Psychiatric Annals

Case Challenge 

Status Epilepticus and Psychosis of Epilepsy

Deepa Hasija, MD; Sree Latha Krishna Jadapalle, MD; Amel Badr, MD

Abstract

This is a case of an 18-year-old, Asian female in 11th grade special education who lives with her family.

The patient was brought to the emergency department (ED) by an ambulance after having a generalized tonic-clonic seizure at home.

Abstract

This is a case of an 18-year-old, Asian female in 11th grade special education who lives with her family.

The patient was brought to the emergency department (ED) by an ambulance after having a generalized tonic-clonic seizure at home.

Deepa Hasija, MD; Sree Latha Krishna Jadapalle, MD; and Amel Badr, MD, are all with Bergen Regional Medical Center, Paramus, NJ. Deepa Hasija, MD, is Associate Chief of Research; Sree Latha Krishna Jadapalle, MD, is research assistant in psychiatry; Amel Badr, MD, is Program Director, Psychiatry Residency Training Program.

Drs. Hasija, Jadapalle, and Badr have disclosed no relevant financial relationships.

Address correspondence to: Deepa Hasija, MD, via email: dhasija@bergen-regional.com.

This is a case of an 18-year-old, Asian female in 11th grade special education who lives with her family.

The patient was brought to the emergency department (ED) by an ambulance after having a generalized tonic-clonic seizure at home.

In the ED, the patient experienced auditory hallucinations of the command type, telling her to hurt herself. She also had visual hallucinations of people changing shapes and colors. She did not report any suicidal ideation, homicidal ideation, or substance abuse.

Three days before presentation, the patient became noncompliant with her medications, resulting in her becoming isolative, having decreased appetite, and being unable to take care of personal hygiene. She also complained of being unable to sleep the night before admission.

The patient’s psychiatric diagnoses included psychotic disorder not otherwise specified (NOS) since 2010 and seizure disorder (unknown etiology) for the past 17 years. She had had one prior in-patient psychiatric hospitalization in the previous year. The patient’s symptoms were well controlled until 4 months before presentation. Her history included one grand mal seizure episode every 3 months, the last one being 1 month prior. For her seizures, she had been switched from levetiracetam to carbamazepine 400 mg oral two times a day and zonisamide 100 mg oral daily as an adjunct.

The patient’s history was negative for suicide attempts, homicidal ideation or attempts, access to firearms; physical, emotional, sexual abuse or any substance use. There was no history of psychiatric illness in her family except that her paternal uncle had epilepsy. The patient was born full term, via C-section, in an uncomplicated pregnancy. All her developmental milestones were normal. Her school performance in special education was good.

On examination, the patient appeared older than her stated age, was unkempt and had poor personal hygiene. Her posture was appropriate and she was restless; she paced in her room and the ED hallway. Her behavior was uncooperative with minimal eye contact and rapid speech. She was anxious, tearful, and had blunted affect. In addition to hallucinations, the patient reported having delusions of persecution and nihilism. The patient believed that everyone was going to die soon and that demons were coming to impregnate her. She was hypervigilant at the time of evaluation but had been previously drowsy after the seizure. Upon examination, she was oriented to person and place but only partially in time. Memory and cognition were not tested in full because the patient became uncooperative during the interview. Her insight was impaired as she denied her mental illness and was non-compliant with medications.

The patient was first admitted to the medical section of the hospital after her seizure episode because laboratory results showed that her carbamazepine level was sub-therapeutic. Her workup included blood work and CT scan, which were both normal. She was transferred to the psychiatric unit because she continued to have disorganized behavior and was unable to care for herself in the hospital after her seizure medications were at therapeutic levels.

The patient was started on aripiprazole 5 mg orally daily; carbamazepine 200 mg oral twice daily; and phenytoin 100 mg oral three times daily. She was taking lorazepam, haloperidol, and benztropine for agitation and extra pyramidal symptoms as needed. Neurology consult was also requested; her EEG was abnormal, consistent with a structural/irritative lesion in the left hemisphere that generalized, possibly contributing to the seizures.

In 4 days of psychiatric hospitalization, the patient experienced another episode of seizure-like activity for less than a minute without loss of consciousness. Laboratory values showed phenytoin level was at the lower end of the therapeutic range and carbamazepine levels were subtherapeutic. Carbamazepine was titrated up to 200 mg oral three times a day.

The patient was started on valproic acid ER 1,000 mg orally every night; lamotrigine 25 mg orally daily; and phenobarbital 120 mg every night. Aripiprazole was discontinued; the patient was started on olanzapine 5 mg orally daily with titration up to 10 mg in 5 days, and 10 mg orally twice daily subsequently. No improvement was noticed after 7 days of being compliant with the treatment.

Olanzapine was gradually discontinued; the patient was started on haloperidol 5 mg orally twice daily with benztropine 0.5 mg oral twice daily. After 4 days of treatment, the patient’s condition was markedly improved, with no reported delusions, hallucinations, or agitation. She was discharged home in stable and overall improved condition with the plan to follow up with a neurologist and psychiatrist. Her discharge medications were haloperidol 5 mg orally twice daily; benztropine 0.5 mg orally twice daily; carbamazepine 200 mg orally three times daily; valproic acid ER 1,000 mg orally every night; and phenobarbital 120 mg orally every night.

Diagnosis

Ictal Psychosis

Discussion

Ictal psychosis [IP] is associated with visual or auditory illusions, hallucinations, and affective changes. Postictal psychosis [PIP] occurs in 2% to 7.8% of epilepsy patients;1 it is often caused by complex partial and secondarily generalized seizures, and causes 25% of epilepsy-related psychosis.

