Welcome to the clinical neurology podcast, where you will learn over 12 episodes, how to localise a lesion in neurology based on history taking and physical examination. The podcast is meant for medical students and to make them enjoy learning neurology. Medicine, paediatrics, psychiatry, critical care, neurology residents, general practitioners and nurse practitioners will find it beneficial. Notes, images and other clinical resources for the podcast are available in the show description and on the neurology teaching club.com website. I am your host Dr Krishnadas N C, and let’s get started.
Weakness is a common symptom with which a patient presents in neurology. In this episode we will see how to approach a patient with weakness. For this we need to know the motor pathway. What happens when you decide to move your leg? Consider you decides to dorsiflex your right foot. Pyramidal cells of Bets in layer 5 of contralateral left primary motor cortex leg area fires. These impulses are carried through corona radiata which is formed by myelinated axons of pyramidal cells and reaches anterior 2/3 of posterior limb of internal capsule. The axons of leg and arm areas are widely separated in the corona radiata but as it reaches the internal capsule the axons are very close to each other. It’s almost like a funnel with the internal capsule forming the bottom of the funnel. This has clinical importance because a lesion in internal capsule is more likely to involve the upper limb and lower limb equally as their fibers are very close together. Then it reaches the middle 3/5 of cerebral peduncles of midbrain and ascends down in the basis pontis and medullary pyramids on the left side. The pyramidal fibers crosses over to the right side at the lower end of medulla at the cervico-medullary junction and forms the lateral corticospinal tract in cervical cord. 5-10% do not cross to opposite side and form the anterior corticospinal tract. Most of these fibers ultimately crossover at lower spinal cord level. Only 2% remain ipsilateral and supply the axial musculature of trunk and proximal muscles.
The crossed over fibers in lateral corticospinal tract ascends down in the cervical, thoracic, and lumbar spine. It synapses with the alpha motor neuron in anterior horn cell of L5 segment on right side. This entire pathway from left motor cortex to right spinal segmental level where the pyramidal cell axon synapse with the segmental alpha motor neuron is the upper motor neuron. Lesion anywhere in this pathway produce clinical features of a Upper motor neuron disorder which includes hypertonia, brisk reflexes, upgoing plantar and a Upper motor neuron pattern of weakness. This means extensor more than flexor weakness in upper limb and flexors more than extensor weakness in lower limb. There is also a distal fine motor more than proximal weakness. There is not much wasting or involuntary movements like fasciculations.
A lesion anywhere in this pathway from leg area in left motor cortex though corona radiata, internal capsule, midbrain, pons, and medulla and then after crossing to right side in right lateral corticospinal tract in cervical, thoracic, and lumbar spine can produce a right foot drop with UMN features like spasticity, hyperreflexia and upgoing plantar. Please note that the images of Corticospinal tract and whatever we are discussing here can be obtained in neurology teaching club.com website
For leg to dorsiflex these impulses from corticospinal tract must reach the Tibialis anterior muscle the main dorsiflexor of foot. How does it reach there?
The pyramidal fibers synapse with alpha motor neurons in anterior horn at L5 level. Alpha motor neuron in anterior horn cell at L5 level gets out as the ventral motor root, forms the common L5 root after joining with dorsal sensory root. L5 root joins with other roots to form the lumbosacral plexus. The nerve fibers to dorsiflexors come out through sciatic nerve. When Sciatic N divides into common peroneal nerve and tibial nerve, they ascend down through Common peroneal nerve and when it divides into deep peroneal and superficial peroneal nerve proceeds in the deep peroneal nerve to reach the Neuro muscular junction of Tibialis Anterior muscle which dorsiflex the foot. This pathway of the alpha motor neuron axon from anterior horn cell of L5 level to the neuro muscular junction of TA is called the lower motor neuron.
Components of lower motor neuron include
Alpha motor neurons in anterior horn cells
Root
Plexus
Peripheral nerve
Neuro muscular junction and
Muscle
NMJ and muscle per say do not form part of the Lower motor neuron but they can be considered as part of the Lower motor neuron syndrome as the clinical features are same. Lesion at any of these levels can also produce a foot drop. This will be associated with clinical features of LMN disorder including
Wasting
Hypotonia
Weakness in a nerve, plexus or root pattern depending on the site of lesion
Decreased or absent reflex
Flexor plantar reflex
Involuntary movements like fasciculations may be present
So, when a patient presents with weakness as in foot drop the site of lesion can be anywhere from motor cortex, corona radiata, internal capsule, mid brain, pons, and medulla of opposite side, or in ipsilateral cervical, thoracic, lumbar spinal cord corticospinal tract. The lesion in any of these sites will be an Upper motor neuron type. The lesion can also be in lower motor neuron extending from anterior horn cell, root, plexus, peripheral nerve, Neuromuscular junction, or muscle with a lower motor neuron type of weakness.
When a patient presents with weakness our job is to localize where exactly is the anatomic site of involvement. It’s like a criminal case investigation where you must find out the culprit site of lesion. It’s easy if you have an approach and can be quite cumbersome if you don’t have one.
Now we will learn how to approach a patient with weakness in a step-by-step manner. When a patient presents with weakness, we need to follow these steps always
STEP 1
Is to see if there is true weakness?
A patient can tell he has weakness and when we examine, the patient might be having ataxia or bradykinesia. Similarly, a patient having severe pain may not move the limb which might be mistaken as weakness. This is called pseudo paralysis. A good example is an elderly with fracture neck of femur. They present as lower limb weakness, and they may not be able to communicate their pain. The diagnosis will be missed if a proper history is not taken and general examination including musculoskeletal examination is not done. Patients with dissociation conversion disorders can also present as weakness.
