Immunoadsorption was used initially to treat the seizures. Once they had ceased, we used 375 mg/m2 intravenous rituximab--a monoclonal anti-CD20 antibody--once-weekly for 4 weeks to stabilize the condition, leading to complete depletion of CD19+ B cells. Rituximab infusions were used again when concentrations of CD19+ B cells rose and focal seizures re-emerged. The patient remained on antiepileptic therapy (levetiracetam, oxcarbazepine, zonisamide and phenobarbital) throughout treatment.
Active immunization with amyloid-β (Aβ) peptide 1–42 reverses amyloid plaque deposition in the CNS of patients with Alzheimer’s disease and in amyloid precursor protein transgenic mice. However, this treatment may also cause severe, life-threatening meningoencephalitis. Physiological responses to immunization with Aβ1–42 are poorly understood. In this study, we characterized cognitive and immunological consequences of Aβ1–42/CFA immunization in C57BL/6 mice. In contrast to mice immunized with myelin oligodendrocyte glycoprotein (MOG)35–55/CFA or CFA alone, Aβ1–42/CFA immunization resulted in impaired exploratory activity, habituation learning, and spatial-learning abilities in the open field. As morphological substrate of this neurocognitive phenotype, we identified a disseminated, nonfocal immune cell infiltrate in the CNS of Aβ1–42/CFA-immunized animals. In contrast to MOG35–55/CFA and PBS/CFA controls, the majority of infiltrating cells in Aβ1–42/CFA-immunized mice were CD11b+CD14+ and CD45high, indicating their blood-borne monocyte/macrophage origin. Immunization with Aβ1–42/CFA was significantly more potent than immunization with MOG35–55/CFA or CFA alone in activating macrophages in the secondary lymphoid compartment and peripheral tissues. Studies with TLR2/4-deficient mice revealed that the TLR2/4 pathway mediated the Aβ1–42-dependent proinflammatory cytokine release from cells of the innate immune system. In line with this, TLR2/4 knockout mice were protected from cognitive impairment upon immunization with Aβ1–42/CFA. Thus, this study identifies adjuvant effects of Aβ1–42, which result in a clinically relevant neurocognitive phenotype highlighting potential risks of Aβ immunotherapy.
Serious neurological complications after diving have increased in the last years because of its increased popularity [1,2,5,7]. Dangerous neurological complications such as ischemic stroke reflecting an acute central nervous system pathology are frequently associated with a dysbaric air embolism or decompression sickness (Caisson's disease), but may also include rarer causes [8]. Due to unspecific clinical presentation, the differential diagnosis of diving-related neurological symptoms may be difficult. A dissection of cervical arteries in young to middle-aged scuba divers has rarely been described. We describe a patient with internal carotid artery dissection after scuba diving, who presented at the emergency department with subacute embolic strokes. In addition, we also summarize the published reports to date of cervical artery dissections associated with scuba diving. Case reportA 51-year-old right-handed man presented with a history of neurological symptoms after having performed a scuba dive in a lake a week earlier. The dive was guided by and performed with a professional diving instructor. The whole dive including pre-and post-diving preparation took 2 h. The uneventful time under water was as follows: 15 min at 5 m, 15 min at 20 m and 15 min at 5 m with a total underwater time of 45 min. The weight of the diving gear did not exceed the usual weight range for recreational diving. There was no trauma during the dive or unusual movements or minor trauma afterwards. He was a certified recreational diver with moderate experience. Three hours after surfacing he noted slurred speech and difficulties finding words for 15 min. After 2 days he noted difficulties with tongue movement and problems with swallowing and expressing words. After that, his food intake was restricted to liquids. He also suffered from an aching throat and leftsided dull temporal-occipital headaches. After 4 days he turned to his GP who initiated further vascular evaluation.On presentation at the Neurological Emergency Unit he showed an incomplete Horner's syndrome with miosis and ptosis on the left eye and dysarthria. He also presented a tongue deviation to the left and a deviation of the uvula. The rest of the neurological examination was normal with no clinical evidence of long-tract disturbances, extrapyramidal or brain-stem dysfunction. No sensory abnormalities, motor deficits or cognitive deficits were observed. The general physical examination revealed normal findings.No relevant past medical or family history could be found. He had smoked 20 cigarettes per day until 1990.The ultrasound of the extra-and intracerebral cerebral vessels showed a resistance profile in the distal extracranial part of the left internal carotid artery. The flow in the left middle cerebral artery was decreased in comparison to the right side, but was collaterally fed via the anterior and posterior communicating arteries and the left (retrograde) ophthalmic artery.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.