MOTOR (CORTICOSPINAL TRACT)
understood by realizing that the first half of a pathway name commonly refers to where the pathway originates and the latter half refers to where the pathway terminates. E.g. the spinothalamic tract originates in the spinal cord and ends in the thalamus.
As may be seen in the figure, a lesion (injury) of the pain-temperature pathway (spinothalamic tract), whether within the brain stem or spinal cord, results in loss of pain-temperature sensation contralaterally (i.e. on the opposite side of the body), below the level of the lesion.
A lesion at the spinal level of the pathway for conscious proprioception (the ability to sense the position and movement of the limbs) and stereognosis (the ability to identify objects by touch) results in loss of these senses ipsilaterally (i.e. on the same side) below the level of the lesion. A unilateral lesion at the brain stem level or above results in contralateral loss of conscious proprioception.
The path for light touch combines features of these two pathways. Consequently, light touch commonly is spared in unilateral spinal cord lesions because there are alternate routes to carry the information.
All of these sensory pathways eventually cross the midline, synapse in the thalamus and terminate in the sensory area of the cerebrum. Therefore, a lesion of the sensory area of the cerebral cortex results in contralateral deficits in pain-temperature, proprioception, stereognosis, and light touch sensation.
Proprioception has a conscious and an unconscious component. The conscious pathway goes to the thalamus and cerebral cortex, enabling one to describe the position of a limb. The unconscious pathway (spinocerebellar tract) connects with the cerebellum, which is considered an unconscious organ, and enables one to walk and perform other complex acts without having to think about which joints to flex and extend. Unlike the other sensory pathways, which cross contralaterally, the spinocerebellar tract primarily remains ipsilateral. In general, one side of the cerebellum influences the same side of the body. Thus, cerebellar lesions tend to produce ipsilateral malfunction, typically presenting as ataxia (awkwardness of movement), whereas cerebral lesions result in contralateral defects, manifested by weakness or sensory loss.
The corticospinal tract and related motor pathways synapse in the spinal cord, just before leaving the cord. This anatomic feature is important because motor neurons above the level of this synapse are upper motor neurons (UMN), whereas the peripheral nerve cell bodies in the anterior horn of the cord, and their axonal extensions outside the cord are lower motor neurons (LMN). Upper and lower motor neuron injuries produce different clinical signs. Although lesions at either level result in weakness, the presentations differ.
Fig. 9-12. Upper motor neuron (UMN) versus lower motor neuron (LMN) lesions.
Cranial nerve functions:
CN1 (Olfactory): Smells CN2 (Optic): Sees
CNs 3,4,6 (Oculomotor, Trochlear, Abducens): Move eyes; CN3 constricts pupils, accommodates CN5 (Trigeminal): Chews and feels front of head CN7 (Facial): Moves the face, tastes, salivates, cries CN8 (Vestibulocochlear): Hears, regulates balance CN9 (Glossopharyngeal): Tastes, salivates, swallows, monitors carotid body and sinus
CIO (Vagus): Tastes, swallows, lifts palate, talks, communication to and from thoracoabdominal viscera CN11 (Accessory): Turns head, lifts shoulders CN12 (Hypoglossal): Moves tongue
An injury to one side of the brain stem that affects the corticospinal tract, spinothalamic tract, or medial lemniscus will cause contralateral neurologic deficits in the extremities, in view of the crossing over of pathways, illustrated in Fig. 9-11. The same injury, if it encompasses an exiting cranial nerve, will cause ipsilateral deficits along the distribution of the affected cranial nerve. In fact, any time a patient presents with the combination of an extremity defect of any type on one side of the body
Upper MN Defect spastic paralysis no significant muscle atrophy Cuciculatioos and fibrillations not present hypemflexia
Babinski reflex may be present
Lower MN Defect flaccid paralysis significant atrophy fasciculations and fibrillations present hyporeflexia
Babinski reflex not present and a cranial nerve deficit on the other side, one must be highly suspect that the lesion is in the brain stem.
