THE CEREBELLUM

Dr. S. Jimnez-Dietsch

"The mystery of the cerebellum lies in the fact that we have a fairly good idea about
what it does -- we just don't know how it manages to it"
C.T. Leonard
In: The Neuroscience of Human Movement

The cerebellum constitutes only 10% of the total volume of the brain, yet it contains more than
half of all the neurons. Estimates suggest that six-sevenths of the cerebellar surface is buried in
the fissures; it would measure a meter across if laid flat.

GROSS FEATURES
---folias:
Transverse convolutions that increase the surface area of the cerebellar cortex.

---divisions:
No clear division is apparent, but shallow furrows delineate a midline vermis from the
right and left cerebellar hemispheres.

---cerebellar peduncles:
1. inferior cerebellar peduncle = restiform body
2. middle cerebellar peduncle = brachium pontis
3. superior cerebellar peduncle = brachium conjunctivum
Important Anatomical Notes:
1. The inferior and middle cerebellar peduncles contain mostly
input fibers; the superior cerebellar peduncle is for the most part
an output pathway.
2. The cerebellofugal fibers which depart through the superior
cerebellar peduncle cross at the level of the mesencephalic
tegmentum before terminating in the red nucleus and thalamus.
This crossing is called the decussation of the superior
cerebellar peduncle.

---longitudinal zones:
1. vermian zone
2. paravermian zone
3. hemispheric (lateral) zone

---lobes and fissures:

1. anterior lobe (related to primary fissure)
2. posterior lobe
3. flocculonodular lobe (related to posterolateral fissure)
Cerebellum --- page 2

HISTOLOGICAL FEATURES:
The cerebellar surface consists of an outer gray matter called the cerebellar cortex and an inner
core of white matter called the medullary substance.

---5 types of neurons in the cerebellar cortex:

1. basket cells
2. stellate cells
3. Purkinje cells
4. granular cells
5. Golgi cells

---3 cortical layers:

1. molecular layer
2. Purkinje cell layer
3. granule cell layer

---principal afferent fibers in the white matter (they outnumber efferents 40:1)
1. climbing fibers ~ they arise from inferior olive as olivocerebellar fibers
2. mossy fibers

---deep cerebellar nuclei:

1. fastigial
2. globose
3. emboliform
4. dentate

they receive excitatory input through collaterals of all afferent cerebellar fibers that
pass by en route to the cerebellar cortex
These neurons are said to be spontaneously active even in animals sitting
quietly, therefore, the Purkinje cells are needed to diminish deep nuclear cells
firing.

Purkinje cell projections to the deep cerebellar nuclei are topographically arranged (refer
to ppt.)
Cerebellum --- page 3

INPUT VIA MOSSY AND CLIMBING FIBERS

---climbing fibers:
They arise from cells in the inferior olive (thus they are olivocerebellar fibers). The
neurons in the inferior olive receive information from many areas of the CNS, including
the cerebral cortex, red nucleus, mesencephalic tectum, spinal cord, reticular
formation, and basal nuclei. The most important input to the inferior olive is from the
spinal cord. The neurons in the inferior olive relay all these information via
olivocerebellar fibers that cross the midline and enter the contralateral cerebellum via the
inferior cerebellar peduncle, and then "climb" along the dendrites of an individual
Purkinje cell. Each Purkinje cell is innervated by one and only one climbing fiber.
However, an individual climbing fiber can innervate between 1 and 10 Purkinje cells.

---mossy fibers:
They are the largest afferent system to the cerebellar cortex. They continuously update
the cerebellum on the status of ongoing movement, primarily through propioceptive
information. This propioceptive information conveyed by the mossy fibers comes mainly
from the spinal cord via spinocerebellar tracts. (Review: The spinocerebellar tracts carry
propioceptive information from muscle and joint receptors, and exteroceptive information
from skin). Mossy fibers send collaterals to the deep cerebellar nuclei, enter the
cerebellar cortex, and branch repeatedly before contacting granule cells. Each mossy
fiber innervates several granule cells, and each granule cell receives input from several
mossy fibers. Mossy fibers excite the granule cells.

