Foot drop denotes a complex issue involving significant weakness in ankle and toe dorsiflexion.
Dorsiflexors of foot and ankle include tibialis anterior and extensors. Muscles assist in foot clearance during swing and control plantarflexion at heel strike.
Muscle weakness leads to equinovarus deformity, where patients exaggerate hip and knee flexion to avoid toe drag during the swing phase of walking.
Heel strike force surpasses body weight, with ground reaction vector directed behind the ankle and knee.
Uncontrolled plantarflexion can lead to a slap in the foot, while the tibialis anterior absorbs heel strike shock.
Foot drop occurs due to injury of dorsiflexors or their neural pathways. The causes of foot drop are divided in three categories as: neurologic, muscular, and anatomic.
Fibers from L4-S1 ventral rami form the peroneal nerve alongside the tibial nerve in the sciatic nerve.
The peroneal nerve curves over the fibular neck to enter the lower leg compartment.
The peroneal nerve’s larger funiculi and reduced protective tissue increase its susceptibility to trauma compared to the tibial nerve.
The peroneal nerve’s superficial path near the fibular neck makes it more vulnerable to injury.
Epidemiology
Peroneal neuropathy from fibular head compression is common, with foot drop as its main symptom.
About 90% of peroneal lesions are unilateral and affect either side equally. Foot drops due to peroneal nerve palsy are concerned after TKA (0.3-4%) and proximal tibial osteotomy (3-13%).
Epidural anesthesia for TKA increases palsy risk 2.8 times compared to others. Seventy percent of hip arthroplasty patients show nerve injury but seldom exhibit symptoms.
Intraoperative neurologic damage might not be immediately noticeable due to epidural anesthesia effects.
Anatomy
Pathophysiology
The axon’s integrity and its target rely on trophic substances made in the neuronal perikaryon.
A double-crush phenomenon occurs when proximal nerve damage heightens injury risk.
A distal lesion impairs axoplasmic flow, which increases foot drop risk post-hip replacement in patients with spinal stenosis.
Spinal stenosis compromises proximal nerves and stretches sciatic nerve distally. The superficial branch runs between the peroneal heads and descends to lie between the peroneal tendon and gastrocnemius.
Etiology
The causes of foot drop are:
Neurological causes
Muscular causes
Mechanical or structural causes
March gangrene arises from edema and small hemorrhages in anterior compartment muscles after strenuous activity in unaccustomed individuals.
Foot drop can result from mononeuropathies of peroneal or sciatic nerves. Foot drop results from habitual leg crossing but resolves with habit cessation.
Genetics
Prognostic Factors
Peripheral compressive neuropathy recovery occurs within 3 months if compression avoided.
Total knee replacement often results in partial peroneal nerve palsy, which generally has a good recovery prognosis.
Partial palsy recovers quickly due to local sprouting; complete axonal loss requires slower proximal-to-distal growth at 1 mm/day.
Study evaluates predictive factors for recovery outcomes post-surgery for lumbar foot drop.
Clinical History
Collect details including the chief complaint, history of present illness, and medical history to understand clinical history of patients.
Physical Examination
Gait Analysis
Sensory Examination
Reflexes
Motor Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Acute symptoms are:
Trauma, nerve compression, vascular events, stroke, tight cast, or fibular fracture, acute onset with back pain.
Chronic symptoms are:
Degenerative, hereditary, or chronic neuropathic conditions, motor neuron disease, fasciculations, mild weakness.
Differential Diagnoses
Peroneal Nerve Palsy
L5 Radiculopathy
Sciatic Nerve Injury
Muscular Dystrophies
Stroke
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Glucose control for diabetics and vitamin B1, B6, B12 supplementation are beneficial.
For non-surgical foot drop, while peroneal nerve stimulation helps with hemiplegia cases.
Foot drop from dorsiflexor trauma needs surgical repair. Minimize narcotic medications despite significant pain experienced.
Foot drop treatment aims to restore nerve continuity through direct repair or remove the nerve insult.
Transdermal capsaicin or diclofenac reduces symptoms locally.
Erythropoietin is an FDA-approved hormone for anemia treatment with potential neuroprotective and neurotrophic effects.
