the fibers present in the cerebellar peduncles the applied anatomy of the cerebellum the microscopic structure of the cerebellum, mossy, and climbing fibers

1. Cerebellum-2

2. Learning objectives
1. List the fibers present in the cerebellar peduncles
2. Explain the applied anatomy of cerebellum
3. Explain the microscopic structure of cerebellum, mossy
and climbing fibres

3. Inferior Cerebellar peduncle(restiform body)
It consists of following afferent
(incoming)and efferent fibers
The afferent fibers (6 groups):
1. Posterior/dorsal spinocerebellar
tract
2. Posterior external arcuate
fibers(cuneo-cerebellar)
3. Anterior external arcuate fibers
4. Vestibulocerebellar ,
5. Olivocerebellar –arise from
contralateral inferior olivary
nucleus,
6. Reticulocerebellar
7. Rostral spinocerebellar tract
8. Trigeminocerebellar tract
Efferent fibers :
1. Cerebello-vestibular
2. Cerebello-olivary
3. Cerebello-reticular

4. Middle cerebellar peduncle
• It consists of entirely
afferent/incoming fibers of
cortico-ponto-
cerebellar pathway
• First order neurons of these
fibers are in the cerebral motor
cortex whereas second order
neurons are in the nuclei
pontis of the opposite side
(crossed ponto- cerebellar
fibres)

5. Superior cerebellar peduncle
It consists of mainly efferent (outgoing)
fibers form the cerebellum(cerebellar
Nuclei).
Efferent(outgoing) fibers
– arise in the dentate nucleus
– pass to the opposite side of the
midbrain and divide into ascending
and descending fibres
• Ascending fibres pass to end in red
nucleus and thalamus
• Descending fibres join the olivary
nucleus and reticular formation
Afferent fibers
1. Anterior(ventral) spinocerbellar
tract
2. Rubrocerebellar

6. Proprioceptive information from muscle spindles and Golgi tendon
organs of ipsilateral lower limb and of trunk enter through the dorsal
roots of the spinal nerves into the ipsilateral Clarke's column(second
order neurons of this tract are here ) in the spinal cord.
The axons(fibers ) of the cells of Clarke's Column or thoracic
nucleus ( which lies just beneath the dorsal horn extending between C8-
L4 cord segments) form this tact and enter the ipsilateral cerebellar
hemisphere through inferior cerebellar peduncle conveying impulses to
the cortex of Paleo(spino)cerebellum.
1. Posterior or Dorsal spinocerebellar tract (DSCT) or
Flechsig's fasciculus:

7. Carry unconscious
proprioception from ipsilateral
side to cerebellum
Anterior spinocerebellar - is
double crossed
Posterior spinocerebellar- is
uncrossed
Anterior
spinocerebellar
tract
Posterior
spinocerebellar
tract

8. 2. Posterior external arcuate
fibers or Cuneocerebellar tract (CCT)
Arise from ipsilateral accessory/external
cuneate nucleus which receives
proprioceptive information from muscle
spindles(primarily) and Golgi tendon
organs of ipsilateral upper limb and neck
via fasciculus cuneatus (from segments
above the C8).
The axons from the 2nd order neurons
situated in this nucleus run to ipsilateral
palaeocerebellar cortex through inferior
cerebellar peduncle as cuneocerebellar
tract.
It is an upper limb and neck analogue to
the dorsal spinocerebellar tract.

9. 9
3.Arcuate nuclei & Anterior external arcuate fibres and
stria medullaris
Curved , interrupted bands, anterior to the pyramids, and are said to be displaced
pontine nuclei (nuclei pontis) and form part of cortico- ponto-cerebellar pathway.
They are the source of anterior external arcuate fibres and fibres of the
striae medullares
Anterior external arcuate fibres are the efferents mainly from the contralateral
but also, ipsilateral arcuate nuclei which run laterally over(covering) the olive
(circumolivary fibres)and enter the cerebellum through the inferior cerebellar
peduncle
A few efferent fibres of arcuate nuclei pass dorsally through the substance of
the medulla and reach the median sulcus over the floor of the 4th ventricle and
decussate with similar fibres of opposite side and run laterally beneath the
ependyma as the striae medullares.

