parietal to the ipsilateral motor areas. Dissociation apraxia results in unrecognizable movement consequent to the dissociation of the praxis network from the language commands for eliciting them. Ideational apraxia is an inability to organize and perform a series of movements in the right order. Conceptual apraxia is an incorrect, but correctly executed, choice of semantic action, such as tool use or tool selection. Clinicians often conflate ideational and conceptual apraxias because they have less specific localization and usually occur together in advanced dementias. Traditionally, the classification of apraxias also includes limb-kinetic apraxia, although this is actually a disturbance in fine finger or motor movements and not a specific disorder of praxis. Finally, the classification of apraxia includes patients with callosal lesions with limb apraxia limited to the nondominant limbs.

TABLE 11.1

Apraxias: Most Likely Finding on Examination

	Ideomotor-Parietal	Ideomotor-Disconnection	Dissociation	Ideational	Conceptual	Limb-Kinetic
Pantomime to verbal command	Abnormal ¹	Abnormal ¹	Abnormal ²	Abnormal ³	Abnormal ⁴	Abnormal ⁵or Normal
Imitation of gestures	Abnormal ¹	Abnormal ¹	Normal	Normal ³	Normal	Abnormal ⁵or Normal
Gesture knowledge	Abnormal	Normal	Normal	Normal	Normal ⁴	Normal
Sequential actions	Normal ¹	Normal	Abnormal	Abnormal	Normal ⁴	Normal
Conceptual knowledge	Normal	Normal	Normal	Abnormal	Abnormal	Normal
Real object use	Abnormal ⁶	Abnormal ⁶	Normal	Abnormal ³^,⁷	Abnormal ⁴	Abnormal ⁵or Normal
Meaning-less gestures	Abnormal	Abnormal ⁶	Normal	Abnormal ³^,⁷	Normal ⁷	Abnormal ⁵or Normal
Limb-kinetic	Normal	Normal	Normal	Normal	Normal	Abnormal ⁵

1 Spatiotemporal production errors on single, individual ideomotor tasks.

2 Unrecognizable movements or attempts.

3 For sequencing errors only, i.e., errors on multiple, serial ideomotor tasks.

4 Abnormal if involves content of tool use/action or tool selection.

5 For decreased dexterity in fine finger movements.

6 Errors depend on severity of apraxia; may perform adequately.

7 But may be abnormal from advanced dementia rather than from apraxia. Modified from Mendez MF, Deutsch MB. The limb apraxias and related disorders. In: Daroff RB, Fenichel GM, Jankovic MD, Mazziotta JC, Pomeroy SL, eds. Bradley’s Neurology in Clinical Practice . 7th ed. New York, NY: Elsevier; 2016, pp. 115–121.

THE EXAMINATION OF APRAXIA

Some guidelines are useful for apraxia testing. First, the examination for apraxia and cortical motor disorders must be part of the complete mental status examination (MSX) and neurological examination. The examiner cannot characterize these disorders without excluding other deficits that might be responsible for disturbances in movement. The examiner needs to exclude other cognitive deficits, such as attentional deficits, language impairment, perceptual or spatial disturbances, or executive dysfunction. The examiner also needs to exclude primary motor or sensory problems, such as weakness, rigidity or spasticity, incoordination and dysmetria, or sensory loss. Second, note any complaints of loss of dexterity and observe for any unusual posturing or movements. Patients with apraxia may be unaware of these deficits, and the examiner needs to specifically inquire about the patient’s ability to perform skilled movements. Although apraxia is not an evident dystonia or dyskinetic movement disorder, it may be evident on attempts at learned motor movements. Finally, start testing with verbal commands. The examination usually focuses on testing both upper limbs, first the dominant hand and then the nondominant hand independently, avoiding going from one hand to the other so as to avoid self-cueing. If the patient fails to perform normally on verbal commands, then the examiner can evaluate imitation, gesture comprehension, sequencing, conceptual knowledge, real object use, and imitation of meaningless gestures.

AXIAL AND LOWER EXTREMITY APRAXIA

Before discussing limb apraxia there should be a screen for apraxia affecting the central axis of the body and the lower extremities ( Table 11.2 ). Orobuccal-facial apraxia is associated with left inferior frontal and insular lesions. Begin evaluating for orobuccal-facial apraxia by asking the patients to pretend to suck through a straw or pretend to blow out a match. Then evaluate responses to whole body commands, such as asking the patient to stand up, bow, or assume a boxer’s stance. Dementia patients with whole body apraxia may have difficulty sitting or standing from a chair or rolling over when in a supine position. Next check for gait apraxia or a “magnetic gait,” reported with normal pressure hydrocephalus, vascular dementia, and other frontal lobe conditions. These patients have a hard time getting started, as if their feet are glued to the ground, with subsequent slow, shuffling gait. The examiner can videotape this whole maneuver and time it for quantification (e.g., Timed Walk or Timed Up and Go Tests). In addition to asking them to initiate a gait, evaluate for the presence of a “foot grasp,” similar to a hand grasp reflex, with curling down of the toes on stroking the plantar aspect of the feet. Further evaluate for lower extremity apraxia with commands such as writing on the floor while sitting, making figure threes or eights with their legs while supine, and other activities as noted in Table 11.2 .

TABLE 11.2

Praxis Testing of the Axis (Including Lower Extremities)

	Transitive Actions	Intransitive Actions
Orobuccal-facial	Suck on straw	Wink
	Blow out match	Blow a kiss
	Sniff flowers	Stick out tongue
	Lick icing from lips	Whistle
Whole body	Pretend to lift weights	Stand up
	Swing imaginary bat	Bow
	Pretend to walk tightrope	Roll over in bed
	Pretend to sweep floor	Assume boxer stance
Gait and lower extremities	Kick imaginary ball	Make a figures “3” or “8” with legs while supine
	Write with foot on floor	Turn around when walking
	Emulate bicycle peddling	Start and continue gait
	Put out cigarette	Timed Walk (10 meters or 30 feet) or Up and Go Test (both can videotaped)