Cerebellar clinical presentation

General

Although the functional anatomy of the cerebellum comprises three separate zones-

A midline,
An intermediate,
A lateral (hemispheric) zone

Only the midline and lateral zones are associated with distinct abnormalities;

No abnormalities that are specifically associated with the intermediate zone have been identified.

Many of the signs that are observed with midline lesions may also be associated with lateral lesions, and vice versa.

By connections/ functional

Vermal (vermis) zone

Send fibres to fastigial nucleus

Paravermal (or paramedian) zone

Send fibers to Globus and emboliform nucleus

Lateral zone

Longitudinal parcellation
Send fibers to dentate nucleus

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Cerebellar clinical features can be grouped into 3 groups

Symptoms of cerebellar disease

The symptoms of cerebellar disease are nonspecific

They include

H/A
N/V
Gait difficulty
Vertigo

Signs of midline cerebellar disease

The midline of the cerebellum

Comprises of the

Anterior and posterior vermis
Flocculonodular lobe
Fastigial nuclei

is responsible for

Equilibrium required during ambulation
Maintenance of truncal posture
Position of the head in relation to the trunk
Control of extraocular eye movements.

Types of deficit

Gait ataxia

An umbrella term that describes the following

A wider than normal base
Unsteadiness
Irregularity of steps
Lateral veering

The steps may be uncertain, some shorter and some longer than intended, and there may be a tendency to stagger or lurch to one side.

There is little localizing value in cerebellar gait disorders to distinguish between midline and lateral cerebellar lesions

Although lateral lesions tend to cause the patient to veer toward the side of the lesion.

Mild cerebellar gait disorders may be exacerbated by asking the patient to tandem walk.

~~The Romberg's sign~~

In which the patient loses balance after closing the eyes, is a result of disordered position sensation secondary to posterior column disease and is not related to cerebellar dysfunction.
If patient's ataxia is arising from the cerebellum even with visual input the cerebellum will not be able to function therefore patient will fall over even with eyes opened

Truncal imbalance

May be manifested during

Walking by a tendency to fall to the right, left, forward, or backward.
Sitting the patient may lean or fall to one side

These tendencies tend to be toward the side of the lesion.

Abnormal head postures

May be due to midline or lateral cerebellar lesions.

Present as a

Head tilt (i.e., lateral deviation of the head) OR
Rotated posture of the head.

Ocular motor dysfunction

May occur in association with midline cerebellar lesions but is also associated with lesions in other parts of the cerebellum.

The cerebellum and brainstem are involved in

Computing the location of targets in space
Deriving temporal information from spatial information for appropriate muscle innervation,
Adjusting the gain on saccadic eye movements to minimize target overshoot and undershoot.

Types of Ocular motor dysfunction

Nystagmus

Definition: Nystagmus consists of rhythmic oscillatory movements of one or both eyes, occurring with the eyes in the primary position or with ocular deviation.

The most common types of nystagmus observed in association with midline cerebellar lesions are

Gaze evoked nystagmus

Gaze-evoked nystagmus occurs when an individual cannot maintain conjugate eye deviation away from the midposition.

Aetiology

Similar to that induced by drugs.
Associated with brainstem or cerebellar disease

Mechanism

Eye is attempted to be kept at an Extreme position (eccentric gaze).
Dysfunction of the neural integrator (as mentioned above)
Thus, the eyes cannot be maintained at an eccentric orbital position and are pulled back toward primary position by the elastic forces of the orbital fascia.
Then, corrective saccade moves the eyes back toward the eccentric position in the orbit.
The result is a to-and-fro oscillation of the eyes involving a fast component in the direction of gaze and a slow component away.

Clinical feature

Conjugate lateral gaze is accompanied by a slow, involuntary drift of the eyes back to midposition, followed by a rapid corrective return of the eyes to the laterally located target.

