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Lower Motor Examination
TZ
Introduction
• Although there is no uniform consent on the distinction between
paresis & plegia, what most clinicians agree on is that paresis is a
mild to moderate weakness of the muscles (with a power of 1,2,3,4),
while plegia is a complete weakness of the muscles (0 power).
• Based on the limbs that are involved by the weakness we
can classify it as;-
• Hemiparesis (involving one half of the body),
• Paraparesis (involving both the lower limbs) and
• Quadriparesis (involving all the 4 limbs).
Lower motor examination
• Position of feet/leg: deviation of the feet implies weakness.
• If the feet are rotated outwards we can expect a spastic paralysis
(upper motor neuron) and if the rotation is to the midline, a flaccid
paralysis (lower motor neuron).
• Muscle bulk: you must first see if there is a visible discrepancy of the
muscle bulk in corresponding areas of the 2 limbs & then measure
with a tape meter 10cm below & 20cm above the tibial tuberosity,
then compare.
• A reduced muscle bulk is suggestive of LMNLs although it can happen
in a long standing UMNLs due to disuse atrophy.
• If there is a difference in the measurement with swelling & tenderness
you should suspect DVT, as limb weakness is a very important risk
factor for its development.
• Fasciculation: are twitching of the muscles visible through the skin
suggesting LMNs.
• You should first see if there is a spontaneous fasciculation and then try
to induce it by tapping on areas of muscle bulk with your hammer
• The tone is the resistance to passive movement of the limbs.
• You should check the tone by moving the feet, the leg and the thigh.
• A decreased tone (hypotonic) is a manifestation of lower motor lesion
and a tone increment (hypertonic) suggests an upper motor lesion.
• You report this as hypertonic, hypotonic or normotonic.
• You can assess the power by seeing the movement of the leg
independent of gravity, against gravity, and with the application of
some resistance.
• You grade power out of 5 as:
• It is often better to start by asking the patient to raise the legs against
gravity and assess the others based on the outcome.
• If he/she couldn’t raise it go down in to assessing side to side
movement (no gravity) and if he/she could raise the legs try assessing
movement with some resistance.
• Another way of assessing the power is checking for each muscle
group;-
• Dorsiflexion & plantarflexion: elevate/press down the feet & toes
against resistance,
• Extension of knee: bend the knee & try to straighten against resistance,
• Flexors of knee: raise the leg from the bed & ask the patient to bend
their knee,
• Extension of hip: raise the leg with the knee extended & ask the
patient to push down against resistance,
• Flexors of hip: extend the knee & ask the patient to raise the leg
against resistance
• Adductor of thigh: abduct the leg & ask the patient to bring the legs
to the midline against resistance
• Abductor of thigh: put the legs together in the midline & ask the
patient to separate them against resistance,
• Rotators of thigh: extend the knee & ask the patient to rotate
internally & externally against resistance
• The presence of sensory level is suggestive of spinal cord lesion and
should be checked.
• The sensory parameters are pain, temperature, vibration and
position senses.
• The lesion is usually 2 levels lower than the spinal cord level as they
cross higher up (for example, if we get a sensory level at C2 then the
lesion is at C4).
Paraparesis
• Acute onset weakness speaks for vascular causes, acute
hydrocephalus, infections like transverse myelitis and trauma.
• Vascular causes can be sagital sinus vein thrombosis, parasagital
cortical vein thrombosis, anterior spinal artery ischemia or
hemmorhage.
• Subacute to chronic onset suggests compressive myelopathy
secondary to TB spondylitis, primary spinal cord tumors or
metastases, degenerative disorders of the spinal cord.
• The types of muscle groups affected can also help us differentiate the
possible cause.
• For example, myopathies tend to affect the proximal muscle groups,
so patients are going to have difficulties with climbing stairs, arising
from squatting position, combing their hair or picking high-sitting
objects.
• Neuropathies affect the distal muscle more, meaning the patient is
going to be complaining of problems with their fine motor skills.
Causes of paraplegia
• Cerebral origin: the lower limbs and the micturition center are
represented in the paracentral lobule (around the upper one inch of
the cerbral cortex) and as a result lesions of this area can give us
paraparesis with bladder disturbance (urine retention, urgency or
incontinence).
• This makes it similar to spinal cord lesions which can also give us
paraparesis with bladder dysfunction.
