Intracranial pressure

Primary stabbing headache: a new dural sinus stenosis-associated primary headache?

Authors: Montella S, Ranieri A, Marchese M, De Simone R.

Primary stabbing headache (PSH) is a primary syndrome of unknown aetiology, characterised by brief, jabbing stabs predominantly felt in the orbital, temporal and parietal areas, whose frequency may vary from one to many per day, usually responding to indomethacin. PSH frequency in the general population is not well defined, but recent evidence suggests it could be more frequent than previously thought. In clinical series, PSH incidence was 33/100,000 per year, while in a population study 35.2 % prevalence was found. PSH was previously described as isolated or associated to other headache syndromes, most frequently with migraine. There is evidence that an idiopathic intracranial hypertension without papilledema, a condition usually associated to significant stenosis of dural sinuses (93 % sensitivity and specificity), is much more prevalent than believed and may run asymptomatically in up to 11 % of otherwise healthy individuals. In migrainous prone people, a sinus stenosis-associated intracranial hypertension without papilledema (ss-IHWOP) comorbidity may represent a powerful risk factor for progression of pain. Besides migraine, significant sinus stenosis has been found overrepresented also in chronic tension type headache as well as in exertional, cough, sexual activity-associated headaches (all indomethacin responsive primary headaches) and in altitude headache (an acetazolamide responsive condition). To explore the possible association between venous outflow disturbances and PSH, we retrospectively investigated the co-occurrence of sinus venous stenosis in patients referring to our headache centre since 2004 diagnosed with PSH who completed the diagnostic protocol. Out of 50 consecutive patients reporting PSH as the main or as accessory complaint, 8 (6 females, 2 males) performed MR venography (MRV). All MRV revealed significant unilateral or bilateral sinus stenosis. Mean age at PSH onset was 35.3 ± 18.9 years (range 11-67 years). Duration of attacks ranged 1-3 s. Median daily frequency of attacks was 4 (range 2-20); median number of days per month with PSH presentation was 14 (range 4-30). Six patients described attacks in temporal or parietal areas, one at the top of the head, and one in the occipital area. Only one patient had isolated PSH; all the others were diagnosed also with migraine without aura. Seven out of eight patients responded to indomethacin 75 mg/die, and one to topiramate 100 mg/die. Interestingly, both drugs share with acetazolamide a CSF pressure lowering effect. Our findings indicate that PSH is associated with central sinus stenosis and suggest that an undiagnosed ss-IHWOP might be involved in PSH pathogenesis.

Use of the CRASH study prognosis calculator in patients with severe traumatic brain injury treated with an intracranial pressure-targeted therapy

Authors: Olivecrona M, Olivecrona Z.

Based on the Corticosteroid Randomisation after Significant Head Injury (CRASH) trial database, a prognosis calculator has been developed for the prediction of outcome in an individual patient with a head injury. In 47 patients with severe traumatic brain injury (sTBI) prospectively treated using an intracranial pressure (ICP) targeted therapy, the individual prognosis for mortality at 14 days and unfavourable outcome at 6months was calculated and compared with the actual outcome. An overestimation of the risk of mortality and unfavourable outcome was found. The mean risk for mortality and unfavourable outcome were estimated to be 44.6±32.5% (95% confidence interval , 35.1-54.2%) and 69.3±23.7% (95% CI, 62.3-76.2%). The actual outcome was 4.3% and 42.6% respectively. The absolute risk reduction (ARR) for mortality was 33.1% and for unfavourable outcome 29.8%. A logistic fit for outcome at 6months shows a statistically significant difference (p<0.01). A receiver operating characteristic (ROC) curve analysis shows an area under the curve (AUC) of 0.691. The CRASH prognosis calculator overestimates the risk of mortality and unfavourable outcome in patients with sTBI treated with an ICP-targeted therapy based on the Lund concept. We do not advocate the use of the calculator for treatment decisions in individual patients. We further conclude that patients with blunt sTBI admitted within 8hours of trauma should be treated regardless of their clinical status as long as the initial cerebral perfusion pressure is >10mmHg.

Cerebrovascular Pressure Reactivity and Cerebral Oxygen Regulation After Severe Head Injury

Authors: Jaeger M, Lang EW.

