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Apraxia
Introduction
Apraxia is an acquired higher-order cognitive-motor disorder characterized by the inability to perform skilled actions or specific purposeful movements, including movements that were previously learned or that can be immediately imitated after observation or instruction, despite adequate strength, sensation, comprehension, coordination, and cooperation.[1][2][3] Diagnosis involves ruling out weakness, sensory dysfunction, comprehension deficits, or incoordination as potential causes.[1][2][4] Initially, Hugo Karl Liepmann classified apraxia into 3 types: limb-kinetic, ideomotor, and ideational.[5] Liepmann's descriptions laid the groundwork for today's characterizations. However, the concept of apraxia now comprises a broader spectrum of subtypes than those originally identified by Liepmann. Broadly, apraxia can be classified based on the performance of specific tasks or general actions.[6] The framework has evolved from a task-based diagnostic approach toward a process-based model that deconstructs the conceptual and production systems of action into multiple cognitive processes, including semantic memory, body schema, visuospatial skills, and motor planning.[1] Unfortunately, the subtypes of apraxia are not defined consistently in the literature.[7]
Major forms of apraxia include:
- General:
- Ideational: Loss of neural encoding of the concept of a previously known skill
- Ideomotor: Impaired connection between the concept of a skill and its motor output
- Limb-kinetic: Loss of the motor output associated with a given skill
- Conceptual: Loss of ability to use tools
- Task-specific
- Speech
- Specific constructional: Difficulty in drawing, constructing, or copying
The term ideational apraxia is sometimes used as an alternative to describe the loss of the ability to perform a sequence of movements. In contrast, conceptual apraxia refers to the loss of the concept itself.[2][7] However, a thorough discussion of these differences in usage is beyond the scope of this article.
Praxis, or the ability to carry out skilled actions, involves the activation or inhibition of neural networks in the brain. The type of apraxia that manifests can vary depending on the neural network involved, arising from dysfunction of specific parietofrontal praxis networks or from deficient interaction between praxis and praxis-related cognitive networks.[4][8] Apraxia can be diagnosed through a comprehensive evaluation, which includes a detailed history, neurological examination, and apraxia-specific testing. However, there is no consensus on the best operational practices for assessing apraxia.[1]
Clinically, apraxia is associated with reduced independence in activities of daily living (ADLs), increased caregiver dependence, unemployment, lower quality of life, and poorer functional outcomes.[3][9][10] The treatment of apraxia involves addressing its underlying causes through physical, occupational, or other task-specific therapies, as well as counseling. Long-term outcomes depend on the type of apraxia and its effect on the patient's activities of daily living. Associated deficits can include acalculia, agraphia, and aphasia, as well as confusion, social anxiety, and low self-esteem. Some individuals with apraxia may require long-term assisted nursing care.
Etiology
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Etiology
Apraxia arises from acquired brain disorders affecting the neural substrates. Some commonly known causes of apraxia include:
- Cerebrovascular disorders: Cortical lesions in the frontal, temporal, or parietal regions, especially within praxis networks in the dominant hemisphere, can cause apraxia. White matter lesions may also cause disconnections between these areas. Subcortical lesions involving the thalamus or basal ganglia may be contributing factors.[11][12][13]
- Neurodegenerative disorders: Apraxia may reflect progressive bilateral network degeneration rather than a single focal lesion. Apraxia is a core feature of Alzheimer disease and corticobasal syndrome. Other associated disorders include progressive supranuclear palsy, frontotemporal dementia, Parkinson disease, Lewy body dementia, and primary progressive aphasia variants.[3][14][15] Progressive apraxia of speech is considered a distinct syndromic entity.[16] Apraxia in Huntington disease is a motor manifestation of dysfunction in corticostriatothalamic circuits rather than of cortical pathology.[17][18]
- Infectious disorders: Apraxia is a common but underrecognized manifestation of prion diseases, such as Creutzfeldt-Jakob disease.[19][20]
- Other etiologies: Multiple sclerosis, brain tumors, schizophrenia, and traumatic brain injury can cause apraxia.[21][22][23] Childhood apraxia of speech is a neurodevelopmental speech disorder seen in the pediatric population.[24]
The risk of developing a specific form of apraxia depends on the risk of developing its associated etiological disorder.
