Clinical utility of EEG in diagnosing and monitoring epilepsy in adults.

Electroencephalography (EEG) remains an essential diagnostic tool for people with epilepsy (PWE). The International Federation of Clinical Neurophysiology produces new guidelines as an educational service for clinicians to address gaps in knowledge in clinical neurophysiology. The current guideline was prepared in response to gaps present in epilepsy-related neurophysiological assessment and is not intended to replace sound clinical judgement in the care of PWE. Furthermore, addressing specific pathophysiological conditions of the brain that produce epilepsy is of primary importance though is beyond the scope of this guideline. Instead, our goal is to summarize the scientific evidence for the utility of EEG when diagnosing and monitoring PWE.

Differential effects of antiepileptic drugs on sexual function and hormones in men with epilepsy.

OBJECTIVE: To compare sexual function and reproductive hormone levels among men with epilepsy who took various antiepileptic drugs (AEDs), untreated men with epilepsy, and normal controls. METHODS: Subjects were 85 men with localization-related epilepsy (25 on carbamazepine [CBZ], 25 on phenytoin [PHT], 25 on lamotrigine [LTG], and 10 untreated for at least 6 months [no AED]) and 25 controls. Sexual function scores (S-scores), hormone levels (bioactive testosterone, estradiol), hormone ratios (bioactive testosterone/bioactive estradiol), and gonadal efficiency (bioactive testosterone/luteinizing hormone) were compared among the five groups. RESULTS: S-scores, bioactive testosterone levels, bioactive testosterone/bioactive estradiol, and bioactive testosterone/luteinizing hormone were significantly greater in the control and LTG groups than in the CBZ and PHT groups. Sex hormone binding globulin was significantly higher in the CBZ and PHT groups than in all other groups. S-scores were below the control range in 20% of the men with epilepsy, including 32.0% on CBZ, 24% on PHT, 20% on no AEDs, and 4% on LTG (chi2: p = 0.08 for all four groups; chi2: p = 0.02 for the three AED groups). Bioactive testosterone was below the control range in 28.2%, including 48% on CBZ, 28% on PHT, 20% on no AEDs, and 12% on LTG (chi2: p = 0.02). Among men with epilepsy who had low S-scores, 70.6% had bioactive testosterone levels below the control range as compared to 17.6% among men with normal S-scores (chi2: p < 0.0001). Among men with epilepsy who had abnormally low bioactive testosterone, 50.0% had low S-scores; among men with normal bioactive testosterone, 8.2% had low S-scores (chi2: p < 0.0001). Bioactive testosterone decline with age was significantly greater among men with epilepsy than among controls and notably greater in the CBZ and PHT groups than in the LTG and untreated groups. CONCLUSIONS: Sexual function, bioavailable testosterone levels, and gonadal efficiency in men with epilepsy who took lamotrigine were comparable to control and untreated values and significantly greater than with carbamazepine or phenytoin treatment.

Oxygen desaturations triggered by partial seizures: implications for cardiopulmonary instability in epilepsy.

PURPOSE: The occurrence of hypoxemia in adults with partial seizures has not been systematically explored. Our aim was to study in detail the temporal dynamics of this specific type of ictal-associated hypoxemia. METHODS: During long-term video/EEG monitoring (LTM), patients underwent monitoring of oxygen saturation using a digital Spo2 (pulse oximeter) transducer. Six patients (nine seizures) were identified with oxygen desaturations after the onset of partial seizure activity. RESULTS: Complex partial seizures originated from both left and right temporal lobes. Mean seizure duration (+/-SD) was 73 +/- 18 s. Mean Spo2 desaturation duration was 76 +/- 19 s. The onset of oxygen desaturation followed seizure onset with a mean delay of 43 +/- 16 s. Mean (+/-SD) Spo2 nadir was 83 +/- 5% (range, 77-91%), occurring an average of 35 +/- 12 s after the onset of the desaturation. One seizure was associated with prolonged and recurrent Spo2 desaturations. CONCLUSIONS: Partial seizures may be associated with prominent oxygen desaturations. The comparable duration of each seizure and its subsequent desaturation suggests a close mechanistic (possibly causal) relation. Spo2 monitoring provides an added means for seizure detection that may increase LTM yield. These observations also raise the possibility that ictal ventilatory dysfunction could play a role in certain cases of sudden unexpected death in epilepsy in adults with partial seizures.

Presentation, evaluation, and treatment of nonconvulsive status epilepticus.

