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Cerebellum

    Thomas Ahn, MD
Department of Neurology
Loyola University Medical
       June 2012
Perspective
              -found in the posterior cranial
              fossa.

              - forms a roof over the 4th
              ventricle.
Embryology




- Evolved out of Vestibular nuclei in the pons and medulla.
Divisions
Simplified Divisions
Tonsils




The tonsils in the posterior lobe.
Tonsils




With increase in intracranial pressure due to hemmorhage, can herniate
through the Foramen Magnum and compress the Medulla, which is a
cardiopulmonary control center, get palsy, and eventually death.
Function
• Gets execution plan from the Motor Cortex
  and actual streaming info from the senses.
• Through comparisons of external & internal
  feedback signals, the cerebellum is able to:
  1. correct ongoing movements when they
  deviate from the intended course.
  2. modify motor programs in the
  supplementary motor cortex so that future
  movements attain their goals, ie. motor
  learning.
- FlocculoNodular lobe (vestibule-cerebellum): oldest, axis proprioceptive info from eye, head, trunk
(via Inferior peduncles).
- Anterior lobe (spino-cerebellum): proprioception from limbs and trunk (via Superior and inferior
peduncles).
- Posterior lobe (cerebro-cerebellum): info from Cortico-ponto-cerebellar (Middle peduncle) and
Olivo-cerebellar pathways.
Inputs
• The cerebellum receives its MAJOR input from the cortex
  which is relayed through the pons.
  The corticopontine tract originates primarily from:
  1. premotor cortex (area 6)
  2. motor cortex (area 4)
  3. somatosensory cortex (areas 3, 1, 2)
  4. higher order somatosensory cortex (area 5)

  Pontocerebellar fibers cross in the pons & reach the
  cerebellum via the middle cerebellar peduncle.
  Therefore, Efferents from pontine nuclei form mossy fibers
  terminating primarily in the contralateral cerebrocerebellum
  due to the crossing they make.
Output from the 4 deep Nuclei
3 Peduncles

          Peduncles connects Cerebellum
          to Pons:
          -Superior (rostral) peduncle:
          Efferent: brachium
          conjunctivum (decussation).
          -Afferent: Spino-cerebellum
          (proprioceptive info from
          neck, trunk, ext.)

          -Middle peduncle:
          (largest), exclusively Ponto-
          Cerebellar path.

          -Inferior peduncle: Spinco-
          cerebellar tracts, Medulla
          (Reticular formation), Vestibular
          nuclei.
Decussation
                                                             A lesion of the RIGHT
                                                             superior cerebellar
                                                             peduncle CAUDAL TO
                                                             (before) the
                                                             decussation ->
                                                             ipsilateral lesion.

                                                             A lesion ROSTRAL to
                                                             the decussation of the
                                                             superior cerebellar
                                                             peduncle ->
                                                             CONTRALATERAL
                                                             motor deficits.


The superior cerebellar peduncle crosses at caudal midbrain (inferior
colliculus) levels, after which most of the fibers ascend to the red nucleus
(rostral midbrain) and dorsal thalamus (ventral lateral and ventral anterior
nuclei).
Symptoms due to lesions of the cerebellar cortex
•   Ataxia, Tremor (intention & positional), Hypotonia, Asthenia
•   difficult to separate from brainstem lesions of cerebellar pathways.
•   Ataxia: broad-based stance and gait, Tandem walk is most sensitive.
•   Tremor: in volitional muscle contraction.
     – Positional = postural = action = static (hands stretched out “stop” sign in volitional muscle
       contraction). Unsteady oscillation of Head and trunk = Titubation.
     – Intentional = end-point = terminal = kinetic (finger-to-nose).
     – Unlike Parkinson’s tremor (resting, not in action).
•   Dysmetria: finger-to-nose.
•   Dysdiadokokinesia: rapid-alternating move.
•   dysarthria : scanning speech from low to high volume at wrong syllables. Children
    less affected but may show period of Mutism after surg.
•   Nystagmus: volitional gaze evoked, slow component toward a null or resting point.
    dysmetric jerky Saccades, slow initiation and skew deviation.
•   Hypotonia: floppy joints and muscles.
•   Asthenia: weak, fatigue, reluctance to move.
•   Personality changes: Silly, illogical, disinhibited, inapproapriate.
    lateral synd (hemisphere): ipislateral UE ataxia and incoordination.
•   midline synd (Vermis): truncal unsteadiness and LE ataxia.
Circulation




