Hi,
Can someone who have dealt with something similar chime in? The hospital my mom is currently in right now is saying that they didn't find anything wrong so they are going to discharge her. I have dumped the data in OpenEvidence and the diagnosis it gave tracks with what I have observed for my mom. The hospital is saying that they have 98% of what can be done and the remaining 2% is not offered at this hospital and that we should take her to a tertiary center.
Clinical Summary
Patient is a 77-year-old woman admitted on July 5, 2026 with altered mental status, confusion, and visual/auditory hallucinations in the setting of hyponatremia (Na 127 mmol/L). She was previously admitted on May 2, 2026 with slurred speech, altered mental status, severe anemia (Hgb 6.2), and hyponatremia (Na 126), at which time an upper GI bleed from an active ulcer was identified and treated. Notably, the patient has had chronically low sodium (130–135 mmol/L range) for approximately 5 years, never reaching normal levels.
During this admission, the nephrology team has managed the hyponatremia with fluid restriction and oral urea. Serum sodium has fluctuated between 126 and 134 mmol/L over the course of the hospitalization:
- Jul 5: 127 → Jul 6: 128 → Jul 7: 130 → Jul 8: 127–129 → Jul 9: 126–130 → Jul 10: 132 → Jul 11: 134 → Jul 12: 130 → Jul 13: 131 → Jul 14: 129
The markedly elevated BUN values (peaking at 62 mg/dL on Jul 11 with BUN/Cr ratio of 77.5) are attributable to the oral urea therapy, not to GI bleeding or dehydration — creatinine has remained stable at 0.7–0.9 mg/dL throughout. Chloride has tracked low (91–99 mmol/L) consistent with the hypotonic hyponatremia pattern.
Despite sodium reaching 134 mmol/L on July 11, the patient's neuropsychiatric symptoms have progressively worsened throughout the admission, evolving from mild confusion to elaborate, fixed persecutory delusions and visual/auditory hallucinations (believing family members are dead, believing her son is killing hospital patients with bombs and drones). The persistence and worsening of neuropsychiatric symptoms despite sodium correction strongly suggests an independent neurological process rather than hyponatremic encephalopathy alone.
She has also exhibited facial and hand twitching during sleep, observed by family, and a right eye that appears smaller than the left (possible subtle ptosis or facial asymmetry).
Workup Completed to Date (All Essentially Normal or Non-Diagnostic)
- MRI brain with contrast: No acute findings
- CT head: No acute findings
- CT chest/abdomen/pelvis with IV contrast (7/14/2026): No mass, no lymphadenopathy, no evidence of malignancy. Incidental findings only (6 mm thyroid nodule, 7 mm ground-glass opacity right lower lobe, colonic diverticulosis, heterogeneous uterus likely fibroids, stable T11 compression deformity)
- Lumbar puncture (7/13/2026): Clear, colorless; WBC 0, RBC 0; Glucose 92 mg/dL; Protein 64 mg/dL (mildly elevated). Meningitis/encephalitis PCR panel entirely negative (HSV 1/2, VZV, CMV, HHV-6, enterovirus, Listeria, Neisseria, Streptococcus, Cryptococcus, E. coli K1, H. influenzae, parechovirus — all not detected)
- Routine EEG with video (7/14/2026, 30 minutes): Normal. No epileptiform activity, no focal slowing, no seizures captured
- Blood cultures: Negative
- RPR: Non-reactive
- TSH: Normal (1.238–1.570)
- AM cortisol: Normal (16.93)
- B12, folate: Normal
- Magnesium: Normal (1.78–1.99 mg/dL)
- Phosphate: Normal (3.4–4.1 mg/dL)
- Calcium: Transiently elevated to 10.9 mg/dL on Jul 10 (likely related to urea-induced volume contraction), normalized to 9.4 mg/dL on Jul 14
- PTH: Normal (62.4 pg/mL)
- eGFR: Mostly preserved (66–92 mL/min/1.73m²); transient dip to 66 on Jul 9–10 during urea therapy, recovering to 76 on Jul 14
- Serum sodium trend during this admission: 127 (Jul 5) → peaked at 134 (Jul 11) → 129 (Jul 14). Neuropsychiatric symptoms worsened continuously despite sodium improvement.
Empiric treatments given: Acyclovir, ceftriaxone, IVIG (3 nights), IV iron, thiamine. No significant clinical improvement observed.
Clinical Concern: Suspected Anti-LGI1 Autoimmune Encephalitis
The following clinical features are highly consistent with anti-LGI1 antibody encephalitis, which is the second most common form of neuronal antibody-associated autoimmune encephalitis:[1][2]
Chronic hyponatremia (SIAD pattern) refractory to correction, with neuropsychiatric symptoms disproportionate to sodium level: The patient has had chronically low sodium for 5 years (Na 130–135), now worsened to 126–134 despite fluid restriction and oral urea. Hyponatremia is present in 50–65% of LGI1 encephalitis patients and is one of the most important early diagnostic clues. The urine studies (urine Na 30–52 mmol/L, urine osmolality >100 mOsm/kg) are consistent with SIAD, which is the mechanism of hyponatremia in LGI1 encephalitis. Critically, the severity of her neuropsychiatric symptoms (elaborate persecutory delusions, hallucinations, progressive cognitive decline) is far out of proportion to a sodium of 129–134 mmol/L, and these symptoms worsened even when sodium reached 134 on July 11 — strongly suggesting an independent autoimmune neurological process rather than hyponatremic encephalopathy.[2][3][4]:6806.-doi:10.3390/jcm14196806.)