Gaze-evoked nystagmus is usually also associated with nystagmus on upgaze, but rarely is there downbeat nystagmus on downgaze.

vs Gaze paretic nystagmus

Feature	Gaze-Evoked Nystagmus	Gaze Paretic Nystagmus
Main Mechanism	Failure of central neural integrator	Weakness or fatigue of extraocular muscles, or incomplete recovery after gaze palsy
Clinical features	In eccentric gaze, sustained or pathologic	After partial recovery from gaze palsy or with neuromuscular weakness
Causes	Brainstem/cerebellar dysfunction, drugs, physiologic at extremes	Myasthenia gravis, Guillain-Barre, recent gaze palsy
Drift Direction	Toward primary position (center)	Toward weak/paralyzed direction, then corrective saccade
Relationship	General category of nystagmus	Subtype of gaze-evoked nystagmus

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Rebound nystagmus

Rebound nystagmus is specific for cerebellar disease, although it is poorly localised within the cerebellum.

Horizontal jerk nystagmus that is associated with cerebellar disease.

A primary position nystagmus

Provoked by prolonged eccentric gaze holding. It appears after the eyes are returned to primary position.

It characteristically appears to fatigue and change direction when lateral gaze is sustained or when the eyes are returned to primary position.

It essentially represents a type of gaze-evoked nystagmus that changes direction after sustained lateral gaze or after refixation to the primary position.

Optokinetic nystagmus

A nonpathological nystagmus that develops normally when an individual attempts to count the stripes on a rotating drum or a moving cloth strip.

Aka pendular nystagmus

Elicited by moving a repetitive visual stimulus through the visual field.

Slow phase of this nystagmus comprises a pursuit movement that follows the moving target.

Fast phase comprises a saccade in the opposite direction.

A lesion that involves the pursuit or saccadic pathways will disrupt this induced form of physiological nystagmus.

In the presence of cerebellar disease, optokinetic nystagmus may become exaggerated, producing unusually large amplitudes of both the fast and the slow components.

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Ocular dysmetria

Defined as the conjugate overshoot of a target with voluntary saccades.

The eyes appear to jerk back and forth because of repeated inaccuracies in saccadic movements intended to bring the target to the fovea.

Characterized by a series of undershooting and overshooting saccades followed by diminishing oscillations until eye “hones in” on target (may be seen in Friedreich’s ataxia)

Like limb dysmetria, it is associated with lesions of the cerebellar pathways.

Signs of lateral (hemispheric) cerebellar disease

The lateral (hemispheric) zone of the cerebellum comprises

Cerebellar hemisphere
Dentate nuclei
Interposed nuclei

The intermediate zone is also included here because it does not appear to be associated with distinct abnormalities.

Compared with the midline zone, the lateral zone is involved in a greater variety of clinical disorders.

Hypotonia

A decrease in resistance to passive movement of the limbs,

Due to lateral cerebellar lesions.

Method: grasping the patient's forearms and shaking the relaxed wrists.

Hypotonic limb is identified as the limb with more of a flail hand.

Hyperreflexia

Examination of the patellar reflex in a hypotonic lower limb may demonstrate an increased duration and amplitude of swing.

This pendular cerebellar reflex should be distinguished from clonus, due to corticospinal tract disease, which occurs at a more rapid rate than the pendular reflex.

Dysarthria

Characterized by slow, laboured, slurred, or garbled speech that may be mistaken, like cerebellar ataxia, as a manifestation of alcohol intoxication.

Comprehension and grammar remain intact.

Limb ataxia

Like gait ataxia, comprises a combination of disturbances in voluntary movement, the most important of which are

Dysmetria

Consists of an error in trajectory and speed of movement.
Upper limb

Finger-to-nose test

As the finger approaches the nose, it may oscillate around the nose and strike the cheek (overshoot) or stop short of touching the nose (undershoot).

Lower limb

In the supine position, to raise the heel of one foot over the knee of the other and to slide the heel smoothly down the shin.
Frequent deviations to one side or the other are indicative of dysmetria in that limb.

Decomposition of movement.

