Hubbry Logo
ApraxiaApraxiaMain
Open search
Apraxia
Community hub
Apraxia
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Apraxia
Apraxia
Apraxia
View on Wikipedia
from Wikipedia
Apraxia
Apraxia is characterized by loss of the ability to execute or carry out learned purposeful movements.
SpecialtyNeurology, psychiatry
TreatmentOccupational therapy, physical therapy

Apraxia is a motor disorder caused by damage to the brain (specifically the posterior parietal cortex or corpus callosum[1]), which causes difficulty with motor planning to perform tasks or movements. The nature of the damage determines the disorder's severity, and the absence of sensory loss or paralysis helps to explain the level of difficulty.[2] Children may be born with apraxia; its cause is unknown, and symptoms are usually noticed in the early stages of development. Apraxia occurring later in life, known as acquired apraxia, is typically caused by traumatic brain injury, stroke, dementia, Alzheimer's disease, brain tumor, or other neurodegenerative disorders.[3] The multiple types of apraxia are categorized by the specific ability and/or body part affected.

The term "apraxia" comes from Ancient Greek ἀ- (a-) 'without' and πρᾶξις (praxis) 'action'.[4]

Types

[edit]

The several types of apraxia include:

  • Apraxia of speech (AOS) is having difficulty planning and coordinating the movements necessary for speech (e.g. potato=totapo, topato).[5] AOS can independently occur without issues in areas such as verbal comprehension, reading comprehension, writing, articulation, or prosody.[6]
  • Buccofacial or orofacial apraxia, the most common type of apraxia, is the inability to carry out facial movements on demand. For example, an inability to lick one's lips, wink, or whistle when requested to do so. This suggests an inability to carry out volitional movements of the tongue, cheeks, lips, pharynx, or larynx on command.[7][8]
  • Constructional apraxia is the inability to draw, construct, or copy simple configurations, such as intersecting shapes. These patients have difficulty copying a simple diagram or drawing basic shapes.[7]
  • Gait apraxia is the loss of ability to have normal function of the lower limbs such as walking. This is not due to loss of motor or sensory functions.[9]
  • Ideational/conceptual apraxia is having an inability to conceptualize a task and impaired ability to complete multistep actions. This form of apraxia consists of an inability to select and carry out an appropriate motor program. For example, the patient may complete actions in incorrect orders, such as buttering bread before putting it in the toaster, or putting on shoes before putting on socks. Also, a loss occurs in the ability to voluntarily perform a learned task when given the necessary objects or tools. For instance, if given a screwdriver, these patients may try to write with it as if it were a pen, or try to comb their hair with a toothbrush.[10][11]
  • Ideomotor apraxia is having deficits in the ability to plan or complete motor actions that rely on semantic memory. These patients are able to explain how to perform an action, but unable to "imagine" or act out a movement such as "pretend to brush your teeth" or "pucker as though you bit into a sour lemon." When the ability to perform an action automatically when cued remains intact, though, this is known as automatic-voluntary dissociation. For example, they may not be able to pick up a phone when asked to do so, but can perform the action without thinking when the phone rings.[10][11]
  • Limb-kinetic apraxia is having the inability to perform precise, voluntary movements of extremities. For example, a person affected by limb apraxia may have difficulty waving hello, tying shoes, or typing on a computer.[12][8] This type is common in patients who have experienced a stroke, some type of brain trauma, or have Alzheimer's disease.[13]
  • Oculomotor apraxia is having difficulty moving the eye on command, especially with saccade movements that direct the gaze to targets. This is one of the three major components of Balint's syndrome.[8]

Causes

[edit]

Apraxia is most often due to a lesion located in the dominant (usually left) hemisphere of the brain, typically in the frontal and parietal lobes. Lesions may be due to stroke, acquired brain injuries, or neurodegenerative diseases such as Alzheimer's disease or other dementias, Parkinson's disease, or Huntington's disease. Also, apraxia possibly may be caused by lesions in other areas of the brain.[11]

Ideomotor apraxia is typically due to a decrease in blood flow to the dominant hemisphere of the brain and particularly the parietal and premotor areas. It is frequently seen in patients with corticobasal degeneration.[11]

Ideational apraxia has been observed in patients with lesions in the dominant hemisphere near areas associated with aphasia, but more research is needed on ideational apraxia due to brain lesions. The localization of lesions in areas of the frontal and temporal lobes would provide explanation for the difficulty in motor planning seen in ideational apraxia, as well as its difficulty to distinguish it from certain aphasias.[14]

Constructional apraxia is often caused by lesions of the inferior nondominant parietal lobe, and can be caused by brain injury, illness, tumor, or other condition that can result in a brain lesion.[14]