Epidemiology
Apraxia prevalence estimates vary widely because studies differ in lesion laterality, chronicity, apraxia subtype, and assessment instrument. Prevalence estimates range from approximately 50% to 80% among individuals with left hemisphere strokes, 30% to 50% among those with right hemisphere strokes, 19% to 45% among those with traumatic brain injuries, 25% among those with multiple sclerosis, and 90% among those with dementia.[25][26] Childhood apraxia of speech is a rare pediatric condition. In a large pediatric outpatient cohort, 2.4% of children received a diagnosis of apraxia, and 1.3% of children with autism spectrum disorder had a comorbid diagnosis of childhood apraxia of speech.[24][27] Apraxia is more common in right-handed individuals with left-hemisphere lesions, especially those with cerebrovascular disorders, reflecting the left hemisphere's dominance for praxis in most individuals.[8] However, population-level incidence and prevalence data for apraxia are unfortunately limited.
Pathophysiology
Praxis has various conceptual subdivisions that are best understood using the dual-system model. The conceptual system includes knowledge of tools or objects, their functions, and their relationships with other objects and actions. The production system is involved in the execution of skilled movements and their spatiotemporal organization.[28][29][30] Although the neural networks that subserve different types of praxis are not identical, specific brain structures, such as the left inferior parietal lobule and frontal motor areas, are involved in both praxis and apraxia.[28][31][32][33]
A typical schema of the structures involved in praxis illustrates how praxis networks can be activated by visual, auditory, verbal, or tactile stimuli. The activated sensory modality provides information to neurons in the left parietal lobe, which selectively fire to commence the praxis process.[34][35] Subsequently, feedforward signaling reaches the supplementary and premotor areas, where corresponding maps of coordinated movements are accessed. The resulting information is sent to the primary motor cortex, which initiates the encoded motor programs by activating the musculature through the pyramidal tracts.[2]
Connections between the superior parietal lobule and the dorsal premotor cortex are involved in visuomotor transformation for reaching and grasping. Lesions in these areas can result in optic apraxia. Connections between the inferior parietal lobule, including the supramarginal gyrus, and the ventral premotor cortex are critical for gesture production, pantomime, and tool use. The supramarginal gyrus is a key structure in which damage leads to persistent pantomime production errors.[36] The temporal cortex is involved in action recognition and semantic processing of gestures.[8]
In Alzheimer disease, apraxia results from cortical tau aggregation in parietofrontal praxis networks, representing a gradual, bilateral neurodegenerative disorder rather than a focal disorder.[3] Models of praxis and their associated networks are continually evolving. Additional structures are implicated, including the thalami, basal ganglia, prefrontal regions, temporal regions, and connecting white matter. Damage to these structures, which constitute the praxis networks, can result in apraxia, depending on the role of the damaged structure within its network.[2] Subcortical lesions associated with apraxia extend into the internal capsule and periventricular white matter, suggesting that disconnection of cortical praxis networks is the primary mechanism.[13]
History and Physical
A clinical history is key to evaluating apraxia and other neurological disorders. In addition to a thorough neurological examination, the history should focus on onset, progression, the functional impact of motor difficulties, language difficulties, behavioral changes, and memory impairment.[3][12][13] Evaluation of apraxia can begin after a comprehensive neurological examination, which excludes sensory, motor, and cognitive dysfunction as potential causes of the observed deficits. Before testing, the patient must demonstrate an understanding of and the ability to perform the tasks used for testing. Although there is no prescribed sequence for testing the extremities, both sides should be evaluated.[2][37]
In general, 2 types of actions are assessed: those that are directly imitated and those that are recalled from memory. These actions can be further subdivided into 3 categories: intransitive gestures, transitive gestures, and pantomime. Intransitive gestures, also known as symbolic gestures, do not depend on the use of an object, such as saluting or waving goodbye. Transitive gestures involve using an object, such as swinging a hammer or flipping a coin. Pantomime involves mimicking or simulating the use of tools or objects without physically using them. In addition, meaningless gestures, such as holding the index finger to the underside of the nose, can be assessed.[2][37] Multistep or sequential actions can be used to assess ideational apraxia.[37]
Examples of abnormal findings associated with apraxia subtypes include:
- Ideomotor apraxia: Patients are unable to pantomime or imitate gestures. Moreover, they experience challenges with spatiotemporal orientation and positioning. Movements involving their digits, hands, and arms display abnormal trajectories.
