Gait Apraxia
Apraxias
Apraxia, Ideomotor
Infarction, Anterior Cerebral Artery
Gait Disorders, Neurologic
Gait Ataxia
Gait apraxia after bilateral supplementary motor area lesion. (1/14)
OBJECTIVES: The study aimed at addressing the issue of the precise nature of gait apraxia and the cerebral dysfunction responsible for it. METHODS: The case of a patient, affected by a bilateral infarction limited to a portion of the anterior cerebral artery territory is reported. The patient's ability to walk was formally assessed by means of a new standardised test. RESULTS: Due to an anomaly within the anterior cerebral artery system, the patient's lesion was centred on the supplementary motor regions of both hemispheres. He presented with clear signs of gait apraxia that could not be accounted for by paresis or other neurological deficits. No signs of any other form of apraxia were detected. CONCLUSIONS: The clinical profile of the patient and the analysis of 49 cases from previous literature suggest that gait apraxia should be considered a clinical entity in its own right and lesions to the supplementary motor areas are responsible for it. (+info)Paraneoplastic chorea: case study with autopsy confirmation. (2/14)
A 67-year-old man presented with a 7-month history of insidiously progressive chorea, ataxia, and vertigo. Neurologic examination revealed deficits referable to the basal nuclei, cerebellar vermis, and vestibular nuclei. Small-cell lung cancer was diagnosed by fine-needle biopsy of a parahilar mass. After chemotherapy, the patient's chorea worsened. Anti-Hu antibodies were present in serum and cerebrospinal fluid. Microscopic examination of the brain at autopsy revealed diffuse perivascular lymphocytic infiltrates, microglial activation, and neuronophagia throughout the neuraxis, including the brainstem, cerebellum, lenticular nuclei, striatum, and cerebral cortex. Prominent loss of Purkinje cells was seen in the cerebellar vermis and hemispheres to a lesser degree. Chorea is extremely rare as a paraneoplastic manifestation of cancer. The florid presentation and the positive findings contrasted with an unremarkable MRI of the brain. This case illustrates the preeminence of symptoms and signs over negative MRI findings in paraneoplastic encephalitis. (+info)A new classification of higher level gait disorders in patients with cerebral multi-infarct states. (3/14)
BACKGROUND: cerebral multi-infarct states may lead to gait disorders in the absence of cognitive impairment. Where these gait disorders occur in the absence of neurological signs they have been termed gait apraxia or more recently higher-level gait disorders. In this paper we hypothesise three main types based on presumptive sites of anatomical damage: (a) Ignition Apraxia, where damage is predominantly in the supplementary motor area and its connections, with good responses to external clues; (b) Equilibrium Apraxia, where damage is predominantly in the pre-motor area in its connections, with poor responses to external cues and (c) Mixed Gait Apraxia. SUBJECTS: the clinical features and measured gait parameters of 13 patients with cerebral multi-infarct states and higher-level gait disorder are described (7 with Ignition Apraxia and 6 with Equilibrium Apraxia) along with those of 6 healthy elderly control subjects. METHODS: baseline gait characteristics were assessed on a walkway, which measured the following: step lengths, width of base and velocity. RESULTS: measured baseline gait parameters support the above hypothesis. CONCLUSIONS: it is suggested, though not proven, that patients with Ignition Apraxia could have problems with internal cueing due to lesions in the supplementary motor area or its connections whereas those with Equilibrium Apraxia could have dysfunction predominantly in the pre-motor area and its connections. (+info)Walking difficulties in patients with Alzheimer's disease might originate from gait apraxia. (4/14)
OBJECTIVES: To investigate whether gait apraxia is a possible cause for some of the walking abnormalities shown by patients with Alzheimer's disease. METHODS: 60 patients with Alzheimer's disease, selected as being free from overt extrapyramidal impairment or other potential causes of walking deficits, were assessed with a new test evaluating aspects of walking and related movements. Norms for this test were collected from a sample of 182 healthy volunteers. RESULTS: 40% of the Alzheimer group performed below the cut off score on this test, and half performed poorly. Performance of the Alzheimer group in the walking skills test correlated highly with scores in a test assessing limb apraxia and with dementia severity. CONCLUSIONS: Gait apraxia may be the cause of walking disorders found in a subgroup of patients with Alzheimer's disease. Its detection is made easier by the use of a standardised test, but still relies heavily on the exclusion of other causes of walking deficits. It is a recognisable and independent form of apraxia. (+info)Apraxia in movement disorders. (5/14)
