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Article ; Online: Post-COVID Small Fiber Neuropathy, Implications of Innate Immunity, and Challenges on IVIG Therapy.

Dalakas, Marinos C

Neurology(R) neuroimmunology & neuroinflammation

2024 Volume 11, Issue 3, Page(s) e200248

MeSH term(s)	Humans ; Immunoglobulins, Intravenous ; Small Fiber Neuropathy ; COVID-19 ; Immunity, Innate
Chemical Substances	Immunoglobulins, Intravenous
Language	English
Publishing date	2024-04-17
Publishing country	United States
Document type	Editorial
ZDB-ID	2767740-0
ISSN	2332-7812 ; 2332-7812
ISSN (online)	2332-7812
ISSN	2332-7812
DOI	10.1212/NXI.0000000000200248
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Article ; Online: Advances in the therapeutic algorithm for myasthenia gravis.

Dalakas, Marinos C

Nature reviews. Neurology

2023 Volume 19, Issue 7, Page(s) 393–394

MeSH term(s)	Humans ; Myasthenia Gravis/therapy ; Myasthenia Gravis/drug therapy ; Immunosuppressive Agents/therapeutic use
Chemical Substances	Immunosuppressive Agents
Language	English
Publishing date	2023-05-29
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	2491514-2
ISSN	1759-4766 ; 1759-4758
ISSN (online)	1759-4766
ISSN	1759-4758
DOI	10.1038/s41582-023-00825-y
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Article ; Online: Therapies in Stiff-Person Syndrome: Advances and Future Prospects Based on Disease Pathophysiology.

Dalakas, Marinos C

Neurology(R) neuroimmunology & neuroinflammation

2023 Volume 10, Issue 3

Abstract: Among the glutamic acid decarboxylase (GAD)-antibody-spectrum disorders, the most common phenotypic subset is the stiff-person syndrome (SPS), caused by impaired GABAergic inhibitory neurotransmission and autoimmunity characterized by very high titers of ...

Abstract	Among the glutamic acid decarboxylase (GAD)-antibody-spectrum disorders, the most common phenotypic subset is the stiff-person syndrome (SPS), caused by impaired GABAergic inhibitory neurotransmission and autoimmunity characterized by very high titers of GAD antibodies and increased GAD-IgG intrathecal synthesis. If not properly treated or untreated because of delayed diagnosis, SPS progresses leading to disability; it is therefore fundamental to apply the best therapeutic schemes from the outset. This article is focused on the rationale of specific therapeutic strategies based on the SPS pathophysiology targeting both the impaired reciprocal GABAergic inhibition to symptomatically improve the main clinical manifestations of stiffness in the truncal and proximal limb muscles, gait dysfunction, and episodic painful muscle spasms and the autoimmunity to enhance improvement and slow down disease progression. A practical, step-by-step therapeutic approach is provided, highlighting the importance of combination therapies with the preferred gamma-aminobutyric acid-enhancing antispasmodic drugs, such as baclofen, tizanidine, benzodiazepines, and gabapentin, that provide the first-line symptomatic therapy, while detailing the application of current immunotherapies with intravenous immunoglobulin (IVIg) plasmapheresis, and rituximab. The pitfalls and concerns of long-term therapies in different age groups, including children, women planning pregnancy, and especially the elderly considering their comorbidities are emphasized, also highlighting the challenges in distinguishing the conditioning effects or expectations of chronically applied therapies from objective meaningful clinical benefits. Finally, the need for future targeted immunotherapeutic options based on disease immunopathogenesis and the biologic basis of autoimmune hyperexcitability are discussed, pointing out the unique challenges in the design of future controlled clinical trials especially in quantifying the extend and severity of stiffness, episodic or startle-triggered muscle spasms, task-specific phobias, and excitability.
MeSH term(s)	Child ; Humans ; Female ; Aged ; Stiff-Person Syndrome/therapy ; Stiff-Person Syndrome/drug therapy ; Autoantibodies ; Autoimmunity ; Baclofen/therapeutic use ; Spasm
Chemical Substances	Autoantibodies ; Baclofen (H789N3FKE8)
Language	English
Publishing date	2023-04-14
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2767740-0
ISSN	2332-7812 ; 2332-7812
ISSN (online)	2332-7812
ISSN	2332-7812
DOI	10.1212/NXI.0000000000200109
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Article: Autoimmune inflammatory myopathies.

Dalakas, Marinos C

Handbook of clinical neurology

2023 Volume 195, Page(s) 425–460

Abstract: The autoimmune inflammatory myopathies constitute a heterogeneous group of acquired myopathies that have in common the presence of endomysial inflammation and moderate to severe muscle weakness. Based on currently evolved distinct clinical, histologic, ... ...

