What are the factors affecting encephalitis survival rates. How can inpatient mortality be predicted among encephalitis patients. What is the importance of a novel admission risk score in encephalitis treatment. How does encephalitis impact healthcare systems globally. What are the challenges in diagnosing and treating encephalitis. How can patient outcomes be improved in encephalitis cases. What are the long-term effects of encephalitis on survivors.

Understanding Encephalitis: A Comprehensive Overview

Encephalitis, an inflammation of the brain tissue, poses significant challenges to healthcare systems worldwide. This condition can be caused by various factors, including viral infections, autoimmune disorders, and in some cases, unknown origins. The complexity of encephalitis often leads to difficulties in diagnosis and treatment, making it crucial for medical professionals to have a deep understanding of the disease and its potential outcomes.

Recent studies have shown that encephalitis hospitalization rates and inpatient mortality in the United States have fluctuated over the years. Between 2000 and 2010, there was a noticeable trend in these rates, highlighting the need for improved management strategies and predictive tools.

Encephalitis Hospitalization Burden

The burden of encephalitis-associated hospitalizations in the United States has been a subject of extensive research. A study covering the period from 1988 to 1997 revealed significant healthcare utilization due to this condition. More recent data from 1998 to 2010 further emphasized the ongoing impact of encephalitis on the healthcare system, with substantial numbers of hospitalizations reported annually.

Causes and Clinical Presentations of Encephalitis

Encephalitis can manifest in various forms, each with its unique set of challenges. Acute encephalitis, as described by Johnson RT in 1996, presents a range of symptoms that can often be mistaken for other neurological conditions. This similarity in presentation adds to the complexity of diagnosis and appropriate treatment initiation.

In non-outbreak situations, the cause of encephalitis often remains a mystery. A systematic review by Granerod et al. in 2010 highlighted the challenges faced by clinicians in identifying the underlying cause of encephalitis in sporadic cases. This uncertainty can lead to delays in treatment and potentially poorer outcomes for patients.

Encephalitis in Older Adults

The clinical epidemiology, risk factors, and outcomes of encephalitis in older adults present unique challenges. A study by Hansen et al. in 2020 shed light on the specific considerations needed when treating elderly patients with encephalitis. The findings emphasized the importance of age-specific approaches in management and prognosis prediction.

Geographical Variations in Encephalitis Presentations

Encephalitis presentations can vary significantly across different regions. A multicentre, population-based prospective study conducted in England revealed distinct differences in clinical presentations and causes of encephalitis. This variability underscores the need for region-specific guidelines and treatment protocols.

• Viral causes (e.g., herpes simplex virus)
• Autoimmune encephalitis
• Bacterial infections
• Unknown etiologies

Predicting Outcomes in Encephalitis Patients

Predicting the outcome of encephalitis cases is crucial for effective patient management and resource allocation. Thakur et al. in 2013 identified several predictors of outcome in acute encephalitis, providing valuable insights for clinicians. These predictors can help in early intervention and potentially improve patient outcomes.

For autoimmune encephalitis, a study by Qiu et al. in 2019 analyzed clinical characteristics and poor prognostic predictors. This research highlighted the importance of early recognition of autoimmune causes and the potential for targeted treatments in improving outcomes.

Specific Encephalitis Types and Their Outcomes

Different types of encephalitis can have varying outcomes and require specific management approaches. For instance, a multicenter cohort study by Jaquet et al. in 2019 focused on functional outcomes in adult patients with herpes simplex encephalitis admitted to the ICU. The study provided valuable data on the long-term prognosis and rehabilitation needs of these patients.

West Nile virus neuroinvasive infection, another form of encephalitis, has been the subject of multinational studies. Popescu et al. in 2020 developed a prediction model for unfavorable outcomes in these cases, offering a tool for clinicians to assess risk and tailor treatment strategies.

Diagnostic Challenges and Management Strategies

Diagnosing encephalitis accurately and promptly remains a significant challenge. Gennai et al. in 2016 developed a clinical and paraclinical score to estimate the probability of herpes simplex virus encephalitis in patients with febrile, acute neurologic impairment. This scoring system aims to assist in rapid diagnosis and treatment initiation.

Management of suspected encephalitis cases, particularly those caused by herpes simplex virus, has been a focus of research. A study by Bell et al. in 2009 examined the management practices in a U.K. teaching hospital, highlighting areas for improvement in diagnostic and treatment protocols.

Importance of Timely Diagnostics

The timing of diagnostic procedures, such as lumbar punctures, can significantly impact the accuracy of diagnosis. Michael et al. in 2010 investigated the effect of delayed lumbar punctures on the diagnosis of acute bacterial meningitis in adults, emphasizing the importance of prompt diagnostic measures in encephalitis cases as well.

