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directly over the sac and dural remnants present in the wall of the sac were dissected free of the overlying skin to create a watertight seal. The high free-floating occipital bones were rotated down and behind the torcula before proceeding with the skin closure.The immediate post-operative weight of the neonate was 2.2 kg implying an occipital encephalocele of 2.6 kg. Postoperative period was uneventful and the neonate was discharged on the tenth post-operative day.

ObjectivesWe recently showed that diminished motor cortical excitability is associated with high levels of poststroke fatigue. Motor cortex excitability impacts movement parameters such as reaction and movement times. We predicted that one or both would be influenced by the presence of post-stroke fatigue. Methods 41 first-time stroke survivors (high fatigue n=21, Fatigue Severity Scale 7 (FSS-7) score >5; low fatigue n=20, FSS-7 score <3) participated in the study. Movement times, choice and simple reaction times were measured in all participants. Results A three way ANOVA with fatigue (high and low), task (movement time, simple reaction time and choice reaction time) and hand (affected and unaffected) as the three factors, revealed a significant difference between affected (but not unaffected) hand movement times in the high compared to low fatigue groups. Reaction times, however, were not different between the high-fatigue and low-fatigue groups in either the affected or unaffected hand. Conclusions Previously, we showed that motor cortex excitability is lower in patients with high post-stroke fatigue. Our current findings suggest that post-stroke fatigue (1) is a problem of movement speed ( possibly a consequence of diminished motor cortex excitability) and not movement preparation, and (2) may have a focal origin confined to the lesioned hemisphere. We suggest that low motor cortex excitability in the lesioned hemisphere is a viable therapeutic target in post-stroke fatigue.

Traumatic brain injury (TBI) consists of varied pathophysiological consequences and alteration of intracranial dynamics, reduction of the cerebral blood flow and oxygenation. In the past decade more emphasis has been directed towards optimizing cerebral perfusion pressure (CPP) in patients who have suffered TBI. Injured brain may show signs of ischemia if CPP remains below 50 mmHg and raising the CPP above 60 mmHg may avoid cerebral oxygen desaturation. Though CPP above 70 mmHg is influential in achieving an improved patient outcome, maintenance of CPP higher than 70 mmHg was associated with greater risk of acute respiratory distress syndrome (ARDS). The target CPP has been laid within 50-70 mmHg. Cerebral blood flow and metabolism are heterogeneous after TBI and with regional temporal differences in the requirement for CPP. Brain monitoring techniques such as jugular venous oximetry, monitoring of brain tissue oxygen tension (PbrO2), and cerebral microdialysis provide complementary and specific information that permits the selection of the optimal CPP. This review highlights the rationale for use CPP directed therapies and neuromonitoring to identify optimal CPP of head injured patients. The article also reviews the evidence provided by various clinical trials regarding optimal CPP and their application in the management of head injured patients.