IntroductionCranial autonomic involvement in episodic cluster headache (ECH) is known. Some vegetative symptoms are part of the diagnostic criteria for ECH and other trigemino-autonomic cephalalgias in the IHS classification [1]. Less is known about systemic autonomic impairment. Some authors [2][3][4][5][6][7] have described a derangement of cardiovascular responses during attacks of ECH. Moreover, a few authors have studied the differences between active and remission phase. We present a case-control study on systemic autonomic nervous activity, in particular its cardiovascular function, in ECH, during cluster periods and during remission phases. MethodsSeventeen ECH patients (14 males, 3 females, mean age 36.2 years, range 22-55) underwent a series of vegetative tests (Table 1), according to Ewing's protocol [8], to evaluate parasympathetic cardiovascular responses: lying to standing test (LST), Valsalva manoeuvre (VM) and deep breathing test (DBT); we also performed two tests, sympathetic skin response (SSR) and measurement of postural changes of blood pressure (PH), to assess vasoactive sympathetic pathway. Each patient was studied during either the active or silent period. We considered as active period when the last attack had occurred no more than 2 days before the study and silent period if the patient had been attack-free for the last 3 months and the following 2 months. Seventeen sex-and agematched healthy subjects were also evaluated as controls. During the active phase patients were drug-free; only symptomatic agents were allowed. The day of the study patients did not take coffee, tea or other foods containing sympathicomimetic amines. No patient suffered from diseases other than ECH; nobody was a smoker. Tables 2 and 3. SSR and PH showed no difference either between the active and the silent period or between ECH and normal controls. On the contrary, we found significant (p<0.01) differences in VM, LST and J Headache Pain (2005) 6:240-243 DOI 10.1007/s10194-005-0196-8 Systemic autonomic involvement in episodic cluster headache: a comparison between active and remission periods Values were then compared with normal controls. Our data show a parasympathetic, but not sympathetic, involvement. Moreover, this impairment seems to be "chronic", as it persists beyond the active period. Results Values are shown in

Epilepsy is a frequent consequence of neonatal hypoxic–ischemic encephalopathy. It is not yet known if the introduction of therapeutic hypothermia modifies the rate and the characteristics of epilepsy. We report on 59 infants who suffered from hypoxic–ischemic encephalopathy and underwent therapeutic hypothermia. Birth, physiological and biochemical data, frequent electroencephalography (EEG) recordings or continuous EEG monitoring, and magnetic resonance imaging (MRI) were documented in the neonatal period. Prechtl's General Movements evaluation was performed and the Griffiths Scales of Mental Development were applied at 3 and 24 months of age, respectively. Children were followed up for at least 3 years (mean 5 ± 1.6 years). Six children (10%) developed epilepsy. All of them had a severe hypoxic–ischemic encephalopathy and were neurologically impaired at 2 years of age. Furthermore, all of them had a severe pattern of MRI injury and poor neonatal EEG backgrounds. Four of them suffered from neonatal status epilepticus. Four out of six showed a similar epileptic pattern: their epilepsy started early; it was drug resistant; it required an aggressive polytherapy; and it showed a spontaneous improvement after 2 years. The rate of epilepsy in our cooled infants was similar to those reported in other studies on noncooled ones. Only severe hypoxic–ischemic encephalopathy predisposed the cooled infants toward epilepsy. Neonatal status epilepticus and persisting poor EEG backgrounds were predictive of the development of epilepsy in our sample.

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