Neuro Gait Abnormalities Flashcards
- What is a flaccid gait?
- What are the underlying neurological or muscular causes
- How does it clinically present during the gait cycle?
- Flaccid gait results from muscle weakness or paralysis.
- Typically due to lower motor neuron lesions.
- Clinical presentation includes a lack of muscle tone, poor control of limb movements, and dragging of the affected limb during the swing phase.
- What is foot drop gait?
- What are the typical causes?
- What compensatory mechanisms are commonly observed?
- Foot drop gait is characterized by the inability to dorsiflex the foot, caused by conditions such as peroneal nerve palsy or anterior tibialis weakness.
- Compensatory mechanisms include exaggerated hip and knee flexion (steppage gait) to avoid dragging the toes.
What characterizes genu recurvatum during the stance phase, what are the common underlying causes, and how does it differ from extensor thrust gait?
Genu recurvatum involves hyperextension of the knee during stance, often caused by quadriceps weakness, plantarflexion contractures, or hamstring weakness. It differs from extensor thrust gait, which shows poor knee control but lacks the dramatic hyperextension.
How does gluteus maximus weakness manifest in a patient’s gait, what are its primary causes, and what compensations are seen in the trunk during the stance phase?
Gluteus maximus weakness causes a lurch gait characterized by a backward trunk lean during early stance to compensate for reduced hip extension strength. Common causes include nerve injury or muscular atrophy.
What is Trendelenburg gait, how does gluteus medius weakness or hip abductor insufficiency cause this pattern, and what compensatory strategies might be observed?
Trendelenburg gait occurs due to gluteus medius weakness, leading to a pelvic drop on the contralateral side during stance. Compensation often includes a lateral trunk lean toward the affected side to maintain balance.
What are the defining characteristics of spastic gait, and what neurological conditions commonly lead to this abnormality?
Spastic gait is marked by stiff, jerky limb movements, often with toe walking or scissoring. It is commonly seen in conditions like cerebral palsy, stroke, or multiple sclerosis, which result in increased muscle tone.
What is toe-walking gait, what are its primary causes, and how does it present differently in children versus adults?
Toe-walking gait is defined by initial contact on the toes rather than the heel. In children, it may be idiopathic or due to cerebral palsy, while in adults it could stem from spasticity or Achilles tendon contractures.
What is hemiplegic gait, what compensatory mechanisms are seen in the swing and stance phases, and what are the common clinical presentations?
Hemiplegic gait presents with circumduction or hip hiking during swing and a stiff, extended lower extremity in stance. It results from unilateral spasticity and is commonly observed in stroke patients.
What defines scissoring gait, what are the primary causes, and how do these patients compensate during the swing phase to clear their feet?
Scissoring gait is characterized by crossing of the legs during swing, caused by hip adductor spasticity. Patients may compensate with a narrowed base of support and exaggerated trunk movements to clear their feet.
What is crouched gait, how do hip or knee flexion contractures contribute to its presentation, and what compensations are observed in the lumbar spine or trunk?
Crouched gait involves flexed hips and knees during stance, often due to contractures or spasticity. Compensations include increased lumbar lordosis and reduced stride length to maintain upright posture.
How does cerebellar dysfunction influence gait patterns, what are the hallmark clinical signs of ataxic gait, and how does it differ from other neurologically impaired gaits?
Ataxic gait is characterized by a wide base of support, staggering, and uneven movements due to poor coordination. It is distinct from other gaits as it often resembles acute alcohol intoxication and may involve exaggerated movements.
What are the defining characteristics of Parkinsonian gait, how does the festinating pattern emerge, and how might it impact the patient’s mobility and safety?
Parkinsonian gait features shuffling steps, reduced arm swing, and forward trunk lean. Festination occurs as the patient’s feet attempt to ‘catch up’ with their center of gravity, increasing fall risk.
What is festinating gait, what causes the forward-leaning posture and rapid short steps, and how does it typically progress during the gait cycle?
Festinating gait involves rapid, short steps and forward-leaning posture, often seen in advanced Parkinson’s disease. It progresses as the patient’s steps become faster without increasing stride length.
What is vaulting gait, what are the underlying causes, and what observable compensations occur in the stance limb?
