What is the function of the cerebellum?
- To make movements of the extremities, trunk and eyes as smooth as possible by continually making small corrections
- coordinated contraction/relaxation of agonist & antagonist muscles
What are the inputs of the cerebellum?
- **Inputs: **sensory (proprioception) pathways from spinal cord, cortex, brainstem
- Motor information from cord ⇒ ventral spinocerebellar tract ⇒ superior cerebellar peduncle ⇒ cerebellum
- Visual, sensory, motor information from cortex ⇒ pontine nuclei ⇒ middle cerebellar peduncle ⇒ cerebellum
- Proprioceptive information from limbs ⇒ fasciculus gracilis/ cuneatus ⇒ dorsal spinocerebellar tract & cuneocerebellar tract ⇒ inferior cerebellar peduncle ⇒ cerebellum
What are the outputs from the cerebellum?
- Outputs: brainstem (that then project back to extremities/trunk & eyes), thalamus
- Cerebellum ⇒ VL thalamus ⇒ primary motor & supplementary motor cortex ⇒ ventral & lateral corticospinal tract ⇒ movement
- Cerebellum ⇒ vestibular nuclei ⇒ head/eye control & posture
- Cerebellum ⇒ medullary & pontine reticular formation ⇒ medullary & pontine reticulospinal tract ⇒ unconscious motor control
Cerebellar deficits are ___________ to the lesion
ipsilateral
- due to:
- ‘doublecrossing’ or
- fibers remain ipsilateral
Acute lesions accompanied by nausea/vomiting due to _______.
vertigo
- vestibular dysfunction similar
- pts are not necessarily ataxic on finger to nose or heel to shin
Ataxia
uncoordinated muscle movement
- errors in speed, range, force, timing
**Truncal ataxia **
wide-based, unsteady gait or difficulty sitting up
- localizes to lesion of vermis
- “drunk-like”
- Walk patient—normal walk & tandem walk
-
Romberg test
- ask patient to stand in place, feet together & close eyes
- if s/he needs to step to stabilize, then deficit could be due cerebellar, proprioceptive, or vestibular dysfunction
- not specific to cerebellar disorders
Appendicular ataxia:
difficulty coordinating an extremity
- manifests as dysmetria & dysrhythmia
- lesion of ipsilateral lateral hemispheres
Appendicular ataxia:
- Dysmetria:
- Dysrhythmia:
- Finger-nose-finger test:
- Heel-to-shin test:
- Finger tapping:
- Dysdiadochokinesia:
- **Dysmetria **= overshoot/undershoot of a body part (limb) during movement toward a target
- Dysrhythmia = abnormal rhythm and timing of movement
- Finger-nose-finger test—alternating between touching nose and examiner’s finger
- abnormal if patient’s finger shakes as it approaches target (either nose or finger)
- Heel-to-shin test—guiding heel along shin when supine
- abnormal if heel shakes
- Finger tapping—watch amplitude, rhythm, speed
- cerebellar disorders cause abnormal rhythm, slowed speed, and varying amplitude
- Dysdiadochokinesia = abnormal speed/rhythm when tapping hand with palm/dorsum alternatively
Tremor:
- Postural Tremor:
- Action/Intention tremor:
- Titubation:
involuntary, rhythmic oscillation of a body part
-
Postural tremor = tremor that occurs when a limb is held in a particular position (eg. open hands held extended)
- lesion of ipsilateral lateral hemisphere
-
Action/intention tremor = tremor that occurs when limb is in motion
- lesion of ipsilateral lateral hemisphere
-
Titubation = tremor of trunk or head
- lesion of vermis
Ocular dysmetria:
**overshoot or undershoot of the eyes as patient focuses on a target **
- lesion of flocculonodular lobe
Eye movements:
- Saccades:
- Slow eye movements:
Eye movements:
- **Saccades: **quick, voluntary movement of eyes onto target
- mediated by cortex—frontal & parietal eye fields
- **Slow eye movements: **involuntary movement of eyes
- mediated by cerebellum, vestibular nuclei & pathways, and extraocular motor nuclei
Nystagmus:
rhythmic oscillations of the eyes
- mediated by cortex
- an attempt by the cortex to correct abnormal signal to brain
- deficit of slow eye movements
- fast-beating phase of eye movements:
- “right beating nystagmus”—fast phase of eye movements are to the right & slow phase of eye movements to left
- What causes a pure vertical nystagmus?
