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Cardiogenic syncope in temporal lobe epileptic seizures
  1. CESARE IANI
  1. Clinica Neurologica, Ospedale S Eugenio
  2. Roma
  3. Clinica Neurochirurgica
  4. Università Cattolica S Cuore,
  5. Dipartimento di Medicina Interna
  6. Universita di Roma “Tor Vergata”
  7. IRCCS “S Lucia”, Roma
  8. Dipartimento di Scienze Neurologiche
  9. Policlinico A. Gemelli, Roma
  10. Università di Roma “La Sapienza” and Istituto
  11. Neurologico, Mediterraneo “Neuromed”
  12. Pozzilli (Isernia)
  1. Professor Mario Manfredi, Dipartimento di Scienze Neurologiche, Viale dell’Universita 30, 00185—Roma (Italy).
  1. GABRIELLA COLICCHIO
  1. Clinica Neurologica, Ospedale S Eugenio
  2. Roma
  3. Clinica Neurochirurgica
  4. Università Cattolica S Cuore,
  5. Dipartimento di Medicina Interna
  6. Universita di Roma “Tor Vergata”
  7. IRCCS “S Lucia”, Roma
  8. Dipartimento di Scienze Neurologiche
  9. Policlinico A. Gemelli, Roma
  10. Università di Roma “La Sapienza” and Istituto
  11. Neurologico, Mediterraneo “Neuromed”
  12. Pozzilli (Isernia)
  1. Professor Mario Manfredi, Dipartimento di Scienze Neurologiche, Viale dell’Universita 30, 00185—Roma (Italy).
  1. ANTONIO ATTANASIO
  1. Clinica Neurologica, Ospedale S Eugenio
  2. Roma
  3. Clinica Neurochirurgica
  4. Università Cattolica S Cuore,
  5. Dipartimento di Medicina Interna
  6. Universita di Roma “Tor Vergata”
  7. IRCCS “S Lucia”, Roma
  8. Dipartimento di Scienze Neurologiche
  9. Policlinico A. Gemelli, Roma
  10. Università di Roma “La Sapienza” and Istituto
  11. Neurologico, Mediterraneo “Neuromed”
  12. Pozzilli (Isernia)
  1. Professor Mario Manfredi, Dipartimento di Scienze Neurologiche, Viale dell’Universita 30, 00185—Roma (Italy).
  1. DONATELLA MATTIA
  1. Clinica Neurologica, Ospedale S Eugenio
  2. Roma
  3. Clinica Neurochirurgica
  4. Università Cattolica S Cuore,
  5. Dipartimento di Medicina Interna
  6. Universita di Roma “Tor Vergata”
  7. IRCCS “S Lucia”, Roma
  8. Dipartimento di Scienze Neurologiche
  9. Policlinico A. Gemelli, Roma
  10. Università di Roma “La Sapienza” and Istituto
  11. Neurologico, Mediterraneo “Neuromed”
  12. Pozzilli (Isernia)
  1. Professor Mario Manfredi, Dipartimento di Scienze Neurologiche, Viale dell’Universita 30, 00185—Roma (Italy).
  1. MARIO MANFREDI
  1. Clinica Neurologica, Ospedale S Eugenio
  2. Roma
  3. Clinica Neurochirurgica
  4. Università Cattolica S Cuore,
  5. Dipartimento di Medicina Interna
  6. Universita di Roma “Tor Vergata”
  7. IRCCS “S Lucia”, Roma
  8. Dipartimento di Scienze Neurologiche
  9. Policlinico A. Gemelli, Roma
  10. Università di Roma “La Sapienza” and Istituto
  11. Neurologico, Mediterraneo “Neuromed”
  12. Pozzilli (Isernia)
  1. Professor Mario Manfredi, Dipartimento di Scienze Neurologiche, Viale dell’Universita 30, 00185—Roma (Italy).

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Cardiac arrhythmias may cause syncopal attacks masquerading as epilepsy. Conversely, epileptic seizures can induce tachyarrhythmias or bradyarrhythmias (and rarely, as a result, fainting). Differentiating between these two possibilities may prove difficult without concomitant ECG and EEG recording.

A 39 year old male lorry driver, without cardiac and neurological disorders and not taking medication, was admitted to a coronary care unit after a cluster of episodes of loss of consciousness preceded by epigastric warm sensation and a bitter taste in the mouth, and followed by pallor, sweating, muscle jerking, and rigidity with arrest of the pulse. The episodes occurred both in orthostatism and clinostatism. Clinical investigation, laboratory tests, clinostatic and orthostatic blood pressures, echocardiography, and ECG at rest, during exercise, and during carotid sinus massage were normal.

He experienced another attack while on continuous ECG monitoring. A nurse stated that the patient complained, while standing, of epigastric discomfort, followed by a fleeting phase of unresponsiveness and purposeless arm and mouth movements. A few seconds later he fell and showed a generalised tonic convulsion. The pulse, apparently normal during the initial phase of the episode, abruptly ceased when the patient collapsed. The ECG recording (fig 1) showed a progressive decrease of heart rate, culminating in a sinus arrest of 9.5 seconds, preceding the fall. Another four episodes of sinus arrest of 4-5 seconds, without tonic convulsions, were recorded on the next day.

