The Brain Stem and Cerebellum

The Spinal Cord | The Brain Stem And Cerebellum | The Diencephalon | The Basal Ganglia | The Cerebral Cortex | The Peripheral Nervous System, Neuromuscular Junction, and Muscle

Long tracts

Long tracts: the motor and sensory tracts described in the spinal cord are present in the brain stem, but in the brain stem they are all contralateral to the side of the body they serve.

1. The pyramidal tract (upper motor neuron) is located in the cerebral peduncles of the midbrain, it courses through the base of the pons in several bundles that rejoin to form the pyramids in the medulla. The pyramids decussate at the junction of the medulla and cervical spinal cord. See figure 4
2. The spinothalamic tracts continue in a lateral position throughout the brainstem on their way to the thalamus (figure 5).
3. The posterior columns end in the medulla where they synapse in the nuclei cuneatus and gracilis (subserving function in the arms and legs respectively). Second order neurons immediately decussate to form the medial lemnisci. The medial lemnisci are medially situated in the medulla, but in the pons they become horizontally oriented and by the midbrain they are situated laterally, near the spinothalamic tracts. These sensory pathways both end in the thalamus (VPL). (figure 5).

Segmental structures

The segmental anatomy of the brainstem is analogous to that of the spinal cord, but it is more complex. We will not attempt to describe brainstem anatomy in detail: please consult your neuroscience notes and texts for details. figure 6 illustrates the approximate location of brainstem sensory and motor nuclei and Table 1 is a rough guide to segmental level.

With the exception of the trochelar nucleus (cranial nerve IV), which crosses to innervate the contralateral superior oblique muscle, each of the brainstem cranial nerve nuclei innervate ipsilateral structures. Since the long tracts discussed above are crossed, lesions confined to one side of the brainstem typically present with cranial nerve findings on one side, and motor and sensory findings on the opposite side of the body. This rule is very helpful in localization. (See section II-G below, and figure 7, figure 8and figure 9, for examples.)

The reticular formation

Although typically thought of as an amorphous background in which brainstem nuclei are arranged, the reticular nuclei and tracts form a complex and detailed structure with diverse functions. In the medulla and pons, reticular nuclei are important in modulating respiration, heart rate and blood pressure. The reticular formation of the rostral pons and midbrain is critical for the maintenance of consciousness (lesions in this area result in coma), and reticular nuclei (such as the PPRF) are important for mediating eye movement. Some brainstem nuclei provide a major source of particular neurotransmitters for large portions of the brain: the locus coeruleus (norepinephrine), the raph nuclei (serotonin), and the substantia nigra (dopamine). These neurotransmitters are important neuromodulators. Reduction in norepinephrine or serotonin probably affects arousal and emotion. Neurological correlates are clearer for dopamine: Parkinsons disease is associated with loss of dopaminergic pigmented neurons in the substantia nigra.

The cerebellum

Lesions of one cerebellar cortex result in ataxia on the same side as the lesion. The cerebellar hemisphere projects to the dentate nucleus of the cerebellum, whose fibers leave the cerebellum in the superior cerebellar peduncle, cross as soon as they reach the brain stem, and synapse in the contralateral red nucleus and thalamus (VA and VL). Collateral fibers from the corticospinal tract synapse in the basis pontis, and fibers from these pontine nuclei project to the opposite cerebellar hemisphere. Thus, for example, the right cerebellar hemisphere projects to the left thalamus and cortex, which in turn projects to the left pontine nuclei, which project back to the right cerebellar hemisphere.

The control of eye movements.

Horizontal eye movements (see Figure 7):

1. Anatomy
   
   A conjugate horizontal eye movement requires simultaneous activation of one lateral rectus muscle and the contralateral medial rectus muscle. The sixth nerve nucleus contains motor neurons that control the lateral rectus muscle. It also contains neurons that project through the medial longitudinal fasciculus (MLF) to the medial rectus subnucleus of the contralateral third nerve nucleus. This subnucleus contains motor neurons that control the medial rectus muscle. Thus activation of the sixth nerve nucleus can cause a conjugate lateral eye movement toward the side of the nucleus stimulated.
2. "Voluntary" horizontal eye movements can be directed by the frontal eye fields. Stimulation of the frontal eye field on one side causes deviation of the eyes to the opposite side. To achieve this, the frontal eye fields are connected with the contralateral pontine lateral gaze center (the paramedian pontine reticular formation or PPRF), the pathway crossing in the caudal midbrain.
   
   
3. Clinical correlation:
   
   Horizontal gaze palsy: Paresis of conjugate eye movements is called a gaze palsy. Horizontal gaze palsy may be caused by lesions in the cerebral hemispheres, which cause paresis of gaze away from the side of the lesion, or from brain stem lesions, which, if they occur below the crossing of the fibers from the frontal eye fields in the caudal midbrain, will cause weakness of gaze toward the side of the lesion. Another way to remember this is that patients with hemisphere lesions look toward their lesion, while patients with pontine gaze palsies look away from their lesions. Note that patients with gaze palsy still have conjugate eye movements and therefore do not complain of diplopia.
   