BACKGROUND: To investigate the relationship between cerebrovascular pressure reactivity and cerebral oxygen regulation after head injury.
METHODS: Continuous monitoring of the partial pressure of brain tissue oxygen (PbrO2), mean arterial blood pressure (MAP), and intracranial pressure (ICP) in 11 patients. The cerebrovascular pressure reactivity index (PRx) was calculated as the moving correlation coefficient between MAP and ICP. For assessment of the cerebral oxygen regulation system a brain tissue oxygen response (TOR) was calculated, where the response of PbrO2 to an increase of the arterial oxygen through ventilation with 100 % oxygen for 15 min is tested. Arterial blood gas analysis was performed before and after changing ventilator settings.
RESULTS: Arterial oxygen increased from 108 ± 6 mmHg to 494 ± 68 mmHg during ventilation with 100 % oxygen. PbrO2 increased from 28 ± 7 mmHg to 78 ± 29 mmHg, resulting in a mean TOR of 0.48 ± 0.24. Mean PRx was 0.05 ± 0.22. The correlation between PRx and TOR was r = 0.69, P = 0.019. The correlation of PRx and TOR with the Glasgow outcome scale at 6 months was r = 0.47, P = 0.142; and r = -0.33, P = 0.32, respectively.
CONCLUSIONS: The results suggest a strong link between cerebrovascular pressure reactivity and the brain's ability to control for its extracellular oxygen content. Their simultaneous impairment indicates that their common actuating element for cerebral blood flow control, the cerebral resistance vessels, are equally impaired in their ability to regulate for MAP fluctuations and changes in brain oxygen.

Magnetic Resonance-Based Estimation of Intracranial Pressure Correlates With Ventriculoperitoneal Shunt Valve Opening Pressure Setting in Children With Hydrocephalus

Authors: Muehlmann M, Koerte IK, Laubender RP, Steffinger D, Lehner M, Peraud A, Heinen F, Kiefer M, Reiser M, Ertl-Wagner B.

OBJECTIVES: The aim of this study was to investigate the relationship between the pressure setting of the ventriculoperitoneal (VP) shunt valve and a magnetic resonance (MR)-based estimate of intracranial pressure (ICP) in children with shunt-treated hydrocephalus without clinical signs of shunt malfunction.
MATERIALS AND METHODS: Institutional review board approval was obtained before the study, and all subjects and/or their legal guardians provided written informed consent. In this prospective study, 15 consecutive patients (median age, 8.25 years; range, 2.2-18.4 years; 6 girls and 9 boys) with shunt-treated hydrocephalus without signs of shunt malfunction were examined with retrospectively gated phase contrast sequences to quantify arterial inflow, venous outflow, and cerebrospinal fluid (CSF) flow to and from the cranial vault. The ratio of the maximal intracranial volume change and the pulse pressure gradient change was used to derive MR-ICP. Spearman ρ was used to test for the association of setting of the shunt valve opening pressure and MR-ICP.
RESULTS: Shunt valve opening pressure settings and MR-ICP were positively correlated (Spearman ρ = 0.64, P < 0.01). Median MR-ICP was 8.67 mm Hg (interquartile range , 1.59 mm Hg) and median setting of the VP-shunt valve was 6.62 mm Hg (IQR, 1.47 mm Hg). The median MR-ICP was 1.9 mm Hg (IQR, 0.73 mm Hg) higher than the setting of the shunt valve.
CONCLUSION: There is a positive correlation between MR-ICP and VP shunt valve opening pressure setting. The systematically higher assessment of MR-ICP is most likely a result of outflow resistance within the shunt tubing system and well within the known fluctuation rates of VP shunt systems.

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Spectral analysis of intracranial pressure signals recorded during infusion studies in patients with hydrocephalus

Authors: García M, Poza J, Santamarta D, Abásolo D, Barrio P, Hornero R.

Hydrocephalus includes a number of disorders characterised by clinical symptoms, enlarged ventricles (observable using neuroimaging techniques) and altered cerebrospinal fluid (CSF) dynamics. Infusion tests are one of the available procedures to study CSF circulation in patients with clinical and radiological features of hydrocephalus. In them, intracranial pressure (ICP) is deliberately raised and CSF circulation disorders evaluated through measurements of the resulting ICP. In this study, we analysed seventy-seven ICP signals recorded during infusion tests using four spectral-based parameters: median frequency (MF) and relative power (RP) in three frequency bands. These measures provide a novel perspective for the analysis of ICP signals in the frequency domain. Each signal was divided into four artefact-free epochs (corresponding to the basal, early infusion, plateau and recovery phases of the infusion study). The four spectral parameters were calculated for each epoch. We analysed differences between epochs of the infusion test and correlations between these epochs and patient data. Statistically significant differences (p<1.7×10-3, Bonferroni-corrected Wilcoxon signed-rank tests) were found between epochs of the infusion test using MF and RP. Furthermore, some spectral parameters (MF in the basal phase, RP for the first frequency band and in the early infusion phase, RP for the second frequency band and in all phases of the infusion study and RP in the third frequency band and in the basal phase) revealed significant correlations (p<0.01) between epochs of the infusion test and signal amplitude in the basal and plateau phases. Our results suggest that spectral analysis of ICP signals could be useful for understanding CSF dynamics in hydrocephalus.


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