Cerebellar Lesions

POSTERIOR VERMIS
Flocculonodular lobe- vestibulocerebellum (eye movements, equilibrium)
o This helps you when you step off of a curve
Vestibular nucleus, no deep cerebellar nuclei involved
Medulloblastoma (children)= headache, vomiting, errors of rhythm/timing of
speech
o Refuse to walk unaided due to constant falling
Nystagmus
Titubation (nodding of the head or body) and truncal ataxia
Ataxic gait that IMPROVES when lying down, the staggering gait affects both
limbs
Ocular signs= bilateral loss of abduction
o Obstructed 4th ventriclepapilledema, presses on petrosphenoidal ligament of
Gruber which pushes down on Abducent Nerve
Bilateral cerebellar sings= dysdiadochokinesia, poor performance on heel-to-shin test
ANTERIOR VERMIS
Vermis of spinocerebellum (balance)
Fastigial nucleus
**The area of this lesion receives input from VESTIBULAR LABYRINTH
Staggering gait, pendular reflexes bilaterally
Poor results bilaterally on heel-to-shin test, poor results bilaterally on tandem walking
test
Patient closes their eyes while standingsways both directions, doesnt fall
(NEGATIVE Romberg)
Homeless- alcoholism
Truncal ataxia and titubation may be seen but not always
Ataxic gait does NOT improve when lying down
Youll see more limb involvement
CEREBELLAR HEMISPHERE SYNDROME
Progressively more clumsy
Dysdiadochokinesia- inability to perform rapid alternating movements (touch
examiners finger)
Tremor
Veers to one side when attempting to walk in tandem, tends to fall to that side
UNILATERAL- ipsilateral to symptoms
CEREBELLO-OLIVARY DEGENERATION OF HOLMES
Bilateral cerebellar dysfunction signs= gait ataxia, dysarthria (scanning speech),
intention tremor
Genetic basis
Purkinje cells of the cerebellum fail to develop
OLIVOPONTOCEREBELLAR DEGENERATION (Dejerine-Thomas syndrome)
Bilateral cerebellar gait ataxia, dysarthria, intention tremor
Genetic basis (autosomal dominant)
Parkinsonian signs- akinesia/ bradykinesia and rigidity- due to loss of substantia nigra
and shrinkage of basis pontis
No sensory changes or weakness/paralysis, negative Romberg test

Lesion of Fastigial nucleus, Nodulus, Flocculus

Unsteady gait
Unable to walk in tandem, no tendency to fall
Successfully performs heel-to-shin test
Truncal tremor, titubation
No intention tremor, dysmetria, decomposition of movement, or dysdiadochokinesia
Lesion of Dentate Nucleus
Dysmetria, decomposition of movement, or dysdiadochokinesia (3Ds)
LATERAL LOBE of cerebellum
Efferent axons from the neurons in the dentate nucleus project to:
o Ventral lateral nucleus of thalamus
o Red nucleus, parvocellular part (cross of SCP) which then projects to
ipsi inferior olivary nucleus then to ICP
Cerebellum talking to cerebellum
Olive= climbing fibers that go to the Purkinje cells. They stimulate
(excitatory) purkinje cells.
Axons from the dentate nucleus pass through the SUPERIOR cerebellar peduncle
Lesion of Interposed Nucleus
Emboliform and globose
Intention tremor
Involves GAIT: lesion causes ataxia of limb movements
Tendency to fall to one side, poor heel-to-shin test on ipsilateral side
Lesion of Superior Cerebellar Peduncle
Symptoms involving cerebrocerebellum (dentate nucleus) and spinocerebellum
(interposed nucleus)
Axons of cells located in the DENTATE NUCLEI are damaged
Dentatorubrothalamic tract is damaged
Compromises communication between the CEREBELLUM and the THALAMUS
Lesion of Middle Cerebellar Peduncle
Axons of cells located in the PONTINE NUCLEI are damaged
Compromises communication between CEREBRUM and CEREBELLUM
Lesion of Inferior Cerebellar Peduncle
Axons of cells located in the INFERIOR OLIVARY NUCLEI are damaged
Tumor that presses on anterior portion of CEREBRAL peduncle
Compromises the ability of the cerebrum to project to the PONTINE NUCLEI
Basket cells
BASKET CELLS synapse on somas of the PURKINJE CELLS. They INHIBIT the Purkinje
cells.
Lesion= reduced inhibition of Purkinje cells
Golgi Cells
GOLGI CELLS inhibit GRANULE CELLS
Lesion= reduced inhibition of granule cells
Inferior olivary nucleus
Excite Purkinje cells
Lesion= reduced excitation of Purkinje cells
**Red nuclei, PARVOCELLULAR portion projects directly to the inferior olivary nuclei
Benedikts

Ability of the cerebellum to communicate with the THALAMUS is compromised

Midbrain tegmentum lesion
Tegmentum connects the cerebellum to the VENTRAL LATERAL nucleus of thalamus
Ipsilateral Oculomotor palsy- abducted, depressed, mydriasis, ptosis
Loss of fine touch, conscious proprioception, vibratory sense on CONTRALATERAL
body
Ataxia, intention tremor (CONTRALATERAL)
Webers
CONTRALATERAL spastic hemiplegia, UMN signs
Ipsilateral Oculomotor palsy- abducted, depressed, mydriasis, ptosis
Unilateral cerebellar signs= brainstem lesion (stroke) so look for CN lesion symptoms
Anterior Spinal Artery
Medial medullary syndrome
Spinal cord lesion: loss of everything except dorsal columns