Diagnosis

[edit]

Although qualitative and quantitative studies exist, little consensus exists on the proper method to assess for apraxia. The criticisms of past methods include failure to meet standard psychometric properties and research-specific designs that translate poorly to nonresearch use.[15]

The Test to Measure Upper Limb Apraxia (TULIA) is one method of determining upper limb apraxia through the qualitative and quantitative assessment of gesture production. In contrast to previous publications on apraxic assessment, the reliability and validity of TULIA was thoroughly investigated.[16] The TULIA consists of subtests for the imitation and pantomime of nonsymbolic ("put your index finger on top of your nose"), intransitive ("wave goodbye"), and transitive ("show me how to use a hammer") gestures.[15] Discrimination (differentiating between well- and poorly performed tasks) and recognition (indicating which object corresponds to a pantomimed gesture) tasks are also often tested for a full apraxia evaluation.[15]

However, a strong correlation may not be seen between formal test results and actual performance in everyday functioning or activities of daily living (ADLs). A comprehensive assessment of apraxia should include formal testing, standardized measurements of ADLs, observation of daily routines, self-report questionnaires, and targeted interviews with the patients and their relatives.[15]

As stated above, apraxia should not be confused with aphasia (the inability to understand language); however, they frequently occur together. Apraxia is so often accompanied by aphasia that many believe that if a person displays AOS, then the patient also having some level of aphasia should be assumed.[17]

Treatment

[edit]

Treatment for individuals with apraxia includes speech therapy, occupational therapy, and physical therapy.[18] Currently, no medications are indicated for the treatment of apraxia, only therapy treatments.[19] Generally, treatments for apraxia have received little attention for several reasons, including the tendency for the condition to resolve spontaneously in acute cases. Additionally, the very nature of the automatic-voluntary dissociation of motor abilities that defines apraxia means that patients may still be able to automatically perform activities if cued to do so in daily life. Nevertheless, patients experiencing apraxia have less functional independence in their daily lives,[20] and that evidence for the treatment of apraxia is scarce.[21] However, a literature review of apraxia treatment to date reveals that although the field is in its early stages of treatment design, certain aspects can be included to treat apraxia.[22]

One method is through rehabilitative treatment, which has been found to positively impact apraxia, as well as ADLs.[22] In this review, rehabilitative treatment consisted of 12 different contextual cues, which were used to teach patients how to produce the same gesture under different contextual situations.[22] Additional studies have also recommended varying forms of gesture therapy, whereby the patient is instructed to make gestures (either using objects or symbolically meaningful and nonmeaningful gestures) with progressively less cuing from the therapist.[23] Patients with apraxia may need to use a form of alternative and augmentative communication depending on the severity of the disorder. In addition to using gestures as mentioned, patients can also use communication boards or more sophisticated electronic devices if needed.[24]

No single type of therapy or approach has been proven as the best way to treat a patient with apraxia, since each patient's case varies. One-on-one sessions usually work the best, though, with the support of family members and friends. Since everyone responds to therapy differently, some patients will make significant improvements, while others will make less progress.[25] The overall goal for treatment of apraxia is to treat the motor plans for speech, not treating at the phoneme (sound) level. Individuals with apraxia of speech should receive treatment that focuses on the repetition of target words and rate of speech. The overall goal for treatment of apraxia should be to improve speech intelligibility, rate of speech, and articulation of targeted words.[26]

See also

[edit]

References

[edit]

