Stiff-person syndrome (SPS) is a rare and disabling central nervous system disorder with no satisfactory treatment. Muscle rigidity, sporadic muscle spasms, and chronic muscle pain characterize SPS. SPS is strongly correlated with autoimmune diseases, and it is usual to find high titers of antibodies against acid decarboxylase (GAD65). Due to its highly disabling nature and complicated treatment, we aim to create a treatment protocol through a narrative review of currently available treatments that show efficacy. We expect to facilitate management based on treatment responses ranging from first-line medication to refractory medication. We conducted a medical subject heading (MeSH) strategy. We used the term SPS with the subheading treatment: "Stiff-Person Syndrome/Therapy" [MeSH]. An initial data gathering of 270 papers came out with the initial research. After using the inclusion criteria, we had 159 articles. We excluded 31 papers for being either systematic reviews, literature reviews, or meta-analysis. From the 128 remaining articles, we excluded another 104 papers because the extraction of the data was not possible or the study outcome did not meet our demands. There are two main treatments for SPS: GABAergic (gamma-aminobutyric acid) therapy and immunotherapy. For treatment, we suggest starting with benzodiazepines as first-line treatment. We recommend adding levetiracetam or pregabalin if symptoms persist. As second-line therapy, we recommend oral baclofen over rituximab and tacrolimus. We also suggest rituximab over tacrolimus. For patients with refractory treatment, we can use intrathecal baclofen, intravenous immunoglobulin (IVIG) , or plasmapheresis. We conclude that intrathecal baclofen and IVIG are more effective than plasmapheresis in patients with refractory symptoms. Propofol may be used as a bridge - temporary therapy before initiating a permanent treatment.

Wilson’s disease (WD) is an autosomal recessive disease that presents mainly with hepatic, neurological, and psychiatric manifestations. Neurological manifestations have been described in the past. Nevertheless, the pathophysiology and the clinical relevance of these manifestations have not been described in great detail in the medical literature. We aim to consolidate the knowledge about the neurological manifestations of WD and present the pathophysiology of each neurological manifestation of the disease. We will give a brief definition, the provenance, and the pathophysiology of the neurological conditions. We collected data from the National Library of Medicine (PubMed) using regular keywords and medical subject headings. Studies were selected applying the following inclusion/exclusion criteria: (1) studies that used exclusively human subjects, (2) papers published in English, and (3) papers from 1990 onward. The exclusion criteria were (1) studies that used animals, (2) papers not published in English, and (3) papers published before 1990. Additional studies were included via reference lists of identified papers and related articles featured in PubMed and Google Scholar. Copper toxicity is the principal factor for brain degeneration seen in WD. Parkinsonism seen in WD has been associated with a nigrostriatal dopaminergic deficit. Resting tremor may have the same pathophysiology as parkinsonism. Action tremor is related to an accumulation of copper in the cerebellum's vermis and hemispheres. At the same time, essential tremor can be explained due to affection of the dentate nucleus. Choreoathetosis is produced due to increased activity of the direct pathway. We did not find specifically associated pathophysiology related to dysarthria. We assume that multiple parts of the brain are involved in that problem. Putamen nucleus damage is the leading cause that explains dystonia seen in WD along with the globus palidus. We did not find a specific localization for seizures in WD, but the pathology seems to be related to decreased levels of B6 and direct toxicity of copper on the brain.

Stroke is a leading cause of death, disability, and dementia worldwide. Strokes can be divided into ischemic strokes and hemorrhagic strokes. At the moment, tissue plasminogen activator (tPA) is the only FDA-approved drug for ischemic stroke. Minocycline (MC) and Magnesium (Mg) are promising therapies for ischemic stroke, especially in the pre-hospital setting. These drugs are readily available, inexpensive, and generally safe. We decided to investigate these drugs' neuroprotective effects in treating ischemic stroke in the acute and chronic setting. We conducted a systematic review of the published literature on MC and Mg's functional outcome in ischemic stroke. This paper's methodology included only clinical trials published in the last 15 years, using PubMed as a database. The systematic review demonstrated that MC infusion in the pre-hospital and hospital setting improved functional outcomes and disability scores. Furthermore, MC also decreased matrix metalloproteinase 9 (MMP-9) levels. MC might have a more significant effect on men than women because different molecular pathways of cerebral ischemia seem to be involved between both genders. The systematic review showed that patients with ischemic stroke did not benefit from magnesium sulfate infusion in the pre-hospital and hospital setting. Nevertheless, patients with lacunar strokes and patients who supplemented their meals with potassium-magnesium salt in the diet had better functional outcomes. Future studies would need a more significant sample of participants and a better selection to increase the study's power and avoid selection bias, respectively. Further publications could benefit from subcategorizing strokes and investigating the gender role in stroke treatment. These directives could give a more robust conclusion regarding the neuroprotective effects of these drugs.

Multiple system atrophy (MSA) is a rare, progressive, fatal, neurodegenerative disorder. There are two main types: the parkinsonian type (MSA-P) and cerebellar type (MSA-C). The disease usually presents with genitourinary dysfunction, orthostatic hypotension, and rapid eye movement (REM) sleep behavior disorder. Patients rapidly develop balance, speech, and coordination abnormalities. We present a review of the clinical picture and the actualized treatment modalities of the MSA cerebellar type. For the study methods, a PubMed search was done using the following medical subject headings (MeSH) terms: “multiple system atrophy/therapy". Inclusion criteria included studies in English, full papers, human studies, and publications in the last 30 years. Case reports and series were excluded. A total of 157 papers were extracted after applying the inclusion and exclusion criteria, and 41 papers were included for the discussion of this review. This review underlines the therapeutic strategies as well as the clinical picture of multiple system atrophy, and how MSA-C and MSA-P differ from each other. We discussed this review in four topics: ataxia, autonomic dysfunction (neurogenic orthostatic hypotension and urinary disorders), parkinsonism, and REM sleep disorder. In conclusion, the treatment of MSA-C is mainly symptomatic; there are not many studies on MSA-C. The ataxic component and fewer parkinsonian symptoms are the main difference of MSA-C as opposed to MSA-P.

Ataxia is a constellation of symptoms that involves a lack of coordination, imbalance, and difficulty walking. Hereditary ataxia occurs when a person is born with defective genes, and this degenerative disorder may progress for several years. There is no effective cure for ataxia, so we need to search for new treatments. Recently, interest in riluzole in the treatment of ataxia has emerged. We conducted this systematic review to analyze the safety and efficacy of riluzole for treating hereditary ataxia in recent clinical trials. We conducted a systematic review using PubMed and Google Scholar as databases in search of this relationship. We used the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) and Meta-analysis of Observational Studies in Epidemiology (MOOSE) protocols to conduct this study. For inclusion criteria, we included full-text clinical trials on humans written in English and found three clinical trials. We excluded case reports, literature reviews, systematic reviews, and meta-analyses for this analysis. We aimed to evaluate the Scale for the Assessment and Rating of Ataxia (SARA) score, the International Cooperative Ataxia Rating Scale (ICARS) score, and the safety of the medication. Two out of the three clinical trials showed statistically significant clinical improvement in the ICARS and SARA scores, while the other trial did not show improvement in the clinical or radiological outcomes. The drug was safe in all clinical trials. Overall, the results of this analysis of riluzole for the treatment of hereditary ataxia are encouraging. Further clinical trials are needed to investigate the efficacy of riluzole on hereditary ataxia.