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Acute bilateral thalamic necrosis in a child with Mycoplasma pneumoniae
C S Ashtekar1, T Jaspan, D Thomas
1Paediatric Intensive Care, Queen's Medical Centre, Nottingham, UK.
Insights
This case report details a child with Mycoplasma pneumoniae infection who developed acute bilateral thalamic necrosis. This rare neurological complication highlights the diverse spectrum of Mycoplasma pneumoniae
Area of Science:
- Neurology
- Infectious Diseases
- Pediatrics
Background:
- Mycoplasma pneumoniae is a common respiratory pathogen.
- Neurological complications of Mycoplasma pneumoniae are rare but can be severe.
- Acute bilateral thalamic necrosis is a distinct clinicoradiological entity.
Observation:
- A previously healthy 5-year-old boy developed Mycoplasma pneumoniae pneumonia.
- He experienced a prolonged seizure leading to intubation and ventilation.
- Brain MRI revealed bilateral thalamic lesions with edema and hemorrhage, consistent with acute bilateral thalamic necrosis.
Findings:
- The patient received antibiotics and corticosteroids for Mycoplasma pneumoniae infection and a suspected autoimmune process.
- He showed slow neurological recovery over two months, with residual dysarthria, drooling, and mild left hemiparesis.
- Persistent dystonia and tremor affected speech and fine motor skills at nine months follow-up.
Implications:
- This is the first reported case of Mycoplasma pneumoniae-associated isolated acute bilateral thalamic necrosis.
- It expands the known neurological manifestations of Mycoplasma pneumoniae.
- Highlights the importance of considering Mycoplasma pneumoniae in cases of acute thalamic injury, even without typical respiratory symptoms.
Abstract:
A previously neurodevelopmentally intact 5-year-old male was admitted to hospital with a right lower lobe pneumonia with pleural effusion, subsequently confirmed to be a Mycoplasma pneumoniae infection. On the seventh day of the illness he had a prolonged generalized tonic or tonic-clonic convulsion, requiring intubation and ventilation. He was slow to regain consciousness (Child's Glasgow Coma Score 7-10 over 6 days) and brain imaging with CT and then MRI demonstrated bilateral thalamic lesions with oedema and central haemorrhage suggestive of acute bilateral thalamic necrosis, without striatal or white-matter involvement. He was treated with a 2-week course of erythromycin, and as an autoimmune process was considered possible, 5 days of intravenous methylprednisolone (20 mg/kg/day) followed by a 4-week oral prednisolone taper. He made a slow recovery over the next few weeks with almost complete neurological recovery by 2 months but with significant dysarthria, drooling, and a mild left hemiparesis. At 9 months, significant dystonia continued to affect his speech and, together with tremor, his upper-limb fine motor function bilaterally. His gait, personality, and higher cognitive functions appeared to have recovered fully. Although acute striatal necrosis, acute disseminated encephalomyelitis, and encephalitis have been reported with Mycoplasma pneumoniae and a similar picture of acute bilateral thalamic necrosis with influenza-A ('acute necrotizing encephalopathy'), this is the first reported case of Mycoplasma pneumoniae-associated isolated acute bilateral thalamic necrosis.