Table 3 Examples of non-neurodegenerative neurological disorders with localized inflammatory response

Isolated seizures [46]

Inflammatory response is usually short-lived.

Increased IL-1β, IL-6, and TNF in brain regions where epileptogenesis and signal spreading occur.

Neuroinflammation can be due to infection, vascular causes (such as ischemia or vasculitis), neoplastic disease, trauma, and severe neurodegeneration.

Epilepsy [47]

Neuroinflammation can differ between ictal and non-ictal status.

Changes in catecholaminergic and serotonergic activity can occur in temporal lobe epilepsy, when increased monoamines and monoamine metabolites in spiking temporal cortex and cerebrospinal fluid may be found.

Epilepsy can be a complication of severe dementia, with traditionally established markers according to the dementia syndrome.

Systemic lupus erythematosus [48]

Neuroinflammation is more intense during neurologic episodes.

Neurological manifestations can be a result of vasculitis or regional inflammation of the brain.

Central nervous system involvement is mostly characterized by seizures, psychosis and movement disorders, with low C-reactive protein but high erythrocyte sedimentation rate in less than half of patients, and abnormal cerebrospinal fluid findings (elevated proteins, lymphocytic pleocytosis, oligoclonal bands) associated with poor prognosis.

Normal pressure hydrocephalus [49, 50]

Neuroinflammation is usually more intense when there is more interstitial oedema.

Mechanisms are common regardless of the etiology, with initially raised cerebrospinal fluid pressure followed by ventricular enlargement and decreased absorption of cerebrospinal fluid at the transcapillary or transvenular level, with interstitial oedema and ischemic damage of the white matter along with further normalization of cerebrospinal fluid pressure.

Normal pressure hydrocephalus can result from trauma, intracranial hemorrhage, meningitis (infectious or not), venous sinus thrombosis, or vasculitis. There has been evidence of a link between normal pressure hydrocephalus and systemic lupus erythematosus, in which the insidious inflammatory process that develops in the meningeal tissues (with deposition of IgG, IgA, IgM, C3 and C1q on the dural vessels) or the vasculitis itself may cause the volume of cerebrospinal fluid to increase. It is also known that patients with normal pressure hydrocephalus with moderate to severe AD burden are significantly less likely to respond to shunting.

Migraine [51, 52]

Neuroinflammation differs in the prodromal phase, during the migraine attack, and in the postdrome phase.

Immune response and inflammatory signaling pathways are triggered at the focus that affects cortical function, and contribute to progression of migraine.

No association with white blood cell-based inflammation markers, though genome-wide analyses of blood gene expression have shown significant associations with immune response and inflammatory signaling pathways.