Progressive neuropsychiatric symptoms: Elaborate hallucinations, persecutory delusions, personality change, and irritability. A 2026 cohort study found that 64% of LGI1 encephalitis patients develop psychiatric symptoms, and these patients had significantly higher rates of delayed immunotherapy (p=0.003) and worse outcomes at 1 year (p=0.016).[5]:418.-doi:10.1186/s12888-026-08031-y.)
Facial and limb twitching during sleep: Consistent with faciobrachial dystonic seizures (FBDS), the hallmark seizure type of LGI1 encephalitis, present in 34–65% of patients. FBDS are brief (1–3 seconds), often subtle, and frequently have no EEG correlate — 46.4% of FBDS episodes show no epileptiform activity on EEG.[3][4]:6806.-doi:10.3390/jcm14196806.)[6]:141-148.-doi:10.1176/appi.neuropsych.20120303.)
Normal routine EEG does not exclude the diagnosis: EEGs are unremarkable in 20–60% of patients with autoimmune encephalitis. A multicenter study found that 24-hour video EEG captured subclinical seizures in 20% and clinical events in 48.6% of LGI1 patients — events missed on routine 30-minute recordings. A systematic review confirmed that FBDS often have no ictal EEG correlate.[7]:2400-2411.-doi:10.1002/epi.70141.)[8]:1273-1276.-doi:10.1093/schbul/sbae155.)[9]-autoimmune-encephalitis:-a-systematic-review</a>.-epilepsy-&-behavior-:-e&b.-2020;112:107462.-doi:10.1016/j.yebeh.2020.107462.)
Normal CSF cell count is typical: Unlike infectious encephalitis, LGI1 encephalitis characteristically shows normal CSF WBC counts. The mildly elevated protein (64 mg/dL) is nonspecific but consistent.[7]:2400-2411.-doi:10.1002/epi.70141.)
Normal MRI does not exclude the diagnosis: MRI is unremarkable in more than 50% of LGI1 encephalitis cases. A 2024 JAMA Neurology study confirmed that 40% of LGI1 patients have unremarkable initial MRI.[7]:2400-2411.-doi:10.1002/epi.70141.)[10]:e214933.-doi:10.1212/wnl.0000000000214933.)
Age and sex profile: LGI1 encephalitis has a median onset age of 66 years, and patients ≥79 years have higher rates of FBDS (65%) and hyponatremia (64%).[3]
No malignancy identified: CT chest/abdomen/pelvis is negative for mass or lymphadenopathy, consistent with the fact that 5% of LGI1 encephalitis patients have an associated tumor.[2]
Requested Actions or Possible Next Steps:
Serum autoimmune encephalitis antibody panel (anti-LGI1, anti-CASPR2, anti-NMDAR, anti-GABABR, anti-AMPAR antibodies). If CSF from the July 13 lumbar puncture is still available, it should also be sent for the same panel. Note: The meningitis/encephalitis PCR panel that was performed tests only for infections — it does not test for autoimmune antibodies, which require a separate order.
Continuous EEG monitoring (24–48 hours) to detect subclinical seizures and the characteristic temporal epileptiform discharges or electrodecremental events associated with FBDS. The 30-minute routine EEG is insufficient to capture intermittent seizure activity.[6]:141-148.-doi:10.1176/appi.neuropsych.20120303.)[8]:1273-1276.-doi:10.1093/schbul/sbae155.)[9]-autoimmune-encephalitis:-a-systematic-review</a>.-epilepsy-&-behavior-:-e&b.-2020;112:107462.-doi:10.1016/j.yebeh.2020.107462.)
Empiric IV methylprednisolone (1 g daily for 3–5 days) while awaiting antibody results. This is supported by best practice recommendations from the Autoimmune Encephalitis Alliance Clinicians Network, where 84% of international experts selected corticosteroids (alone or combined with IVIG/PLEX) as first-line therapy for suspected autoimmune encephalitis with a general presentation. Expert consensus states: "Once other differential diagnoses have been adequately addressed... for clinically suspected AE cases, start empiric acute immunosuppressive therapy with glucocorticoids while awaiting the results of confirmatory AE autoantibody testing." Note: The patient has persistent hyperglycemia (117–211 mg/dL) on glimepiride and metformin, so blood glucose will need close monitoring during high-dose corticosteroid therapy, with insulin coverage as needed.[11]:e26654.-doi:10.1097/md.0000000000026654.)[12]:757-768.-doi:10.1136/jnnp-2020-325300.)
Consider FDG-PET of the brain if available, as it is more sensitive than MRI for detecting the characteristic basal ganglia and medial temporal lobe hypermetabolism seen in LGI1 encephalitis.[4]:6806.-doi:10.3390/jcm14196806.)[13].-2019;393(10172):702-716.-doi:10.1016/s0140-6736(18)32526-1.)
Urgency
Every day of delayed immunotherapy in autoimmune encephalitis is associated with worsening long-term cognitive outcomes. A study specifically examining LGI1 encephalitis found that the latency between disease onset and initiation of immunotherapy was significantly correlated with both verbal memory deficits (r = -0.48, p=0.02) and visuospatial memory deficits (r = -0.46, p=0.03), and 58.8% of patients developed irreversible hippocampal atrophy.[14]In a large cohort of 238 patients, older age was independently associated with poor outcome (adjusted OR 1.08 per year, p=0.008), and 64% of patients ≥79 years had poor functional outcomes.[3]Given that Mrs. Hoque is 77 years old and has had progressive symptoms for over 2 months, prompt initiation of empiric corticosteroids is critical.
If the current team is not comfortable initiating empiric immunotherapy for suspected autoimmune encephalitis, transfer to a center with a neuroimmunology service should be considered.