- What causes a direction-changing nystagmus?
- What causes a horizontal or rotary nystagmus?
-
Pure vertical nystagmus:
- ALWAYS CNS lesion
-
Direction-changing nystagmus:
- CNS lesion
-
Horizontal or rotatory nystagmus:
- CNS or PNS lesion
Lesion of vermis/flocculonodular lobe can cause _______, _________, or ______ nystagmus
vertical, horizontal, or rotatory
- R beating horizontal nystagmus on R gaze, upgaze, downgaze ⇒
- R beating horizontal nystagmus on R gaze, L beating horizontal nystagmus on left gaze, vertical nystagmus on upgaze ⇒
-
L VOR or L vestibular nuclear lesion
- lesion could be CNS or PNS w/ horizontal nystagmus
- lesion is likely to be cerebellum or one of its pathways
- Slow saccades:
- Scanning (ataxic) speech:
- Hypotonia of ipsilateral limb:
- Impaired VOR Suppression:
- **Slow saccades: **slowness in eye movements when trying to quickly look at target
-
Scanning (or ataxic) speech: slow, effortful speech with difficulty articulating
- lesion of lateral hemispheres
- **Hypotonia of ipsilateral limb: **b/c cerebellum influences corticospinal tracts
- pt falls to weak side (ipsilateral to lesion)
-
Impaired VOR suppression:
- L VOR activated (i.e. head moving left) ⇒ moves eyes to the right
- if you want to move head to L and eyes to L ⇒ need to suppress VOR
- done by the L cerebellum (L flocculonodular)
- L cerebellar lesion ⇒ no L VOR suppression ⇒ **cannot track movements moving R to L **
Lateral Hemispheres:
- Function:
- Motor pathway influenced:
- Deficit if Lesioned:
- **Function: **Motor planning for extremities
- Motor pathway influenced: LCST
- **Deficit if lesioned: **Appendicular ataxia
Intermediate hemispheres:
- Function:
- Motor pathway influenced:
- Deficit if Lesioned:
- **Function: **Distal limb coordination
- **Motor pathway influenced: **LCST, rubrospinal tract
- **Deficit if lesioned: **Appendicular ataxia
- **Vermis **
- Function:
- Motor pathway influenced:
- Deficit if Lesioned:
-
Flocculonodular lobe
- Function:
- Motor pathway influenced:
- Deficit if Lesioned:
- **Vermis **
- Function: Proximal limb & trunk coordination
- Motor pathway influenced: VCST, reticulospinal tract, vestibulospinal tract
- Deficit if Lesioned: Truncal ataxia
-
Flocculonodular lobe
- Function: Balance & vestibuloocular reflexes
- Motor pathway influenced: Medial longitudinal fasciculus
- Deficit if Lesioned: Nystagmus/slow saccades
Differential diagnosis for cerebellar dysfunction:
-
Vestibular dysfunction
- also causes vertigo, difficulty walking, N/V, nystagmus
- usually no dysmetria or ataxia on finger to nose or heel to shin
-
Corticospinal tract dysfunction
- also causes hypotonia & weakness
- can be mistaken for ataxia
-
Impaired proprioception
- these pts have a sensory ataxia
- Ex: proprioceptive loss in feet makes walking difficult
Acute causes for cerebellar dysfunctions:
- Cerebellar stroke (ischemic or hemorrhagic)
- Alcohol intoxication
- Drug overdose (eg. phenytoin)
- Multiple sclerosis
Chronic causes for cerebellar dysfunctions:
- Essential tremor
- Spinocerebellar ataxia
- Tumor (eg. astrocytoma)
- Chronic alcoholism
What can cause a cerebellar stroke?