Abstract	The autoimmune inflammatory myopathies constitute a heterogeneous group of acquired myopathies that have in common the presence of endomysial inflammation and moderate to severe muscle weakness. Based on currently evolved distinct clinical, histologic, immunopathologic, and autoantibody features, these disorders can be best classified as dermatomyositis, necrotizing autoimmune myositis, antisynthetase syndrome-overlap myositis, and inclusion body myositis. Although polymyositis is no longer considered a distinct subset but rather an extinct entity, it is herein described because its clinicopathologic information has provided over many years fundamental information on T-cell-mediated myocytotoxicity, especially in reference to inclusion body myositis. Each inflammatory myopathy subset has distinct immunopathogenesis, prognosis, and response to immunotherapies, necessitating the need to correctly diagnose each subtype from the outset and avoid disease mimics. The paper describes the main clinical characteristics that aid in the diagnosis of each myositis subtype, highlights the distinct features on muscle morphology and immunopathology, elaborates on the potential role of autoantibodies in pathogenesis or diagnosis , and clarifies common uncertainties in reference to putative triggering factors such as statins and viruses including the 2019-coronavirus-2 pandemic. It extensively describes the main autoimmune markers related to autoinvasive myocytotoxic T-cells, activated B-cells, complement, cytokines, and the possible role of innate immunity. The concomitant myodegenerative features seen in inclusion body myositis along with their interrelationship between inflammation and degeneration are specifically emphasized. Finally, practical guidelines on the best therapeutic approaches are summarized based on up-to-date knowledge and controlled studies, highlighting the prospects of future immunotherapies and ongoing controversies.
MeSH term(s)	Humans ; Myositis, Inclusion Body/diagnosis ; Myositis, Inclusion Body/therapy ; COVID-19 ; Myositis/diagnosis ; Myositis/therapy ; Autoimmune Diseases/diagnosis ; Autoimmune Diseases/therapy ; Inflammation ; Autoantibodies
Chemical Substances	Autoantibodies
Language	English
Publishing date	2023-08-10
Publishing country	Netherlands
Document type	Review ; Journal Article
ISSN	0072-9752
ISSN	0072-9752
DOI	10.1016/B978-0-323-98818-6.00023-6
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Article: Objectivity, practicality, and significance of practice guidelines for the practicing neurologists: What we learnt from consensus criteria in CIDP, Myasthenia Gravis and Inflammatory Myopathies.

Dalakas, Marinos C

Therapeutic advances in neurological disorders

2023 Volume 16, Page(s) 17562864231194821

Abstract: ... the case; and (c) relying on web-based registries or retrospective data collections from heterogeneous ...

Abstract	The value of practice guidelines in the three most common autoimmune neuromuscular disorders, namely Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Myasthenia Gravis (MG) and Autoimmune Inflammatory Myopathies (AIM), has been extensively debated regarding their usefulness in clinical practice, objectivity and universal value considering that guidelines are also established regionally in certain countries. This commentary highlights common concerns on how guidelines are presently generated, pointing out: (a) non-sufficient diversity among Task-Force members to identify and address not only routine clinical and electrophysiology issues but also immunology, imaging, pathology, biomarkers, epidemiology or treatment economics; (b) Task-Force being often comprised by the same or seemingly like-minded members conveying the erroneous impression that experts with opposing views might have been excluded, even if this is clearly not the case; and (c) relying on web-based registries or retrospective data collections from heterogeneous sources. As a result, the existing practice guidelines in CIDP, MG and AIM remain an unfinished business but an excellent base for further enhancement. Guidelines can be extremely helpful not only for clinical trials but also in clinical practice if viewed as a living document with continuously updated versions by experts even with opposing views with precise information on diagnostics, pathomechanisms, therapeutic schemes, evolving biomarkers and economics of new therapies with validation of the post-guidelines criteria. Geographic diversity should be taken into consideration because the availability of biomarker testing, and therapies differ among countries. Patient preferences need to be also considered in therapeutic guidelines because newly marketed drugs offer more options steadily changing the therapeutic algorithms in autoimmune neuromuscular diseases generating also questions as to whether they also influence decisions on insurance coverage. Collectively, these startup considerations are aimed to make practice guidelines more objective, widely acceptable worldwide and more practical or easier to follow in clinical practice.
Language	English
Publishing date	2023-09-04
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2442245-9
ISSN	1756-2864 ; 1756-2856
ISSN (online)	1756-2864
ISSN	1756-2856
DOI	10.1177/17562864231194821
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Article ; Online: Severe Stiff-Person Syndrome After COVID: The First Video-Documented COVID Exacerbation and Viral Implications

Dalakas, Marinos C

Neurology(R) neuroimmunology & neuroinflammation

2023 Volume 11, Issue 2, Page(s) e200192

Abstract: Objectives: To describe a patient with mild GAD-positive stiff-leg syndrome (SLS) who developed severely disabling stiff-person syndrome (SPS) 1 week after mild COVID-19 and discuss the impact of viral implications.: Methods: Video-documented serial ... ...