Erythropoietin is administered as 5000 U/kg in three doses weekly post-nerve injury.
Ankle-Foot Orthosis assists foot drop without surgery or during recovery phases.
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
use-of-non-pharmacological-approach-for-foot-drop
Foot drop patients face high fall risk and mobility limitations. All tripping hazards should be removed and use non-slip flooring.
Use highchairs with armrests to make standing position easier. Use bright lights in hall area, stairs, and bathrooms.
Use assistive devices and orthotics including walking aids and footwear adaptations.
Proper awareness about foot drop should be provided and its related causes with management strategies.
Appointments with surgeon and preventing recurrence of disorder is an ongoing life-long effort.
Use of Antidepressants
Amitriptyline:
It decreases pain to inhibit spinal neurons involved in pain perception.
Desipramine:
It inhibits reuptake of noradrenaline at synapses in central descending pain modulating pathways.
Duloxetine:
It inhibits neuronal serotonin and norepinephrine uptake, and antidepressant action.
Use of Anticonvulsants
Gabapentin:
It exerts their action via the alpha2-delta1 and alpha2-delta2 auxiliary subunits.
Use of Hematopoietic Growth Factors
In acute phase, the goal is to prevent further nerve damage, address acute causes, and ensure safety of patients.
Pharmacologic therapy is effective in the treatment phase as it includes the use of antidepressants, anticonvulsants, and hematopoietic growth factors.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and surgical interventional therapies.
The regular follow-up visits with the surgeon are scheduled to check the improvement of patients along with treatment response.
Foot drop denotes a complex issue involving significant weakness in ankle and toe dorsiflexion.
Dorsiflexors of foot and ankle include tibialis anterior and extensors. Muscles assist in foot clearance during swing and control plantarflexion at heel strike.
Muscle weakness leads to equinovarus deformity, where patients exaggerate hip and knee flexion to avoid toe drag during the swing phase of walking.
Heel strike force surpasses body weight, with ground reaction vector directed behind the ankle and knee.
Uncontrolled plantarflexion can lead to a slap in the foot, while the tibialis anterior absorbs heel strike shock.
Foot drop occurs due to injury of dorsiflexors or their neural pathways. The causes of foot drop are divided in three categories as: neurologic, muscular, and anatomic.
Fibers from L4-S1 ventral rami form the peroneal nerve alongside the tibial nerve in the sciatic nerve.
The peroneal nerve curves over the fibular neck to enter the lower leg compartment.
The peroneal nerve’s larger funiculi and reduced protective tissue increase its susceptibility to trauma compared to the tibial nerve.
The peroneal nerve’s superficial path near the fibular neck makes it more vulnerable to injury.
Peroneal neuropathy from fibular head compression is common, with foot drop as its main symptom.
About 90% of peroneal lesions are unilateral and affect either side equally. Foot drops due to peroneal nerve palsy are concerned after TKA (0.3-4%) and proximal tibial osteotomy (3-13%).
Epidural anesthesia for TKA increases palsy risk 2.8 times compared to others. Seventy percent of hip arthroplasty patients show nerve injury but seldom exhibit symptoms.
Intraoperative neurologic damage might not be immediately noticeable due to epidural anesthesia effects.
The axon’s integrity and its target rely on trophic substances made in the neuronal perikaryon.
A double-crush phenomenon occurs when proximal nerve damage heightens injury risk.
A distal lesion impairs axoplasmic flow, which increases foot drop risk post-hip replacement in patients with spinal stenosis.
Spinal stenosis compromises proximal nerves and stretches sciatic nerve distally. The superficial branch runs between the peroneal heads and descends to lie between the peroneal tendon and gastrocnemius.
The causes of foot drop are:
Neurological causes
Muscular causes
Mechanical or structural causes
March gangrene arises from edema and small hemorrhages in anterior compartment muscles after strenuous activity in unaccustomed individuals.
Foot drop can result from mononeuropathies of peroneal or sciatic nerves. Foot drop results from habitual leg crossing but resolves with habit cessation.
Peripheral compressive neuropathy recovery occurs within 3 months if compression avoided.
Total knee replacement often results in partial peroneal nerve palsy, which generally has a good recovery prognosis.
