CPEO

Chronic progressive external ophthalmoplegia (CPEO)

Clues
- Common adult presentations of mitochondrial disease

Clinical features
- Classic: ophthalmoparesis + ptosis
> Pupil sparing
- Possible: proximal limb myopathy + bulbar involvement + reduced respiratory muscle strength

Presentations
- Isolated CPEO vs CPEO-plus
> Isolated→ only eyes; with anything else is CPEO-plus
> Kearns-Sayre syndrome triad
(CPEO + pigmentary retinopathy + onset before 20yo)

Genetics
- Half of cases→ 4977-bp mtDNA deletion
- Other half is multiple deletions in mtDNA
> Common: POLG, TWNK (C10orf2), SLC25A4

Workup
- Labs: can ↑CK & ↑lactate
- EMG: myopathic changes
- Muscle biopsy→ ragged-red fibers & COX-negative fibers
- Cardiac eval→ ECG & TTE
> Cardiac conduction block→ KSS
- oMRI→ EOM atrophy

DDx
- Seronegative MG
- OPMD
- Congenital myasthenic syndromes
- Myotonic dystrophy

Ttx
- Supportive
- If ptosis→ surgery/ prisms
- CoQ10 and others, evidence is limited
Avoid mitochondrial-toxic medications

General advice for mito myoapthies
1) Succinylcholine→ ↑HyperK adn rhabdo
2) Propofol↑Propofol syndrome
3) Volatile anesthetics→ prefer sevo
4) Avoid LR→ impaired lactate metabolism 

Forensic Psych

Forensic Psych

Visual hallucinations
- VH→ Olfactory→ Tactile
> Low probability of being psychiatry (olfactory & tactile), usually malingering, rarely neurological
> Drugs of abuse withdrawal

Orthostatic hypotension

Orthostatic hypotension (OH)

Management

Meds
Midodrine
-2nd dose before 0600PM to avoid nocturnal supine HTN

Stroke - Mortality

Stroke - Mortality

< 24h→ stroke severity
>24h→ quality hospital metric

Stroke - DVT prophylaxis

Stroke - DVT prophylaxis

Current ICH
- If rCTH (6h) is stable, theoretically okay to start DVT prophylaxis
*Guidelines say rCTH in 24, if stable okay to restart DVT prophylaxis

If starting full AC in-hospital
-There is no need for DVT prophylaxis

241. Minimal Hepatic Encephalopathy: A Narrative Review

Article type: Literature Review
Article title: Minimal Hepatic Encephalopathy: A Narrative Review

Journal: Cureus
Year: 2026
Authors: Jamir Pitton Rissardo, Fatemeh Rashidi, Hania Moharam, Ibrahim Khalil, Meryem Bahar, Masoumeh Rashidi, Basem Ahmed, Saleh Salem, Ana Leticia Fornari Caprara, Abhishek A. Chouthai, Ahmed M. Kedwany, Hagar H. Sayed, Omesh Prathiraja, Maleesha Jayasinghe
E-mail: jamirrissardo@gmail.com

ABSTRACT
Minimal hepatic encephalopathy (MHE) is primarily a cognitive disorder linked to chronic liver disease that often remains underdiagnosed due to the subtlety of its clinical manifestations. These symptoms are frequently overlooked or dismissed as inconsequential in clinical practice, leading to many undiagnosed cases. The standard neurological examination is usually normal in individuals with MHE. Regular and systematic screening for MHE is essential for early detection, which can improve cognitive outcomes and prevent progression to a more serious and debilitating condition known as overt hepatic encephalopathy. The pathophysiology of MHE is very complex and multifactorial, involving several interacting mechanisms. Mainly, hyperammonemia, systemic inflammation, gut-derived neurotoxins, oxidative stress, and mitochondrial dysfunction are at its root. Any of these factors may interfere with the normal functioning of neurotransmitters, giving rise to the typical subtle cognitive impairments that are hallmarks of MHE. The Animal Naming Test and EncephalApp-Stroop test are practical, rapid, and easily administered tools for screening for minimal hepatic encephalopathy in outpatient and bedside settings. Emerging diagnostic technologies, including advanced neuroimaging techniques and novel biomarkers, have also been investigated and show promise for improving the early detection and diagnosis of MHE.
Keywords: chronic liver diseases, driving impairment, electroencephalography, hepatic encephalopathy, minimal hepatic encephalopathy, neurocognitive testing, neuropsychological testing, psychometric tests, quality of life

Full text available at:

