A 63‐year‐old Man With Dementia, Ataxia and Vi Nerve Palsy

Patients suffering from abducent nerve palsy are usually primary seen by a conservative medical Specialist. In most cases the ENT specialist is secondary involved for treatment. In the majority of cases abducent nerve palsy is a temporary symptom associated with neurologic or vascular diseases. Rarely inflammation, neoplasm or fracture of the skull base cause this symptom and lead to an intervention done by the ENT surgeon. This case series describes retrospectively the abducent palsy seen through the eyes of an ENT surgeon. From 2008 to 2011 15 patients suffering from abducent nerve palsy. One patient suffering from a temporal bone fracture has been treated conservatively while 14 patients needed surgery. 6 patients had a complicated inflammation of the skull base. In 7 patients skull base neoplasms were found in endoscopic surgery. In one case the underlying pathology remained unclear. 2 third of the patients that suffered from complications of inflammatory diseases completely recovered after a combined operative and conservative therapy. The patients who suffered from neoplasms of the skull base partially recovered in only one third, none, achieved full recovery. The patient with the temporal bone fracture achieved a partial recovery after 3 months. If the leading symptom of abducent palsy is caused by a severe extracranial inflammation, neoplasm or trauma an experienced skull base surgeon is mandatory. The recovery rate of abducent palsy in our case series was 60 %. The prognosis of abducent palsy in skull base inflammation is much better compared to patients with skull base neoplasm.

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“…Im Bereich der Felsenbeinspitze finden sich Schwannome [12,13], M. Paget [14], Metastasen [9,10], Lymphome [15] und Arachnoidalzysten [16,17].…”

unclassified

Abduzensparese mit Ursache im HNO-Fachgebiet

2017

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“…This potentially reflects gluten sensitivity (GS), which is a newly characterized syndrome defined by some intestinal but mostly extra-intestinal symptoms related to the ingestion of gluten-containing food (i.e., wheat, barley, or rye) distinct from celiac disease (CD) and wheat allergy (26, 27). High levels of AGA IgG have also been observed in brain conditions such as ataxia (28–30). This provides further support for the gut–brain inflammation linkage.…”

Section: Introductionmentioning

confidence: 99%

Antigliadin Antibodies (AGA IgG) Are Related to Neurochemistry in Schizophrenia

et al. 2017

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Inflammation may play a role in schizophrenia; however, subgroups with immune regulation dysfunction may serve as distinct illness phenotypes with potential different treatment and prevention strategies. Emerging data show that about 30% of people with schizophrenia have elevated antigliadin antibodies of the IgG type, representing a possible subgroup of schizophrenia patients with immune involvement. Also, recent data have shown a high correlation of IgG-mediated antibodies between the periphery and cerebral spinal fluid in schizophrenia but not healthy controls, particularly AGA IgG suggesting that these antibodies may be crossing the blood–brain barrier with resulting neuroinflammation. Proton magnetic resonance spectroscopy (MRS) is a non-invasive technique that allows the quantification of certain neurochemicals in vivo that may proxy inflammation in the brain such as myoinositol and choline-containing compounds (glycerophosphorylcholine and phosphorylcholine). The objective of this exploratory study was to examine the relationship between serum AGA IgG levels and MRS neurochemical levels. We hypothesized that higher AGA IgG levels would be associated with higher levels of myoinositol and choline-containing compounds (glycerophosphorylcholine plus phosphorylcholine; GPC + PC) in the anterior cingulate cortex. Thirty-three participants with a DSM-IV diagnosis of schizophrenia or schizoaffective disorder had blood drawn and underwent neuroimaging using MRS within 9 months. We found that 10/33 (30%) had positive AGA IgG (≥20 U) similar to previous findings. While there were no significant differences in myoinositol and GPC + PC levels between patients with and without AGA IgG positivity, there were significant relationships between both myoinositol (r = 0.475, p = 0.007) and GPC + PC (r = 0.36, p = 0.045) with AGA IgG levels. This study shows a possible connection of AGA IgG antibodies to putative brain inflammation as measured by MRS in schizophrenia.

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