Hallucinations result from the activation of a localized group of neurons, and are investigated by cerebral recording and cerebral stimulation. Tests for psychosis in epilepsy include EEG, structural magnetic resonance imaging, and stereoelectroencephalography, which show semicontinuous/continuous epileptic activity in limbic structures. Preventing this activity can help prevent the psychotic episodes.

Antipsychotic Treatment

Antipsychotic medications can lower the seizure threshold and exacerbate seizures; they should be prescribed with utmost care. Hallucinations and delusions respond best to antipsychotics. Ziprasidone is preferred to treat and prevent postictal and chronic interictal psychosis because of its affective and anxiolytic qualities. Risperidone, quetiapine, and aripiprazole are also commonly used agents.1

Our patient did not respond to aripiprazole and olanzapine, making the treatment more complicated. Haloperidol stabilized the patient and resolved her psychotic symptoms. Haloperidol has best antipsychotic action without decreasing epileptogenic threshold.2 It is indicated mainly for acute and severe psychotic states that require rapid onset of action for a short time period.2 Antiepileptic drugs increase the metabolism of antipsychotics, requiring higher doses of antipsychotics for treating the psychosis of epilepsy and increasing the risk of side effects.2

Despite many available treatment options, almost 30% of epilepsy patients still continue to have seizures.3 Deep brain stimulation technique is being investigated as a prospective epilepsy treatment. It could avoid functional deficits associated with epilepsy surgery and minimize side effects of antiepileptic medications.4 Deep brain stimulation may cause kindling antagonism; ie, stimulation in one area can inhibit the formation of kindled seizures from another site.5 Intermittent stimulation is less likely to cause neural tissue damage and functional disruption or habituation.

Experimental research indicates that altering the specific timing of stimulation might be more efficient than continuous, scheduled, or random stimulation.3

Stimulation is most effective if they were applied early and at the primary seizure onset zones.6 The key is detecting of electrographic seizures and applying electrical stimulus to stop them and prevent onset of symptoms.4 Responsive stimulation targets the seizure onset zone in the cortex or hippocampus. It can target two spatially separated seizure onset zones, making it the best treatment option for multifocal or bilateral epilepsy.4 Responsive stimulation is known to have temporal and spatial specificity.

Studies of responsive stimulation on small populations showed reduced seizures; responsive stimulation was found to be safe and well tolerated.7–9

Conclusion

More thorough investigation and detection is needed for the epileptogenic foci causing abnormal electrical discharges that lead to the development of psychotic syndromes in these patients. Responsive neurostimulation is displaying favorable preliminary results in treatment-resistant patients by targeting the seizure onset zones, preventing the occurrence of epilepsy and associated psychotic syndromes. In the meantime, haloperidol is a reasonable option to manage psychosis associated with epilepsy.

References

  1. Nadkarni S, Arnedo V, Devinsky O. Psychosis in epilepsy patients. Epilepsia. 2007;48Suppl 9:17–19. doi:10.1111/j.1528-1167.2007.01394.x [CrossRef]
  2. Guarnieri R, Hallak JE, Walz R, et al. [Pharmacological treatment of psychosis in epilepsy]. Rev Bras Psiquiatr. 2004;26(1):57–61. doi:10.1590/S1516-44462004000100014 [CrossRef]
  3. Sun FT, Morrell MJ, Wharen RE Jr, . Responsive cortical stimulation for the treatment of epilepsy. Neurotherapeutics. 2008;5(1):68–74. doi:10.1016/j.nurt.2007.10.069 [CrossRef]
  4. Jobst BC, Darcey TM, Thadani VM, Roberts DW. Brain stimulation for the treatment of epilepsy. Epilepsia. 2010;51Suppl 3:88–92. doi:10.1111/j.1528-1167.2010.02618.x [CrossRef]
  5. Bertram E. The relevance of kindling for human epilepsy. Epilepsia. 2007;48Suppl 2:65–74. doi:10.1111/j.1528-1167.2007.01068.x [CrossRef]
  6. Motamedi GK, Lesser RP, Miglioretti DL, et al. Optimizing parameters for terminating cortical afterdischarges with pulse stimulation. Epilepsia. 2002;43(8):836–846. doi:10.1046/j.1528-1157.2002.24901.x [CrossRef]
  7. Anderson WS, Kossoff EH, Bergey GK, Jallo GI. Implantation of a responsive neurostimulator device in patients with refractory epilepsy. Neurosurg Focus. 2008;25(3):E12. doi:10.3171/FOC/2008/25/9/E12 [CrossRef]
  8. Kossoff EH, Ritzl EK, Politsky JM, et al. Effect of an external responsive neurostimulator on seizures and electrographic discharges during subdural electrode monitoring. Epilepsia. 2004;45(12):1560–1567. doi:10.1111/j.0013-9580.2004.26104.x [CrossRef]
  9. Osorio I, Frei MG, Sunderam S, et al. Automated seizure abatement in humans using electrical stimulation. Ann Neurol. 2005;57(2):258–268. doi:10.1002/ana.20377 [CrossRef]
Authors

Deepa Hasija, MD; Sree Latha Krishna Jadapalle, MD; and Amel Badr, MD, are all with Bergen Regional Medical Center, Paramus, NJ. Deepa Hasija, MD, is Associate Chief of Research; Sree Latha Krishna Jadapalle, MD, is research assistant in psychiatry; Amel Badr, MD, is Program Director, Psychiatry Residency Training Program.

Drs. Hasija, Jadapalle, and Badr have disclosed no relevant financial relationships.

Address correspondence to: Deepa Hasija, MD, via email: .dhasija@bergen-regional.com

10.3928/00485713-20111229-03

Sign up to receive

Journal E-contents