Cerebellar disorders and coordination
Cerebellar ataxia develops upon damage to the organ itself or its conducting tracts (afferent and efferent pathways). The clinical picture strictly depends on the lesion location:
- Cerebellar hemisphere lesion: coordination disorders develop in the limbs strictly on the homolateral side (side of the lesion). In the Romberg test and during walking, the patient deviates toward the affected hemisphere.
- Cerebellar vermis lesion: trunk stability and gait are isolatedly impaired (truncal ataxia), nystagmus and dysarthria appear. Limb ataxia is absent in this case.
Pseudobulbar palsy and oral automatism
This syndrome occurs with bilateral lesions of the corticonuclear tracts. Typical damage areas include the pons, as well as obligatory symmetric involvement of subcortical basal ganglia or frontal lobes on both sides.
The key marker of subcortical structure disinhibition is primitive reflexes (oral automatisms):
- Palmomental reflex (Marinesco-Radovici sign): stroking the skin of the thenar eminence causes contraction of the mentalis muscle (m. mentalis).
- Snout reflex: tapping the upper lip with a reflex hammer leads to lip pursing due to contraction of the m. orbicularis oris.
Amnestic syndrome and memory impairment
In amnestic syndrome, long-term memory is selectively impaired, while short-term memory (assessed by digit span), procedural memory, and higher intellect (speech, logic) remain intact. Personality and motivation changes may occur (e.g., in Korsakoff syndrome or bilateral thalamic infarctions).
Differential diagnosis with dementia: dementia, unlike pure amnestic syndrome, is accompanied by a drop in intelligence quotient (IQ) as well as the addition of focal deficits—aphasia and agnosia.
Lateralization of memory disorders:
- Left-sided lesions impair verbal memory.
- Right-sided lesions selectively block visual memory.
- Bilateral processes lead to the loss of both types of information encoding.
Etiological factors include vascular events, TBI, metabolic disorders (Wernicke-Korsakoff syndrome), neurosurgical temporal lobe resections, and electroconvulsive therapy.
Brainstem alternating syndromes
Medulla oblongata lesions produce distinct alternating symptoms:
Medial medullary syndrome (Dejerine syndrome):
| Side / Zone | Affected structure | Clinical manifestations |
|---|---|---|
| Ipsilaterally (side of the lesion) | Hypoglossal nerve (XII cranial nerve) | Paralysis of one half of the tongue with hemiatrophy |
| Ipsilaterally | Inferior olivary nucleus | Myorhythmia of the soft palate and pharynx |
| Contralaterally (opposite side) | Pyramidal tract | Central hemiplegia (without spasticity), Babinski sign |
| Contralaterally | Medial lemniscus | Loss of deep, tactile, and vibration sensitivity |
| Brainstem level | Medial longitudinal fasciculus | Nystagmus |
Another brainstem example is Wallenberg syndrome, presenting with acute vertigo, ipsilateral ataxia, and asynergia combined with crossed (contralateral) loss of pain and temperature sensitivity. Furthermore, CT may fail to visualize ischemia in the early stages, requiring MRI.
The rule of cerebellar hemispheres: "Where you fall is where the lesion is" (body deviation occurs homolaterally to the affected hemisphere).
Class and exam questions
How to distinguish psychogenic motor disorders from true cerebellar ataxia?
Psychogenic disorders manifest with bizarre, demonstrative gait (e.g., "tightrope walking") and a history of hysteria in the complete absence of objective neurological symptoms.
Which area of the palm is stroked to elicit the Marinesco-Radovici reflex?
Stroking is applied to the skin of the hand's thenar eminence, provoking contraction of the chin muscle.
What is the main functional difference between Dejerine syndrome and pseudobulbar palsy?
Dejerine syndrome produces an alternating deficit (peripheral XII nerve palsy on the side of the lesion and contralateral spastic hemiparesis), whereas pseudobulbar syndrome requires obligatory bilateral disruption of corticonuclear pathways and is accompanied by oral automatisms.
What else to study on this topic
- Clinical and tomographic dynamics of Wallenberg syndrome in the hyperacute period
- Iatrogenic amnesias following electroconvulsive therapy and temporal lobe resections
- Anatomical relationships of the red nucleus and spinothalamic tract at the brainstem level
- Metabolic mechanisms of Wernicke-Korsakoff syndrome development
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