DOI

Citation
Rissardo JP, Rashidi F, Moharam H, Khalil I, Bahar M, Rashidi M, Ahmed B, Salem S, Fornari Caprara AL, Chouthai AA, Kedwany AM, Sayed HH, Prathiraja O, Jayasinghe M. Minimal Hepatic Encephalopathy: A Narrative Review. Cureus 18(8): e113978. doi:10.7759/cureus.113978.
Figure 1. Grades of hepatic encephalopathy.
Figure 2. Role of ammonia in the pathophysiology of hepatic encephalopathy.
Figure 3. The algorithm for arriving at the diagnostically appropriate diagnosis of minimal hepatic encephalopathy.
Figure 4. Proposed clinical algorithm for the diagnosis of minimal hepatic encephalopathy.
Table 1. Diagnostic methods for the detection of MHE. ANT: Animal Naming Test, CFF: critical flicker frequency testing, CHE: covert hepatic encephalopathy, CRT: Continuous Response Time test, EEG: electroencephalography, HRQOL: health-related quality of life, ICT: Inhibitory Control Test, MHE: minimal hepatic encephalopathy, PHES: Psychometric Hepatic Encephalopathy Score, RBANS: Repeatable Battery for the Assessment of Neuropsychological Status, SIP: Sickness Impact Profile, 3-NT: 3-nitrotyrosine.
Table 2. Precipitating factors diagnosis and management. BRTO: Balloon-Occluded Transvenous Retrograde TIPS: transjugular intrahepatic portosystemic shunt, SPSS: spontaneous portosystemic shunt, BRTO: balloon-occluded retrograde transvenous obliteration, CARTO: coil-assisted retrograde transvenous obliteration, PARTO: plug-assisted retrograde transvenous obliteration, HE: hepatic encephalopathy, IV: intravenous, BMI: body mass index, DEXA: dual-energy X-ray absorptiometry, GI: gastrointestinal, PPI: proton pump inhibitor.Obliteration, CARTO: Coil-Assisted Retrograde Transvenous Obliteration, PARTO: Plug-assisted BRTO.
Table 3. Published studies on the management of minimal hepatic encephalopathy. BCAA: branched-chain amino acids, BDT: block design test, CFF: critical flicker frequency, CEP: cognitive evoked potentials, DST: digit symbol test, EEG: electroencephalogram, FOS: fructooligosaccharide, HRQOL: health-related quality of life, ICT: inhibitory control test, LTT: line tracing test, MHE: minimal hepatic encephalopathy, NCT-A: number connection test-A, NCT-B: number connection test-B, NfL: Neurofilament light, OHE: overt hepatic encephalopathy, PHES: psychometric hepatic encephalopathy score, SDT: serial dotting test, SIBO: small intestinal bacterial overgrowth.

240. Effects of subthalamic nucleus deep brain stimulation on sleep quality and daytime sleepiness in Parkinson’s disease: a systematic review and meta‑analysis

Article type: Systematic Review
Article title: Effects of subthalamic nucleus deep brain stimulation on sleep quality and daytime sleepiness in Parkinson’s disease: a systematic review and meta‑analysis

Journal: Neurological Research
Year: 2026
Authors: Jamir Pitton Rissardo, Mansi Jain, and Ana Letícia Fornari Caprara
E-mail: jamirrissardo@gmail.com

ABSTRACT
Background: Subthalamic nucleus deep brain stimulation (STN-DBS) is an established treatment for motor symptoms in Parkinson’s disease (PD), but its effects on sleep remain uncertain. This study evaluated changes in nocturnal sleep quality and daytime sleepiness following STN-DBS. Methods: Four databases were searched for longitudinal studies assessing sleep outcomes after STN-DBS in PD. Sleep was evaluated using the Parkinson’s Disease Sleep Scale (PDSS) and Epworth Sleepiness Scale (ESS). Study quality was assessed with the Newcastle-Ottawa Scale. Pooled mean differences (MDs) were calculated using inverse-variance fixed-effects models, and heterogeneity was assessed with I2 statistics. Results: Nine studies reporting PDSS outcomes (n = 286) and eight reporting ESS outcomes (n = 190) were included. Most patients underwent bilateral STN-DBS (93.7%). Pooled analyses demonstrated significant improvements in PDSS scores (MD 21.23 points, 95% CI 11.59–30.87; p < 0.01) and reductions in ESS scores (MD − 3.62 points, 95% CI − 5.09 to −2.14; p < 0.01). Heterogeneity was negligible for both outcomes (τ = 0; I2 = 0%). The 95% prediction intervals remained favorable for PDSS (9.61–32.86) and ESS (−5.46 to −1.77), suggesting consistent findings across studies. Conclusion: Current evidence suggests that STN-DBS is associated with improved subjective sleep quality and reduced daytime sleepiness in patients with PD. However, these findings should be interpreted cautiously because they are derived primarily from observational studies with limited sample sizes and potential confounding factors. Prospective studies specifically designed to evaluate sleep outcomes are needed to clarify the independent effects of STN-DBS on sleep.
Keywords: Parkinson’s disease; subthalamic nucleus; deep brain stimulation; sleep quality; daytime sleepiness; non‑motor symptoms.

Full text available at:

DOI

Citation
Rissardo J P, Jain M, Fornari Caprara AL. Effects of subthalamic nucleus deep brain stimulation on sleep quality and daytime sleepiness in Parkinson’s disease: a systematic review and meta‑analysis. Neurol Res 2026, 1–19. https://doi.org/10.1080/01616412.2026.2717709
Figure 1. PRISMA screening flow diagram.
Figure 2. Forest plot of pooled mean change from baseline in MD of PDSS scores after STN-DBS.
Figure 3. Forest plot of pooled mean change from baseline in MD of ESS scores after STN-DBS.
Table 1. Study characteristics of meta-analysis studies.
Table 2. NOS.
Table 3. Certainty of evidence.
Table 4. Quantitative evidence on sleep outcomes after STN‑DBS in PD.

239. Accepted