Figure 1

Two lead Holter recording of a syncopal attack (three uninterrupted minutes). During nausea and epigastric discomfort (minute 11.30) the sinus rhythm, superimposed by sweating and movement artifacts, progressively slows down. The syncope (minute 11.31) coincides with a sinus arrest of 9.5 seconds, intermingled with sporadic junctional escape beats and followed by a sinus rhythm (end of minute 11.31), that progressively accelerates up to 110 bpm (minute 11.32). Muscle artifact at the end of asystole indicates the occurrence of a tonic spell. CM1 = V1, CM5 = V5.

A permanent demand ventricular pace maker programmed to trigger at 40 beats per minute (bpm) was applied, but episodes of epigastric discomfort with lack of respon siveness and automatisms, not followed by syncope or convulsions, recurred on the next day and prompted his transfer to a neurological unit. A standard EEG showed focal spike and wave with delta slowing on the right centrotemporal region (C4-T4). A Medilog 9000 ambulatory EEG-ECG recording captured a seizure (fig 2) beginning with right centrotemporal recruiting sharp waves, followed by a progressive sinus bradycardia and culminating in a junctional escape rhythm at 47 bpm. The sinus rhythm was recaptured by a transient sinus tachycardia. Other episodes of psychomotor type occurred in subsequent days, but there were no falls or tonic convulsions. The epileptic seizures were secondary to a right anterior temporal low grade astrocytoma, and subsided after treatment with carbamazepine and removal of the mass. The pacemaker was left in place, and the patient has been free of seizures, without anticonvulsants, for three years.

Figure 2

Simultaneous 15 lead EEG and one lead ECG recording of a partial complex seizure. A paroxysmal right temporal discharge (horizontal arrow), preceded by interictal spikes and sharp waves, is followed five seconds later by progressive bradycardia (vertical arrow). Thirteen seconds afterwards a junctional escape rhythm occurs (tract between stars, enlarged in the bottom tracing) at a mean rate of 47 bpm. Recapturing by the sinus rhythm (first beat after right star) takes place 34 seconds from the onset of the EEC discharge, and culminates in a sinus tachycardia at 120 bpm, which rapidly subsides after the cessation of the EEC paroxysm. The entire seizure lasted 54 seconds. F=frontal, C=central, P=parietal, O=occipital, T=temporal EEG; even numbers=right; odd numbers=left; calibration: major time divisions 10 s.

Epileptic seizures often cause disturbances in cardiac rhythm, generally consisting of mild changes in heart rate such as sinus tachycardia. The possibility of life threatening cardiac arrhythmias has been suggested by the higher incidence of sudden unexpected deaths among patients with epilepsy than in the normal population.1 Males, young adults with anatomical causes of seizure disorder, patients not receiving or receiving subtherapeutic levels of antiepileptic medication, with concomitant heart disease, and with alcohol misuse present the major risks.1 Generalised tonic-clonic seizures, alone or in combination with partial complex seizures, are usually involved, and among proposed mechanisms is an intense sympathetic discharge to the heart, possibly time locked with vagal impulses and resulting in disordered cardiac rate, rhythm, or output.1 There are only a few proved observations of epileptic bradycardia and asystole, and only in isolated cases2-4 has the cardioinhibitory effect of a seizure been documented by simultaneous EEG and ECG.

In animals, neuromediated bradycardia has been elicited by electrical stimulation of various regions of the limbic system. In humans, repeated observations pioneered by Van Buren5 have shown that seizure related bradyarrhythmias accompany electrical discharges originating from the temporal lobe, strengthening the hypothesis that neural structures within or adjacent to this lobe mediate cardioinhibition. A right-left hemispheric asymmetry for heart innervation has been suggested, but in the reported cases of ictal cardiac arrest right sided, left sided, and bilateral epileptic foci can be found.

Our case resembles that described by Smaje et al,6 in which temporal lobe seizures secondary to a right hemispheric intracranial tumour induced recurrent episodes of sinus arrest, followed by syncope and muscle jerking; in this patient as well, surgical removal of the tumour reversed the epileptic seizures and the secondary cardiac involvement. Patients 1 and 2 of Constantinet al are similar.7 In these patients, monitoring led to the false diagnosis of primary cardiac arrest and to the implantation of a permanent pace-maker.

In our patient, the presence of epigastric sensations and purposeless arm and mouth movements preceding the fall should have suggested the diagnosis of partial complex seizures, but clinical clues were disregarded in the face of a repeated documentation of sinus arrest. Actually, only simultaneous EEG and ECG recording makes it possible to recognise the concurrence and the timing of cerebral and cardiac disturbances, and this examination should be recommended in patients with episodes of loss of consciousness of an unclear nature. Finally, it is likely that falling and tonic convulsions after sinus arrest were anoxic rather than epileptic in origin, as they did not show when sinus arrest was shorter than nine seconds, nor after pacemaker implantation. Besides, in the episode shown in fig 1 the fall and tonic spell occurred at the end of the period of asystole, whereas in the episode reported in fig 2 there was no EEC generalisation of the paroxysmal activity. However, simultaneous ECG-EEG recording of a tonic seizure could not be obtained.

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