Case report: Anti-NMDA receptor encephalitis manifesting as rapid weight loss and abnormal movement disorders with alternating unilateral ptosis and contralateral limb tremor.

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis, associated with immunoglobulin G (IgG) autoantibodies against the GluN1 subunit of the NMDAR, is one of the most common types of autoimmune encephalitis. In patients with anti-NMDAR encephalitis, movement disorders (MDs) are often frequent, mainly presenting as facial dyskinesias and stereotyped movements. The alternating clinical manifestation of limb tremor with unilateral ptosis is rare. Here, we report an interesting case of a 22-year-old woman with rapid weight loss presenting with staged dyskinesia. Interestingly, she typically showed persistent tremor of the right upper limb, which would stop when her left upper eyelid drooped uncontrollably, a phenomenon that lasted for a few seconds, followed by automatic upper eyelid lift and continued persistent tremor of the upper limb. Moreover, it was fortunate to find anti-NMDAR antibodies in her cerebrospinal fluid (CSF), which indicated the patient had anti-NMDAR encephalitis. And abnormal apparent diffusion coefficient (ADC) hyperintense signals on the left midbrain interpeduncular fossa explained this manifestation of focal neurological deficit. After the systematic administration of immunotherapy (intravenous immunoglobulin, IVIG), steroid pulse therapy, and symptomatic treatment, the initial symptoms were significantly relieved except for limb tremor. The MDs were becoming less visible for the next six months under topiramate prescriptions. Noteworthy, there are no specific MD phenotypes in anti-NMDAR encephalitis. We describe the young women with unique MDs and rapid weight loss to help us get a more comprehensive understanding of anti-NMDAR encephalitis.

Coexistence of anti-SOX1 and anti-GABAB receptor antibodies with paraneoplastic limbic encephalitis presenting with seizures and memory impairment in small cell lung cancer: A case report.

Purpose: Paraneoplastic neurological syndromes associated with autoantibodies are rare diseases that cause abnormal manifestations of the nervous system. Early diagnosis of paraneoplastic neurological syndromes paves the way for prompt and efficient therapy. Case report: we reported a 56-year-old man presenting with seizures and rapidly progressive cognitive impairment diagnosed as paraneoplastic limbic encephalitis (PLE) with anti-SRY-like high-mobility group box-1 (SOX-1) and anti-γ-aminobutyric acid B (GABAB) receptor antibodies and finally confirmed by biopsy as small cell lung cancer (SCLC). At the first admission, brain magnetic resonance imaging (MRI) showed no abnormal signal in bilateral hippocampal regions and no abnormal enhancement of enhanced scan. The serum anti-GABAB receptor antibody was 1:100 and was diagnosed as autoimmune encephalitis (AE). The computed tomography (CT) scans of the chest showed no obvious tumor signs for the first time. Although positron emission tomography-computed tomography (PET-CT) revealed hypermetabolism in the para mid-esophageal, the patient and his family declined to undertake a biopsy. The patient improved after receiving immunoglobulin, antiepileptic therapy, and intravenous methylprednisolone (IVMP) pulse treatment. However, after 4 months, the symptoms reappeared. Brain MRI revealed abnormal signals in the hippocampal regions. Reexamination of the cerebral fluid revealed anti-GABAB receptor and anti-SOX-1 antibodies, which contributed to the diagnosis of PLE. SCLC was found in a para mid-esophageal pathological biopsy. Antiepileptic medications and immunoglobulin were used to treat the patient, and the symptoms were under control. Conclusion: Our findings increase the awareness that patients with limbic encephalitis with cognitive dysfunction and epileptic seizures should be enhanced to detect latent malignancy. Our case also highlights the importance of anti-SOX1 antibodies in the detection of underlying neoplasm, particularly SCLC. Our findings raise awareness of the cognitive impairment seen by patients with limbic encephalitis.

White Matter Alterations in Depressive Disorder.

Depressive disorder is the most prevalent affective disorder today. Depressive disorder has been linked to changes in the white matter. White matter changes in depressive disorder could be a result of impaired cerebral blood flow (CBF) and CBF self-regulation, impaired blood-brain barrier function, inflammatory factors, genes and environmental factors. Additionally, white matter changes in patients with depression are associated with clinical variables such as differential diagnosis, severity, treatment effect, and efficacy assessment. This review discusses the characteristics, possible mechanisms, clinical relevance, and potential treatment of white matter alterations caused by depressive disorders.

Cerebral blood flow self-regulation in depression.

BACKGROUND: Depression is a common neuropsychiatric disease with a high prevalence rate. Sleep problems, memory decline, dizziness and headaches are the most common neurological symptoms in depressed patients. Abnormality of cerebral blood flow (CBF) has been observed in depressive patients, but those patients did not have intracranial structural damage. Both of those phenomena might be related to cerebral blood flow self-regulation (CBFSR: cerebral blood flow self-regulation). CBFSR can maintain CBF relatively stable in response to changes in neurological and metabolic factors. Therefore, this review aimed to discuss CBFSR in depression. METHODS: We searched for keywords such as "depression", "cerebral blood flow", "cerebral autoregulation", "cerebrovascular reactivity" and the words related to depression. We analyzed whether there is a change in the CBFSR in depression, further explored whether there is a relationship between the pathogenesis of depression and the CBFSR, and discussed the possible mechanism of impaired CBFSR in patients with depression. RESULTS: Discovered by the literature review, CBFSR is significantly impaired in depressed patients. The level of circulating markers of endothelial dysfunction, nitric oxide, inflammatory cytokines, glucocorticoid and monoamine neurotransmitters is mostly abnormal in depression, which affected the CBFSR to varying degrees. LIMITATIONS: Limitations include the small number of direct studies about depression and CBFSR mechanisms. CONCLUSION: CBFSR is impaired in depression. The underlying mechanisms include endothelial dysfunction, overactivation of microglia and changes of cytokines, hyperactivation of the HPA axis, increased oxidative stress, monoamine neurotransmitter disorders, etc. These deepened our understanding of the clinical symptoms of depressed patients.

Renin-angiotensin system: The underlying mechanisms and promising therapeutical target for depression and anxiety.

Emotional disorders, including depression and anxiety, contribute considerably to morbidity across the world. Depression is a serious condition and is projected to be the top contributor to the global burden of disease by 2030. The role of the renin-angiotensin system (RAS) in hypertension and emotional disorders is well established. Evidence points to an association between elevated RAS activity and depression and anxiety, partly through the induction of neuroinflammation, stress, and oxidative stress. Therefore, blocking the RAS provides a theoretical basis for future treatment of anxiety and depression. The evidence for the positive effects of RAS blockers on depression and anxiety is reviewed, aiming to provide a promising target for novel anxiolytic and antidepressant medications and/or for improving the efficacy of currently available medications used for the treatment of anxiety and depression, which independent of blood pressure management.