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Beware Ictal Activity That Mimics Psychiatric Illness How to Detect and Halt Nonconvulsive Status Epilepticus

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Beware Ictal Activity That Mimics Psychiatric Illness How to Detect and Halt Nonconvulsive Status Epilepticus N ew Investigators Beware ictal activity that mimics psychiatric illness How to detect and halt nonconvulsive status epilepticus Joseph S. Goveas, MD Assistant professor Department of psychiatry and behavioral medicine ® Dowden Health Media Medical College of Wisconsin, Milwaukee Stanley N. Caroff, MD Copyright Professor of psychiatry For personal use only University of Pennsylvania School of Medicine Veterans Affairs Medical Center, Philadelphia Silvana Riggio, MD Associate professor Department of psychiatry Mount Sinai School of Medicine Bronx Veterans Affairs Medical Center, New York onconvulsive status epilepticus (NCSE) N is marked by neurobehavioral distur- bances that resemble primary psychiatric disor- ders. Mistaken diagnosis and delayed treatment increase the risk of neurologic damage, so recog- nizing 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. continued © Bill Brooks/Masterfile VOL. 5, NO. 7 / JULY 2006 69 For mass reproduction, content licensing and permissions contact Dowden Health Media. New Investigators Box Status epilepticus: Risk of death, brain injury from nonconvulsive forms tatus epilepticus (SE) is an acute medical (CPSE).5 CPSE also has resulted in prolonged Semergency. Both forms—convulsive (CSE) and neurologic deficits, although concomitant nonconvulsive (NCSE)—require early recognition medical illnesses might have contributed to the and treatment. In the United States, 60 SE cases deficits.6 In one study, some patients gradually occur per 100,000 population/year, with mortality returned to baseline cognitive function after rates of 20% in adults and 38% in the elderly.1,2 CPSE stopped, but they were not tested with 7 Mortality risk. Data suggest patients with NCSE standardized neuropsychological tools. are unlikely to die unless NCSE co-occurs with No significant postictal memory impairment CSE or severe medical illness such as delirium was observed on neuropsychological testing in or acute complications. Mortality risk does not patients with NCSE of frontal origin.8 A >5-year appear linked with a type of EEG discharge.3 follow-up study of absence status epilepticus Neurologic injury risk. Prolonged NCSE may (ASE) found no evidence of long-term cognitive cause permanent neurologic damage.4 Transient or behavioral decline, even though most patients memory impairment has been reported after had recurrent ASE.9 Similarly, no long-term cessation of complex partial status epilepticus sequelae were seen in patients with ASE.10,11 TRIGGERS, NEUROLOGIC SYMPTOMS Table 1 NCSE is an acute but treatable medical Clinical factors that may precipitate NCSE emergency that calls for assessing and supporting cardiac and respiratory func- Medical Recent infection, hyperventilation, tion, monitoring vital signs, temperature trauma, menstruation, pregnancy, reduction, and fluid replacement. renal dialysis, postoperative period, Prognosis is usually good unless NCSE is sleep deprivation associated with a serious medical illness (Box).1-11 Metabolic Hypoparathyroidism, renal failure, Many metabolic, neurologic, phar- hyper/hyponatremia, hyper/ macologic, and medical abnormalities hypoglycemia, hypocalcemia can precipitate NCSE (Table 1). The Neurologic Mental retardation, dementia, stroke most common causes are hypoxia/ anox- ia, stroke, infection, subtherapeutic anti- Pharmacologic Low serum levels or abrupt epileptic levels, alcohol and benzodi- discontinuation of anticonvulsants, azepine intoxication/withdrawal, and alcohol intoxication/withdrawal, metabolic abnormalities.4,7,10,12 benzodiazepine withdrawal NCSE manifests as absence status lithium and neuroleptic use, epilepticus (ASE) or complex partial sta- psychotropic overdose tus epilepticus (CPSE). A generally Source : References 9,10,12,16 accepted diagnostic definition is ≥30 minutes of behavioral change from base- continued on page 75 70 Current VOL. 5, NO. 7 / JULY 2006 p SYCHIATRY Current p SYCHIATRY continued from page 70 Promising New Investigator: Joseph S. Goveas, MD This paper was among those entered in the 2006 Promising New Investigators competition sponsored by the Neuroleptic Malignant Syndrome Information Service (NMSIS). The