The PICA arises from the vertebral a. and courses transversely and
downward along the medulla. The common trunk gives rise to the
medial branch (medPICA) and the lateral branch (latPICA).
• The PICA infarctions: most common Cerebellar infarct, but
  only ~2% of all ischemic strokes.
• medPICA territory infarct -> vestibular
  signs, dizziness, vertigo, truncal ataxia, axial
  lateropulsion, and nystagmus.
   – Because the medial branch of PICA participates in the blood
     supply of the medulla in its rostral region, up to 30% of the PICA
     distribution infarctions also involve the lateral medulla, resulting
     in ipsilateral Horner syndrome, decreased sensation in the
     ipsilateral trigeminal distribution, and contralateral hypesthesia
     to pain and temperature in limbs and trunk.
   – By contrast, 10% of patients with a pure lateral medullary infarct
     have an associated PICA distribution cerebellar infarction.
• latPICA infarct -> dizziness, vertigo, and dysmetria without
  truncal ataxia or axial lateropulsion.
• A pseudotumor occurs in 10-25% of cases of
  cerebellar infarction.
• Commonly in PICA and SCA infarctions.
• factors: >1/3 of the cerebellar hemisphere;
  vascular occlusion at the origin of the SCA and
  PICA with no collateral flow; vasogenic edema
  secondary to reperfusion; and a massive SCA
  distribution infarct with a location that favors
  the development of hydrocephalus such as
  the vermis
• Of patients with cerebellar hemorrhage, 10-
  20% present with AMS.
• If noncomatose on admission deterioration
  can be predicted. Higher risk are SBP
  >200, absent corneal reflexes, impaired
  oculocephalic responses, vermian hemorrhage
  or hemispheric hemorrhage extending to the
  vermis, and patients with early hydrocephalus.
CASE!!
• A 46 M in a motorcycle accident w/o helmet.
  Following the fall, transient LOC and vomitted
  x2-3. No seizures or bleeding from the
  ear, nose, or mouth. Gen Exam nl. He was
  drowsy but arousable. The GCS was E3V5M6.
  The pupils equal and reactive to light. CN
  exam was nl. No focal motor deficits. The
  initial CT scan (performed 6 h after injury) was
  nl. X-ray C-spine was normal.
• Follow-up CT scan showed a large low-density area
  occupying the most of the left cerebellum. The fourth
  ventricle was shifted to the right, and the third and fourth
  ventricles were dilated. These features were suggestive of
  cerebellar infarction and obstructive hydrocephalus.
• In view of the rapid neurological deterioration and the
  presence of a large cerebellar infarct, the patient
  underwent an emergency left paramedian suboccipital
  craniectomy and decompression of the infarcted
  cerebellum.
• He made an uneventful recovery. Follow-up CT scan
  showed opening up of the fourth ventricle and reduction in
  the size of the ventricles.
• Follow-up color Doppler study of the neck
  vessels, electrocardiogram, and echocardiography were all
  normal.
• Pt was managed conservatively. the next day his
  sensorium improved. He, however, complained of
  headache. Forty-eight hours after the injury, the
  patient became progressively drowsy and had
  multiple episodes of vomiting. The GCS was
  E2V4M5. The pupils were equal and reacting to
  light. The full range of ocular movements was
  present and he was moving all four limbs.
• What do you think is happening?
• What would you do next?
(a)CT scan showing right cerebellar infarction
(b)follow-up CT scan showing infarction
(c)postoperative scan showing the opened up ventricle
       From:
       J Emerg Trauma Shock. 2010 Apr-Jun; 3(2): 207–209.
       doi: 10.4103/0974-2700.62102

