An accumulating body of evidence point to the significance of neuroinflammation and immunogenetics also in schizophrenia. Recent genome-wide studies in schizophrenia suggest immune involvement in schizophrenia. Microglia are the resident macrophage of the brain and major players in innate immunity in the CNS. They respond rapidly to even minor pathological changes in the brain and may contribute directly to the neuronal degeneration by producing various pro-inflammatory cytokines and free radicals. In many aspects, the neuropathology of schizophrenia is closely associated with microglial activation. We and other researchers have shown the inhibitory effects of some typical or atypical antipsychotics on the release of inflammatory cytokines and free radicals from activated microglia, both of which are not only directly toxic to neurons but also cause a decrease in neurogenesis as well as white matter abnormalities in the brains of the patients with schizophrenia. The treatment through the inhibition of microglial activation may shed new light on the therapeutic strategy of schizophrenia.

Neuroinflammation in schizophrenia especially focused on the role of microglia.

Catatonia and the immune system: a review

Medical comorbidity in bipolar disorder: The link with metabolic-inflammatory systems.

Only a very few systematic studies have investigated the frequency of neurologic disorders in patients with Crohn's disease (CD) and ulcerative colitis (UC), which are the two main types of inflammatory bowel disease (IBD). Results have been inconsistent and variable, owing to differences in case-finding methods and evaluated outcomes in different studies. The most frequent neurologic manifestations reported in CD and UC populations are cerebrovascular disease (with either arterial or venous events), demyelinating central nervous system disease, and peripheral neuropathy (whether axonal or demyelinating); however, the literature describes numerous nervous system disorders as being associated with IBD. The pathogenesis of nervous system tissue involvement in IBD has yet to be elucidated, although it seems to be related to immune mechanisms or prothrombotic states. The recently-introduced tumor necrosis factor (TNF) inhibitors have proven successful in controlling moderate to severe IBD activity. However, severe neurologic disorders associated with TNF inhibitors have been reported, which therefore raises concerns regarding the effect of anti-TNF-α antibodies on the nervous system. Although neurological involvement associated with IBD is rarely reported, gastroenterologists should be aware of the neurologic manifestations of IBD in order to provide early treatment, which is crucial for preventing major neurologic morbidity.

Inflammatory bowel disease: An increased risk factor for neurologic complications

Patients with inflammatory bowel disease (IBD) can be affected by other unrelated diseases. These are called comorbid conditions, and can include any secondary health problem that affects a person suffering from a primary or main disease, and which is neither linked physiopathologically to the primary condition, nor is it due to the treatments used for the primary condition or to its long-term anatomical or physiological consequences. Different comorbid conditions, as well as their influence on IBD, are discussed.

Comorbidity in inflammatory bowel disease.

Zopiclone is a cyclopyrrolone derivative belonging to the group of selective benzodiazepine receptor agonists, which was introduced in Germany in 1991 for the treatment of insomnia. Zopiclone is chemically unrelated to benzodiazepines, but has a similar effect of potentiating the function of γ-aminobutyric acid (GABA) at the GABAA receptor complex (Karle and Nielsen, 1998). It is an effective hypnotic in sleep disorders of various aetiologies, and is considered to have an advantageous side-effect profile (Hesse et al., 2003; Karle and Nielsen, 1998; Noble et al., 1998). It has a weaker muscle-relaxant potential compared to benzodiazepines (Karle and Nielsen, 1998).

/pdf/zopiclone-dependence-after-insomnia-related-to-torticollis-453o7ikyod.pdf

Zopiclone dependence after insomnia related to torticollis.

The imidazopyridin Zolpidem belongs to the group of non-benzodiazepins. There have already been published many case reports of zolpidem dependence but little has been published about the management of Zolpidem detoxification. We report a case of Zolpidem dependence and describe the drug treatment of withdrawal. Our withdrawal management of a female patient included administeration of Diazepam, Carbamazepin and earacupuncture (protocol of NADA). With a former daily dose of 60 mg Zolpidem we started the patient on 25 mg Diazepam so that 10 mg Zolpidem would be equivalent to 4.15 mg Diazepam. In the following Zolpidem was discontinued and a daily reduction of Diazepam over 8 days was performed. The patient tolerated this detoxification with mild symptoms so that we suggest a higher Diazepam dosis (for 10 mg Zolpidem 5 mg Diazepam).

Medikaments gesttzter Entzug bei einer Zolpidem-Abhngigkeit

Successful treatment of psychosis with infliximab in a patient with Crohn's disease.

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Zopiclone dependence after insomnia related to torticollis.

Medikaments gesttzter Entzug bei einer Zolpidem-Abhngigkeit

Successful treatment of psychosis with infliximab in a patient with Crohn's disease.