Neuro Gait Abnormalities Flashcards

1
Q
  • What is a flaccid gait?
  • What are the underlying neurological or muscular causes
  • How does it clinically present during the gait cycle?
A
  • 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.
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2
Q
  • What is foot drop gait?
  • What are the typical causes?
  • What compensatory mechanisms are commonly observed?
A
  • 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.

  • Flaccid/Muscle Weakness Dysfunctions
  • Video #2
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3
Q
  • What characterizes genu recurvatum during the stance phase
  • What are the common underlying causes
  • How does it differ from extensor thrust gait?
A
  • 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.

  • Flaccid/Muscle Weakness Dysfunctions
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4
Q
  • How does gluteus maximus weakness manifest in a patient’s gait
  • What are its primary causes
  • What compensations are seen in the trunk during the stance phase?
A
  • 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.
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5
Q
  • What is Trendelenburg gait
  • What is the cause of this pattern
  • What compensatory strategies might be observed?
A
  • 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

  • Flaccid/Muscle Weakness Dysfunctions
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6
Q
  • What are the defining characteristics of spastic gait
  • What neurological conditions commonly lead to this abnormality?
A
  • 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.
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7
Q
  • What is toe-walking gait
  • What are its primary causes
  • How does it present differently in children versus adults?
A
  • 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.
  • Toe first/Toe walking: Inadequate dorsiflexor assist: inadequate plantar flexion stop: inadequate heel lift, heel pain, extensor spasticity, pes equinus, short leg
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8
Q
  • What is hemiplegic gait
  • What compensatory mechanisms are seen in the swing and stance phases
  • What are the common clinical presentations?
A
  • 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.

  • Spastic/Higher tone Dysfunctions
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9
Q

What defines scissoring gait
What are the primary causes
How do these patients compensate during the swing phase to clear their feet?

A
  • 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.
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10
Q
  • What is crouched gait
  • How do hip or knee flexion contractures contribute to its presentation
  • What compensations are observed in the lumbar spine or trunk?
A
  • 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.

  • Spastic/Higher tone Dysfunctions
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11
Q
  • How does cerebellar dysfunction influence gait patterns
  • What are the hallmark clinical signs of ataxic gait
  • How does it differ from other neurologically impaired gaits?
A
  • 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.

  • Cerebellar Dysfunction
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12
Q
  • What are the defining characteristics of Parkinsonian gait
  • How does the festinating pattern emerge
  • How might it impact the patient’s mobility and safety?
A
  • 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.
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13
Q
  • What is festinating gait
  • What causes the forward-leaning posture and rapid short steps
  • How does it typically progress during the gait cycle?
A
  • 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.

  • Basal Ganglia Dysfunction
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14
Q
  • What is vaulting gait
  • What are the underlying causes
  • What observable compensations occur in the stance limb?
A
  • 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.
  • Circumduction or Vaulting: locked knee, excessive plantar flexion (inadequate stop, plantar flexion contractures), Weak hip flexors or weak dorsiflexors
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15
Q
  • How do hip hiking and circumduction gait patterns compensate for swing limb clearance deficits
  • What are the typical causes
  • How can you differentiate between the two clinically?
A
  • 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.

  • Spastic/Higher tone Dysfunctions
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16
Q

What are the biomechanical mechanisms behind foot slap, and how does it manifest during gait?

A
  • 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.
  • Foot Slap: inadequate dorsiflexion assist: inadequate plantarflexion stop; weak dorsiflexors

  • Flaccid/Muscle Weakness Dysfunctions
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17
Q

What are the primary causes of toe-walking gait, and how does it affect the phases of gait?

A
  • 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.
  • Toe first/Toe walking: Inadequate dorsiflexor assist: inadequate plantar flexion stop: inadequate heel lift, heel pain, extensor spasticity, pes equinus, short leg

  • Spastic/Higher tone Dysfunctions
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18
Q
  • How does quadriceps weakness contribute to genu recurvatum
  • What is the resulting effect on knee stability?
A
  • 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.
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19
Q

What is the role of hamstring weakness in extensor thrust gait, and how does it affect the swing and stance phases?

A

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.

