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See my cranial nerves summary to work out the answers to this SG.

Case 1

A sixty-three year old woman, while working about the house, suddenly fell to the floor and was unable to get up. She had difficulty speaking and her left arm and leg were paralysed. An examination made two months after the onset of the symptoms showed paralysis of the left upper and lower limbs. The tone of the muscles in these limbs was increased and the tendon reflexes were exaggerated. When the tongue was protruded it deviated to the right. The right half of the tongue was wrinkled due to atrophy.

  • Symptoms:
    • Speaking
    • Left arm paralysed
    • Tone increasing
    • Reflexes exaggerated
    • Deviated right tongue
  • Explanation
    • Right side intrinsic tongue muscles paralysed (so protruding the tongue pushes only the left side forwards)
    • Atrophy due to paralysis and disuse
      • XII hypoglossal nerve affected
    • Motor tract is the (right) corticospinal tract causing left arm paralysis. This tract transmits messages about intended movements from the cerebral cortex (in the forebrain) down to motor neurons in the spinal cord, which in turn supply (bring about movement in) muscles of the trunk and limbs. As these tracts pass down through lower part of the brainstem (the medulla) they form a swelling on each side called the pyramids. The hypoglossal nerve emerges from the brain as a series of little rootlets along the outer edge of these pyramids (preolivary sulcus). These two structures share the same blood supply, so if this is interrupted, both the hypoglossal nerve and the corticospinal tracts will be affected, as in this case.
    • Course and distribution of nerve: Nerve travels downwards behind internal carotid before turning anteriorly over the top of it (note ICA is posterior to ECA). Crosses the lateral side of the external carotid reaching the sides of the tongue. Supplies the intrinsic muscles of the tongue.
    • Tone and reflexes is due to an upper motor neuron lesion (myotactic stretch reflex: spindle fibre afferents take control without descending inhibition)
      • Loss of control by the brain
    • Location of lesion - right side
      • In the medulla, because this is the only place where the hypoglossal nerve and corticospinal tract are located together and consequently the only place where they could both be injured at once. (Before the pyramidal decussation)
    • Paralysis of the limbs occurs on the opposite side to that of the tongue
      • When the fibres of the (right) corticospinal tract reach the bottom of the medulla (junction between the brain and the spinal cord) they cross over (decussate) to descend down the opposite (left) side of the cord and end up supplying motor neurons on that side (left).
    • Cranial nerves vs spinal nerves
    • Recovery is unlikely
      • Although there may be some improvement with rehabilitation, the patient is unlikely to recover full function, particularly in the distal muscles of the limbs. This is because neurons in the central nervous system that have been severely injured do not have the power to repair themselves and will eventually die off. Although some progress has been made in recent years into developing techniques which might promote central nerve regeneration, there is still a very long way to go before full functional recovery could confidently be predicted.
  • Note you can have a lesion of the corticospinal tract up in the midbrain that will affect the right side of the tongue and the right side of the body, because of the decussation of the corticobulbar tracts, which occurs above the pons. This would result in weakness rather than paralysis, because in the corticobulbar tracts, both sides supply both sides (so upper motor neuron lesions on this side are not unilateral and not all or nothing)
    • The upper motor neuron in the cranial nerves is the corticobulbar tract
    • The lower motor neuron is the nerve itself

Case 2

A woman, fifty-eight years old, suddenly fell to the floor, and when she tried to get up realised she couldn't move her right arm or leg. Weeks later, neurological examination revealed that she was unable to open her left eye fully because of drooping of the upper eyelid (ptosis) and the left eyeball was turned outward and slightly downward. The left pupil was dilated and did not react to light, although the consensual light reflex in the other eye was present. When protruded, the tongue turned somewhat to the right, showing a weakness of the musculature of that side, but there was no atrophy. Also on the right side, there was a paralysis of the muscles of the lower part of the face, causing drooping of the right side of the mouth, but the muscles around her eye and forehead were not affected. The paralysis of the right limbs was accompanied by increased muscle tone and exaggerated reflexes.

