Spinal adhesive arachnoiditis is a rare pathology involving pia mater of the spinal cord and nerve roots. It can potentially lead to disability—many patients end up wheelchair-bound due to subsequent paraparesis. It is an infrequent but possible cause of lower extremities weakness in patients with a history of spinal surgery, epidural anaesthesia, myelography or spinal tumors. Three patients, one male and two females, admitted to our unit due to paraparesis presented at least one of the above mentioned risk factors. Each of them had a severe course of illness—progressive paresis of lower extremities. All above cases were diagnosed with spinal adhesive arachnoiditis confirmed with Magnetic Resonance Imaging (MRI) scan—the most sensitive and specific diagnostic tool. Despite conservative treatment and intensive rehabilitation none of the presented patients preserved the ability to mobilise independently. Considering spinal adhesive arachnoiditis in patients with paraparesis and history of typical risk factors should be included in clinical diagnostic procedure.

The sensation of pain is common to both animals and human beings. Its threshold, intensity, tolerability, and characteristics are variable and depend on ethnicity, gender, stress exposure, co-existing mental disorders, such as depression or anxiety, social and economical background, as well as on genetic factors. It is estimated that about 5 and 20 percent of population suffer from acute and chronic pain, respectively, which results in the search for medical advice in healthcare facilities, and causes great expenses in health care budgets worldwide. Research aimed at identifying the causative agents of pain syndromes include single nucleotidepolymorphism (SNP), family history studies, twin siblings' genetic diversity studies, and recently, also a genome-wide association study (GWAS). Clinical syndromes of derangement of pain sensation are generally caused by single gene mutations (e.g. erythromelalgia and paroxysmal extreme pain disorder caused by mutations of SCN9A), but can also be associated with multiple gene mutations, as happens in migraine, fibromyalgia or hereditary sensory and autonomic neuropathies. Structural changes of proteins caused by gene mutations involve various cellular element, such as ion channels, receptors, scaffolding proteins, enzymes, transporting proteins, eventually leading to numerous clinical entities in which pain or its lack remain the leading symptoms. The sensation of pain is initiated by a stimulus, which activates the free nerve endings via chemical mediators, and the mechanical stimuli is then transmitted to the brain along the neurons and spinal tracts. Synaptic neurotransmitters and cell structures take part in this process and eventually affect the intensity of pain sensation.