Antiseizure Medication Use and Outcomes After Suspected or Confirmed Acute Symptomatic Seizures.

Importance: Antiseizure medications (ASMs) are frequently prescribed for acute symptomatic seizures and epileptiform abnormalities (EAs; eg, periodic or rhythmic patterns). There are limited data on factors associated with ASM use and their association with outcomes. Objectives: To determine factors associated with ASM use in patients with confirmed or suspected acute symptomatic seizures undergoing continuous electroencephalography, and to explore the association of ASMs with outcomes. Design, Setting, and Participants: This multicenter cohort study was performed between July 1 and September 30, 2021, at 5 US centers of the Post Acute Symptomatic Seizure Investigation and Outcomes Network. After screening 1717 patients, the study included 1172 hospitalized adults without epilepsy who underwent continuous electroencephalography after witnessed or suspected acute symptomatic seizures. Data analysis was performed from November 14, 2023, to February 2, 2024. Exposure: ASM treatment (inpatient ASM continuation ≥48 hours). Main Outcomes and Measures: Factors associated with (1) ASM treatment, (2) discharge ASM prescription, and (3) discharge and 3-month Glasgow Outcome Scale score of 4 or 5 were ascertained. Results: A total of 1172 patients (median [IQR] age, 64 [52-75] years; 528 [45%] female) were included. Among them, 285 (24%) had clinical acute symptomatic seizures, 107 (9%) had electrographic seizures, and 364 (31%) had EAs; 532 (45%) received ASM treatment. Among 922 patients alive at discharge, 288 (31%) were prescribed ASMs. The respective frequencies of inpatient ASM treatment and discharge prescription were 82% (233 of 285) and 69% (169 of 246) for patients with clinical acute symptomatic seizures, 96% (103 of 107) and 95% (61 of 64) for electrographic seizures, and 64% (233 of 364) and 48% (128 of 267) for EAs. On multivariable analysis, acute and progressive brain injuries were independently associated with increased odds of inpatient ASM treatment (odds ratio [OR], 3.86 [95% CI, 2.06-7.32] and 8.37 [95% CI, 3.48-20.80], respectively) and discharge prescription (OR, 2.26 [95% CI, 1.04-4.98] and 10.10 [95% CI, 3.94-27.00], respectively). Admission to the neurology or neurosurgery service (OR, 2.56 [95% CI, 1.08-6.18]) or to the neurological intensive care unit (OR, 7.98 [95% CI, 3.49-19.00]) was associated with increased odds of treatment. Acute symptomatic seizures and EAs were significantly associated with increased odds of ASM treatment (OR, 14.30 [95% CI, 8.52-24.90] and 2.30 [95% CI, 1.47-3.61], respectively) and discharge prescription (OR, 12.60 [95% CI, 7.37-22.00] and 1.72 [95% CI, 1.00-2.97], respectively). ASM treatment was not associated with outcomes at discharge (OR, 0.96 [95% CI, 0.61-1.52]) or at 3 months after initial presentation (OR, 1.26 [95% CI, 0.78-2.04]). Among 623 patients alive and with complete data at 3 months after discharge, 30 (5%) had postdischarge seizures, 187 (30%) were receiving ASMs, and 202 (32%) had all-cause readmissions. Conclusions and Relevance: This study suggests that etiology and electrographic findings are associated with ASM treatment for acute symptomatic seizures and EAs; ASM treatment was not associated with functional outcomes. Comparative effectiveness studies are indicated to identify which patients may benefit from ASMs and to determine the optimal treatment duration.

Paroxysmal Hypothermia With Prominent Parkinsonian Features After Suprachiasmatic Tumor Resection.

Paroxysmal hypothermia (PH) is a rare syndrome of stereotyped episodes of hypothermia, bradycardia, and altered mental status occurring in patients with hypothalamic lesions. Prior cases have mentioned bradykinesia, ataxia, and dysarthria, but parkinsonism has not been described as a specific feature of PH. We report two patients, an adult and a child, who developed PH after suprachiasmatic tumor resection, both with clinical presentations notable for prominent parkinsonian features despite no evidence of parkinsonism during the intervening months and years. We propose a diagnostic algorithm and scoring tool to aid in the clinical diagnosis of PH presenting as parkinsonism.

Cardiac sarcoidosis requiring ICD placement and immune thrombocytopenia following alemtuzumab treatment for multiple sclerosis.

Alemtuzumab, an effective disease-modifying therapy for multiple sclerosis, carries a significant risk of secondary autoimmunity. We present a case of cardiac sarcoidosis and immune thrombocytopenia diagnosed in an MS patient two years after completing alemtuzumab treatment. We hypothesize that alemtuzumab-induced changes to the T regulatory cell population may be implicated in the development of sarcoidosis in MS patients.

Teriflunomide Safety and Efficacy in Advanced Progressive Multiple Sclerosis.