Mossy fibers also carry information from the cerebral cortex (mostly from sensory,
motor, and visual areas of cortex). The pontine nuclei serve as relay for this cortical
input. Pontocerebellar fibers then travel through the middle cerebellar peduncle to reach
the contralateral cerebellar cortex.

Mossy fibers also brings vestibular information to the cerebellum. This vestibular
information reaches the cerebellum, along with visual information. Integration of these
signals allows the cerebellum to control balance and equilibrium and to influence head
and eye movements relative to gaze.

---subdivisions according to input:

Although investigators disagree somewhat. the cerebellum can be subdivided into three
different areas according to the input or information received.
1. vestibulocerebellum (archicerebellum) = mainly flocculonodular lobe
Is the portion of the cerebellum that receives its primary input
from the vestibular nuclei. This input enters the cerebellum via
the inferior cerebellar peduncle.

Vestibular information reaches the vestibulocerebellum by way of the vestibular

nerve (primary vestibulocerebellar fibers) and vestibular nuclei
(secondary vestibulocerebellar fibers). The vestibular information reports
head position and allows the vestibulocerebellum to control balance and
equilibrium.
Cerebellum --- page 4

2. spinocerebellum (paleocerebellum) = mainly anterior lobe

Is the portion of the cerebellum that receives its principal input from
the spinocerebellar tracts. The spinocerebellar tracts carry mainly
propioceptive information relating to joint position and movement
(that is, information from stretch receptors, Golgi tendon organs,
as well as from skin receptors -- this propioception is sometimes referred
to as "unconscious propioception" ). The propioceptive information informs
the cerebellum on position, velocity, and force of muscle contractions. The
spinocerebellum uses this input to adjust muscle tone.

3. pontocerebellum (neocerebellum) = mainly posterior lobe

Is the portion of the cerebellum that receives its principal input
from the pontine nuclei. The neurons in the pontine nuclei receive
input from corticopontine fibers that originate in the ipsilateral
cerebral cortex. The areas of cortex that provide input to the
pontine nuclei are mainly the sensory and motor cortices. Axons
from neurons in the pontine nuclei cross the midline as pontocerebellar
fibers, ascend into the contralateral cerebellar cortex via the middle cerebellar
peduncle, and terminate as mossy fibers. The cerebellum is thus informed of
the motor commands being issued from the cerebral cortex by a flow of neuronal
impulses through this cortico-ponto-cerebellar pathway.

Important Fact:
Almost all sensory modalities reach the cerebellum (including tactile information, vision, and
audition). The vast majority of the sensory input is propioceptive information from the
joints and muscles of the limbs and trunks. The sensory information is needed to furnish a
constant account of the progress of motor activity.

EFFERENT CEREBELLAR CONNECTIONS

---output from deep cerebellar nuclei:
***from the fastigial nucleus:
1.to vestibular nuclei
2.to the reticular formation

***from the nucleus interpositus:

1. to the red nucleus (magnocellular portion) -- main target
2. to the thalamus

***from the dentate nucleus (dentate-rubro-thalamic tract):

1. to the red nucleus (parvocellular portion)
2. to the thalamus -- main target
Cerebellum --- page 5

CLINICAL CORRELATIONS
Lesions to the cerebellum do not produce paralysis, weakness, nor do they affect the ability to
initiate or terminate voluntary movement. Although cerebellar lesions do not cause paralysis or
loss of sensation, they do cause devastating changes in the ability to produce smooth,
coordinated, complex movements. During cerebellar disorders posture and balance deteriorate,
eye-hand coordination is disrupted, and motor tasks reflect errors in direction, force, velocity,
amplitude, and timing.

---signs of cerebellar disorders:

The signs of cerebellar lesions are a myriad of motor deficits described generally as
ataxia (G. without order). In general terms, ataxia is lack of coordination of muscular
activity. It is a disordered contractions of agonist and antagonists muscles. The
movements will err in rate, range, force, and duration. Skilled movements originating in
the cerebral motor cortex become inaccurate and poorly controlled. Ataxia may affect the
limbs, the trunk, or gait. Ataxia secondary to cerebellar injury characteristically persists
in spite of visual cues (motor ataxia).

