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Motor nervous pathway function is impaired after treatment of childhood acute lymphoblastic leukemia: a study with
A H Harila-Saari1, U E Huuskonen, U Tolonen
1Department of Pediatrics, Oulu University Central Hospital, Oulu, Finland. Arja.Harila-Saari@oulu.fi
Insights
Childhood acute lymphoblastic leukemia (ALL) treatment affects motor pathways, causing nerve damage and motor difficulties. Motor evoked potentials (MEPs) reveal these neurotoxic effects, prompting further study in survivors.
Area of Science:
- Neuroscience
- Pediatric Oncology
- Clinical Electrophysiology
Background:
- Childhood acute lymphoblastic leukemia (ALL) treatment may impact motor nervous system pathways.
- Understanding these effects is crucial for long-term patient outcomes.
Purpose of the Study:
- To evaluate motor nervous pathway involvement in children treated for ALL.
- To assess neurotoxicity using motor evoked potentials (MEPs).
Main Methods:
- Studied 32 children with ALL post-treatment using transcranial and peripheral magnetic stimulation (MS) for MEPs.
- Conducted detailed neurological examinations and compared results with 32 healthy controls.
Main Results:
- ALL patients showed prolonged MEP latencies, indicating demyelination.
- Reduced MEP amplitudes suggested loss of motor or muscle fibers.
- Neurological deficits were common, including reflex issues and motor difficulties.
- Peripheral nerve delays correlated with vincristine, CNS lesions with methotrexate.
Conclusions:
- ALL treatment adversely affects the entire motor nervous system.
- MEPs via MS offer an objective method to assess neurotoxicity.
- Findings highlight the need to investigate long-term motor effects in ALL survivors.
Background:
The objective was to evaluate whether motor nervous pathways are affected when patients are treated for childhood acute lymphoblastic leukemia (ALL).
Procedure:
Thirty-two children with ALL were studied at the end of treatment by means of motor evoked potentials (MEPs) elicited by magnetic stimulation (MS) transcranially and peripherally and underwent a detailed neurological examination. Thirty-two healthy children matched with them for age, sex, and height served as a control group.
Results:
The latencies of the MEPs were significantly prolonged along the entire motor nervous pathway in the patients with ALL compared with the healthy controls, indicating demyelination in the thick motor fibres. The MEP amplitudes of the distal extremities elicited by stimulation at the brachial plexus and LV spinal level were significantly lowered in the patients treated for ALL, also indicating anatomical or functional loss of descending motor fibres and/or muscle fibres. The MEP amplitudes elicited by cortical MS showed wider variation and no clear abnormalities were found. Neurological signs and symptoms were common after treatment: 41% of the patients had depressed deep tendon reflexes, 31% had fine motor difficulties and 63% gross motor difficulties, and 34% had dysdiadochokinesia. The conduction delay within the peripheral nerve was related to the post-therapeutic interval after administration of vincristine and the lesions within the CNS to the number of injections of intrathecal methotrexate.
Conclusions:
The present results show adverse effects of the ALL treatment on the entire motor nervous pathways. In our experience, the measurement of MEPs by MS provides an objective, painless, and practical tool for assessing the treatment-related neurotoxicity in both the CNS and the peripheral nerves. These disturbances in the motor nervous pathways at the end of treatment raise the question of the long-term effects of ALL treatment on the motor nerve tracts, and have led us to employ MEPs to study these effects in long-term survivors of ALL.