Cerebellar examination

Introduction

Introduce yourself, confirm the patient's name and date of birth. Obtain consent and a chaperone and then proceed to wash hands.

To truly appreciate the pathologies behind cerebellar signs, it is important to have a good understanding of the functional anatomy of the cerebellum. Presenting signs often depend on the location of the responsible cerebellar lesion. In this page, lesions with a defined location will be coloured with red text.

The cerebellum is located at the back of the brain, within the posterior cranial fossa. It lies posterior to the pons.

The cerebellum can be grossly divided into the anterior, posterior and flocculolobular lobes. The anterior lobe lies rostral to the primary fissure of the cerebellum, and the posterior lobe lies dorsal to this.

The midline region which runs through all three lobes is known as the vermis (shaded blue in the image below). Lateral to the vermis, on either side lie the hemispheres. The “intermediate” part of the hemispheres, immediately lateral to either side of the vermis is known as the paravermis (shaded red in the image below).

Functional anatomy of the cerebellum



Spinocerebellum: The majority of the vermis and the paravermis (i.e. the anterior lobe and medial posterior lobe) functionally give rise to the spinocerebellum, which receive somatosensory signals from the spinal cord to regulate movement and posture. The vermis receives proprioceptive input from the trunk and proximal limbs whereas the paravermis receives input from the distal limbs. Therefore, a “midline cerebellar lesion” affects the spinocerebellum. There will be issues with posture and gait, such as truncal ataxia.

Neocerebellum (cerebrocerebellum): The lateral aspects of the hemispheres (i.e. the parts of posterior lobe lateral to the paravermis) functionally give rise to the neocerebellum, which connect to the corticospinal tract and are involved in motor planning. Therefore, a “lateral cerebellar lesion” is present in one of the hemispheres and affects the neocerebellum. There will be issues with limb coordination such as dysmetria, dysdiadochokinesia, intention tremor and the rebound phenomenon.

Vestibulocerebellum: The floculolobular lobe and the remaining inferior vermis functionally give rise to the vestibulocerebellum, which communicates with the vestibular system and superior colliculi to regulate balance and vision respectively. Hence, lesions to this area or connecting pathways can cause diplopia, nystagmus and vertigo.

Functional anatomy of the cerebellum

General inspection

Begin the examination by inspecting the patient whilst they are seated. Ensure that the patient is completely exposed from the shoulder to the hand, and from the waist downwards such that all four limbs can be seen.

Ask the patient about pain and comfort. Look for any abnormalities in posture. If the patient is unable to support their trunk independently this suggests they may have truncal ataxia, which can be caused by a midline cerebellar lesion. Such patients may also present with titubationspasmodic nodding or shaking) of the head. Carefully inspect the back of the head for scarswhich may indicate previous surgery.

Look for paraphernalia around the bed which may indicate cerebellar disease such as a catheter (patients in the progressive stage of multiple sclerosis may be incontinent) or mobility aids (walking sticks or wheelchairs).

Truncal ataxia is a result of dysfunction of the spinocerebellum due to a midline cerebellar lesion. (See “functional anatomy of the cerebellum” in the introduction).

The patient is unable to support their trunk independently when sitting upright or when standing. This is clearly apparent when performing Romberg’s test; the patient will not be able to complete the test as they will lose balance even with their eyes open. When seated, the patient may need to steady themselves with their hands. When walking, the patient’s gait will be broad-based and lumbering.



Some patients may have had a previous operation to resect part, or all of a cerebellar tumour, or otherwise following a cerebellar stroke. A posterior craniotomy will result in a midline scar, commonly found in the sub-occipital region at the back of the head. Such a scar may be difficult to see, as it can be masked by the patient’s hair.

Gait

Ask the patient to stand, and then walk 5m, turn around sharply, and walk back towards you. Patients with a cerebellar lesion will have an ataxic gait. A midline cerebellar lesion will present with a broad based, lumbering, truncal gait (see truncal ataxia above). On the other hand, if the patient appears to be veering towards one side, this would suggest that the ataxia is due to a unilateral lesion of the ipsilateral cerebellar hemisphere.

