1. The Cerebellum
Clinical Examination

2. Objectives
To be knowledgeable about the aspects of the neurological examination pertaining to the cerebellum
To understand how to localize lesions within the cerebellum on the basis of clinical findings
To develop a framework about the presentation of nervous system illness

3. Cerebellar Examination
Midline cerebellar function
Cerebellar hemispheric function

4. Clinical localization in the cerebellum
For purpose of localization, cerebellum can be viewed as a saggitally-oriented structure containing 3 zones on each side:
Midline
Intermediate
Lateral

5. Midline zone
Consists of the anterior and posterior parts of the vermis, fastigial nucleus and associated input and output projections
concerned with posture, locomotion, position of head relative to trunk, control of EOM’s
Cerebellar signs resulting from midline cerebellar disease
disorders of stance/gait, truncal postural disturbances, rotated postures of the head, disturbances of eye movements

6. Intermediate zone
Consists of paravermal region of cerebellum and interposed nuclei (emboliform, globose)
concerned with control of velocity, force and pattern of muscle activity
Clinical disorders related to disease of this zone not clearly delineated

7. Lateral zone cerebellar hemisphere and dentate nucleus on each side
concerned with the planning of movement in connection with neurons in the Rolandic region of the cerebral cortex (fine, skilled)
Lesions result in abnormalities of skilled voluntary movements: hypotonia, dysarthria, dysmetria, dysdiadochokinesia, excessive rebound, impaired check, kinetic and static tremors, past-pointing

8. Midline Cerebellar Function
Observation
Posture, head position
Gait
Eye movements
Rhomberg Test
Tests of gait- tandem, toe + heel walking, walking backward
Hop on each foot

9. Cerebellar Hemispheric Function
Finger-to-nose test
Rapidly alternating movements
Heel-to-shin test

10. Cardinal Features of Cerebellar Dysfunction
Hypotonia
Ataxia
Dysarthria
Tremor
Ocular Motor Dysfunction

11. Classic signs of cerebellar damage
Depending on extent, an individual may have one symptom or a combination
In all cases, symptoms from unilateral damage appear on the side ipsilateral to the injury
Ascending spinocerebellar pathways are uncrossed and descending corticoopontocerebellar fibers are crossed; thus motor deficits from cerebellar damage are ipsilateral to the lesion whereas motor deficits from damage to motor areas of the cerebral cortex are contralateral to the lesion

12. postural instability
delayed initiation and termination of motor actions
inability to perform continuous, repetitive movements
errors in smoothness and direction of a movement
lack of coordingation or synergy of movement, especially complex movements
lack of motor plasticity or learning

14. Hypotonia usually accompanies acute hemispheric lesions
Interestingly less often seen in chronic lesions
Ispilateral to the side of a cerebellar lesion
More noticeable in upper limbs and proximal muscles
(beware of increased tone with a cerebellar lesion—may reflect compression of brainstem/corticospinal tracts)!!
Probably due to  fusimotor activity, secondary to cerebellar injury (especially the dentate), with a  response to stretch in muscle spindle afferents

15. Ataxia
Defective timing of sequential contraction of agonist /antagonist muscles
Results in a disturbance in smooth performance of voluntary acts (errors in rate, range, force, duration)
Without cerebellar modulation, skilled movements originating in cerebral cortex are inaccurate, poorly controlled
May affect limbs, trunk, gait (depends on part of cerebellum involved)
usually persists despite visual cues (unlike ataxia due to posterior column disease affecting the spinal cord)

16. Asynergia= lack of synergy of various muscles while performing complex movements ( movements are broken up into isolated, successive parts-- decomposition of movement)
Dysmetria= abnormal excursions in movement
Dysdiadochokinesia= impaired performance of rapidly alternating movement
Past-pointing
Excessive rebound when an opposed motion is suddenly released

17. Cerebellar Dysarthria
Abnormalities in articulation and prosody (together or independent)
“scanning”, “slurring”, “staccato”, “explosive”, “hesitant”, “garbled”
May result from a generalized hypotonia (disorder of muscle spindle function)
Hemisphere lesions are associated with speech disorders more often than vermal lesions

18. Posterior Fossa Syndrome
Acute, bilateral injury to both cerebellar paravermal regions, including the dentate, may lead to transient muteness
Seen in up to 20% of posterior fossa tumor resections in children (“cerebellar mutism syndrome”)
May last for several months, with severe dysarthria after return of speech

19. Cerebellar affective disorder
Impaired executive function, personality, emotional and behavioral changes
Can be seen as part of the mutism syndrome