OBJECTIVES: To explore the safety and efficacy profile of teriflunomide in progressive multiple sclerosis. METHODS: We conducted a single-center retrospective observational analysis of a progressive multiple sclerosis population, assessing safety and efficacy in patients treated at least one year with teriflunomide or glatiramer acetate. Sustained progression of expanded disability status scale and sustained worsening of timed 25-foot walk were compared using a Cox proportional hazards model. RESULTS: Teriflunomide group (n = 29) mean characteristics: age = 58 years (SD ± 7.6), disease duration = 16.7 years (SD ± 9.5), expanded disability status score = 5.9 (SD ± 1.3), and follow - up = 32.4 months (SD ± 13.6). Glatiramer acetate group (n = 30) mean characteristics: age = 52.4 years (SD ± 11.3), disease duration = 15.1 years (SD ± 10.4), expanded disability status score = 5.7 (SD ± 1.6), and follow - up = 46.9 months (SD ± 43.9). Both treatments were well tolerated without serious side effects. After adjustment for age, sex, and baseline expanded disability status score, sustained expanded disability status score progression did not differ between groups (hazard ratio = 1.17; 95% confidence interval: 0.45, 3.08; p = 0.75). Sustained timed 25-foot walk worsening after adjustment also did not differ (hazard ratio = 0.56; 95% confidence interval: 0.2, 1.53; p = 0.26). CONCLUSION: In an advanced progressive multiple sclerosis population, no substantial differences in tolerability, safety, sustained EDSS progression, or sustained T25FW worsening over time were observed between glatiramer acetate and teriflunomide-treated groups. The small sample precluded definitive determination.

Ganglion Cell Complex Loss in Chiasmal Compression by Brain Tumors.

BACKGROUND: Patterns of ganglion cell complex (GCC) loss detected by optical coherence tomography provide an objective measure of optic nerve injury. These patterns aid in early diagnosis and localization of chiasmal lesions. METHODS: Twenty-three patients with chiasmal compression seen between 2010 and 2015 were imaged with the Cirrus high-definition optical coherence tomography macular cube 512 × 128, retinal nerve fiber layer (RNFL) scan protocols and automated (30-2 Humphrey) visual fields (VFs). Age-matched controls were included for comparison. Generalized estimating equations were performed comparing RNFL and GCC thicknesses between patients and their controls. Effect size (d) was calculated to assess the magnitude of difference between patients and controls. The average GCC and RNFL thicknesses also were correlated with VF mean deviation (MD). Pre operative average GCC thickness was correlated to post operative VF MD. RESULTS: Patterns of GCC thinning corresponded to VF defects. The average GCC thickness was 67 ± 9 µm in patients and 86 ± 5 µm in controls (P < 0.001). The effect size was the greatest for GCC thickness (d = 2.72). The mean deviation was better correlated with GCC thickness (r =0.25) than RNFL thicknesses (r =0.15). Postoperatively, VF MD improved in 7 of 8 patients with persistent nasal GCC thinning. Six patients had no VF defect and showed statistically significant loss of GCC compared with controls (P = 0.001). CONCLUSIONS: Distinct patterns of GCC loss were identified in patients with chiasmal compression. Binasal GCC loss was typical and could be seen with minimal or no detectable VF loss. Thinning of the GCC may be detected before loss of the RNFL in some patients. After decompression, the majority of patients showed improvement in VF despite persistent GCC loss. Patients with less GCC loss before decompression had better postoperative VFs. Therefore, GCC analysis may be an objective method to diagnose and follow patients with chiasmal lesions.

The Optical Coherence Tomographic Profile of Leber Hereditary Optic Neuropathy.

The objective of this study was to describe the changes in the retinal ganglion cell complex (GCC) relative to the retinal nerve fibre layer (RNFL) over time in Leber hereditary optic neuropathy (LHON) patients. Average RNFL and GCC thickness was measured in seven patients in the early acute (123, 68.4 µm), late acute (113.5, 57.4 µm), and chronic (72.7, 50.8 µm) phases. Patients showed thinning of the GCC with RNFL swelling in the early acute phase. GCC thinning became severe within weeks and persisted. RNFL swelling normalised during the late acute phase with eventual thinning in the chronic phase. GCC changes appear at the commencement of visual loss and in some cases prior to vision loss. These findings define an optical coherence tomography (OCT) profile in LHON.

Distinguishing ischaemic optic neuropathy from optic neuritis by ganglion cell analysis.

PURPOSE: To determine whether a pattern of altitudinal ganglion cell loss, as detected and measured by optical coherence tomography (OCT), can be used to distinguish non-arteritic ischaemic optic neuropathy (NAION) from optic neuritis (ON) during the acute phase, and whether the rate or severity of ganglion cell loss differs between the two diseases. METHODS: We performed a retrospective, case-control study of 44 patients (50 eyes) with ON or NAION and 44 age-matched controls. Non-arteritic ischaemic optic neuropathy and ON patients had OCT at presentation and four consecutive follow-up visits. Controls had OCT at one point in time. The ganglion cell complex (GCC) was evaluated in the macula, and the retinal nerve fibre layer (RNFL) was evaluated in the peripapillary region. Ganglion cell complex thickness, RNFL thickness and GCC mean superior and inferior hemispheric difference were compared between NAION and ON patients at each time-point using unpaired t-tests and between disease and control subjects at first measurement using paired t-tests. RESULTS: Mean time from onset of symptoms to initial presentation was 10.7 ± 6.6 days in NAION and 11.7 ± 8.6 days in ON (p = 0.67). There was a significantly greater vertical hemispheric difference in GCC thickness in NAION patients than ON patients at all time-points (5.5-10.7 µm versus 3.1-3.6 µm, p = 0.01-0.049). Mean GCC thickness was significantly decreased at less than 2 weeks after onset in NAION compared to age-matched controls (72.1 µm versus 82.1 µm, p < 0.001), as well as in ON compared to age-matched controls (74.3 µm versus 84.5 µm, p < 0.001). Progression and severity of GCC and RNFL loss did not differ significantly between NAION and ON. CONCLUSION: A quantitative comparison of mean superior and inferior hemispheric GCC thickness with OCT may be used to distinguish NAION from ON.