Carefully observe the patient as they turn; patients with an identified ataxic gait will have particular difficulty maintaining balance with this manoeuvre. Poor balance is seen most commonly in lesions of the anterior vermis and is often the only sign seen in patients with alcoholic cerebellar degeneration.

Next, ask the patient to walk heel-to-toe in a straight line to the end of the room. Walking heel-to-toe lowers the stride width, so any finer ataxia will be revealed with this more sensitive test.

It is important that at all times you are standing by the patient ready to catch them if they begin to fall. If the patient has a cortical or cerebellar lesion, then they may start to fall even when getting off the bed.

An ataxic, or cerebellar gait is the most common manifestation of cerebellar disease in patients. The list below summarises the important features of the ataxic gait:



Alcoholic cerebellar degeneration is a common neurological complication seen in alcoholics. The toxic and metabolic effects of ethanol combined with thiamine (B1) deficiency is thought to cause atrophy of the anterior and/or superior vermis. Damage to the cerebellum is irreversible, so signs will persist even with abstinence from alcohol.

Romberg’s test

Ask the patient to stand upright with their feet together and arms by their side. A patient with a midline cerebellar lesion will have truncal ataxia, and will have difficulty maintaining their balance at this point.

If the patient is able to stand without issue, then ask them to maintain this position while they close their eyes. If there is a loss of balance at this point, only then does the patient test "positive" for Romberg's sign, and they have a loss of vestibular function (for example in Ménière’s disease) or proprioception (for example in peripheral neuropathy).

Romberg’s test looks for a loss of vestibular or proprioceptive function. It is not a measure of cerebellar function. If you suspect any imbalance in a patient, you should perform Romberg’s test to establish if the cause is sensory in origin rather than cerebellar. Be aware that some patients may have both cerebellar and sensory ataxia (multiple sclerosis can cause both).

Romberg's test is performed on the premise that the body requires at least two out of the following three senses to be functioning adequately to maintain balance while standing: vision, vestibular function and proprioception. If the patient can stand with their eyes open, then it can be said that vision and either one of vestibular function or proprioception are intact.

Once the eyes are closed, then the patient is purely reliant on the latter two senses to maintain balance, and so if they fall, then this indicates that there is a problem with vestibular function, proprioception or otherwise the dorsal columns which communicate proprioception.

Face

Eyes

Ask the patient to keep their head still and focus on a white pin in front of them. Move the pin in an H pattern. Beforehand, ask them to report any diplopia (double vision) which can be caused by vestibulocerebellar syndrome or a posterior circulation stroke (affecting the brainstem, cerebellum and occipital cortex). Inspect for nystagmus, usually present with lesions to the vestibulocerebellum or associated pathways.

Place your right hand on the left side of the patient’s peripheral vision. Ask the patient to look at your right hand, and then to your nose, whilst keeping their head still. Here you are looking for a saccadic dysmetria, which if present suggests an ipsilateral cerebellar hemisphere lesion. The patient’s eyes will either ‘undershoot’ or ‘overshoot’ the target, before correcting and fixing onto the target. Perform the same test on the other side using your left hand.

When testing the eyes, it may be helpful to place the back of your hand on the patient’s forehead to limit movement whilst they are following your finger.

Nystagmus is characterised by fast and slow saccades, it may be helpful to watch videos of this to familiarise yourself with the different phases. The ‘direction’ of the nystagmus will be the same as that of the fast saccade.

Physiological nystagmus: Some patients will have nystagmus at the extremes of vision (i.e. looking far to the left or right). This is normal and is termed physiological nystagmus. Be careful not to confuse this with the pathological nystagmus you might see in patients with cerebellar lesions.

Cerebellar nystagmus: The vestibulocerebellum is involved in the vestibulo-ocular reflex. Hence, a lesion to the floculonodular lobe (which forms the vestibulocerebellum) or any associated cerebellar pathways can lead to impaired visual fixation. The type of cerebellar lesion often leads to a specific identifiable sign in the patient. For example, a defect in the flocculus will cause a saccadic, downbeat nystagmus. Paraneoplastic cerebellar degeneration will cause irregular saccades in all directions.

Cerebellar pathology is only one of the many causes of pathological nystagmus. Nystagmus can be observed in patients with a vestibular disease, such as benign paroxysmal positional vertigo, and also in patients with toxicity (e.g. phenytoin).



