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.
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
