Pituitary tumor apoplexy is an uncommon event heralded by abrupt onset of severe headache, restriction of visual fields, deterioration of visual acuity, and weakness of ocular motility frequently coupled with clinical indications of decreased endocrine function. Hemorrhage into or necrosis of a preexisting sellar mass, usually a pituitary macroadenoma, produces an expansion of sellar contents. Compression of adjacent structures elicits the variable expression of symptoms referable to displacement of the optic nerves and chiasm and impingement of the third, fourth, and sixth cranial nerves. Damage to or destruction of the anterior pituitary leads to multiple acute and/or chronic hormone deficiencies in many patients. Medical management may be used in rare cases in which the signs and symptoms are mild and restricted to meningismus or ophthalmoplegia deemed to be stable. In patients with visual or oculomotor lability or an altered level of consciousness, expeditious surgical decompression, accomplished most commonly through a transsphenoidal approach, should be performed to save life and vision and to optimize the chance of regaining or maintaining pituitary function.

Though a pastime rarely considered rough or dangerous, sledding is not risk-free. The presentation of several serious injuries to Rainbow Babies and Children’s Hospital in Cleveland, Ohio, led us to examine our emergency department and admitting records to determine the incidence of neurological injury among children involved in sledding accidents. We discovered 24 children who had sustained brain or spine injuries as sequelae to sledding mishaps during a 5-year period. The ages ranged from 3 months to 15 years. Injuries included multiple skull fractures, 2 epidural hematomas, 1 subdural hematoma, 1 odontoid fracture and 1 anoxic brain injury. There was 1 death. Twenty-one of 24 patients incurred their injuries by colliding with fixed objects. Both improvised crafts and models intended for sledding were involved in the injuries. Only 3 sleds possessed steering capability. Eight of the 9 children who sustained a serious neurosurgical injury were supervised by an adult. Only 2 children had received instruction before sledding. The lack of awareness of the potential for injury together with the dearth of instruction and lack of control over a vehicle dashing down a hill studded with obstacles can change a carefree pastime into a hazardous activity.

✓ Two children who were 13 months and 3 years old and who had suffered traumatic atlantooccipital dislocation were each treated by being placed in a halo orthosis for 10 weeks. Because of a continued loss of reduction due to the poor fit of the halo vest, a dual-strap augmentation was developed. This strap augmentation allowed consistent reduction to be maintained. Both children were therefore successfully treated nonsurgically with a halo vest. One child remained neurologically intact and the other had improvement in motor strength. There were no complications from the use of strap augmentation for halo vest fixation.

Hypertension-induced encephalopathy is a recognized pathological process commonly focused in the parietal and occipital lobes of the cerebral hemispheres. The parenchyma of the posterior fossa is infrequently involved. The authors report on two cases of isolated edema of the cerebellar hemispheres, which occurred in the setting of hypertensive crisis and led to complete obstruction of or significant impingement on the fourth ventricle and potentially lethal hydrocephalus. To the best of the authors' knowledge, these are the first reported cases of hypertensive encephalopathy centered in the posterior fossa. Two patients presented with profound decreases in neurological status subsequent to development of malignant hypertension. Imaging studies revealed diffusely edematous cerebellar hemispheres with effacement of the fourth ventricle, causing dilation of the lateral and third ventricles. Following emergency placement of external ventricular drains, control of systemic blood pressure was accomplished, and neurological functioning returned to baseline. Although neurological deterioration resolved swiftly following placement of ventricular catheters and administration of diuretic agents, systemic blood pressure did not fluctuate with the release of cerebrospinal fluid and resolution of increased intracranial pressure. Decrease in systemic blood pressure lagged well behind improvement in neurological status; the patients remained morbidly hypertensive until systemic blood pressure was controlled with multiple parenteral medications. The authors hypothesize that the development of hypertension beyond the limits of cerebral autoregulation led to breakdown of the blood-brain barrier in the cerebellum and development of posterior fossa edema secondary to the focal transudation of protein and fluid. Correction of the elevated blood pressure led to amelioration of cerebellar edema. In the appropriate clinical setting, hypertension as the inciting cause of cerebellar encephalopathy should be considered.