Alphabetical list of currently known Human Neurological Conditions Infantile spasms (a form of seizures) Lesions or "lacunae" of the retina of the eye that The onset is predominantly in the first year of life, typically between months. of conditions resulting from overuse of a tool, eg. computer, guitar, knife, etc. or. Seizures are the most common acute neurologic problem in the United States States. Epilepsy (recurrent Six types of generalized seizures and their presenting signs are described in table 1 Excessive use of stimulants, cocaine, etc. Epilepsy, A disease of the brain defined by any of the following conditions: (1) at An external file that holds a picture, illustration, etc. .. Herpes viruses such as human herpes virus type 6 (HHV-6) have been associated with.
Neurological (Seizures, 6. etc) Disorders
West Nile Virus, another emerging virus associated with encephalitis and seizures, has spread across the USA since the late s [ ]. Magnetic resonance imaging MRI of the brain in the coronal plane demonstrating signal hyperintensity and swelling on the FLAIR sequence involving the insula cortices, mesial and inferior temporal regions a in a patient with herpes simplex HSV encephalitis.
There is associated T1-weighted hyperintensity within the mesial temporal structures on the pre-contrast T1-weighted imaging suggestive of haemorrhagic change b , and some further enhancement on the post-contrast T1-weighted sequence c. MRI images contributed by Dr.
Photomicrographs were kindly provided by Profs. Viruses within the Picornaviridae Family, such as enteroviruses, Coxsackieviruses A and B, parechoviruses and echoviruses, have been associated with the development of febrile seizures. Enteroviruses are a leading cause of viral encephalitis in children. Cases of enterovirus infection are increasing and infection can cause an acute flaccid paralysis similar to polio [ 73 ]. One hundred and twenty-six people with status epilepticus who presented in a neurological intensive care unit were evaluated [ ].
People with encephalitis are more likely to develop later seizures [ 15 ]. Following viral encephalitis complicated with acute seizures, there is a fold increase in developing unprovoked seizures [ 90 ]. This risk for seizures is most evident within the first 5 years after viral encephalitis. Animal models are useful to study the mechanisms involved in infection-induced epileptogenesis, but most infectious agents that cause encephalitis in rodents are associated with high mortality, so that the processes leading to epilepsy cannot be investigated [ 72 ].
One exception is a recently developed animal model virus encephalitis that mirrors many of the features of viral encephalitis-induced epilepsy [ 69 ]. This has advantages over other earlier experimental animal models of virus-induced seizures and epilepsy. Rabbits, rats and mice have been infected with viruses and develop seizures, but most die following the acute viral encephalitis phase making the study of epilepsy limited [ ].
Prior to and including day 5, neuronal loss was minimal and similar between mice with seizures and mice without seizures. Motor function and coordination were impaired in the animals with seizures [ 69 ] and mice demonstrated impaired cognitive ability and anxiety-like behaviours [ ].
Since the acute seizures start at day 3 p. The innate immune system is made up of effector cells such as neutrophils, macrophages and natural killer NK cells. Brain resident innate immune cells include microglia and astrocytes. These cells can produce many proinflammatory cytokines that can contribute to the inflammation observed in the CNS.
Complement is also a critical component of the innate immune response to infection. Data suggest that C3 in the CNS is important for the development of seizures [ 5 , ]. In the expanded traces [ 1 — 4 ], epileptic activity associated with behavioural arrest [ 3 ] or no behavioural arrest [ 4 ] is present in TMEV mice but not in PBS mice [ 1 ]. Activity observed during a generalised convulsive seizure is expanded for comparison [ 2 ].
Figures were compiled from Stewart et al. Higher magnification of the hippocampal layer c shows severe loss of pyramidal cells in the CA1 sector arrows , while the dentate gyrus DG seems to be relatively intact. Note also the inflammatory lympho-histiocytic predominantly perivascular cells in the hippocampus in c arrowheads. These cytokines have been detected in sera from people with TLE [ 12 , ] and from resected brain tissue from people with intractable epilepsy [ 48 , 49 , , ].
Over 20 years ago, transgenic mice overexpressing IL-6 driven by the glial fibrillary acidic protein GFAP promoter were found to develop spontaneous seizures [ 27 ]. A subset of these mice went on to develop spontaneous recurrent seizures Fig.
Depletion of PMNs and NK cells did not alter numbers of infected mice developing seizures, but depletion of macrophages did. To determine which cells were producing these cytokines, macrophages and microglia were isolated and intracellular cytokine staining using flow cytometry was used.
