Apraxia

What Causes Apraxia?

Acquired apraxia may be caused by various diseases or injuries that cause damage to the parts of the brain controlling memory and voluntary movements. Common causes of apraxia include:

• Stroke
• Brain tumors
• Traumatic brain injuries
• Dementia
• Alzheimer’s disease
• Corticobasal degeneration
• Other degenerative brain diseases
• Hydrocephalus

Is Apraxia Hereditary?

Apraxia usually occurs sometime after birth and results from a disease or injury. When it is present at birth, it is most often the result of a malformation of the central nervous system that is not inherited. However, one type of apraxia, oculomotor apraxia (OMA), sometimes has a genetic cause inherited by a child from one of their parents.

Inherited OMA seems to be passed on in an autosomal dominant pattern. This means that children may develop the condition if they inherit even one copy of the mutated gene from either of their parents. If a parent carries the disorder-causing mutation, they will have a 50 percent chance of having an affected child with each pregnancy.

How Is Apraxia Detected?

The early signs of acquired apraxia are generally apparent when a person becomes unable to produce or control specific movements. Early symptoms of common types of apraxia that affect speech include:

• Slow speech
• Pauses in the middle of words
• Difficulty with proper stress of syllables
• Distortion of speech sounds
• Movements of the mouth, lips, or tongue without speaking

How Is Apraxia Diagnosed?

Diagnosis of apraxia begins with determining whether the patient has a cluster of symptoms that meet the diagnostic criteria for the disorder. A doctor will start with a physical exam to rule out other problems that may be causing the symptoms, such as aphasia or dyspraxia. After these exams, if the doctor suspects that apraxia is the cause of the symptoms, they may recommend an assessment by specialists to solidify the diagnosis.

Diagnostic steps may include:

• A physical exam. This exam aims to rule out physical conditions that could be causing the symptoms.
• Assessment by a speech-language pathologist. This assessment will attempt to understand the person’s ability to speak and understand language.
• Imaging exams. Magnetic resonance imaging (MRI) or computerized tomography (CT) scans may be used to look for signs of brain damage causing acquired apraxia.

PLEASE CONSULT A PHYSICIAN FOR MORE INFORMATION.

How Is Apraxia Treated?

There is no cure for apraxia. Treatment of the disorder focuses on treating underlying diseases or injuries and providing therapies to help the patient cope with the disabilities of apraxia.

Common treatment approaches include:

• Physical therapy to improve impairments in coordination and movement
• Occupational therapy to assist in accomplishing daily tasks and routines
• Speech therapy
• Special education to confront educational challenges

How Does Apraxia Progress?

The long-term outlook for people with apraxia varies widely from case to case. Sometimes symptoms improve over time. For example, apraxia caused by a stroke often resolves within weeks.

However, many people with apraxia experience significant impairments that do not improve. With therapy, some people with relatively mild impairments can learn to compensate for their symptoms and live independently. Others with severe impairments of movement or speech may be unable to perform essential daily tasks or communicate effectively, making the help of a full-time caregiver necessary.

How Is Apraxia Prevented?

There is no known way to prevent apraxia.

Apraxia Caregiver Tips

Many people with apraxia also suffer from other brain-related issues, a condition called co-morbidity. Here are a few of the disorders commonly associated with apraxia:

• Apraxia is often associated with another speech-related brain disorder called aphasia.
• Apraxia of speech in children is sometimes associated with Down syndrome, autism, or epilepsy.

Apraxia Brain Science

Apraxia is often caused by damage to the brain’s parietal lobe, an area in the upper back part of the brain. The parietal lobe is responsible for interpreting and managing sensory input and uses these inputs to contribute to a wide range of functions. Among other things, this area helps to give us a perception of where our body is in space, make a visual map of the world around us, plan and coordinate our movements, and process language.

Scientists believe the spatial functions of the parietal lobe allow us to create and remember three-dimensional models enabling us to perform complex movements and tasks such as speaking. Damage to this part of the brain may interfere with our ability to access those models, thus making it difficult or impossible to perform the tasks described.

Apraxia Research

Title: Apraxia in Parkinson’s Disease Patients With Deep Brain Stimulation (Apraxia DBS)

Stage: Recruiting

Principal investigator: Bhavana Patel, DO 

University of Florida

Gainesville, FL

Deep brain stimulation (DBS) of the subthalamic nucleus or globus pallidus internus can improve motor symptoms of Parkinson’s disease (PD). However, it is not known whether DBS can help reduce the signs and symptoms of the limb-kinetic, ideomotor or ideational apraxia associated with PD or if apraxia can exist as a stimulation-induced side effect from DBS therapy. In this study, researchers will conduct a pilot study to examine the feasibility of characterizing the prevalence of apraxia in PD patients with chronic, stable DBS.

