Pontine Syndromes

Sections

Clinical Cases
Answer Explanations

Pontines Syndromes

Clinical Cases

Case 1:

• Patient is found in an apparent comatose state.
• Exam reveals normal pupil reactivity, normal vertical eye movements, volitional blinks, complete bilateral face and body paralysis, normal sleep–wake states, and an absent gag reflex.

Case 2:

• Patient presents with slurred speech and clumsiness of the right hand.
• Exam reveals impaired smile on the right; dysarthria; dysphagia; loss of fine motor movements in the right hand; and mild weakness of the right arm with normal right leg strength.

Answer Explanations

CASE 1:

• In the basis, draw representative groups of scattered descending corticonuclear (aka corticobulbar) and corticospinal tracts.
  • Paralysis of the body and of the lower cranial nerves (tongue movements, gag, and swallow) results from damage to the descending corticospinal and corticonuclear tracts.
• Draw the reticular formation in the pontine tegmentum.
  • The normal sleep–wake states are maintained because the majority of the reticular formation is spared.
• Include the the paramedian pontine reticular formation (PPRF) in the paramedian ventral pontine tegmentum: the pontine circuitry for horizontal eye movements.
• Then, show the medial longitudinal fasciculus (MLF) in the contralateral dorsal tegmentum.
• Draw the abducens nucleus of cranial nerve 6.
• And then draw the facial nucleus of cranial nerve 7.

Show that cranial nerve 7 forms an internal genu around the abducens nucleus, which creates a bump in the floor of the fourth ventricle, called the facial colliculus.

• Paralysis of the face results from destruction of the exiting facial motor nerve fibers. The facial nucleus, itself, lies within the dorsal pons and is spared.
• Indicate that the PPRF stimulates the abducens nucleus, which sends efferent nerve fibers through the medial pons to produce ipsilateral eye abduction.
• Then, also show that the abducens nucleus sends ascending interneuronal fibers up the contralateral MLF, which innervate the oculomotor nucleus and cause the ipsilateral eye (the eye contralateral to the abducens nucleus) to adduct.
  • Paralysis of horizontal eye movements in this case results from destruction of the PPRF. Note that although most of the reticular formation is spared, this small portion is injured. Volitional vertical eye movements are spared because the center for volitional vertical eye movements lies within the midbrain (above the level of the lesion).
  • The patient's ability to blink results from the ability to elevate and retract the upper eyelids through spared third nerve innervation of the levator palpebrae and through third nerve relaxation, which passively closes the eyelids. Orbicularis oculi is required for forced eyelid closure; it is innervated by the facial nerve, which is injured in this syndrome.
• Encircle the pontine basis and ventral paramedian pontine tegmentum and indicate that injury here produces the aforementioned constellation of symptoms, called locked-in syndrome. In locked-in syndrome, the pontine basis and ventral tegmentum are injured, causing devastating paralysis, which is often misperceived as coma when in reality consciousness is preserved.

CASE 2:

• Indicate that within the basis of the pons, from medial to lateral, lie the face, arm, and leg fibers.
• Encircle the face and arm fibers and show that injury here results in dysarthria-clumsy hand syndrome: a syndrome of contralateral face and upper extremity weakness with preserved lower extremity strength due to restricted paramedian pontine injury.