After reviewing the literature, a personal series of 10 adult patients with cerebellar infarction diagnosed by CT scan is described. The clinical picture in young adult men is characterized by rapid onset of headache, vomiting, vertigo, ataxia and blurred vision. After this sudden onset the patients may present a stable course or a rapid or delayed onset of brain stem compression, revealed by impairment of consciousness. CT scan is the diagnostic method of choice. The correlation between angiographic and CT localization of the infarction is not good. For therapy the following policy is suggested: in alert and clinically stable patients: medical treatment (mannitol, glycerol, dexamethason), ICP and serial CT monitoring; in alert patients with hydrocephalus or mass effect: medical treatment and monitoring as mentioned before; ventricular drainage if ICP surpasses 350 mm H2O; in patients with impaired consciousness and hydrocephalus or mass effect: immediate ventricular drainage. If it is not followed by prompt improvement of the level of consciousness, an emergency suboccipital craniectomy with removal of the infarcted tissue should be done.
Activation of the Na+/H+ antiport mechanism was studied in human neutrophils by monitoring intracellular pH with a carboxyfluorescein derivative. N-formyl-methionyl-leucyl-phenylalanine (FMLP) and phospholipase C (PLC) induced biphasic pH changes. Amiloride, which inhibits the antiport, completely blocked alkalinization but enhanced acidification. Polymyxin B, which inhibits protein kinase C, only blocked alkalinization. Activation with phorbol 12-myristate 13-acetate (PMA) led to alkalinization only; this was inhibited by amiloride or polymyxin B. Thus, during polymorphonuclear leukocyte (PMN) activation, intracellular alkalinization appears to be mediated by an amiloride-sensitive Na+/H+ antiport. Antiport activity can also be blocked indirectly by inhibition of protein kinase C activity. Early intracellular acidification does not appear to require kinase activity but is observed when phospholipids are remodeled with PLC. The antiport was also activatable by hypertonic buffered media. This response did not appear to be mediated by protein kinase C because it was unaffected by polymyxin B. Finally, superoxide generation was investigated. It is affected by, but not soley controlled by, either antiport or protein kinase C activity.
Diagnostic work-up and management of intracranial arachnoid cysts are still controversial. The authors have standardized a therapeutic protocol based on the information derived from CSF contrast flow studies. The report concerns 16 cases of intracranial arachnoid cysts treated according to their protocol.
Analysing 12 cases of cavernous sinus meningiomas the authors conclude that: the clinical history is characteristic; CT scan has proved to be more sensitive than carotid angiography in detecting small lesions. However in large lesions the vascular supply pattern is the only feature that exactly identifies the site of the lesion. Both angiography and CT scan allow a near definitive diagnosis of meningioma; because of their location it is almost always impossible to remove these tumours completely. Actually the best treatment is a piecemeal subtotal microsurgical removal via a subtemporal approach. Radiotherapy is indicated for partially resected lesions. On the basis of the revision of the anatomy of this region and looking forward to a widespread use of the Cavitron in neurosurgery, a more radical approach to this lesion is foreseen.
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