Partial palsy recovers quickly due to local sprouting; complete axonal loss requires slower proximal-to-distal growth at 1 mm/day.
Study evaluates predictive factors for recovery outcomes post-surgery for lumbar foot drop.
Collect details including the chief complaint, history of present illness, and medical history to understand clinical history of patients.
Gait Analysis
Sensory Examination
Reflexes
Motor Examination
Acute symptoms are:
Trauma, nerve compression, vascular events, stroke, tight cast, or fibular fracture, acute onset with back pain.
Chronic symptoms are:
Degenerative, hereditary, or chronic neuropathic conditions, motor neuron disease, fasciculations, mild weakness.
Peroneal Nerve Palsy
L5 Radiculopathy
Sciatic Nerve Injury
Muscular Dystrophies
Stroke
Glucose control for diabetics and vitamin B1, B6, B12 supplementation are beneficial.
For non-surgical foot drop, while peroneal nerve stimulation helps with hemiplegia cases.
Foot drop from dorsiflexor trauma needs surgical repair. Minimize narcotic medications despite significant pain experienced.
Foot drop treatment aims to restore nerve continuity through direct repair or remove the nerve insult.
Transdermal capsaicin or diclofenac reduces symptoms locally.
Erythropoietin is an FDA-approved hormone for anemia treatment with potential neuroprotective and neurotrophic effects.
Erythropoietin is administered as 5000 U/kg in three doses weekly post-nerve injury.
Ankle-Foot Orthosis assists foot drop without surgery or during recovery phases.
Orthopaedic Surgery
Foot drop patients face high fall risk and mobility limitations. All tripping hazards should be removed and use non-slip flooring.
Use highchairs with armrests to make standing position easier. Use bright lights in hall area, stairs, and bathrooms.
Use assistive devices and orthotics including walking aids and footwear adaptations.
Proper awareness about foot drop should be provided and its related causes with management strategies.
Appointments with surgeon and preventing recurrence of disorder is an ongoing life-long effort.
Orthopaedic Surgery
Amitriptyline:
It decreases pain to inhibit spinal neurons involved in pain perception.
Desipramine:
It inhibits reuptake of noradrenaline at synapses in central descending pain modulating pathways.
Duloxetine:
It inhibits neuronal serotonin and norepinephrine uptake, and antidepressant action.
Orthopaedic Surgery
Gabapentin:
It exerts their action via the alpha2-delta1 and alpha2-delta2 auxiliary subunits.
Orthopaedic Surgery
In acute phase, the goal is to prevent further nerve damage, address acute causes, and ensure safety of patients.
Pharmacologic therapy is effective in the treatment phase as it includes the use of antidepressants, anticonvulsants, and hematopoietic growth factors.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and surgical interventional therapies.
The regular follow-up visits with the surgeon are scheduled to check the improvement of patients along with treatment response.
Foot drop denotes a complex issue involving significant weakness in ankle and toe dorsiflexion.
Dorsiflexors of foot and ankle include tibialis anterior and extensors. Muscles assist in foot clearance during swing and control plantarflexion at heel strike.
Muscle weakness leads to equinovarus deformity, where patients exaggerate hip and knee flexion to avoid toe drag during the swing phase of walking.
Heel strike force surpasses body weight, with ground reaction vector directed behind the ankle and knee.
Uncontrolled plantarflexion can lead to a slap in the foot, while the tibialis anterior absorbs heel strike shock.
Foot drop occurs due to injury of dorsiflexors or their neural pathways. The causes of foot drop are divided in three categories as: neurologic, muscular, and anatomic.
Fibers from L4-S1 ventral rami form the peroneal nerve alongside the tibial nerve in the sciatic nerve.
The peroneal nerve curves over the fibular neck to enter the lower leg compartment.
The peroneal nerve’s larger funiculi and reduced protective tissue increase its susceptibility to trauma compared to the tibial nerve.
The peroneal nerve’s superficial path near the fibular neck makes it more vulnerable to injury.
Peroneal neuropathy from fibular head compression is common, with foot drop as its main symptom.
About 90% of peroneal lesions are unilateral and affect either side equally. Foot drops due to peroneal nerve palsy are concerned after TKA (0.3-4%) and proximal tibial osteotomy (3-13%).