Prognostic Factors and Treatment Outcomes

Understanding prognostic factors is crucial for predicting outcomes and tailoring treatment strategies. Raschilas et al. in 2002 conducted a multicenter study on the outcome and prognostic factors for herpes simplex encephalitis in adult patients. Their findings provide valuable insights into the factors influencing patient survival and recovery.

In cases of autoimmune encephalitis, immune therapy has shown promising results. A systematic review by Nosadini et al. in 2015 explored various immune therapy options, offering guidance on treatment choices for this specific form of encephalitis.

Long-term Care and Socio-medical Trajectory

The care of encephalitis patients extends beyond the acute hospital phase. Cooper et al. in 2017 investigated the socio-medical trajectory of herpes simplex virus encephalitis, highlighting the need for comprehensive, long-term care strategies. This research emphasized the importance of considering the broader impact of encephalitis on patients’ lives and their families.

Long-term outcomes of patients with acute infectious encephalitis have been studied across various causes. Mailles et al. in 2012 conducted research in France, providing insights into the long-term prognosis and quality of life of encephalitis survivors.

Epidemiological Trends and Challenges

Recent epidemiological studies have shed light on the prevalence and distribution of encephalitis cases. Hasbun et al. in 2017 analyzed the epidemiology of meningitis and encephalitis in the United States from 2011 to 2014, offering updated information on disease trends and demographics.

Comparing prospective studies with hospital discharge data can reveal discrepancies in epidemiological assessments. Bernard et al. in 2013 highlighted these differences, emphasizing the need for comprehensive and accurate data collection methods in encephalitis research.

Standardizing Encephalitis Definitions and Algorithms

To improve diagnosis and research in encephalitis, standardized case definitions and diagnostic algorithms are essential. The International Encephalitis Consortium, as reported by Venkatesan et al. in 2013, developed consensus statements on these aspects, providing a framework for consistent approach to encephalitis cases globally.

These standardized definitions and algorithms aim to:

1. Enhance diagnostic accuracy
2. Facilitate comparative research
3. Improve treatment protocols
4. Aid in epidemiological studies

The development of a novel admission risk score for predicting inpatient mortality among encephalitis patients represents a significant advancement in the field. This tool, based on the comprehensive analysis of various factors influencing encephalitis outcomes, offers clinicians a valuable resource for early risk assessment and treatment planning.

By incorporating factors such as age, comorbidities, initial clinical presentation, and laboratory findings, the risk score provides a more nuanced approach to patient management. This can lead to more personalized treatment strategies and potentially improved outcomes for encephalitis patients.

Implications for Healthcare Policy and Resource Allocation

The insights gained from recent encephalitis research have significant implications for healthcare policy and resource allocation. Understanding the burden of encephalitis on healthcare systems can inform decisions on:

• Allocation of specialized neurological care resources
• Training programs for healthcare professionals
• Public health initiatives for prevention and early detection
• Research funding priorities in neurology and infectious diseases

As our understanding of encephalitis continues to evolve, so too must our approaches to its management and treatment. The development of predictive tools like the novel admission risk score represents a step forward in this ongoing journey to improve patient care and outcomes in encephalitis cases.

Emerging Research and Future Directions

The field of encephalitis research is continuously evolving, with new studies shedding light on various aspects of the disease. Emerging areas of research include:

• Advanced neuroimaging techniques for early detection and prognosis
• Genetic factors influencing susceptibility and outcomes
• Novel therapeutic approaches, including targeted immunotherapies
• The role of the microbiome in encephalitis development and progression

These research directions hold promise for further improving our understanding and management of encephalitis. As new data emerges, it will be crucial to integrate these findings into clinical practice and update guidelines accordingly.

The Role of Artificial Intelligence in Encephalitis Management

Artificial intelligence (AI) and machine learning are increasingly being explored as tools to enhance encephalitis diagnosis and management. Potential applications include:

• Automated analysis of brain imaging to detect subtle changes indicative of encephalitis
• Predictive models for patient outcomes based on large datasets
• Decision support systems for clinicians in treatment selection
• Real-time monitoring of patient data for early detection of complications

While these technologies are still in developmental stages for encephalitis applications, they represent an exciting frontier in improving patient care and outcomes.