This pilot study will assess the safety and feasibility of an apraxia testing protocol in chronically implanted PD DBS patients. Researchers hypothesize that apraxia testing in the DBS ON and OFF states will be a safe and well-tolerated testing protocol. They also hypothesize that DBS will affect the severity of limb-kinetic, ideomotor, and ideational apraxia in PD patients. This will set the foundation for more extensive prospective trials to further characterize apraxia in relation to DBS and whether or not DBS programming can modulate this phenomenon.

In this study, researchers will recruit 60 PD patients with chronic, stable DBS of either the subthalamic nucleus (STN) or globus pallidus interna (GPi). Both unilateral and bilateral DBS patients are eligible for this study. For this study, “chronic, stable DBS” will be defined as patients with at least six months of optimization programming at the University of Florida. The subjects will be recruited to the Fixel clinic for a 1-day study visit in the medication ON state. The patients will undergo testing for limb-kinetic, ideomotor, and ideational apraxia of both upper extremities in the DBS ON-state at home therapeutic settings.

Title: Treating Primary Progressive Aphasia and Apraxia of Speech Using Non-invasive Brain Stimulation

Stage: Recruiting

Principal Investigator: John Hart, MD 

The University of Texas at Dallas

Dallas, TX

The purpose of the study is to test whether low-level electric stimulation, called transcranial Direct Current Stimulation (tDCS), on the part of the brain (i.e., pre-supplementary motor area) thought to aid in memory will improve speech and language difficulties in patients with primary progressive aphasia (PPA) and progressive apraxia of speech (PAOS). The primary outcome measures are neuropsychological assessments of speech and language functions, and the secondary measures are neuropsychological assessments of other cognitive abilities and electroencephalography (EEG) measurements.

This pilot study has one treatment arm with open-label treatment. It will examine the improvement of speech output, verbal fluency, and other cognitive deficits associated with primary progressive aphasia (PPA) and progressive apraxia of speech (PAOS), by utilizing (1) milliamp transcranial direct current stimulation (tDCS) active treatment applied to the pre-supplementary motor area for 20 minutes over 10 sessions. There will be baseline testing, and follow-up testing immediately after and 8 weeks after completion of treatment.

All patients with a clinical diagnosis of PPA or PAOS will be assigned to one open-label group to receive active tDCS. Primary outcome speech and language measures, secondary neuropsychological and electroencephalography (EEG) measures and pre-screening assessments for study medical history and contraindications for treatment will be collected prior to the treatment (i.e., baseline).

Primary outcome speech and language function measures and secondary neuropsychological and electroencephalography (EEG) measures will be collected after treatment session 10 and following treatment competition (i.e., 8-week).

Title: The Neurobiology of Two Distinct Types of Progressive Apraxia of Speech (SLD4T)

Stage: Recruiting

Principal Investigator: Keith Josephs, MD 

Mayo Clinic

Rochester, MN

Apraxia of speech (AOS) is a motor speech disorder reflecting a problem with the programming and/or planning of speech. AOS is well recognized in the context of stroke where onset is acute and the condition improves or is stable and chronic. AOS that is insidious in onset and progresses over time because of neurodegeneration is less well recognized and understood. For the past decade, investigators have studied patients with primary progressive apraxia of speech (PAOS). They have demonstrated that it can be the earliest manifestation of an underlying neurodegenerative disease and have recently reported that the profile of PAOS characteristics can differ among affected patients. In some instances, the speech pattern is dominated by distorted sound substitutions and additions, and other features attributable to articulatory difficulty, while in other cases, the pattern is dominated by slow, prosodically segmented speech. We have designated the first profile as Phonetic PAOS (Ph-PAOS) and the second as Prosodic PAOS (Pr-PAOS; previously referred to in our studies as type 1 and 2, respectively). Importantly, it appears that the AOS pattern type may have prognostic implications. In a recent longitudinal study, the investigators observed that in some PAOS patients, the AOS remained the most salient feature over an average of seven years of the neurodegenerative disease. Other patients developed a severe extrapyramidal syndrome, resembling progressive supranuclear palsy, within five years, causing significant morbidity, including the inability to ambulate and a shortened life span; interestingly, this more aggressive course was associated with the Pr- PAOS type. At present, little is known about these types. To address the main aim to better understand the neurobiology and clinical associations of PAOS types, they will perform longitudinal speech, language, and neurocognitive testing, acoustic analyses, neuroimaging, and autopsy in a cohort of 47 new PAOS patients (for 80 PAOS patients total) and healthy controls.