• As a result presence of certain conditions should tip
us some information to localize the lesion to the
cerebral cortex.
• We get lower motor neuron type lesion at the level of compression as
anterior horn cells are affected but we get upper motor neuron type
of lesion below the compression because of corticospinal tracts
affection.
• Intramedullary spinal cord compressions are mostly secondary to an
intramedullary tumor.
• But the extramedullary compressions have many differentials.
Hemiparesis
• Hemiparesis results from an UMNL above the mid cerivcal cord (most
are above the foramen magnum).
• Presence of other neurologic deficits will help us localize the lesion.
• For example, presence of language disorders, cortical sensory
disturbance, cognitive abnormalities, apraxia, seizure and disorders of
visual-spatial integration indicate cortical lesions while homonymous
visual field defects indicate a cortical or subcortical hemispheric
lesion.
• A pure motor hemiparesis of face, arm and leg is mostly due to
lesions in the internal capsule or brainstem.
• The absence of cranial nerve deficits indicate that the lesion is in the
cervical spinal cord, especially if it is associated with ipsilateral loss of
proprioception (as this fibers cross high up in the medulla) and
contralateral loss of pain and temperature.
• In acute hemiparesis, we usually evaluate the patient
with CT scan and lab tests, and do MRI of the brain or spine if the CT
doesn’t show any abnormality.
• In subacute hemiparesis, the first investigation should be brain MRI
and if it is normal do MRI of the spine
Quadriparesis
• Weakness of all 4 limbs may occur secondary to disorders of the CNS
(quadriparesis) or motor unit (generalized weakness).
• Causes of episodic weakness:
Hyperthyroidism
Myasthenia Gravis
GBS
• Causes of pure motor paraplegia:
Cerebral causes of paraplegia
Spinal cord lesions such as:
- Heriditary spastic paraplegia
- Lathyrism
- ALS
Acute demyelinating polyneuropathy
Myopathy
Periodic paralysis (hypokalemic, hyperkalemia, hypercalcemia, hyponatremia,
hypernatremia)
Conn’s syndrome also known as primary hyper-aldosteronism
Botulinum poisoning
CNS disorders (transient ischemic attack of the brain stem, Transient global
cerebral ischemia, Multiple sclerosis)

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Lower Limb Weakness Exam

  • 2. Introduction • Although there is no uniform consent on the distinction between paresis & plegia, what most clinicians agree on is that paresis is a mild to moderate weakness of the muscles (with a power of 1,2,3,4), while plegia is a complete weakness of the muscles (0 power). • Based on the limbs that are involved by the weakness we can classify it as;- • Hemiparesis (involving one half of the body), • Paraparesis (involving both the lower limbs) and • Quadriparesis (involving all the 4 limbs).
  • 3. Lower motor examination • Position of feet/leg: deviation of the feet implies weakness. • If the feet are rotated outwards we can expect a spastic paralysis (upper motor neuron) and if the rotation is to the midline, a flaccid paralysis (lower motor neuron).
  • 4. • Muscle bulk: you must first see if there is a visible discrepancy of the muscle bulk in corresponding areas of the 2 limbs & then measure with a tape meter 10cm below & 20cm above the tibial tuberosity, then compare. • A reduced muscle bulk is suggestive of LMNLs although it can happen in a long standing UMNLs due to disuse atrophy. • If there is a difference in the measurement with swelling & tenderness you should suspect DVT, as limb weakness is a very important risk factor for its development. • Fasciculation: are twitching of the muscles visible through the skin suggesting LMNs. • You should first see if there is a spontaneous fasciculation and then try to induce it by tapping on areas of muscle bulk with your hammer
  • 5. • The tone is the resistance to passive movement of the limbs. • You should check the tone by moving the feet, the leg and the thigh. • A decreased tone (hypotonic) is a manifestation of lower motor lesion and a tone increment (hypertonic) suggests an upper motor lesion. • You report this as hypertonic, hypotonic or normotonic. • You can assess the power by seeing the movement of the leg independent of gravity, against gravity, and with the application of some resistance. • You grade power out of 5 as:
  • 6. • It is often better to start by asking the patient to raise the legs against gravity and assess the others based on the outcome. • If he/she couldn’t raise it go down in to assessing side to side movement (no gravity) and if he/she could raise the legs try assessing movement with some resistance. • Another way of assessing the power is checking for each muscle group;- • Dorsiflexion & plantarflexion: elevate/press down the feet & toes against resistance, • Extension of knee: bend the knee & try to straighten against resistance,
  • 7. • Flexors of knee: raise the leg from the bed & ask the patient to bend their knee, • Extension of hip: raise the leg with the knee extended & ask the patient to push down against resistance, • Flexors of hip: extend the knee & ask the patient to raise the leg against resistance • Adductor of thigh: abduct the leg & ask the patient to bring the legs to the midline against resistance • Abductor of thigh: put the legs together in the midline & ask the patient to separate them against resistance, • Rotators of thigh: extend the knee & ask the patient to rotate internally & externally against resistance
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  • 10. • The presence of sensory level is suggestive of spinal cord lesion and should be checked. • The sensory parameters are pain, temperature, vibration and position senses. • The lesion is usually 2 levels lower than the spinal cord level as they cross higher up (for example, if we get a sensory level at C2 then the lesion is at C4).
