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Year : 2018  |  Volume : 7  |  Issue : 3  |  Page : 204-206

A rare presentation of complex partial seizures

Department of Psychiatry, JSS Medical College and Hospital, JSS Academy of Higher Education and Research, Mysore, Karnataka, India

Date of Web Publication20-Jul-2018

Correspondence Address:
Dr. M Kishor
Department of Psychiatry, JSS Medical College and Hospital, JSS Academy of Higher Education and Research, Mysore, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijhas.IJHAS_155_17

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Complex partial seizures occur when an epileptic discharge arises from a localized region of a cerebral hemisphere along with involvement of some degree of impaired consciousness. They have varied clinical presentations and mimic many clinical syndromes. We hereby report a case of a 39-year-old man who presents with symptoms suggestive of mania and was treated with antipsychotics with minimal improvement in symptoms. Subsequently, following a detailed evaluation, he was diagnosed to have temporal lobe epilepsy. The case presents the diagnostic dilemma involved in dealing with atypical presentations of epilepsy.

Keywords: Atypical presentations of epilepsy, behavioral disturbances in the postictal phase, mania, temporal lobe epilepsy

How to cite this article:
Bhargava S, Chandran S, Manohar J S, Kishor M. A rare presentation of complex partial seizures. Int J Health Allied Sci 2018;7:204-6

How to cite this URL:
Bhargava S, Chandran S, Manohar J S, Kishor M. A rare presentation of complex partial seizures. Int J Health Allied Sci [serial online] 2018 [cited 2023 Jun 6];7:204-6. Available from: https://www.ijhas.in/text.asp?2018/7/3/204/237257

  Introduction Top

Complex partial seizures (CPSs) occur when an epileptic discharge arises from a localized region of a cerebral hemisphere along with involvement of some degree of impaired consciousness.[1] CPSs have varied clinical presentations which mimic many clinical syndromes such as absence seizures, panic disorder, adult petit mal epilepsy or epilepsia partialis continua. One presentation of temporal lobe epilepsy (TLE) is a complex partial seizure which produces the most diverse and complex auras of all and accounts for 4–10 cases per 1000 of all epilepsy cases.[2] Patients with TLE often have a brief postictal state with slow gradual recovery characterized by confusion and disorientation.[3] Common postictal phenomenons include postictal delirium, nose wiping, hypersalivation, and headache. Less common postictal behaviors include violence, wandering, psychosis, and Todd's paresis.[4] Features of aggressive behaviors have also been observed in epileptic seizures with particular reference to the act of biting.[5] Other reports of homicidal behavior, experiential, and affective phenomenon have also been recorded. We hereby report a case of a 39-year-old man who presented with symptoms of mania, but following a detailed evaluation, he was diagnosed to have TLE.

  Case Report Top

A 39-year-old male patient, Mr. D, came with the complaints of menacing posturing, loud exclamation of abusive words, constantly screaming at family members, talking to himself, taking currency notes from his wallet and throwing it all over the floor, hallucinatory behavior such as muttering to self, blankly staring at the wall, smacking his hands together, and punching nearby objects. He had brief episodes of wandering away from home and was found circling a tree and repeatedly entering and exiting his car along with throwing away his car keys. The concerned family members took him to a local hospital where he was admitted for a day with minimal improvement in symptoms and subsequently was brought to the casualty of our hospital. The symptoms of the patient were rapidly progressive and evolved within a span of 2 days.

On examination, the patient was restless and was aimlessly walking around the ward. He had increased psychomotor activity and increased rate of speech with frequent repetition of words. A provisional diagnosis of mania was made and the patient was started on antipsychotics for a span of 2 days with no improvement in symptoms.

Subsequently, on the second day of admission, the staff noticed a similar episode where the patient was throwing keys on the floor and picking them up in the ward. The behavior was episodic and lasted for about 2–3 min. During this episode, on examination, his pupils were dilated. Subsequently, the patient was found screaming at his caregiver with the use of abusive language and pacing around in the ward.

With no response to antipsychotics, nil significant history of psychiatric disorders, nil significant family history of psychiatric illnesses, no associated legal and financial stressors, no history of any altercations, and no history of substance use combined with collection of collateral data from multiple family members, other differential diagnosis were considered.