Global Collaboration and Knowledge Sharing

The complex nature of encephalitis and its varied presentations across different populations underscore the importance of global collaboration in research and clinical practice. International consortia and collaborative research networks play a crucial role in:

• Sharing data and resources across borders
• Conducting large-scale, multi-center studies
• Developing standardized protocols and guidelines
• Addressing regional variations in encephalitis epidemiology and management

Such collaborative efforts are essential for advancing our understanding of encephalitis and improving patient care worldwide.

Patient-Centered Approaches and Quality of Life Considerations

As survival rates for encephalitis improve, there is an increasing focus on the quality of life of survivors. Research is now expanding to include:

• Long-term cognitive and psychological outcomes
• Rehabilitation strategies for encephalitis survivors
• Support systems for patients and caregivers
• Integration of patient-reported outcomes in clinical trials and practice

These patient-centered approaches aim to address the holistic needs of encephalitis survivors and improve their overall well-being beyond mere survival.

The development of the novel admission risk score for predicting inpatient mortality among encephalitis patients represents a significant step forward in personalizing patient care. By providing clinicians with a tool to assess risk early in the admission process, it enables more targeted interventions and resource allocation. This approach has the potential to significantly improve patient outcomes and optimize healthcare resource utilization.

As research in encephalitis continues to advance, it is likely that we will see further refinements in diagnostic techniques, treatment strategies, and prognostic tools. The integration of these advancements into clinical practice will be crucial in improving the care and outcomes for patients affected by this complex and challenging condition.

The field of encephalitis research and management is at an exciting juncture, with new discoveries and innovations promising to transform patient care. As we move forward, the continued collaboration between researchers, clinicians, and patients will be essential in translating these advancements into tangible improvements in encephalitis survival rates and quality of life for those affected by this condition.

Predicting Inpatient Mortality Among Encephalitis Patients: A Novel Admission Risk Score

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Prognostic factors in childhood acute encephalitis

. 1991 Jun;10(6):441-6.

doi: 10.1097/00006454-199106000-00005.

J Rautonen 
¹
, M Koskiniemi, A Vaheri

Affiliations

Affiliation

• ¹ Children’s Hospital, Helsinki, Finland.

• PMID:

  1906597

• DOI:

  10.1097/00006454-199106000-00005

J Rautonen et al.

Pediatr Infect Dis J.

1991 Jun.

. 1991 Jun;10(6):441-6.

doi: 10.1097/00006454-199106000-00005.

Authors

J Rautonen 
¹
, M Koskiniemi, A Vaheri

Affiliation

• ¹ Children’s Hospital, Helsinki, Finland.

• PMID:

  1906597

• DOI:

  10.1097/00006454-199106000-00005

Abstract

We have studied the prognostic factors in 462 children, from 1 month to 16 years old, with acute encephalitis. Death occurred in 2.8% patients, 6.7% were severely damaged and 90.5% were cured with no or only minor sequelae. The risk of death or severe damage in patients less than 1 year of age was 5.0-fold (95% confidence limits, 2.2 to 11.6; P less than 0.001) greater than that of older children. When compared with those children whose level of consciousness had been normal before admission, children who had been disoriented before admission had a 3.9-fold (1.1 to 14.3, P less than 0.05) risk and those who had been unconscious had a 25.4-fold (7.3 to 88.1, P less than 0.001) greater risk of death or severe damage. The risk of death or severe damage in patients with herpes simplex virus encephalitis was 11.7-fold (3.8 to 35.8, P less than 0.001) and in patients with Mycoplasma pneumoniae encephalitis it was 7.0-fold (2.6 to 18.7, P less than 0.001) that of other children. All patients with none of the above mentioned risk factors were cured without any major sequelae. We conclude that specific attention should be paid to the youngest patients, especially to those with an impaired level of consciousness, and all available measures should be focused on early detection of herpes simplex virus or M. pneumoniae infection.

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MeSH terms

Encephalitis: rehabilitation, symptoms, consequences, treatment

Encephalitis rehabilitation

Encephalitis is an inflammation of the brain caused by an infection (infectious encephalitis) or an immune system reaction affecting the brain (autoimmune or post-infectious encephalitis). Potentially, any virus can cause encephalitis, but not every person infected with the virus will suffer from this disease.

Encephalitis can be caused by:

• Herpes simplex: types 1 and 2
• Varicella: mumps, measles, rubella
• Influenza, enteroviruses
• Enteric viruses
• Insect-borne viruses: Japanese encephalitis, West Nile virus, tick-borne encephalitis.

Bacteria, fungi and parasites can also cause encephalitis, although less frequently. For example:

• Bacteria: mycoplasma, meningococcus, pneumococcus, listeria.
• Fungi: histoplasma, cryptococcus, candida.
• Parasites: Plasmodium, which causes malaria, Toxoplasma.

