The incidence of acute symptomatic seizures is the highest reported in patients with first stroke with prospective follow-up. Hemorrhagic stroke and cortical lesion were independent predictors of acute symptomatic seizures. Hyperlipidemia was a protective factor for hemorrhagic stroke.
Super-refractory status epilepticus appears clearly less prevalent in this cohort than previously reported, probably as it is not restricted to intensive care unit. SRSE emerges in younger patients with marked consciousness impairment, pointing to the underlying severe clinical background, but these variables do not predict most SRSE developments. There is currently a knowledge gap for prediction of SRSE occurrence that needs to be filled.
Fever is frequent after CA, and Tmax in ICU is associated with worsened neurological outcome. This association becomes stronger as the timing of Tmax extends further from the CA.
A 74 year old male with a history of plasma cell leukaemia, treated with VMP (bortezomib, melphalan, prednisolone) presented with a 2 week history of lumbar back pain and weakness of the hands and ankles.Clinical examination confirmed asymmetric weakness in the hands and ankles. Sensory examination was initially normal, reflexes preserved and plantars mute. Other than the known IgG paraproteinaemia and longstanding hyponatraemia, bloods, including a vasculitis screen, were unremarkable. MRI brain and spine were non-contributary. CSF examination revealed paired bands consistent with the presence of an IgG paraprotein, but was otherwise bland. Nerve conduction studies showed a severe sensorimotor axonal neuropathy.The patient was treated with plasma exchange followed by IV methylprednisolone but continued to progress developing more proximal weakness and sensory loss to the knees and elbows, with loss of deep tendon reflexes within 2 weeks. Sural nerve biopsy showed axonal degeneration but no vasculitis or malignant infiltration. The patient became increasingly fatigued and cachectic and the decision was made jointly with the haematologists to palliate.Plasma cell leukaemia is a rare and aggressive subtype of multiple myeloma with a poor prognosis which has been associated with malignant nerve infiltration. Bortezomib may also cause a peripheral neuropathy.o.poole@nhs.net
IntroductionThe management of new-onset refractory status epilepticus (NORSE) in pregnancy may be complicated by anti-seizure medication (ASM) polytherapy-associated teratogenicity. We aim to demonstrate the safety and efficacy of vagal nerve stimulation (VNS) in a pregnant patient presenting with NORSE.Case descriptionA 30-year old female, at 5-weeks' gestation presented with drug-refractory myoclonic status epilepticus, responsive only to high levels of anesthetic agents. The severity of seizures did not allow extubation, and the patient remained ventilated and sedated. VNS was implanted 26 days after seizure onset. The immediate post-operative output was 0.25 mA, which was rapidly titrated up to 0.5 mA the next morning, and to 0.75 mA that afternoon. This was further increased to 1.0 mA on 3rd day post-operation, and to 1.25 mA 7 days post-op. Myoclonic jerks diminished significantly 7 days post-op, allowing extubation. Twenty days after VNS implantation, no myoclonic jerks were observed. There was also a notable neurological improvement including increased alertness and mobility, and ability to obey commands. Drug overdose was subsequently found to be the most likely etiology of her NORSE. An early pregnancy assessment 17 days after VNS implantation showed a normally sited pregnancy, normal fetal heart activity and crown-rump length. The patient remained seizure free, gained functional independence and delivered a premature but otherwise healthy baby at 33 weeks' gestation.ConclusionNORSE is challenging to manage, further compounded in pregnancy due to the teratogenicity of ASMs and ASM polytherapy. This is the first case-study to report the safe implantation and use of VNS during the first trimester of pregnancy for the management of NORSE.
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