The definition of apraxia specifies that the disturbance of performed skilled movements cannot be explained by the more elemental motor disorders typical of patients with movement disorders. Generally this does not present a significant diagnostic problem when dealing with 'higher-level' praxic disturbances (e.g. ideational apraxia), but it can be a major confound in establishing the presence of limb-kinetic apraxia. Most motor disturbances characteristic of extrapyramidal disorders, particularly bradykinesia and dystonia, will compromise the ability to establish the presence of loss of dexterity and deftness that constitutes this subtype. The term 'apraxia' has also been applied to other motor disturbances, such as 'gait apraxia' and 'apraxia of eyelid opening', that perhaps are misnomers, demonstrating the lack of a coherent nomenclature in this field. Apraxia is a hallmark of corticobasal degeneration (CBD) and historically this has received the most attention among the movement disorders. Corticobasal degeneration is characterized by various forms of apraxia affecting limb function, particularly ideomotor apraxia and limb-kinetic apraxia, although buccofacial and oculomotor apraxia can be present as well. The syndrome of parkinsonism and prominent apraxia, designated the 'corticobasal syndrome' (CBS), may be caused by a variety of other central nervous system pathologies including progressive supranuclear palsy (PSP), Alzheimer's disease, dementia with Lewy bodies and frontotemporal dementias. Distinct from the CBS, PSP and Parkinson's disease can demonstrate varying degrees of apraxia on selected tests, especially in those patients with more severe cognitive dysfunction. Diseases that cause the combination of apraxia and a primary movement disorder most often involve a variety of cerebral cortical sites as well as basal ganglia structures. Clinical-pathological correlates and functional imaging studies are compromised by both this diffuse involvement and the confusion experienced in the clinical evaluation of apraxia in the face of the additional elemental movement disorders. Finally, although apraxia results in clear disability in patients with the CBS, it is not clear how milder ideomotor apraxia found on specific testing contributes to patients' overall day-to-day motor disability. (+info)Lengthening and transfer of hamstrings for a flexion deformity of the knee in children with bilateral cerebral palsy: technique and preliminary results. (6/14)
Between July 2000 and April 2004, 19 patients with bilateral spastic cerebral palsy who required an assistive device to walk had combined lengthening-transfer of the medial hamstrings as part of multilevel surgery. A standardised physical examination, measurement of the Functional Mobility Scale score and video or instrumented gait analysis were performed pre- and post-operatively. Static parameters (popliteal angle, flexion deformity of the knee) and sagittal knee kinematic parameters (knee flexion at initial contact, minimum knee flexion during stance, mean knee flexion during stance) were recorded. The mean length of follow-up was 25 months (14 to 45). Statistically significant improvements in static and dynamic outcome parameters were found, corresponding to improvements in gait and functional mobility as determined by the Functional Mobility Scale. Mild hyperextension of the knee during gait developed in two patients and was controlled by adjustment of their ankle-foot orthosis. Residual flexion deformity > 10 degrees occurred in both knees of one patient and was treated by anterior distal femoral physeal stapling. Two children also showed an improvement of one level in the Gross Motor Function Classification System. (+info)Association between the metabolic syndrome and its components and gait speed among U.S. adults aged 50 years and older: a cross-sectional analysis. (7/14)
BACKGROUND: To examine the relationship between the metabolic syndrome and its components and gait speed among older U.S. men and women. Whether these associations are independent of physical activity was also explored. METHODS: Eight hundred and thirty-five men and 850 women aged > or =50 years from the continuous National Health and Nutrition Examination Survey 1999-2002 were examined. We used the definition of the metabolic syndrome developed by the U.S. National Cholesterol Education Program Adult Treatment Panel III. Gait speed was measured with a 6.10-meter timed walk examination. RESULTS: The prevalence of the metabolic syndrome was 40.2% in men and 45.6% in women (P = .127). The prevalence of gait speed impairment was 29.3% in men and 12.5% in women (P < .001). No association was found between the metabolic syndrome and