Nonconvulsive status epilepticus (NCSE) is much more common than is generally appreciated. It is certainly underdiagnosed, but its presentation is protean. Diagnostic criteria and treatment are controversial. Absence status is characterized by confusion or diminished responsiveness, with occasional blinking or twitching, lasting hours to days, with generalized spike and slow wave discharges on the EEG. Complex partial status consists of prolonged or repetitive complex partial seizures (with a presumed focal onset) and produces an "epileptic twilight state" with fluctuating lack of responsiveness or confusion. There is a clear overlapping of syndromes. Other confused, stuporous, or comatose patients with rapid, rhythmic, epileptiform discharges on the EEG may have "electrographic" status and should be considered in the same diagnostic category. NCSE typically occurs following supposedly controlled convulsions or other seizures, but with persistent neurologic dysfunction despite apparently adequate treatment. Confusion in the elderly or among emergency room patients is also a typical setting. The diagnosis of NCSE usually involves an abnormal mental status with diminished responsiveness, a supportive EEG, and often a response to anticonvulsant medication. All patients have clinical neurologic deficits, but the EEG findings and response to seizure medication are variable and are more controversial criteria. The response to drugs can be delayed for up to days. Experimental models and pathologic studies showing neuronal damage from status epilepticus pertain primarily to generalized convulsive status. Most morbidity from NCSE appears due to the underlying illness rather than to the NCSE itself. Some cases of prolonged NCSE or those with concomitant systemic illness, focal lesions, or very rapid epileptiform discharges may suffer more long-lasting damage. Although clinical studies show little evidence of permanent neurologic injury, the prolonged memory dysfunction in several cases and the similarities to convulsive status suggest that NCSE should be treated expeditiously. The diagnosis is important to make because NCSE impairs the patient's health significantly, and it is often a treatable and completely reversible condition.

Focal status epilepticus: clinical features and significance of different EEG patterns.

PURPOSE: Focal status epilepticus is typically diagnosed by the observation of continuous jerking motor activity, but many other manifestations have been described. EEG evidence of focal status may take several forms, and their interpretation is controversial. We detailed the clinical spectrum of focal status in patients diagnosed by both clinical deficit and EEG criteria and contrasted clinical manifestations in patients with different EEG patterns. METHODS: Patients were diagnosed with a neurologic deficit and discrete recurrent focal electrographic seizures or rapid, continuous focal epileptiform discharges on EEG. Clinical findings were determined by chart review. RESULTS: Of 41 patients with focal status, acute vascular disease was the cause in 21; 10 of 41 had exacerbations of prior epilepsy. A variety of clinical seizure types occurred, both before and after the EEG diagnosis, but the diagnosis was not expected in 28 patients before the EEG. Three had no obvious clinical seizures. Focal motor seizures and an abnormal mental status were the most common manifestations at the time of the EEG. With antiepileptic drugs, almost all had control of clinical seizures, and most improved in mental status. Patients with rapid continuous focal epileptiform discharges were nearly identical in presentation, likelihood of diagnosis, subsequent seizures, response to medication, and outcome to those with discrete seizures on EEG. CONCLUSIONS: Focal status epilepticus may be seen with a wide variety of clinical seizure types or without obvious clinical seizures. The diagnosis is often delayed or missed and should be considered after strokes or clinical seizures when patients do not stabilize or improve as expected. The diagnosis should be made equally whether patients have discrete electrographic seizures or continuous rapid focal epileptiform discharges on the EEG, and the same response to medications and outcome should be anticipated for the two groups.

Evidence against permanent neurologic damage from nonconvulsive status epilepticus.

