Raised intracranial pressure and seizures in the neurological intensive care unit

B. McNamara1, J. Ray1, D. Menon2 and S. Boniface*,1

1 Department of Clinical Neurophysiology, Addenbrookes Hospital, Cambridge, UK. 2 Department of Anaesthesia, University of Cambridge, Cambridge, UK Department of Clinical Neurophysiology, Box 124, Addenbrookes Hospital, Cambridge CB2 2QQ, UK. E-mail: sjb80@cam.ac.uk

Accepted for publication: July 21, 2002


    Abstract
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 Abstract
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 Methods
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 Discussion
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Background. The relationship between changes in intracranial pressure and incidence of subclinical seizures in patients requiring neurological intensive care is not fully understood. The aim of this study was to investigate if acute increases in intracranial pressure were accompanied by subclinical seizures.

Methods. We prospectively studied 17 intensive care patients (11 male, aged 3–66 yr) who were selected from 85 patients requiring intracranial pressure measurement. Patients were selected to have a 30 min, 16-channel electroencephalogram (EEG) recorded when intracranial pressure remained increased despite preliminary treatments.

Results. Diagnoses included head injury, intracranial haemorrhage, subarachnoid haemorrhage and sagittal sinus thrombosis. All patients had at least one acute episode of intracranial pressure increase. Pressures ranged from 90 to 440 mm H2O. Encephalopathic features (delta/theta rhythms and burst suppression) were noted on all EEGs. No seizure activity was recorded.

Conclusions. We conclude from this pilot study that seizures are an uncommon cause of acute raised intracranial pressure. To determine whether raised intracranial pressure causes seizures, long-term monitoring in a large cohort of intensive care patients would be necessary, studying patients with similar diagnoses and ages.

Br J Anaesth 2003; 90: 39–42

Keywords: brain, intracranial pressure; complications, seizure; head, injury; intensive care; monitoring, electroencephalography


    Introduction
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
One reason for monitoring in neurological intensive care is to identify subclinical causes of secondary brain injury, to allow prompt treatment. Seizures are an important cause of morbidity in neurological intensive care patients.1 Early identification and treatment of seizures is a key part of management but it is often difficult to identify such seizures. Patients are often paralysed, and seizures in patients with acute brain injury are often non-convulsive seizures of partial origin.1 In patients in the first 2 weeks after head injury, seizures occur in 30% of cases and most of these are non-convulsive.2 Important differences in head injury management in Europe in general, and the UK in particular, can cause variations in incidence. The infrequent use of prophylactic anticonvulsants (e.g. phenytoin) might increase the incidence of seizures, but the far more common use of benzodiazepines and i.v. anaesthetics (especially propofol) for sedation could reduce seizure incidence. A large study using continuous electroencephalogram (EEG) monitoring in all patients with head injury would provide the best measure of such incidence, but this would be expensive and difficult.

As a first step, however, we could study patients at high risk of seizures, and measure the incidence of non-convulsive seizures. Increases in intracranial pressure (ICP) can be a useful surrogate marker of seizures on the intensive care unit if they occur in association with changes in heart rate and arterial pressure.3 Increases in ICP are associated with partial and generalized seizures.4 5 These increases are attributed to alterations in cerebral blood flow occurring during a seizure.57 However, we do not know how many increases in ICP are caused by seizures. Here we set out to measure the incidence of seizures during increases in ICP in patients receiving neurological intensive care.


    Methods
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
We prospectively studied patients for 6 months in the neurological intensive care unit at Addenbrookes Hospital, Cambridge. Management was standardized. ICP was monitored with a micromanometer (Codman, Johnson and Johnson Professional Inc., Raynham, MA, USA). When ICP >250 mm H2O, patients were managed according to a standard plan (Fig. 1). Those patients in whom ICP remained increased despite these treatments were entered into this study, irrespective of diagnosis; there were no exclusion criteria. All of these patients had a 30 min, 16-channel EEG. EEG was digitally acquired using a PL-EEG system (Walter Graphtek Ltd, Surrey, UK). The EEGs were examined for epileptiform features (spikes and sharp waves) and electrographic evidence of seizures (continuous spike and slow wave activity or evolving slow wave activity). In those patients who had ICP spikes during the recording, frequency topographical analysis was performed before, during and after the peak in ICP.



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Fig 1 Summary of management plan for patients with elevated ICP on the neurological intensive care unit at Addenbrookes Hospital.

 

    Results
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Patient characteristics
Eighty-five patients required ICP monitoring during the study period. Of these, 17 patients had episodes of raised ICP of uncertain aetiology requiring EEG investigation (six patients had multiple EEGs). All of the patients were ventilated at the time of the study. Patient details and the drug treatment are summarized in Table 1 (i.v. medication included atracurium 300–600 µg h–1, fentanyl 50–200 µg as needed, midazolam <=0.1 mg kg–1 h–1, phenytoin 15 mg kg–1 given as a loading dose, and propofol 3–5 mg kg–1 h–1). Most patients (13) had ICP increases within the first 5 days of admission to the intensive care unit, the rest were affected in their second week of admission. The duration of all EEG monitoring of all patients was 14 h.