Magnetic resonance imaging (MRI) was done to screen for organic causes which indicated no abnormality. Subsequently, an electroencephalography (EEG) was done which showed spikes and sharp waves in both the temporal lobes.

On the basis of presence of ambulatory and cursive automatisms, a characteristic feature of complex partial seizure and an aid from the EEG the diagnosis of TLE was made. The patient was started on fosphenytoin iv (150 mg BD) and levetiracetam iv (500 mg BD) and his condition showed significant improvement over the course of a couple of days. He was then put on maintenance therapy with phenytoin (300 mg) and levetiracetam (1 g) orally.

  Discussion Top

Seventy million cases of epilepsy have been recorded globally out of which 12 million cases are from India, attributing to 1% of disease burden in the country.[6] Out of the global prevalence of epilepsy, 36% is attributed to CPS. Patients with CPS may manifest a wide variety of symptoms, including paroxysmal anxiety or somatic symptoms, stereotyped movements or behaviors, bizarre or incongruous affect, and changes in cognition. Because of these effective, behavioral, and cognitive symptoms, patients with CPS are frequently misdiagnosed with psychiatric illnesses. Often, these symptoms present with unusual qualities that are atypical for primary psychiatric syndromes. These can include gustatory and olfactory hallucinations; micropsia or macropsia.[7]

Some phenomena are well known as peculiar epileptic experiences with intense delusions such as deja vu, deja vecu, and dreaming state or sometimes patients also complain of out-of-body experiences.[8] CPSs have also been associated with certain personality features including moral rigidity, hyperreligiosity, hypergraphia, and stickiness of skin. At times, they experience difficulty in ending conversations.[9] Unfortunately, there are few epidemiological studies in TLE. The best available epidemiological data were provided by Hauser and Kurland who estimated the prevalence of TLE in 1960 to be 1.7/1000 people.[10]

Mood disorders are common in people with epilepsy with prevalence rate of 20%–50%; the higher prevalence rates have been typically identified in patients with poorly controlled epilepsy.[11] During the phase of altered sensorium in patients with CPS, the patient commonly engages in repetitive semi-purposeful activities known as automatisms. The most common are oroalimentary automatisms, which include, chewing, swallowing movements, and lip smacking. Gestural automatisms which are repetitive fidgeting, picking at, or adjusting of clothing or handling or objects within easy reach are also frequent. Preservative automatisms might represent continuation of complex motor acts initiated before seizure onset, for example, opening and closing a door repeatedly. Vocal automatisms may include perseverative utterances sometimes known as epileptic palilalia or gelastic seizures such as humming, singing, and laughing.[12]

Features of aggressive behaviors have also been observed in the postictal phase with particular reference to the act of biting which was confirmed by videotape recordings. The recordings synchronized with the EEG recordings, and when subjected to further behavioral data analysis, it was observed that an ictal discharge has to develop into the brain, disrupting frontotemporal limbic networks.[5]

Wandering is commonly noticed in these cases and may seem semi-purposeful, as if though patient is searching for something or trying to escape. These are referred to as ambulatory automatisms. Another phenomenon noticed is that of cursive seizures, wherein the patient is seen walking or running in circles.[1] In this case, the patient's behavior of circling a tree and repeatedly entering and exiting his car along with throwing away his car keys could probably have been automatisms.

Altered perceptual experiences are also reported which include both distortions of real perceptions (illusions) and spontaneous hallucinations. Sounds may seem suddenly remote or intensely loud. Auditory hallucinations may be simple or complex, ranging from ringing and buzzing noises to organized experiences such as music or voices [1]

Patients with TLE often have a brief postictal state with slow gradual recovery characterized by confusion and disorientation. However, cases have been reported with less common postictal phenomenon of wandering and symptoms of mania in about 22% of patients and are often with associated psychotic phenomenology as seen in this case.[13]

In this case, the patient was constantly screaming at family members and talking to himself and had increased rate of speech with frequent repetition of words and loud exclamation of abusive words, which could be suggestive of a postictal phenomenology. A prolonged postictal phase can lead to high degree of cognitive deficits such as mental slowness, memory difficulties, and attention deficits, and hence, early diagnosis and intervention is necessary.[14]

Pandya et al. reported a rare case of a patient with intractable epilepsy and escalating aggression, resulting in homicide, who had complete resolution of her seizures and explosive behavior following a right temporal lobectomy.[15]