These cells were isolated at day 3 p. In contrast higher numbers of macrophages were positive for IL In other studies, mice were treated with minocycline or wogonin and numbers of microglia versus macrophages were determined.
Both wogonin and minocycline reduced the numbers of infiltrating macrophages into the CNS by twofold [ 34 ]. These data are consistent with mononuclear cell infiltration in mesial TLE. Preliminary data suggest that the adoptive transfer of bone marrow-derived monocytes into TMEV-infected mice increases the number of mice developing seizures. In addition to being an important platform for studying the mechanisms underlying viral-induced epilepsy, the TMEV mouse is an important etiologically relevant model for assessing the impact of acute interventions on epileptogenesis and the comorbidities associated with epilepsy [ 11 ].
More CBZ-treated mice presented with acute seizures. VPA-treated mice also showed improved motor performance 15 days p. CBZ-treated mice, but not VPA-treated mice, displayed an anxiety-like profile in the open field test when tested at 36 days p.
Ongoing investigations are aimed at further characterisation of these observations and the characterisation of other acute interventions on the acute and long-term changes associated with TMEV-induced encephalomyelitis.
An interesting example of an experimental model of infection-induced acute seizures has recently been reported by Buckingham et al. However, as with most models of infection-induced seizures, only early seizures could be recorded following infection, because mice died or became moribund within 1—2 weeks. Interestingly, Buckingham et al. The data suggest a role for the membrane attack complex MAC of complement in malaria-induced seizures and that inhibition of the terminal complement pathway may reduce seizures and seizure-related neurocognitive deficits.
Sterile inflammation is a homeostatic tissue response to injury triggered by endogenous molecules called danger signals DS or alarmins. Virtually every cell type can release these molecules when the tissue is exposed to biological stressors, to alert the environment of imminent or ongoing damage, and consequently to activate homeostatic programmes for tissue repair and healing.
DS activate the so-called pattern recognition receptors PRR , namely toll-like receptors TLR and nucleotide-binding oligomerization domain receptors NOD -like receptors that are typically expressed by innate immunity cells, and recognise damage-associated molecular pattern DAMP motifs expressed by danger signals.
Notably, PRR also recognise pathogens during infection pathogen-associated molecular patterns, PAMPs , and this dual recognition role identifies PRR as a key nodal regulator of homeostatic tissue responses to damage or infection. Activation of PRR both by DS or pathogens results in the transcriptional activation of NFkB-sensitive inflammatory genes, thereby leading to the generation and rapid amplification of the inflammatory cascade that is instrumental for the recognition and removal of the injurious agent and for promoting tissue healing and repair.
As with every homeostatic response, however, if the activation of PRR is protracted and not strictly controlled by endogenous anti-inflammatory mechanisms, it may lead to tissue damage or dysfunction [ ]. In the normal brain, PRR are expressed at barely detectable levels in neurons, glia and endothelial cells of microvessels, but they are rapidly induced in these cells following an epileptogenic insult e.
This evidence supports the suggestion that PRR are activated by DS in epilepsy in the absence of infections, and raises the crucial question of the pathophysiological role of this phenomenon. Pharmacological studies in experimental models have been instrumental in demonstrating that sterile inflammation may have profound effects on seizures and possibly plays a role in epileptogenesis [ ]. This phenomenon has a rapid onset within min to hours , persists after the inciting event has elapsed days to weeks , and is still detectable in chronic epilepsy tissue characterised by spontaneous recurrent seizures [ , ].
The persistence of these inflammatory events suggests that the endogenous mechanisms that should be activated to promote rapid resolution, thus preserving the homeostatic response, are instead inefficient. The inflammatory molecules that persist in brain tissue may become detrimental for brain function and cell survival, as demonstrated in experimental models. To understand the role of inflammation in acute seizure generation mechanisms and in epileptogenesis, two main approaches have been developed.
In the first approach, seizure susceptibility and epileptogenesis were assessed in transgenic mice with deletion or amplification of specific neuroinflammatory signallings. Conversely, molecules and drugs mimicking or blocking PRR activation by DS were intracerebrally or systemically applied to animals either before provoking acute seizures or during recurrent spontaneous seizures in established chronic epilepsy, or after epileptogenic events and before the onset of the disease.
