Anatomy clinical correlates: Cerebellum and brainstem

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Introduction0:00–0:51

The cerebellum, which is latin for ‘little brain’, is a part of the brain that plays a major role in posture, balance, maintenance of muscle tone and coordination of skilled voluntary motor activities.
The brainstem, on the other hand, is a trunk-like structure that connects the higher parts of the central nervous system with the spinal cord and serves as a center for life sustaining reflexes, such as breathing and our heartbeat.
Injury and disease to these parts of our brain can result in a variety of complex neurological problems, which can even have life threatening consequences.
First off, let’s look at lesions of the cerebellum, which can be caused by a variety of things such as stroke, space occupying lesions, infections, or drug toxicities.

Cerebellar lesions0:51–4:06

Remember that the cerebellar cortex can be divided into three functional regions that are positioned longitudinally: the lateral zone; the intermediate or paravermal zone; and the median or vermal zone.
One type of lesion is a lateral lesion of the cerebellum, which affects the lateral and intermediate zone of the cerebellum and their associated cerebellar nuclei, which impairs voluntary movements of the extremities.
Think Lateral lesions affect Lateral structures! The lateral zone assists in motor planning, and the intermediate zone has been shown to control muscles of the distal parts of the limbs, particularly the hands and feet.
Clinically, lateral cerebellar lesions can cause ipsilateral limb ataxia, meaning loss of coordination of the limb on the same side as the lesion.
This can manifest as: intention tremor, which are involuntary, trembling movements that occur with voluntary targeted movements; dysmetria, which is when individuals overshoot or undershoot an intended position of the extremities for example during the finger to nose test; dysdiadochokinesia which is the inability to perform fast alternating movements; a loss of balance with a tendency to fall to the same side as the lesion, and finally reduced muscle tone on the ipsilateral side.Next, there are medial lesions to the cerebellum, which affects the vermis or median zone; the flocculonodular lobe, or the fastigial nucleus.
These areas modulate posture and coordination of the trunk and proximal limbs, which are medial structures. So now remember a Medial lesion affects the Medial structures!
Clinically, medial lesions cause truncal ataxia, which is when individuals have an unsteady and wide based gait, sometimes referred to as drunken sailor gait.
Lesions of the flocculonodular lobe tend to cause vestibular symptoms, such as nystagmus, vertigo and vomiting. One of the most common causes of medial cerebellar degeneration in adults is chronic alcohol abuse, while in children damage is often caused by brain tumors such as medulloblastomas or ependymomas.Let’s take a short break and see if you can compare clinical symptoms of the lateral versus medial lesions to the cerebellum.Now, the cerebellum sits in the posterior cranial fossa, covered by a fold of dura mater called the tentorium cerebelli.

