ABSTRACT
Since their introduction in 1999, anti-tumour necrosis factor-α (anti-TNF-α) therapies have been suspected repeatedly to be associated with the occurrence of central nervous system (CNS) demyelinating disorders, including multiple sclerosis (MS). However, recent publications were restricted to descriptions of monophasic demyelinating events or cases of relapsing-remitting MS (RRMS). We here provide the first case report of primary progressive MS (PPMS) onset upon anti-TNF-α therapy as well as a literature review of previously published cases of anti-TNF-α therapy-associated MS onset. The 51-year old male patient was treated with adalimumab due to psoriasis arthritis. About 18 months after treatment initiation, he developed slowly progressing neurological deficits including gait impairment, paraesthesia of the lower limbs, strangury and visual impairment, which led to the discontinuation of adalimumab therapy. Magnetic resonance imaging of the brain and the spinal cord revealed multiple inflammatory lesions and cerebrospinal fluid examination showed slight pleocytosis and positive oligoclonal bands. Thus, PPMS was diagnosed according to the 2017 revision of the McDonald criteria. As PPMS often causes only subtle symptoms in the beginning and early treatment discontinuation of anti-TNF-α therapy seems essential to improve the patient's outcome, we think that it is important to increase the awareness of slowly progressing neurological deficits as a potential adverse event of anti-TNF-α therapy among all clinicians involved in the initiation and monitoring of these drugs. In addition, the occurrence of both RRMS and progressive MS upon anti-TNF-α therapy might suggest a shared TNF-α-mediated pathophysiological mechanism in the evolution of all MS subtypes.
ABSTRACT
Background and Purpose- Patients with large-vessel stroke frequently need to be transferred to comprehensive stroke centers for endovascular treatment. An update of physiological perfusion parameters and stroke progression on arrival is desirable. We examined the reliability of preinterventional pooled blood volume (PBV)-maps acquired by flat-panel detector computed tomography (CT) in the interventional angiography suite. Methods- The volumes of preinterventional perfusion deficit in flat-panel detector CT-PBV source images were compared with final infarct volume on follow-up multislice-CT after endovascular treatment of 29 consecutive patients with occlusion of the middle cerebral artery (MCA) or the distal internal carotid artery (ICA). Results- Endovascular treatment was successful in 26 patients (Thrombolysis in Cerebral Infarction, 2b-3). Overall, the median preinterventional PBV-deficit was 9×larger than median final infarct volume on multislice-CT (86.4 mL [10.3; 111.6] versus 9.6 mL [3.6; 36.8]). This was especially evident in the subgroup of successful recanalization (PBV-deficit: 87.5 mL [10.6; 115.1], final infarct: 8.7 mL [3.6; 29]). In futile recanalization, the final infarct tended to be underestimated (PBV-deficit: 86.4 mL [5.9; -] and final infarct: 116.4 mL [3.5; -]). Conclusions- Flat panel detector CT-PBV is not reliable in predicting the final infarct volume and should not be used in clinical decision making for endovascular treatment of acute cerebral artery occlusions.
