Cerebellum and Basal Ganglia

What do cerebellar lesions do?

Impair balance, coordination, muscle tone

What don’t do cerebellar lesions do?

Impair strength and sensation

What are the pathways of the cerebellum?

Superior, middle, inferior peduncles

Massive WM tracts that connect to brainstem

What are the anatomical sections of the cerebellum?

Vermis (midline), medial, and lateral hemispheres

What is the largest region of the cerebellum?

Lateral hemisphere

What are the functional sections of the cerebellum?

Vestibulocerebellum (underside; responsible for vestibulo coordination) (flocculonodular lobe)

Spinocerebellum (vermis and medial)

Cerebrocerebellum (lateral)

Where are the deep nuclei of the cerebellum?

Fastigial (midline), interposed (medial), dentate (lateral)

Output nuclei

What are the major cerebellar fiber and cell types?

Afferents

Intracerebellar

Efferents

Afferent cerebellar fibers

Climbing fibers (from inferior olive to purkinje cells)

Mossy fibers (from SC and brainstem to granule cells) - from pons, reticular formation, vestibular regions

Intracerebellar fibers

Granule cells (within cerebellar cortex and between pontine inputs and purkinje dendrites) - majority of cells

Purkinje cells (only cell to exit cerebellum, most deep) to deep nuclei

Efferent cerebellar fibers

Deep cerebellar nuclei (SCP or ICP to motor thalamus, red nucleus, inferior olive, vestibular nuclei) (motor and coordination projections)

Function of vestibulocerebellum

Visual reflexes (vestibuloculor reflex, smooth eye movement with posture changes)

Postural control (regulates muscle tone to postural muscles; balance)

What are the afferents to the vestibulocerebellum?

Vestibular nuclei, CN VIII; enters through the ICP (most common pathway to cerebellum)

Where do the afferents of the vestibulocerebellum travel to?

To flocculonodular node and vermis to fastigial nucleus to efferents via ICP

From the ICP, where do efferents of the vestibulocerebellum travel to?

Reticular and vestibular nuclei on CL (decussate)

Contributes to vestibulospinal tracts

Symptoms of lesions to vestibulocerebellum

Disequilibrium

Hypotonia - loss of tone in trunk or proximal leg

Nystagmus or altered VOR

Strabismus (heterotropia) - cross eyed

Function of the spinocerebellum

*Feedback system*

Motor coordination of posture and IPS limbs (compares intended movement with actual movement) → fine tuning

Function of vermis in spinocerebellum

Coordinates axial/trunk muscles

Function of medial hemispheres in spinocerebellum

Coordinates limb movement

Afferents of the spinocerebellum

Proprioceptive information from spinocerebellar tract (LE), cuneocerebellar tract (UE), and spinal trigeminal nucleus (head)

Travels to ICP

What are the two pathways of the spinocerebellum

Vermis or medial hemispheres

What is the pathway through the vermis for the spinocerebellum?

Vermis (midline) to deep cerebellar nuclei (fastigial nuclei) to efferents via SCP

Decussate to motor thalamus to motor cortex (left cortex if right arm)

What is the pathway through the medial hemisphere for the spinocerebellum?

Medial hemisphere (distal limbs) to deep cerebellar nuclei (interposed nuclei) to efferents via SCP

Decussate to motor thalamus to motor cortex

What are the symptoms of lesions to the spinocerebellum?

Decomposition of movement

Truncal ataxia

Rebound phenomena (loss of check reflex)

Speech scanning

Random volume emphasis of words

Check reflex

prevents arm from hitting self if resistance is removed

Cerebrocerebellum function

Feedforward system

Motor learning (skilled movements)

Planning of motor movements (neurons fire before neurons in M1 but after S1)

Cognition

Afferents to cerebrocerebellum

CL cortico-pontine-cerebellar pathway

Synapse in pontine nuclei (bulge in pons) → all info comes from pons and into MCP

Pathway of cerebrocerebellum

Pons → MCP → Lateral hemispheres → Dendate nucleus → efferents via SCP to CL motor thalamus (VA/VL) and cortex

Where are deficits usually in lesions in cerebrocerebellum?

IPS to cerebellar damage

Symptoms of lesions to cerebrocerebellum

Dyssnergia (sequential movement)

Change in timing regulation

Hypotonia

Reduced spinal reflexes

Dysmetria (wrong length → over/undershoot; type of ataxia)

What is similar to dysmetria?

Intention tremors

Where is the inferior olivary nucleus located?

Rostral medulla

Where do the efferents of the IO nucleus travel?

project to CL cerebellar cortex (climbing fibers) via ICP

Where do the afferents of the IO nucleus come from?

SC, cerebral cortex, red nucleus

Where are the basal ganglia located?

between cortex and thalamus; also in midbrain and near thalamus

General function of the basal ganglia?

Helps refine movement signal from cortex by inhibiting “incorrect” motor activity; brake hypothesis

Modifies initiation and execution of motor activity

Disinhibition

System wants to be on (neurons firing APs at all times) but is kept turned off by constant inhibitory signals

To activate the system, stop the inhibition

What are the components of the basal ganglia?

Striatum (caudate nucleus, nucleus accumbens, putamen)

Globus pallidus (external and internal)

Subthalamic nucleus (STN)

Substantia nigra

Direct pathway (+ excite, - inhibit)

Motor cortex + striatum - GPi/SNr - thalamus + motor cortex

Function of the direct pathway

Facilitates movement and disinhibits thalamus

Increased thalamic drive

What leads to hypokinetic disorders?

Damage in direct pathway

Indirect pathway

Motor cortex + striatum - GPe - STN + GPi - thalamus - motor cortex

Function of indirect pathway

Inhibits movement and thalamus

Decreases thalamic drive

What leads to hyperkinetic disorders?

Damage to indirect pathway

Chorea

involuntary, constant, rapid, complex body movements that flow from one body part to another

Choreiform

involuntary “dance like” movement of the limbs

Athetosis

slow, writhing movements of the fingers and hands

Ballismus

violent, flailing movements

Damage to STN results in hemiballismus

Dystonia

a persistent spasm/posture of a body part which can result in grotesque movements and distorted positions of the body

Resting tremor

occurs when body part is at complete rest against gravity (decreases with voluntary activity)

Postural tremor

occurs during maintenance of a position against gravity and increases with action

Essential tremor

occurs in a person who is moving or trying to move; no cause

Intentional tremor

manifests as a marked increase in tremor amplitude during a terminal portion of targeted movement

Example of hyperkinetic and hypokinetic disease

Huntington’s

Parkinson’s

Bradykinesia

slowing of voluntary movement

Lead-pipe rigidity

resistance persists throughout the ROM

Cogwheel rigidity

periodic resistance at different points throughout ROM (ratcheting)

Difference between spasticity and rigidity

Spasticity is speed dependent (can move limb through full ROM if slow)

Rigidity (can’t move through ROM either slow or fast)

Parkinson’s

Degenerative hypokinetic disorder

Cell loss in SNc (pars compacta substantia nigra) → reduced dopamine loss → inhibits direct pathway and allows indirect pathway to become dominant

Symptoms of parkinson’s

Bradykinesia

Increased muscle tone

Resting tremor

Decreased voluntary movement

Dysautonomic symptoms (incontinence, constipation)

Huntington’s disease

Genetic degenerative hyperkinetic disorder with the loss of GABA-ergic neurons in GPe (disinhibition)

Inhibits indirect pathway which increases thalamic drive (more cortex excitement)

Symptoms of huntington’s

Dementia

Chorea (fidgeting and worsens)