Hypometric saccades refer to the eyes undershooting the target (i.e. don’t reach it). Hypermetric saccades are where the eyes overshoot the target (i.e. go past it).

Speech

Ask the patient to repeat a couple of short phrases, the same ones used in the cranial nerve examination, (for example, ‘baby hippopotamus’ or ‘British constitution’). Lesions to the cerebellum and associated pathways can present with ataxic dysathria, which presents in many ways:

Most patients with an ataxic dysarthria have an injury to the left cerebellar hemisphere from a previous stroke. It is thought that there is damage to areas involved in coordination of articulatory movement of the tongue and orofacial muscles.

This is a type of dysarthria where sentences may be broken up into syllables, with pauses in between them, and unusual stress placed on the syllables. It forms one of the three symptoms in Charcot's neurologic triad of multiple sclerosis

Upper Limb

Tone

First assess the tone of the muscle groups at the shoulder, elbow and wrist joints, comparing each side like for like. Ensure the patient is relaxed and support their arm and shoulder.

Circumduce the shoulder (glenohumeral) joints. Circumduction assesses all of the possible movements at this joint: flexion, extension, abduction, adduction and rotation. Next, flex and extend the elbow joints. If there is any rigidity, carefully assess what type. Finally, pronate, supinate and circumduce the wrists.

Look for signs of hypotonia, which can be caused by an ipsilateral cerebellar lesion.

Use caution when presenting hypotonia as a finding. It is a very subjective finding and is difficult to detect, so don’t put too much weight on it when presenting.

Pronator drift and the rebound phenomenon

Test for pronator drift. Ask the patient to hold their arms fully extended in front of them, palms facing upwards, and observe. If they can maintain this position without pronating their arms, ask them to close their eyes, and observe once again. If there is pronation at any point during this exercise, the patient is positive for pronator drift (lesion in ipsilateral cerebellum or ipsilateral dorsal column).

Test for the rebound phenomenon. Ask the patient to keep their arms in the same outstretched and extended position with their eyes closed. Next, instruct them to keep their arms steady as you lightly push their arms down near the forearms. In a positive test, the patient’s arms will overshoot when repositioning (i.e. reposition too far up). This is the rebound phenomenon (cerebellar disease).

Pronator drift is a sign of an upper motor neurone lesion, and lesions to the cerebellum itself fall under this category. In cerebellar pathology, the arms will also drift upwards slightly, secondary to hypotonia.

Coordination

Ask the patient to place their right palm on top of the left. Next, instruct them to repeatedly flip their right hand at an increasing pace. After about 5 seconds of continual movement ask them to do the same with the left hand. This exercise tests for dysdiadochokinesia, which is indicative of an ipsilateral cerebellar lesion.

Then test for past pointing. Ask the patient to touch their index finger to their nose. Hold your own finger at an arm's length distance away and instruct the patient to touch your index finger with theirs, before touching their nose once again. Ask them to repeat this motion with both hands. This will test for dysmetria and intention tremor, also indicative of an ipsilateral cerebellar lesion.

Dysdiadochokinesia is a term for the inability to perform rapid alternating movements. It is a feature of cerebellar ataxia. As with intention tremor and dysmetria, dysdiadochokinesia occurs due to a lateral cerebellar lesion affecting the neocerebellum.

Intention tremor is a type of tremor that appears with target-directed movement. The amplitude of the tremor will increase closer to the target (i.e. the patient’s tremor will become more obvious as their finger gets closer to yours).

Dysmetria is a term for a lack of coordination movement when there is purposeful movement, that is to say, when there is undershoot or overshoot when trying to reach a certain position. Dysmetria is also a feature of cerebellar ataxia.

Lower Limb

Tone

To assess tone, assess the muscle groups at the hip, knee and ankle joints, comparing each side like for like. Ensure the patient is relaxed, place your hands on their knee and roll the leg such that there is rotation at the hip. Repeat with the other leg. Lift each knee briskly at least 30cm off the bed and then release - the knee should drop and the leg straighten.