Fungal encephalitis is caused by a fungal infection that enters the bloodstream and attacks the spinal cord. This type of encephalitis is especially dangerous for people with a weakened immune system, such as those infected with HIV.

Toxoplasmic encephalitis is caused by protozoan parasites that mainly live on cats, but you can get infected not from them, but by eating unwashed vegetables or raw meat. It is also dangerous for HIV-infected people or people with weakened immune systems.

Autoimmune encephalitis can be triggered by an attack by the immune system on the brain or develop as a result of infection – this is called “post-infectious” encephalitis. Other types of encephalitis are associated with the activity of specific antibodies in the blood.

Symptoms of encephalitis

Infectious encephalitis in the first symptoms resembles the flu or a cold: a person experiences a headache, increased fatigue and drowsiness. More severe symptoms may appear over a period of hours to days.

These include:

• altered state of consciousness (uncharacteristic behavior, general feeling of confusion or hallucinations),
• loss of consciousness,
• fever,
• convulsions,
• inability to speak or control movements ,
• aversion to bright lights,
• loss of sleep.

Tick-borne encephalitis

This type of encephalitis is the most famous and well-known. It is seasonal and is carried by parasites. Not all ticks are carriers of encephalitis, but they can be carriers of other dangerous infections. Therefore, residents of endemic areas (for example, Kemerovo, Irkutsk, Tomsk regions, Krasnoyarsk and Altai Territories), as well as people planning trips to regions that are unfavorable for this disease, doctors recommend vaccinating against tick-borne encephalitis.

Recently, cases of the disease have become more frequent in Europe, as not only ticks, but also birds, rodents, cows and dogs can be carriers. Tick-borne encephalitis manifests itself in the same way as other types of infectious encephalitis – first through flu or cold symptoms, and after about a week – neurological symptoms.

Treatment of encephalitis

The first thing a patient receives with infectious encephalitis is antiviral drugs aimed at eliminating the root cause of the disease. These include antibiotics, acyclovir, and immunomodulatory drugs. It is necessary to eliminate the symptoms and consequences of the disease, that is, try to return the body to normal functioning.

It is important to support the person psychologically and create a comfortable environment for him – due to increased sensitivity, it is necessary to minimize contacts and visits, reduce noise levels, provide a calm and comfortable environment and treat unusual and sometimes aggressive behavior with care and understanding. It is necessary to consult with specialists in time and do not be shy to ask for help from loved ones.

Sequelae of encephalitis

Encephalitis affects the brain, so neurons (brain nerve cells) suffer. People who have had encephalitis experience consequences similar to those of a stroke, head injury, and other brain diseases. As a rule, they are associated with impaired cognitive and speech functions.

At the same time, each patient has his own consequences of the transferred encephalitis, depending on individual factors.

The most common effects are listed below:

• fatigue,
• memory problems,
• headaches, some parts of the body, loss of control over the body,
• speech problems,
• slow reaction times,
• hormonal disorders.

All these effects are long-term: do not underestimate their impact on a person’s life and social relationships. Therefore, it is important to be attentive to a loved one who has had encephalitis. For many, returning to a normal life, to work or school, can be difficult. In children, the consequences may not appear immediately, but as the body grows and develops, therefore it is important to be observed by a doctor and be attentive to any changes in the child’s behavior. It is especially worth paying attention to any cognitive impairment and fatigue.

Rehabilitation methods

Whatever form of encephalitis a person has, it is very important to create an environment for a natural recovery process. In addition to a favorable environment and environment, the help of rehabilitation specialists is important for a person, since the disease affects cognitive, behavioral, social, emotional and medical aspects. In all aspects, it is important to give support to the patient and his family.

In rehabilitation, it is important to take into account psychological and human assistance:

• try to regain cognitive skills,
• work with motivation and emotional state,
• develop physical and mental endurance,
• improve the quality of life,
• develop social skills.

You can discuss with your doctor the rehabilitation program and the profile of specialists to be involved. Usually, a neurologist, psychologist and neuropsychologist, speech therapist, physiotherapist and occupational therapist help the recovery process after encephalitis. Their joint efforts are aimed at restoring body functions or their compensation by possible methods.

Neuropsychological therapy

The neuropsychologist’s task is to determine the degree of brain damage and cognitive capabilities at the start of the rehabilitation process. A neuropsychologist evaluates the work of attention and memory, the speed of thinking and speech using specially designed tests. The work of a neuropsychologist with a patient is very important, as the doctor helps to restore brain function or minimize disturbances in its work.