Quiz4:06–4:25

Central transtentorial herniation4:25–8:56

This fold separates the cranial cavity into the infratentorial space containing the cerebellum and parts of the brainstem, and the supratentorial space containing the cerebrum.
On the anterior part of the tentorium, there is an opening called the tentorial incisure or notch, through which the brainstem passes.
Since the cranium is a hard structure that can’t expand, if supratentorial intracranial pressure rises, it can force parts of the brain to protrude through the tentorial incisure, causing a transtentorial herniation.In a central or downward transtentorial herniation, the whole brainstem is pushed downward, or caudally, through the tentorial notch.
This can occur because of severe cerebral edema, like after a traumatic head injury. Other possible causes are space occupying lesions of the brain particularly in the supratentorial space, such as tumors or hemorrhages.
When herniation develops rapidly, it can tear off small paramedian basilar artery branches that supply the medulla and pons.
These small parenchymal bleedings are called Duret hemorrhages. Unfortunately, these are usually fatal, seeing as the brainstem plays a vital role in breathing and regulating heartbeat.
Another type of transtentorial herniation is called an uncal herniation, where the medial part of the temporal lobe, called the uncus, is pushed through the tentorial notch where it compresses on the midbrain of the brainstem.
It’s usually caused by an expanding mass such as hematomas, tumors, or abscesses in the temporal lobe. One of the first structures that can become compressed is the oculomotor nerve, or cranial nerve III, on the ipsilateral side.
This nerve arises from the midbrain between the cerebral peduncles, providing motor control to the eye muscles, as well as relaying parasympathetic innervation for the constriction of the iris and accommodation of the lens.
Since the parasympathetic fibers are positioned superficially to the motor fibers, they’re the first to become compressed, resulting in a dilated and fixed pupil often referred to as a ‘blown pupil’ and paralysis of accommodation of the ipsilateral eye.
As compression progresses, the motor fibers get affected as well, causing oculomotor nerve palsy, resulting in the eye being pulled downwards and outwards due to unopposed action of the superior oblique and lateral rectus muscles which are innervated by cranial nerve IV and cranial nerve VI respectively.
This can cause symptoms like double vision, diplopia, as well as potential ptosis as the oculomotor nerve supplies the upper eyelid muscle.
The uncus can also compress on the cerebral peduncle where descending corticospinal fibers decussate, which may lead to contralateral hemiparesis.
In severe cases of midline shift due to uncal herniation, the brainstem can become compressed on the contralateral edge of the tentorium cerebelli, called the Kernohan notch.
This can result in the Kernohan phenomenon, resulting in damage to the contralateral oculomotor nerve and cerebral peduncle which causes a fixed and dilated contralateral pupil with oculomotor palsy, and ipsilateral hemiparesis.Last but not least, there’s cerebellar tonsillar herniation, which can be caused by tumours or bleeds leading to elevated intracranial pressure in the posterior cranial fossa.

Cerebellar tonsillar herniation8:56–9:32

This increased intracranial pressure causes the cerebellar tonsils to herniate down through the foramen magnum. The tonsils can then compress the brainstem and its respiratory and cardiac centers, leading to coma and potential death.Let’s take another short break and see if you can recall three most common types of herniations involving the brainstem and cerebellum.Let’s switch gears and talk about the lesions of the brainstem, starting with the midbrain.

Quiz9:32–9:45

Parinaud syndrome9:45–11:36

Lesions or compression of the tectum or dorsal part of the midbrain at the level of the superior colliculi can lead to dorsal midbrain syndrome, also known as the Parinaud syndrome.
They involve the vertical gaze center causing vertical gaze palsy, where individuals are unable to perform upward or downward conjugate gaze.
Lesions also involve the Edinger Westphal nuclei, causing light-near dissociation, where pupils do not react to light but react to accommodation.
Damage to the dorsal midbrain in Parinaud Syndrome can also cause bilateral eyelid retraction, revealing the sclera above the superior corneal limbus, which is known as the Collier sign.
This mechanism is not fully understood, but is thought to be due to overstimulation of the upper eyelid muscles. Finally when an individual tries to look upwards, there may be irregular, jerky nystagmus that is associated with convergence and retraction of both eyes, particularly with upward gaze, and this is called convergence-retraction nystagmus.
This can happen because of sustained contraction of the medial rectus and other extraocular muscles. Parinaud syndrome can be caused by a stroke to the dorsal midbrain, a tumour of the pineal gland, called a pinealoma, and hydrocephalus.Now, the midbrain is home to many structures, one of which is the medial longitudinal fasciculus, or MLF for short.

