Inflammatory CNS lesions

Multiple sclerosis (MS) is a complex inflammatory disease of the central nervous system (CNS) that is variable in terms of symptoms and presentation. The name refers to two features of the disease multiple describes the number of CNS lesions and sclerosis refers to the demyelinated lesions. Today, these lesions are usually called plaques, rather than scleroses. Although scientific understanding of MS has progressed at a rapid pace, there are still many areas of evolving knowledge. 

An upregulation of ICAM-1 and VCAM-1 on the surface of endothelial cells is generally attributed to the activity of inflammatory cytokines such as TNF-a, IL-1, IL-4, and IFN-y.43-83-86 All of these cytokines are readily identifiable in the CNS lesions of MS,87-90 particularly in close proximity to blood vessel walls.82-91 In EAE, disease activity is exacerbated by TNF-a,92-93 antagonised by specific neutralising antibodies,94 and injection of TNF-a into rat spinal cord induces mononuclear cell infiltrates.95 However, several of the cytokines identified in MS lesions are also present in the CNS of normal and noninflammatory disease controls91 and therefore caution must be applied in interpreting cytokine expression and localisation to a particular phase of demyelination. 

Association of Pain, neuropathic pain is defined as pain initiated or caused by a primary lesion, dysfunction in the nervous system". Neuropathy can be divided broadly into peripheral and central neuropathic pain, depending on whether the primary lesion or dysfunction is situated in the peripheral or central nervous system. In the periphery, neuropathic pain can result from disease or inflammatory states that affect peripheral nerves (e.g. diabetes mellitus, herpes zoster, HIV) or alternatively due to neuroma formation (amputation, nerve transection), nerve compression (e.g. tumours, entrapment) or other injuries (e.g. nerve crush, trauma). Central pain syndromes, on the other hand, result from alterations in different regions of the brain or the spinal cord. Examples include tumour or trauma affecting particular CNS structures (e.g. brainstem and thalamus) or spinal cord injury. Both the symptoms and origins of neuropathic pain are extremely diverse. Due to this variability, neuropathic pain syndromes are often difficult to treat. Some of the clinical symptoms associated with this condition include spontaneous pain, tactile allodynia (touch-evoked pain), hyperalgesia (enhanced responses to a painful stimulus) and sensory deficits. 

Antithrombin HI in cerebrospinal fluid can be easily denoted as an inflammatory marker. Correlations with levels of immunoglobulins, their intrathecal oligo-clonal synthesis, complement components, and acute-phase reactants confirm such concepts. Correlations with apolipoproteins and with the presence of lipophagic macrophages in cytological preparations confirm the elevation of CSF AT III levels when a destructive lesion of the CNS is present. 

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