The resulting data show that PRR activation by DS, and specific effector members of the inflammatory cascade, contribute to the mechanisms of seizure generation and recurrence, and may also be implicated in the development of the disease [ 87 , 88 , ]. In particular, genetic ablation or pharmacological antagonism of TLR3 Gross et al. Reduction of cell loss and reduction of comorbidities were also beneficial effects observed when COX-2 and prostaglandin E2 were antagonised during epileptogenesis [ ].
The mechanisms of the generation of acute symptomatic seizures after infections vary with the type of infection and are often multifactorial [ ]. The triggering of the inflammatory cascade with release of inflammatory cytokines appears to be a common underlying factor in most CNS infections and has been well studied in meningitis and encephalitis [ ].
As described below for sterile inflammation, prolonged stimulation of proinflammatory signals either by chronic inflammation or by seizures themselves may lead to a residual pathological state such as damaged BBB, neuronal death, and persistent neuronal hyperexcitability—all of which may contribute to epileptogenesis. In general, however, the mechanisms of epilepsy following CNS infections are not well established, although data from experimental models, as exemplified by the TEMV model described above, may advance our knowledge about the mechanisms of acute and late seizures following brain infection.
In individuals with brain infections, structural damage such as cortical necrosis with herpes simplex virus, infarction in meningitis, hypoxic—ischaemic injury in cerebral malaria, and gliosis around calcified NCC may all constitute epileptogenic foci [ ].
Hyperthermia associated with various CNS infections can also itself lead to neuronal hyperexcitability [ 77 ] as discussed below. The induction of inflammatory mediators in seizure-prone brain areas is induced by cell injury, seizures, or their combination. The presence of degenerating neurons amplifies the inflammatory response, but cell death is not instrumental in the induction of sterile inflammation in the brain.
For example, the activation of IL-1R1 and TLR4 expressed by microglia and astrocytes by their endogenous ligands mediates NFkB- and activator protein 1 AP-1 -dependent inflammatory gene transcription, thereby perpetuating inflammatory events that involve the release of cytokines and chemokines, the induction of COX-2 and the complement system, and may subsequently lead to the brain recruitment of leukocytes.
The same receptors activated in endothelial cells of the BBB contribute to its increased permeability to serum macromolecules, such as IgG and albumin, by promoting the break-down of tight junctions [ 92 ], and may favour leukocytes brain extravasation by inducing adhesion molecules on microvessels.
PRR and IL-1R1 activation in neurons may rapidly increase neuronal excitability via post-translational modification of receptor-gated or voltage-dependent ion channels, mostly mediated by activation of protein kinase C PKC and proto-oncogene, nonreceptor tyrosine kinase Src family of protein kinases [ , ].
This molecule is physiologically bound to nuclei in every cell type but can rapidly be translocated following brain injury and during seizures to the cytoplasm from where it is extracellularly released.
Chromatin-bound HMGB1 regulates gene transcription, and recent evidence in macrophages and fibroblasts showed that, on its nuclear-to-cytoplasmatic translocation, the cell phenotype is significantly altered Marco Bianchi, personal communication. If the same effects are induced in brain cells, HMGB1 translocation during epileptogenesis may lead to epigenetic changes in neurons and glia with a possible impact on cell function and disease outcomes [ 67 ].
Febrile seizures in experimental models trigger sterile inflammation: The brain increase in inflammatory molecules mainly occurs in microglia [ 51 , ] and astrocytes [ 42 ], and there is recent evidence of HMGB1 translocation in neurons [ 29 ]. The data prove that is the seizure activity per se, and not the increment in core or brain temperature, that provokes neuroinflammation. These data show that sterile inflammation determines the threshold for the occurrence of experimental febrile seizures, and possibly also contributes to the progression of disease.
Febrile seizures in children often, but not always, occur in the context of an ongoing systemic infection. This clinical setting has been reproduced in immature rodents by systemic administration of lipopolysaccharide LPS to mimic Gram-negative infections or Poly I: C to mimic viral infections, and the associated fever. This acute challenge imposed in a specific developmental window PN7-PN14 promotes convulsions in immature rats exposed to doses of kainic acid that are ineffective in naive animals, thus showing that seizure threshold is decreased [ 51 , ].
The increased susceptibility to provoked seizures was maintained in the animals until their adulthood. Pre-exposure of immature rodents to LPS before inducing status epilepticus enhances cell loss in forebrain [ 6 ], and LPS alone increases the severity of epilepsy when the animal is exposed to status epilepticus in adulthood [ 7 ].