MLF lesion11:36–13:57

Damage to the MLF can cause what's called internuclear ophthalmoplegia, which is an impairment of horizontal conjugate gaze.
Remember that for horizontal gaze, the frontal eye field sends a signal to the contralateral paramedian pontine reticular formation, which then communicates with the abducens nucleus on that side to act on the contralateral lateral rectus muscle of the frontal eye field where the signal was sent.
Simultaneously, fibers from that abducens nucleus also sends fibers through the MLF tract to communicate with the oculomotor nucleus on the ipsilateral side of the original signal from the frontal eye field to act on the medial rectus muscle of the ipsilateral eye, allowing both eyes to coordinate horizontal gaze together in the same direction.
Unilateral damage to the MLF causes the inability to adduct the ipsilateral eye, while the contralateral eye can still perform abduction.
So, for example, if the right MLF gets damaged and the individual tries to look to the left, the right eye stays fixed while the left eye abducts, causing diplopia.
The abducted eye may also undergo nystagmus. Unilateral damage of the MLF is usually due to lacunar infarcts of pontine arteries from the basilar artery in the area of the midbrain and dorsal pons.
Bilateral MLF damage can also occur, and it’s usually associated with multiple sclerosis. Bear in mind that convergence and pupillary light reflex are not affected by MLF damage, because they use different pathways.Lower in the pons, we can also have a lesion to the paramedian pontine reticular formation, or PPRF, which is the subcortical lateral gaze center.

PPRF lesion13:57–15:34

As we said, the PPRF receives input from the contralateral frontal eye field and sends signals to the abducens nucleus on the same side to stimulate the lateral rectus muscle of that ipsilateral eye.
The signal is simultaneously sent through the medial longitudinal fasciculus to the contralateral oculomotor nuclei to stimulate the medial rectus muscle of the contralateral eye.
When there is a lesion to the PPRF both eyes deviate to the contralateral side, away from the brainstem lesion. This is in contrast to frontal eye field lesions where both eyes will deviate to the ipsilateral side of the lesion, or towards the side of the lesion.
So, for example, when eyes are deviated to the right, the lesion can either involve the left PPRF or the right frontal eye field.
Some possible causes for lesions to the PPRF include ischemic or hemorrhagic stroke involving the paramedian branches of the basilar artery that supply it.
Now, let’s take a look at the ventricular system, which is a network of cavities housing cerebrospinal fluid, or CSF for short, within the brain.

Noncommunicating hydrocephalus15:34–17:21

When there is an increase of CSF volume, this can lead to a dilation of the ventricles resulting in a condition called hydrocephalus.
Normally, CSF is produced by the choroid plexuses of the ventricles and flows from the two lateral ventricles, through the third and fourth ventricles, and ultimately to the subarachnoid space to be reabsorbed.
The narrowest aspect of the ventricular system is the cerebral aqueduct, also called the aqueduct of Sylvius, which can be found within the midbrain and connects the third to the fourth ventricle.
This is the most common site of obstruction that can lead to buildup of CSF and subsequent hydrocephalus. The cerebral aqueduct can be blocked due to intraventricular hemorrhages, bacterial and fungal infections, or due to congenital aqueductal stenosis.
Other possible causes are tumors or masses, like a glioma or a colloid cyst, that compress and further narrow the cerebral aqueduct.
Clinically, this can result in noncommunicating or obstructive hydrocephalus, which causes headaches, nausea, vomiting, papilledema, coma and even death.Let’s take another break and see if you can recall two conditions and their clinical features that can develop from the compression of the dorsal midbrain by pinealoma.Alright!

Quiz17:21–17:40

Reticular activating system lesions17:40–18:51

Now let’s move on to the reticular activating system, or RAS for short, which is a complex processing center found in the midbrain in an ill defined area called the reticular formation.
The reticular formation is responsible for controlling consciousness and arousal, receiving afferent information from multiple sensory pathways such as auditory, visual, and somatosensory centers, and relaying this information to the cerebral cortex which processes this information.
It is thought our degree of wakefulness and awareness of oneself in the environment is related to the degree of activity coming from the reticular formation, where things such as pain sensation may stimulate the reticular formation and subsequently increase arousal.
Therefore, lesions of the midbrain, such as bilateral pontine hemorrhage, can damage the RAS, reducing levels of arousal and consciousness.