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Table 1 Age, reason for admission to the intensive care unit, and drug treatment at the time of the EEG examination (n=17). Background EEG activity and EEG activity during any elevations in ICP
 
EEG findings
None of the EEGs showed spikes or sharp waves. There were no electrographic seizures on any of the records examined. Thirteen of the patients showed continuous slow or mid-frequency activity. The remaining four patients showed a burst suppression pattern. Five of the patients developed peaks of ICP during the EEG recording. There was no alteration in the EEG record during the ICP increase in any of these cases (e.g. Fig. 2). Topographical spectral analysis was performed on the EEG before, during and after the ICP peaks in all of these cases. There was no change in the quantitative EEG findings during the ICP spikes.




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Fig 2 (A) Background EEG activity in patient 5, showing a non-specific pattern of generalized delta activity. Vertical lines are at 1 min intervals. (B) EEG activity during a 100 mm H2O elevation in ICP. There is no visible alteration in the distribution or frequency of EEG activity. The frequency distribution map did not change.

 

    Discussion
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 Methods
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We wished to find if seizures caused raised ICP in brain-injured patients. We found no EEG evidence of seizures in these patients with raised ICP, even when increases in ICP were multiple. There are a number of possible explanations for this. Firstly the assumption that seizures can increase ICP may be false. The association between seizures and raised ICP seen in previous studies could have been coincidental. This is unlikely because animal experiments suggest that prolonged seizures can increase ICP.8 Alternatively, increases in ICP may be a real, but late, complication of seizures. Anticonvulsant agents and sedatives may stop seizures before alterations in ICP develop. For example, in our study group, all but three of the patients were on medication with anticonvulsant action. It has also been proposed that the EEG may be a useful surrogate marker for alterations in ICP. However, our findings imply that the EEG is insensitive to acute alterations in ICP and has little practical application as a means of monitoring changes in ICP within the limits studied here.

The time when ICP increases occurred was variable. Seizure activity that increases ICP could depend on the time of these events. Most ICP increases occurred relatively early in a patient’s admission. A larger study is required to address the significance of seizure activity as a cause of late (after 7 days) increases in ICP.

We conclude, from this pilot study of a variety of patients, that seizures are an uncommon cause of acute raised ICP, probably because of the treatment plans used. The study does not show if any particular diagnostic category or age group is more susceptible to seizures that could increase ICP.

Our data do not address the more general issue of the incidence of seizure in severe head injury. Perhaps patients with less severe intracranial hypertension are at lower risk of seizure activity. I.V. anaesthetics and benzodiazepines could thus counterbalance the smaller use of anticonvulsants (in comparison to North American practice). Patients with less severe intracranial hypertension could receive less i.v. sedative drugs and benzodiazepines, and could possibly be at greater risk of seizures in the absence of prophylactic anticonvulsant medication. To determine whether raised ICP causes seizures, long-term monitoring in a large cohort of intensive care patients would be necessary, preferably recruiting patients with similar diagnoses and ages. To facilitate this, automated spike and wave detection could be utilized. It is conceivable that seizures do not cause raised ICP during a short ictus, but that loss of auto-regulation after a seizure could cause increased pressure. In this instance, monitoring after raised ICP has occurred would miss the electrical event.


    References
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 Abstract
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 Methods
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 Discussion
 References
 
1 Young GB, Jordan KG, Doig GS. An assessment of non-convulsive seizures in the intensive care unit using continuous EEG monitoring: an investigation of variables associated with mortality. Neurology 1996; 47: 83–9[ISI][Medline]

2 Lee ST, Lui TN, Wong CW, et al. Early seizures after severe closed head injury. Can J Neurol Sci 1997; 24: 40–3[ISI][Medline]

3 Jordan KG. Neurophysiologic monitoring in the neuroscience intensive care unit. J Clin Neurophysiol 1995; 13: 579–626

4 Caldarelli MC, Di Rocco, Iannelli A. Effects of artificially induced increases in intracranial pressure on epileptic activity. Epilepsia 1980; 21: 587–96[ISI][Medline]

5 Gabor AJ, Brooks AG, Scobey RP, et al. Intracranial pressure during epileptic seizures. Electroencephalogr Clin Neurophysiol 1984; 57: 497–506[CrossRef][ISI][Medline]

6 Brodersen P, Paulson OB, Bolwig TG, et al. Cerebral hyperaemia in electrically induced epileptic seizures. Arch Neurol 1973; 28: 334–8[CrossRef][ISI][Medline]

7 Plum F, Posner JB, Troy B. Cerebral metabolic and circulatory responses to induced convulsions in animals. Arch Neurol 1968; 18: 1–13[CrossRef][ISI][Medline]

8 Knoblich OE, Gaab M, Weber W, et al. Intracranial pressure and electrical activity of the brain in various forms of experimental and clinical seizures. Neurosurg Rev 1980; 3: 243–9[Medline]





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