Nonconvulsive status epilepticus (NCSE) is much more common than is generally appreciated and is certainly underdiagnosed, but its long-term effects are largely undetermined and remain controversial. There is increasing experimental evidence that generalized convulsive status epilepticus produces lasting neuropathologic damage in the hippocampus, but experimental models often include provocation of status epilepticus (SE) by physical (e.g., electrical stimulation) and chemical (including excitotoxic) agents that may induce damage independent of the epileptiform discharges. Also, damage appears to be related to the intensity and duration of electrical stimulation. Such models usually include high-frequency discharges sustained over long periods, somewhat different from the electrical activity of typical human NCSE. Pathologic studies in humans pertain primarily to patients who have had generalized convulsive status epilepticus. Clinical studies of the effects of NCSE are mandatory, but conclusions are difficult to come by, in part because of diverse definitions of NCSE. An altered mental status is obligatory, but the pertinent EEG and medication response criteria are controversial. Response to medication can be delayed by many hours or even days. Absence SE appears to cause no lasting effects. Complex partial SE is less uniform. Most reported cases have returned to baseline neurologic function, but several well-described patients have had prolonged memory deficits. The significance of other deficits is difficult to interpret in light of concomitant vascular and other diseases causing neurologic dysfunction. Clinical series usually lack premorbid neurologic and neuropsychologic assessment. The few exceptions are complicated by preexisting mental retardation and other deficits, by the coexistence of progressive illness, by the later effects of recurrent seizures, and almost always by the confounding influence of anticonvulsant medications. Most morbidity appears attributable to the underlying illnesses rather than to the NCSE itself. It is possible that relatively infrequent cases of prolonged NCSE or those with the synergistic effect of concomitant systemic illness, focal lesions, or very rapid excitatory epileptiform discharges may suffer more long-lasting damage, but these observations are still preliminary. NCSE should be treated expeditiously because of the acute neurologic impairment of the patients, because of the attendant morbidity including physical injury, and because it may go on to generalized convulsions. There is reasonable concern about possible long-term effects, but permanent neurologic damage from NCSE has not yet been established as a mandate for urgent treatment.

Depth of EEG suppression and outcome in barbiturate anesthetic treatment for refractory status epilepticus.

PURPOSE: Barbiturate anesthetic treatment of patients with refractory status epilepticus (RSE) is often titrated to a burst-suppression record on the EEG. We sought to determine whether the depth of EEG suppression correlated with persistent seizure control in such patients. METHODS: We reviewed the EEGs and clinical course of patients treated with pentobarbital (PTB) for RSE. Persistent seizure control or relapse to status epilepticus after the taper of PTB was determined with reference to the depth of EEG suppression during treatment. RESULTS: Of 35 patients tapering PTB, persistent seizure control was achieved in six of 12 patients reaching a burst-suppression record at greatest depth of EEG suppression and in 17 of 20 patients reaching a "flat" record; three patients with neither pattern had persistent control. Survival also was somewhat better in the more suppressed group. Isolated epileptiform discharges during the barbiturate infusion did not correlate with outcome. Recurrence of electrographic status after PTB taper predicted clinical relapse. CONCLUSIONS: The EEG is important in managing PTB treatment for patients with RSE. Some period of intense seizure and EEG suppression may help in preventing relapse of status after the PTB taper. It is not necessary to suppress all epileptiform discharges, but persistent clinical and EEG monitoring is necessary to avoid relapses.

Assessing suspected spinal cord compression: a multidisciplinary outcomes analysis of 342 episodes.

The object of this work was to evaluate the assessment and document the outcomes of cancer patients with suspected spinal cord compression (SCC). In a retrospective cohort study of 342 episodes of suspected SCC in cancer patients evaluated by computed tomography (CT) of the spine, a multidisciplinary team of neurologists, radiologists, and oncologists assessed the impact of varying the anatomical criterion for SCC and including new SCC diagnosed shortly after definitive radiographical imaging. We developed a logistic regression model to identify independent clinical predictors of SCC, including the natural history of the underlying cancer as well as neurological and radiological risk factors. Management of suspected SCC infrequently involved neurology consultation (21% of episodes). The frequency of SCC increased more than four-fold when the definition was expanded to include epidural cancer rather than spinal cord displacement only (36% vs. 8%), and 90-day clinical follow-up identified few new lesions not evident on definitive imaging studies. Clinical information about the course of cancer (documentation and duration of metastatic cancer) added independent predictive information to that yielded by neurological assessment and prior imaging studies in a multiple regression model. The a priori predicted risk of SCC, which ranged from 4% to 87% in this study, may vary enough to affect treatment strategies, although our population may have excluded very-low-risk patients. Consistent anatomical definitions of SCC, clinical follow-up of definitive imaging studies and the addition of information on the natural history of cancer to traditional neurological and radiographical evaluation may all improve clinical assessment of suspected SCC in cancer patients.

Incidence of spikes and paroxysmal rhythmic events in overnight ambulatory computer-assisted EEGs of normal subjects: a multicenter study.