Further reading

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Apraxia

View on Grokipedia
from Grokipedia
Apraxia is a neurological disorder characterized by the loss of the ability to execute or perform skilled, purposeful movements or tasks, despite intact sensory function, comprehension, and basic motor capabilities. This condition arises from disruptions in the brain's motor planning and execution processes, distinguishing it from conditions involving muscle weakness or paralysis. Apraxia manifests in various forms, each affecting different aspects of motor control. Key types include ideomotor apraxia, where individuals have difficulty imitating gestures or using objects correctly on command; ideational apraxia, involving challenges in planning and sequencing multi-step actions; limb-kinetic apraxia, which impairs the precise control of limb movements; and conceptual apraxia, affecting the understanding of action concepts. Additional subtypes encompass buccofacial (or orofacial) apraxia, impacting movements of the mouth and face, such as pretending to blow out a candle, and apraxia of speech, a motor speech disorder that hinders the planning and coordination of speech movements. These types often co-occur and are commonly triggered by brain damage from causes such as stroke, traumatic brain injury, dementia, neurodegenerative diseases like Alzheimer's or corticobasal degeneration, brain tumors, or, less frequently, schizophrenia. In children, childhood apraxia of speech may stem from unknown origins or associations with genetic syndromes, cerebral palsy, or other neurological conditions, without evident structural brain damage. Symptoms of apraxia vary by type and severity but typically involve inconsistent errors in task performance, such as struggling to mime brushing teeth or wave goodbye, even when the person understands the request and has no sensory or strength deficits. For limb apraxias, individuals may misuse tools, sequence actions incorrectly (e.g., putting toothpaste on a toothbrush before applying it to teeth), or exhibit groping behaviors during attempts. In apraxia of speech, common signs include distorted or inconsistent pronunciation, slow and effortful speech, difficulty transitioning between sounds or syllables, and groping movements of the lips, jaw, or tongue, which can range from mild occasional errors to severe mutism. Diagnosis generally involves neurological examinations, observation of motor tasks, and sometimes imaging like MRI to identify underlying brain lesions, while ruling out aphasia or other disorders. Treatment for apraxia focuses on rehabilitation rather than , emphasizing repetitive practice and cueing to rebuild motor plans. Speech-language pathologists or occupational therapists deliver targeted interventions, such as gesture training for or dynamic temporal and tactile cueing for speech apraxia, often involving intensive sessions to improve accuracy and speed. Outcomes depend on the underlying cause and timeliness of therapy; while recovery is possible after or , progressive forms linked to neurodegeneration may worsen over time, requiring ongoing support to maintain function and .

Overview

Definition

Apraxia is a neurological disorder characterized by the inability to execute purposeful, skilled, and learned movements despite intact muscle strength, sensation, coordination, and comprehension of the task. This condition specifically disrupts the planning and organization of motor actions, rather than the basic execution of movements. The term "apraxia" was introduced by German philologist Heymann Steinthal in 1871, but German neurologist Hugo Liepmann provided a foundational description in 1900, portraying it as a higher-order deficit in motor control arising from brain lesions, distinguishing it from mere paralysis or sensory loss. Liepmann's foundational work emphasized that apraxia involves a breakdown in the conceptual and sequential aspects of movement, often linked to left-hemisphere dominance for praxis. Apraxia must be differentiated from related impairments such as , which affects ; , which involves impaired coordination due to cerebellar or sensory issues; and or , which stem from muscle or nerve dysfunction rather than planning deficits. At its core, apraxia reflects damage to key brain regions responsible for motor praxis, including the (for conceptualization), (for execution), and (for interhemispheric communication). Apraxia can affect various domains, such as limb movements or .

Signs and Symptoms

Apraxia manifests as an inability to execute purposeful, skilled movements despite preserved comprehension, strength, sensation, and coordination, often evident in tasks requiring production or tool use. Primary symptoms include difficulty performing gestures on command or by , such as pantomiming the use of a tool like pretending to hammer a nail or brush teeth, even when the patient understands the instruction and has no basic motor deficits. Patients may produce incorrect or spatial errors, such as using the wrong hand orientation or body part for the action, highlighting a disruption in motor rather than execution. Common presentations involve errors in sequencing multi-step actions, for example, reversing the order of steps when simulating making a sandwich by applying before spreading it, or exhibiting where movements lack appropriate positioning relative to an imagined object. is frequent, with patients repeating an incorrect gesture across different tasks, such as continuing a waving motion when asked to mime using a . These errors can occur in both transitive gestures (related to object use, like handling utensils) and intransitive gestures (communicative, like saluting), aiding in clinical differentiation during assessment. In speech apraxia, a subtype, individuals show inconsistent articulation errors, such as groping for sounds or distorting syllables without underlying or . The functional impact is significant, impairing daily activities like dressing (e.g., inability to sequence buttoning a ), using eating utensils properly, or writing legibly, leading to reduced . In speech-related cases, it results in slow, effortful speech with variable errors, affecting communication. Patients often exhibit frustration and awareness of their deficits, expressing distress over failed attempts, which distinguishes apraxia from conditions with . These symptoms are frequently associated with left hemisphere damage, particularly involving parietal regions critical for spatial-motor integration.