EEGs, which detect abnormal patterns of cortical electrical activity, can be helpful in characterizing and localizing many types of seizures. However, because electrical discharges due to CPS may involve only subcortical brain regions, EEG findings may appear nonspecific or unremarkable even during active seizures. Thus, without further diagnostic workup, patients with CPS may be incorrectly assumed to carry a primary psychiatric diagnosis. Hence, it should be kept in mind that a normal EEG report does not rule out the presence of a seizure episode.[9]

Reports have confirmed that most ictal psychiatric symptoms seem to be related to the activation of the nondominant hemisphere. Differential diagnoses should be formulated with appropriate consideration of stereotypy and accompanying automatisms.[8]

Some cases have a presentation of mania masking an underlying seizure episode. The concept of complex partial seizure mimickers is hence important. They have varied clinical presentations such as those of absence seizures, aphasia, apraxia, and related syndromes, panic disorder, TLE, frontal lobe epilepsy, adult petit mal epilepsy, epilepsia partialis continua, epileptic and epileptiform encephalopathies, and psychogenic nonepileptic seizures.[16]

  Conclusion Top

Rarely, psychiatric abnormalities reported in patients with epilepsy are mood disorders but are likely to occur in TLE and hence present as a diagnostic dilemma. It should always be kept in mind that a lack of suspicion of CPS leads to trial of different drugs which causes side effects and delay in recovery process. Furthermore, different modalities of presentation of CPS intertwined with prominent behavioral symptoms require a detailed evaluation.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

David A. Lishman's Organic Psychiatry. Chichester, U.K.: Wiley-Blackwell; 2012. p. 309-22.  Back to cited text no. 1
Téllez-Zenteno JF, Hernández-Ronquillo L. A review of the epidemiology of temporal lobe epilepsy. Epilepsy Res Treat 2012;2012:630853.  Back to cited text no. 2
Grant AC, Koziorynska E, Lushbough C, Maus D, Mortati K. Acute postictal confusion and violence: Two cases with unfortunate outcomes. Epilepsy Behav Case Rep 2013;1:71-3.  Back to cited text no. 3
Caicoya AG, Serratosa JM. Postictal behaviour in temporal lobe epilepsy. Epileptic Disord 2006;8:228-31.  Back to cited text no. 4
Tassinari CA, Tassi L, Calandra-Buonaura G, Stanzani-Maserati M, Fini N, Pizza F, et al. Biting behavior, aggression, and seizures. Epilepsia 2005;46:654-63.  Back to cited text no. 5
Amudhan S, Gururaj G, Satishchandra P. Epilepsy in India I: Epidemiology and public health. Ann Indian Acad Neurol 2015;18:263-77.  Back to cited text no. 6
[PUBMED]  [Full text]  
Roffman JL, Stern TA. A complex presentation of complex partial seizures. Prim Care Companion J Clin Psychiatry 2006;8:98-100.  Back to cited text no. 7
Mula M. Epilepsy-induced behavioral changes during the ictal phase. Epilepsy Behav 2014;30:14-6.  Back to cited text no. 8
Geschwind N. Behavioural changes in temporal lobe epilepsy. Psychol Med 1979;9:217-9.  Back to cited text no. 9
Hauser WA, Kurland LT. The epidemiology of epilepsy in Rochester, Minnesota, 1935 through 1967. Epilepsia 1975;16:1-66.  Back to cited text no. 10
Kanner AM. Epilepsy and mood disorders. Epilepsia 2007;48 Suppl 9:20-2.  Back to cited text no. 11
Blair RD. Temporal lobe epilepsy semiology. Epilepsy Res Treat 2012;2012:751510.  Back to cited text no. 12
Mula M, Monaco F. Ictal and peri-ictal psychopathology. Behav Neurol 2011;24:21-5.  Back to cited text no. 13
Gaitatzis A, Trimble MR, Sander JW. The psychiatric comorbidity of epilepsy. Acta Neurol Scand 2004;110:207-20.  Back to cited text no. 14
Pandya NS, Vrbancic M, Ladino LD, Téllez-Zenteno JF. Epilepsy and homicide. Neuropsychiatr Dis Treat 2013;9:667-73.  Back to cited text no. 15
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