The principal signs of cerebellar lesions are:

1. Truncal and/or appendicular ataxia
Patients with lesions confined to the cerebellar vermis have an unsteady posture during
sitting and standing and unsteady, staggering, broad-based, "drunk-like" gait (ataxic
gait) with no other significant abnormalities on exam. The gait is unsteady, with a
tendency to fall to the side, forward, or backward but movements of the arms and legs
are normal when the trunk is supported (e.g., when pt. is lying in bed). This condition is
referred to as truncal ataxia. In contrast, lesions to the cerebellar hemispheres affect
movements of the extremities, a condition referred to as appendicular ataxia.

Appendicular ataxia is always ipsilateral to the lesion. In contrast, truncal ataxia

is a bilateral disorder.

Clinical Note:
Cerebellar lesions often extend to involve both the vermis and the cerebellar
hemispheres, and truncal and appendicular ataxia frequently coexist in the same
patient.

Testing for Truncal Ataxia:

Truncal ataxia can be demonstrated by having the patient perform a
tandem gait, in which the patient walks a straight line touching the toes of one
foot with the heel of the other with each step. Patients with truncal ataxia
caused by damage to the cerebellum or associated pathways will have particular
difficulty with this task, since they tend to have a wide-based, unsteady gait
and become more unsteady when attempting to keep their feet close together.

Important to know.............
An ataxic gait may result from motor incoordination due to cerebellar disease,
or from lack of propioception in the lower extremities due to disease in the
dorsal column-medial lemniscal system. An ataxic gait secondary to
cerebellar injury characteristically persists in spite of visual cues (unlike
ataxia secondary to posterior column involvement which is called
sensory ataxia and is visually compensated).
Cerebellum --- page 6

Regarding the Romberg (swaying) sign..

The pt. is asked to stand with the feet together. Note whether the patient
sways. Then ask the pt. to close the eyes, and note whether the swaying
increases. Normally, subjects will sway minimally with the eyes closed but
not fall.
Patients with dorsal column lesions, such as tabes dorsalis, sway much
more with eyes closed and may fall unless supported. They do not
compensate with time. This sign is the result of loss of propioceptive
afferents via dorsal roots and dorsal columns. In these patients, Rombergs
test shows that vision can substitute for propioception.
Patients with vestibular lesions initially tend to sway to the side of the
lesion, but the nervous system compensates with time. In fact, many
patients with vestibular disease perform well on the Romberg test.
Students often mistakenly consider the swaying test as a test of cerebellar
function, but the cerebellum does not depend on vision to do its job of
muscle coordination. The cerebellum can coordinate muscular contractions
only if it receives the proper propioceptive information. Therefore, in
cerebellar lesions, patients will sway or lose their balance with the eyes
open or closed.

Remember
During the swaying test (Rombergs test), loss of dorsal column
modalities, as in tabes dorsalis, causes the most severe swaying with
eyes closed.

2. Decomposition of movement (also referred to as asynergia)

There is lack of synergy of the various muscle components in performing complex
movements so that the movements are broken up into isolated successive parts. The
various components of a motor act are then performed in a jerky and irregular rather than
in a smooth sequence. Decomposition of movement is an adopted strategy that
compensates for the inability to make complex movements accurately. The pt. with
a cerebellar disorder learns to make movements more accurate by moving one joint at a
time in a serial manner.

3. Dysmetria
This is a disturbance of the trajectory or placement of a body part during active
movements. The limb may fall short of its goal (hypometria), or it may extend beyond
its goal (hypermetria or past-pointing phenomenon).

4. Dysarthria
Speech disorder during cerebellar lesions has been described as slow, slurred,
scanning, staccato, explosive, garbled, and hesitant, but comprehension
remains intact and grammar does not suffer. Speech abnormalities is caused by
irregular fluctuations in both rate and volume.
Cerebellum --- page 7

5. Dysdiadochokinesis (Adiadochokinesis)
Inability to perform rapidly alternating or fine repetitive movements.

6. Hypotonia
Results in a floppy, loose-jointed, rag-doll appearance with pendular reflexes.
Hypotonia often decreases with time.
Regarding pendular reflexes..
While testing the stretch reflex and as a result of hypotonia, a limb may
swing back and forth after the reflex contraction.

