Related Experiment Video

Updated: Jul 20, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
07:36

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

11.3K

Delayed Neurological Sequelae of Carbon Monoxide Intoxication Initially Treated as Infectious Meningo Encephalitis

Xavier Jannot1, Alpha Oumar Diallo1, Judicaelle Didierjean2

  • 1Service de Médecine Interne, Hôpitaux Universitaires de Strasbourg, Strasbourg, France.

European Journal of Case Reports in Internal Medicine
|March 7, 2025
PubMed

Insights

Carbon monoxide intoxication can cause a delayed neurological syndrome, known as post-interval syndrome, even after an initial recovery period. This poorly understood condition has a poor prognosis and requires advanced imaging for diagnosis.

Area of Science:

  • Neurology
  • Toxicology
  • Internal Medicine

Background:

  • Carbon monoxide (CO) intoxication can lead to delayed neurological complications.
  • Post-interval syndrome (PIS) is a rare but serious delayed neurological sequela following CO exposure.
  • PIS is characterized by neuropsychiatric disorders after an asymptomatic interval.

Purpose of the Study:

  • To report a case of PIS following CO intoxication.
  • To highlight the diagnostic challenges and poor prognosis of PIS.
  • To raise awareness among clinicians about this underrecognized condition.

Main Methods:

  • Case report of a 75-year-old woman with delayed neurological symptoms after CO exposure.
  • Initial misdiagnosis of infectious meningoencephalitis.
  • Diagnosis confirmed by serial magnetic resonance imaging (MRI) and clinical evaluation.
  • Exclusion of other neurological causes.

Main Results:

  • The patient presented with confusion, gait disturbances, and mutism 3 weeks after CO intoxication.
  • Initial treatment for meningoencephalitis was ineffective.
  • Serial MRI revealed findings consistent with PIS, distinguishing it from acute cytotoxic edema.
  • No neurological improvement was observed at 6-month follow-up.

Conclusions:

  • Post-interval syndrome is an underrecognized complication of CO intoxication that warrants consideration in patients with delayed neurological symptoms.
  • Repeated MRI, performed more than a month after symptom onset, is crucial for differentiating PIS from cytotoxic edema.
  • The prognosis for PIS is poor, with no established effective treatments currently available.
Keywords:
Carbon monoxide intoxicationdelirummeningo-encephalitis

More Related Videos

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease04:23

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease

Published on: April 28, 2019

6.5K
Early Pathological and Magnetic Resonance Detection of Cerebral Injury Using a Rat Model of Neonatal Hypoxic Ischemic Encephalopathy05:52

Early Pathological and Magnetic Resonance Detection of Cerebral Injury Using a Rat Model of Neonatal Hypoxic Ischemic Encephalopathy

Published on: October 28, 2022

731

Related Concept Videos

Viral Meningitis01:18

Viral Meningitis

Viral meningitis is the most common form of meningitis and is often referred to as aseptic meningitis to indicate the absence of bacterial involvement. It is generally milder than bacterial meningitis, with symptoms including fever, headache, stiff neck, drowsiness, nausea, photophobia, and vomiting. Rarely, more severe manifestations or death may occur. Common causative agents include enteroviruses, particularly coxsackie A and B viruses and echoviruses, all members of the Enterovirus genus...
Bacterial Meningitis I: Introduction01:22

Bacterial Meningitis I: Introduction

Bacterial meningitis is a severe, life-threatening inflammation of the meninges, particularly the pia mater and arachnoid mater, affecting the subarachnoid space, ventricles, and cerebrospinal fluid (CSF). If untreated, it can lead to significant neurological complications or death.Causative AgentsCommon pathogens vary with age and immune status. In adults, major organisms include Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. Streptococcus agalactiae (group B...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
Encephalitis l: Introduction01:19

Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...