Defining a Taxonomy of Intracranial Hypertension: Is ICP More Than Just a Number?

Intracranial pressure (ICP) monitoring and control is a cornerstone of neuroanesthesia and neurocritical care. However, because elevated ICP can be due to multiple pathophysiological processes, its interpretation is not straightforward. We propose a formal taxonomy of intracranial hypertension, which defines ICP elevations into 3 major pathophysiological subsets: increased cerebral blood volume, masses and edema, and hydrocephalus. (1) Increased cerebral blood volume increases ICP and arises secondary to arterial or venous hypervolemia. Arterial hypervolemia is produced by autoregulated or dysregulated vasodilation, both of which are importantly and disparately affected by systemic blood pressure. Dysregulated vasodilation tends to be worsened by arterial hypertension. In contrast, autoregulated vasodilation contributes to intracranial hypertension during decreases in cerebral perfusion pressure that occur within the normal range of cerebral autoregulation. Venous hypervolemia is produced by Starling resistor outflow obstruction, venous occlusion, and very high extracranial venous pressure. Starling resistor outflow obstruction tends to arise when cerebrospinal fluid pressure causes venous compression to thus increase tissue pressure and worsen tissue edema (and ICP elevation), producing a positive feedback ICP cycle. (2) Masses and edema are conditions that increase brain tissue volume and ICP, causing both vascular compression and decrease in cerebral perfusion pressure leading to oligemia. Brain edema is either vasogenic or cytotoxic, each with disparate causes and often linked to cerebral blood flow or blood volume abnormalities. Masses may arise from hematoma or neoplasia. (3) Hydrocephalus can also increase ICP, and is either communicating or noncommunicating. Further research is warranted to ascertain whether ICP therapy should be tailored to these physiological subsets of intracranial hypertension.

Could there be any merit in lumping primary open-angle glaucoma, idiopathic intracranial hypertension and Meniere's disease into a novel and discrete category of fluid tension disorders?

Open-angle glaucoma, idiopathic intracranial hypertension, and Meniere's disease are disorders managed by different specialties in medicine viz. ophthalmology, neurology, and otorhinolaryngology respectively. By working in silos, the similarity of these disorders is overlooked. Close inspection of these disorders reveals the presence of signs and symptoms triggered by fluid under high pressure within relatively closed chambers. There is a similarity in the capillary production of fluid, which then circulates and drains into the venous system. Management practices that reduce fluid production, decrease fluid pressure or enhance fluid drainage are employed for the treatment of all three disorders. A search for a unifying mechanism explaining the pathophysiology of all three disorders may unlock effective and perhaps curative measures for these disorders.

Raised intracranial pressure and brain edema.

Acutely increased intracranial pressure (ICP) is a life-threatening neurosurgical emergency. Optimal management strategy is selected according to the causative process. Typical causes are intracranial bleeds like traumatic subdural, epidural, or intracerebral hematoma (ICH); spontaneous ICH, intraventricular hemorrhage, subarachnoid hemorrhage, and hydrocephalus. When occurring without significant brain injury and treated effectively before herniation, a full recovery can be expected. In intraparenchymal injuries a full recovery is unlikely since dead cells in the central nervous system leave an "empty hole," to be replaced by cerebrospinal fluid. The clinical recovery is based on the surviving cells that are able to make new synapses. Surgery may decrease ICP by removing significant mass effect. In all conditions, when notable injury of brain parenchyma occurs, brain edema may gradually increase ICP and further worsen the clinical condition. This is seen typically in large brain infarctions when the formation of brain edema may lead to increased ICP for hours and days. Brain edema is traditionally classified as vasogenic or cytotoxic but according to current knowledge is rather a continuum, starting with cytotoxic cell swelling followed by ionic edema and then vasogenic edema. Here we review the causes of increased ICP, including mechanisms of brain edema, with clinical examples.

Intracranial hypertension without headache in children.

