Case Presentation:

The patient is a previously healthy two–year–old female. While eating in a restaurant with her family, she had a temper tantrum. She then became limp with her eyes rolling back. She recovered in 15 min. She had a second similar but unprovoked episode at home 2 h later. After the second episode, she was unable to use the right side of her body and unable to walk. Prior to these events she had no history of trauma, ingestion, fever, vomiting, diarrhea or respiratory symptoms. She has no history of seizure or breath–holding spells. She was taken to an urgent care center for evaluation. She was noted to be mild tachycardic, pale and had a small bruise on her right lower leg. Once triaged she was able to walk again but still had right leg weakness. Plain films of the leg were normal as was a head CT. Labwork showed a Hgb of 4.2 g/dL with normal MCV and RDW and reticulocyte count of 0.2%. Platelet count was 285,000 and ANC was 2554. The differential for her anemia included Diamond Blackfan Syndrome, Aplastic Anemia, Transient Erythroblastopenia of Childhood (TEC) and malignancy. Additional labwork showed a normal ferritin, LDH, nonelevated lead level, and negative serology for CMV, EBV and parvovirus. Her peripheral smear demonstrated a few atypical lymphocytes, felt to be reactive. While hospitalized she was transfused with packed red blood cells. Her leg weakness resolved and she had no other neurologic deficits. She was followed in the hematology clinic for the subsequent two months with normalization of her labwork.


TEC is a temporary red cell aplasia seen in young children first described in 1970 with an annual incidence of 4.3 per 100,000. It is the most common cause of decreased red blood cell production in childhood. The majority of children present with pallor, and approximately 50% follow a viral infection. Anemia typically resolves over one to two months. Severe anemia may require transfusion. In 1983 the first case of TEC with associated neurologic symptoms was reported. The author hypothesized that the neurologic deficits resulted from the profound anemia leading to inadequate oxygenation of the brain. Since this initial report other case series have been unable to show a relationship between the hemoglobin level and the observed neurologic events. Other authors have suggested that immune dyregulation may be initiated by the same viral infection that causes TEC. The true incidence of neurologic symptoms with TEC is unknown but appears to be infrequent. However in all cases the deficits have been transient and resolved spontaneously, typically sooner than the hematologic abnormalities. Head CT and angiography, when obtained, have been normal.


TEC has a rare but known association with neurologic deficits. While focal neurologic findings are always concerning, in all reported case series the neurologic findings of TEC have been transient and resolved without specific therapies.