Etiology and Pathophysiology

Causes

Apraxia is most commonly an acquired disorder resulting from damage to regions involved in motor planning, with cerebrovascular accidents, particularly affecting the left hemisphere, accounting for the majority of cases. Apraxia occurs in approximately 50% to 80% of individuals with left-hemisphere and is especially prevalent among right-handed patients due to hemispheric dominance for praxis functions. Traumatic brain injuries represent another significant acquired cause, often leading to apraxia through diffuse or focal damage to frontal and parietal lobes. Neurodegenerative diseases, such as and , frequently manifest apraxia as a core feature, with progressive deterioration of neural pathways impairing gesture and tool use. Less frequently, is associated with gesture deficits and apraxia. Developmental forms of apraxia are rare and typically congenital, arising from genetic mutations or early insults. For instance, mutations in the gene, as well as more recently identified genes such as ASH1L and KDM5B, are linked to childhood , disrupting speech motor programming from early development. Perinatal hypoxia can also contribute to congenital apraxia by causing hypoxic-ischemic injury that affects praxis-related areas. Iatrogenic causes include post-surgical complications, such as those following tumor resection in praxis-dominant brain regions, and infections like that inflame and relevant neural tissues. Overall of apraxia is estimated at 28% to 37% among patients with first-ever left-hemisphere in rehabilitation or settings. Risk factors for stroke-related apraxia include age over 65 years, , and a history of , which elevate the likelihood of cerebrovascular events.

Neurological Mechanisms

Apraxia arises from disruptions in the neural circuits responsible for planning and executing purposeful movements, primarily involving the left hemisphere in right-handed individuals. Key brain regions implicated include the left parietal lobe, particularly the , which is crucial for the representation of praxis or learned motor actions. The plays a central role in the execution of these actions by translating representations into motor commands. Additionally, the facilitates interhemispheric transfer of praxis information from the dominant left hemisphere to the right hemisphere, enabling bilateral coordination. Pathophysiological models of apraxia emphasize disconnections within these networks. Hugo Liepmann's early 20th-century disconnection theory posits that apraxia results from lesions that sever the pathways linking sensory input—such as visual or conceptual representations of actions—from motor output centers, preventing the activation of stored motor programs. Modern perspectives extend this to broader network disruptions in frontoparietal circuits, where damage impairs the distributed processing required for gesture selection and execution, often triggered by events like . Lesion localization studies indicate that unilateral damage to the left hemisphere, especially in parietal and frontal areas, typically produces limb apraxia affecting both sides of the body, with greater severity in the right limb. Bilateral lesions exacerbate the deficit, leading to more profound impairments, while isolated callosal lesions in right-handers result in left-hand apraxia due to failed transfer of praxis engrams to the right . Neuroimaging evidence supports these mechanisms by revealing functional and structural alterations in praxis networks. Functional MRI (fMRI) studies demonstrate reduced activation in left frontoparietal regions during gesture production tasks in apraxic patients, indicating impaired recruitment of areas for action planning and execution. Diffusion tensor imaging (DTI) further shows damage to white matter tracts, such as the superior longitudinal fasciculus, which connect parietal representation areas to premotor and motor regions, correlating with the severity of apraxia. Theoretical frameworks provide conceptual underpinnings for these observations. The engram theory, rooted in Liepmann's work, views praxis as reliant on stored motor engrams—neural traces of learned actions—that are disrupted by lesions, leading to errors in kinematics and sequencing. Complementing this, the dual-route model of gesture production distinguishes a direct pathway for visuomotor transformation of observed actions into immediate motor output and an indirect pathway involving semantic processing and lexical retrieval for meaningful gestures, with apraxia arising from selective damage to one or both routes.

Classification

Ideomotor Apraxia

Ideomotor apraxia is characterized by an impairment in the execution of learned gestures despite preserved comprehension of the task, intact strength, sensation, and coordination. Patients struggle to translate conceptual knowledge of an action into appropriate motor output, resulting in errors when performing pantomimes on verbal command or imitation, such as incorrectly orienting a gesture or disrupting its temporal sequence. This form of apraxia is the most prevalent subtype, commonly observed in individuals with left-hemisphere brain damage from stroke or neurodegenerative conditions, where voluntary gesture production fails while automatic or habitual movements remain relatively intact. Key features include spatial errors, such as misaligning the hand in a tool-use (e.g., holding an imaginary with the wrong grip), and temporal errors, like hesitating or incorrectly sequencing the motion of hammering a nail. Transitive gestures, involving tool use, elicit more errors than intransitive ones, such as waving goodbye, and the deficit can manifest in limb (upper extremity) or buccofacial (oral-facial, e.g., difficulty imitating blowing a kiss) variants. A classic clinical example is a who understands the command to "pretend to comb your hair" but instead performs an unrelated action, such as scratching the head, or uses an imprecise sweeping motion without the proper combing . In contrast, the same may successfully hammer a real nail when the tool is provided, highlighting the dissociation between voluntary and actual performance. Lesion correlates primarily involve the left , particularly the , along with the , , and connecting pathways such as the superior longitudinal fasciculus. These regions form a critical for execution, and damage here disrupts the translation from intention to movement without affecting the underlying motor representations or limb kinetics. frequently accompanies left-hemisphere strokes, occurring in a substantial proportion of cases due to the vulnerability of these parietal and frontal structures. Testing typically employs standardized assessments like the De Renzi Test, a 24-item battery evaluating to verbal command and , scoring for accuracy in spatial, temporal, and content errors. Patients are asked to demonstrate actions such as using or saluting, with performance compared across limbs and modalities to distinguish ideomotor deficits from other impairments; errors are more pronounced in non-dominant hand use or tasks.