Physical therapy

A physiotherapist helps to cope with the physiological consequences of the disease, such as difficulty in controlling one’s body, loss of balance and coordination in space, and numbness in the limbs. To do this, the specialist develops a program of physical exercises using special equipment or without it.

Cognitive and Behavioral Therapy

Therapy is aimed at regaining the skills of self-control, decision-making, independence of action. For this, games, tests, specially designed tasks can be used.

It is important not only for the patient to receive psychological help, but also for his family members. It is also worth consulting about ways to improve communication within the family in new circumstances after illness.

It is necessary to be prepared for the fact that the process of recovery from encephalitis can take months or even years. Properly selected therapy and subsequent rehabilitation, started on time, in some cases can restore not only the physical health of a person, but also his psychological state and relationships in the family and society.

The rehabilitation center “Three Sisters” has all the comfortable conditions for staying. The wards are equipped with panic buttons for calling staff, functional beds that make it easier for the patient to move, there are handrails and railings, and automatically opening doors. You can learn more about rehabilitation after infectious diseases here.

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Autoimmune nature of neurological and neuropsychiatric disorders

Author:
T.N. Slobodin

04/25/2018

TO ZMISTU NUMBER

In more and more data about the autoimmune nature of some neurological and neuropsychiatric disorders have recently appeared. The purpose of this review is to consider in the movement disorders section a palette of autoimmune encephalitis (or encephalopathies), the triggering factor of which is infectious agents, tumors or other causes that provoke the synthesis of autoantibodies to various brain structures, including its diverse receptors. The main outline of the review is taken from the article by Baizabzl-Carvallo and Jankovic [1].

It should be noted that the insidiousness of autoimmune encephalitis lies in the fact that they can mimic infectious, toxic-metabolic, neurodegenerative and demyelinating diseases, which leads to their erroneous or late diagnosis, while a timely diagnosis and prescription of immunotropic therapy (glucocorticoids, plasmapheresis, intravenous immunoglobulins) in most cases cause a positive effect. Encephalitis lethargica, long described as a disease with subacute onset, parkinsonian, neuropsychiatric and oculomotor manifestations, is now considered as a syndromic diagnosis, combining diseases caused by various causes, including post-infectious and autoimmune (encephalitis caused by antibodies to NMDA or dopamine receptors) [2–4].

According to the etiological principle, autoimmune encephalitis is divided into paraneoplastic, post-infectious and idiopathic (when the cause is unclear, but often associated with the presence of other autoimmune diseases).

The mechanism of development of autoimmune encephalitis depends on the characteristics of autoantibodies, which can be pathogenic (targeting antigens on the surface of brain cells), and autoantibodies directed to intracellular antigens with the involvement of elements of cellular immunity (T-cells) in the pathogenesis, which causes, in contrast to first, their poor response to immunotropic therapy. Regardless of the triggering factor and the nature of the autoantibodies synthesized in response to it, various clinical variants of disorders can form in accordance with the region of application of the autoimmune process: limbic encephalitis, cerebellar degeneration, striatal (subcortical), stem encephalitis, leukoencephalopathy. According to the age of onset of the disease, autoimmune encephalitis of childhood and adults is distinguished.

Thus, among the entire spectrum of extrapyramidal diseases, united in this group solely on the principle of external manifestations, a subtype is singled out, the pathogenesis of which is based on autoimmune mechanisms, the early recognition of which can turn them into potentially curable diseases.

Autoimmune neuropsychiatric disorders associated with streptococcal infection

Sydenham’s chorea (CS) was first described in 1686 by T. Sydenham, and its association with rheumatism was discovered only in 1810 [4–5]. Despite the fact that cholesterol is only one of the many extrapyramidal and neuropsychiatric manifestations of this disease, it is still called chorea, and not, for example, Sydenham’s disease. CS is the prototype of disorders in which an infectious agent (in this case, β-hemolytic streptococcus) becomes a trigger for an autoimmune response that causes a variety of motor and neuropsychiatric symptoms [6-11]. Antibodies to the basal ganglia are detected in the acute period of CS in 100% of cases and only in 12% of patients with rheumatism without extrapyramidal manifestations [12]. Suspicion of this pathology is justified in each case of acutely developed chorea in a child. A previous streptococcal infection in the throat, elevated titers of antistreptolysin O (ASLO) support the diagnosis. A timely diagnosis determines the success of treatment not only in terms of prescribing specific therapy, but also from the standpoint that in patients with CS, the risk of developing acute dystonic reactions and other extrapyramidal complications in response to taking antipsychotics that block dopamine receptors is too high, comparing, in particular, , with patients with Tourette syndrome (TS) [13].

