Lecture Motor 0 Cerebellar

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CMS 301 ; MOTOR

SYSTEM- ATAXIA

Imane Yassine

F A C U L T Y O F
M E D I C I N E
Agenda
I. Anatomy of the motor system (pyramidal and
extrapyramidal)

II. Anatomy of the cerebellum

III. Clinical findings in motor system disorders

IV. Clinical findings in cerebellar disorders


Anatomy of the pyramidal tract
• Cerebral cotrex
• Internal capsule
• Brainstem
• Motor decussation Loading…
• Coticospinal tracts
• AHC
• Roots
• Plexus
• Peripheral nerves
• MNJ
• muscles
Motor system pathway
• The upper motor neurons
originate in the cerebral cortex
and travel down to the brain stem
or spinal cord,
• while the lower motor neurons
begin in the spinal cord and go
on to innervate muscles and
glands throughout the body.
Anatomy of the extrapyramidal tracts
• Rubrospinal tract
• Tectospinal tract
• Vestibulospinal tracts (medial and lateral)
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• Reticulospinal tracts (Medullary and pontine)
Clinical Significance
• An upper motor neuron lesion is a
lesion anywhere from the cortex to
the corticospinal tract; (cortex,
internal capsule, pyramidal tract,
lateral corticospinal tract)
• This lesion causes ;
o Weakness :distal > proximal & pro gravity > anti
gravity
o hyperreflexia: (abnormally brisk reflexes)
o spasticity, (a brisk stretch of muscles causes a sudden
increase in tone followed by decreased muscle
resistance)
o and a positive Babinski reflex, presenting as an upward
response of the big toe when the plantar surface of the
foot is stroked, with other toes fanning out.

• Negative features include impaired motor control,


easy fatiguability, weakness, and loss of dexterity
• lower motor neuron lesions are
lesions anywhere from
o the anterior horn of the spinal cord,
o peripheral nerve,
o neuromuscular junction,
o or muscle.
• This type of lesion causes
o hyporeflexia,
o flaccid paralysis,
o Fasculations,
o and atrophy.
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Pattern recognition in motor weakness
Cerebellum
• The cerebellum, located under the
posterior cerebral cortex in the
posterior cranial fossa, just
posterior to the brainstem, has
diverse connections to the brain
stem, cerebrum, and spinal cord.

• The cerebellum subdivides into


two hemispheres connected by
the vermis, a central midline part
• Any midline cerebellar lesions manifest as imbalance, while
hemispheric cerebellar lesions result mainly in incoordination.

• The cerebellum maintains our motor equilibrium and calibration of


movements.

• It is an essential region of the brain playing a central role in


maintaining our gait, stance, and balance, as well as the coordination
of goal-directed movements and complex movements.
Anatomic Basis of Clinical Signs
•Midline lesions—The middle zone of the cerebellum— the
vermis and flocculonodular lobe and their associated subcortical
(fastigial) nuclei—is involved in the control of axial functions,
including eye movements, head and trunk posture, stance, and gait.
Midline cerebellar disease therefore
results in a clinical syndrome
characterized by
• Gaze-evoked nystagmus and
hypo- or hypermetric
saccadic eye movements: on
looking to either side, the
fast-phase of nystagmus will
be in the direction of gaze,
and on the generation of
saccadic eye movements, the
patient may under- or
overshoot, with resultant
small corrective saccades.
• Cerebellar ‘staccato’ speech (in music, staccato refers to unconnected
or detached notes)

• Upper limb signs of intention tremor (tremor that increases in


amplitude as a finger approaches the target)
o past-pointing,
o dysmetria and
o dysdiadochokinesis (difficulties with making rapid alternating movements,
such as pronation-supination (an early sign may be that the patient moves their
hand as if they are turning the pages of a book).
o The finger–nose test should be undertaken slowly and carefully as carrying out
the test in a rapid fashion tends to miss early cerebellar signs.
• Rebound phenomenon: the patient is asked to maintain his arms in
the outstretched position with eyes closed. Downward pressure is
applied to the arms and is released suddenly. In a cerebellar syndrome,
the arms will shoot upward when pressure is released and will oscillate
before returning to the original position. The cerebellum functions as a
calibrator of forces, and dysfunction results in the generation of
inappropriate muscle forces to fix the limb in a particular position

• Hypotonia of arms and legs (reduced tone of limbs)


• Look for evidence of a sensory rather than cerebellar ataxia:
positive Romberg’s test or pseudoathetosis (apparent writhing of
fingers of outstretched hands when eyes are closed, due to
proprioceptive impairment). If sensory ataxia is suspected, look for
sensory impairment (especially joint position sense) and distal
weakness associated with a peripheral sensory or sensorimotor
neuropathy.

• Ataxic gait (examination of gait is needed to exclude other gait


disorders too )
• Heel–shin ataxia (ask the patient to make a circular movement, with the
heel raised off the shin once it has reached the ankle, before placing it on
the knee again. Simply gliding one heel up and down the opposite shin
will miss early ataxia)

• Truncal ataxia (demonstrable in sitting position or while standing)

• Pendular reflexes: the movement elicited by percussion is not


dampened, resulting in swinging back and forth of the limb. Once again,
this is due to a failure of calibration of muscle forces, resulting in
abnormal ‘dampening.’
•Hemispheric lesions—The lateral zones of the cerebellum (cerebellar
hemispheres) help to coordinate movements and maintain tone in the
ipsilateral limbs.

• The hemispheres also have a role in regulating ipsilateral gaze.

• Disorders affecting one cerebellar hemisphere cause ipsilateral hemiataxia


and hypotonia of the limbs as well as nystagmus and transient ipsilateral gaze
paresis (inability to look voluntarily toward the affected side).

• Involvement of the medial (paravermian) portion of either cerebellar


hemisphere can also produce dysarthria.
Thank you

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