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Paroxysmal hypertension during a complex partial seizure
  1. DL JARDINE,
  2. I G CROZIER,
  3. H IKRAM
  1. Department of Cardiology, Christchurch Hospital, New Zealand
  2. Department of Neurology
  1. Dr D L Jardine, Department of General Medicine, Christchurch Hospital, Private Bag 4710, Christchurch, New Zealand davidj{at}chhlth.govt.nz
  1. T J ANDERSON
  1. Department of Cardiology, Christchurch Hospital, New Zealand
  2. Department of Neurology
  1. Dr D L Jardine, Department of General Medicine, Christchurch Hospital, Private Bag 4710, Christchurch, New Zealand davidj{at}chhlth.govt.nz

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The autonomic mechanisms involved in neurogenic paroxysmal hypertension are not understood. We present the first demonstration of the precise haemodynamic and autonomic changes during a complex partial seizure.

A 50 year old headmaster was investigated for an 8 year history of recurrent absence attacks, stereotyped in nature and of sudden onset, each lasting about half a minute. He became pale, sweaty, and mentally withdrawn but did not fall down. Recovery was rapid and associated with transient headache. Previous neurological investigations, including repeated EEG and MRI, were negative. Electrocardiographic Holter monitoring disclosed only sinus bradycardia so he underwent head up tilt testing to exclude vasovagal syncope. Intra-arterial blood pressure and ECG were recorded continuously. Microneurography needles were positioned in the peroneal nerve of the right leg for recording efferent postganglionic MNSA.1 This technique allows beat to beat monitoring and quantification of MNSA (bursts/min) which controls vascular tone in skeletal muscle. MNSA in turn is modulated by changes in blood pressure via the baroreflexes. Blood pressure is normally maintained during head up tilt by increased MNSA and vasocontriction.2

The patient showed normal blood pressure, heart rate, and MNSA responses to tilt initially, but after 10 minutes, he suddenly became pale, sweaty, and withdrawn for …

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