11. 4.Vestibulocerebellar tract
Conveys the vestibular fibres to the cerebellar cortex.
1st order vestibular afferents come from the cell bodies of the
neurons in the vestibular (Scarpa’s) ganglion and synapse in the
medial and inferior vestibular nuclei, from where the 2nd order
afferents begin and ascend to the cerebellum through the inferior
cerebellar peduncle. Most of these afferents reach the cortex of
the flocculonodular lobe.
Few of the 1st order vestibular afferents go directly also to the
flocculonodular lobe through the inferior cerebellar peduncle
without relaying in the vestibular nuclei.

12. 5.Olivocerebellar fibers or Climbing fibers
Have their cell bodies in the inferior olivary nucleus.
Their axons leave medially through the hilum, cross the midline, and ascend
into the contralateral cerebellar hemisphere via the inferior cerebellar
peduncle.
Once they enter the cerebellum, they are referred to as the climbing fibers.
Finally, they terminate by in the cerebellar cortex of the vermis, paramedian
zone, and also the lateral zone belonging to the neocerebellum.
6. Reticulocerebellar tract
Originates in different levels of the reticular formation and terminates mainly
in vermis.

13. 7.Rostral spinocerebellar tract- Cervical equivalent to the
Ventral/anterior spinocerebellar tract(i.e transmits information
from the golgi tendon organs of the cranial half of the body ).
Originates from neurons (lamina V -intermediate gray zone of
the spinal cord) rostral to Clarke's column and sends uncrossed
axons through the lateral funiculus to the cerebellum.
It reaches the cerebellum partly through the brachium
conjunctivum ( superior cerebellar peduncle) and partly through
the restiform body, terminating bilaterally in the anterior lobe of
the cerebellum.

14. The ventral(indirect) or Gowers' spinocerebellar
tract
• Like the dorsal spinocerebellar tract, it also involves two neurons.
Originates from lumbosacral spinal levels
• Unlike the dorsal spinocerebellar tract, the ventral
spinocerebellar tract will cross to the opposite side first in the
spinal cord in its anterior white commissure and then cross backs
again (in the deep white matter of the cerebellum) so that it ends
in the ipsilateral cerebellar hemisphere (referred to as a "double-
cross").
• The ventral tract gets its proprioceptive/fine touch/vibration
information from a first order neuron, whose cell body is in the
dorsal ganglion. The axons runs via the dorsal root and enter the
posterior horn of the grey matter, synapse with the 2nd order
neurons.

15. Carry unconscious
proprioception from ipsilateral
side to cerebellum
Anterior spinocerebellar - is
double crossed
Posterior spinocerebellar- is
uncrossed
Anterior
spinocerebellar
tract
Posterior
spinocerebellar
tract

16. Applied anatomical aspects

17. Cerebellar functions
3 Chief functions- each has been attributed to one
functional lobe
1. Equilibrium (balance & eye movement) by
vesitibulocerebellum
2. Muscle tone (walking-gait and pŌsture maintenance) by
spinocerbellum
3. Coordination of fine voluntary movements(motor skills ) by
cerebrocerebellum. It correlates movement in
progression and the intended movement

18. Functions – Equilibrium, Muscle tone, Coordination

19. Vestibulocerebellar (Flocculonodular)lesions
Mainly produce stance, gait abnormalities and Nystagmus
1. Stance(the way in which someone stands) – broad-based stance
is seen due to loss of equilibrium
2. Gait- a broad-based, slow, staggering, and unsteady gait is
seen. Truncal instability during walking, causes falls (Truncal ataxia)
In unilateral cerebellar disease, patients will veer towards the side
of the lesion.
Ask the patient to walk to the end of the examination room and
then to turn back whilst you paying attention to the gait and
turning (patients with cerebellar disease will find the turning
maneuver particularly difficult).
3. Tandem walking (ask to walk in a straight-line heel-to-toe) -
sensitive in identifying dysfunction of the cerebellar vermis and is
often the earliest abnormality .
4. Titubation -rhythmic body and or head nodding (tremor)
5. Nystagmus