Traditionally, the vast majority of encephalitides have been ascribed a microbiological aetiology. However, more recently it has been recognised that many are due to immunological, often autoimmune, mechanisms. Antibody-mediated limbic encephalitis is an increasingly recognised cause of seizures in acquired epilepsy, most commonly localised to the temporal lobe [ 32 ]. Acute inflammation of the mesial temporal regions during limbic encephalitis can lead to hippocampal atrophy consistent with mesial temporal sclerosis on magnetic resonance imaging [ 32 ].
Antibody-associated encephalitis is either classified as paraneoplastic PE or non-paraneoplastic limbic encephalitis [ 13 , 17 ]. Paraneoplastic neurological disorders can harm any part of the CNS, such as brainstem, the limbic system or just single cell types, i. Purkinje cells in paraneoplastic cerebellar degeneration. Although multiple areas of the CNS can be involved, PE most often affects the limbic system and termed already in as limbic encephalitis by Corsellis [ 33 ].
Antibodies can react with both, the nervous system and the underlying cancer, but some evidence suggests a correlation between neurological deficits and antibody targets rather than with an underlying specific tumour [ 13 ].
These studies have supported the concept of non-paraneoplastic antibody-mediated encephalitis NPE , in which encephalitic patients present with similar neurological deficits, including epilepsy, but extensive diagnostic tests and follow-up failed to detect cancer. Nowadays, antibody-mediated encephalitis can be classified according to serum antibodies and their specific targets see Table 3: Most of these antibody-associated encephalitides can occur with or without an underlying neoplasm.
However, their pathogenic role is still matter of ongoing investigations. Generally, it is assumed that antibodies against intracellular antigens are less or not pathogenic [ 56 ] as antibodies will hardly reach intracellularly located neural antigens in normal brain.
Exceptions may be antibodies to GAD65 [ 82 ] or to amphiphysin [ 54 ]. In neuropathological studies of PE with anti-Hu, anti-Yo, or anti-Ma antibodies, CD8-positive T-cells dominate inflammatory infiltrates [ ], which possess cytotoxic granules and are in close apposition to neurons suggesting that cytotoxic T-lymphocytes play a role in neuronal cell death. Antibodies are directed to potassium channel complex proteins, such as contactin-associated protein-like 2 Caspr2 and leucine-rich, glioma-inactivated 1 LGI1 [ ].
Antibodies against LGI1 are more often found than antibodies against Caspr2 [ 60 ]. Clinically, these patients present with memory loss, confusion, behavioural changes and seizures [ ]. In addition, patients with LGi1 antibodies present with facio-brachial dystonic seizures preceding limbic encephalitis [ 62 ]. Histopathologically, surgical specimens obtained from patients with anti-VGKC complex reveal neuronal cell loss in the presence of infiltrating T-cells and perivascular B-cells [ ]. Patients with antibodies specific for LGI1 or caspr2 show inflammation and severe degeneration in the hippocampus.
Importantly, antibody lowering treatments like plasma exchange have been found to improve neurological deficits in these patients, suggesting that antibodies directed against the VGKC complex are responsible for clinical symptoms Ramanathan et al. Histopathology findings in patients with antibodies directed against the NMDAR, a subtype of glutamate receptors in the brain, differ from most other antibody-associated encephalitidides. It is important to note that neuronal loss is remarkably mild in these patients.
It occurs mainly in young females with a peak of age at onset between 19 and 24 years [ 91 , ]. Clinically, a prodromal stage with symptoms such as fever, nausea, vomiting or diarrhoea may be found in retrospect. After few weeks, patients develop seizures, partial status epilepticus, short-term memory loss and, in addition, psychiatric symptoms such as anxiety, insomnia, fear, mania and paranoia. This phase is followed by the initiation of abnormal movements of limb and trunk and oro-lingual-facial dyskinesias, a sudden spontaneous fall in consciousness and autonomic manifestations such as tachy- or bradycardia, hyperventilation and central hypoventilation [ 91 , ].
At this stage, patients need to be managed in intensive care units. However, most patients completely recover, and follow-up MRI studies do not detect permanent brain atrophy [ 91 , ]. The clinical syndrome of NMDAR encephalitis was first reported in in patients with paraneoplastic encephalitis resulting from ovarian teratomas harbouring antibodies to hippocampal neuropil [ 1 ].
