Correction to: Subdural hemorrhage rebleeding in abused children: frequency, associations and clinical presentation.

The original article included a statement which is not fully accurate. This correction clarifies the original statement.

Subdural hemorrhage rebleeding in abused children: frequency, associations and clinical presentation.

BACKGROUND: Limited documentation exists about how frequently radiologically visible rebleeding occurs with abusive subdural hemorrhages (SDH). Likewise, little is known about rebleeding predispositions and associated symptoms. OBJECTIVE: To describe the frequency of subdural rebleeding after abusive head trauma (AHT), its predispositions and clinical presentation. MATERIALS AND METHODS: We evaluated children with SDHs from AHT who were reimaged within a year of their initial hospitalization, retrospectively reviewing clinical details and imaging. We used the available CT and MR images. We then performed simple descriptive and comparative statistics. RESULTS: Fifty-four of 85 reimaged children (63.5%) with AHT-SDH rebled. No child had new trauma, radiologic evidence of new parenchymal injury or acute neurologic symptoms from rebleeding. From the initial presentation, macrocephaly was associated with subsequent rebleeding. Greater subdural depth, macrocephaly, ventriculomegaly and brain atrophy at follow-up were associated with rebleeding. No other radiologic findings at initial presentation or follow-up predicted rebleeding risk, although pre-existing brain atrophy at initial admission and initial chronic SDHs barely missed significance. Impact injuries, retinal hemorrhages and clinical indices of initial injury severity were not associated with rebleeding. All rebleeding occurred within chronic SDHs; no new bridging vein rupture was identified. The mean time until rebleeding was recognized was 12 weeks; no child had rebleeding after 49 weeks. CONCLUSION: Subdural rebleeding is common and occurs in children who have brain atrophy, ventriculomegaly, macrocephaly and deep SDHs at rebleed. It usually occurs in the early months post-injury. All children with rebleeds were neurologically asymptomatic and lacked histories or clinical or radiologic findings of new trauma. Bleeds did not occur outside of chronic SDHs. We estimate the maximum predicted frequency of non-traumatic SDH rebleeding accompanied by acute neurological symptoms in children with a prior abusive SDH is 3.5%.

Posterior fossa tumors and their impact on sleep and ventilatory control: a clinical perspective.

The cerebellum, classically viewed as a motor structure of the brain, may play a role in respiration. Brainstem dysfunction has been implicated in sleep disordered breathing (SDB), but apnea after surgery of brain tumors in the posterior fossa, not involving the brainstem has been reported. We report four cases with posterior fossa tumors without brainstem invasion who suffered SDB after surgery diagnosed by polysomnography (PSG). Advanced MRI techniques with DTI were used to find correlations with SDB. Abnormal signals in the superior, middle and inferior cerebellar peduncles were seen in these patients with the most severe changes in the inferior peduncle. SDB may be under diagnosed in the setting of posterior fossa tumors without brainstem involvement. Damage to the cerebellar peduncles, especially the inferior cerebellar peduncle, without brainstem involvement, can cause significant disruption of respiration.

Epilepsy surgery after treatment of pediatric malignant brain tumors.

Epilepsy surgery is common in the face of benign brain tumors, but rarely for patients with a history of malignant brain tumors. Seizures are a common sequelae in survivors of malignant pediatric brain tumors. Medical management alone may not adequately treat epilepsy, including in this group. We report four cases of patients who previously underwent gross total resection, radiation therapy, and chemotherapy for successful treatment of malignant brain neoplasia, yet suffered from medically intractable seizures. All underwent surgery for treatment of epilepsy with extension of the original resection. Despite the aggressive primary treatment of the neoplasm, and the potential for diffuse cerebral insults, all benefited from focal surgical resection. Aggressive surgical management of intractable epilepsy can be considered in survivors of malignant brain tumors.

Cerebral blood flow and metabolism following decompressive craniectomy for control of increased intracranial pressure.

OBJECTIVE: Decompressive craniectomy (DC) is a common practice for control of intracranial pressure (ICP) following traumatic brain injury (TBI), although the impact of this procedure on the fate of operated patients is still controversial. METHODS: Cerebral blood flow (CBF) and metabolic rates were monitored prospectively and daily as a surrogate of neuronal viability in 36 TBI patients treated by DC and compared with those of 86 nonoperated patients. DC was performed either on admission (n=29) or within 48 hours of admission (n=7). RESULTS: DC successfully controlled ICP levels and maintained CBF within a normal range although the cerebral metabolic rate of oxygen (CMRO2) was significantly lower in this group. In 7 patients, pre- and postoperative recordings showed a significant ICP decrease that correlated with CBF augmentation but not with concurrent improvement of CMRO2 that remained particularly low. Logistic regression analysis of all investigated variables showed that DC was not associated with higher mortality despite more severe injuries in this group. However, operated patients were 7-fold more likely to have poor functional outcomes than nonoperated patients. Good functional outcome was strongly associated with higher CMRO2 but not with higher CBF values. CMRO2 levels were significantly lower in the DC group, even after adjustment for injury severity, and showed a progressive and sustained trend of deterioration significantly different from that of the non-DC group. CONCLUSION: These results suggest that DC may enhance survival in the presence of severe brain swelling, although it is unlikely to represent an adequate answer to mitochondrial damage responsible for cellular energy crisis and edema.