Decomposition of movement involves errors in the sequence and speed of the component parts of a movement.
An affected limb is unable to execute a movement, such as reaching out to grasp a glass of water, in a smooth and fluid manner. Instead, the movement is halting, imprecise, and jerky.
Test

Finger-to-nose test
Dys-diadochokinesis

Asking the patient to perform a series of rapidly alternating or fine repetitive movements, such as a sequence of pronation and supination movements of the hand. The presence of decomposition of movement during this maneuver is referred to as

Intention tremor

An irregular, more or less rhythmic, interruption of a voluntary movement that begins and increases as the patient approaches a target.

Test

Finger-to-nose test

Rest tremor of parkinsonism, which only occurs at rest
Action tremor of familial or essential origin, which characteristically occurs during a sustained posture and from the beginning to the end of a movement.

Impaired check

An impaired check response is characterized by the wide excursion of an affected limb following an involuntary displacement of the limb by an examiner.

Tested

By tapping the wrists of a patient with outstretched, pronated arms. With the patient's eyes closed, normally there is a small displacement of the arm that has been tapped, followed by a rapid, accurate return to the original position.

In a patient with cerebellar disease, the displaced arm demonstrates an unusually wide excursion, followed by an overshoot of the original position.
The original position is finally reached only after considerable oscillation about it.

Provide resistance against a patient's flexed arm

On abrupt release of an affected arm, the arm will continue unchecked in the direction of its force and will strike the patient's chest.

Oculomotor disorders

Associated with both lateral and midline cerebellar disorders but defy more specific localization.

Several of these disturbances have already been described, such as gaze-evoked nystagmus, rebound nystagmus, ocular dysmetria, and optokinetic nystagmus.

Other oculomotor disorders:

Constant, random, conjugate saccades of unequal amplitudes in all directions.

Frequently, they are most marked immediately before and after a fixation.

Defined as rapid to-and-fro oscillations of the eyes.

These abnormal movements may develop abruptly, last for only seconds, and disturb vision for the duration of the episode.

Comprises intermittent (abrupt) downward displacement of the eyes, followed by a slow, synchronous return to the primary position.

The relatively quick downward displacement is slower than the fast component of nystagmus;

This disorder should therefore be distinguished from downbeat nystagmus, which is associated with lesions in the cervicomedullary junction.

Horizontal eye movements are typically paralyzed.

Is defined as a rhythmic, pendular oscillation of the eyes that is associated with synchronous oscillation of the plate (palatal myoclonus).

Examination techniques for cerebellar motor syndrome

Clinical Maneuver	Evaluation
Ocular stability	Nystagmus, saccadic intrusions
Ocular pursuit	Saccadic pursuit
Saccades	Dysmetric saccades
Head-impulse test (HIT)	Impaired vestibulo-ocular response (VOR)
Ocular alignment	Skew deviation, esotropia
Speech	ㅤ
Repeating a sentence or normal conversation	Dysarthric speech
Upper limb movements	ㅤ
Finger-to-nose test	Decomposition of movement, dysmetria, kinetic tremor, intention tremor
Finger chase	Dysmetria
Finger-to-finger test (index-index test)	Kinetic tremor, intention tremor
Fast alternating movements	Adiadochokinesia
Stewart-Holmes maneuver	Rebound phenomenon
Lower limb movements	ㅤ
Heel-to-shin test (knee-tibia test)	Decomposition of movement, kinetic tremor, dysmetria
Trunk movements	ㅤ
Quality of sitting	Increased sway of the trunk
Muscle tone	ㅤ
Passive stretch of joints	Hypotonia
Knee jerk	Pendular knee jerk
Stance and gait	ㅤ
Standing (feet together)	Ataxia of stance, titubation, lateropulsion
Regular gait / walking	Ataxic gait
Tandem gait (heels to toes)	Ataxic gait
Handwriting	ㅤ
Standard sentence	Irregular writing, megalographia, kinetic tremor
Archimedes' spiral	Kinetic tremor, dysmetria