Soon after, it was discovered that this particular syndrome was associated with antibodies against the NR1 subunit of the NMDAR [ 35 ].
Anti-NMDAR encephalitis was also found in the absence of a tumour in a large number of patients [ 91 , ]. However, there is yet no evidence for complement-mediated or cytotoxic T-cell-mediated neuronal cell death in this disease. GAD antibodies are associated with a broad spectrum of diseases, i. Neurological diseases are associated with very high GAD antibody concentrations being two to three log ranks higher than in the diabetic population [ ].
The spectrum of neurological conditions associated with GAD antibodies ranges is broad [ ], including stiff-man syndrome, cerebellar ataxia, limbic encephalitis and pharmacoresistant TLE, which is probably the chronic form of GAD antibody-associated limbic encephalitis. Some experimental conditions have provided evidence that these antibodies might contribute to a loss of GABAergic inhibition [ 81 , 82 ]. Histopathological studies have shown neuronal loss and axonal dystrophy in the hippocampi of these patients, whereas Ig and complement deposition were absent from these brains.
Since the antigen is intracellular, a T-cell-mediated pathology would be a likely mechanism. Autoimmune encephalitis is a rapidly growing field and new antibodies targeting receptor or channel complexes are increasingly identified. Discussion of all these antibodies is beyond the scope of this review. Examples for recently identified antibodies that cause encephalitis and epilepsy include antibodies against AMPA receptors another sub-type of glutamate receptors , GABA B receptors, dopamine-D2 receptors and glycine receptors [ ].
Understanding the molecular details of autoantibody actions on receptor and channel complexes is highly desirable and may open the path to develop specific therapies to treat humoral autoimmune encephalitis. With respect to the discussion on autoimmune encephalitis in the context of our review, there is an important caveat.
In our review, we aim at showing that infections can promote seizures and epileptogenesis by activating overlapping pathways with classical sterile inflammation, which by definition occurs in association with a brain damage or tissue injury.
Autoimmune diseases likely act by different mechanisms in promoting seizures, most of which are largely unknown or still under evaluation, such as autoantibody-mediated inactivation of ion channels and others. It is still unknown and mostly unexplored if autoantibodies would also indirectly activate sterile mechanisms of inflammation in the brain as discussed above.
In principle, there are at least three strategies to prevent epilepsy after brain infections or other epileptogenic brain insults Fig.
Appropriate treatment of the CNS infection and correction of predisposing factors such as fluid and electrolyte imbalance would modify the initial insult and thereby may reduce the risk of long-term consequences. Antiepileptogenesis or disease modification after the infection includes treatments that directly target the complex mechanisms underlying epileptogenesis [ 80 ]. As discussed above, the available experimental evidence supports the idea that inflammation in brain caused by either sterile injuries or by infections may contribute to acute seizures and epilepsy development using partially overlapping mechanisms, therefore, highlighting putative common target for therapeutic interventions which may not only suppress the symptoms of the disease but also interfere with key pathogenic mechanisms.
One can envisage the use of specific anti-inflammatory drugs blocking the key pathogenic inflammatory mechanisms [ ]. The advantage of this approach is that some of these drugs are already available in the clinic for the treatment of auto-inflammatory or autoimmune diseases [e.
The challenge, however, is to design an intervention that blocks the detrimental arm of brain inflammation without interfering with the homeostatic mechanisms; in this context, the implementation of resolving anti-inflammatory mechanisms rather than the prevention of the inflammatory cascade from occurring may be a better strategy. Preventing inflammation may also be difficult due to the rapid onset and amplification of the cascade after the first inciting event.
The development of a biomarker of brain inflammation would be of great help to monitor the efficacy of an anti-inflammatory intervention, and determine when the treatment can be stopped [ ]. Several infections, mostly preventable, are associated with seizures and epilepsy. The exact risks of developing seizures are poorly understood, but appear to relate to the pathogen, the degree of cortical involvement, maturation of the brain, genetic makeup and the cytokine-mediated inflammatory response.
This is clearly an area of great clinical importance requiring further investigation. Insight into the mechanisms of seizures and epilepsy in CNS infections could help in evolving innovative antiepileptogenic interventions.
In this respect, it is important to note that both infectious and non-infectious causes of inflammation share common molecular pathways and mechanisms that are critically involved in the processes leading to epilepsy Figs.
