|Year : 2013 | Volume
| Issue : 2 | Page : 153-155
Non-convulsive status epilepticus presenting with catatonia and suicidal behavior
Balaji Bharadwaj, Sugaparaneetharan Ayyanar, Jayant Mahadevan, Ravi P Rajkumar
Department of Psychiatry, Neuropsychiatry Clinic, JIPMER, Puducherry, India
|Date of Submission||10-May-2012|
|Date of Acceptance||20-May-2012|
|Date of Web Publication||3-Jun-2013|
Neuropsychiatry Clinic, Department of Psychiatry, JIPMER, Puducherry- 605 006
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Non-convulsive status epilepticus (NCSE) is an uncommon clinical entity. An electroencephalogram (EEG) helps in diagnosis of NCSE, in cases without overt motor manifestations of seizures such as automatisms. We describe an 18-year-old patient with NCSE, who had presented with catatonia and suicidal attempts. There were no automatisms or eye signs indicative of seizure. He had an episode of tonic neck deviation followed by incontinence, which first alerted us to the possibility of epilepsy. An abnormal EEG and a clinical response along with correction of EEG abnormalities with diazepam clarified the diagnosis. Management and hospital course are described in brief. The patient had residual symptoms, suggestive of a postictal state at discharge. The case shows the importance of keeping NCSE as a differential diagnosis, in cases presenting with catatonic symptoms, perplexity, and confusion. The presence of fleeting hallucinations and behavioral disturbances indicate limbic seizures in such cases, presenting in a catatonic state.
Keywords: Catatonia, delayed diagnosis, electroencephalogram, Non-convulsive status epilepticus
|How to cite this article:|
Bharadwaj B, Ayyanar S, Mahadevan J, Rajkumar RP. Non-convulsive status epilepticus presenting with catatonia and suicidal behavior. Int J Nutr Pharmacol Neurol Dis 2013;3:153-5
|How to cite this URL:|
Bharadwaj B, Ayyanar S, Mahadevan J, Rajkumar RP. Non-convulsive status epilepticus presenting with catatonia and suicidal behavior. Int J Nutr Pharmacol Neurol Dis [serial online] 2013 [cited 2020 Jun 6];3:153-5. Available from: http://www.ijnpnd.com/text.asp?2013/3/2/153/112846
| Introduction|| |
An epileptic seizure was defined by Chadwick  as, "an intermittent, stereotyped, disturbance of consciousness, behavior, emotion, motor function, or sensation that on clinical grounds is believed to result from cortical neuronal discharge." 'Complex partial seizures' are partial seizures with impairment of consciousness.  The diagnosis of complex partial seizures depends on the history of typical oro-motor or other automatisms. Limbic seizures without overt automatisms can occur commonly, as they are localized to the ipsilateral lobe in two-thirds of the cases. Such cases may present with an aura consisting of psychiatric symptoms. Automatisms occur only in 22% of the ipsilateral temporal lobe seizures and in 77% of the cases, when there is a spread of seizure activity to the contralateral side.  In a previous report of three cases, catatonic symptoms have appeared during a non-convulsive status, but the cases were noted to have a past history of generalized seizures. 
There may be a few cases of status epilepticus where the convulsive movements are not obvious. Such a condition is known as non-convulsive status epilepticus (NCSE) and may mimic psychiatric illness in its presentation. We describe the case of a boy with NCSE, presenting to Psychiatry in a catatonic state, with a history of febrile seizures in childhood.
| Case Report|| |
An 18-year-old boy presented with a one-month history of motiveless wandering, perplexity, poor speech output, and three attempts of suicide. One attempt was by pouring kerosene over himself and attempting to immolate himself, while two other attempts were to drown himself by walking neck-deep into a canal near his home. He was admitted to Psychiatry with a provisional diagnosis of acute psychotic illness. He had a history of appearing absent-minded, being confused when he was asked to fetch objects, and sometimes not responding to name call, in the preceding two years.
The patient had a past history of two episodes of febrile seizures at the age of three years. There was no subsequent history of seizures. Childhood and early developmental milestones were normal. He was an average student at school. There was no family history of seizures or mental illness.