Risperidone is better tolerated than haloperidol or pimozide, but tetrabenazine (monoamine-depleting) is preferred because it does not lead to the risk of tardive dyskinesias [14]. Valproate and carbamazepine can be considered as symptomatic therapy for CS [6, 15]. Corticosteroids, plasmapheresis and intravenous immunoglobulin are prescribed in severe refractory cases [16]. But in rare cases, spontaneous remissions can occur. To prevent the recurrence of streptococcal infection, monthly courses of penicillin are prescribed for 10 years or until the age of 40 in case of cardiac complications, and also for a 5-year period or up to 21 years of age in the absence of heart damage [17].

PANDAS

In 1997, the term “pediatric autoimmune disorders associated with streptococcal infection” (PANDAS) was proposed. Suggested criteria for this nosology included [18]:

• onset from 3 years of age to puberty;
• having an obsessive-compulsive (OCD) and/or tic disorder;
• acute onset of symptoms, exacerbations and remissions;
• neurological disorders without choreiform manifestations;
• temporary association with streptococcal infection.

The proposed association between a wide range of neuropsychiatric manifestations and a possible autoimmune response provoked by streptococcal infection, as in patients with CS, has caused heated debate regarding the real existence of PANDAS and its relationship with TS, and this topic remains a subject of controversy to this day.

However, a number of studies confirm the high predominance of ASLO titers and antibodies to the basal ganglia in patients with TS compared with healthy controls [19–27]. The results of retrospective observations also prove a high frequency of streptococcal infection during the year preceding the development of tics or OCD [28–29].

However, there is evidence that does not support this relationship. Since no correlation was found between the presence of antibodies to the basal ganglia and the prefrontal cortex, an increase in cytokines in the cerebrospinal fluid, and an exacerbation of neurological symptoms in the form of tics and OCD, which maintains the status of controversy for the existence of this nosology [30-33].

Although other movement disorders, such as tremor, dystonia, stereotypes, myoclonus, opsoclonus, paroxysmal choreoathetosis, and catatonia, have been described in patients with streptococcal infection, the pathogenetic relationship between them has not yet been reliably established [34-36]. The positive outcome of treatment with intravenous immunoglobulins and plasmapheresis has been studied in a small number of patients with PANDAS, therefore, immunomodulatory treatment of this pathology, the existence of which is still in doubt, cannot be widely recommended, although each individual case should be considered individually [37-39].

Autoimmune encephalitis of paraneoplastic and non-paraneoplastic origin

Patients with paraneoplastic lesions usually subacutely develop the following syndromes alone or in combination [40]:

• encephalitis or encephalomyelitis;
• stem encephalitis;
• limbic or cerebellar encephalitis;
• paraneoplastic degeneration of the cerebellum;
• syndromes of lesions of the peripheral or autonomic nervous system.

The target antigen in paraneoplastic syndromes can be both intracellular and localized on the surface of cell membranes [41]. The intracellular group of antigens is also known as classical paraneoplastic onconeural antigens, since in patients with these syndromes, the presence of a tumor is associated with their specific intrathecal synthesis [42]. The pathogenetic role of these antibodies in the development of neurological disorders remains controversial after unsuccessful experimental studies, although there is strong evidence of T-cell immune attack against neural antigens, which may explain the poor response to immunotherapy [41–45].

Examples from this category of disorders are paraneoplastic cerebellar degeneration with anti-Yo, anti-Tr, anti-Ri and anti-Hu antibodies [46–48]. Atypical parkinsonism is associated with anti-Ma antibodies, chorea with anti-CV2/CRMP5, and opsoclonus-myoclonus with anti-Ri [49–55].

The second group of disorders is caused by antibodies directed against antigens on the surface of nervous system cells and is associated with the presence of tumors in 70% of patients [56-58]. Convincing experimental evidence exists for these antibodies of their pathogenetic role in the development of neurological disorders, since they significantly reduce the number of synaptic receptors in brain structures [56, 59]. Patients with these syndromes show improvement with intravenous immunoglobulin treatment and tumor removal [41]. Examples include a wide range of conditions associated with sodium channel antibodies (VGKC), including parkinsonism, tremor, myoclonus, and chorea [60]. In addition, it has recently been proven that these antibodies are directed against LGI1 or CASPR2, proteins that are part of the transsynaptic complex that provides synaptic transmission [61]. One of the typical manifestations of encephalopathy caused by antibodies to VGKC is limbic encephalitis, which manifests itself as severe memory impairment, disorientation, and epileptic seizures. In particular, it can be paraneoplastic, but more often it is a non-paraneoplastic (non-tumor) process. Moreover, optimal immunotherapy results in a decrease in CSF VGKC antibodies, which correlates with clinical improvement but does not rule out residual cognitive impairment.