Ideational Apraxia

Ideational apraxia is characterized by a deficit in the conceptual organization and planning of multi-step actions, where individuals struggle to formulate the overall idea or sequence required for completing familiar, complex tasks despite understanding the individual objects involved. Patients can typically recognize and name tools but fail to integrate them into a coherent , leading to errors such as missequencing steps or omitting key actions altogether. This disorder is more severe than , as it impairs higher-level conceptualization rather than just gesture execution, and it affects performance equally when using actual objects and when pantomiming actions. It frequently co-occurs with following left hemisphere strokes. Lesions associated with are typically located in the dominant (left) hemisphere, particularly involving the , , and surrounding parietal regions, which are critical for action sequencing and semantic integration of tools with their purposes. These deficits are also prevalent in neurodegenerative conditions such as , where widespread cortical involvement disrupts conceptual praxis networks. Diagnosis involves specific testing of multi-step sequences, such as demonstrating the use of everyday objects in a logical order, where errors like object misuse or become evident. Single-object use tasks may reveal subtler issues, but complex sequences best highlight the planning impairment. For instance, a might correctly identify a and but strike the match against the cigarette instead of a , or attempt to pour from a without first placing a underneath. Another common example is the inability to mail an , where the individual names the stamp and envelope but cannot sequence affixing the stamp and inserting the letter.

Other Types

Orofacial apraxia, also known as buccofacial apraxia, refers to the inability to perform volitional, non-verbal movements of the , face, and on command, such as blowing a kiss, coughing, or protruding the tongue, despite preserved comprehension and muscle strength. This form is frequently associated with lesions in the left frontal operculum and is commonly observed in individuals with Broca's aphasia, where it contributes to difficulties in imitating orofacial gestures. Unlike simple motor weakness, orofacial apraxia reflects a disruption in the planning of skilled facial movements, often linked to inferior and deep damage. Limb-kinetic apraxia involves a loss of dexterity and precision in performing skilled, coordinated hand and finger movements, such as buttoning a or manipulating small objects, resulting in clumsy or uncoordinated actions without underlying weakness or . It arises primarily from damage to the contralateral , particularly its ventral portions involved in grasp control, and can also involve lesions, distinguishing it from conditions like , which feature involuntary oscillations rather than impaired fine motor planning. This apraxia impacts activities requiring independent finger control, leading to reduced hand deftness that is not attributable to bradykinesia or rigidity alone. Constructional apraxia manifests as an inability to assemble, draw, or copy two- or three-dimensional objects, such as arranging blocks or replicating a , often resulting in distorted or incomplete spatial arrangements despite intact basic motor function. It is typically linked to lesions in the right , where disruptions in visuospatial processing impair the organization of elements into coherent wholes, and frequently overlaps with visuospatial , persisting even after initial neglect symptoms resolve following right parietal . This variant highlights parietal involvement in integrating visual and motor information for constructive tasks, differing from general planning deficits by its emphasis on spatial synthesis. Conceptual apraxia involves a deficit in the semantic knowledge and understanding of action concepts, where individuals may misuse tools or fail to grasp the purpose of gestures and actions, even if they can perform simpler movements. It is distinguished from by focusing on the loss of conceptual meaning rather than sequencing alone, and is often associated with lesions in the . is a motor speech disorder characterized by deficits in planning and programming the sequences of movements needed for accurate speech sound production, leading to groping behaviors, slow speech rate, and inconsistent errors across repeated attempts at the same words or syllables. In some childhood cases, it can be associated with genetic factors, including rare mutations in the gene, which disrupt neural pathways for articulatory coordination and sequencing. These errors are not due to or coordination issues alone but stem from impaired sensorimotor transformation for phonemes, resulting in distorted vowels, sound prolongations, and trial-and-error articulations. Among rarer variants, gait apraxia involves a profound disturbance in the automatic execution of walking patterns, often described as a "magnetic gait" where feet seem stuck to the floor, short shuffling steps, and widened base, commonly seen in as part of its classic triad with and incontinence. This form reflects frontal-subcortical dysfunction affecting locomotion initiation and sequencing, without primary sensory or motor deficits. Dressing apraxia, another specialized variant, entails spatial and sequencing errors in donning or doffing clothes, such as putting arms in the wrong sleeves or mismatching garments, typically arising from damage that impairs and visuospatial orientation during complex, multi-step tasks.