The incidences of spikes and paroxysmal rhythmic events (PREs) in 10-h overnight EEGs of normal adult volunteers (n=135) were studied at 11 sites with a computer-assisted ambulatory EEG monitoring system with automatic spike and PRE detection. Spikes were evident in the overnight EEG of 1 subject (0.7%), and PREs were apparent in the overnight EEG of the same subject (0.7%). The incidences of spikes of 24 other subjects with a history of migraine and/or a family history of epilepsy were 12.5 and 13.3%, respectively. The overnight EEGs of these subjects were significantly more likely to show spikes than the overnight EEGs of subjects without migraine or a family history of epilepsy.

Seizures.

Seizures are one of the most common neurologic emergencies. This article reviews the emergency evaluation and treatment of seizures, including status epilepticus. Pseudoseizures related to drugs, alcohol, and pregnancy are also discussed.

Suspected spinal cord compression in breast cancer patients: a multidisciplinary risk assessment.

Breast cancer is the most common cause of metastatic epidural spinal cord compression (SCC) in women, and this condition results in significant neurologic dysfunction and morbidity. Prior studies of patients with suspected SCC did not employ multivariate analysis techniques, often included persons with a wide variety of malignancies, and generally focused on identifying associated neurologic and radiologic features. We therefore conducted a study examining a more comprehensive set of potential clinical risk factors in breast cancer patients with suspected SCC. We retrospectively analysed 123 episodes of suspected SCC among 93 breast cancer patients evaluated by spine computed tomography (CT) scanning. Multiple logistic regression analysis was employed to identify independent predictors of SCC. Clinically significant metastatic epidural cancer was defined as thecal sac compression (TSC), which occurred in 33 episodes (27%). Four independent predictors of TSC were identified and included oncologic features (known bone metastases > or = 2 years, metastatic disease at initial diagnosis) in addition to neurologic and radiologic features (objective weakness, vertebral compression fracture on spine radiograph). These four predictors stratified episodes into subgroups with widely varying risks of TSC, ranging from 12% (0 risk factors) to 85% (> or = 3 risk factors). These results suggest that the evaluation of breast cancer patients with suspected SCC should include clinical information about their disease course in addition to neurologic examination and prior imaging studies. If confirmed, these predictors may help clinicians assess risk in this patient population.

Multifocal cerebral hemorrhage in eclampsia and severe pre-eclampsia.

Eclampsia and severe pre-eclampsia have often been associated with transient cortical blindness and with bilateral occipital CT hypodensities or increased T2-weighted signal abnormalities on MRI. Petechial hemorrhages have been reported pathologically and on MRI, but major hemorrhages have been infrequent. Symptoms and radiologic findings are usually reversible and the prognosis good. We reviewed the clinical and radiologic findings in four patients with eclampsia or severe pre-eclampsia who had multifocal cerebral hemorrhages found acutely on CT. Hemorrhages were usually bilateral and often in posterior areas. Two patients had hemorrhages discovered after earlier normal scans. One patient died, and others had prolonged neurologic residua including visuospatial and other cognitive deficits. The posterior CT and MRI abnormalities in eclampsia and severe pre-eclampsia are not always benign and reversible but may precede or include multifocal hemorrhages with long-term neurologic complications. The affected areas suggest an increased posterior circulation vulnerability to the hypertensive vascular disease of eclampsia.

Technical implementation and clinical findings/results of monitoring oxygen saturation in patients referred for long-term EEG monitoring.

Recent technical developments allow the recording of a patient's oxygen saturation (SpO2) simultaneously with intensive long-term EEG monitoring (LTM). Clinically significant information from this enhanced multi-system physiological monitoring device can contribute to more accurate diagnoses in patients referred for LTM. This report covers the technical usage of combined SpO2/EEG recordings in a small group of patients. Clinically, the findings on the SpO2 monitor helped to define the diagnosis in many of these patients. In a few, the SpO2 changes were diagnostic in their own right and prompted referral to our Sleep Disorders Laboratory. From a research aspect, the details of the morphology and timing of the oxygen desaturations and EEG show several interesting relationships with respect to the dynamics of seizure semiology and respiratory physiology.

Nonconvulsive status epilepticus in thrombotic thrombocytopenic purpura.

Fluctuating neurologic symptoms, including confusion, stupor, and convulsions, are common signs in thrombotic thrombocytopenic purpura (TTP). We describe a patient with TTP who had a clinical seizure, intermittent stupor, and a declining course despite aggressive treatment. An EEG showed continuous rhythmic epileptiform discharges, and she improved with anticonvulsants. Fluctuating stupor in TTP has generally been attributed to microvascular occlusive disease, but nonconvulsive status epilepticus is a treatable condition that can cause similar symptoms.