  • Symptoms
    • Right arm/leg paralysis
    • Ptosis on the left side
    • Left eyeball is down and abducted
    • Droopy mouth
  • Explanations
    • Movement of the eye is due to medial rectus and the oculomotor nerve (CN3)
    • Eyelid drooping is due to levator palpebrae superioris
    • The eye is moved in a medial (nasal) direction by the medial rectus muscle and in the lateral (outwards) direction by the lateral rectus muscle. Both of these muscles act together to keep the eye in the neutral position (looking forwards). When the two muscles are pulling against each other one muscle is said to oppose the other. If the medial rectus muscle is paralysed the lateral rectus muscle draws the eye outwards because it no longer being opposed by the paralysed medial rectus muscle. This condition is described clinically as lateral strabismus. The opposite would occur if the lateral rectus muscle was paralysed (causing medial strabismus).
      • Or sympathetic nervous system – horner’s syndrome
    • Emerges from occulomotor and Edinger-Westphal nuclei at the interpeduncular fossa. Pierces the dura. Runs along wall of cavernous sinus and enters orbit through superior orbital fissure at common tendinous ring. Recall the picture of the cavernous sinus.
    • Double vision: Movements between the two eyes are coordinated, so that both eyes look at the one object or scene. When muscles in one eye are paralysed the movements of that eye can no longer be coordinated with the other eye, particularly when they try to use the paralysed muscles. For example, as in this case, when the patient tries to look to the right, his normal right eye turns to the right but his left eye is unable to look in that direction. Consequently the image entering the two eyes is different (because they are looking in different directions) and the patient perceives this as ‘seeing double’.
    • Drooping of eye: The muscle that elevates the eye, the levator palpebrae superioris m., contains both skeletal and smooth muscle fibres. The skeletal muscle fibres, which make up the bulk of the muscle, are supplied by the oculomotor nerve. When these fibres lose their nerve supply, the eyelid droops (ptosis).
    • Other possible cause: The smooth muscle fibres in the levator palpebrae superioris m. are supplied by sympathetic nerves. Consequently loss of sympathetic nerve supply to these fibres in the upper eyelid will also cause ptosis, although it is not usually as severe as that seen with an oculomotor nerve lesion. Loss of sympathetic supply to the head causes a cluster of symptoms (ptosis, miosis, enophthalmos and anhidrosis) that are referred to as Horner’s syndrome.
    • Pupillary reflex: In a normal person, when light is shone onto the pupil of one eye, both pupils constrict to regulate the amount of light entering the eye. The response in the eye that is stimulated is known as the direct pupillary reflex and the response in the opposite eye is known as the consensual reflex. The optic nerve (2nd cranial nerve) carries the sensory (light) stimulus into the brain. The oculomotor nerve transmits a message from the brain which causes the pupil to constrict (via its parasympathetic division). Note that in this case the indirect light reflex is working for this case. Note also there would be very different responses between Horner's syndrome (can't dilate) and a CN3 lesion (can't constrict)
    • Facial muscles, which is supplied by corticobulbar tract
    • Facial nerve would cause paralysis of all the muscles of the face, so we know it's not a lesion of facial nerve.
    • Occulomotor nerve comes out well above where the facial nerve comes out. Hence you'd have had a lesion to the corticobulbar tract of hte facial nerve.
      • In the facial nerve, only the nerves supplying the upper part of the face are supplied by both sides. For the lower part of the face, only the contralateral nervous side supplies it. Therefore, upper motor neuron disease = can move above eye only (e.g. brainstem tract), but lower motor neuron disease = facial paralysis (e.g. Bell's palsy)
      • Paralysis of the muscles of the lower half of the face was on contralateral side (muscles of upper face are supplied bilaterally and not affected). Weakness (but not paralysis) of tongue muscles and muscles of mastication on the contralateral side (These muscles are supplied bilaterally but the input from the contralateral side is a bit stronger, hence some weakness).

Case 3

A 22 year-old medical student, who had suffered from influenza-like symptoms the week before, experienced aching around his left ear. The next morning, when shaving, he noticed that his mouth was drooping and he was unable to move the left side of his face. His left eye was starting to feel painful and itchy. Neurological examination showed that he could not wrinkle his forehead on the left side, nor could he purse his lips or show his teeth on that side. He had trouble closing his left eye. Taste sensation was abnormal on the left side of his tongue and loud sounds caused him discomfort. Otherwise he was normal and in good health.


