Evidence-Based Reviews

Beware ictal activity that mimics psychiatric illness

Current Psychiatry. 2006 July;5(7):69-86

Joseph S. Goveas, MD

Stanley N. Caroff, MD

Silvana Riggio, MD

How to detect and halt nonconvulsive status epilepticus.

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References

1. DeLorenzo RJ, Hauser WA, Towne AR, et al. A prospective, population-based epidemiologic study of status epilepticus in Richmond, Virginia. Neurology 1996;46(4):1029-35.

2. Shorvon S. Status epilepticus: Its clinical features and treatment in children and adults Cambridge, UK: Cambridge University Press, 1994.

3. Shneker BF, Fountain NB. Assessment of acute morbidity and mortality in nonconvulsive status epilepticus. Neurology 2003;61:1066-73.

4. Walker M, Cross H, Smith S, et al. Nonconvulsive status epilepticus: Epilepsy research foundation workshop reports. Epileptic Disord 2005;7(3):53-296.

5. Engel J, Ludwig BI, Fetell M. Prolonged partial complex status epilepticus: EEG and behavioral observations. Neurology 1978;28:863-9.

6. Krumholz A, Sung GY, Fisher RS, et al. Complex partial status epilepticus accompanied by serious morbidity and mortality. Neurology 1995;45:1499-1504.

7. Ballenger CE, King DW, Gallagher BB. Partial complex status epilepticus. Neurology 1983;33:1545-52.

8. Thomas P, Zifkin B, Migneco O, et al. Nonconvulsive status epilepticus of frontal origin. Neurology 1999;52:1174-83.

9. Guberman A, Cantu-Reyna G, Stuss D, Broughton R. Nonconvulsive generalized status epilepticus: Clinical features, neuropsychological testing, and long-term follow-up. Neurology 1986;36:1284-91.

10. Thomas P, Beaumanoir A, Genton P, et al. ‘De novo’ absence status of late onset: Report of 11 cases. Neurology 1992;42:104-10.

11. Andermann F, Robb J. Absence status: a reappraisal following review of thirty-eight patients. Epilepsia 1972;13:177-87.

12. Kaplan PW. Nonconvulsive status epilepticus in the emergency room. Epilepsia 1996;37(7):643-50.

13. Riggio S. Nonconvulsive status epilepticus: Clinical features and diagnostic challenges. Psychiatr Clin N Am 2005;28(3):653-64.

14. Drislane FW. Presentation, evaluation, and treatment of nonconvulsive status epilepticus. Epilepsy Behav 2000;1(5):301-14.

15. Tomson T, Lindbom U, Nilsson BY. Nonconvulsive status epilepticus in adults: Thirty-two consecutive patients from a general hospital population. Epilepsia 1992;3(5):829-35.

16. Dunne JW, Summers QA, Stewart-Wynne EG. Non-convulsive status epilepticus: A prospective study in an adult general hospital. Q J Med 1987;62(238):117-26.

17. Kaplan PW. Behavioral manifestations of nonconvulsive status epilepticus. Epilepsy Behav 2002;3(2):122-39.

18. Mann SC. Malignant catatonia. In: Mann SC, Caroff SN, Keck PE Jr, Lazarus A, eds. Neuroleptic malignant syndrome and related conditions (2nd ed). Washington, DC: American Psychiatric Publishing Inc, 2003:121-43.

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Nonconvulsive status epilepticus (NCSE) is marked by neurobehavioral disturbances that resemble primary psychiatric disorders. Mistaken diagnosis and delayed treatment increase the risk of neurologic damage, so recognizing NCSE symptoms early is important.

To help you make a timely diagnosis, this article describes:

neuropsychiatric manifestations of NCSE
how to narrow the differential diagnosis by reviewing clinical symptoms and using electroencephalography (EEG)
techniques used to rapidly halt ictal activity.

Box

Status epilepticus: Risk of death, brain injury from nonconvulsive forms

Status epilepticus (SE) is an acute medical emergency. Both forms—convulsive (CSE) and nonconvulsive (NCSE)—require early recognition and treatment. In the United States, 60 SE cases occur per 100,000 population/year, with mortality rates of 20% in adults and 38% in the elderly.^1,2

Mortality risk. Data suggest patients with NCSE are unlikely to die unless NCSE co-occurs with CSE or severe medical illness such as delirium or acute complications. Mortality risk does not appear linked with a type of EEG discharge.³