Relapse and survival after barbiturate anesthetic treatment of refractory status epilepticus.

PURPOSE: Pentobarbital is standard treatment for refractory status epilepticus (SE) and is almost uniformly effective, but the morbidity of treatment and the mortality of refractory SE are high. Recurrence of SE after pentobarbital discontinuation may predict a worsened outcome. We sought to determine the optimal use of barbiturate anesthetic treatment of refractory SE. METHODS: We reviewed 44 episodes of barbiturate anesthetic treatment for refractory SE in 40 patients, seeking factors predicting freedom from relapse to clinical or electrographic SE after treatment and predicting survival. RESULTS: Eight of 9 patients with relapse of seizures after barbiturate treatment died, whereas only 9 of 26 with persistently controlled seizures died (p < 0.005). Both likelihood of relapse and survival correlated strongly with etiology, with 19 of 20 patients with chronic epilepsy, infections, or focal lesions having good control as compared with 2 of 9 with multiple medical problems (p < 0.001). Treatment delay did not predict a worsened outcome. Hypotension caused dose reduction but never required treatment discontinuation. Patients with more prolonged treatment and those receiving phenobarbital (PB) at the time of pentobarbital taper were less likely to relapse. CONCLUSIONS: Relapse of SE after barbiturate anesthetic treatment is a poor prognostic sign and should be prevented, if possible. Etiology was the primary predictor of outcome, but more prolonged treatment and the use of PB during pentobarbital withdrawal appeared to provide protection against relapse.

Comparison of coronal sphenoidal versus standard anteroposterior temporal montage in the EEG recording of temporal lobe seizures.

Chronic sphenoidal electrodes were developed to facilitate the recording and localization of temporal lobe seizures during long term monitoring. Many reports demonstrate their utility in displaying temporal interictal epileptiform activity, but there have been few direct comparisons of sphenoidal electrodes and surface temporal recordings actually. We compared simultaneous portions of 74 EEG recordings of temporal lobe seizures (from 42 patients), with one portion including sphenoidal electrodes in a coronal montage and one with a standard anterior posterior temporal montage. Separated tracings were reviewed by readers blinded to the other portion of the tracing. The coronal sphenoidal montage allowed recognition of temporal lobe seizures inapparent with standard surface temporal electrodes in 19% of seizures and led to an earlier identification (usually by > or = 5 s) of the onset in 70% of seizures. Indwelling, flexible sphenoidal electrodes assist in ambulatory recording of temporal lobe seizures, both in demonstrating the presence of seizures and in determining the localization and time of seizure onset.

Nonconvulsive status epilepticus in patients with cancer.

Patients with systemic cancer may have altered mental status without evidence of metastases, strokes, or metabolic encephalopathies. Six such patients are described whose EEGs showed continuous generalized epileptiform discharges in the absence of clinical signs of seizures. Two patients had never had any clinical evidence of seizures, and four had seizures that were thought to have stopped before the EEG. Three patients were confused, and three were stuporous or comatose. In some patients the nonconvulsive epileptic activity may have been directly related to the cancer; three had findings suggestive of possible paraneoplastic encephalopathies. Anticonvulsants led to an improved mental status in four patients, but all except one died. Nonconvulsive generalized status epilepticus may explain altered mental status in some patients with cancer, and anticonvulsant medication treatment can be beneficial.

Clinical implications of generalized electrographic status epilepticus.

We reviewed clinical features of 48 patients without prior epilepsy who had generalized electrographic status epilepticus (ESE) identified from EEG readings. Clinical status epilepticus (SE) had occurred in 40%, but most were thought to have stopped seizing. Overall, ESE was unsuspected in 81% of patients. Many types of seizures were present before the EEG, but clinical seizures recurred in only 17 patients after diagnosis, and 18 patients (38%) never had clinical evidence of seizures. Most patients (60%) were comatose. The cause of ESE often remained uncertain though many patients had serious medical illnesses. Eighty-eight percent died, and a poor outcome was predicted by coma at the time of diagnosis (29 of 29), anoxia (15 of 15), an invariantly discharging, low-voltage background EEG (15 of 16), and refractory electrographic or clinical seizures (29 of 31). Seizure type did not predict outcome, and mortality was as high for patients without clinical evidence of seizures (89%) as for the series as a whole. ESE is often unanticipated and signifies neurologic disease with a prognosis worse than convulsive SE or the typical nonconvulsive SE; the absence of clinical seizures confers no advantage.