gait speed impairment. After including the individual components of the metabolic syndrome in a logistic model adjusted for age and leisure-time physical activity, abdominal obesity, low HDL cholesterol, and high fasting glucose were significantly associated with gait speed impairment among women (adjusted odds ratio [AOR] = 0.48, 95% confidence interval [CI] = 0.26 to 0.89; AOR = 2.26, 95% CI = 1.08 to 4.75; and AOR = 2.05, 95% CI = 1.12 to 3.74, respectively). Further adjustment for race/ethnicity, education, smoking status, alcohol consumption, arthritis status, and use of an assistive device attenuated these associations; among women, abdominal obesity and low HDL cholesterol remained significantly associated with gait speed impairment (AOR = 0.37, 95% CI = 0.18 to 0.76 and AOR = 2.45, 95% CI = 1.07 to 5.63, respectively) while the association between hyperglycemia and impaired gait speed attenuated to nonsignificance. CONCLUSION: Among women, gait speed impairment is associated with low HDL cholesterol and inversely with abdominal obesity. These associations may be sex-dependent and warrant further research. (+info)Backward walking in Parkinson's disease. (8/14)
(+info)Gait apraxia is a neurological disorder that affects an individual's ability to perform coordinated and complex movements required for walking, despite having the physical capability to do so. It is not caused by weakness or sensory loss, but rather by damage to the brain areas responsible for motor planning and execution, particularly in the frontal lobes.
Gait apraxia is characterized by a wide-based, hesitant, and unsteady gait pattern. Individuals with this condition may have difficulty initiating walking, changing direction, or adjusting their stride length and speed. They may also exhibit symptoms such as freezing of gait, where they are unable to move their feet forward despite intending to walk.
This disorder is often associated with various neurological conditions, including cerebrovascular accidents (strokes), degenerative diseases such as Parkinson's disease and multiple sclerosis, traumatic brain injuries, and infections of the central nervous system. Treatment typically involves physical therapy, gait training, and the use of assistive devices to improve mobility and safety.
Apraxia is a motor disorder characterized by the inability to perform learned, purposeful movements despite having the physical ability and mental understanding to do so. It is not caused by weakness, paralysis, or sensory loss, and it is not due to poor comprehension or motivation.
There are several types of apraxias, including:
1. Limb-Kinematic Apraxia: This type affects the ability to make precise movements with the limbs, such as using tools or performing complex gestures.
2. Ideomotor Apraxia: In this form, individuals have difficulty executing learned motor actions in response to verbal commands or visual cues, but they can still perform the same action when given the actual object to use.
3. Ideational Apraxia: This type affects the ability to sequence and coordinate multiple steps of a complex action, such as dressing oneself or making coffee.
4. Oral Apraxia: Also known as verbal apraxia, this form affects the ability to plan and execute speech movements, leading to difficulties with articulation and speech production.
5. Constructional Apraxia: This type impairs the ability to draw, copy, or construct geometric forms and shapes, often due to visuospatial processing issues.
Apraxias can result from various neurological conditions, such as stroke, brain injury, dementia, or neurodegenerative diseases like Parkinson's disease and Alzheimer's disease. Treatment typically involves rehabilitation and therapy focused on retraining the affected movements and compensating for any residual deficits.
Ideomotor apraxia is a neurological disorder that affects the ability to perform learned, purposeful movements in the absence of muscle weakness or paralysis. It results from damage to specific areas of the brain that are responsible for motor planning and execution.
In ideomotor apraxia, the person has difficulty translating an intention or idea into the appropriate movement. For example, if asked to pantomime using a toothbrush, they may not be able to recall and execute the correct sequence of movements required for this task, even though they understand what is being asked of them and have no problem moving their arm or hand.
This disorder can manifest as awkward, poorly coordinated, or incomplete movements, often with inconsistent errors. Ideomotor apraxia is typically seen following lesions to the left hemisphere of the brain, particularly in regions associated with language and motor function, such as Broca's area and the parietal lobe. Treatment usually involves occupational therapy and strategies to help compensate for the impaired motor skills.
