We report the case of a patient with akinetic mutism, which transiently recovers the verbal interaction after Midazolam administration. The man, 46 years-old, affected by post traumatic encephalopathy (traffic accident in 2006), TC of the brain collected in March 2012 showed focal damage in right temporal basal lobe and in left temporo-polar basal lobe, very little damage of the white matter left frontal lobe have also been detected. In February 2012, the patient was mildly sedated with Midazolam (10 mg i.v.) to perform brain computed tomography. Upon waking from sedation he interacted with family, talking on the phone with a relative, congratulating his brother because of his recent graduation, and recognized the road leading to his home and his home itself. He did not remember anything of what happened after the accident. All this took about two hours, after which the patient fell in the previous akinetic mutism state. Administration of Midazolam was repeated under electroencephalographic (EEG) monitoring and video recording. The patient showed the same behavioural modifications. The EEG showed the disappearance of diffuse activity at 7 Hz present at the baseline, and a significant diffuse increment of activity in alfa 3 and beta 1 bands. To our knowledge there are no reported cases of "awakening" induced by the administration of Midazolam. Midazolam is, as Zolpidem, a "GABA A" agonist. That effect could be explained by the hypothesis forwarded by Clauss: temporary resolution of diaschisis, or that proposed by Schiff: restoration of striatal pallidal inhibition with thalamo-cortical facilitation. A further hypothesis relate to this patient, would consider the possible coexistence of the catatonic syndrome in severe brain injury (Sutten et al 1959), which is usually reversed by benzodiazepines.
Post traumatic akinetic mutism unexpectedly reversed by midazolam: case report
Formichi B;
2012
Abstract
We report the case of a patient with akinetic mutism, which transiently recovers the verbal interaction after Midazolam administration. The man, 46 years-old, affected by post traumatic encephalopathy (traffic accident in 2006), TC of the brain collected in March 2012 showed focal damage in right temporal basal lobe and in left temporo-polar basal lobe, very little damage of the white matter left frontal lobe have also been detected. In February 2012, the patient was mildly sedated with Midazolam (10 mg i.v.) to perform brain computed tomography. Upon waking from sedation he interacted with family, talking on the phone with a relative, congratulating his brother because of his recent graduation, and recognized the road leading to his home and his home itself. He did not remember anything of what happened after the accident. All this took about two hours, after which the patient fell in the previous akinetic mutism state. Administration of Midazolam was repeated under electroencephalographic (EEG) monitoring and video recording. The patient showed the same behavioural modifications. The EEG showed the disappearance of diffuse activity at 7 Hz present at the baseline, and a significant diffuse increment of activity in alfa 3 and beta 1 bands. To our knowledge there are no reported cases of "awakening" induced by the administration of Midazolam. Midazolam is, as Zolpidem, a "GABA A" agonist. That effect could be explained by the hypothesis forwarded by Clauss: temporary resolution of diaschisis, or that proposed by Schiff: restoration of striatal pallidal inhibition with thalamo-cortical facilitation. A further hypothesis relate to this patient, would consider the possible coexistence of the catatonic syndrome in severe brain injury (Sutten et al 1959), which is usually reversed by benzodiazepines.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