20. Tremor rhythmic, alternating, or oscillatory movements
can be a normal exaggeration of movement, a primary disorder, or a symptom of a cerebellar disorder or Parkinson's disease
Diagnosis is usually clinical
Treatment varies by etiology

21. Tremor- Framework/ Categories
Trigger: Resting or action-- includes postural tremors and intention tremors (triggered by a purposeful movement)
Cause: Physiologic, essential, parkinsonism, or secondary to drugs or other disorders (including cerebellar disorders)
Amplitude of oscillation: Fine or coarse

22. Tremor- General features
Resting tremor : maximal at rest, decreases with activity; usually a symptom of Parkinson's disease
Postural tremor : maximal with limb in a fixed position against gravity; gradual onset suggests physiologic or essential tremor; acute onset suggests toxic / metabolic disorder
Intention tremor : maximal during movement toward a target (finger-to-nose testing) ; suggests a cerebellar disorder but may result from other diseases (MS, Wilson’s)

23. Tremor- Physiologic
Physiologic tremor: present normally -- usually so slight that it is noticeable only under certain conditions ; predominantly postural, fine and rapid (8 to 13 Hz)
most visible when hands are outstretched
Amplitude may be increased (enhanced) by
Anxiety
Stress
Fatigue
Metabolic disorders (eg, hyperadrenergic states such as alcohol or drug withdrawal or thyrotoxicosis)
Certain drugs (eg, caffeine, other phosphodiesterase inhibitors, β-adrenergic agonists, corticosteroids)
Alcohol and other sedatives usually suppress it

24. Tremor- Essential tremor
benign hereditary tremor, senile tremor
coarse or fine, medium frequency (4 to 8 Hz); min or absent at rest
usually bilateral
can affect the hands, head, voice
tends to increase with aging
In 50% of patients, inheritance is autosomal dominant
may be enhanced by any factor that enhances physiologic tremor (not always required)
Some consider essential tremor a variant of physiologic tremor

25. Tremor- Cerebellar Disease
an intention tremor; no effective drug available; physical measures (eg, weighting the affected limbs or teaching patients to brace the proximal limb during activity) sometimes helps
Asterixis: not a tremor; muscle tone lapses when wrist extension is attempted, resulting in repetitive, nonrhythmic, non-oscillatory wrist flexion; a sign of chronic renal or liver failure (differentiate from tremor)
3-5 Hz
Usually bilateral
Can be a sign of hepatic encephalopathy (inability of liver to metabolize ammonia to urea)
Patient is usually drowsy or stuporous

27. Oculomotor dysfunction
Nystagmus frequently seen in cerebellar disorders
Gaze-evoked nystagmus, upbeat nystagmus, rebound nystagmus, opticokinetic nystagmus may all be seen in midline cerebellar lesions
Other ocular lesions seen include opsoclonus, skew deviation, ocular bobbing
Most of the disorders giving rise to these affect brainstem structures, too: cerebellar role in their onset not well-defined
Overall, most “cerebellar” eye signs cannot be localized to specific areas of the cerebellum

28. Features to Examine

29. Gait
Ataxia
In cerebellar disease, the walk is staggering/lurching/wavering
Not benefitted by patient’s view of his surroundings
Lesion in mid-cerebellum: movements are in all directions
Lesion in lateral cerebellum: staggering/falling are toward the side of the lesion
Somewhat steadied by standing or walking on a wide base
(ataxia secondary to vestibular disease may appear similar)

30. Gait Gait have patient walk across room under observation
Watch for normal posture + coordinated arm movements
ask patient to walk heel-to-toe across room, walk on toes to test for plantar flexion weakness, and on heels to test for dorsiflexion weakness
Abnormalities in heel to toe walking: ethanol intoxication, weakness, poor position sense, vertigo -- exclude before poor balance is attributed to a cerebellar lesion
elderly patients have difficulty with tandem gait (heel to toe walking) -- general neuronal loss impairs combination of position sense, strength, coordination

32. blumentandemgait

33. blumenTipToeGaitandHopping

34. impairedTandemGait.flv

35. CerebGait.flv

36. Testing of Station (equilibratory coordination)
Position of Feet
Ataxia from spinocerebellar disease is less when the patient stands on a broad base (feet widely apart)
Eyes open or closed
Cerebellar ataxia is not improved by visual orientation; ataxia from posterior column disease (disordered proprioception) is worsened with the eyes closed
Direction of Falling
Disease of lateral lobe of cerebellum causes falling to ispilateral side
Lesions of midline/vermis cause indiscriminate falling, depending on initial stance of the patient