Neurologic injury risk. Prolonged NCSE may cause permanent neurologic damage.⁴ Transient memory impairment has been reported after cessation of complex partial status epilepticus (CPSE).⁵ CPSE also has resulted in prolonged neurologic deficits, although concomitant medical illnesses might have contributed to the deficits.⁶ In one study, some patients gradually returned to baseline cognitive function after CPSE stopped, but they were not tested with standardized neuropsychological tools.⁷

No significant postictal memory impairment was observed on neuropsychological testing in patients with NCSE of frontal origin.⁸ A >5-year follow-up study of absence status epilepticus (ASE) found no evidence of long-term cognitive or behavioral decline, even though most patients had recurrent ASE.⁹ Similarly, no long-term sequelae were seen in patients with ASE.^10,11

Triggers, neurologic symptoms

NCSE is an acute but treatable medical emergency that calls for assessing and supporting cardiac and respiratory function, monitoring vital signs, temperature reduction, and fluid replacement. Prognosis is usually good unless NCSE is associated with a serious medical illness (Box).^1-11

Many metabolic, neurologic, pharmacologic, and medical abnormalities can precipitate NCSE (Table 1). The most common causes are hypoxia/anoxia, stroke, infection, subtherapeutic antiepileptic levels, alcohol and benzodiazepine intoxication/withdrawal, and metabolic abnormalities.^4,7,10,12

NCSE manifests as absence status epilepticus (ASE) or complex partial status epilepticus (CPSE). A generally accepted diagnostic definition is ≥30 minutes of behavioral change from baseline, with diagnostic EEG findings.^4,13 EEG is indispensable because the clinical manifestations of NCSE are predominantly behavioral, with minimal or no motor activity.

Table 1

Clinical factors that may precipitate NCSE

Medical	Recent infection, hyperventilation, trauma, menstruation, pregnancy, renal dialysis, postoperative period, sleep deprivation
Metabolic	Hypoparathyroidism, renal failure, hyper/hyponatremia, hyper/hypoglycemia, hypocalcemia
Neurologic	Mental retardation, dementia, stroke
Pharmacologic	Low serum levels or abrupt discontinuation of anticonvulsants, alcohol intoxication/withdrawal, benzodiazepine withdrawal lithium and neuroleptic use, psychotropic overdose
Source : References 9,10,12,16

ASE, a primary generalized process, is characterized by confusion or diminished responsiveness; it may be associated with occasional blinking or other minor motor activity and can last for hours to days. It usually occurs in patients with known epilepsy, particularly absence seizures.

ASE is reported primarily in children, although de novo cases have been described in elderly patients with no history of epilepsy.^10,14

CPSE is usually associated with a history of focal epilepsy and vascular disease. CPSE has a focal onset, with subsequent secondary generalization. Onset is usually temporal in origin but also can be extratemporal.

Patients with CPSE often cycle between an “epileptic twilight state” with confusion and complete unresponsiveness with stereotyped automatisms. It can present with marked behavioral fluctuation or a change in mental status and is generally followed by a prolonged postictal state.^4,7,13-15 Several NCSE cases have occurred in patients with no history of seizures.^9,10,16

Historically, CPSE was reported to be less common than ASE, but this misconception was most likely caused by failure to recognize CPSE’s clinical presentation and rapid generalization on EEG.^7,15

Neuropsychiatric features

Patients with NCSE may be referred for evaluation of an array of behavioral changes commonly seen in psychiatric practice. The differential diagnosis is extensive (Table 2) and includes neurologic and medical conditions often associated with catatonic syndrome.^17,18

In a retrospective study, Kaplan¹² assessed clinical presentations and reasons for diagnostic delay in 23 adults eventually diagnosed with NCSE. Presenting symptoms included:

confusion, agitation, aggressive behavior
lethargy, mutism, verbal perseveration, echolalia
delirium, blinking, staring, chewing or picking behaviors
tremulousness or myoclonus
bizarre behavior (inappropriate laughing, crying, or singing)
rigidity with waxy flexibility
delusions, hallucinations.

Clinicians mistook hallucinations and mood lability for a primary psychiatric condition in 7 patients, presumed catalepsy was psychogenic in 3 patients, and thought obtundation was caused by alcohol or drug intoxication in 4 cases.

A prospective study of 22 patients with NCSE found that 7 had a history of psychotic depression, schizophrenia, self-mutilation, bipolar disorder, or episodic severe aggression; 12 of 18 with ASE had a history of epilepsy, and 3 of 4 with CPSE had experienced seizures associated with cerebrovascular accident, right cerebral embolus, and thiazide-induced hyponatremia, respectively.¹⁶