Red nucleus lesions18:51–21:13

This can cause lethargy, stupor, and coma. Okay, let’s look at another midbrain structure called the red nucleus, which helps coordinate muscle tone and body posture.
The red nucleus is located in the tegmentum or ventral part of the midbrain, and gives rise to the rubrospinal tract that descends and acts on the flexor muscles of the upper limb.
Severe lesions of the proximal midbrain above the red nucleus damages the descending inhibitory signals from the cortex to the spinal cord and red nucleus.
As a result, the red nucleus is overstimulated, sending signals to the flexor muscles of the upper extremities through the rubrospinal tract, increasing their tone.
Furthermore, other descending motor tracts such as the vestibulospinal and reticulospinal tracts also lose inhibitory control, and they also overstimulate the extensor muscles of the body.
This leads to a characteristic pathological posturing, called decorticate, or flexor posturing, where upper extremities are flexed with the wrists and hands flexed into fists near the chest, while the lower extremities are extended and internally rotated with foot plantarflexion.On the other hand, lesions at or below the red nucleus damage the rubrospinal tract, so the flexors of the upper limbs are no longer stimulated.
In turn, the vestibulospinal and reticulospinal tracts overstimulate the extensor muscles of the entire body, causing the characteristic decerebrate, or extensor posturing, where the upper extremities are adducted, extended and in hyperpronation, while the lower extremities are also extended with foot plantarflexion.
Decerebrate posturing is associated with a worse prognosis. Pro tip: to easily differentiate between these two postures, just remember that in decorticate posturing the arms are close to the heart, or cor in latin.Let’s take a final break and see if you can differentiate between lesions to the frontal eye field, paramedian pontine reticular formation and medial longitudinal fasciculus.Lastly, let’s look at the vomiting center of the brain, which is responsible for our vomiting reflex.

Quiz21:13–21:33

Brain vomiting center21:33–23:12

The vomiting center is coordinated by the nucleus tractus solitarius, or solitary nucleus, found in the medulla oblongata, and it receives input from multiple sources to initiate the vomiting reflex.
First, it receives information from the chemoreceptor trigger zone, or CTZ which is located on the dorsal surface of the medulla on the floor of the fourth ventricle in an area called the area postrema, or area ‘puke’- strema.
The CTZ doesn’t have a well developed blood-brain barrier which means that it can be exposed to chemical substances found in the blood and CSF which can directly activate it and initiate the vomiting reflex.
These substances include toxins, hormones, and drugs such as chemotherapy drugs, as well as alcohol. It also receives input from visceral afferent fibers coming from the GI tract via the vagus nerve.
For example, Chemotherapy drugs can stimulate vagal afferent nerve fibers receptors in the bowel wall of the gastrointestinal tract, which ascend and trigger the vomiting reflex in the CTZ.

Review23:12–25:51

Additionally, it also receives input from the vestibular system, which can explain car and boat sickness.##SummaryAlright, as a quick recap… Lateral lesions to the cerebellum cause limb ataxia and loss of balance, while the medial lesions cause truncal ataxia and nystagmus.
Increased intracranial pressure can cause central or downwards transtentorial herniation of the brainstem, tearing basilar artery branches supplying the medulla and pons, and may be life threatening.
In uncal transtentorial herniation, the uncus compresses the ipsilateral oculomotor nerve and the descending motor pathways to the contralateral body in the midbrain.
In cerebellar tonsillar herniations, the respiratory and cardiac centers of the brainstem are compressed, which can lead to coma and death.
Parinaud syndrome refers to a lesion of the dorsal midbrain that causes vertical gaze palsy, light-near dissociation, Collier sign and convergence-retraction nystagmus.
Lesions of the medial longitudinal fasciculus cause internuclear ophthalmoplegia and impaired horizontal gaze characterized by inability to adduct the ipsilateral eye, diplopia and nystagmus of the contralateral eye.
Lesion of the paramedian pontine reticular formation leads to the deviation of the eyes to the contralateral side. Blockage of the cerebral aqueduct in the midbrain can lead to noncommunicating hydrocephalus that presents with headaches, nausea, vomiting, papilledema, coma and even death.
Lesions of the reticular activating system of the midbrain reduce level of consciousness and may lead to coma. Lesions above the red nucleus present with decorticate posturing while lesions below it present with decerebrate posturing.
The vomiting center of the brain activates our vomiting reflex, and receives input from the chemoreceptor trigger zone in the