The human brain is increasingly seen as a dynamic neural system, the function of which relies on a diverse set of connections between brain regions. To assess these complex dynamical interactions, formalism of complex networks was suggested as one of the most promising tools to offer new insight into the brain's structural and functional organization, with a potential also for clinical implications. Irrespective of the brain mapping technique, modern network approaches have revealed fundamental aspects of normal brain-network organization, such as small-world and scale-free patterns, hierarchical modularity, and the presence of hubs. Moreover, the utility of these approaches, to gain a better understanding of neurological diseases, is of great interest. In the present contribution, we first describe the basic network measures and how the brain networks are constructed on the basis of brain activity data in order to introduce clinical neurologists to this new theoretical paradigm. We then demonstrate how network formalism can be used to detect changes in EEG-based functional connectivity patterns in six paediatric patients with childhood absence epilepsy. Notably, our results do not only indicate enhanced synchronicity during epileptic episodes but also reveal specific spatial changes in the electrical activity of the brain. We argue that the network-based evaluation of functional brain networks can provide clinicians with more detailed insight into the activity of a pathological brain and can also be regarded as a support for objective diagnosis and treatment for various neurological diseases.
Antiglutamic acid decarboxylase antibody-associated cerebellar ataxia (GAD-Abs CA) is a rare, but increasingly detected, autoimmune neurological disorder characterized by the clinical presence of a cerebellar syndrome concomitant with positive GAD-Abs levels in serum and cerebrospinal fluid (CSF). It represents 3% of all immune-mediated sporadic CAs. Low-titre GAD-Abs CA is an even rarer subtype of GAD-Abs CA. We report on a 68-year-old woman with a 3-year history of progressive gait ataxia. In addition to the modified Rankin Scale (mRS), we used two other objective scales to evaluate CA severity, i.e. the International Cooperative Ataxia Rating Scale (ICARS) and the Scale for Assessment and Rating of Ataxia (SARA). Series of CT and MRI showed atrophy of the cerebellum. Except for the glycated haemoglobin (HbA) levels, all other routine laboratory examinations were within normal limits. Autoimmune laboratory examinations showed positive (25.8 U/mL) serum GAD-Abs levels. The GAD antibody index was <1.0. The CSF analysis showed no oligoclonal immunoglobulin bands. Intravenous immunoglobulin (IVIg) therapy was started and significant improvement was observed. The diagnosis of low-titre GAD-Abs CA was established.
Statins or 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors are a mainstay of cardiovascular disease therapy. In addition to their lipid-lowering capabilities, they exhibit several pleiotropic effects. Their adverse reactions such as myalgias are not uncommon, but in rare cases, the resulting rhabdomyolysis can be fatal. Recently, more insight has been brought into the pathogenesis of statin-induced rhabdomyolysis, and immune-mediated necrotizing myopathies are diagnosed more frequently. We present a case of a female patient who was on chronic rosuvastatin therapy and developed necrotizing myopathy. The disease progressed to acute kidney and liver injury. We discontinued the drug, started supportive measures, and initiated renal replacement therapy with a high cutoff dialysis membrane once. Her recovery was prompt, with a normal control electromyography 2 weeks after discharge.
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