Mortality among patients with idiopathic intracranial hypertension enrolled in the IH Registry.

OBJECTIVE: To determine (1) if mortality among patients with idiopathic intracranial hypertension (IIH) enrolled in the Intracranial Hypertension Registry (IHR) is different from that of the general population of the United States and (2) what the leading underlying causes of death are among this cohort. METHODS: Mortality and underlying causes of death were ascertained from the National Death Index. Indirect standardization using age- and sex-specific nationwide all-cause and cause-specific mortality data extracted from the Centers for Disease Control and Prevention Wonder Online Database allowed for calculation of standardized mortality ratios (SMR). RESULTS: There were 47 deaths (96% female) among 1437 IHR participants that met inclusion criteria. The average age at death was 46 years (range, 20-95 years). Participants of the IHR experienced higher all-cause mortality than the general population (SMR, 1.5; 95% confidence interval [CI], 1.2-2.1). Suicide, accidents, and deaths from medical/surgical complications were the most common underlying causes, accounting for 43% of all deaths. When compared to the general population, the risk of suicide was over 6 times greater (SMR, 6.1; 95% CI, 2.9-12.7) and the risk of death from accidental overdose was over 3 times greater (SMR, 3.5; 95% CI, 1.6-7.7). The risk of suicide by overdose was over 15 times greater among the IHR cohort than in the general population (SMR, 15.3; 95% CI, 6.4-36.7). CONCLUSIONS: Patients with IIH in the IHR possess significantly increased risks of death from suicide and accidental overdose compared to the general population. Complications of medical/surgical treatments were also major contributors to mortality. Depression and disability were common among decedents. These findings should be interpreted with caution as the IHR database is likely subject to selection bias.

[Management of craniocerebral trauma in a neurosurgery center]. / Versorgung des Schädel-Hirn-Traumas im neurochirurgischen Zentrum.

Aggressive treatment of patients with severe head injury increases the chance for survival and good functional outcome in most cases. To prevent irreversible cerebral lesions, the key point of treatment is the management of intracranial hypertension caused by intracranial hematomas, brain edema and impaired circulation of cerebrospinal fluid (CSF). Therapeutic standards are surgery of traumatic hematoma, osmotherapy and mild hyperventilation for brain edema, and CSF drainage. In highly elevated intracranial pressure (ICP) administration of barbiturates and forced hyperventilation can be considered.

[Epidural cerebrospinal fluid pressure measurement and therapy of intracranial hypertension in "malignant" middle cerebral artery infarct]. / Epidurale Hirndruckmessung und Hirndrucktherapie bei "malignem" Mediainfarkt.

BACKGROUND AND PURPOSE: A permanent elevation of ICP after severe brain injury for instance in subarachnoid or intracerebral hemorrhage or neurotrauma is associated with a poor clinical outcome. Although increasingly being used in the intensive care of patients with elevated ICP, continuous epidural ICP monitoring in ischemic stroke has not been firmly established yet. PATIENTS AND METHODS: We prospectively evaluated the clinical course and outcome of patients with raised ICP due to space occupying ischemic middle cerebral artery (MCA) infarction as seen in CT, who underwent continuous ICP monitoring. Epidural ICPprobes were inserted ipsilaterally (all patients) and contralaterally (additional in 7 patients) to the side of infarctation. Glasgow Coma and Scandinavian Stroke Scales (GCS and SSS) were obtained initially and in the further clinical course. All patients were subjected to a standardized treatment protocol for raised ICP. ICP values were correlated with clinical presentation at the time point of deterioration, with outcome and CT findings. Effectiveness of different treatment modalities to lower ICP were analyzed and discussed. RESULTS: 9 of 48 patients survived the MCA infarct (19%), with the cause of death being transtentorial herniation with subsequent brain death in all 39 patients. Mean SSS at admission was 20.6 (survivors 21.5 +/- 5.6, nonsurvivers 19.8 +/- 6.5). All patients showed clinical signs of herniation before the increase of ICP. All 39 patients who died developed ICP values higher than 35 mmHg and no patient with ICP values of more than 35 mmHg survived. CCT changes dit not necessarily reflect the absolute measured ICP values. All treatment modalities for raised ICP including osmotherapy, controlled hyperventilation, tromethamol and barbiturates were initially effective, but only in a minority of patients ICP control could be sustained. CONCLUSIONS: We conclude that ICP monitoring in large hemispheric infarction may predict clinical outcome. ICP monitoring was not helpful in guiding long term treatment of ICP. It remains doubtful, whether ICP monitoring has a positive influence on clinical outcome of acute severe ischemic stroke.

Significance of intracranial pressure waveform analysis after head injury.