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Cerebellum

  • 1. Cerebellum Thomas Ahn, MD Department of Neurology Loyola University Medical June 2012
  • 2. Perspective -found in the posterior cranial fossa. - forms a roof over the 4th ventricle.
  • 3. Embryology - Evolved out of Vestibular nuclei in the pons and medulla.
  • 6. Tonsils The tonsils in the posterior lobe.
  • 7. Tonsils With increase in intracranial pressure due to hemmorhage, can herniate through the Foramen Magnum and compress the Medulla, which is a cardiopulmonary control center, get palsy, and eventually death.
  • 8. Function • Gets execution plan from the Motor Cortex and actual streaming info from the senses. • Through comparisons of external & internal feedback signals, the cerebellum is able to: 1. correct ongoing movements when they deviate from the intended course. 2. modify motor programs in the supplementary motor cortex so that future movements attain their goals, ie. motor learning.
  • 9. - FlocculoNodular lobe (vestibule-cerebellum): oldest, axis proprioceptive info from eye, head, trunk (via Inferior peduncles). - Anterior lobe (spino-cerebellum): proprioception from limbs and trunk (via Superior and inferior peduncles). - Posterior lobe (cerebro-cerebellum): info from Cortico-ponto-cerebellar (Middle peduncle) and Olivo-cerebellar pathways.
  • 10. Inputs • The cerebellum receives its MAJOR input from the cortex which is relayed through the pons. The corticopontine tract originates primarily from: 1. premotor cortex (area 6) 2. motor cortex (area 4) 3. somatosensory cortex (areas 3, 1, 2) 4. higher order somatosensory cortex (area 5) Pontocerebellar fibers cross in the pons & reach the cerebellum via the middle cerebellar peduncle. Therefore, Efferents from pontine nuclei form mossy fibers terminating primarily in the contralateral cerebrocerebellum due to the crossing they make.
  • 11. Output from the 4 deep Nuclei
  • 12.
  • 13. 3 Peduncles Peduncles connects Cerebellum to Pons: -Superior (rostral) peduncle: Efferent: brachium conjunctivum (decussation). -Afferent: Spino-cerebellum (proprioceptive info from neck, trunk, ext.) -Middle peduncle: (largest), exclusively Ponto- Cerebellar path. -Inferior peduncle: Spinco- cerebellar tracts, Medulla (Reticular formation), Vestibular nuclei.
  • 14. Decussation A lesion of the RIGHT superior cerebellar peduncle CAUDAL TO (before) the decussation -> ipsilateral lesion. A lesion ROSTRAL to the decussation of the superior cerebellar peduncle -> CONTRALATERAL motor deficits. The superior cerebellar peduncle crosses at caudal midbrain (inferior colliculus) levels, after which most of the fibers ascend to the red nucleus (rostral midbrain) and dorsal thalamus (ventral lateral and ventral anterior nuclei).
  • 15.
  • 16. Symptoms due to lesions of the cerebellar cortex • Ataxia, Tremor (intention & positional), Hypotonia, Asthenia • difficult to separate from brainstem lesions of cerebellar pathways. • Ataxia: broad-based stance and gait, Tandem walk is most sensitive. • Tremor: in volitional muscle contraction. – Positional = postural = action = static (hands stretched out “stop” sign in volitional muscle contraction). Unsteady oscillation of Head and trunk = Titubation. – Intentional = end-point = terminal = kinetic (finger-to-nose). – Unlike Parkinson’s tremor (resting, not in action). • Dysmetria: finger-to-nose. • Dysdiadokokinesia: rapid-alternating move. • dysarthria : scanning speech from low to high volume at wrong syllables. Children less affected but may show period of Mutism after surg. • Nystagmus: volitional gaze evoked, slow component toward a null or resting point. dysmetric jerky Saccades, slow initiation and skew deviation. • Hypotonia: floppy joints and muscles. • Asthenia: weak, fatigue, reluctance to move. • Personality changes: Silly, illogical, disinhibited, inapproapriate. lateral synd (hemisphere): ipislateral UE ataxia and incoordination. • midline synd (Vermis): truncal unsteadiness and LE ataxia.