A unilateral cerebral cortex lesion commonly results in weakness and sensory loss in the contralateral extremities. There may also be contralateral deficits in certain cranial nerve functions. However, unilateral cerebral cortex lesions do not affect all cranial nerves, because of bilateral representation of function. That is, one side of the cerebrum, rather than just connecting with cranial nerves on the opposite side of the body, connects with most cranial nerves on both sides of the body. Therefore, a lesion to one side of the cerebrum will cause little, if any, deficit, in certain cranial nerve functions, because connections from the other side of the cerebrum maintain function. For example, hoarseness may occur with a lesion of the 10th cranial nerve (vagus) but will not result from a unilateral cerebral lesion. Deafness many occur with a lesion to the cochlear nerve, but will not occur with a unilateral cerebral lesion.
Cerebral lesions do affect the cranial nerves as follows:
Olfactory Nerve (CN1). This nerve does not cross the midline. Consequently, a unilateral cortical lesion results in ipsilateral anosmia (loss of sense of smell).
Optic (CN2), Oculomotor (CN3), Trochlear (CN4) and Abducens (CN6) Nerves. Destruction of a cerebral hemisphere does not result in visual loss or ocular paralysis that is confined to the contralateral eye. Rather, both eyes are partially affected. Neither eye can move to the contralateral side (the eyes "look toward the lesion"), and neither eye sees the contralateral environment. (Mechanisms are explained in Figs. 9-13 and 9-17.)
Trigeminal Nerve (CN5). A cerebral lesion results in loss of sensation on the opposite side of the face.
Facial Nerve (CN7). Cerebral lesions generally only result in paralysis of the lower half of the face (below the eye) contralateral^, due to the strictly contralateral connections from each cerebral hemisphere to the opposite lower face. The upper face usually is not significantly involved in unilateral cerebral lesions, such as a cerebral stroke, because of bilateral connections to the forehead and eyelids from each hemisphere. The patient can raise his eyelids and close his eyes. When the facial nerve itself is damaged, as in Bell's palsy, there is total ipsilateral hemifacial paralysis, including the forehead and the eyelids; the patient cannot raise the eyebrow or close the eyelids on the side of the nerve lesion.
Vestibulocochlear Nerve (CN8). Hearing deficits result from local lesions between the ear and the brain-
stem. A lesion in one hemisphere results in little deficit, because auditory information from each ear is represented bilaterally. That is, auditory fibers, upon entering the brainstem, immediately divide into ipsilateral and contralateral routes that go to both cerebral hemispheres.
Glossopharyngeal (CN9), Vagus (CN10), Accessory (CN11) and Hypoglossal (CN12) Nerves. Except for CN12, these nerves usually are not significantly affected by unilateral cerebral lesions. However, weakness of one half of the tongue may sometimes occur with a contralateral cerebral lesion, but is more striking with a direct lesion of CN12.
Fig. 9-13. The visual pathways seen from above. Optic fibers temporal (lateral) to the fovea connect with the brain ipsilaterally. Fibers nasal to the fovea cross over to the opposite side at the optic chiasm. A lesion of the optic tract on the left, therefore, results in loss of the right visual field in each eye.
Fig. 9-14. Lateral view of the visual pathways. Note (Fig. 9-13) that the right visual field falls on the left half of each retina. The superior visual field falls on the inferior retina. The right visual field projects to the left side of the brain. Similarly, the superior visual field projects below the calcarine fissure in the occipital lobe. In other words, everything is upside down and backwards, provided you think in terms of visual fields. For example, a patient with a lesion inferior to the right calcarine fissure will experience a left superior field defect (Figs. 9-13, 9-14).
The center of the retina (the fovea) projects to the tips of the occipital lobe (Fig. 9-14). Thus, a patient with a severe blow to the back of the head may experience bilateral central scotomas (visual field defects) if both occipital poles are destroyed. This fortunately is extremely rare.
Fig. 9-15. Pathway for the pupillary reflexes to light and accommodation. The pupillary light reflex is consensual; that is, light information from one eye reaches
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