We wish to thank Drs. Finsterer and Stöllberger for the interest in our work. As suggested, in the present letter we focus on the medical history and neurological background of the patient described in our previous case report [1]. The latter dealt with a 73year old female with a cryptogenic epilepsy who had experienced a triple occurrence of Takotsubo syndrome (TTS). The first manifestation of the neurological disease occurred in 2000, resulting in a generalized tonic–clonic crisis at the age of 55years old. At that time the cerebral magnetic resonance imaging (MRI) and the electroencephalography (EEG) were completely negative. Neither family history positive for epilepsy nor previous birth trauma, childhood epilepsy, meningitis, traumatic brain injury, alcoholism, or drug abuse were found. After the first seizure the patient was treated with phenobarbital, at a dosage of 100mg per day, which was discontinued in 2006 before the first TTS. More precisely, the first occurrence of TTS was most probably triggered by the loss of her husband and was associated with tonic–clonic seizures. The second episode of TTS was not apparently triggered by any stressful events; the patient was actually reading a book at home when the chest oppression started. The third TTS was not apparently triggered by any significant events and was associated with a concomitant short-term memory disturbance; specifically, at presentation the patient was confused and agitated and she could not remember the past events of few hours before. Twenty-four hours later, the EEG only showed isolated bisynchronous high-voltage delta-wave activity, which was more pronounced anteriorly, but no paroxysmal activation. On that occasion, a cerebral computed tomography (CT) scan was also performed and did not show any abnormalities. The neurological evaluation actually hypothesized a complex partial crisis with post-ictal amnesia ruling out other differential diagnoses. No neuromuscular disorders (NMDs) were observed by the multiple neurological examinations; over the time, the patient did not ever develop any symptoms related to neuromuscular disorders. Also mitochondrial disorders were properly excluded.
Mugnai, G., Pasqualin, G., Danese, A., Prati, D., Menegatti, G., Vassanelli, C. (2016). Response to: Triple occurrence of seizure-associated Takotsubo syndrome. INTERNATIONAL JOURNAL OF CARDIOLOGY, 209, 334-334 [10.1016/j.ijcard.2016.02.105].
Response to: Triple occurrence of seizure-associated Takotsubo syndrome
Pasqualin G.Secondo
;
2016
Abstract
We wish to thank Drs. Finsterer and Stöllberger for the interest in our work. As suggested, in the present letter we focus on the medical history and neurological background of the patient described in our previous case report [1]. The latter dealt with a 73year old female with a cryptogenic epilepsy who had experienced a triple occurrence of Takotsubo syndrome (TTS). The first manifestation of the neurological disease occurred in 2000, resulting in a generalized tonic–clonic crisis at the age of 55years old. At that time the cerebral magnetic resonance imaging (MRI) and the electroencephalography (EEG) were completely negative. Neither family history positive for epilepsy nor previous birth trauma, childhood epilepsy, meningitis, traumatic brain injury, alcoholism, or drug abuse were found. After the first seizure the patient was treated with phenobarbital, at a dosage of 100mg per day, which was discontinued in 2006 before the first TTS. More precisely, the first occurrence of TTS was most probably triggered by the loss of her husband and was associated with tonic–clonic seizures. The second episode of TTS was not apparently triggered by any stressful events; the patient was actually reading a book at home when the chest oppression started. The third TTS was not apparently triggered by any significant events and was associated with a concomitant short-term memory disturbance; specifically, at presentation the patient was confused and agitated and she could not remember the past events of few hours before. Twenty-four hours later, the EEG only showed isolated bisynchronous high-voltage delta-wave activity, which was more pronounced anteriorly, but no paroxysmal activation. On that occasion, a cerebral computed tomography (CT) scan was also performed and did not show any abnormalities. The neurological evaluation actually hypothesized a complex partial crisis with post-ictal amnesia ruling out other differential diagnoses. No neuromuscular disorders (NMDs) were observed by the multiple neurological examinations; over the time, the patient did not ever develop any symptoms related to neuromuscular disorders. Also mitochondrial disorders were properly excluded.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