  • Symptoms
    • Aching left ear (so it must be high up in the facial nerve, as this is before it heads off in the facial canal)
    • Mouth drooping of the left
    • Left eye sore (lacrimal nerve is gone too)
    • No muscle on the left side
    • Taste affected (hence chorda tympani affected)
  • Explanations
    • Facial nerve – pontomedullary internal acoustic meatus, facial canal, stylomastoid foramen
      • The facial nerve (7th cranial nerve). It emerges from the pons at the pontomedullary junction and enters the internal acoustic meatus within the petrous temporal bone and travels towards the inner ear. It then enters the facial canal and emerges from the skull through the stylomastoid foramen, to enter the parotid gland, where it breaks up into its terminal branches that are distributed to the face.
      • Main branch) passes through facial canal(from internal acoustic meatus to stylomastoid foramen), then enters the parotid gland
      • Chorda tympani path: Exits the skull through the internal acoustic meatus as part of the facial nerve, then it travels through the middle ear, where it runs from posterior to anterior across the tympanic membrane. It passes between the malleus and the incus, on the medial surface of the neck of the malleus. The nerve continues through the petrotympanic fissure, after which it emerges from the skull into the infratemporal fossa. It soon combines with the larger lingual nerve, a branch of the mandibular nerve The fibers of the chorda tympani travel with the lingual nerve to the submandibular ganglion. Here, the preganglionic fibers of the chorda tympani synapse with postganglionic fibers which go on to innervate the submandibular and sublingual salivary glands. Special sensory (taste) fibers also extend from the chorda tympani to the anterior 2/3 of the tongue via the lingual nerve.
    • Muscles of facial expression
      • Obicularis oculi
      • The facial nerve supplies the muscles of facial expression which include the muscles of the lips and the muscle that closes his eyes. Paralysis of lip muscles would result in inability to show his teeth or purse his lips. Paralysis of the orbicularis oculi muscle would result in an inability to close the eye.
    • Painful/itchy – glands of the orbit
      • No secretions
      • dry
      • This occurs because the glands of the orbit, including the lacrimal (tear) gland, which functions to lubricate the eye, are supplied by a branch of the facial nerve. When they lose their nerve supply they no longer produce secretions, causing the surface of the eye to dry out, resulting in a painful itchy sensation. Inability to close his eye, particularly when sleeping, will also contribute to the drying of the eye.
    • Sensitive to loud noises
      • Tympanic ossicles - stapedius muscle
      • The facial nerve also supplies a small muscle in the middle ear cavity called the stapedius muscle. This muscle normally dampens excessive vibrations of the ossicles (little ear bones involved in transmitting sound waves to the inner ear), thereby reducing the volume of excessively loud sounds. When this muscle is paralysed this function is lost and the patient complains of sensitivity to loud sounds (hyperacusis).
    • Taste – facial nerve + V3
      • Taste fibres leave the facial nerve as it passes through the facial canal to form a branch called the chorda tympani, which hitches a ride with branches of the mandibular nerve to reach taste buds on the surface of the tongue.
    • Bell’s palsy due to viral infection
      • Recover quickly, in one month
      • Bell’s palsy is a common condition caused by inflammation (neuritis) of the facial nerve as it passes through the petrous temporal bone. It is frequently associated with preceding viral infection.
  • Aetiology: The inflammation of the nerve in this patient was probably caused by the viral infection suffered a week earlier.
  • Recovery: Four out of five patients with Bell’s palsy recover within a month, once the inflammation subsides. In the remaining 20% of sufferers the nerve undergoes some degeneration - recovery usually takes 3 months or more and may be incomplete.

Case 4

A man, aged sixty five, was working in his garden when he suddenly became dizzy and nauseous and started vomiting. His wife had to help him walk back to the house because he had become unsteady on his feet. His wife noticed that his voice had changed. Neurological examination revealed that the strength and tone of the muscles and the deep reflexes were normal and equal on the two sides, but there was a paralysis of the left vocal cord and of the left side of the soft palate. The finer movements of the left upper and lower limbs were not well coordinated. When walking or when standing with his eyes closed he would tend to fall to the left. There was a complete loss of pain and temperature sensation over the left side of the face and the right side of the body below the head. Tactile sensation was normal over the entire body. It was also noted that his left pupil was constricted and his left eyelid drooped slightly.

Spinal cord tracts
  • Symptoms
    • 65, dizzy/nauseous
    • unsteady
    • voice hoarse – paralysis of left vocal cord and left side of soft palate
    • reflexes and tone normal
    • finer movements of left upper and lower limbs not coordinated
    • fall to the left
    • loss of pain and temperature sensation on left face and right body below head
    • tactile unaffected
    • left pupil constricted, left eyelid drooped slightly
  • Explanations
    • Vestibular system controls balance
      • Cerebellum + brainstem are involved
    • Coordination of fine movements – cerebellum
    • Loss of pain and temperature sensation but not tactile
      • Spinothalamic involved in pain and temperature (decussates at its own vertebral level and runs up the lateral spinothalamic tract)
      • Tactile, proprioception and vibration travels in the dorsal horn and medial lemnisci (decussates at the sensory decussation from the gracile/cuneate fasciculi; in closed medulla above pyramidal decussation)
      • Because these two tracts decussate at different levels, you can get lesions affecting one modality and not the other
    • Trigeminal nerve carries pain and temperature sensations of the face (CN V)
    • Left face and right body - we have an injury that affects the spinal trigeminal nucleus and the spinothalamic tract before it crosses
      • Spinothalamic decussates
      • Cranial nerves don’t
      • The peripheral sensory information (both medial lemniscus/c.+g. fasciculi and the spinothalamic tract) is uniformly cut when a lesion occurs above the sensory decussation
    • Cranial nerve to the laryngeal muscles - X: vagus (recurrent laryngeal nerve)
      • Vagus nerve has bilateral supply (one vagus on each side), so may not see effects:
        • Heart rate increase
        • Digestion problems
    • Target of lesion: Brainstem – medulla (dorsolateral part - ) and cerebellu
      • X,V
    • Artery that may have been occluded: PICA. This lesion is known as lateral medullary (Wallenberg's) syndrome and usually results from occlusion of PICA. Similar symptoms can also occur from occlusion of the left vertebral artery.
    • Note that medial medullary syndrome affects everything else as well (bigger symptoms)
      • Note: need to memorize the cross sections of the spinal cord and which vessels supply which wedge-shaped areas.