A Central nervous system (CNS) hemorrhage is bleeding in or around the brain and spinal cord. Reasons of CNS hemorrhage include high blood pressure, cancers, drug abuse, abnormally weak blood vessels that leakage, and trauma. Regression of CNS bleeding was confirmed to be relatively repetitive in patients with severe FV, FX, FVII and FXIII deficiencies. Generally in CNS hemorrhage, radiological evaluations are necessary, for example a magnetic resonance imaging (MRI) scan or computed tomography (CT) scan. The MRI or CT scan highlight different features and location of CNS bleeding. Several patterns of MicroRNA (miRNA) expression occur in blood and CNS 24 h after CNS hemorrhage, kainite seizures, brain ischemia, and even surgeries. A number of miRNAs were considerably regulated more than 1.5-fold in blood and brain after each CNS damage. Several miRNAs were down regulated or upregulated in both CNS and blood after a given damage; and a few miRNAs, containing mir-155, mir-362- 3p, miR-298, etc, were down regulated or upregulated in both CNS and blood after several variety damages. The ‘cell cycle’ was among the top-ranked roles for miRNA regulated in both CNS and blood, and for mRNAs and miRNAs that changed in CNS and blood one day after injury. The miRNAs induced in blood related to the ‘cell cycle’ may relate to the blood inflammatory response and the proliferation of white blood cells (WBCs) to acute CNS injury. Cell cycle re-entry in neurons has been confirmed in a lot of CNS diseases, including stroke, CNS bleeding, epilepsy, and traumatic CNS injury.

Inflammation is portion of the body's immune response and it is basically a host protective response to tissue ischemia, injury, autoimmune responses or infectious agents. Although the information presented so far points to a detrimental role for inflammation in central nervous system (CNS) disease, it may also be useful. CNS demonstrates characteristic of inflammation, and in response to damage, disease or infection, resident CNS cells generate inflammatory mediators, including prostaglandins (PGs), pro-inflammatory cytokines, free radicals and complement, which in turn induce chemokines and adhesion molecules, recruit immune cells, and activate glial cells. In response to a brain injury, astrocytes become activated, increasing expression of glial fibrillary acidic protein, and producing cytokines. Cytokines including both tumor necrosis factor-α (TNF-α) and IL-1 are strongly implicated in neuronal loss during acute and chronic neurodegenerative disease, but also participate in repair and recovery. Although TNF-α is found associated with active MS lesions, induces death of oligodendrocytes. TNF-α appears not to be needed for mast cell–dependent pelvic pain. TNF-α, is released from Schwann cells immediately after nerve damage. IL-1 can also attach nerve terminals and influence substance P release and migration of polymorphonuclear White blood cells (WBCs). IL-1β is also selectively upregulated in astrocytes in the spinal trigeminal nucleus, spinal cord and rostral ventromedial medulla in models of inflammation, cancer pain and nerve damage. IL-1β is an important messenger between neurons and glia.