High-Pressure Headaches, Low-Pressure Syndromes, and CSF Leaks: Diagnosis and Management

Authors: Graff-Radford SB, Schievink WI.

BACKGROUND: Headache resulting from idiopathic intracranial hypertension (IIH) in a population of moderately to obese women of childbearing age. The causes overall remain unclear. With this review, we provide an overview of clinical treatment and management strategies.
RESULTS: IIH management is dependent on the signs and symptoms presented. Symptomatic treatment should attempt to lower intracranial pressure, reduce pain, and protect the optic nerves. Consideration for lumbar puncture and draining fluid as an option for reducing pressure may be helpful; however, repeated treatment is not usually favored by patients. Traditional prophylactic medications used in migraine may help reduce the primary headache often induced by raised intracranial pressure. We suggested surgical intervention for patients experiencing visual loss or impending visual loss and not responding to medication therapy.
CONCLUSION: In this review, we discuss headache associated with IIH and spontaneous intracranial hypotension. Much needs to be learned about treatment options for patients with cerebrospinal fluid leaks including methods to strengthen the dura.

Pathophysiology of cerebral oedema in acute liver failure

Authors: Scott TR, Kronsten VT, Hughes RD, Shawcross DL.

Cerebral oedema is a devastating consequence of acute liver failure (ALF) and may be associated with the development of intracranial hypertension and death. In ALF, some patients may develop cerebral oedema and increased intracranial pressure but progression to life-threatening intracranial hypertension is less frequent than previously described, complicating less than one third of cases who have proceeded to coma since the advent of improved clinical care. The rapid onset of encephalopathy may be dramatic with the development of asterixis, delirium, seizures and coma. Cytotoxic and vasogenic oedema mechanisms have been implicated with a preponderance of experimental data favouring a cytotoxic mechanism. Astrocyte swelling is the most consistent neuropathological finding in humans with ALF and ammonia plays a definitive role in the development of cytotoxic brain oedema. The mechanism(s) by which ammonia induces astrocyte swelling remains unclear but glutamine accumulation within astrocytes has led to the osmolyte hypothesis. Current evidence also supports an alternate 'Trojan horse' hypothesis, with glutamine as a carrier of ammonia into mitochondria, where its accumulation results in oxidative stress, energy failure and ultimately astrocyte swelling. Although a complete breakdown of the blood-brain barrier is not evident in human ALF, increased permeation to water and other small molecules such as ammonia has been demonstrated resulting from subtle alterations in the protein composition of paracellular tight junctions. At present, there is no fully efficacious therapy for cerebral oedema other than liver transplantation and this reflects our incomplete knowledge of the precise mechanisms underlying this process which remain largely unknown.

Predictability of intracranial pressure level in traumatic brain injury: features extraction, statistical analysis and machine learning-based evaluation

Authors: Chen W, Cockrell CH, Ward K, Najarian K.

This paper attempts to predict Intracranial Pressure (ICP) based on features extracted from non-invasively collected patient data. These features include midline shift measurement and textural features extracted from Computed axial Tomography (CT) images. A statistical analysis is performed to examine the relationship between ICP and midline shift. Machine learning is also applied to estimate ICP levels with a two-stage feature selection scheme. To avoid overfitting, all feature selections and parameter selections are performed using a nested 10-fold cross validation within the training data. The classification results demonstrate the effectiveness of the proposed method in ICP prediction.

Rebound Intracranial Hypertension: A Complication of Epidural Blood Patching for Intracranial Hypotension

Authors: Kranz PG, Amrhein TJ, Gray L.

Rebound intracranial hypertension is a complication of epidural blood patching for treatment of intracranial hypotension characterized by increased intracranial pressure, resulting in potentially severe headache, nausea, and vomiting. Because the symptoms of rebound intracranial hypertension may bear some similarity to those of intracranial hypotension and literature reports of rebound intracranial hypertension are limited, it may be mistaken for refractory intracranial hypotension, leading to inappropriate management. This clinical report of 9 patients with confirmed rebound intracranial hypertension reviews the clinical characteristics of patients with this condition, emphasizing factors that can be helpful in discriminating rebound intracranial hypertension from refractory spontaneous intracranial hypotension, and discusses treatment.

