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TonsilsWith increase in intracranial pressure due to hemmorhage, can herniatethrough the Foramen Magnum and compress the Medulla, which is acardiopulmonary 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 inferiorpeduncles).- Posterior lobe (cerebro-cerebellum): info from Cortico-ponto-cerebellar (Middle peduncle) andOlivo-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.
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 (inferiorcolliculus) levels, after which most of the fibers ascend to the red nucleus(rostral midbrain) and dorsal thalamus (ventral lateral and ventral anteriornuclei).
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.
CirculationThe PICA arises from the vertebral a. and courses transversely anddownward along the medulla. The common trunk gives rise to themedial 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