Circumduce the ankle joints. Circumduction assess all of the possible movements at this joint: flexion, extension, abduction, adduction and rotation.

As with the upper limb, look for signs of hypotonia (damage to lateral cerebellar hemispheres; damage will be ipsilateral to the side of the lesion).

Again, use caution when presenting hypotonia as a finding.

Reflexes

Test the patellar reflex (L3-4) in both legs: Take the weight of the leg and ask the patient to relax. Tap the patellar tendon, which is superior to the tibial tuberosity and inferior to the patella. Patients with a cerebellar lesion may have ‘pendular’ reflexes.

Pendular reflexes will be slow, and the leg will continue to swing back and forth (like a pendulum). Again, use this sign with caution when presenting, as it can be difficult to detect.

Coordination

Place your palms just below the patient's feet and ask them to tap your palms with their left foot only, right foot only, both feet together and then both feet interchangeably. Inability to do this with ease suggests dysdiadochokinesia.

Ask the patient to place their right heel on their left knee whilst you place your hand half a metre above their left foot. Next, instruct them to move their right heel down to their left ankle, and then lift their foot in the air such that their toes touch your hand. Then ask the patient to repeat this motion. After about 5 seconds of continuous movement ask them to do the same using the left heel instead. This exercise tests for dysmetria.

Conclusion

Complete your examination by offering to take a full history, perform a full neurological and speech examination and offering to perform fundoscopy.

Further imaging may include an MRI scan, which is key in identifying any structural damage.

Papilloedema may be seen in cases of raised intracranial pressure. Also check for optic atrophy, which may be present in cases of multiple sclerosis.

Additional Information

When presenting, it may be helpful to know the key signs of cerebellar disease and some causes. The acronyms DANISH (signs) and PASTRIES (causes) can help with remembering these:

Dysdiadochokinesia
Ataxia
Nystagmus
Intention tremor
Slurred /scanning speech
Hypotonia/hyporeflexia



Paraneoplastic syndrome
Abscess/atrophy
Stroke/sclerosis (multiple sclerosis)
Trauma
Raised ICP
Infection
Ethanol and poisons
Spinocerebellar ataxia (progressive degenerative genetic disease)

Interactive markscheme


When assessing each other, please click on each list item as you go along. Doing so will turn the list item green. Make careful note of any steps missed at the end.
We recommend completing any examination or procedure in under 10 minutes, but you can adjust the timer to suit your needs.
:

  1. Introduction: “Hello, I’m SimpleOSCE and I am a medical student. I’ve been asked to perform an examination to test your speech, eyes and coordination today, would that be okay? Can I confirm your name and DOB? Thank you.”
  2. "For the purpose of this examination the examiner will act as a chaperone."
  3. Wash hands.
  4. Ask the patient to expose themselves from shoulder to the hand, and from the waist downwards such that all four limbs can be seen.
  5. Ask about pain and discomfort.
  6. Inspect the patient whilst seated for truncal ataxia, scars and titubation and then inspect their surroundings (mobility aids, catheter).
  7. Gait I: Ask the patient to stand and inspect whilst they walk 5m, turn around sharply and walk back.
  8. Gait II: Carefully observe the patient’s movement as they turn, specifically looking for poor balance.
  9. Gait III: Ask the patient to walk in a straight line heel-to-toe.
  10. Gait IV: Be ready to catch the patient at all times in case they fall.
  11. Perform Romberg’s test.
  12. Test for diplopia and nystagmus.
  13. Test for saccadic dysmetria.
  14. Test speech using short phrases (e.g. British constitution).
  15. Assess tone in the upper limbs.
  16. Assess for pronator drift, asking the patient to close their eyes.
  17. With the patient’s eyes still closed, test for the rebound phenomenon.
  18. Test coordination in the upper limbs for dysdiadochokinesia and dysmetria.
  19. Assess tone in the lower limbs.
  20. Assess the knee jerk reflex in both limbs, looking for pendular reflexes.
  21. Test coordination in the lower limbs for dysdiadochokinesia and dysmetria.
  22. Thank the patient and ask if they need help redressing.
  23. “To complete my examination, I would like to perform a full neurological examination, take a full neurological history and perform fundoscopy.
  24. Present findings.
Overall: 0/28