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20
Q

How does gluteus maximus weakness impact hip stability during gait, and what compensatory strategies are used?

A

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.

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21
Q

How do spasticity and hypertonia alter joint motion in spastic gait, and what are the resulting biomechanical deviations?

A

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.

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22
Q

How does cerebellar dysfunction lead to ataxic gait, and what compensatory mechanisms are observed?

A

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.

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23
Q

What causes scissoring gait, and how does adductor spasticity influence the biomechanics of the lower extremities?

A

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.

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24
Q

What mechanisms lead to hip hiking and circumduction, and how do they compensate for reduced limb clearance during swing?

A
  • 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.
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25
Q

What causes vaulting gait, and how does it alter the biomechanics of the stance leg?

A

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.

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26
Q

How does Parkinson’s disease affect stride length and posture in Parkinsonian gait?

A

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.

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27
Q

What is the biomechanical cause of crouched gait, and how do hip flexion and knee flexion contractures contribute?

A

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.

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28
Q

How does pelvic drop in Trendelenburg gait affect the center of gravity and overall balance?

A

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.

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29
Q

What biomechanical factors lead to festinating gait in Parkinson’s disease, and how does it progress over time?

A
  • 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.
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30
Q

How do neurological impairments affect the timing and rhythm of gait in hemiplegic patients?

A

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.

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31
Q

How would you clinically identify foot drop gait during gait analysis, and what tests can confirm its underlying cause?

A

Foot drop gait is identified by observing high steppage gait or toe drag during swing. Tests like manual muscle testing (MMT) for dorsiflexors or nerve conduction studies can confirm conditions like peroneal nerve palsy.

32
Q

What clinical observations would indicate Trendelenburg gait, and how can you confirm gluteus medius weakness?

A

Trendelenburg gait is observed when the pelvis drops on the contralateral side during stance. Confirmation involves a positive Trendelenburg test or MMT of the hip abductors.

33
Q

How can you differentiate between circumduction and hip hiking during gait observation?

A

Circumduction involves an outward swing of the leg, while hip hiking elevates the pelvis on the swing side. Observation of pelvis and limb movement during swing helps differentiate the two.

34
Q

What signs during gait observation would suggest spasticity as the primary impairment, and how can you assess its severity?

A

Signs include stiff-legged movement, scissoring, or toe-walking. Severity can be assessed with tools like the Modified Ashworth Scale or spasticity-specific gait analysis.

35
Q

How does cerebellar ataxic gait appear during clinical evaluation, and what additional tests can confirm cerebellar dysfunction?

A

Ataxic gait presents with a wide base of support, irregular steps, and staggering. Finger-to-nose tests or heel-to-shin tests can confirm cerebellar involvement.

36
Q

What are the clinical features of Parkinsonian gait, and how does it differ from other hypokinetic gait patterns?

A

Parkinsonian gait features shuffling steps, reduced arm swing, and festination. It differs by the hallmark bradykinesia and forward-leaning posture specific to Parkinson’s disease.

37
Q

How would you observe and diagnose a patient with scissoring gait, and what are the key spasticity-related impairments involved?

A

Scissoring gait is observed by crossing of the legs during swing. Key impairments include hip adductor spasticity and reduced hip abduction during gait.

38
Q

What are the primary clinical cues for diagnosing hemiplegic gait, and how do you differentiate mild from severe cases?

A

Hemiplegic gait presents with circumduction, hip hiking, or toe drag on the affected side. Severity is differentiated by the degree of spasticity and loss of reciprocal arm swing.

39
Q

How can you identify crouched gait during gait analysis, and what musculoskeletal impairments are typically involved?

A

Crouched gait is identified by flexed hips and knees during stance. Impairments include hip and knee flexion contractures or spasticity in the hip flexors and quadriceps.

40
Q

What are the observable compensations for vaulting gait, and what conditions should be suspected based on this finding?

A

Vaulting involves rising onto the toes of the stance leg. Conditions like leg length discrepancy, reduced knee flexion, or ankle dorsiflexion limitations should be suspected.

41
Q

What clinical observations would lead you to suspect festinating gait, and how does it impact functional mobility?