Diagnosis

Clinical Assessment

Clinical assessment of apraxia primarily involves behavioral and structured tasks to evaluate the patient's to perform purposeful movements, distinguishing apraxia from deficits in basic motor function, sensation, or comprehension. These methods are conducted at the bedside or in clinical settings without relying on advanced instrumentation, focusing on limb, oral, or buccofacial praxis through verbal commands, , and . Standardized tests such as the Florida Apraxia Battery (FAB) provide a comprehensive framework for assessing limb apraxia, incorporating subtests for production to verbal command, imitation (both meaningful and meaningless), and actual use of common objects like tools. The extended version, FABERS, expands these to include additional items for transitive (tool-related) and intransitive (communicative, non-tool) , ensuring evaluation across semantic categories to identify specific impairments. Bedside evaluations typically begin with simple verbal command tasks, such as instructing the patient to "show how to use " or "pretend to a nail," to assess of transitive actions. tasks follow, where the examiner demonstrates gestures (e.g., waving or saluting for intransitive actions) without verbal cues, followed by actual object manipulation, providing the patient with real items like a or key to demonstrate use. These approaches help isolate apraxic errors, such as incorrect sequencing in multi-step actions like brushing teeth. Scoring in these assessments categorizes errors into types including content errors (selecting an incorrect gesture, e.g., miming instead of pouring), spatial errors (misoriented hand position relative to an imagined object), and temporal errors (disrupted timing or sequence of movements). Severity is often rated on a 0-3 scale per item, where 0 indicates no apraxia (accurate performance), 1 mild (minor errors correctable with cues), 2 moderate (frequent errors affecting functionality), and 3 severe (complete inability to perform). Tools like the Apraxia Screen of TULIA (AST) aggregate scores across 12 imitation items, with totals of 10-12 indicating no apraxia, 6-9 mild, and 5 or less severe. Patient-specific considerations include testing with the preferred (dominant) hand first to minimize confounding from , and adapting for comprehension deficits by prioritizing or demonstration-based tasks over verbal commands to avoid conflating apraxia with . Inter-rater reliability for these methods is generally high, around 0.85-0.99 across scales, supporting consistent . In patients, such assessments detect apraxia in approximately 25-50% of cases where left-hemisphere lesions are present, aiding early identification of functional impairments.

Diagnostic Tools

Neuroimaging techniques play a crucial role in identifying structural and functional abnormalities associated with apraxia, particularly by visualizing lesions in the praxis network, which includes perisylvian regions such as the left and . Conventional computed tomography (CT) scans are often used in acute settings, such as post-stroke evaluation, to detect early ischemic changes or hemorrhages that may underlie apraxic symptoms. provides higher resolution for delineating lesions in tracts and cortical areas implicated in production and comprehension, helping to confirm apraxia in cases of focal . Functional MRI (fMRI) extends this by assessing activation deficits during praxis tasks, revealing reduced BOLD signals in the and parietal lobes during or , which supports the of ideomotor or . Electrophysiological methods offer insights into the neural dynamics of motor planning without relying on structural imaging. Transcranial magnetic stimulation (TMS) evaluates motor cortex excitability by measuring motor evoked potentials in response to praxis-related stimuli, often showing prolonged latencies or reduced amplitudes in apraxic patients, indicating disrupted corticospinal pathways. Electroencephalography (EEG), particularly event-related potentials (ERPs), captures temporal aspects of gesture processing; for instance, diminished P300 components during tool-use imitation tasks can differentiate apraxia from intact motor function. These tools are particularly useful in distinguishing apraxia from conditions like alien hand syndrome, where abnormal excitability patterns emerge. To rule out mimics, differential diagnostic tools are integrated alongside primary assessments. Language evaluations, such as the Diagnostic Aphasia Examination (BDAE), help exclude by testing comprehension and naming without interference, as apraxia often co-occurs but is gesture-specific. Manual muscle strength testing and dynamometry assess for , ensuring that observed movement errors stem from planning deficits rather than weakness, with normal strength preserving the apraxia diagnosis. Advanced imaging techniques provide deeper insights into connectivity and metabolic underpinnings. Diffusion tensor imaging (DTI) quantifies the integrity of the arcuate fasciculus, a key tract linking parietal and frontal regions, often revealing reductions in apraxia patients with left-hemisphere damage. (PET) detects hypometabolism in temporoparietal junctions in dementia-related apraxia, such as in , aiding in etiological classification. Despite their utility, these diagnostic tools have limitations. may appear normal in functional apraxia or mild cases without overt lesions, necessitating reliance on clinical correlation. Cost-effectiveness analyses indicate that advanced modalities like fMRI or PET should follow initial clinical and basic tests, as they are resource-intensive and not always superior for routine confirmation.

