The suprachiasmatic nucleus (SCN) mediates the circadian rhythms [14], which control a variety of biological processes, such as sleep-wake cycle, core body temperature, glucose homeostasis hormone secretion and cell-cycle regulation. The disturbance of circadian rhythms can result in internal desynchronization [15].
The present study showed that there were both circadian and seasonal patterns of stroke onset and indicated that such temporal variability was influenced by different combinations of cardiovascular risk factors. Most studies Casetta et al. [16], Kario et al. [17] and Butt et al. [18] confirmed our findings and documented the peak of stroke onset between 6:01 am and 12:00 pm. On the other hand, Nahrir et al. [19] found that most strokes occur from 12.01 am to 6 am. We also did not agree with Kallet [20] in their finding that there was no difference in circadian variation regarding the aetiologic distribution or in the clinical stroke subtypes. The methodology of the previous studies had not been uniformed, as some investigators chose to divide the clock into quartiles, as we did, while others narrowed the time epochs further into 2-h subunits.
Fasting (no food or fluid intake) during the holy Ramadan month is mandatory for all healthy adult Muslims from dawn to sunset for a period of one lunar month. Changes in lifestyle during Ramadan month affect the circadian rhythm and influence the timing of presentation of cerebral stroke [21].
In patients presented with stroke during Ramadan month, there was a significant shift with the higher frequency of stroke onset time which was mainly in the third quartile (12.01 pm–6 pm). This was in concordance with the previous studies Anderson et al. [22] Manfredini et al. [2] and El Mitwalli et al. [10]. During Ramadan, the changes in food intake and sleep timing and then shift of cortisol profile affect the circadian rhythm and influence the timing of presentation of cerebral stroke.
Variety of abnormal diurnal variation patterns had been found among our patients. There was loss of normal nocturnal dipping of BP in 59 patients. Our finding was in accordance with Chrousos [7], who found that the normal diurnal variation in BP was abolished in stroke patients and this non-dipping was equally seen in both ischaemic and haemorrhagic groups. Diminished nocturnal blood pressure decline could be explained by disturbance of the central autonomic nervous system with nocturnal reduction of sympathetic activity and increased parasympathetic activity. Excess secretion of cortisol and epinephrine in the acute phase of stroke attenuates the fall of blood pressure.
The results of this study revealed the abolition of the circadian rhythm of HRV and a loss of the relative vagal nocturnal dominance in patients with acute stroke. Our results agreed with the previous findings of reduced HRV after both types of stroke. Barron et al. [23] and Naver et al. [24] found that both ischaemic and haemorrhagic lesions located either hemispheric or in the brainstem may result in impaired HRV. The circadian variation in HRV seems more likely to be a result of sympathetic inhibition rather than a parasympathetic effect as the presence of vagal neuropathy did not affect it.
The low CBFV in the morning is thought to be a consequence of the fall in the overall reduced metabolic level and reduced cognitive processing. Additionally, recumbent sleeping position with reduction of physical activity contributes to the decline in CBFV [5]. The results of this study revealed that in normal subjects, there was circadian periodicity in CBFV with significant difference; it was lower in the morning (second quartile) than in the evening (fourth quartile).
In comparison between different groups, we found that group A showed significantly lower levels of CBF velocity. Our findings were in accordance with Novak et al. [25], who found that BFVs were lower by approximately 30% in the patients with ischaemic stroke compared with the control subjects. These findings also agreed with Salinet et al. [26], who found that recordings revealed a significantly lower CBFV in the affected hemisphere within 72 h after stroke compared to controls.
Follow-up of patients after 3 months revealed that HRV values returned to normal. These results agreed with findings of Binici et al. [27], who reported that the abolition of the circadian rhythm of HRV and a loss of the relative vagal nocturnal dominance in patients with acute stroke seemed to be reversible.
In stroke patients, the plasma cortisol level returned to normal values with reappearance of normal circadian rhythm. Butt et al. [18] found that cerebral stroke induced abnormalities of cortisol circadian secretion while in convalescent period, these cortisol abnormalities were transient.
Follow-up of clinical severity according to stroke onset by NIHSS is as follows: our results showed that sleep stroke (first quartile) had worst prognosis and worse functional outcome after 3 months (measured by mRS). Our study has been in accordance with Jiménez-Conde et al. [28], who found that sleep stroke had high severity and worse prognosis.
Follow-up of clinical severity according to BP changes by NIHSS is as follows: the reverse dippers and extreme dippers had worse functional outcome after 3 months (measured by mRS). This agreed with Kario et al. [29], who found that the fatal stroke incidence was significantly higher in reverse dippers. These results suggest that nocturnal extreme dippers are more liable to ischaemic strokes due to the associated cerebral hypoperfusion during the night.