The authors have investigated the relationships between the amplitude of the ICP pulse wave, the mean values of ICP and CPP, and the outcome of 56 head injured ventilated patients. The ICP was monitored continuously using a Camino transducer (35 patients) or subdural catheter (21 patients). The mean Glasgow Coma Score was 6 (range 3-13; 5 patients had a GCS > 8 after resuscitation). Patients were grouped according to their Glasgow Outcome Score assessed at 12 months after injury. The amplitude of ICP pulse waveform was assessed using the fundamental harmonic of the pulse waveform (AMP) to avoid distortion caused by different frequency responses of the pressure transducers used in the study. Statistical analysis revealed that in patients with fatal outcome the ICP pulse amplitude increased when the mean ICP increased to 25 mmHg and then began to decrease. The upper breakpoint of the AMP-ICP relationship was not present in patients with good/moderate outcome. The moving correlation coefficient between the fundamental harmonic of ICP pulse wave and the mean ICP (RAP: R-symbol of correlation between A-amplitude and P-pressure) was introduced to describe the time-dependent changes in correlation between amplitude and mean ICP. The RAP was significantly lower in patients who died or remained in the vegetative state. In 7 patients who died from uncontrollable intracranial hypertension RAP was oscillating or decreased to 0 or negative values well before brain-stem herniation. The combination of an ICP above 20 mmHg for a period longer than 6 hours with low correlation between the amplitude and pressure (RAP < 0.5) was described as an predictive index of an unfavourable outcome.

[Incidence of ophthalmologic complications in acute intracranial hypertension]. / Inzidenz ophthalmologischer Komplikationen bei akuter intrakranieller Drucksteigerung.

Although Terson's syndrome has been diagnosed more frequently since the early 1960s because of improved intensive-care facilities, these reports are single case reports or retrospective studies. Therefore, we examined prospectively 20 patients (11 male, 9 female), aged between 23 and 77 years, with subarachnoid hemorrhages or rapid increase in intracranial pressure (ICP) of other origin (tumor-associated, post-traumatic) to evaluate ocular changes. In all patients the increase in ICP was confirmed by computed tomography. Additionally, in 16 patients permanent monitoring of ICP was performed. Twelve patients presented with subarachnoid hemorrhage, 6 had a post-traumatic increase in ICP, and 2 more presented with a tumor-associated intracranial hemorrhage. A total of 8 patients (40%) presented with intraocular changes; 6 presented with uni- or bilateral intraretinal hemorrhage, 1 patient had a bilateral papilledema and 1 more patient had bilateral vitreal hemorrhage. When ocular hemorrhage occurred, the mortality was 2.5 times as high as in patients without ocular hemorrhage. For this prognostic feature of the ophthalmological status all patients with rapid increase in ICP should be monitored early for intraocular hemorrhage. The possibility of intraocular hemorrhage is elevated in high-degree subarachnoid hemorrhage, whereas a rapid increase in ICP also found when the pressure has other causes (tumor-associated, posttraumatic).

The use of lobectomy in the management of severe closed-head trauma.

A retrospective review is presented of 20 patients with traumatic brain injury who were treated during the course of their illness by lobectomies either after a herniation or other significant deterioration or to reduce elevated intracranial pressure. All the patients suffered from blunt head trauma. Patient ages ranged from 19 to 59 years (average, 34 yr). The initial Glasgow Coma Scale score ranged from 3 to 15 (average, 8.2). There were 14 frontal lobectomies, 2 temporal, 3 frontal and temporal, and 1 occipital. Surgery was performed between 0 and 8 days after injury (average, 2.8). Outcome was favorable (good or moderately disabled) in 11 patients and unfavorable (severely disabled, persistently vegetative, or dead) in 9. No patients survived in a persistently vegetative state. A higher initial Glasgow Coma Scale score was positively correlated with a more favorable outcome (P < 0.03). Younger patients also showed a significant positive relationship to outcome (P < 0.0005). Better pupillary reactivity showed a significant trend toward a more favorable outcome (P < 0.04). The type of lesions identified on computed tomographic scans had no association with outcome. A lobectomy can be a useful adjuvant in the management of severe brain injury, especially in younger patients with relatively higher initial Glasgow Coma Scale scores who subsequently deteriorate or develop elevated intracranial pressure.

Management of intracranial hypertension.

Intracranial hypertension is the final common denominator of morbidity and mortality for diverse neurologic problems, and its proper treatment requires the heuristic application of the available therapeutic alternatives when the clinical situation and patient's prognosis warrants treatment. The initial therapeutic focus for ICP reduction should be control of factors that may aggravate intracranial hypertension such as inappropriate head and body position, elevated body temperature, pain, noxious stimuli, elevated airway pressure, elevated blood pressure, seizures, and hypotonic intravenous fluids. The appropriate conventional therapies (e.g., hyperventilation, osmotic agents, sedatives, barbiturates, and cerebrospinal fluid removal) should be selected based on the details of each individual case. Surgical removal of intracranial mass lesions may be indicated in some circumstances, particularly for intractable intracranial hypertension and progressive, severe brain tissue shifts.