38. blumenRhombergTest

39. Diadochokinesia
Normal coordination includes ability to arrest one motor impulse and substitute the opposite
Loss of this = dysdiadochokinesia
Characteristic of cerebellar disease
Many simple tests for this:
Alternating movements (pronate and supinate forearm + hand quickly): in cerebellar disease, movements overshoot, undershoot be irregular or inaccurate
Rapidly tap fingers on table
Open and close fists
Stewart-Holmes rebound sign

40. blumenFineFingerTap.rm

41. blumenRapidlyAltMovements.rm

42. dysdiadochokinesiamovie

43. Dysmetria Finger to nose test Heel to Shin test
With eyes open, have pt partially extend elbow and rapidly bring tip of index finger in a wide arc to tip of his nose
In cerebellar disease, the action may have an intention tremor
With eyes closed, sense of position in the shoulder and elbow is tested
Heel to Shin test
Pt places one heel on opposite knee and slides heel down the tibia with foot dorsiflexed
Movement should be performed accurately
In cerebellar disease, the arc of the movement is jerky/wavering
The slide down the shin has an action tremor

46. blumenFingerNoseTest.rm

47. Coordinationwithpuppets.mp4

48. Cerebellarintentiontremor.mp4

49. Heelshintest.mp4

50. Heelshinabnormal.mp4

51. Checkreflexmovie.mp4

52. Checkreflexabnorvideo.mp4

53. Spasticspeech.flv

54. Cerebellar Syndromes
In general, precise clinical localization is difficult in the cerebellum
Some syndromes can be classified anatomically:
Rostral vermis syndrome (anterior lobe)
Caudal vermis syndrome (flocculonodular, posterior lobe)
Hemispheric syndrome (posterior lobe, variably anterior too)
Pancerebellar syndrome

55. Cerebellar Syndromes- rostral vermis
Wide-based stance and gait
Ataxia of gait, proportionally little ataxia on heel-shin with pt lying down
Normal or slightly impaired arm cooordination
Infrequent hypotonia, nystagmus, dysarthria
alcoholics (restricted form of cerebellar cortical degeneration)

56. Cerebellar Syndromes- caudal vermis
Axial dysequilibrium, staggering gait
Little or no limb ataxia
Sometimes spontaneous nystagmus
Rotated postures of head
Seen in diseases that damage the flocculonodular lobe (esp medulloblastoma in children)—as tumor grows, a hemispheric cerebellar syndrome may be superimposed
Need to also consider other signs of  ICP (obstruction of CSF)

57. Cerebellar Syndromes- hemispheric
Incoordination of ipsilateral limb movements
More noticeable with fine motor skills
Incoordination affects most noticeably muscles involved in speech and finger movements
Etiologies include infarcts, neoplasms, abscesses

58. Cerebellar Syndromes- pancerebellar
Combination of all the other syndromes
Bilateral signs of cerebellar dysfunction involving trunk, limbs, cranial musculature
Etiologies usually infectious/parainfectious processes, hypoglycemia, paraneoplastic disorders, toxic-metabolic disorders

59. Cerebellum: 4th ventricle
The fourth ventricle is ventral to the cerebellum
Anatomically and clinically important
Mass lesions located in the cerebellum, or swelling of the cerebellum (eg. Edema from an infarct) can compress the 4th ventricle and result in obstructive hydrocephalus

60. My patient: Tamra 15 yr, R-handed ♀ previously healthy from Woodstock
3 wk progressive gait unsteadiness, ataxia, dizziness
6 wk H/A, holocephalic, worse when coughing or sneezing, 5/10, takes Advil
20 lbs weight loss over 3 wks
admitted to Woodstock General
Dx Mono, D/C home,next day H/A 10/10

61. HR 76, RR 16, BP 135/76 mmHg, T-35.9
Awake, alert, oriented x3, speech OK
Pupils 4mm bilat., brisk, full EOM
Nystagmus up & lateral gaze
Bilateral papilledema
Symetrical facial features
N bulk & tone, full power arms & legs 5/5
Reflexes symmetric, Plantars equivocal
Difficulty pointing bilat., dysmetric, past pointing, heel to shin good
Broad based gait

65. Cerebellar dysarthria video clip

66. Nystagmus video clip

67. Finger to nose- Tamra

68. Heel to shin- Tamra

69. Lower extremity ataxia- Tamra

70. Upper extremity ataxia- Tamra