In addition, prevention of CNS infections such as meningitis and encephalitis through immunisation and eradication of parasitic infections by increasing public awareness and improving sanitation are the definitive steps towards reducing the burden of epilepsy [ ]. JWS receives research support from the Dr. We are grateful to Dr. Gail S Bell for critically reviewing the manuscript. National Center for Biotechnology Information , U. Author manuscript; available in PMC Feb 1.
Annamaria Vezzani , 1 Robert S. Fujinami , 2 H. Author information Copyright and License information Disclaimer. The publisher's final edited version of this article is available at Acta Neuropathol. See other articles in PMC that cite the published article. Abstract Epilepsy is the tendency to have unprovoked epileptic seizures. Table 1 Glossary of terms used in this review.
Early seizures are typically felt to represent acute symptomatic i. Mechanisms of early and late seizures are thought to differ. Open in a separate window. Interactions of infectious agents and the central nervous system. Bacterial infections as a cause of epilepsy Bacterial infections of the CNS involve mainly the meninges and the cerebral parenchyma; almost any CNS bacterial infection can result in acute symptomatic seizures and later acquired epilepsy [ 19 , 38 , , ].
Acute bacterial meningitis Acute symptomatic seizures and the late development of epilepsy in survivors of acute bacterial meningitis are well known, although there have been few attempts to characterise the risk of seizures according to the infective agent [ 19 ].
Intracranial abscesses Cerebral abscesses Figs. Intracranial empyemas These are usually the consequence of direct spread of an adjacent focus of infection such as sinusitis or otitis media and are mostly caused by anaerobic agents.
Parasitic infections as a cause of epilepsy Almost all parasitoses can be associated with seizures and epilepsy Table 2 either by a diffuse encephalitis or encephalopathy, or by intracerebral location of the parasite.
Neurocysticercosis NCC Cysticercosis is the infestation by the larval form of Taenia solium , with pigs as the intermediate host [ ]. Cerebral malaria Malaria is the most common tropical parasitic disease. Toxoplasmosis Toxoplasmosis is a common parasitic infection Fig. Toxocariasis Human toxocariasis is the infestation caused by the larval stages of Toxocara canis and, less frequently, Toxocara cati.
Combination of parasites Concomitant infections are possible in areas endemic for several parasites. Fungal infections Seizures may also be a consequence of fungal CNS infections [ 19 , , ]. Viral infections as a cause of epilepsy Viral infection in humans can result in infection of the CNS. Experimental models to study mechanisms of epileptogenesis after brain infections Animal models are useful to study the mechanisms involved in infection-induced epileptogenesis, but most infectious agents that cause encephalitis in rodents are associated with high mortality, so that the processes leading to epilepsy cannot be investigated [ 72 ].
The sterile non-infectious inflammatory response that occurs following brain insults and its potential role in epileptogenesis Definition and key molecules of sterile inflammation Sterile inflammation is a homeostatic tissue response to injury triggered by endogenous molecules called danger signals DS or alarmins. Sterile inflammation in the CNS In the normal brain, PRR are expressed at barely detectable levels in neurons, glia and endothelial cells of microvessels, but they are rapidly induced in these cells following an epileptogenic insult e.
How should we explain the development of early and late seizures after brain infections and sterile inflammation? Mechanisms mediating the pathological consequences of sterile inflammation The induction of inflammatory mediators in seizure-prone brain areas is induced by cell injury, seizures, or their combination. Long-term consequences of systemic and CNS inflammation on immature brain function, and their role in experimental febrile seizures Febrile seizures in experimental models trigger sterile inflammation: Antibody-mediated encephalitis and epilepsy Traditionally, the vast majority of encephalitides have been ascribed a microbiological aetiology.
Table 3 Spectrum of antibody-associated epileptic encephalitides. NMDA receptor-associated encephalitis Histopathology findings in patients with antibodies directed against the NMDAR, a subtype of glutamate receptors in the brain, differ from most other antibody-associated encephalitidides. Autoantibodies targeting other receptor or channel complexes Autoimmune encephalitis is a rapidly growing field and new antibodies targeting receptor or channel complexes are increasingly identified.
Strategies to prevent epilepsy resulting from brain infections and non-infectious inflammation In principle, there are at least three strategies to prevent epilepsy after brain infections or other epileptogenic brain insults Fig. Conclusions Several infections, mostly preventable, are associated with seizures and epilepsy. Treatment-responsive limbic encephalitis identified by neuropil antibodies: The risk of unprovoked seizures after encephalitis and meningitis.