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  • 12. Paraparesis • Acute onset weakness speaks for vascular causes, acute hydrocephalus, infections like transverse myelitis and trauma. • Vascular causes can be sagital sinus vein thrombosis, parasagital cortical vein thrombosis, anterior spinal artery ischemia or hemmorhage. • Subacute to chronic onset suggests compressive myelopathy secondary to TB spondylitis, primary spinal cord tumors or metastases, degenerative disorders of the spinal cord.
  • 13. • The types of muscle groups affected can also help us differentiate the possible cause. • For example, myopathies tend to affect the proximal muscle groups, so patients are going to have difficulties with climbing stairs, arising from squatting position, combing their hair or picking high-sitting objects. • Neuropathies affect the distal muscle more, meaning the patient is going to be complaining of problems with their fine motor skills.
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  • 16. Causes of paraplegia • Cerebral origin: the lower limbs and the micturition center are represented in the paracentral lobule (around the upper one inch of the cerbral cortex) and as a result lesions of this area can give us paraparesis with bladder disturbance (urine retention, urgency or incontinence). • This makes it similar to spinal cord lesions which can also give us paraparesis with bladder dysfunction.
  • 17. • As a result presence of certain conditions should tip us some information to localize the lesion to the cerebral cortex.
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  • 20. • We get lower motor neuron type lesion at the level of compression as anterior horn cells are affected but we get upper motor neuron type of lesion below the compression because of corticospinal tracts affection.
  • 21. • Intramedullary spinal cord compressions are mostly secondary to an intramedullary tumor. • But the extramedullary compressions have many differentials.
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  • 26. Hemiparesis • Hemiparesis results from an UMNL above the mid cerivcal cord (most are above the foramen magnum). • Presence of other neurologic deficits will help us localize the lesion. • For example, presence of language disorders, cortical sensory disturbance, cognitive abnormalities, apraxia, seizure and disorders of visual-spatial integration indicate cortical lesions while homonymous visual field defects indicate a cortical or subcortical hemispheric lesion. • A pure motor hemiparesis of face, arm and leg is mostly due to lesions in the internal capsule or brainstem.
  • 27. • The absence of cranial nerve deficits indicate that the lesion is in the cervical spinal cord, especially if it is associated with ipsilateral loss of proprioception (as this fibers cross high up in the medulla) and contralateral loss of pain and temperature. • In acute hemiparesis, we usually evaluate the patient with CT scan and lab tests, and do MRI of the brain or spine if the CT doesn’t show any abnormality. • In subacute hemiparesis, the first investigation should be brain MRI and if it is normal do MRI of the spine
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  • 29. Quadriparesis • Weakness of all 4 limbs may occur secondary to disorders of the CNS (quadriparesis) or motor unit (generalized weakness).
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  • 31. • Causes of episodic weakness: Hyperthyroidism Myasthenia Gravis GBS • Causes of pure motor paraplegia: Cerebral causes of paraplegia Spinal cord lesions such as: - Heriditary spastic paraplegia - Lathyrism - ALS Acute demyelinating polyneuropathy Myopathy Periodic paralysis (hypokalemic, hyperkalemia, hypercalcemia, hyponatremia, hypernatremia) Conn’s syndrome also known as primary hyper-aldosteronism Botulinum poisoning CNS disorders (transient ischemic attack of the brain stem, Transient global cerebral ischemia, Multiple sclerosis)