Treatment and Management

Therapeutic Approaches

Rehabilitation therapies form a of apraxia , emphasizing repetitive practice to restore motor and execution. Gesture training, particularly for , involves targeted drills to improve and meaningful gesture production, often incorporating paradigms that minimize incorrect responses to build accurate motor memories. These approaches have demonstrated moderate in systematic reviews, with improvements in gesture accuracy observed across multiple studies. complements this by focusing on , such as dressing or tool use, where restricts the unaffected limb to promote intensive use of the impaired one, enhancing functional in limb apraxia. For , speech-language pathology interventions target articulatory motor programming through structured sound production therapy, which progresses from simple to complex sound targets using visual, auditory, and tactile cues to facilitate accurate production. A related method, PROMPT (Prompts for Restructuring Oral Muscular Phonetic Targets), employs hands-on tactile-kinesthetic guidance to the face and jaw, improving speech and intelligibility in individuals with severe motor speech delays. These therapies are typically delivered intensively, with evidence from randomized trials showing gains in speech clarity and word production. Pharmacological options play a limited role in apraxia treatment, primarily as adjuncts in cases linked to . Cholinesterase inhibitors, such as donepezil, enhance transmission to support cognitive functions, potentially alleviating apraxic symptoms like impaired or tool use in dementias such as Alzheimer's or by improving overall executive and visuospatial abilities. Clinical guidelines recommend their use cautiously, with monitoring for side effects like gastrointestinal upset, as benefits for apraxia specifically remain secondary to broader cognitive stabilization. Non-invasive brain stimulation techniques, including (tDCS), offer promising augmentation to behavioral therapies. Anodal tDCS applied over the increases cortical excitability in this key region for praxis, leading to enhanced and performance when combined with training; randomized controlled trials report significant improvements, with some patients showing gains of around 17% in apraxia imitation subscores post-intervention. These effects are attributed to strengthened neural connectivity, though optimal protocols vary by apraxia subtype and location. A multidisciplinary approach, integrating neurologists, occupational therapists, speech-language pathologists, and physical therapists, optimizes apraxia recovery by addressing interconnected deficits holistically. Early intervention post-stroke, initiated within weeks of onset, facilitates and yields superior functional outcomes compared to delayed therapy, as evidenced by guideline recommendations and cohort studies.

Prognosis

The prognosis for apraxia varies depending on the underlying cause, such as , and individual factors, but many patients experience spontaneous improvement in the acute phase. Following , apraxia often recovers substantially within the first few months, with the majority of spontaneous gains occurring in the initial 3 months due to resolution of and natural neural reorganization. Initial can be high, around 30-50% in left-hemisphere , but declines over time, with a notable proportion of cases showing persistent deficits, particularly those involving larger lesions. Several factors influence recovery trajectories, including the timing of therapeutic intervention, lesion characteristics, and patient-specific variables. Early rehabilitation enhances outcomes by promoting , while smaller lesions in frontal regions generally yield better compared to extensive parietal involvement, which correlates with greater severity and slower resolution. Older age and comorbid cognitive impairments further hinder recovery, whereas younger patients or those with preserved tend to show more favorable progress. Long-term effects of persistent apraxia include heightened dependency in (ADLs), such as dressing or using utensils, potentially necessitating ongoing support. In pediatric cases of speech apraxia, intensive leads to significant resolution in most children, with many achieving functional communication levels; however, some may have persistent speech sound errors into adulthood, particularly with severe cases. Prognostic indicators, such as higher baseline severity on standardized praxis assessments, predict poorer outcomes, while evidence of brain plasticity—like increased contralesional hemisphere activation—signals potential for greater recovery. Chronic apraxia is associated with elevated rates of depression and reduced due to communication barriers and functional limitations. Adaptive strategies, including visual cues and environmental modifications, can mitigate these impacts by enhancing independence and daily functioning over time.