Autoimmune encephalitis in children. Complement activation in experimental and human temporal lobe epilepsy. Inflammation exacerbates seizure-induced injury in the immature brain.
Inflammation enhances epileptogenesis in the developing rat brain. Tumor necrosis factor-alpha inhibits seizures in mice via p75 receptors. The dual role of TNF-alpha and its receptors in seizures. Evaluating an etiologically relevant platform for therapy development for temporal lobe epilepsy: J Pharmacol Exp Ther.
Etiology and site of temporal lobe epilepsy influence postictal cytokine release. Recommendation for a definition of acute symptomatic seizure. Revised terminology and concepts for organization of seizures and epilepsies: Viral, bacterial, fungal and parasitic infections associated with seizure disorders.
Handbook of clinical neurology, The epilepsies. International consensus classification of hippocampal sclerosis in temporal lobe epilepsy: N Engl J Med.
Subdural empyema presenting with seizure, confusion, and focal weakness. West J Emerg Med. Epilepsy and neurocysticercosis in Latin America: Complement C5-deficient mice are protected from seizures in experimental cerebral malaria. Potassium channel antibodies in two patients with reversible limbic encephalitis. Neurologic disease induced in transgenic mice by cerebral overexpression of interleukin 6. Proc Natl Acad Sci. Epilepsies associated with hippocampal sclerosis.
A novel, noninvasive, predictive epilepsy biomarker with clinical potential. Inflammatory processes, febrile seizures, and subsequent epileptogenesis. Nodding syndrome since Trop Med Int Health. Curr Neurol Neurosci Rep. Infiltrating macrophages are key to the development of seizures following virus infection. Inflammatory cytokines and related genes are induced in the rat hippocampus by limbic status epilepticus.
Infections and inflammatory diseases. Herpes simplex encephalitis as a potential cause of anti- N -methyl-D-aspartate receptor antibody encephalitis: Detection of human herpesvirus-6 in mesial temporal lobe epilepsy surgical brain resections.
Interleukin-1beta contributes to the generation of experimental febrile seizures. Epileptogenesis provoked by prolonged experimental febrile seizures: A year prospective study of childhood herpes simplex encephalitis: Human herpesvirus 6 and 7 in febrile status epilepticus: Increased expression of mRNA encoding interleukin-1beta and caspase-1, and the secreted isoform of interleukin-1 receptor antagonist in the rat brain following systemic kainic acid administration.
Large-scale analysis of viral nucleic acid spectrum in temporal lobe epilepsy biopsies. Overexpression of mucalpain in the anterior temporal neocortex of patients with intractable epilepsy correlates with clinicopathological characteristics. Chemotactic and mitogenic stimuli of neuronal apoptosis in patients with medically intractable temporal lobe epilepsy.
Cytokines and brain excitability. Clinical symptoms, diagnosis, and treatment of neurocysticercosis. Stiff person syndrome-associated autoantibodies to amphiphysin mediate reduced GABAergic inhibition. Contributions of astrocytes to epileptogenesis following status epilepticus: Neuronal surface antigen antibodies in limbic encephalitis: Blood-brain barrier dysfunction, TGFbeta signaling, and astrocyte dysfunction in epilepsy.
Receptor for advanced glycation endproducts is upregulated in temporal lobe epilepsy and contributes to experimental seizures. Faciobrachial dystonic seizures precede Lgi1 antibody limbic encephalitis. Case-control studies on the relationship between onchocerciasis and epilepsy: Clinical profile and outcome of Japanese encephalitis in children admitted with acute encephalitis syndrome. Exposure to multiple parasites is associated with the prevalence of active convulsive epilepsy in sub-Saharan Africa.
The brain serves as the organic basis of cognition and exerts centralized control over the other organs of the body. The brain is protected by the skull ; however, if the brain is damaged , significant impairments in cognition and physiological function or death may occur.
Addiction is a disorder of the brain's reward system which arises through transcriptional and epigenetic mechanisms and occurs over time from chronically high levels of exposure to an addictive stimulus e. Arachnoid cysts are cerebrospinal fluid covered by arachnoidal cells that may develop on the brain or spinal cord. However, if there is a large cyst, symptoms may include headache, seizures, ataxia lack of muscle control , hemiparesis , and several others. Macrocephaly and ADHD are common among children, while presenile dementia, hydrocephalus an abnormality of the dynamics of the cerebrospinal fluid , and urinary incontinence are symptoms for elderly patients 65 and older.