Vaulting gait occurs when the patient rises on the toes of the stance limb to clear a longer swing leg, often due to limited knee or hip flexion or leg length discrepancy.
How do hip hiking and circumduction gait patterns compensate for swing limb clearance deficits, what are the typical causes, and how can you differentiate between the two clinically?
Hip hiking raises the pelvis on the affected side, while circumduction swings the leg outward. Both compensate for reduced limb clearance caused by weak hip flexors or knee stiffness, but circumduction has a semicircular swing pattern.
What are the biomechanical mechanisms behind foot slap, and how does it manifest during gait?
Foot slap occurs due to weak dorsiflexors, often caused by conditions like peroneal nerve injury. It manifests as a rapid and audible drop of the forefoot during the loading response phase of gait.
What are the primary causes of toe-walking gait, and how does it affect the phases of gait?
Toe-walking gait is caused by conditions such as spasticity, cerebral palsy, or Achilles tendon contractures. It affects initial contact by bypassing the heel and places more demand on the forefoot during stance.
How does quadriceps weakness contribute to genu recurvatum, and what is the resulting effect on knee stability?
Quadriceps weakness leads to genu recurvatum by failing to control knee flexion during loading response. This results in excessive knee hyperextension, compromising stability during the stance phase.
What is the role of hamstring weakness in extensor thrust gait, and how does it affect the swing and stance phases?
Hamstring weakness reduces knee flexion control, causing the knee to snap into extension (extensor thrust) during stance. It may also impact terminal swing by failing to decelerate knee extension.
How does gluteus maximus weakness impact hip stability during gait, and what compensatory strategies are used?
Gluteus maximus weakness affects hip extension during stance, causing the trunk to lean backward to shift the center of gravity posteriorly and reduce hip extensor demand.
How do spasticity and hypertonia alter joint motion in spastic gait, and what are the resulting biomechanical deviations?
Spasticity and hypertonia restrict joint mobility, leading to stiff-legged movement, toe-walking, and scissoring gait patterns. These deviations impair shock absorption and swing phase limb clearance.
How does cerebellar dysfunction lead to ataxic gait, and what compensatory mechanisms are observed?
Cerebellar dysfunction impairs coordination, causing ataxic gait with a wide base of support and irregular, staggering steps. Patients often use exaggerated movements to maintain balance.
What causes scissoring gait, and how does adductor spasticity influence the biomechanics of the lower extremities?
Scissoring gait is caused by adductor spasticity, leading to excessive hip adduction during swing. This narrows the base of support and causes the legs to cross midline.
What mechanisms lead to hip hiking and circumduction, and how do they compensate for reduced limb clearance during swing?
Hip hiking raises the pelvis, while circumduction swings the leg outward. Both compensate for insufficient knee or hip flexion, or dorsiflexion, to clear the foot during swing.
What causes vaulting gait, and how does it alter the biomechanics of the stance leg?
Vaulting gait occurs when the patient rises on the toes of the stance leg to clear a longer swing limb. This places increased load on the calf muscles and stance leg joints.
How does Parkinson’s disease affect stride length and posture in Parkinsonian gait?
Parkinson’s disease reduces stride length due to bradykinesia and causes a forward-flexed posture. This leads to shuffling steps and a decreased ability to stop or turn quickly.
What is the biomechanical cause of crouched gait, and how do hip flexion and knee flexion contractures contribute?
Crouched gait is caused by hip and knee flexion contractures, which maintain the limbs in a flexed position during stance. This increases the energy cost of walking and shortens stride length.
How does pelvic drop in Trendelenburg gait affect the center of gravity and overall balance?
Pelvic drop shifts the center of gravity toward the contralateral side, leading to poor balance. Patients often compensate by leaning their trunk laterally toward the affected side.
What biomechanical factors lead to festinating gait in Parkinson’s disease, and how does it progress over time?
Festinating gait results from impaired postural control and forward-leaning trunk posture. Over time, the patient’s steps become shorter and quicker as they try to ‘catch up’ with their center of gravity.
How do neurological impairments affect the timing and rhythm of gait in hemiplegic patients?
Neurological impairments disrupt reciprocal movement patterns, causing delays in swing phase and abnormal timing of limb movements. This often leads to circumduction or hip hiking on the affected side.