A separate group is encephalitis caused by the synthesis of antibodies to NMDA receptors. As a rule, they occur in young women, starting with a prodromal stage in the form of headache and fever, followed by psychoses, epileptic seizures, hypoventilation, autonomic disorders and dyskinesias, mainly involving the orofacial region. In these patients, antibodies to NMDA receptors in high titers are found in the cerebrospinal fluid [62]. There is an undoubted connection with tumors of the ovaries or less often testicles in men. A positive effect is observed against the background of immunotherapy and after removal of the tumor, however, a fatal resolution is also possible with a late diagnosis.

Another group of tumor-associated autoimmune disorders is the “stiff person syndrome” (SPS) caused by antibodies to glutamic acid decarboxylase [63–67]. Some of these patients have another autoimmune disease — thymoma, diabetes mellitus, vitiligo, or pernicious anemia [68]. In the paraneoplastic variant, the face with SPS is in most cases older than in the non-paraneoplastic variant, and are characterized by predominant stiffness in the muscles of the neck and upper extremities [69]. The most severe variant is caused by antibodies to glycine receptors and is manifested by progressive encephalomyelitis, rigidity, myoclonus, and progressive epilepsy with mental retardation [70, 71]. However, special attention should be paid to the steroid-responsive encephalopathy associated with autoimmune thyroiditis, known as Hashimoto’s encephalitis.

This disease begins subacutely – in the form of progressive cognitive impairment in combination with myoclonus, tremor, ataxia, high titers of antibodies to thyroperoxidase and, as a rule, without concomitant hypothyroidism. In some cases, the first episodes of the disease are detected in the form of short-term myoclonic twitches in the muscles of the face and limbs, periods of speech and thought processes slowing down, lasting from several days to weeks, and may be preceded by several years of violent manifestations with impaired consciousness and tonic-clonic convulsions, who require urgent hospitalization. Most often, MRI shows no changes, and the EEG shows generalized or paroxysmal slow-wave activity without epileptiform symptoms. High titers of antibodies to thyroperoxidase, even with euthyroidism, suggest Hashimoto’s autoimmune encephalopathy. Immunosuppressive therapy, starting with steroids, usually results in complete remission in 80–96% of cases.

Rasmussen’s encephalitis is a disease of childhood that manifests with partial seizures, including focal myoclonus, dementia (cognitive decline), extrapyramidal disorders, and unilateral cerebral atrophy. This pathology is associated with a possible viral infection, but there is more data on the pathogenetic role of T cells [72–74]. In particular, in paraneoplastic autoimmune disorders, detection and removal of tumors is the main approach to stop autoimmunization, and in combination with immunotherapy (corticosteroids, plasmapheresis, intravenous immunoglobulin, rituximab) [75, 76]. And in diseases associated with antibodies to surface antigens, the response to immunotropic therapy is obvious even before tumor removal. When antibodies directed to intracellular antigens are activated, cyclophosphamide, tacrolimus, cyclosporine, or mycophenolate mofetil are the drugs of choice [41]. Symptomatic treatment may include short courses of antipsychotics or tetrabenazine for paraneoplastic chorea, GABAergic drugs (benzodiazepines, barbiturates) for SPS, botulinum toxin for myoclonus dystonia in Rasmussen’s encephalitis [14, 16, 77–79].

Systemic lupus erythematosus and antiphospholipid syndrome

Systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APC) is a complex autoimmune disease often manifested by movement disorders. Chorea is the most common manifestation of SLE, occurring within the first year after diagnosis and can often precede it [80]. Among 2-3% of patients with SLE, 96% of the pathology is observed in women, and in half of the cases it is unilateral. Chorea is often accompanied by other manifestations: epileptic seizures, strokes, cognitive impairment, personality disorders and psychosis [81, 83]. Signs of chorea in the background of antiphospholipid syndrome do not differ from those in SLE, but begin at an earlier age (under 15 years). The role of estrogens in the pathogenesis of the disorder is possible, since women predominate, exacerbations occur during pregnancy and while taking contraceptives [81, 82, 84]. It is assumed that in both disorders, antiphospholipid antibodies enter the CNS through the blood-brain barrier and bind to brain structures rich in phospholipids, in particular the basal ganglia. Clinical improvement in patients with chorea on the background of SLE and ARS is observed when taking haloperidol and tetrabenazine, valproic acid and clonidine, as well as corticosteroids, anticoagulants and aspirin [85-87]. In refractory chorea, intravenous immunoglobulins and plasmapheresis have been successfully used. In addition to chorea, parkinsonism has been described in individuals with SLE, the origin of which is associated with antibodies to dopamine receptors [88–90]. Successful treatment has been observed with corticosteroids, azathioprine, cyclophosphamide, dopamine receptor agonists, and levodopa [91-94]. Cerebellar involvement has been reported in 2% of patients with SLE. Subacutely, most patients develop ataxia without neuropsychiatric disorders, and in some cases, isolated tremor, blepharospasm, cervical dystonia, and SPS occur [95–97]. But in all episodes, improvement occurred against the background of cyclophosphamide and intravenous immunoglobulins. And with antiphospholipid syndrome, there are single descriptions of various motor phenomena: paroxysmal dyskinesia, hemidystonia, writing spasm, parkinsonism, corticobasal syndrome and ataxia.