theme of this year’s competition was “New insights on psychotropic drug safety and side effects.” CURRENT PSYCHIATRY is honored to publish this peer- reviewed, evidence-based article on a clinically important topic for practicing psychiatrists. NMSIS is dedicated to reducing morbidity and mortality of NMS by improving medical and psychiatric care of patients with heat-related disorders; providing support information for medical professionals, patients and families; and improving scientific understanding of these conditions through research. line, with diagnostic EEG findings.4,13 EEG is indispensable because the clinical manifestations of NCSE are predominantly behavioral, with minimal or no motor activity. ASE, a primary generalized process, is character- ized 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 behav- ioral fluctuation or a change in mental status and VOL. 5, NO. 7 / JULY 2006 75 Current New Investigators p SYCHIATRY Table 2 • confusion, agitation, Cerebrovascular dis- Table 3 Differential diagnosis of NCSE aggressive behavior ease, tumors, and trauma Clinical features that raise suspicion of NCSE • lethargy, mutism, verbal are the most common caus- Domain Features Metabolic disorders Hypo/hyperglycemia, hypercalcemia, perseveration, echolalia es of late-life NCSE.4,19 De Addison’s disease, Cushing’s disease, • delirium, blinking, star- novo NCSE occasionally Cognitive changes Prolonged confusion, executive dysfunction, uremia ing, chewing or picking presents: obtundation, attention/memory difficulties, Neurologic disorders Stroke, CNS tumors, closed head trauma, behaviors • after benzodiaze- lack of initiative, perseveration, stupor transient global amnesia, seizures, • tremulousness or myo- pine withdrawal Speech Poverty of speech with monosyllabic inflammatory and infectious clonus • with neuroleptic, answers, verbal perseveration, echolalia, encephalopathies • bizarre behavior (in- tricyclic antide- palilalia, aphasia, paraphasic errors, Psychiatric disorders Schizophrenia, mood disorders, catatonia, appropriate laughing, pressant, or lithi- confabulation, mutism malignant catatonia, somatoform disorders, 10,16 crying, or singing) um treatment Affective Prolonged fear, affective indifferent state conversion disorder, Asperger’s syndrome, • rigidity with waxy flexibility • with metabolic ab- with blank facial expression, hypomania, malingering • delusions, hallucinations. normalities and psychotic depression, inappropriate Toxic disorders Toxic encephalopathy, neuroleptic malignant Clinicians mistook hal- nonpsychotropic laughing and crying, anxiety states syndrome, serotonin syndrome, alcohol and lucinations and mood labili- medications.10 Psychosis Visual, auditory and cenesthetic sedative-hypnotic withdrawal, drugs (lithium ty for a primary psychiatric hallucinations, delusions toxicity, tricyclics, baclofen, tiagabine, condition in 7 patients, pre- CLINICAL SYMPTOMS overdose) sumed catalepsy was psy- Clinical features of NCSE Impulse control Hostility, agitation, violence, groping, Source: Reference 17,18 chogenic in 3 patients, and include cognitive changes, genital manipulation, picking, posturing thought obtundation was speech abnormalities, af- Others Catatonic signs, autonomic disturbances caused by alcohol or drug fective disturbances, psy- Source: References 5,7-9,12,15-17,20-23 is generally followed by a prolonged postictal intoxication in 4 cases. chosis, poor impulse con- state.4,7,13-15 Several NCSE cases have occurred in A prospective study of 22 patients with trol, and bizarre behaviors patients with no history of seizures.9,10,16 NCSE found that 7 had a history of psychotic (Table 3). Some patients develop ictal phenome- diagnosis of psychogenic catatonia as NCSE. Historically, CPSE was reported to be less depression, schizophrenia, self-mutilation, bipo- na resembling catatonia or clinical and EEG EEG is necessary to exclude NCSE in these cases. common than ASE, but this misconception was lar disorder, or episodic severe aggression; 12 of changes that mimic neuroleptic malignant syn- NMS. Yoshino et al27 described two patients taking most likely caused by failure to recognize 18 with ASE had a history of epilepsy, and 3 of 4 drome (NMS).20-23 neuroleptics who met criteria for NMS and had CPSE’s clinical presentation and rapid general- with CPSE had experienced seizures associated Catatonia. Lim et al24 described three patients with EEG changes
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