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK585110/
  2. https://medlineplus.gov/ency/article/007472.htm
  3. https://www.nidcd.nih.gov/health/apraxia-speech
  4. https://www.mayoclinic.org/diseases-conditions/childhood-apraxia-of-speech/symptoms-causes/syc-20352045
  5. https://www.mayoclinic.org/diseases-conditions/childhood-apraxia-of-speech/diagnosis-treatment/drc-20352051
  6. https://emedicine.medscape.com/article/1136037-overview
  7. https://www.medlink.com/articles/apraxia
  8. https://pmc.ncbi.nlm.nih.gov/articles/PMC4953459/
  9. https://www.thejcn.com/pdf/10.3988/jcn.2017.13.4.317
  10. https://pmc.ncbi.nlm.nih.gov/articles/PMC5619285/
  11. https://www.ahajournals.org/doi/10.1161/STROKEAHA.122.037948
  12. https://link.springer.com/article/10.1007/s11910-024-01391-6
  13. https://academic.oup.com/brain/article/128/7/1480/307101
  14. https://pmc.ncbi.nlm.nih.gov/articles/PMC7945048/
  15. https://www.ncbi.nlm.nih.gov/books/NBK368474/
  16. https://medlineplus.gov/genetics/condition/foxp2-related-speech-and-language-disorder/
  17. https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2024.1396240/full
  18. https://pubmed.ncbi.nlm.nih.gov/10763789/
  19. https://pmc.ncbi.nlm.nih.gov/articles/PMC8139361/
  20. https://www.thejcn.com/DOIx.php?id=10.3988/jcn.2017.13.4.317
  21. https://pmc.ncbi.nlm.nih.gov/articles/PMC2696397/
  22. https://www.thieme-connect.com/products/ejournals/html/10.1055/s-2000-13180
  23. https://jamanetwork.com/journals/jamaneurology/fullarticle/773544
  24. https://pmc.ncbi.nlm.nih.gov/articles/PMC8833454/
  25. https://academic.oup.com/braincomms/article/3/4/fcab263/6414617
  26. https://www.frontiersin.org/journals/human-neuroscience/articles/10.3389/fnhum.2016.00039/full
  27. https://pmc.ncbi.nlm.nih.gov/articles/PMC5653618/
  28. https://pubmed.ncbi.nlm.nih.gov/25936541/
  29. https://www.merckmanuals.com/professional/neurologic-disorders/function-and-dysfunction-of-the-cerebral-lobes/apraxia
  30. https://pmc.ncbi.nlm.nih.gov/articles/PMC4341309/
  31. https://www.physio-pedia.com/Apraxia
  32. https://pmc.ncbi.nlm.nih.gov/articles/PMC8803819/
  33. https://pmc.ncbi.nlm.nih.gov/articles/PMC4187334/
  34. https://pmc.ncbi.nlm.nih.gov/articles/PMC6866284/
  35. https://www.sciencedirect.com/topics/medicine-and-dentistry/constructional-apraxia
  36. https://academic.oup.com/brain/article/133/4/1239/313402
  37. https://pubmed.ncbi.nlm.nih.gov/20375139/
  38. https://www.asha.org/practice-portal/clinical-topics/acquired-apraxia-of-speech/
  39. https://medlineplus.gov/ency/article/000752.htm
  40. https://pubmed.ncbi.nlm.nih.gov/3969202/
  41. https://pubmed.ncbi.nlm.nih.gov/19358011/
  42. https://pmc.ncbi.nlm.nih.gov/articles/PMC3759515/
  43. https://www.sralab.org/rehabilitation-measures/apraxia-screen-tulia
  44. https://www.sciencedirect.com/topics/[neuroscience](/page/Neuroscience)/apraxia
  45. https://www.e-arm.org/journal/view.php?number=4117
  46. https://pmc.ncbi.nlm.nih.gov/articles/PMC3390701/
  47. https://pubmed.ncbi.nlm.nih.gov/25347756/
  48. https://pmc.ncbi.nlm.nih.gov/articles/PMC4942853/
  49. https://pmc.ncbi.nlm.nih.gov/articles/PMC7979536/
  50. https://www.ahajournals.org/doi/10.1161/01.str.0000091396.95360.e1
  51. https://neurolrespract.biomedcentral.com/articles/10.1186/s42466-019-0042-0
  52. https://www.ahajournals.org/doi/10.1161/str.0000000000000098
  53. https://pmc.ncbi.nlm.nih.gov/articles/PMC4590569/
  54. https://strokengine.ca/en/consequences/apraxia/
  55. https://pmc.ncbi.nlm.nih.gov/articles/PMC8044583/
  56. https://pmc.ncbi.nlm.nih.gov/articles/PMC9511731/
  57. https://www.ahajournals.org/doi/10.1161/STROKEAHA.125.051414
  58. https://pubmed.ncbi.nlm.nih.gov/6206911/
  59. https://neurolrespract.biomedcentral.com/articles/10.1186/s42466-022-00211-x
  60. https://my.clevelandclinic.org/health/diseases/17911-childhood-apraxia-of-speech
  61. https://pubmed.ncbi.nlm.nih.gov/37734154/
  62. https://pubs.asha.org/doi/10.1044/2022_JSLHR-22-00347
  63. https://onlinelibrary.wiley.com/doi/10.1111/ene.16184
Add your contribution
Related Hubs
User Avatar
No comments yet.