We aimed to determine the frequency of intracranial hypertension without headache in children. We retrospectively analyzed patients evaluated in a pediatric intracranial hypertension referral center. Patients were divided into 2 groups depending on whether they complained of headache at the time of presentation. Age, body mass index, and opening cerebrospinal fluid pressures were considered continuous variables and compared by Wilcoxon rank-sum test because of non-normality. A P value of .05 was considered significant. A total of 228 charts were reviewed; 152 patients met the criteria for intracranial hypertension and 22/152 patients (14.5%) met the criteria of optic nerve edema without headache. There were clinically significant differences in age and body mass index between the 2 groups. The group without headache was typically younger and not obese. The opening pressure and modified opening pressure were not clinically significant between the 2 groups.

Transsylvian-transinsular approach for the removal of basal ganglia hemorrhage under a Modified Intracerebral Hemorrhage score.

BACKGROUND: Spontaneous intracerebral hemorrhages account for 20% of all strokes. The Modified Intracerebral Hemorrhage (MICH) score provides a simple, reliable system for decision making regarding surgical treatment. The transsylvian-transinsular approach had previously been neglected because of the dependence on great surgical experience. We believe this approach not only compares favorably with the minimally invasive surgery concept but also preserves most of the cerebral functional cortex with a maximum hematoma evacuation rate. METHODS: From May 2007 to September 2008, a single surgeon treated 32 patients with basal ganglia hemorrhage using the transsylvian-transinsular approach. Of these, 20 had MICH scores of 2 to 3; 5 had MICH scores of 4; and 7 had MICH scores of 5. After 24 postoperative hours, we evaluated the hematoma evacuation rate by a computed tomography scan. The functional recovery was evaluated by the Barthel Index at 1, 3, and 6 months postoperatively. RESULTS: All data were analyzed according to MICH score. The hematoma evacuation rates were in the following order: MICH scores 2 to 3 (97%) > MICH score 4 (92%) > MICH score 5 (90%). Surgery-related mortality was MICH2, 3 (0%) < MICH4 (20%) < MICH5 (43%). The Barthel Index of the MICH2, 3 patients (n = 18) improved from 16.9 at 1 postoperative month to 41.94 at 6 postoperative months. CONCLUSIONS: The transsylvian-transinsular approach for the removal of an ICH was not difficult, and it was found to be a safe method for treating a spontaneous basal ganglion ICH. In addition, this approach conformed with the spirit of minimally invasive surgery.

[Benign intracranial hypertension: history, definition, and physiopathology]. / Hypertension intracrânienne bénigne: historique, définition et physiopathologie.

Benign intracranial hypertension (BIH) is a rare condition in which the pathophysiology remains unclear. Multiple theories have been proposed in the past to explain BIH. Today it is widely accepted that the condition occurs in situations where alteration of cerebrospinal fluid (CSF) reabsorption is encountered. The venous system is therefore involved and may be the common denominator of the pathophysiological theories. A distinction must be made between idiopathic benign intracranial hypertension and BIH resulting from drugs, other pathological conditions, or toxics (secondary BIH), which are reported in this paper. We emphasize the crucial role of exhaustive clinical, biological, and neuroradiological investigations aiming to establish the diagnosis of BIH.

[Classification and therapy of craniocerebral injury (CCI)]. / Einteilung und therapie des schädel-hirn-traumas (SHT).