A

Festinating gait is observed as rapid, short steps with a forward-leaning posture. It reduces functional mobility by impairing balance and increasing fall risk.

42
Q

How can you clinically distinguish between a wide-based ataxic gait and a narrow-based spastic gait?

A

Ataxic gait has a wide base of support and irregular steps, while spastic gait shows a narrow base with stiff, scissoring movements. Observation of stride regularity and base width helps differentiate them.

43
Q

What are the observable differences between toe-walking due to spasticity and toe-walking due to idiopathic causes?

A

Spasticity-related toe-walking involves hypertonic calf muscles and other signs of neurological dysfunction, while idiopathic toe-walking is typically isolated without associated spasticity.

44
Q

How does pelvic drop in Trendelenburg gait manifest during dynamic gait analysis, and what tests can further evaluate the affected muscles?

A

Pelvic drop on the contralateral side is observed during stance. Tests like the Trendelenburg test or single-leg stance can evaluate hip abductor strength.

45
Q

What are the common compensatory strategies observed in patients with weak quadriceps, and how does this affect knee stability during gait?

A

Compensations include forward trunk lean or hand assistance to extend the knee. These strategies reduce knee flexion demand but may compromise balance and stability during gait.

46
Q

What are the causes and clinical presentations of lateral trunk bending in patients using orthotics?

A

Lateral trunk bending is caused by medial side uprights set too high, hip pain, weak or tight hip abductors, short leg, or poor balance. It presents as a visible side-to-side trunk shift during gait.

47
Q

How do locked knee joints in orthotics contribute to circumduction or vaulting during gait?

A

Locked knee joints prevent knee flexion, causing circumduction or vaulting as compensations to clear the advancing limb during swing.

48
Q

What causes anterior trunk bending in orthotic users, and how does it affect gait biomechanics?

A

Anterior trunk bending occurs due to weak quadriceps, hip or knee flexion contractures, or inadequate knee locks. It shifts the center of gravity forward to compensate for reduced knee stability.

49
Q

How does posterior trunk lean occur in patients using orthotics, and what compensatory mechanisms are observed?

A

Posterior trunk lean results from weak gluteus maximus or inadequate hip locks. It shifts the center of gravity posteriorly to reduce demand on the hip extensors during stance.

50
Q

What leads to hyperextension of the knee in patients with orthotic devices, and what biomechanical factors are involved?

A

Knee hyperextension is caused by inadequate plantarflexion stop, inadequate knee lock, or weak quadriceps. It results in excessive posterior knee stress during stance.

51
Q

What causes knee instability in orthotic users, and how does it affect gait?

A

Knee instability is caused by inadequate dorsiflexion stop, weak quadriceps, or knee pain. It leads to unsteady knee movements during stance and swing phases.

52
Q

How does inadequate dorsiflexion assist in orthotics lead to foot slap, and what are the compensations observed?

A

Inadequate dorsiflexion assist causes foot slap by failing to control forefoot descent during loading response. Patients may compensate with exaggerated hip or knee flexion.

53
Q

What are the biomechanical causes of toe-first or toe-walking patterns in patients using orthotics?

A

Toe-first patterns are caused by inadequate dorsiflexion assist, plantarflexion contractures, or heel pain. It increases forefoot loading and alters push-off mechanics.

54
Q

How does excessive pronation occur in orthotic users, and what are the contributing factors?

A

Excessive pronation is caused by weak invertors, valgus alignment, or transverse plane malalignment. It results in medial foot collapse during stance.

55
Q

What leads to excessive supination in orthotic users, and how does it impact foot mechanics during gait?

A

Excessive supination is caused by weak evertors, varus alignment, or high arches. It creates lateral foot loading and reduced shock absorption.

56
Q

How does a KAFO with a medial upright set too high contribute to excessive stance width during gait?

A

A high medial upright in a KAFO forces the leg outward, increasing stance width and altering balance and foot placement during gait.

57
Q

What are the implications of inadequate plantarflexion stop in orthotics, and how does it affect the gait cycle?

A

Inadequate plantarflexion stop leads to excessive plantarflexion during stance, causing instability and impaired limb clearance during swing.