STEP 2
Once you are sure there is true weakness the second question is, Is it Upper motor neuro or lower motor neuron?
If the patient has spasticity, hyperreflexia or upgoing plantar its Upper motor neuron
If the patient has wasting, hypotonia, decreased reflex or fasciculation it suggests lower motor neuron involvement.
For example, in the patient with foot drop
If tone increased, reflex brisk and plantar upgoing it suggest a UMN lesion
If there is wasting, hypotonia or absent reflex with or without fasciculation it suggests a lower motor neuron problem
If Upper motor neuron how to localize between cortex, corona radiata, internal capsule, brainstem, and spinal cord?
It’s based on associated findings with weakness
If along with weakness patient has Cortical features like aphasia, apraxia, neglect, agnosia- lesion is in cortex e.g., Patient with right hemiparesis has aphasia, lesion is in left cortex
If along with weakness patient has crossed cranial nerve palsy lesion is in brainstem. For example, if patient with right hemiparesis has left 3rd cranial nerve palsy the lesion is in left midbrain
In Corona radiata and internal capsule there is no cortical or cranial nerve involvement other than the upper motor neuron facial nerve involvement. In internal capsule severity of weakness is equal in upper limb and lower limb as the pyramidal fibers are close together. In Corona radiata the weakness will be more in upper limb than lower limb or vice versa as the pyramidal fibers are far apart and a lesion tend to involve one group more than the other.
Cervical cord lesion produces quadriparesis if lesion is extensive or brown Sequard like if the lesion is patchy involving one side only with weakness and posterior column on same side and pain and temperature lost in the opposite side
Thoracic cord lesion produces paraparesis with sensory level on trunk
We will discuss these in detail when we learn localization of hemiplegia, brainstem, and spinal cord disorders.
If lower motor neuron is involved how to localize further?
Lower motor neuron includes
Alpha motor neurons in anterior horn cells
Root
Plexus
Peripheral nerve
Neuromuscular junction
Muscle
Anterior horn cell, muscle and NMJ are pure motor syndromes meaning lesions in these will not produce any sensory symptoms or signs or in other word if patient has any sensory symptoms or signs, we can rule out these three components of lower motor neuron
Lesions in Root, plexus and peripheral nerve will produce a motor sensory syndrome where patient will be having sensory signs and symptoms along with weakness
STEP 3- If the lesion is lower motor neuron the next question to ask is if it is pure motor or a motor sensory syndrome?
The pure motor syndrome of anterior horn cell, neuro muscular junction and muscle can be further localized based on weather its symmetrical or asymmetrical, fatiguability or diurnal variation is present, wasting or fasciculation is present etc. which we will discuss in detail when we discuss lower motor neuron disorders.
Proximal pure motor with fatiguability and diurnal variation suggest Neuromuscular junction disorder like myasthenia. Proximal pure motor without fatiguability and diurnal variation suggest muscle disease. Asymmetric pure motor with wasting and fasciculations suggest anterior horn cell disease like motor neuron disease
Motor sensory syndrome include root plexus and peripheral nerve. Pattern of distribution of weakness and sensory helps to differentiate between nerve, plexus, and root. For example, in the foot drop case if the patient has hypotonia, absent reflex, flexor plantar or wasting we know it is lower motor neuron involvement. Then see if the patient has any sensory symptoms. If yes, it is either root, plexus, or nerve. See the pattern of motor and sensory involvement and based on that we differentiate between the three.
If dorsiflexion alone is lost and decreased sensation in first web space. This is in the distribution of deep peroneal nerve.
If eversion is also lost and decreased sensation in dorsum of foot. So along with deep peroneal nerve the lateral compartment supplied by superficial peroneal nerve is also involved and sensory is in the distribution of common peroneal nerve.
So, this suggest the cause of foot drop is common peroneal nerve palsy.
If plantar flexion is also weak this suggest tibial nerve is also involved. That means lesion is in Sciatic nerve or proximal in plexus or root
If hip extension also weak gluteus maximus is affected, inferior Gluteal nerve is involved- multiple nerves in a limb involved so possibly lumbosacral plexus lesion
Foot drop with hip abduction weakness and radicular pain – tibialis anterior and gluteus Medius both supplied by L5 root. So, lesion is probably in L5 root.
Thus, further localization of a motor sensory lower motor syndrome into nerve, root and plexus is based on the pattern of motor and sensory involvement
Don’t worry if you could not follow completely. It’s just a curtain raiser to approach to lower motor neuron disorders which we will discussing as a separate episode.
Before we finish, we will revise what we learnt today once again
We learned the motor pathway
Upper motor neuron from motor cortex to anterior horn cell of segmental level in spinal cord including cortex, corona radiata, internal capsule, brain stem and spinal cord
The lower motor neuron from anterior horn cell to muscle including anterior horn cell, root, plexus, peripheral nerve, neuro muscular junction and muscle.
The clinical features of upper motor neuron and lower motor neuron lesions
Then we learned the approach to localize a case of weakness
Step 1 – Is there true weakness?
Step 2- Is the weakness upper motor neuron or lower motor neuron type based on bulk, tone, power, and reflex
Step 3- If upper motor neuron is involved, where? based on the associated symptoms like aphasia in cortical lesion and crossed cranial nerve palsy in brainstem
Step 3- If lower motor neuron is involved then, is it pure motor or motor sensory?
If pure motor symmetrical or asymmetrical, is there fatiguability and diurnal variation Based on these anterior horn cell, neuromuscular disease, or muscle.
If motor sensory the pattern of sensory and motor weakness. Based on that root, plexus, or peripheral nerve
In the next episode we will see how to localize lesion in a hemiplegia case.
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