In spite of great success in research severe traumatic brain injury (TBI) remains the most frequent cause for morbidity and mortality in the age < 45 years. The primary lesion emerges at the moment of trauma. Due to several pathophysiological mechanisms secondary lesions occur that enlarge size of contusions significantly. As a consequence of intracranial bleedings and brain edema intracranial pressure (ICP) increases and threaten the patient. Extent of severity (declared in Glasgow Coma Scale Score [GCS]), expansion and type of bleedings (acute and chronic subdural hemorrhage, epidural bleeding, contusion bleedings and intracerebral hemorrhage) determinate operative and conservative therapy as well as intensive care medicine. A specific feature represents frontobasal lesions that, apart of penetrating injuries, are treated interdisciplinary not before ICP is stable, brain edema declining and coagulation sufficient several days after trauma. A persisting rhinoliquorrhoe cause meningitis up to 85 % within 10 years. Patient with GCS < 8 have to be intubated and controlled ventilated. Basic monitoring does not differ from those of other patients treated at the intensive care ward (sufficient breathing [pO (2), pCO (2)], arterial blood pressure, CBC and coagulation parameters, fluid monitoring and nutrition). Additionally, ICP have to be measured and be treated corresponding to the algorithm of ICP treatment. Complementary, oxygen saturation of brain tissue (ptiO (2)), local cerebral blood flow (r-CBF) and cerebral metabolism (micro dialysis) can be measured. Just the combination of the single monitoring parameters gives evidence of the functional condition of the injured brain and relieved planning and performing of the appropriate therapy.

Intracranial hypertension: classification and patterns of evolution.

Intracranial hypertension (ICH) was systematized in four categories according to its aetiology and pathogenic mechanisms: parenchymatous ICH with an intrinsic cerebral cause; vascular ICH, which has its actiology in disorders of cerebral blood circulation: ICH caused by disorders of cerebro-spinal fluid dynamics and idiopathic ICH. The increase of intracranial pressure is the first to happen and then intracranial hypertension develops from this initial effect becoming symptomatic: it then acquires its individuality, surpassing the initial disease. The intracranial hypertension syndrome corresponds to the stage at which the increased intracranial pressure can be compensated and the acute form of intracranial hypertension is equivalent to a decompensated ICH syndrome. The decompensation of intracranial hypertension is a condition of instability and appears when the normal intrinsic ratio of intracranial pressure time fluctuation is changed. The essential conditions for decompensation of intracranial hypertension are: the speed of intracranial pressure increase over normal values, the highest value of abnormal intracranial pressure and the duration of high ICP values. Medical objectives are preventing ICP from exceeding 20 mm Hg and maintaining a normal cerebral blood flow. The emergency therapy is the same for the acute form but each of the four forms of ICH has a specific therapy, according to the pathogenic mechanism and if possible to aetiology.

Quantification of secondary CPP insult severity in paediatric head injured patients using a pressure-time index.

This paper describes and validates a new Cumulative Pressure-Time Index (CPT) which takes into account both duration and degree of cerebral perfusion pressure (CPP) derangement and determines critical thresholds for CPP, in a paediatric head injury dataset. Sixty-six head-injured children, with invasive minute-to-minute intracranial pressure (ICP) and blood pressure monitoring, had their pre-set CPP derangement episodes (outside the normal range) identified in three childhood age-bands (2-6, 7-10, and 11-16 years) and global outcome assessed at six months post injury. The new cumulative pressure-time index more accurately predicted outcome than previously used summary measures and by varying the threshold CPP values, it was found that these physiological threshold values (< or = 48, < or = 52 and < or = 56 mmHg for 2-6, 7-10, and 11-16 years respectively) best predicted brain insult in terms of subsequent mortality and morbidity.

Study of clinical features of amyloid angiopathy hemorrhage and hypertensive intracerebral hemorrhage.

OBJECTIVE: The purpose of this study was to differentiate between cerebral amyloid angiopathy (CAA) and hypertension (HTN) based on hemorrhage pattern interpretation. METHODS: From June 1994 to Oct., 2000, 83 patients admitted to our service with acute intracerebral hemorrhage (ICH) were investigated retrospectively; 41 patients with histologically proven diagnosis of cerebral amyloid angiography and 42 patients with clear history of hypertension were investigated. RESULTS: Patients with a CAA-related ICH were significantly older than patients with a HTN-related ICH (74.0 years vs 66.5 years, P < 0.05). There was a significantly higher number of hematomas > or = 30 ml in CAA (85.3%) when compared with HTN (59.5%). No basal ganglional hemorrhage was seen in CAA, but in 40.5% in HTN. In CAA-related ICH, subarachnoid hemorrhage (SAH) was seen in 26 patients (63.4%) compared to only 11 patients (26.2%) in HTN-related ICH. Intraventricular hemorrhage was seen in 24.4% in CAA, and in 26.2% in HTN. Typical features of CAA-related ICH included lobar distribution affecting mainly the lobar superficial areas, lobulated appearance, rupture into the subarachnoid space, and secondary IVH from the lobar hemorrhage. More specifically, multiplicity of hemorrhage, bilaterality, and repeated episodes also strongly suggest the diagnosis of CAA. Multiple hemorrhages, defined as 2 or more separate hematomas in multiple lobes, accounted for 17.1% in CAA-related ICH. CONCLUSION: There are certain features in CAA on CT and MRI and in clinical settings. To some extent, these features may contribute to distinguishing CAA from HTN related ICH.

