I. Superior, middle, lower and medial or lateral. This is the classification used in the textbook Neurology in Clinical Practice: Principles of Diagnosis and Management, by Bradley, Daroff, Fenichel, and Mardsen. It divides pontine stroke syndromes into the following groups:
– Superior medial pontine syndrome (arterial territory: median branches of the basilar artery). This can present with ipsilateral ataxia, internuclear ophthalmoplegia (MLF), and myoclonus of the palate pharynx and vocal cords (? central tegmental tract to inferior olive), and contralateral motor weakness (corticospinal tract). – Superior lateral pontine syndrome (arterial territory:
branches from superior cerebellar artery). This can present with: ipsilateral ataxia, ipsilateral Horner’s syn- drome (preganglionic sympathetic fibers), facial hemia- nesthesia, and masticator motor weakness (nuclei and fibers of cranial nerve five), as well as contralateral hemi- anesthesia and loss of vibration and proprioception (medial lemniscus, trigeminothalamic tract, spinothala- mic tract).
– Middle medial pontine syndrome (arterial territory: med- ian branches of the basilar artery). This can present with ipsilateral ataxia, conjugate gaze paresis to the side of the lesion (PPRF or sixth nerve nucleus), internuclear ophthalmoplegia (MLF), and contralateral weakness (cor- ticospinal tract).
– Middle lateral pontine syndrome (arterial territory: long lateral branches of the basilar artery). This can present with contralateral hemisensory loss (spinothalamic tract) and ipsilateral ataxia, paralysis of muscles of mas- tication (fifth motor nucleus), facial hemianesthesia (spinal trigeminal tract and nucleus), and Horner’s syndrome.
– Inferior medial pontine syndrome (arterial territory: median branches of the basilar artery). This presents with contralateral weakness (corticospinal tract), con- tralateral impairment of proprioception and tactile sense over half the body (medial lemniscus), ipsilateral paresis of conjugate gaze (sixth nerve nucleus), lower motor neuron facial palsy (fibers of seventh nerve at the facial colliculus or in the tegmentum), and one-and- a-half syndrome (sixth nerve nucleus and MLF).
– Inferior lateral pontine syndrome (arterial territory: anterior inferior cerebellar artery). This may present with contralateral loss of pain and temperature over the body, possibly including the face (spinothalamic and trigeminothalamic tracts) and ipsilateral deafness (eighth nerve), facial paralysis (seventh nerve), ataxia, impaired sensation over face (spinal trigeminal tract). II. Ventromedial, ventrolateral and tegmental. Drs. Bassetti,
Bogousslavsky, Barth, and Regli advanced this classifica- tion in a paper titled ‘‘Isolated Infarcts of the Pons’’ (Neurology, 46: 165, January 1996). The classification scheme is based on four main arterial territories: anteromedial pontine arteries (ventromedial infarcts), anterolateral
pontine arteries (ventrolateral infarcts), lateral pontine arteries (tegmental infarcts) and posterior pontine arteries (tegmental infarcts).
– Ventromedial pontine infarcts are in the territory of the anteromedial pontine arteries (paramedian arteries of Foix and Hillemand), which supply the medial portion of the corticospinal tract and medial portion of the teg- mentum, such as the medial lemniscus, and cranial nerve nuclei. These infarcts tend to present with signifi- cant contralateral hemiparesis, often accompanied by dysarthria and ipsilateral ataxia (ataxic hemiparesis). Some of the patients also have contralateral lower extremity ataxia. Many patients will also show symp- toms or signs of tegmental involvement, such as eye movement disorders, and lemniscal sensory loss, but the tegmental involvement is usually transient. – Ventrolateral pontine infarcts are in the territory of the
anterolateral pontine arteries (branches of the parame- dian arteries and short circumflex arteries of Foix and Hillemand), which supply the lateral portion of the cor- ticospinal tracts, and portions of the medial tegmentum. These patients present with a constellation of findings, including ataxic hemiparesis with dysarthria, ataxic hemiparesis, dysarthria–clumsy hand, and cranial nerve palsies. However, the hemiparesis is milder than ventro- medial infarcts. The hemiparesis and ataxia are contra- lateral to the lesion. Most patients show mild symptoms of tegmental involvement, and some patients also experience vertigo.
– Tegmental infarcts are in the territory of the lateral pon- tine arteries (branches of the short circumflex and med- ial branches of the long circumflex arteries of Foix and Hillemand, such as arising from the anterior inferior cerebellar artery and superior cerebellar artery). These patients present with vertigo, diplopia, eye movement disturbances, cranial nerve palsies, especially 6th and 7th cranial nerves, and body, or face and body sensory loss involving the lemniscal or spinothalamic tracts. Some motor deficits are present, but they are usually mild. Bilateral tegmental infarcts are often characterized by acute pseudobulbar palsy, somnolence, facial or abdu- cens palsy, and unilateral or bilateral sensorimotor dysfunction.
From these various classifications, several conclusions may be drawn.
(1) In our mind, the best approach is a knowledge of the rele- vant clinical neuroanatomy of the basis pontis and pontine tegmentum, with an ability to correlate lesions visualized on MRI with the corresponding structures and the expected symptoms and signs.
(2) In general, infarcts of the basis pontis tend to present with involvement of the corticospinal tract, leading to motor weakness, which is more pronounced with ventromedial than ventrolateral basis pontis infarcts. There is also invol- vement of the cortico cerebellar fibers, often leading to an ataxia, again predominantly ipsilateral to the motor weak- ness. There may be involvement of the sixth cranial nerve
along its course in the basis pontis, leading to ipsilateral sixth nerve palsy, and possibly also involvement of the 7th nerve along its course within the basis pontis, leading to ipsilateral lower motor neuron facial palsy, such as in the Millard–Gubler syndrome.
However, it is important to remember that basis pontis infarcts may interrupt corticobulbar fibers, including those to the 7th nerve. Thus, it is in fact more common to have homolateral body and facial weakness (i.e., on the same side), rather than a crossed brainstem syndrome with con- tralateral body weakness and ipsilateral facial weakness, as in original descriptions of Millard–Gubler.
(3) As infarcts become more lateral in the basis pontis, the motor weakness becomes less pronounced. Contralateral hemisensory loss becomes more pronounced, as does cere- bellar ataxia. Ventrolateral infarcts may also give 5th nerve findings, including both fifth nerve motor weakness and
impaired sensation over the ipsilateral face, as well as a Horner’s syndrome.
(4) Infarcts of the tegmentum often present with eye movement disorders, including conjugate gaze palsy, from involvement of the sixth nerve nucleus, internuclear ophthalmoplegia, one-and-a-half syndrome (possibly asso- ciated ipsilateral peripheral 7th nerve findings), and mild contralateral motor weakness, such as the Raymond–Foville syndrome. Also, sensory lemniscal findings, such as con- tralateral body pain and temperature loss from involve- ment of the spinothalamic tract, contralateral body proprioception loss from involvement of the medial lem- niscus, ipsilateral or contralateral facial anesthesia from involvement of the spinal trigeminal tract and nucleus (ipsilateral to the lesion), or 5th nerve nucleus or nerve fibers (ipsilateral to the lesion), or the ascending trigemi- nothalamic tract (contralateral to the lesion).