20. Examination of Ataxic Patient
Ataxia- Imperfect coordination :
- Kinetic ataxia:
• Tandem walk,
• walk on toes,
• walk on heels
• Hopping
-Static ataxia:
• Head, shoulder, pelvic position,
• Truncal ataxia,
• Standing on one foot,
• Romberg's sign ( With feet together, ask the patient to close
his/her eyes. CARE!! Patient may fall).

21. Romberg's test, Romberg's sign, or the Romberg
manoeuvre
A test used in an exam of neurological function based on that a person requires at
least two of the three following senses to maintain balance while standing:
1. proprioception (the ability to know one's body position in space);
2. vision (which can be used to monitor and adjust for changes in body position).
3. vestibular function (the ability to know one's head position in space) and
A patient who has a problem with proprioception can still maintain balance by using
vision and vestibular function.
In the Romberg test, the standing patient is asked to close his or her eyes. Loss of
balance on closing the eyes is interpreted as a positive Romberg’s sign and it suggests
that the ataxia is sensory (proprioceptive or it could be vestibular in nature) due to
pathology of the dorsal columns -medial lemniscal system or vestibular system.
If a patient is ataxic and but the Romberg’s sign is negative ( no fall on closing the eyes),
then it indicates that the ataxia is cerebellar in nature (cerebellar ataxia).

22. Lesions of paleocerebellum
Dysfunction of the spinocerebellum may also be present as :
1. Loss of balance while walking - broad-based, slow, staggering,
and unsteady gait described as an ataxic gait (because walking
is uncoordinated and appears to be 'not ordered’).
2. Disturbances of tendon jerks(deep tendon reflexes) – Assess
the knee-jerk reflex (L2, L3, L4,) in each of the patient’s lower
limbs. In cerebellar disease, reflexes are described as
‘pendular’, which means less brisk and slower in their rise and
fall. However, like reduced tone, this sign is very subjective
3. Flail joints –unstable joints(Appendicular ataxia)

23. Neocerebellar lesions
1. Intention tremor
2. Hypotonia- Decreased muscle tone
3. Asynergy- defective or absent co-ordination
between organs, muscles, limbs or joints, resulting in a loss
in movement or speed
4. Dysmetria (past pointing)- Inability to judge the distance
5. Dysdiadochokinesis-Inability to do the rapid alternating
movements-
6. Dysarthria - Slurred speech (speech ataxia)
7. Gaze disturbances-
8. Rebound Phenomenon of Holmes

24. Intention tremor:
• Low frequency (below 5 Hz) tremor of the hand on purposive
movement is the most common, with coarse, rapid, side-to-side
oscillations that increase as the movement goal is approached.
• The amplitude of the tremor increases as an extremity
approaches the endpoint of deliberate and visually guided
movement (hence the name intention tremor). Be careful not to
mistake an action tremor (which occurs throughout the
movement)
• Peculiar writing abnormalities (large, unequal letters, irregular
underlining) depending on the side of the lesion.

25. Hypotonia
Normal resting muscle tone is reduced, leading to abnormal positions of
parts of the body. There is diminished resistance to passive movement.
Assess the tone in the muscle groups of upper and lower extremities on both the sides.
For example, in upper limb- shoulder, elbow and wrist on comparing each
side as you go.
1. Support the patient’s arm by holding their hand and elbow.
2. Ask the patient to relax and allow you to fully control the movement of their arm.
3. Move the muscle groups of the shoulder (circumduction), elbow (flexion/extension)
and wrist (circumduction) through their full range of movements.
4. Feel for abnormalities of tone as you assess each joint (e.g., hypotonia).
Interpretation
• Hypotonia can be caused by an ipsilateral cerebellar lesion. However, the ability to
detect reduced muscle tone is highly subjective and, in many cases, tone can feel
‘normal’ in cerebellar disease.
• As a result, it is advisable not to put too much weight on this sign or the lack of it.