Spontaneous sphenoid lateral recess cerebrospinal fluid leaks arise from intracranial hypertension, not Sternberg's canal

Authors: Illing E, Schlosser RJ, Palmer JN, Curé J, Fox N, Woodworth BA.

BACKGROUND: Spontaneous cerebrospinal fluid (CSF) leaks/encephaloceles are proven to be associated with intracranial hypertension by objective measurements of CSF pressure during or following endoscopic repair. A common area of involvement is a pneumatized lateral recess of the sphenoid (LRS) sinus, where prolonged intracranial pressures lead to arachnoid pits and subsequent development of skull-base defects. Even though the LRS is never present at birth, a "congenital" cause of these leaks due to a persistent Sternberg's (lateral craniopharyngeal) canal continues to be erroneously perpetuated in the literature. The objective of this study was to eliminate the myths defining these leaks as congenital in nature.
METHODS: Evaluation of LRS CSF leaks present within a multiinstitutional case series was performed. Data regarding demographics, body mass index (BMI), radiologic evaluation of intracranial hypertension, and direct intracranial pressure measurements (when available) were collected.
RESULTS: Data evaluation identified 77 LRS CSF leaks in 59 patients (mean age 52 years). Obesity was present in 83% of individuals (mean BMI 36) and 81% were females. Radiologic evidence of intracranial hypertension (eg, empty sella, dilated optic nerve sheaths, and scalloped/attenuated bone) was present on 96% of preoperative computed tomography (CT) and/or magnetic resonance imaging (MRI) scans. Opening or postsurgical lumbar drain or ventriculostomy pressure measurements were elevated in 95% of patients (mean 27.7; range, 9-50 cmH2 O).
CONCLUSION: This study provides objective evidence that LRS CSF leaks are secondary to erosions from intracranial hypertension and refutes the myth regarding a congenital origin from Sternberg's canal.

Effect of sevoflurane on cerebral perfusion pressure in patients with internal hydrocephalus

Authors: Karwacki Z, Witkowska M, Niewiadomski S, Wiatr A, Dzierżanowski J, Słoniewski P.

BACKGROUND: Due to its confirmed neuroprotective properties, sevoflurane is one of a few anaesthetics used for neuroanaesthesia. Its effects on the cerebral and systemic circulations may be of particular importance in patientswith intracranial pathology. This study aimed to evaluate the effect of sevoflurane at concentrations lower than 1 MAC on cerebral perfusion pressure (CPP) in patients with internal hydrocephalus.
METHODS: The study was conducted on14 patients with internal hydrocephalus, who underwent ventriculo-peritoneal shunt implantation. After inserting the catheter into the lateral cerebral ventricle, sevoflurane, at 1.1 and 2.2 vol%, was initiated at two successive 15-minute intervals. The intracranial pressure (ICP) was continuously measured; special attention was focused on the values prior to and at the end of each observation period. The following parameters were monitored: mean arterial pressure (MAP), CPP, heart rate, end-tidal CO₂ concentration, core body temperature, and the inspiratory and end-expiratory concentrations of sevoflurane.
RESULTS: The HR and MAP decreased during successive observation intervals compared to baseline values. Likewise, the CPP decreased from 75.6 ± 2.8 mm Hg to 72.2 ± 2.6 mm Hg to 70.2 ± 0.8 mm Hg. The baseline value for ICP was 16.3 ± 0.6 mm Hg and increased to 17.7 ± 0.8 and 18.9 ± 0.5 mm Hg during the next observation periods.
CONCLUSIONS: Sevoflurane administered ata concentration below 1MAC to patients with internal hydrocephalus increases the ICP and decreases the MAP, which leads to adecrease in CPP. The CPP decrease is more dependent on depressing the systemic circulatory system than an increased ICP.

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