Pathogenesis:
- main arteries supplying blood: SCA, PICA, AICA
- diseased due to atherosclerosis
- penetrating arteries from the main arteries undergo arteriolosclerosis ⇒ blood flow compromised ⇒ ischemic stroke
- from chronic HTN & other vascular risk factors (diabetes, smoking, high cholesterol)
- severe spike in blood pressure causes brittle vessel to rupture ⇒ hemorrhagic stroke
What are some clinical signs & symptoms you expect to see from a cerebellar stroke? How would you localize them?
-
Sudden/acute onset
- within seconds to minutes
- improves over weeks
-
Symptoms
- inability to walk and frequent falls, nausea, vomiting, vertigo
-
Signs
- dysmetria of ipsilateral arm/leg on finger-to-nose & heel-to-shin
- mild ipsilateral dysdiadochokinesia
- mild dysarthria
- horizontal & vertical nystagmus
-
Localization
- ipsilateral cerebellar hemisphere (lateral & flocculonodular lobes) & vermis
-
Other clues for diagnosis: vascular risk factors
- HTN, smoking, diabetes, high cholesterol
How can you differentiate between chronic and acute alcohol intoxication affecting the cerebellum?
One of the most common causes of ataxia
-
Acute symptoms:
- inability to walk with frequent falls
- no ‘checking’ of loss of balance
- slurred speech
- caused by cerebellar neuronal dysfunction
-
Chronic symptoms:
- ataxia with walking/maintaining balance
- difficulty with finger dexterity
- caused by Purkinje cell destruction & subsequent atrophy of vermis
-
Signs:
- difficulty walking/tandem gait, dysarthria, dysmetria of limbs, nystagmus
-
Localization:
- cerebellar vermis
What would you expect to see with an essential tremor? How is it localized?
Most common movement disorder
-
Usually symmetric, bilateral, postural or action tremor that is persistent & visible:
- no other cause found
- usually **autosomal dominant **
- involves arms/hands, voice, head
- chronic neurodegenerative disorder
- gradual loss of Purkinje cells
-
Signs:
- dysmetria, ataxic gait, head titubation
-
Localization:
- cerebellar hemispheres & vermis
Cerebellar ataxia:
- Group of autosomal dominant ataxic disorders
- degeneration of afferent & efferent cerebellar pathways
- destruction of Purkinje cells
- CAG triplet repeat expansion at different genetic loci
- Slowly progressive ataxia of limbs/trunk, scanning speech, slowed saccades
- Profound cerebellar atrophy
- Higher morbidity & mortality than essential tremor
-
Localization:
- entire cerebellum
Astrocytoma:
Most common childhood primary brain tumor
- low grade tumor composed of astrocytes
-
Localization:
- tumor usually grows in cerebellar hemisphere
-
Slowly progressive ipsilateral:
- limb/truncal ataxia, scanning speech, nystagmus due to tumor compressing on adjacent cerebellar parenchyma
-
Signs of increased intracranial pressure
- morning headaches, blurred vision, may culminate in nausea/vomiting, difficulty concentrating in school
- ↑ICP occurs because of any lesion that takes up space in a closed calvarium
What is multiple sclerosis?
-
autoimmune/inflammatory disorder affecting CNS white matter
- Predilection for young (25-40’s), white females
- Each lesion is referred to as a ‘plaque’
Which regions of white matter are attacked in a multiple sclerosis patient?
Regions of CNS that are attacked:
- **Optic nerves **⇒ causes sudden (over 1 day or so) vision loss
- usually cloudy, hazy, blurry that improves over weeks
- no double vision
-
Cerebral white matter regions
- all tracts descending/ascending to cortex
-
Cerebellar white matter
- especially the middle cerebellar peduncle
-
Medial longitudinal fasciculus
- mediates eye movements
- lesion causes internuclear ophthalmoplegia
- **Spinal cord **⇒ complete or incomplete spinal cord lesion in transverse section affecting ascending/descending tracts
- called a transverse myelitis