Abstract	Objectives: To describe a patient with mild GAD-positive stiff-leg syndrome (SLS) who developed severely disabling stiff-person syndrome (SPS) 1 week after mild COVID-19 and discuss the impact of viral implications. Methods: Video-documented serial clinical observations at baseline, after acute COVID-19, and after IVIG treatments. Results: A 39-year-old man with left-SLS was stable during a 2-year follow-up with low-dose antispasmodics, working fully and functioning normally, even able to run. One week after mild COVID-19, he started to experience generalized SPS symptomatology that steadily worsened the following 2-3 weeks, becoming unable to walk, requiring a walker, with significant thoracolumbar and bilateral leg stiffness and spasms. GAD ab were very high. After 3 monthly IVIg infusions he showed improvements, but his gait remains significantly stiff. All clinical changes, from baseline to post-Covid, and then post- IVIg have been video-documented. Discussion: This is the first, clearly documented, severe GAD-positive SPS after COVID-19. Although viral or postviral causation can be incidental, the temporal connection with acute COVID-19, the severe disease worsening after symptom-onset, and the subsequent steady improvement after IVIg, suggest viral-triggered autoimmunity. Because COVID-19 reportedly can trigger or worsen GAD-associated diabetes type 1 through proinflammatory mediators, and SPS has been reportedly triggered by West Nile Virus, possibly through molecular mimicry, this case of acutely converting GAD-SLS to GAD-SPS suggest the need to explore viral etiologies in patients with GAD-SPS experiencing acute, long-lasting episodic exacerbations of stiffness and spasms.
MeSH term(s)	Male ; Humans ; Adult ; Stiff-Person Syndrome/complications ; Stiff-Person Syndrome/diagnosis ; Immunoglobulins, Intravenous ; COVID-19/complications ; Spasm/complications ; Spasm/therapy
Chemical Substances	Immunoglobulins, Intravenous
Language	English
Publishing date	2023-12-26
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	2767740-0
ISSN	2332-7812 ; 2332-7812
ISSN (online)	2332-7812
ISSN	2332-7812
DOI	10.1212/NXI.0000000000200192
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Article ; Online: Unconvincing Evidence of SARS-CoV-2-Associated Myositis in Autopsied Muscles.

Dalakas, Marinos C

JAMA neurology

2022 Volume 79, Issue 1, Page(s) 92

MeSH term(s)	Autopsy ; COVID-19 ; Humans ; Muscles ; Myositis ; SARS-CoV-2
Language	English
Publishing date	2022-01-13
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2702023-X
ISSN	2168-6157 ; 2168-6149
ISSN (online)	2168-6157
ISSN	2168-6149
DOI	10.1001/jamaneurol.2021.4336
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Article ; Online: Complement in autoimmune inflammatory myopathies, the role of myositis-associated antibodies, COVID-19 associations, and muscle amyloid deposits.

Dalakas, Marinos C

Expert review of clinical immunology

2022 Volume 18, Issue 4, Page(s) 413–423

Abstract: Introduction: The inflammatory myopathies (IM) have now evolved into distinct subsets requiring clarification about their immunopathogenesis to guide applications of targeted therapies.: Areas covered: Immunohistopathologic criteria of IM with a ... ...

Abstract	Introduction: The inflammatory myopathies (IM) have now evolved into distinct subsets requiring clarification about their immunopathogenesis to guide applications of targeted therapies. Areas covered: Immunohistopathologic criteria of IM with a focus on complement, anti-complement therapeutics, and other biologic immunotherapies. The COVID19-triggered muscle autoimmunity along with the correct interpretation of muscle amyloid deposits is discussed. Expert opinion: The IM, unjustifiably referred as idiopathic, comprise
MeSH term(s)	COVID-19 ; Dermatomyositis/diagnosis ; Humans ; Muscles/pathology ; Myositis/diagnosis ; Plaque, Amyloid ; SARS-CoV-2
Language	English
Publishing date	2022-03-27
Publishing country	England
Document type	Journal Article
ZDB-ID	2274260-8
ISSN	1744-8409 ; 1744-666X
ISSN (online)	1744-8409
ISSN	1744-666X
DOI	10.1080/1744666X.2022.2054803
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Article ; Online: Role of complement, anti-complement therapeutics, and other targeted immunotherapies in myasthenia gravis.