26. Decomposition of movement occurs with disease of the
lateral zones of the cerebellum. This is reflected in difficulty
with both simple and compound movements. Movement
initiation and termination is affected.
• Dysmetria - placement falls short of or extends beyond
the initial goal, (undershoot or overshoot/past pointing)as
in the finger to nose test(upper limb co-ordination). The
heel–knee–shin test (Lower limb co-ordination). also
demonstrates error in placement, as well as force. The
lateral zone of the cerebellum is felt to be responsible for
normal placement.
• Repetitive movements are also affected with dysfunction
of the lateral zone of the cerebellum. The result is
dysdiadochokinesis( Disorder of the rhythm of rapid
alternating movements). Thigh slapping test- Use the
sitting position and ask the patient to strike first with the
palm and then with the dorsum of the hand upon the
thigh just above the knee

27. EXAMINATION OF COORDINATION IN THE UPPER LIMB
Finger to nose test

28. EXAMINATION OF COORDINATION IN THE LOWER LIMB:
1. Heel-shin test-
Ask the patient to place their right heel
on their left knee and then run it
down their shin in a straight line. Ask to
perform on both sides and Compare
sides
2.FOOT TAPPING TEST:
Ask the patient to tap their foot
against the examiners hand
Compare sides

29. Dysarthria
Dysarthria - In a sense, it is ataxia of speech heard in cerebellar disease. It can
present in the following ways as:
Slurred speech -Enunciation (saying clearly) is difficult (indistinctly the sounds
run into one another).
Scanning speech (also known as staccato speech) : Charcot applied this
term. Words are produced slowly and in a "measured" fashion and are
broken down into separate syllables, often separated by pauses and also spoken
with variations in pitch and loudness. Rhythm changes are prominent.
Assess speech by asking the patient to repeat the following phrases:
“British constitution”
“Baby hippopotamus”

30. Gaze disturbances
Dysmetric saccades
• Position your hand approximately 30cm to the side of your head.
• Ask the patient to look at your hand, then back to your nose. Repeat
this assessment on both sides.
• The movement of the patient’s eyes should be quick and accurate. In
cerebellar lesions, there will often be overshoot (i.e., the eyes will go too far
past the target, then correct themselves back to the target).
This overshoot and subsequent correction are known as dysmetric saccades.
Impaired smooth pursuit
• When the patient is tracking your finger, the eyes should move
smoothly (known as ‘smooth pursuit’). In cerebellar lesions, pursuit can be
“jerky” or “saccadic”( i.e., made up of lots of small movements).

31. Rebound phenomenon
Rebound phenomenon is a reflex that occurs when a patient attempts to move a
limb against resistance that has been suddenly removed.
Assessment
1. Ask the patient to close their eyes and position their arms outstretched in
front of them with their palms facing upwards.
2. Explain to the patient that you are going to apply some downward resistance
on each arm and that they should try to maintain the current position of their
arms as you apply that resistance.
3. Push downwards on one of the patient’s forearms and then immediately
remove the resistance and observe the movement of the limb being assessed.
• In healthy individuals, when the resistance is removed the limb will usually
move a short distance upwards(rebounds) .This is the normal reflex .
• An exaggerated rebound phenomenon suggests of spasticity (e.g., stroke
affecting the cerebrum).
• A complete absence of the phenomenon, caused by a failure of the
antagonist muscles to contract, is suggestive of cerebellar disease.