Celiac disease and gluten sensitivity

Celiac disease is characterized by an immune response to dietary gluten and a variety of gastrointestinal and other systemic manifestations. Neurological disorders are observed in 10–50% of patients [98, 99]. However, there are frequent cases of isolated neurological manifestations without gastrointestinal pathology, but with serological confirmation of gluten sensitivity. The most common is cerebellar or gluten ataxia [100]. It is characterized by progressive cerebellar symptoms (usually in the 5th decade of life), less often there is a decrease in deep sensitivity. Cerebellar atrophy is detected on MRI in 60–80% of cases [101]. The mechanism of ataxia development is associated with the leukocyte antigen of the DQ2 and DQ8 alleles [102]. These patients also have circulating anti-gliadin antibodies (AGAs). Moreover, in patients with hereditary (spinocerebellar ataxia types 1, 2, 3, 4, 6 and 7, Friedreich’s ataxia) and sporadic ataxias, as well as multisystem atrophy, the detection rate of AGAs reaches 41% compared to 12–15% in the control group. . However, the issue of the causal role of AGAs remains controversial; moreover, there is an opinion that they are secondary to cerebellar degeneration [103–104]. The autoimmune pathophysiology of gluten ataxia is supported by the appearance of ataxia in experimental animals after transfusion of AGAs. Other movement disorders associated with gluten hypersensitivity include paroxysmal dyskinesia, ataxia-associated chorea, myoclonus, and parkinsonism [105–107]. Despite controversial issues in understanding the pathogenetic relationships between damage to the structures of the nervous system and certain antibodies, patients show significant clinical improvement after switching to a gluten-free diet for a year [101]. Additional effective measures were the administration of vitamin E and intravenous immunoglobulins [108].

Sjögren’s syndrome

Sjögren’s syndrome (SS) refers to an autoimmune disorder characterized by lymphocytic infiltration and damage to the salivary and lacrimal glands, with the presence of SSA/Ro and SSB/La antibodies, of which the latter is more specific. Neurological complications are observed in 1.5–25% of cases, including parkinsonism with predominant akinesia, poor response to levodopa in combination with subcortical vascular lesions on MRI, or asymmetric parkinsonism with a good response to levodopa and no changes on MRI [109–113]. Some scientists associate these manifestations with cerebral vasculopathy [113-115]. Other extrapyramidal disorders in SS include chorea and dystonia [116-119]. Corticosteroid therapy is justified, and in the case of parkinsonism, additional levodopa [112, 114].

Terminals

Although there are many unanswered questions regarding the autoimmune pathogenetic causes of some movement disorders, knowledge of their existence will make it possible to identify them among the many extrapyramidal diseases that are currently considered idiopathic. With a better understanding of the mechanisms of autoimmune movement disorders, it will be possible to use pathogenetically targeted, and therefore effective therapy.

An autoimmune origin of movement disorders should be suspected in cases of subacute onset, rapid progression of symptoms, combination of movement phenomena with neuropsychiatric and behavioral disorders, and in all cases where the patient has another autoimmune disease. Identification of a current infection or an existing tumor, in combination with typical phenomenological manifestations described in the literature, will allow timely prescribing of the correct treatment, including glucocorticoids, intravenous immunoglobulin or plasmapheresis, in addition to specifically targeted therapy (antibacterial, antiviral, operations to remove tumors). It should be emphasized that the absence of an infection or tumor by no means excludes the possibility of an autoimmune disease, which in this case would be included in the category of idiopathic. In addition, the detection of specific antibodies confirms the assumption of the presence of an autoimmune disease.

References are under revision.

Journal “NeuroNEWS: Psychoneurology and Neuropsychiatry” special issue No. 1 ‘2018 “Sickness of the frail and old age”

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