Long-term observations of intracranial pressure after severe head injury. The phenomenon of secondary rise of intracranial pressure.

The long-term course of intracranial pressure (ICP) was studied in 53 patients from a group of 90 patients with severe head injury treated over a 3-year period. In 49 of these, ICP was significantly elevated during the observation period. The maximum in ICP was usually observed 24 to 96 hours posttrauma. A subgroup of patients developed a second rise of ICP. Such a course was observed in 15 (31%) of the 49 patients with intracranial hypertension. In these cases, ICP increased initially to 20 to 30 mm Hg but could be controlled. Thereafter, ICP was decreased again for at least 12 hours. The secondary ICP rise occurred 3 to 10 days after trauma. In six patients, intracranial hypertension became uncontrollable and eventually caused brain death. The outcome of patients with a secondary rise of ICP was worse when compared with that of patients without this complication. A cause of the secondary ICP rise could only be identified in some cases. Delayed traumatic intracerebral hemorrhage, traumatic vasospasm, hypoxia, and hyponatremia were diagnosed in seven cases. In seven other patients, the secondary ICP rise coincided with a pronounced leukocytosis, which was not associated with apparent infections. Because the occurrence and degree of a secondary rise of ICP after severe head injury are important factors affecting outcome, monitoring of ICP after severe head injury should be prolonged.

Intracranial pressure in African children with cerebral malaria.

Opening lumbar cerebrospinal fluid (CSF) pressure was measured with a paediatric spinal fluid manometer in 26 of 61 Kenyan children (mean age 39 months) with cerebral malaria. In all cases pressure was above normal (mean [SD]22.6 [7.4] cm CSF, range 10.5-36). Clinical features of our patients suggest that intracranial hypertension is important in the pathogenesis of cerebral malaria in children, especially as a cause of death. We suggest that raised intracranial pressure is secondary to increased cerebral blood volume. Lowering intracranial pressure may significantly reduce the mortality and morbidity of cerebral malaria. The potential risks and benefits of lumbar puncture should be considered carefully in patients with suspected cerebral malaria.

Dimethyl sulfoxide in the management of patient with brain swelling and increased intracranial pressure after severe closed head injury.

The results of a prospective study on the effects of dimethyl sulfoxide (DMSO) in patients with severe closed head injuries causing brain edema and increase in intracranial pressure (ICP) are presented. 10 patients were selected and carefully analyzed according to Glasgow coma scale (GCS) scores and severity of brain edema. The results demonstrate that DMSO rapidly reduces the raised ICP, increases the cerebral perfusion pressure (CPP) and improves the neurological course and outcome without affecting the systemic blood pressure and patient responsiveness except only in one patient. We also point out that the rebound effect does not occur.

Thiopental infusion in the treatment of intracranial hypertension complicating fulminant hepatic failure.

Intracranial hypertension complicating fulminant hepatic failure has a mortality in excess of 90% in the presence of renal failure if not rapidly responsive to mannitol and ultrafiltration. Based on data which suggest that barbiturates can be of value in controlling the intracranial hypertension of head injury, intravenous thiopental was assessed in 13 patients with fulminant hepatic failure. All had developed acute renal failure complicated by intracranial hypertension unresponsive to other modes of therapy and were likely by all published criteria to have little chance of survival. The dosage of thiopental was adjusted incrementally until intracranial pressure, measured by extradural transducers, fell to within normal limits or adverse hemodynamic changes occurred. The intracranial pressure was reduced, in each case, by 185 to 500 mg (median: 250 mg) thiopental given over 15 min, and in eight cases continuing infusion achieved stable normal intracranial pressure and cerebral perfusion pressure. Five of the patients made a complete recovery and there were only three deaths from intracranial hypertension. Side effects were few and included minor hypotension controlled by dose reduction. The response of otherwise intractable intracranial hypertension and the 38% survival rate was remarkable for a group of patients with such a poor prognosis.

Contrast sensitivity testing in pseudotumor cerebri.

Twelve patients with pseudotumor cerebri underwent sensory visual testing and the results were analyzed. Contrast sensitivity loss was detected with use of Arden gratings in nine of the twelve patients (75%) and in 13 of 24 eyes (54%). Snellen acuity was worse than 20/20 in 21% of eyes. Contrast sensitivity scores improved with resolution of the patient's papilledema whereas there was no significant improvement of Snellen acuity. Contrast sensitivity testing with Arden plates is a useful procedure for detecting visual loss and serially following patients with pseudotumor cerebri.