Over forty different catatonic symptoms have been described to date [2, 7, 12]. These may be subdivided into the following four categories: motor phenomena (stupor, catalepsy, rigidity, flexibilitas cerea), withdrawal (mutism, staring gaze, negativism, refusal to eat and drink), excitement (hyperactivity, combativeness, autonomous instability, undirected potentially dangerous aggression) and odd repetitive behaviour (grimacing echolalia, echopraxia, stereotypies, manierisms, perseveration, command-automatism, Mitmachen and Gegenhalten, and ambitendency) [7, 9, 13].

Catatonia can be divided into four types [5, 7, 13, 14]. There is the hyperkinetic type of catatonia, characterized by agitation, combativeness [15], verbigeration, stereotypies, echolalia and echopraxia. The stuporous type is characterized by stupor, mutism, posturing and negativism. A third type is lethal or malignant catatonia: an often acutely emerged state involving alterations in consciousness, fever, severe rigidity and autonomous instability. The fourth type is periodic catatonia, characterized by the cyclic return of symptoms of catatonia. These episodes last an average of four to 10 days and can return within weeks or years [9].

The differential diagnosis may be challenging given the current lack of biomarkers and symptom aspecificity. The following conditions need to be considered in the differential diagnosis: malignant antipsychotic syndrome, extrapyramidal side effects of psychopharmacological medication, hyperammonemic encephalopathy [16], acute dystonia, tardive dyskinesia, akathisia, manic episodes, delirium, compulsory movement disorders, conversion disorder, certain compulsions in OCD, serotonin syndrome, locked-in syndrome, vegetative state and stiff person syndrome, kinetic disorders with hypocalcemia, tetanus, strychnine toxicity, rabies and complex partial epilepsy, nonconvulsive status epilepticus [2, 4, 9, 17–19].

In our differential diagnosis we also considered the following: complex partial epileptic seizures [9, 18, 19], postictal akinesia [20], postictal delirium [19], hypoactive delirium [9], nonconvulsive status epilepticus [4, 9], postictal psychosis [21, 22] and non-psychiatric stupor (characterized by immobility, mutism, absence of response to stimuli; this kind of stupor has other causes than catatonia, such as head trauma, anoxia, epilepsy and encephalopathy of unknown origin) [18].

First we would like to address whether it was an ES and not a psychogenic epileptic seizure (PNES) the patient had suffered from. We could not obtain a video EEG, so there is no certainty since video-EEG is the gold standard for such differentiation. We detected however, after the first and second seizures, the last of which was observed by medical staff, a substantial increase in CK which, according to experts, could be a diagnostic instrument for differentiating between ES and PNES [23, 24]. So there is reason to assume it were ES and not PNES.

Another important distinction that must be made in this case is between postictal delirium (occurring in 35% of seizure cases and reported to last sometimes up to 10 days) [25–27] and postictal catatonia as it may substantially influence treatment decision-making [28–30]. Whereas benzodiazepines are used first in cases of catatonia, in delirium such compounds may aggravate symptoms [28–30]. The distinction between the two may be cumbersome given clinical overlap. According to the DSM-5 it is impossible for the two to co-occur since catatonia cannot be diagnosed in the presence of delirium; others question this notion [30]. In addition, Grover [28] found that 12 to 30% of patients with delirium showed symptoms matching the criteria for catatonia.

Another distinction that has to be made is between postictal catatonia and postictal psychosis [21, 22, 31]. Although psychosis as such can be accompanied by catatonic features, this was not the case here as, firstly, except for the psychomotor symptoms, there were no other symptoms of psychosis. Secondly, postictal psychosis is rarely seen with idiopathic generalized epilepsy [21]. And thirdly, postictal psychosis is mostly characterized by delusions of the grandiose or religious type, aggression, pressured speech and excessive emotional response [31].

In our case a diagnosis of catatonia was considered most plausible based on symptomatology (e.g. lack of day-night differences in symptomatology), absence of adverse effects after the lorazepam ‘challenge test’ and repetitive EEGs showing no signs of epileptic activity. Moreover, our observation that the patient remained well-oriented and attentive argued against delirium and that in combination with the absence of delusions or hallucinations none of the above mentioned characteristics of postictal psychosis were present, against postictal psychosis.

The treatment of catatonia initially consists of benzodiazepines [4, 5, 7, 9, 13, 14, 18, 32–35] (effective in 70–80% of all cases) and only when this is ineffective ECT. When ECT is of little help, transcranial magnetic stimulation [18] and NMDA antagonists such as amantadine and memantine [33, 36] may be considered. When these are still ineffective, anticonvulsants can be tried. In some cases, atypical antipsychotics are combined with benzodiazepines [33, 36]. Our patient was treated with valproic acid for epilepsy.

In our case, it was necessary to increase the dose of Lorazepam to 17 mg/d. before we saw clear amelioration of the symptoms. Improvement could in theory also have been attributed to simply time or to the restarted AED since AEDs are also effective in catatonia. But we like to mention that when the AEDs were restarted, the catatonia did not go into remission, and only did so when we augmented the lorazepam to 17 mg/d. Moreover, the fact that the symptoms remained unchanged the first days of occurrence without lorazepam pleads against resolving as a natural course.

The question then arises if ECT would also be a treatment option for our patient. We believe this is since ECT can be given when a patient has a status epilepticus and for catatonia, as mentioned above. There are, to our knowledge, however, no reports of ECT treatment for postictal catatonia.

We searched articles written in Dutch or English in pubmed with the terms ‘post-ictal catatonia’, OR ‘ictal catatonia’ OR ‘catatonia seizures’, OR ‘catatonia postictal state’ OR ‘catatonia and delirium’ as well as cross-references retrieved by our search. We thus found a case series in which four patients developed catatonia during ECT treatment for affective or psychotic disorders [37, 38]. The cause of the catatonia could have been withdrawal of benzodiazepines, besides affective and psychotic disorders, which is supported by the fact that catatonic symptoms disappeared after reinstating benzodiazepines. Two other case reports describe the development of catatonia after ECT, both in patients with a history of bipolar disorder [39, 40], while our patient had no medical history of other psychiatric disorders, except for drug abuse. It is beyond dispute that there is a clear difference between ECT and ES. ECT occurs in a safe environment under controlled circumstances and under narcosis. Furthermore, ECT is often given for conditions that may themselves be accompanied by catatonia. Finally, we found another case report in which catatonia developed postictally, but this patient was known to suffer from schizophrenia [41]. We also found an article by Herman published in 1942 [42], reporting the case of a man stating himself that he suffers from epilepsy. Seizures were, however, not observed and catatonic symptoms were not described clearly.