Acessibilidade / Reportar erro

Recurrent post-ictal hyperthermia

Hipertermia pós-ictal recorrente

LETTERS

Recurrent post-ictal hyperthermia

Hipertermia pós-ictal recorrente

Sofia Rocha; Filipa Sousa; João Pinho; Ricardo Maré; Álvaro Machado

Department of Neurology, Hospital of Braga, Braga, Portugal

Correspondence Correspondence: Sofia Rocha Serviço de Neurologia, Hospital de Braga Sete Fontes / São Victor 4710-243 Braga - Portugal E-mail: sofiarocha99@hotmail.com

Hyperthermia is a well-known precipitant of seizures, especially in susceptible individuals and in children1,2. Its occurrence following epileptic seizures or exclusively peri-ictally is rarely described2.

CASE REPORT

An 80-year-old hypertensive man, with epileptic seizures of unknown etiology, since his 70th's, was observed for 3 times in 4 years with self-limited right focal motor seizures with impairment of consciousness. In all these episodes, he had post-ictal global aphasia, right homonymous hemianopsia, right hemiparesis and hyperthermia (38–39.6°C). Complete clinical workups during these events (including C reactive protein, sedimentation rate, leukocyte count, thorax radiograph, urinalysis, and lumber puncture) ruled out an infection. Brain magnetic resonance imaging and computerized tomography showed old lacunar basal ganglia infarcts and generalized atrophy. Electroencephalogram (EEG) obtained in two of these episodes revealed in one of them slow background activity of 6–7 Hz, with continuous slow theta/delta activity in left fronto-temporal region, with paroxysmal activity (spikes and sharp waves) in the same localization. The patient was treated with valproate and antipyretics (paracetamol and lysine acetylsalicylate). The hyperthermia did not respond to these drugs, but resolved spontaneously in 12–18 hours and the neurological deficits recovered within 24 hours.

DISCUSSION

Transient post-ictal hyperthermia may follow generalized convulsive status epilepticus2,3. In our case, over four years of follow-up, the patient presented three episodes of right focal motor seizures with consciousness impairment and a prolonged post-critic with aphasia, right homonymous hemianopsia, right hemiparesis, and hyperthermia. There was no fever preceding seizures or convulsive status epilepticus. In all of them, an infectious cause of hyperthermia was exhaustively investigated. Such research was always negative. Therefore, we interpreted hyperthermia as a post-ictal manifestation.

Post-ictal hyperthermia seems to be a quite infrequent symptom and it has been rarely described2. Rossetti et al.2 reported two cases and reviewed the literature of the last 40 years. They found another eight reports of peri-ictal fever, which were mainly related to non-convulsive seizures, involving all age groups (5–83 years old), display a relatively short duration (8–96 hours) and showed mostly bi-temporal EEG alterations.

The exact mechanisms that underlie the onset of hyperthermia in the peri-ictal period are not well established. It seems possible that the thermoregulatory center in the hypothalamic pre-optic area may be affected by spreading epileptic activity, and thus cause elevated body temperature3-5. The mesial temporal lobe structures have extensive connections with the neuroendocrine hypothalamus portion, and a discharging temporal focus can possibly alter hypothalamic function3. Another mechanism may involve vagal nerve nuclei (nucleus tractus solitarius) modulation during seizures2. Seizure-induced production of pyrogens in several brain regions, such as neocortex, amygdala, and hippocampus, appears as an alternative2.

The knowledge of the existence of post-ictal hyperthermia could improve the medical management of subjects presenting with. Indeed, fever does not always imply infection, inflammation or malignancy, even though they are still the most common causes4. Whilst a seizure occurring in a febrile context should generally prompt investigations to detect an infectious etiology, repetitive occurrence of this feature should raise the suspicion of a post-ictal symptom.

Received 14 May 2012

Received in final form 18 May 2012

Accepted 29 May 2012

Conflict of interest: There is no conflict of interest to declare.

  • 1. Kang J, Shen W, Macdonald R. Why does fever trigger febrile seizures? GABAA receptor γ2 subunit mutations associated with idiopathic generalized epilepsies have temperature-dependent trafficking deficiencies. J Neurosci 2006;26:2590-2597.
  • 2. Rossetti A, Tosi C, Despland P, Staedler C. Post-ictal fever: a rare symptom of partial seizures. Eur J Neurol 2007;14:586-590.
  • 3. El-Ad B, Neufeld M. Periodic febrile confusion as a presentation of complex status epilepticus. Acta Neurol Scand 1990;82:350-352.
  • 4. Chan K. Epilepsy another cause of intermittent fever with confusion. Postgrad Med J 1992;68:119-120.
  • 5. Meo R, Bilo L, Striano S, Ruosi P, Estraneo A, Nocerino C. Transient global amnesia of epileptic origin accompanied by fever. Seizure 1995;4:311-317.
  • Correspondence:

    Sofia Rocha
    Serviço de Neurologia, Hospital de Braga
    Sete Fontes / São Victor
    4710-243 Braga - Portugal
    E-mail:
  • Publication Dates

    • Publication in this collection
      03 Jan 2013
    • Date of issue
      Dec 2012
    Academia Brasileira de Neurologia - ABNEURO R. Vergueiro, 1353 sl.1404 - Ed. Top Towers Offices Torre Norte, 04101-000 São Paulo SP Brazil, Tel.: +55 11 5084-9463 | +55 11 5083-3876 - São Paulo - SP - Brazil
    E-mail: revista.arquivos@abneuro.org