Point
7
Intro
You have already heard of corticospinal axons. By their
name, they arise from cortical neurons and end in the spinal
cord. Another important group of axons that arise from
cortical neurons do not reach the spinal cord. Instead, they
end in motor nuclei of cranial nerves. These axons
are called CORTICOBULBAR ("bulb" is a term that some
neuroanatomists use when referring to the medulla because of
its appearance as a bulb-like expansion of the spinal
cord).
The corticobulbar input to the hypoglossal nucleus arises
from motor cortex (you can voluntarily move your tongue) and
is predominantly CROSSED. Thus, a lesion in motor
cortex will result in deviation of the tongue toward the
opposite side or CONTRALATERAL to the lesion. In
contrast to the atrophy and fasciculations seen in lesions
of the hypoglossal nucleus and nerve (lower motor neuron),
NO such signs are present after lesions of the
corticobulbar tract (remember, the neurons in the
hypoglossal nucleus are still alive). A lesion of the
corticobulbar input to the hypoglossal nucleus is called
a supranuclear lesion (i.e., above or
rostral to the hypoglossal nucleus). In a lesion of the
motor cortex there is also involvement of corticospinal
fibers. For example, a lesion in the LEFT motor
cortex (which involves both corticospinal and corticobulbar
axons) would result in a RIGHT hemiplegia and
deviation of the tongue to the RIGHT. There would
NOT be any atrophy.
Weakness of the tongue manifests itself as a slurring of speech. The patient's tongue feels "thick" and lingual sounds are slurred. This is called dysarthria (dys-articulation) and is more apparent in hypoglossal nerve lesions but can occur following supranuclear lesions.