58
Q

How does a poorly fitting calf band contribute to knee hyperextension in orthotic users?

A

A poorly fitting calf band fails to provide adequate support, allowing excessive knee extension forces during stance, leading to hyperextension.

59
Q

What causes inadequate dorsiflexion stop in orthotic devices, and what impact does it have on knee stability?

A

Inadequate dorsiflexion stop allows excessive tibial advancement, destabilizing the knee and increasing the risk of buckling during stance.

60
Q

How does a short leg or poor balance affect gait patterns in patients using orthotics?

A

A short leg or poor balance causes uneven weight distribution, leading to compensations such as lateral trunk bending or increased step width.

61
Q

What are the primary treatment goals for managing foot drop gait, and which interventions are most effective?

A

Treatment goals include restoring dorsiflexion and preventing compensatory movements. Effective interventions include strengthening anterior tibialis, using ankle-foot orthoses (AFOs), and functional electrical stimulation (FES).

62
Q

How can Trendelenburg gait be improved through strengthening exercises or assistive devices?

A

Strengthening exercises for the gluteus medius, such as side-lying hip abductions or resistance band walks, can improve Trendelenburg gait. Assistive devices like canes may help with balance.

63
Q

What interventions are effective for addressing circumduction gait caused by hip flexor weakness?

A

Strengthening hip flexors with exercises like straight leg raises or resisted marching can improve circumduction gait. Gait training and functional electrical stimulation may also be beneficial.

64
Q

How can spasticity-related gait abnormalities, such as toe-walking or scissoring, be managed?

A

Management includes stretching tight muscles, using medications like botulinum toxin, orthotics to control foot position, and strengthening antagonist muscles to reduce spasticity.

65
Q

What strengthening and stretching exercises are recommended for patients with crouched gait?

A

Strengthening quadriceps and gluteal muscles, along with stretching hip flexors and hamstrings, can address crouched gait. Task-specific training may also help improve functional gait.

66
Q

What are the best strategies for managing hemiplegic gait, and how do assistive devices play a role?

A

Strategies include strengthening the affected limb, improving balance, and using assistive devices like AFOs or canes to enhance safety and stability during gait.

67
Q

How can cerebellar ataxic gait be addressed through balance training or coordination exercises?

A

Balance training with tools like balance boards, coordination exercises like tandem walking, and proprioceptive training can improve cerebellar ataxic gait.

68
Q

What are the key interventions for reducing knee hyperextension during gait?

A

Interventions include strengthening the quadriceps, using AFOs with a dorsiflexion stop, and gait training to encourage proper knee flexion during stance.

69
Q

How can therapy target compensatory strategies like vaulting or hip hiking?

A

Therapy can focus on improving limb clearance through hip and knee flexor strengthening, stretching tight muscles, and using orthotic devices to enhance swing phase mechanics.

70
Q

What is the role of orthotics in managing gait deviations caused by neurological conditions?

A

Orthotics, such as AFOs or KAFOs, provide stability, improve limb positioning, and correct compensatory gait patterns in patients with neurological impairments.

71
Q

How does cueing and task-specific training improve Parkinsonian gait and reduce festination?

A

External cues like rhythmic auditory stimulation and task-specific training enhance stride length, improve coordination, and reduce festination in Parkinsonian gait.

72
Q

What interventions are recommended to manage lateral trunk bending in orthotic users?

A

Interventions include adjusting orthotic alignment, strengthening hip abductors, and providing balance training to improve trunk control during gait.

73
Q

How can stretching programs address joint contractures contributing to gait abnormalities?

A

Stretching programs targeting tight muscle groups, such as hamstrings or hip flexors, help reduce contractures and restore joint range of motion for improved gait mechanics.

74
Q

What is the role of functional electrical stimulation (FES) in improving gait patterns?

A

FES stimulates weak muscles like dorsiflexors or quadriceps, enhancing limb clearance, stride length, and overall gait pattern in neurological patients.

75
Q

How can gait training programs be individualized for patients with combined neurological and musculoskeletal impairments?

A

Individualized programs address specific deficits through strengthening, stretching, balance training, and task-specific practice, incorporating assistive devices as needed.