Background: The nodulus lies in the midline cerebellum between the inferior medullary velum and the uvula, and constitutes the vestibulocerebellum along with the flocculus and ventral uvula. The nodulus receives afferent inputs from the vestibular system, and controls eye movements and adjusts the posture to gravity. Previously, patients with nodular infarction presented with isolated vertigo and moderate to severe imbalance. However, There has been little report of isolated hypoperfusion rather than infarction.

The aim of this study was to evaluate the effect of motor point block by botulinum toxin type A on spasticity and the change of motor function in spastic diplegic cerebral palsy children. Ten children with spastic diplegic cerebral palsy were recruited for this study. Pre-injection and 6 months follow-up evaluations including Modified Ashworth Scale, popliteal angle and passive range of motion of ankle joint and Gross Motor Function Measure were done for the measurement of spasticity, musculotendinous shortening and functional status. We injected botulinum toxin type A (Botox (R), Allergan Inc., USA) into gastrocnemius muscle. All the patients were treated with neurodevelopmental treatment, range of motion exercise, stretching exercise, and functional electrical stimulation. The motor point block by botulinum toxin type A showed the improvement in spasticity and functional status in children with spastic diplegic cerebral palsy.

Immobility in stroke patients increases the risk of thromboembolisin, and the pulmonary embolism following deep vein thrombosis (DVT) may lead to life-threatening state. In stroke patients, DVT is 10 times more common in the involved extremities than in the uninvolved extremities. In nonambulatory stroke patients, DVT is five times more frequent than in patients who can walk more than 50 feet (4.6). We experienced a rare case of DVT and pulmonary thromboembolism in ambulatory stroke patient. Initial physical examination showed skin. temperature increase and limb girth increase with ankle dorsiflexor weakness. After confirm diagnosis, we performed inferior vena caval filter placement and anticoagulant therapy. The follow-up result was achieved satisfactorily.

The role of peripheral vestibular receptors in acute hypotension was investigated in anesthetized rats. In animals with intact labyrinths, acute hypotension induced by either i.v. infusion of sodium nitroprusside or hemorrhage produced excitation of electrical activity in two-thirds of type I neurons and inhibition in two-thirds of type II neurons recorded in the medial vestibular nuclei. In unilaterally labyrinthectomized animals, two-thirds of type I neurons ipsilateral to the lesion showed an inhibitory response, and two-thirds of contralateral type I neurons showed an excitatory response after the induction of acute hypotension. The response patterns of type II neurons were opposite to those of type I neurons. These results suggest that blood flow changes are detected by peripheral vestibular receptors, and that this might suggest a mechanism for control of blood pressure.

We used single photon emission computed tomography (SPECT) with technetium-99m hexamethylpropylene amine oxime (99mTc-HM-PAO) in 14 studies on 6 patients with delayed neurologic sequelae from carbon monoxide (CO) poisoning to determine whether any changes in cerebral blood flow could be correlated with clinical or computed tomographic evidence of delayed deficits. Among the six initial CT brain scans, two showed low density of both basal ganglia and two showed decreased density of the cerebral white matter. There was no correlation between the clinical outcome and the findings of the follow-up CT brain scans. Of the two SPECTS with 99mTc-HM-PAO performed during acute anoxic insult, one showed focal hypoperfusion which appeared 20 days prior to the onset of delayed neurologic sequelae after CO poisoning. Seven SPECTs in the six patients performing the delayed phase showed diffuse patched patterns of hypoperfusion which improved on follow-up images. There was good correlation between the clinical outcome and the findings of the 99mTc-HM-PAO SPECT. In preliminary conclusion, 9Tc-HM-PAO brain SPECT can be used for predicting or evaluating the outcome of delayed neurologic sequelae after CO poisoning. Cerebral vascular changes may be the possible cause of hypoperfusion in patients with CO poisoning.