Can you tell a Bell’s palsy from a stroke?

In this post, I will be discussing the neuroanatomical differentiation between an upper motor neuron (UMN) and lower motor neuron (LMN) facial palsy. The two pathologies in the title could also be differentiated in other ways, for example, the speed of onset, additional symptoms and signs, etc.; however understanding the neuroanatomy in the context of the clinical picture, is the best way of avoiding making a grave error.

The left hand is connected to the…

When you wave your left hand, the relevant left-sided spinal nerves are receiving signals from the right side of the motor cortex, the opposite is true of the right side of your body. Hence we say spinal nerves receive motor signals from the motor cortex in a contralateral fashion. Cranial nerves are interesting, because they receive bilateral motor inputs, from both left and right motor cortices. Like I always say, there are exceptions, the facial nerve, hypoglossal and accessory nerves are each a little different and not fully bilateral. For the purpose of this post, I am going to concentrate on the facial nerve (cranial nerve VII).

A hypothetical patient

So let us take a hypothetical but not unlikely situation, a patient has a major right middle cerebral artery bleed affecting the right cerebral motor cortex. In this patient, we would predict that there would be a significant loss of motor function (ignoring sensory, speech and visual symptoms for the purpose of this post) affecting the left side of their body, in fact, they would have a left-sided hemiparesis (weakness affecting one side of the body). As we discussed above, spinal nerves are innervated in a contralateral fashion. How about the muscles of the pharynx? These are innervated by the pharyngeal plexus (cranial nerve IX & X), now as the cranial nerves are bilaterally represented, a bleed damaging the right motor cortex, will not have an effect on the left-sided pharyngeal muscles because the left-sided muscles also receive motor inputs from the left motor cortex. Read that again until its crystal clear then keep calm and carry on reading.

Now let’s take the facial nerve in this patient, it innervates the muscles of facial expression; like most of the other cranial nerves, it has bilateral representation from both cortices. There is an exception, only the muscles of the upper half of each side of the face are bilaterally innervated, the lower half of each side of the face is unilateral and contralateral. What does this mean? So the left frontalis has innervation from both the right and left motor cortices. However, all the other facial muscles on the left side of the face are innervated only by the right motor cortex. So in our hypothetical patient with the left-sided hemiparesis affecting his body, let us see if we can work out what has happened to his face. The bleed is affecting his right motor cortex, and we know the right cortex will be innervating the left lower and upper facial muscles, we also know the upper¬†left half of the face will get additional innervation from the left cortex, so the insult results in facial paralysis, affecting the lower left face. The upper left face has been spared, as it also receives inputs from the left cortex. So this patient will have a left-sided facial palsy with left upper face sparing (forehead) and a left-sided hemiparesis affecting the rest of the body.

UMN and LMN lesions

Up until this point, we have only discussed an upper motor neuron lesion (in this case a stroke affecting the right motor cortex). We will now consider a LMN and try to understand how to differentiate it from a UMN lesion of the facial nerve. The basic voluntary motor pathway layout in our nervous system starts with an upper motor neuron cell body, its axon travelling down the CNS, and synapsing with a LMN cell body, then the LMN axon travelling in a cranial or spinal nerve until it forms a neuromuscular junction.

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Figure 1, Facial nerve diagram, adapted from Neuroanatomy draw it to know it

The LMN cell bodies for the facial nerve are grouped in the brainstem to form the facial nerve nucleus; this is located at the pontomedullary junction in the brainstem. Let’s take the left facial nerve nucleus, where is it getting all of its motor inputs from? The left facial nucleus is innervated by the right motor cortex which provides motor signals for the left upper and lower muscles of the face; the left facial nucleus also gets motor signals for the muscles of the left upper face from the left motor cortex. Look at Figure 1 and take a minute and think about that. We have already discussed a UMN lesion, what if I destroy the left facial nucleus (LMN lesion), what happens? We no longer get any signals going to the entire left side of the face, we lose both upper and lower contralateral facial signals (from the right cortex), and we also lose ipsilateral upper facial signals (from the left cortex). Therefore we have a complete left-sided facial palsy (upper and lower left sided facial muscles affected).

Localising a LMN lesion.

Now depending on where the lesion affects the LMN circuitry, will determine which specific branches of the facial nerve will be affected and what other specific symptoms the patient will experience. To localise lesions you must understand the path of the facial nerve, it’s twists and turns and where it’s various branches come off, see Figure 2. By the way, if you are looking at Figure 2 and thinking the pes anserinus is in the leg, yes it is, but its also in the face; the branching of the facial nerve in the parotid gland is also known as the pes anserinus.

Intracranial lesion

So a lesion between the facial nerve nucleus and the internal acoustic meatus (functionally this is the same up to and including the geniculate ganglion) will knock out all the distal branches. This includes all of the muscles of facial expression, parasympathetic supply (via the great petrosal nerve) to the lacrimal glands and to the mucous glands in the nasal cavity. It will also knock out the parasympathetic carried via the chorda tympani, hitching a ride with the lingual nerve to the sublingual and submandibular salivary glands. Gustatory afferents coming back via the chorda tympani from the anterior 2/3 of the tongue will also be impaired. Inside the middle ear, the branch to stapedius which dampens the vibrations transmitted to the inner ear will be affected. The patient will thus become exquisitely sensitive to normal sounds, known as hyperacusis.

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Figure 2, Schematic representation of the facial nerve and its branches, adapted from Master Medicine: Clinical Anatomy

Lesion in the middle ear

A lesion in the middle ear including the geniculate ganglion will be similar to the lesion described above. However, a lesion distal to the geniculate ganglion will spare the greater petrosal nerve and its parasympathetic efferent fibres destined to the lacrimal gland via the pterygopalatine ganglion. So lacrimation will not be affected. The lesion in the middle ear, depending on its size will potentially affect the nerve to stapedius, resulting in hyperacusis, the chorda tympani, resulting in impairment of taste from the anterior 2/3 of the tongue. As the facial nerve exits the stylomastoid foramen, branches are given off innervating the posterior belly of digastric, stylohyoid and the muscles of facial expression, these will all be affected.

Lesion in the parotid gland

Such a lesion (e.g., a parotid tumour) will spare all the branches proximal to the parotid gland. Hence the only branches to be affected should be those of facial expression arising from within the gland itself. Motor supply to the posterior belly of digastric and stylohyoid should be spared as they arise proximal to the lesion. All branches even more proximal, i.e. those in the middle ear, geniculate ganglion will also be spared.

Summary

LMN facial nerve lesion blocks contralateral and ipsilateral signals to that side of the face, resulting in a complete (upper and lower face) ipsilateral facial palsy. An UMN facial nerve lesion knocks out contralateral signals (contralateral upper and lower parts of the face), but ipsilateral UMN signals are still intact, resulting in contralateral facial palsy only affecting the lower half of the face, the forehead is spared.

Before you leave…

We have seen how a stroke affecting the motor cortex can give an UMN palsy, what would happen if a patient had a pontine stroke? What type of palsy would you see?

References

  • Neuroanatomy draw it to know it, Adam Fisch
  • Master Medicine: Clinical Anatomy, Stanley Monkhouse
  • A textbook of neuroanatomy, Patestas and Gartner

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