[Craniocerebral trauma]. / Schädel-Hirn-Trauma.

In cases of craniocerebral trauma there may be primary and secondary cerebral lesions. The principal goal of treatment is to minimize secondary cerebral trauma by optimized therapy. In the primary treatment phase monitoring of vital signs (blood pressure and respiration) is of crucial importance. CT diagnosis is followed by treatment of any increase in intracranial pressure by relief of hematomas, CSF drainage and appropriate intensive care measures.

A new classification and a synergetical pattern in intracranial hypertension.

Intracranial hypertension develops from the initial cerebral effect of increased intracranial pressure and becomes symptomatical; then it acquires its individuality, surpassing the initial disease. The intracranial hypertension syndrome corresponds to the stage at which the increases in intracranial pressure (ICP) can be compensated and the ICH disease is in its acute form, equivalent to a decompensated ICH syndrome. Based on the etiopathogenesis of intracranial hypertension, a new classification is proposed: parenchymatous intracranial hypertension with an intrinsic cerebral cause; vascular intracranial hypertension, which has its etiology in disorders of the cerebral blood circulation; and essential or idiopathic intracranial hypertension, the former pseudotumor cerebri, an incomplete ICH syndrome. A synergetical pattern of the ICH is based on the relation between ICP and the period of high-pressure action: the critical pressure--time fluctuation causes the autoregulation of the cerebral blood flow to decrease or determines the brain herniation. The decompensation is a state of instability and appears when the intrinsic ratio of pressure--time fluctuation is changed: the high ICP lasts longer than the corresponding normal ICP, or the ICP is higher than the one that normally lasts the same period of time.

Incidence of intracranial hypertension after severe head injury: a prospective study using the Traumatic Coma Data Bank classification.

UNLABELLED: Intracranial hypertension (ICH) is a frequent finding in patients with a severe head injury. High intracranial pressure (ICP) has been associated with certain computerized tomography (CT) abnormalities. The classification proposed by Marshall et al. based on CT scan findings, uses the status of the mesencephalic cisterns, the degree of midline shift, and the presence or absence of focal lesions to categorize the patients into different prognostic groups. Our aim in this study was to analyze the ICP evolution pattern in the different groups of lesions of this classification. PATIENTS AND METHODS: We present the results of a prospective study in 94 patients with severe head injury, in whom ICP was monitored for at least 6 hours. ICP evolution was classified into three different categories: 1) ICP always < 20 mm Hg, 2) Intracranial hypertension at some time during monitoring, but controlled by medical or surgical treatment, 3) Uncontrollable ICP. The ICP pattern was correlated with the final CT diagnostic category. CONCLUSIONS: 3 patients had a normal CT scan, and none of them presented intracranial hypertension. In diffuse injury type II, the ICP evolution may be quite different. Patients with bilateral brain swelling (Diffuse Injury III) have a high risk of increased ICP (63.2%). Although in our study the frequency of Diffuse Injury IV was low, all patients in this category had a refractory ICP. In the category of evacuated mass lesions, two thirds of the patients presented an intracranial hypertension. In one third, ICP was refractory to treatment. 85% of patients with a non-evacuated mass lesion showed an increased ICP.