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 Table of Contents    
LETTER TO EDITOR  
Year : 2017  |  Volume : 59  |  Issue : 3  |  Page : 387-388
Nonconvulsive status epilepticus and central paralysis after modified electroconvulsive therapy in a schizophrenic patient


1 Department of Psychiatry, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, P. R. China
2 Department of Neurology, The Second People's Hospital of Zhengzhou, Zhengzhou, P. R. China
3 Department of Psychiatry, Tianjin Anding Hospital, Tianjin, P. R. China

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Date of Web Publication6-Oct-2017
 

How to cite this article:
Deng P, Wang X, Sui J, Pang J, Liu Q, Li H. Nonconvulsive status epilepticus and central paralysis after modified electroconvulsive therapy in a schizophrenic patient. Indian J Psychiatry 2017;59:387-8

How to cite this URL:
Deng P, Wang X, Sui J, Pang J, Liu Q, Li H. Nonconvulsive status epilepticus and central paralysis after modified electroconvulsive therapy in a schizophrenic patient. Indian J Psychiatry [serial online] 2017 [cited 2019 Oct 22];59:387-8. Available from: http://www.indianjpsychiatry.org/text.asp?2017/59/3/387/216183




Sir,

Modified electroconvulsive therapy (mECT) is an effective treatment for schizophrenia, which has a few complications, including delayed suffocation and severe arrhythmia.[1] There has been little information about convulsive status epilepticus (nonconvulsive status epilepticus [NCSE]) and central paralysis induced by mECT.

A 31-year-old woman had been diagnosed with schizophrenia at the age of 18 years. Generalized tonic-clonic seizures occurred while she was once under treatment with clozapine (100 mg/day), whereby electroencephalogram (EEG) examinations revealed that spike-slow complex waves were located in the right hemisphere [Figure 1].
Figure 1: The first time of electroencephalogram showed 1 Hz spike-slow complex waves on her right hemisphere

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She was admitted to the hospital because of a relapse of schizophrenia and was treated with mECT. A series of symptoms occurred within 1 h after the 6th time mECT, including loss of consciousness, intermittent trembling, muscular twitching in half of her face, limb stiffness, and incontinence. Tonic-clonic seizures occurred abruptly after 2 weeks. Her consciousness recovered after 8-week treatment of magnesium valproate (500 mg/day).

She underwent mECT again without complete withdrawal of magnesium valproate after 16 days. After the 7th time mECT, loss of consciousness, intermittent eye gaze, and limb twitching occurred. At that time, the EEG showed increased β-waves. Magnetic resonance imaging showed brain atrophy. She regained consciousness after 4-week treatments of magnesium valproate (750 mg/day) and levetiracetam (500 mg/day). She remained with unclear articulation and muscle hypertonia of the four limbs. Moreover, she could neither hold things nor walk.

Magnesium valproate (500 mg/day) was used continuously with withdrawal of levetiracetam gradually. After 2 years of functional training, her communication was established. Coordinated movement of the upper limbs returned to normal. Muscle tension of the lower limbs was still elevated in the absence of muscular dystrophy of four limbs. She could walk with the help of others.

These results supported the diagnosis of central paralysis as follows: impaired consciousness, muscle hypertonia of the four limbs, catalepsy, unclear articulation, and brain atrophy on brain magnetic resonance imaging. In addition, the paralysis lasted almost 2 years without muscular dystrophy. Motor function of the four limbs recovered from the upper to the lower limbs. Central paralysis, also called motor neuron palsy, is caused by damage to the cortical motor area and the central pathway (corticospinal tract and cortex–brainstem tract). Since the fibers and cells constituting a fiber bundle in these areas are arranged quite closely, motor neuron paralysis is extensive; it affects the whole body or one side of the body.[2],[3]

Moreover, the lack of reasonable recognition of NCSE causing central paralysis was highly suspected. The definition of NCSE often involves a history of preexisting epilepsy and response to treatment.[4] Furthermore, the features of NCSE are different degrees of impaired consciousness lasting for several weeks or months, myoclonias, catalepsy, mutism, seizures, minor facial twitching, and subtle limb jerks.[4],[5],[6] In this case, mutism and intermittent facial and limb twitches appeared. Unconsciousness continued for several weeks. These were consistent with clinical manifestations described above.

In NCSE, electroencephalographic changes are important. However, only increased β-waves were captured in this case, probably because of treatment with magnesium valproate, which mainly reduces the frequency of interictal discharge and shows no significant effect on the discharge duration, as well as the initiation site and propagation speed.[7]

Financial support and sponsorship

This study was funded by grants from the National Natural Science Foundation of China (81371494).

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Biedermann F, Pfaffenberger N, Baumgartner S, Kemmler G, Fleischhacker WW, Hofer A. Combined clozapine and electroconvulsive therapy in clozapine-resistant schizophrenia: Clinical and cognitive outcomes. J ECT 2011;27:e61-2.  Back to cited text no. 1
    
2.
Adams M, Cavanagh JF. International Campaign for Cures of Spinal Cord Injury Paralysis (ICCP): Another step forward for spinal cord injury research. Spinal Cord 2004;42:273-80.  Back to cited text no. 2
    
3.
Jang SH, Park SM, Kim SH, Ahn SH, Cho YW, Ahn MO. The effect of selective tibial neurotomy and rehabilitation in a quadriplegic patient with ankle spasticity following traumatic brain injury. Yonsei Med J 2004;45:743-7.  Back to cited text no. 3
    
4.
Maganti R, Gerber P, Drees C, Chung S. Nonconvulsive status epilepticus. Epilepsy Behav 2008;12:572-86.  Back to cited text no. 4
    
5.
Kaplan PW. The EEG in metabolic encephalopathy and coma. J Clin Neurophysiol 2004;21:307-18.  Back to cited text no. 5
    
6.
Kaplan PW. The clinical features, diagnosis, and prognosis of nonconvulsive status epilepticus. Neurologist 2005;11:348-61.  Back to cited text no. 6
    
7.
Shi YJ, Gong XW, Gong HQ, Liang PJ, Zhang PM, Lu QC. Effect of the entorhinal cortex on ictal discharges in low-Mg2+-induced epileptic hippocampal slice models. Neural Plast 2014;2014:205912.  Back to cited text no. 7
    

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Correspondence Address:
Hengfen Li
Department of Psychiatry, The First Affiliated Hospital of Zhengzhou University, Zhengzhou
P. R. China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/psychiatry.IndianJPsychiatry_301_16

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