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Case and Discussion: Chronic and Acute Confusional States

Explore a case presentation, differential diagnoses, clinical approach, results, and findings of a patient with chronic and acute confusional states. Learn about the clinical approach and the importance of considering various differential diagnoses in such cases.

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Case and Discussion: Chronic and Acute Confusional States

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  1. Case and Discussion:Chronic and Acute Confusional States Connie Chen, MD Neurology Consultants of Dallas

  2. Overview • Case presentation • Differential diagnosis • Clinical approach • Results and findings • Follow-up • Discussion

  3. Case Presentation • 61 yo woman • episode of presyncope • “wobbly” when standing • “slow thinking” over 6 months • noted after administration of BP meds (SBP 200’s lowered to 120’s) • NRO exam non-focal. MS not extensively tested, some memory loss noted • Hyponatremic: Na=117

  4. Case Continued • Diuretic stopped • BP raised slightly • PT d/c’d to home after Na normalized

  5. Case Continued • 2 weeks later • Episodic worsening of confusion • Lost while driving • Worsening short-term memory • Episodes of paranoia • New delusions: • CT scanner trying to transport her to the future • Aliens trying to abduct daughter • After watching “Manchurian Candidate,” she was also involved in a conspiracy

  6. Case Continued • NRO exam: • MS: • Poor memory, attention, not oriented • Labile affect • Intact calculations, language • Delusional • CN, motor, sensation, cerebellar, and gait are normal

  7. Differential diagnosis: Chronic confusional state • Progressive decline of memory, cognition: • Degenerative dementias • Multi-infarct dementia • Chronic infection (TB meningitis, syphilis, HIV) • Hypothyroidism • Vitamin deficiencies (B12, thiamine) • Toxins • Other: seizures, neoplastic, paraneoplastic, “pseudo-dementia”

  8. Differential diagnosis: Acute confusional state • Delirium • “Metabolic states”: • Medications/drugs • Endocrine: thyroid, glucose, hyper/hypoadrenalism • Electrolytes: Na, Ca • Vitamins: B12, thiamine • Organ failure: liver, renal (uremia, “dialysis disequilibrium”), respiratory failure (hypoxia)

  9. Acute Confusional State • Cerebrovascular: • stroke/TIA • hypertensive encephalopathy, hypotension • DIC, TTP • Infectious: meningitis • Seizures • Head trauma • Neoplasm • Other: (Systemic disease: rheumatologic, paraneoplastic)

  10. Clinical approach • Systematic approach • Indications for studies • Don’t stop with one diagnosis: • “Think outside the box” • “What am I missing?” • Tailor your work-up, you can always expand later

  11. Our case: Results and Findings • Chronic confusional state (>6 month decline) • Degenerative dementias: • Diagnosis of exclusion • Requires memory loss in addition to another “cognitive sphere” with functional decline • Multi-infarct dementia: no evidence of infarction. • Chronic infection: LP negative ( mild protein elevation), RPR negative, HIV negative. • Hypothyroidism: nl TSH • Vitamin deficiencies (B12, thiamine): low B12, normal homocysteine • Toxins: negative tox screen

  12. Results Continued • Acute confusional state: • Metabolic: • Meds: none • Endocrine: TSH normal, normo-glycemia • Infections: LP negative except elevated protein, RPR negative, HIV negative. • Vitamins: B12 low but homocysteine normal (MMA pending), thiamine given. • Electrolytes: Na 131, dropped to 127. • Organ failure: organs normal, no respiratory failure.

  13. Results Continued • Cerebrovascular: no focality to suggest stroke/TIA, not hyper or hypotensive, no evidence DIC/TTP. • Seizure: left temporal sharp wave. No seizure. • Neoplasm: normal head CT.

  14. What else am I missing? • Delirium with new onset pyschosis : • Antiphospholipid antibody syndrome • Limbic encephalitis (paraneoplastic syndrome) • Porphyria

  15. More Results • ESR, ANA, anticardiolipin antibodies negative.

  16. More Results • Chest CT: • right paratracheal node • 0.8 cm nodular opacity right upper lobe. • Biopsy of node: small cell lung cancer.

  17. Follow-up • Treatment with XRT and CMTx. • Psychotic symptoms resolved. • Memory loss remains.

  18. Discussion • Limbic encephalitis: “a paraneoplastic syndrome marked by degeneration of neurons in the medial temporal lobe.”

  19. Limbic encephalitis • Incidence: unknown (rare) • Symptoms: • Acute confusional states • Memory loss • Seizures • “Psychiatric” symptoms • Dementia • Antineuronal antibodies: anti-Hu, anti-Ta, (anti-Ma, others)

  20. Limbic encephalitis • Often presents before tumor diagnosis • Tumor associations • Lung (small cell, non-small cell) • Testicular • Breast

  21. Limbic encephalitis: Studies • EEG: temporal lobe seizures, sharp waves, normal. • CSF: (can be normal) • Mild pleocytosis • Mildly elevated protein • Radiographic: • MRI: (can be normal) • medial temporal lobe: “bright” on T2, enhances with contrast. • brainstem • hypothalamus • ** r/o HSV encephalitis**

  22. Limbic encephalitis:Treatment • Treatment: underlying tumor • Immune modulatory treatments attempted: • Steroids • Cyclophosphamide • IV IG • Plasmapheresis • Improvement of symptoms only with tumor treatment • If diagnosed- search for tumor!

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