Sleep paralysis in medieval Persia – the Hidayat of Akhawayni (? –983 AD)

Samad EJ Golzari,1 Kazem Khodadoust,5 Farid Alakbarli,6 Kamyar Ghabili,2 Ziba Islambulchilar,3 Mohammadali M Shoja,1 Majid Khalili,1 Feridoon Abbasnejad,1 Niloufar Sheikholeslamzadeh,7 Nasrollah Moghaddam Shahabi,4 Seyed Fazel Hosseini,2 Khalil Ansarin11Tuberculosis and Lung Disease Research Center, Tabriz University of Medical Sciences; 2Medical Philosophy and History Research Center, Tabriz University of Medical Sciences; 3Department of Pharmaceutics, Tabriz University of Medical Sciences; 4Students' Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran; 5Azerbaijan National Academy of Sciences; 6Institute of Manuscripts of the Azerbaijan National Academy of Sciences, Baku, Azerbaijan; 7Faculty of Law, Central Tehran Branch, Islamic Azad University, Tehran, IranAbstract: Among the first three manuscripts written in Persian, Akhawayni's Hidayat al-muta`allemin fi al-tibb was the most significant work compiled in the 10th century. Along with the hundreds of chapters on hygiene, anatomy, physiology, symptoms and treatments of the diseases of various organs, there is a chapter on sleep paralysis (night-mare) prior to description and treatment of epilepsy. The present article is a review of the Akhawayni's teachings on sleep paralysis and of descriptions and treatments of sleep paralysis by the Greek, medieval, and Renaissance scholars. Akhawayni's descriptions along with other early writings provide insight into sleep paralysis during the Middle Ages in general and in Persia in particular.Keywords: sleep paralysis, night-mare, Akhawayni, Persi

The impact of cortical lesions on thalamo-cortical network dynamics after acute ischaemic stroke: a combined experimental and theoretical study

The neocortex and thalamus provide a core substrate for perception, cognition, and action, and are interconnected through different direct and indirect pathways that maintain specific dynamics associated with functional states including wakefulness and sleep. It has been shown that a lack of excitation, or enhanced subcortical inhibition, can disrupt this system and drive thalamic nuclei into an attractor state of low-frequency bursting and further entrainment of thalamo-cortical circuits, also called thalamo-cortical dysrhythmia (TCD). The question remains however whether similar TCD-like phenomena can arise with a cortical origin. For instance, in stroke, a cortical lesion could disrupt thalamo-cortical interactions through an attenuation of the excitatory drive onto the thalamus, creating an imbalance between excitation and inhibition that can lead to a state of TCD. Here we tested this hypothesis by comparing the resting-state EEG recordings of acute ischaemic stroke patients (N = 21) with those of healthy, age-matched control-subjects (N = 17). We observed that these patients displayed the hallmarks of TCD: a characteristic downward shift of dominant α-peaks in the EEG power spectra, together with increased power over the lower frequencies (δ and θ-range). Contrary to general observations in TCD, the patients also displayed a broad reduction in β-band activity. In order to explain the genesis of this stroke-induced TCD, we developed a biologically constrained model of a general thalamocortical module, allowing us to identify the specific cellular and network mechanisms involved. Our model showed that a lesion in the cortical component leads to sustained cell membrane hyperpolarization in the corresponding thalamic relay neurons, that in turn leads to the de-inactivation of voltage-gated T-type Ca2+-channels, switching neurons from tonic spiking to a pathological bursting regime. This thalamic bursting synchronises activity on a population level through divergent intrathalamic circuits, and entrains thalamo-cortical pathways by means of propagating low-frequency oscillations beyond the restricted region of the lesion. Hence, pathological stroke-induced thalamo-cortical dynamics can be the source of diaschisis, and account for the dissociation between lesion location and non-specific symptoms of stroke such as neuropathic pain and hemispatial neglect.This work was supported by the European Research Council under the European Union's Seventh Framework Programme FP7/2007-2013/ERC grant agreement n. 341196 [CDAC], and the Research and Technological Development Programme FP7-ICT-612139 in the WYSIWYD project to PFMJV. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript