Lead poisoning

Toxicosis

General description

Lead poisoning results from the abnormal intake of lead, which inhibits mitochondrial cellular respiration and enzymes involved in heme synthesis. Lead poisoning occurs when lead accumulates in the body over time and can severely impact health, even at low levels. Children are especially vulnerable, as lead exposure can impair mental and physical development; common sources include lead-based paint and contaminated dust in older buildings. Adults exposed to inorganic lead compounds—often through occupations involving dust inhalation, such as battery manufacturing or renovation work—are also at risk of adverse health effects.

In children, lead poisoning can cause developmental delays, learning difficulties, irritability, loss of appetite, fatigue, abdominal pain, and seizures. At very high levels, it may lead to acute encephalopathy, presenting symptoms such as increased intracranial pressure, restlessness, anxiety, generalized seizures, and, in severe cases, coma or even death within days. In newborns, prenatal lead exposure can result in premature birth, low birth weight, and slowed growth.

For adults, lead poisoning can result in high blood pressure, joint and muscle pain, memory issues, headaches, mood disturbances, and reproductive issues, including reduced sperm count and risk of miscarriage. Initially, lead poisoning can be difficult to detect, as symptoms often appear only after dangerous levels have accumulated in the body, making awareness and early intervention crucial.

Acute phase

Anatomical regions
  • Cerebrum
    Cerebral white matter
    Subcortical white matter
  • Cerebellum
  • Putamen
  • Claustrum
  • Cerebrum
    Insula
  • Thalamus
  • External capsule
Symmetric
Bilateral
T2WI
Hyperintensity
FLAIR
Hyperintensity

In the acute phase, T2WI and FLAIR show bilateral hyperintensity in the corticomedullary junction of the cerebrum, cerebellum, lateral putamen, claustrum, insula, and thalamus, reflecting edematous changes.

Chronic phase

Anatomical regions
  • Cerebrum
    Cerebral white matter
    Subcortical white matter
  • Cerebellum
    Vermis
  • Putamen
  • Thalamus
Bilateral
Multiple
Plain CT
Calcified attenuation
T2WI
Hypointensity
FLAIR
Hypointensity
T2*WI
Hypointensity
SWI
Hypointensity

In the chronic phase, CT reveals calcium deposition in the corticomedullary junction of the cerebrum, thalamus, putamen, bilateral cerebellar vermis.