Mental status examination revealed no delusions or hallucinations, despite an apparently perplexed and fearful facial expression. He showed catatonic features including mutism, posturing, and staring. He responded well to an initial trial of Lorazepam up to 16 mg per day, with improvement of all his symptoms. We tapered Lorazepam and planned to initiate an antipsychotic if the patient reported any psychotic symptoms. On discontinuing Lorazepam, however, the patient had an event, where during an interview with us, he stopped talking, suddenly rose from his chair, turned his head to one side, appeared fearful, and then became incontinent. He subsequently went back to his bed, but there was no drowsiness, and a neurological examination was unremarkable following the event, except for muted plantars. An EEG showed slowing in the frontal and temporal leads intermittently during hyperventilation [Figure 1]a. Computed tomography (CT) of the brain, thyroid function tests, and other biochemical parameters were unremarkable. We initiated treatment with Carbamazepine in view of the witnessed adversive seizure and abnormal EEG. The patient responded well to Carbamazepine at a dose of 600 mg per day, but reported occasional auditory hallucinations of, "ghosts speaking to him," at discharge.
|Figure 1: (a) Delta range slowing during hyperventilation in the initial record. The patient was on lorazepam. (b) Generalized slowing of background, with frontal spike and wave discharges [Arrows) during the second admission [NCSE], when he had discontinued carbamazepine. There was clinical improvement, with normalization|
of EEG (c), after a 5 mg bolus of diazepam was given intravenously
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He developed a generalized maculopapular rash about ten days after discharge, which prompted the family members to stop the drug immediately. The rash was evaluated and treated with oral steroids. The discontinuation also coincided with a worsening of symptoms, which prompted us to do a repeat video-EEG study. This revealed sharp waves in Fp1/F7 leads (Arrows) and slowing in the right frontal leads and generalized slow waves [Figure 1]b. Both the clinical and EEG abnormalities resolved [Figure 1]c when a bolus dose of 5 mg Diazepam was administered. An MRI study of the brain was normal. Due to lack of affordability for tests of anti-NMDA receptor antibody or anti-thyroid antibody, these tests were not done. Hence, autoimmune encephalopathy could not be effectively ruled out in this case.
He was given phenytoin with only partial control of symptoms, the catatonic state persisted. The patient was given an empirical trial of methylprednisolone (1 g) IV for five days. Subsequently, the patient showed good control of his seizures with adequate doses of phenytoin and levetiracetam, with a residual catatonic state, which was treated with diazepam and olanzapine. The patient showed a partial response, without complete recovery. Informed consent was obtained from the father, as the patient was not in clear sensorium, to obtain a valid consent.
| Discussion|| |
This case illustrates the importance of keeping a high-index of suspicion for epileptic etiology, in cases presenting with catatonia. The presence of confusion and an impaired mental state, the episode of urinary incontinence, and the absence of classical psychiatric symptoms, such as, persistent hallucinations or delusions, alerted us to a possible epileptic etiology in this case. The preceding two-year history of episodes of unresponsiveness to simple commands and febrile seizures in childhood was not forthcoming in the initial history, leading to a delayed diagnosis.
The three episodes of fugue and suicidal attempts within a span of one month, without suicidal intent or a plan, was unlike the suicidal attempts seen in psychiatric disorders. There were no persistent psychiatric symptoms except fleeting auditory hallucinations. The patient had catatonic features such as mutism, posturing, negativism, and impulsive behavior (wandering away). However, the lack of contact with surroundings and inappropriate responses to environmental cues, with incomprehensible mumbling or echolalia were very much unlike the usual picture of catatonia. The episode of tonic neck deviation and incontinence alerted us to the epileptic etiology in this case. Severely impaired mental state and remote risk factors for seizures have been seen to predict NCSE, in a previous study. 
Episodes of epileptic fugue (poriomania) have been described in literature.  Whether the episodes of wandering constitute a postictal phenomenon or are part of a complex partial status is a matter of debate.
The initial EEG had shown only non-specific changes and was taken to be indicative of epileptic etiology, due to the witnessed tonic seizure. Even in the second EEG, there was a gross abnormality of EEG in the form of slowing, but no typical spike and wave discharges suggestive of epilepsy. The clinical and EEG improvement after diazepam was strongly indicative of a complex partial status.
Epileptic states as well as catatonia can respond to lorazepam. However, the maintenance of improvement with carbamazepine monotherapy is supportive of an epileptic etiology. The patient had a relapse when carbamazepine was discontinued due to a hypersensitivity reaction.
He subsequently showed only a partial improvement with a combination of phenytoin and levetiracetam. The residual state was possibly postictal confusion, which was treated with olanzapine. The patient was not available for post-discharge follow-up.
| Conclusions|| |
A high index of suspicion for an epileptic etiology should be maintained in cases presenting with a catatonic feature and impaired mental state.
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