32. Left cerebellar tumor
- Ataxic gait
a. Sways to the right in
standing position
b. Steady on the
right leg
c. Unsteady on the
left leg
d. ataxic gait
a b c
d

33. Cerebellar tumors involving vermis
cause:
- Truncal Ataxia( Falls on
standing)
The child in this picture:
- would not try to stand
unsupported
- would not let go of the bed rail
if she was stood on the floor.

34. Microscopic structure of
cerebellum

35. • Has outer(surface) grey matter
called the cortex & inner white
matter.
• Deep nuclei (grey matter) are
embedded inside the white
matter.
• The cortex (grey matter) is
divided into :
1. Outer molecular layer
2. Middle Purkinje cell
layer
3. Inner granular layer

39. 1.Molecular layer
consists of:
1. Dendrites of Purkinje and
Golgi cells
2. Axons of granule cells
which are T shaped
3. Stellate and basket cells

41. 2.Purkinje layer
• Purkinje cells are large flask
shaped cells at the junction of
molecular and granule layers
• They are the principal output
neurons of cerebellar cortex
• Axons arise from bottom and
pass through granule layer
and end in the cerebellar
nuclei
• Their dendrites arise from
neck and pass into above
lying molecular layer

42. Purkinje cells

43. 3.Granule cell layer
• Contain numerous Granule
cells
• Granule cells axons project into
the superficial molecular layer
and divide into in T shape
manner( bifurcate) and extend
parallel to the long axis of each
folium (parallel fibers).
• Granule cells have a few short
dendrites

44. White matter of cerebellum
The white matter is made up of:
• The intrinsic fibres:
– do not leave the cerebellum
– connect different regions
• Afferent (incoming) fibres:
– enter through inferior ,middle, superior cerebellar peduncles
as climbing and mossy fibers
• Efferent fibres:
– constitute the output of the cerebellar nuclei which leave the
cerebellum through the superior and inferior cerebellar
peduncles

45. Climbing and mossy fibers
• Climbing fibers are
olivocerebellar fibres (Afferents
from inferior olivary nucleus) .They
end on the Purkinje cells in the
molecular layer. Axons of purkinje
cells end in the cerebellar
nuclei
• Mossy fibers- All afferent fibres
other than olivocerebellar fibres
are called Mossy fibers. They end
in granular cell layer over the
dendrites of granule cells .
• Both mossy and climbing fibers are
excitatory

46. Inputs:
• Climbing fiber (“+”, excitatory,
from inferior olive nucleus)
• Mossy fiber (+, excitatory,from
spinal cord & brain stem)
Output:
• Purkinje cell axon (“-”, inhibitory)
Input and output of the cerebral cortex

47. Molecular layer
Purkinje layer
Granular layer

48. Cerebellum- magnified
Pia mater
Purkinje neurons
Granular layer
Molecular layer
Notes

49. Cerebellum
Pia mater
Purkinje
neurons
Granular
layer
Molecular
layer
White matter
Notes

51. Ataxia Types
Cerebellar Vestibular Sensory
Dysarthria May be present Absent Absent
Nystagmus Often present Present Absent
Vertigo May be present Present Absent
Limb
ataxia
Usually, present Absent Present(only in the legs)
Stance Unable to stand
with feet
together
May be able to
stand with feet
together
Able to stand with feet together
with eyes are open, but unable
when the eyes closed
Vibratory
and
position
sense
Normal Normal Impaired
22
June
2021

52. Localizing Cerebellar lesions
Cerebellar lesion Signs
Posterior
(Flocculo-nodular lobe;
Archicerebellum)
Eye movement disorders: Nystagmus;
Vestibulo-ocular reflex (VOR)
Postural and gait dysfunction
Midline
(Vermis; paleocerebellum)
Truncal & gait ataxia, Flail joints
Hemisphere
(Neocerebellum)
Dysmetria, Limb ataxia
Dysdiadochokinesis,
"intention" tremor
Dysarthria
Hypotonia

54. Thank you