Increased ICP and Its Cerebral Haemodynamic Sequelae.

OBJECTIVES: Increased intracranial pressure (ICP) is a pathological feature of many neurological diseases; however, the local and systemic sequelae of raised ICP are incompletely understood. Using an experimental paradigm, we aimed to describe the cerebrovascular consequences of acute increases in ICP. MATERIALS AND METHODS: We assessed cerebral haemodynamics [mean arterial blood pressure (MAP), ICP, laser Doppler flowmetry (LDF), basilar artery Doppler flow velocity (Fv) and estimated vascular wall tension (WT)] in 27 basilar artery-dependent rabbits during experimental (artificial lumbar CSF infusion) intracranial hypertension. WT was estimated as the difference between critical closing pressure and ICP. RESULTS: From baseline (~9 mmHg) to moderate increases in ICP (~41 mmHg), cortical LDF decreased (from 100 to 39.1%, p < 0.001), while mean global Fv was unchanged (from 47 to 45 cm/s, p = 0.38). In addition, MAP increased (from 88.8 to 94.2 mmHg, p < 0.01 and WT decreased (from 19.3 to 9.8 mmHg, p < 0.001). From moderate to high ICP (~75 mmHg), both global Fv and cortical LDF decreased (Fv, from 45 to 31.3 cm/s, p < 0.001; LDF, from 39.1 to 13.3%, p < 0.001) while MAP increased further (94.2 to 114.5 mmHg, p < 0.001) and estimated WT was unchanged (from 9.7 to 9.6 mmHg, p = 0.35). CONCLUSION: In this analysis, we demonstrate a cortical vulnerability to increases in ICP and two ICP-dependent cerebro-protective mechanisms: with moderate increases in ICP, WT decreases and MAP increases to buffer cerebral perfusion, while with severe increases of ICP, an increased MAP predominates.

Cerebral haemodynamics during experimental intracranial hypertension.

Intracranial hypertension is a common final pathway in many acute neurological conditions. However, the cerebral haemodynamic response to acute intracranial hypertension is poorly understood. We assessed cerebral haemodynamics (arterial blood pressure, intracranial pressure, laser Doppler flowmetry, basilar artery Doppler flow velocity, and vascular wall tension) in 27 basilar artery-dependent rabbits during experimental (artificial CSF infusion) intracranial hypertension. From baseline (∼9 mmHg; SE 1.5) to moderate intracranial pressure (∼41 mmHg; SE 2.2), mean flow velocity remained unchanged (47 to 45 cm/s; p = 0.38), arterial blood pressure increased (88.8 to 94.2 mmHg; p < 0.01), whereas laser Doppler flowmetry and wall tension decreased (laser Doppler flowmetry 100 to 39.1% p < 0.001; wall tension 19.3 to 9.8 mmHg, p < 0.001). From moderate to high intracranial pressure (∼75 mmHg; SE 3.7), both mean flow velocity and laser Doppler flowmetry decreased (45 to 31.3 cm/s p < 0.001, laser Doppler flowmetry 39.1 to 13.3%, p < 0.001), arterial blood pressure increased still further (94.2 to 114.5 mmHg; p < 0.001), while wall tension was unchanged (9.7 to 9.6 mmHg; p = 0.35).This animal model of acute intracranial hypertension demonstrated two intracranial pressure-dependent cerebroprotective mechanisms: with moderate increases in intracranial pressure, wall tension decreased, and arterial blood pressure increased, while with severe increases in intracranial pressure, an arterial blood pressure increase predominated. Clinical monitoring of such phenomena could help individualise the management of neurocritical patients.

Spontaneous pediculolysis with associated contralateral laminar fracture. A case report.

The authors report the case of a 38 year-old female with a rare combination of spontaneous pediculolysis with an associated contralateral laminar fracture of the lumbar spine. Multimodal radiological examinations of the whole lumbar spine are recommended in the case of a symptomatic patient with low back pain who is not responding to basic physiotherapy and pain management modalities. This will provide the unsuspecting clinician a method to diagnose this rare cause of low back pain and avoid unnecessary surgical intervention.