ADHD is an organic disorder of the nervous system. Many people with ADHD continue to have symptoms well into adulthood.
Autism is a neurodevelopmental disorder that is characterized by restricted and repetitive patterns of behavior and persistent deficits in social interaction and communication. Bipolar disorder is a serious illness of the nervous system. Mood swings from the highs of mania to the lows of deep depression usually occurs over several weeks to months. New research suggests that bipolar disorder is actually a neurological disease genetically related to Parkinson's disease .
Catalepsy is a nervous disorder characterized by immobility and muscular rigidity, along with a decreased sensitivity to pain. Catalepsy is considered a symptom of serious diseases of the nervous system e. Cataleptic fits can range in duration from several minutes to weeks. Catalepsy often responds to Benzodiazepines e.
Major depressive disorder, otherwise known as depression, is a disorder that is characterized by a pervasive and persistent low mood that is accompanied by low self-esteem and by a loss of interest or pleasure in normally enjoyable activities. Encephalitis is an inflammation of the brain. It is usually caused by a foreign substance or a viral infection. Symptoms of this disease include headache, neck pain, drowsiness, nausea, and fever. If caused by the West Nile virus ,  it may be lethal to humans, as well as birds and horses.
Epilepsy is an unpredictable, serious, and potentially fatal disorder of the nervous system, thought to be the result of faulty electrical activity in the brain. Epileptic seizures result from abnormal, excessive, or hypersynchronous neuronal activity in the brain.
Epilepsy becomes more common as people age. Onset of new cases occurs most frequently in infants and the elderly. Epileptic seizures may occur in recovering patients as a consequence of brain surgery. A number of different pathogens i. A medical condition, Locked-in syndrome usually resulting from a stroke that damages part of the brainstem, in which the body and most of the facial muscles are paralysed but consciousness remains and the ability to perform certain eye movements is preserved.
Meningitis is an inflammation of the meninges membranes of the brain and spinal cord. It is most often caused by a bacterial or viral infection. Fever, vomiting, and a stiff neck are all symptoms of meningitis. A chronic, often debilitating neurological disorder characterized by recurrent moderate to severe headaches, often in association with a number of autonomic nervous system symptoms. Multiple sclerosis MS is a chronic, inflammatory demyelinating disease , meaning that the myelin sheath of neurons is damaged.
Symptoms of MS include visual and sensation problems, muscle weakness, numbness and tingling all over, muscle spasms, poor coordination, and depression. Also patients with MS have reported extreme fatigue and dizziness, tremors, and bladder leakage. Alzheimer's is a neurodegenerative disease typically found in people over the age of 65 years.
The ultimate cause is unknown. The clinical sign of Alzheimer's is progressive cognition deterioration. Huntington's disease is a degenerative neurological disorder that is inherited. Degeneration of neuronal cells occurs throughout the brain, especially in the striatum. There is a progressive decline that results in abnormal movements. Parkinson's disease, or PD, is a progressive illness of the nervous system. Caused by the death of dopamine-producing brain cells that affect motor skills and speech.
Symptoms may include bradykinesia slow physical movement , muscle rigidity, and tremors. Behavior, thinking, sensation disorders, and the sometimes co-morbid skin condition Seborrheic dermatitis are just some of PD's numerous nonmotor symptoms. Tourette's syndrome is an inherited neurological disorder.
Early onset may be during childhood, and it is characterized by physical and verbal tics. The exact cause of Tourette's, other than genetic factors, is unknown. There is a wide range of treatments for central nervous system diseases. These can range from surgery to neural rehabilitation or prescribed medications.
From Wikipedia, the free encyclopedia. List of central nervous system infections. This section is missing information about a number of brain disorders   that not currently listed here.
Please expand the section to include this information. Further details may exist on the talk page. For a more comprehensive list, see List of infections of the central nervous system. This section is empty. You can help by adding to it.
Infections, inflammation and epilepsy
programmes and resources for their management (4–6). introduction aspects of the following neurological disorders: dementia, epilepsy, headache disorders. Brain, Volume , Issue 6, 1 June , Pages –, Neurologists appreciate the embodied nature of neurological disorders in terms of diagnosis, effects of a lesion/insult etc. and the effects of (possibly delayed) secondary . For example in epilepsy (Cooray et al., ), seizure activity can. Epilepsy is a central nervous system (neurological) disorder in which brain activity becomes Six types of generalized seizures exist. Absence.