Dalakas, Marinos C

Expert review of clinical immunology

2022 Volume 18, Issue 7, Page(s) 691–701

Abstract: Introduction: Several patients with myasthenia gravis (MG) do not adequately respond to available drugs or exhibit poor tolerance, necessitating the need for new therapies.: Areas covered: The paper discusses the rapidly evolving target-specific ... ...

Abstract	Introduction: Several patients with myasthenia gravis (MG) do not adequately respond to available drugs or exhibit poor tolerance, necessitating the need for new therapies. Areas covered: The paper discusses the rapidly evolving target-specific immunotherapies that promise long-standing remissions in the management of MG. It is specifically focused on the role of complement, anti-complement therapeutics, and the anti-FcRn and B cell monoclonals. Expert opinion: Anti-AChR antibodies cause internalization of the receptors and activate complement leading to
MeSH term(s)	Autoantibodies/metabolism ; Biological Products/therapeutic use ; Complement C5 ; Complement System Proteins ; Humans ; Immunotherapy ; Myasthenia Gravis/drug therapy ; Peptides, Cyclic ; Receptors, Cholinergic/metabolism ; Receptors, Cholinergic/therapeutic use
Chemical Substances	Autoantibodies ; Biological Products ; Complement C5 ; Peptides, Cyclic ; Receptors, Cholinergic ; Complement System Proteins (9007-36-7) ; zilucoplan (YG391PK0CC)
Language	English
Publishing date	2022-06-23
Publishing country	England
Document type	Journal Article
ZDB-ID	2274260-8
ISSN	1744-8409 ; 1744-666X
ISSN (online)	1744-8409
ISSN	1744-666X
DOI	10.1080/1744666X.2022.2082946
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Article ; Online: Stiff-person Syndrome and GAD Antibody-spectrum Disorders: GABAergic Neuronal Excitability, Immunopathogenesis and Update on Antibody Therapies.

Dalakas, Marinos C

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics

2022 Volume 19, Issue 3, Page(s) 832–847

Abstract: Although antibodies against Glutamic Acid Decarboxylase (GAD) were originally associated with Stiff Person Syndrome (SPS), they now denote the "GAD antibody-spectrum disorders (GAD-SD)" that include Cerebellar Ataxia, Autoimmune Epilepsy, Limbic ... ...

Abstract	Although antibodies against Glutamic Acid Decarboxylase (GAD) were originally associated with Stiff Person Syndrome (SPS), they now denote the "GAD antibody-spectrum disorders (GAD-SD)" that include Cerebellar Ataxia, Autoimmune Epilepsy, Limbic Encephalitis, PERM and eye movement disorder. In spite of the unique clinical phenotype that each of these disorders has, there is significant overlapping symptomatology characterized by autoimmune neuronal excitability. In addition to GAD, three other autoantibodies, against glycine receptors, amphiphysin and gephyrin, are less frequently or rarely associated with SPS-SD. Very high serum anti-GAD antibody titers are a key diagnostic feature for all GAD-SD, commonly associated with the presence of GAD antibodies in the CSF, a reduced CSF GABA level and increased anti-GAD-specific IgG intrathecal synthesis denoting stimulation of B-cell clones in the CNS. Because anti-GAD antibodies from the various hyperexcitability syndromes recognize the same dominant GAD epitope, the clinical heterogeneity among GAD-SD patients remains unexplained. The paper highlights the biologic basis of autoimmune hyperexcitability connected with the phenomenon of reciprocal inhibition as the fundamental mechanism of the patients' muscle stiffness and spasms; addresses the importance of high-GAD antibody titers in diagnosis, pinpointing the diagnostic challenges in patients with low-GAD titers or their distinction from functional disorders; and discusses whether high GAD-antibodies are disease markers or pathogenic in the context of their association with reduced GABA level in the brain and CSF. Finally, it focuses on therapies providing details on symptomatic GABA-enhancing drugs and the currently available immunotherapies in a step-by-step approach. The prospects of future immunotherapeutic options with antibody therapies are also summarized.
MeSH term(s)	Autoantibodies ; GABAergic Neurons ; Glutamate Decarboxylase ; Humans ; Stiff-Person Syndrome/diagnosis ; Stiff-Person Syndrome/drug therapy ; gamma-Aminobutyric Acid
Chemical Substances	Autoantibodies ; gamma-Aminobutyric Acid (56-12-2) ; Glutamate Decarboxylase (EC 4.1.1.15)
Language	English
Publishing date	2022-01-27
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2316693-9
ISSN	1878-7479 ; 1933-7213
ISSN (online)	1878-7479
ISSN	1933-7213
DOI	10.1007/s13311-022-01188-w
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