Anterior cerebral artery infarction refers to the death of brain tissue (also known as an infarct) in the territory supplied by the anterior cerebral artery (ACA) due to insufficient blood flow. The ACA supplies oxygenated blood to the frontal lobes of the brain, which are responsible for higher cognitive functions such as reasoning, problem-solving, and decision-making, as well as motor control of the lower extremities.
An infarction in this territory can result from various causes, including atherosclerosis, embolism, thrombosis, or vasospasm. Symptoms of an ACA infarction may include weakness or paralysis on one side of the body (usually the lower extremities), difficulty with coordination and balance, urinary incontinence, changes in personality or behavior, and impaired cognitive function. The severity of symptoms depends on the extent and location of the infarct. Immediate medical attention is necessary to prevent further damage and improve the chances of recovery.
Gait is a medical term used to describe the pattern of movement of the limbs during walking or running. It includes the manner or style of walking, including factors such as rhythm, speed, and step length. A person's gait can provide important clues about their physical health and neurological function, and abnormalities in gait may indicate the presence of underlying medical conditions, such as neuromuscular disorders, orthopedic problems, or injuries.
A typical human gait cycle involves two main phases: the stance phase, during which the foot is in contact with the ground, and the swing phase, during which the foot is lifted and moved forward in preparation for the next step. The gait cycle can be further broken down into several sub-phases, including heel strike, foot flat, midstance, heel off, and toe off.
Gait analysis is a specialized field of study that involves observing and measuring a person's gait pattern using various techniques, such as video recordings, force plates, and motion capture systems. This information can be used to diagnose and treat gait abnormalities, improve mobility and function, and prevent injuries.
A gait disorder is a disturbance in the ability to walk that can't be attributed to physical disabilities such as weakness or paralysis. Neurologic gait disorders are those specifically caused by underlying neurological conditions. These disorders can result from damage to the brain, spinal cord, or peripheral nerves that disrupts communication between the muscles and the brain.
Neurologic gait disorders can present in various ways, including:
1. **Spastic Gait:** This is a stiff, foot-dragging walk caused by increased muscle tone (hypertonia) and stiffness (spasticity). It's often seen in conditions like cerebral palsy or multiple sclerosis.
2. **Ataxic Gait:** This is a broad-based, unsteady, and irregular walk caused by damage to the cerebellum, which affects balance and coordination. Conditions such as cerebellar atrophy or stroke can cause this type of gait disorder.
3. **Parkinsonian Gait:** This is a shuffling walk with small steps, flexed knees, and difficulty turning. It's often seen in Parkinson's disease.
4. **Neuropathic Gait:** This is a high-stepping walk caused by foot drop (difficulty lifting the front part of the foot), which results from damage to the peripheral nerves. Conditions such as diabetic neuropathy or Guillain-Barre syndrome can cause this type of gait disorder.
5. **Choreic Gait:** This is an irregular, dance-like walk caused by involuntary movements (chorea) seen in conditions like Huntington's disease.
6. **Mixed Gait:** Sometimes, a person may exhibit elements of more than one type of gait disorder.
The specific type of gait disorder can provide important clues about the underlying neurological condition and help guide diagnosis and treatment.
Gait ataxia is a type of ataxia, which refers to a lack of coordination or stability, specifically involving walking or gait. It is characterized by an unsteady, uncoordinated, and typically wide-based gait pattern. This occurs due to dysfunction in the cerebellum or its connecting pathways, responsible for maintaining balance and coordinating muscle movements.
In gait ataxia, individuals often have difficulty with controlling the rhythm and pace of their steps, tend to veer or stagger off course, and may display a reeling or stumbling motion while walking. They might also have trouble performing rapid alternating movements like quickly tapping their foot or heel. These symptoms are usually worse when the person is tired or attempting to walk in the dark.
Gait ataxia can be caused by various underlying conditions, including degenerative neurological disorders (e.g., cerebellar atrophy, multiple sclerosis), stroke, brain injury, infection (e.g., alcoholism, HIV), or exposure to certain toxins. Proper diagnosis and identification of the underlying cause are essential for effective treatment and management of gait ataxia.