   Internuclear ophthalmoplegia:
   
   Lesions of the medial longitudinal fasciculus (MLF) between the sixth and third nerve nuclei cause weakness of adduction on attempts at horizontal gaze, but not with convergeance. For example, a lesion of the right MLF will cause weakness of adduction of the right eye on attempted leftward gaze. One can demonstrate that this weakness is not caused by medial rectus paralysis, because this muscle functions normally during convergeance (which is coordinated entirely in the midbrain).
4. Vertical eye movements: These are coordinated in the midbrain. There are centers for vertical gaze in the mesencephalic reticular formation just above the third nerve nuclei.

Influence on posture

Brain stem lesions can affect numerous descending influences on the motor system. Tectospinal, reticulospinal and vestibulospinal pathways influence axial muscle tone and movement. In contrast, corticospinal and rubrospinal pathways innervate limb muscles more than axial muscles. The corticospinal pathways are phylogenetically newer, and mediate the most highly differentiated limb movements, such as individual finger movements. Lesions that upset the balance among these systems can produce abnormal posturing.

Lesions in the brain stem above the pontomedullary junction can result in disinhibition of lateral vestibulospinal and caudal reticulospinal systems that normally promote extensor tone in all extremities. The result is extensor posturing in all extremities (decerebrate posturing). Lesions above the brain stem that interfere with cortical and basal ganglia modulation of all brain stem motor systems may result in decorticate posturing, in which there is flexion of the upper extremities and extension of the lower extremities. Flexor tone in the upper extremities is probably mediated at least in part by rubrospinal and reticulospinal pathways.

Classic syndromes

The following are examples of brainstem syndromes. You are not responsible for knowing the names of these syndromes, but you should try to understand how these lesions are localized.

Mid-brain syndromes:

Weber's syndrome (see Figure 8)

The critical structures involved are the descending corticospinal and corticobulbar fibers in the cerebral peduncle, and the fibers of the third nerve that traverse the peduncle on exiting the midbrain. With a lesion on the right, the patient will have a left hemiparesis and a right third nerve palsy (ptosis, inability to move the eye up, down or medially, and [if fibers from the Edinger-Westphal nucleus are involved] pupillary dilitation).

Benedikt's syndrome

unilateral third nerve palsy with contralateral ataxia, from a midbrain stroke involving the third nerve as it travels near the red nucleus. A lesion of the red nucleus interrupts fibers from the opposite cerebellar hemisphere (dentate nucleus of the cerebellum superior cerebellar peduncle crossing in midbrain red nucleus VA/VL thalamus).

Medial pontine syndromes

Lesions of the sixth nerve nucleus cause paralysis of gaze to the side of the lesion. If fibers from the opposite 6th nerve nucleus are involved as they cross to the MLF, there is also weakness of the ipsilateral medial rectus muscle. The ipsilateral seventh nerve can be involved since its fibers course around the sixth nerve nucleus. Lesions involving the fibers of the sixth nerve as they travel through the pons can also involve the medial lemniscus (producing unilateral abducens weakness and contralateral loss of position and vibration), or descending corticospinal fibers in the base of the pons (producing unilateral abducens weakness and contralateral hemiparesis).

Lateral medullary syndrome (Wallenberg syndrome)

This is the commonest of the brain stem strokes. Involvement of the spinothalamic tract results in contralateral loss of pain and temperature sensation below the neck. Involvement of the descending nucleus and tract of V results in loss of pain and temperature sensation on the face ipsilateral to the lesion. Involvement of descending autonomic fibers results in an ipsilateral Horner's syndrome (ptosis, meiosis, and anhidrosis). Involvement of the nucleus ambiguus causes palatal weakness and dysphagia. Involvement of the inferior cerebellar peduncle (restiform body) causes ipsilateral ataxia. See figure 9.

The locked in syndrome (infarction of the base of the pons)

Corticospinal and corticobulbar tracts in the basis pontis are interrupted, causing quadriplegia and paralysis of all cranial nerve muscles except for those controlling eye movements. If the lesion extends into the tegmentum of the caudal pons, horizontal eye movements may also be affected (so only vertical eye movements are possible), and sensation can be affected. The critical feature of these lesions is that they spare the reticular formation above the caudal pons, and therefore the patients remain awake. The only way to communicate with these unfortunate patients is to ask them to move their eyes in response to questions.

Pontine hemorrhage

Hemorrhage into the pons (usually the result of hypertensive vascular disease) results in coma (from involvement of the reticular formation), decerebrate posturing (lesion between red nucleus and vestibular nucleus), and small pupils (involvement of descending sympathetic fibers).