Epidural anesthesia for TKA increases palsy risk 2.8 times compared to others. Seventy percent of hip arthroplasty patients show nerve injury but seldom exhibit symptoms.
Intraoperative neurologic damage might not be immediately noticeable due to epidural anesthesia effects.
The axon’s integrity and its target rely on trophic substances made in the neuronal perikaryon.
A double-crush phenomenon occurs when proximal nerve damage heightens injury risk.
A distal lesion impairs axoplasmic flow, which increases foot drop risk post-hip replacement in patients with spinal stenosis.
Spinal stenosis compromises proximal nerves and stretches sciatic nerve distally. The superficial branch runs between the peroneal heads and descends to lie between the peroneal tendon and gastrocnemius.
The causes of foot drop are:
Neurological causes
Muscular causes
Mechanical or structural causes
March gangrene arises from edema and small hemorrhages in anterior compartment muscles after strenuous activity in unaccustomed individuals.
Foot drop can result from mononeuropathies of peroneal or sciatic nerves. Foot drop results from habitual leg crossing but resolves with habit cessation.
Peripheral compressive neuropathy recovery occurs within 3 months if compression avoided.
Total knee replacement often results in partial peroneal nerve palsy, which generally has a good recovery prognosis.
Partial palsy recovers quickly due to local sprouting; complete axonal loss requires slower proximal-to-distal growth at 1 mm/day.
Study evaluates predictive factors for recovery outcomes post-surgery for lumbar foot drop.
Collect details including the chief complaint, history of present illness, and medical history to understand clinical history of patients.
Gait Analysis
Sensory Examination
Reflexes
Motor Examination
Acute symptoms are:
Trauma, nerve compression, vascular events, stroke, tight cast, or fibular fracture, acute onset with back pain.
Chronic symptoms are:
Degenerative, hereditary, or chronic neuropathic conditions, motor neuron disease, fasciculations, mild weakness.
Peroneal Nerve Palsy
L5 Radiculopathy
Sciatic Nerve Injury
Muscular Dystrophies
Stroke
Glucose control for diabetics and vitamin B1, B6, B12 supplementation are beneficial.
For non-surgical foot drop, while peroneal nerve stimulation helps with hemiplegia cases.
Foot drop from dorsiflexor trauma needs surgical repair. Minimize narcotic medications despite significant pain experienced.
Foot drop treatment aims to restore nerve continuity through direct repair or remove the nerve insult.
Transdermal capsaicin or diclofenac reduces symptoms locally.
Erythropoietin is an FDA-approved hormone for anemia treatment with potential neuroprotective and neurotrophic effects.
Erythropoietin is administered as 5000 U/kg in three doses weekly post-nerve injury.
Ankle-Foot Orthosis assists foot drop without surgery or during recovery phases.
Orthopaedic Surgery
Foot drop patients face high fall risk and mobility limitations. All tripping hazards should be removed and use non-slip flooring.
Use highchairs with armrests to make standing position easier. Use bright lights in hall area, stairs, and bathrooms.
Use assistive devices and orthotics including walking aids and footwear adaptations.
Proper awareness about foot drop should be provided and its related causes with management strategies.
Appointments with surgeon and preventing recurrence of disorder is an ongoing life-long effort.
Orthopaedic Surgery
Amitriptyline:
It decreases pain to inhibit spinal neurons involved in pain perception.
Desipramine:
It inhibits reuptake of noradrenaline at synapses in central descending pain modulating pathways.
Duloxetine:
It inhibits neuronal serotonin and norepinephrine uptake, and antidepressant action.
Orthopaedic Surgery
Gabapentin:
It exerts their action via the alpha2-delta1 and alpha2-delta2 auxiliary subunits.
Orthopaedic Surgery
In acute phase, the goal is to prevent further nerve damage, address acute causes, and ensure safety of patients.
Pharmacologic therapy is effective in the treatment phase as it includes the use of antidepressants, anticonvulsants, and hematopoietic growth factors.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and surgical interventional therapies.
The regular follow-up visits with the surgeon are scheduled to check the improvement of patients along with treatment response.
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