Apraxia

Clinical presentation and gait features

Patients with frontal apraxia exhibit a very characteristic movement pattern. When standing, a flexed posture is observed, and the base of support (distance between the feet) is slightly widened to compensate for instability.

Gait becomes extremely slow. The patient moves in small, shuffling steps. A diagnostic marker of moderate impairment is the reaction to an external rhythm: the patient's gait noticeably improves if they start walking strictly in step with a healthy assistant.

Deficit progression and associated symptoms

Gait apraxia tends to progress steadily, passing through several severe stages:

1. Initial manifestations: specific difficulties emerge specifically at the start of walking (the patient finds it hard to take the first step).
2. Astasia: complete loss of the ability to stand without support.
3. Abasia: complete loss of the ability to walk.
4. Severe stage: inability to sit independently or even turn over in bed.

Because the etiology involves frontal lobe damage, motor impairments are rarely isolated. They are frequently accompanied by reduced insight into the condition and cognitive decline up to severe dementia. Neurological examination reveals classic frontal signs: oral automatism signs, the grasp reflex, and the gegenhalten phenomenon (paratonia).

Differential diagnosis with cerebellar ataxia

To establish an accurate topographic diagnosis, gait apraxia must be differentiated from other forms of incoordination. In cerebellar ataxia (damage to the cerebellum and its pathways), symptoms are observed that are absent in frontal apraxia:

• Intention tremor: limb tremor whose amplitude increases as the target is approached (revealed in the finger-to-nose test).
• Nystagmus: involuntary rhythmic movements of the eyeballs.
• Dysarthria: specific scanning speech, where words are pronounced fragmentarily, syllable by syllable.
• Babinski's asynergia: inability to sit up from a lying position with crossed arms due to the involuntary lifting of the legs.

Differences from sensory, vestibular, and psychogenic ataxias

• Sensory ataxia: occurs when proprioceptive pathways are damaged. Unlike frontal apraxia, coordination here depends critically on vision (the patient constantly looks down at their feet and sharply loses balance in the dark). The gait is stamping, with a loud slapping sound. In apraxia, joint-position sense is preserved, and there is no such strong dependence on visual control.
• Vestibular ataxia: accompanied by systemic vertigo, nausea, and vomiting. Instability increases sharply with head movements. These autonomic complaints are not characteristic of frontal apraxia.
• Psychogenic (hysterical) ataxia: lacks an organic nervous system lesion. The gait is bizarre (e.g., crossing legs like braiding hair), the patient is demonstrative, whereas in frontal apraxia the deficit has a clear organic etiology.

Class and exam questions

What else to study on this topic

• Cerebellar ataxia: intention tremor and Babinski's asynergia
• Sensory ataxia and loss of joint-position sense
• Vestibular ataxia and vestibulocochlear nerve lesion
• Visual and somatosensory agnosias in cortical lesions
• Amnestic syndromes: Korsakoff's syndrome and transient global amnesia

Other topics in Chapter 2. Movement Disorders

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