7. Intentional tremor
It is demonstrated by asking the pt. to extend the arms parallel to the floor with the hands
open. A rhythmic oscillation generated at the shoulder is seen. Tremor can also be
produced by having the pt. alternately touch his or her nose and then touch the
examiner's finger, which is held at a full arm's length away from the pt. (this is called
"finger-to-nose test"). Tremor is most marked at the end of the movement.

8. Rebound phenomenon
The pt. is asked to maintain the arms extended forward while the examiner taps the
patient's wrist enough to displace the arm. Normally, the arm returns rapidly to the
resting position, but with cerebellar disease, the limb is markedly displaced and
repeatedly overshoots when returning to the original position.

9. Ocular motor disorders

A number of disturbances of ocular function result from cerebellar disease, the most
prominent of which is nystagmus.
Nystagmus:
Is a rhythmical, involuntary oscillation of the eyes. Nystagmus is a normal
response to stimulation of the vestibular or visual system, but spontaneous or
exaggerated nystagmus can indicate dysfunction somewhere in the posterior
cranial fossa, that is, vestibular system, brain stem, or cerebellum. In
cerebellar disease, nystagmus is due to ataxia of the oculogyric muscles (i.e.,
there is lack of coordination between agonists and antagonists involved in the
eyeball movement).

Very important to know:

Cerebellar defects gradually improve with time after sudden lesions such as traumatic injury or
loss of blood supply (CVA = cerebrovascular accident caused by hemorrhage, embolism, or
thrombosis of a cerebellar artery). Improvement of motor function over time occurs partially
because the patient learns compensatory strategies and partially because of plasticity of the
central nervous system (plasticity is the capacity to form new connections or to use
existing connections differently).

It is clear that the right side of the body is under the influence of the right cerebellar
hemisphere and that any symptoms occurring unilaterally are found on the same side as the
lesion in the cerebellum. This contrasts strikingly with cerebral lesions, which produce
contralateral effects.
Cerebellum --- page 8

---medulloblastomas:
malignant tumor of childhood and adolescence arising from the roof of the fourth
ventricle (i.e., lingula) or from the inferior vermis (nine of ten cases are located in the
inferior vermis)
affected individuals have truncal ataxia with both reflexes and muscle tone remaining
normal
medulloblastomas represent 20% of brain tumors in young subjects and they are the
most common cause of damage to the flocculonodular lobe
the tumor infiltrates the fourth ventricle thereby hindering CSF outflow causing obstructive
(noncommunicating) hydrocephalus
patients may present with symptoms and signs of increased intracranial pressure,
including papilledema, strabismus, and diplopia
this tumor is highly malignant and carries a bad prognosis, even after radical operative
removal and radiation recurrences are inevitable after months or years, frequently
metastasizing to other parts of the CNS

---Arnold-Chiari malformation:
congenital defect in the formation of the brainstem
consists of elongation of the cerebellar tonsils, which protrude through the foramen
magnum
hydrocephalus may result from blockage of the fourth ventricle foramina for CSF outflow
this malformation may occur alone, but is frequently associated with spina bifida

Y, finalmente, para todos los que gustan de empinar el codo .....................

Alcoholic intoxication can mimic cerebellar ataxia,
although the effects are bilateral.

---Alcoholic cerebellar degeneration:

A characteristic cerebellar syndrome may develop in chronic alcoholics, probably as a
result of malnutrition.

Degenerative changes of the cerebellar cortex typically start at the superior vermis and
anterior lobe and spread backwards. The pathologic changes are as distinctive as the
stereotyped clinical syndrome. There is marked degeneration of all neurocellular
elements, particularly the Purkinje cells of the cerebellar cortex.

Clinically, patients demonstrate a wide-based gait, varying degrees of truncal instability

(i.e., disturbance of stance), and ataxia of the legs with relatively preserved upper
extremity coordination. Gait ataxia is a universal feature and is almost always the
problem that initially commands medical attention.

Alcoholic cerebellar degeneration usually has its onset between the ages of 40 and 60
years. It is usually insidious in onset; and it is gradually progressive. No specific
treatment is available for alcoholic cerebellar degeneration. Abstinence from alcohol,
combined with adequate nutrition, leads to stabilization in most cases.