- Ideational apraxia: Patients struggle to identify the correct sequence of actions necessary to accomplish a task. Even when provided with a list of required steps, they may encounter difficulties organizing them accurately.
- Limb-kinetic apraxia: Patients exhibit incorrect fine motor actions, particularly with their hands, when attempting to perform a learned task. For instance, they may struggle to rotate a coin with their first, second, and third digits.
- Conceptual apraxia: Patients face challenges identifying the appropriate tool for a given task. When presented with a tool, they may struggle to discern its purpose. Additionally, they may experience difficulty pantomiming the correct use of a tool.[2]
Formal testing tools for limb apraxia include the Florida Apraxia Battery–Extended and Revised Sydney (FABERS), the Apraxia Battery for Adults-2, the Short Screening Test for Ideomotor Apraxia (STIMA), the Cologne Apraxia Screening (KAS) or Revised Cologne Apraxia Screening (KAS-R), the Diagnostic Instrument for Limb Apraxia (DILA) or the Diagnostic Instrument for Limb Apraxia-Short Version (DILA-S), and the Test of Upper Limb Apraxia (TULIA).[38][39][40][41][42] The examiner can observe error types to further assist in diagnosis, such as spatial, temporal, content, body-part-as-object, and perseverative errors.[29][30]
Evaluation
Thorough assessment methods, including detailed history-taking, physical examination, and neuropsychological testing, are used to identify and classify apraxia. Additional testing is used not to describe the apraxia further but to determine its etiology. Apraxia may develop acutely after a neurological insult such as stroke or traumatic brain injury. Alternatively, apraxia may develop insidiously, as observed in neurodegenerative disorders. Patients are often unaware of their inability to perform previously learned skills and activities.
Radiological and laboratory evaluations can assist in identifying the etiology of apraxia, including cerebrovascular disease, neurodegenerative disorders, traumatic brain injury, tumors, and multiple sclerosis. Imaging modalities such as MRI and positron emission tomography can identify associated brain lesions. Voxel-based lesion-symptom mapping studies using MRI have elucidated the specific lesion correlates of different apraxia subtypes.[12][36] Positron emission tomography with specific tracers, such as tau tracers, can demonstrate cortical aggregation patterns associated with Alzheimer disease–related apraxia.[3][43]
Treatment / Management
The primary treatment for apraxia involves focused rehabilitation using various therapies, such as occupational therapy, speech therapy, and physical therapy, alongside treatment of the underlying disorder. Apraxia can significantly impair independent functional capacity, with its presence often indicating the level of caregiver assistance needed after stroke, whereas its absence may predict an early return to work.[44] Patients are taught internal compensatory strategies or external strategies to overcome functional barriers during ADLs.[45] This type of strategy training has statistically significant effects on ADL performance.[46] Gesture training can improve praxic ability and independence in activities of daily living.[10](A1)
Currently, no widely accepted treatment strategy for apraxia exists. The challenge of creating task-specific therapies with generalizable benefits is illustrated in the work of Buxbaum et al.[47] Rehabilitation is ideally initiated promptly following a diagnosis of apraxia, particularly in cases stemming from acute lesions.[48][49] Newer technologies, such as transcranial magnetic stimulation, have shown promise in treating apraxia.[50] Additional emerging approaches include virtual reality–based training, noninvasive brain stimulation, and closed-loop artificial intelligence–based rehabilitation for the treatment of apraxia.[51]
Differential Diagnosis
Movement and speech disorders that can be mistaken for apraxia include aphasia, nonapraxic dysarthria, alien limb phenomenon, akinesia, magnetic grasp, grope reflex, motor preservation, and motor impersistence.
