Mechanisms of development and general topy
The development of any alternating syndrome is based on the interruption of descending and ascending pathways combined with the destruction of cranial nerve nuclei at a specific level of the brainstem.
The main descending motor pathways include:
- Corticospinal tract (tractus corticospinalis). Originates from the limb representation areas in the cortex. Its damage before the decussation causes spastic (upper motor neuron) hemiplegia on the side opposite to the lesion.
- Corticonuclear tract (tractus corticonuclearis). Originates from the face and tongue representation areas. Provides supranuclear innervation.
Topographic diagnosis is based on identifying the affected cranial nerve. It is the nerve that indicates the level of the lesion (ipsilaterally), while long pathways (pyramidal tract, lemniscus medialis, tractus spinothalamicus) produce contralateral symptoms.
Midbrain lesion syndromes (cerebral peduncles)
The lesion is localized at the level of the oculomotor nerve nuclei (cranial nerve III).
The classic clinical picture includes:
- Ipsilaterally: lower motor neuron lesion of the third cranial nerve (interruption of fibers running from the oculomotor nerve nucleus), which may be accompanied by mydriasis and paralysis of external eye muscles.
- Contralaterally: spastic hemiplegia (due to involvement of the pyramidal tract) and upper motor neuron lesion of the facial (cranial nerve VII) and hypoglossal (cranial nerve XII) nerves.
Midbrain alternating syndromes also include Benedikt syndrome (red nucleus lesion — nucleus ruber), which occurs with occlusion of the interpeduncular branches of the basilar and posterior cerebellar arteries.
Pontine syndromes
Symptom complexes depend on which part of the pons (basilar part or tegmentum, oral or caudal divisions) is involved in the pathological process.
Lesion of the caudal part of the basis pontis (Millard-Gubler and Foville syndromes): Occurs upon occlusion of the circumferential branches of the basilar artery.
- On the side of the lesion: lower motor neuron paralysis of the abducens (cranial nerve VI) and flaccid paralysis of the facial nerve (cranial nerve VII).
- On the opposite side: hemiplegia, analgesia, loss of temperature, tactile, proprioceptive, and vibratory sensitivity.
Lesion of the middle part of the basis pontis: Characterized by involvement of the trigeminal nerve (cranial nerve V). On the affected side, there is flaccid paresis of the masticatory muscles, facial hemianesthesia, and cerebellar ataxia (middle cerebellar peduncle lesion). Contralaterally — spastic hemiparesis.
When the pontine tegmentum is involved, lesions of the medial longitudinal fasciculus (nystagmus, gaze paresis), sympathetic tract (Horner syndrome), as well as hearing impairments due to damage to the lateral lemniscus (lemniscus lateralis) are added.
Medulla oblongata alternating syndromes
At the level of the medulla oblongata, two classic symptom complexes are distinguished, depending on the blood supply territory.
Dorsolateral syndrome (Wallenberg syndrome): Resulting from occlusion of the posterior inferior cerebellar artery (PICA).
- Ipsilaterally: nystagmus (inferior vestibular nucleus), ataxia (inferior cerebellar peduncle), Horner syndrome (sympathetic tract), paresis of the soft palate, pharynx, and larynx (nucleus ambiguus), facial analgesia (nucleus of the spinal tract of cranial nerve V).
- Contralaterally: loss of pain and temperature sensitivity on the trunk and limbs (lateral spinothalamic tract).
- Additionally: hiccups (respiratory center of the reticular formation), tachycardia (dorsal motor nucleus of the vagus nerve).
Medial syndrome (Dejerine syndrome): Occurs with a lesion of the paramedian branches of the vertebral or basilar artery.
- Ipsilaterally: peripheral flaccid paralysis of half of the tongue (lesion of the hypoglossal nerve nucleus).
- Contralaterally: central paralysis (hemiplegia) without the development of spasticity with a positive Babinski sign, as well as impaired deep sensation (medial lemniscus lesion).
Briefly: answers to topical questions
How does Weber syndrome differ from Benedikt syndrome?
The syndromes differ in the localization of the lesion in the midbrain and the symptoms on the side opposite to the lesion. In both syndromes, oculomotor nerve palsy occurs on the side of the lesion.
| Sign | Weber syndrome | Benedikt syndrome |
|---|---|---|
| Localization | Cerebral peduncle | Midbrain tegmentum |
| Contralateral symptoms | Central hemiplegia | Cerebellar ataxia (hemiataxia) |
What alternating syndromes occur with midbrain lesions?
Midbrain lesions result in the following alternating syndromes:
- Weber syndrome — oculomotor nerve palsy on the side of the lesion and central hemiplegia on the opposite side.
- Benedikt syndrome — oculomotor nerve palsy on the side of the lesion and cerebellar ataxia (hemiataxia) on the opposite side.
What is included in the clinical picture of Benedikt syndrome?
The clinical picture of Benedikt syndrome includes symptoms of cranial nerve damage and coordination disorders.
- On the damaged side — oculomotor nerve palsy occurs.
- On the opposite side — cerebellar ataxia (hemiataxia) develops.
This symptomatology is caused by a unilateral lesion of the midbrain tegmentum, specifically, the involvement of the rubro-cerebellar pathway in the pathological process.
How does Foville syndrome differ from Millard-Gubler syndrome?
The main difference lies in the presence or absence of abducens nerve involvement on the side of the lesion.
| Sign | Foville syndrome | Millard-Gubler syndrome |
|---|---|---|
| Ipsilateral symptoms | Peripheral paresis of facial muscles and paralysis of the lateral rectus muscle of the eye | Peripheral facial paralysis |
| Contralateral symptoms | Central hemiplegia | Central hemiplegia |
In Millard-Gubler syndrome, the nucleus or root of the abducens nerve is not involved in the pathological process.
Class and exam questions
Why does hemiplegia occur without spasticity in Dejerine syndrome?
In the classical description of Dejerine syndrome, pyramidal tract lesion at the medullary level causes contralateral hemiplegia without the development of spasticity, but with the presence of the Babinski sign.
Which diagnostic imaging method is preferred when brainstem infarction is suspected?
In the first hours of the disease, brain CT often fails to show acute ischemia in the brainstem. MRI is required: diffusion-weighted MRI (DWI) clearly demonstrates the lesion area, and T2-weighted MRI shows signal hyperintensity in the infarction zone.
What is the cause of sensory loss on the face in Wallenberg syndrome?
Ipsilateral analgesia and loss of temperature sensitivity on the face, as well as the absence of the corneal reflex, occur due to a lesion of the nucleus of the spinal tract of the trigeminal nerve (cranial nerve V).
What else to study on this topic
- MRI semiotics of brainstem infarctions: DWI and T2-weighted sequences.
- Topographic anatomy of cranial nerves on sagittal sections of the brainstem.
- Differential diagnosis of bulbar alternating syndromes.
- The role of the medial lemniscus (lemniscus medialis) in conducting proprioceptive sensation.
- Blood supply to the pons: paramedian and circumferential branches of the basilar artery.
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