  • 17. Circulation The PICA arises from the vertebral a. and courses transversely and downward along the medulla. The common trunk gives rise to the medial branch (medPICA) and the lateral branch (latPICA).
  • 18.
  • 19. • The PICA infarctions: most common Cerebellar infarct, but only ~2% of all ischemic strokes. • medPICA territory infarct -> vestibular signs, dizziness, vertigo, truncal ataxia, axial lateropulsion, and nystagmus. – Because the medial branch of PICA participates in the blood supply of the medulla in its rostral region, up to 30% of the PICA distribution infarctions also involve the lateral medulla, resulting in ipsilateral Horner syndrome, decreased sensation in the ipsilateral trigeminal distribution, and contralateral hypesthesia to pain and temperature in limbs and trunk. – By contrast, 10% of patients with a pure lateral medullary infarct have an associated PICA distribution cerebellar infarction. • latPICA infarct -> dizziness, vertigo, and dysmetria without truncal ataxia or axial lateropulsion.
  • 20. • A pseudotumor occurs in 10-25% of cases of cerebellar infarction. • Commonly in PICA and SCA infarctions. • factors: >1/3 of the cerebellar hemisphere; vascular occlusion at the origin of the SCA and PICA with no collateral flow; vasogenic edema secondary to reperfusion; and a massive SCA distribution infarct with a location that favors the development of hydrocephalus such as the vermis
  • 21. • Of patients with cerebellar hemorrhage, 10- 20% present with AMS. • If noncomatose on admission deterioration can be predicted. Higher risk are SBP >200, absent corneal reflexes, impaired oculocephalic responses, vermian hemorrhage or hemispheric hemorrhage extending to the vermis, and patients with early hydrocephalus.
  • 22. CASE!! • A 46 M in a motorcycle accident w/o helmet. Following the fall, transient LOC and vomitted x2-3. No seizures or bleeding from the ear, nose, or mouth. Gen Exam nl. He was drowsy but arousable. The GCS was E3V5M6. The pupils equal and reactive to light. CN exam was nl. No focal motor deficits. The initial CT scan (performed 6 h after injury) was nl. X-ray C-spine was normal.
  • 23. • Follow-up CT scan showed a large low-density area occupying the most of the left cerebellum. The fourth ventricle was shifted to the right, and the third and fourth ventricles were dilated. These features were suggestive of cerebellar infarction and obstructive hydrocephalus. • In view of the rapid neurological deterioration and the presence of a large cerebellar infarct, the patient underwent an emergency left paramedian suboccipital craniectomy and decompression of the infarcted cerebellum. • He made an uneventful recovery. Follow-up CT scan showed opening up of the fourth ventricle and reduction in the size of the ventricles. • Follow-up color Doppler study of the neck vessels, electrocardiogram, and echocardiography were all normal.
  • 24. • Pt was managed conservatively. the next day his sensorium improved. He, however, complained of headache. Forty-eight hours after the injury, the patient became progressively drowsy and had multiple episodes of vomiting. The GCS was E2V4M5. The pupils were equal and reacting to light. The full range of ocular movements was present and he was moving all four limbs. • What do you think is happening? • What would you do next?
  • 25. (a)CT scan showing right cerebellar infarction (b)follow-up CT scan showing infarction (c)postoperative scan showing the opened up ventricle From: J Emerg Trauma Shock. 2010 Apr-Jun; 3(2): 207–209. doi: 10.4103/0974-2700.62102