Prognosis
Patients with apraxia can have significant difficulty performing learned skills, which can profoundly affect their independence and ability to carry out activities of daily living. Appropriate safety precautions must be implemented for objects and activities in the surrounding environment that may cause injury. When the inability to perform certain learned skills is debilitating, patients may require skilled nursing care. The prognosis varies depending on the patient and the underlying etiologic disorder.
Complications
Potential sequelae of apraxia include:
- Inability to perform activities of daily living
- Difficulty functioning at work
- Injury caused by improper tool use
- Social isolation
- Social anxiety
- Low self-esteem
Deterrence and Patient Education
The most common causes of apraxia include stroke, dementia, and traumatic brain injury. Apraxia is often a sign of a complex underlying neurological condition that poses challenges for treatment. Education regarding modifiable risk factors should be prioritized whenever possible. Pharmacological interventions and lifestyle measures targeting hypertension, diabetes mellitus, sleep apnea, atrial fibrillation, tobacco use, and alcohol consumption can contribute to better outcomes.
Regardless of the underlying cause, the inability to perform specific tasks due to apraxia can evoke frustration, potentially resulting in reduced functional capacity, diminished motivation, depression, and further deterioration of function. Educational resources, effective communication with caregivers, and counseling for family members can be crucial for establishing realistic expectations, understanding goals of care, and anticipating challenges during the recovery process. Active participation by patients, caregivers, and family members can significantly facilitate the rehabilitation process.
Pearls and Other Issues
Key facts to keep in mind about apraxia include:
- Apraxia is a neurological disorder characterized by the inability to perform learned or purposeful movements.
- Types of apraxia include ideomotor, ideational, limb-kinetic, and conceptual forms.
- Common causes of apraxia include stroke, traumatic brain injury, dementia, neurodegenerative disorders, tumors, and schizophrenia.
- Although occupational, physical, and speech therapy may improve functional impairments caused by apraxia, addressing the underlying cause is necessary.
- The prognosis depends on the underlying cause and promptness of intervention.
Enhancing Healthcare Team Outcomes
Apraxia poses a challenge for clinicians due to the complexity of its identification and testing. The presence of concurrent neurological and psychological factors can obscure symptoms. Causes of apraxia range from acute disorders such as stroke and traumatic brain injury to chronic conditions such as neurodegenerative disorders or schizophrenia. Furthermore, apraxia can be mistaken for neurological conditions such as aphasia, abulia, and extremity akinesia.
The lack of broad consensus concerning screening and diagnosis can frustrate clinicians. However, a detailed history, physical examination, and targeted testing can facilitate early identification and treatment. Despite inconsistencies in subtype definitions, clinicians prioritize an interdisciplinary approach to diagnosing and treating apraxia, emphasizing seamless communication and collaboration within the healthcare team to gain valuable insights into its complexities.
The involvement of interdisciplinary and interprofessional teams is paramount for treating apraxia and enhancing patient outcomes. The healthcare team can include the patient, family members, nurses, occupational therapists, physical therapists, primary care clinicians, radiologists, neurologists, physiatrists, psychiatrists, counselors, social workers, and caseworkers. Each healthcare team member should maintain open communication with the rest of the team and be responsible for accurate, detailed records of interactions, interventions, and testing. An interprofessional approach significantly enhances patient outcomes.
In both inpatient and outpatient settings, a primary care clinician or neurologist can assess for apraxia through a comprehensive examination and detailed history. Nurses caring for patients can identify deficiencies in extremity function, knowledge of tool use, and changes in general demeanor. Family members can help identify functional deficits during rehabilitation. Therapists can assist in improving extremity function and help patients acquire new skills for extremity function and tool use. Psychological support during the recovery and rehabilitation phases is vital for long-term patient well-being.
Establishing a supportive environment at home and work can facilitate recovery. The long-term outcome depends on the etiology and duration of the illness. However, prompt identification and treatment of the condition by an interprofessional healthcare team can lead to an improved prognosis.
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