12.1 Neurological Acute, Chronic, and Late Effects

CPHON Test Content Outline (TCO) IV.A.1 tests neurologic acute, chronic, and late effects of chemotherapy, radiation, corticosteroids, and central-nervous-system (CNS) surgery. It is not the emergency chapter. Full algorithms for increased intracranial pressure (ICP), status epilepticus, and posterior reversible encephalopathy syndrome (PRES) live later. Here the nurse names the exposure, watches the function that is failing, and keeps the child from falling or aspirating while the team holds, reduces, or rescues the drug.

A 4-year-old on acute lymphoblastic leukemia (ALL) induction who will not climb stairs, a 12-year-old who becomes confused during ifosfamide, and a 7-year-old who stops speaking two days after medulloblastoma resection are all neurologic-effect patients. Compare them with last week's developmental baseline, not with an adult Glasgow script and not with "chemo fatigue."

Vincristine neuropathy

Vincristine binds tubulin and injures long axons. Three maps matter at the chairside:

• Peripheral motor and sensory: lost Achilles reflexes, foot drop, a steppage gait, difficulty climbing stairs or rising from the floor, stocking-glove paresthesias. A preschooler may simply refuse to walk.
• Autonomic: constipation that progresses to ileus, abdominal distention, urinary retention. Constipation after vincristine is a neurologic effect, not a dietary inconvenience.
• Cranial: jaw pain during or after the dose, ptosis, hoarseness, vocal-cord paresis.

Start a bowel regimen (polyethylene glycol, senna as ordered) the day vincristine starts, not after three days without stool. Institute fall precautions. Involve physical therapy; an ankle-foot orthosis may be needed when foot drop appears. Report new foot drop, ileus, or jaw pain so the protocol can hold or reduce vincristine. Do not keep hanging the Friday dose because "everyone gets neuropathy." Recovery can take months and may be incomplete—that is a chronic effect. Hearing loss is a cochlear and eighth-cranial-nerve problem taught in the otologic chapter; mention it here only so you do not mislabel vincristine jaw pain as ototoxicity or skip audiology when platinum or cochlear radiation is also on the roadmap.

Methotrexate leukoencephalopathy and ifosfamide encephalopathy

Methotrexate given intrathecally (IT) or as high-dose intravenous therapy can injure white matter. Acute leukoencephalopathy appears during or shortly after a dose: stroke-like weakness, aphasia, seizures, or an abrupt change in school-age speech. Many episodes are transient; they are still not "attention-seeking." Hold further methotrexate, obtain urgent imaging as ordered, use seizure precautions, and continue serial neurologic checks. Subacute and chronic leukoencephalopathy—especially after methotrexate plus cranial radiation—leaves lasting white-matter change, processing-speed loss, and sometimes a stepwise cognitive decline. An 8-year-old who was bilingual and now searches for words weeks after high-dose methotrexate needs a neurologic workup, not a pep talk.

Ifosfamide encephalopathy is a different clock. The chloroacetaldehyde metabolite causes somnolence, confusion, hallucinations, cerebellar signs, or seizures during or within hours of the infusion. Renal impairment, prior platinum, and low albumin raise risk. Stop the remaining ifosfamide, protect the airway, and give methylene blue when the team orders it. Do not attribute new confusion on an ifosfamide day to hospital sleep or to an opioid dose that has not changed. Rising ICP can look sleepy too: a new unequal pupil, Cushing triad, or a falling Glasgow Coma Scale (GCS) is an emergency-chapter problem, not methylene blue by habit.

Steroid myopathy and mood

Dexamethasone and prednisone cause proximal myopathy and mood lability. Dexamethasone is often harsher on both. A 5-year-old on ALL induction who cannot rise from the toilet, who rages at night, and who has not slept is not "noncompliant." Teach families the mood window, pad the environment, do not force competitive physical education, and involve physical therapy. Do not stop corticosteroids abruptly—adrenal insufficiency is a separate endocrine trap. Psychosis and severe insomnia are reportable, not a reason to skip the next protocol day without the team.

Posterior fossa syndrome and radiation somnolence

After medulloblastoma or other midline posterior-fossa resection, posterior fossa syndrome (cerebellar mutism) often declares itself one to two days later. The child who spoke after anesthesia becomes mute or severely dysarthric, ataxic, hypotonic, emotionally labile, and may stop swallowing. This is not emergence delirium and not stubbornness. Protect the airway, treat aspiration risk, keep the child nothing-by-mouth until swallow is assessed, and start speech-language pathology, occupational therapy, and physical therapy. Tell the family that recovery takes weeks to months and may be incomplete. That teaching is TCO IV.A.1 symptom management; the tumor-staging chapter does not replace it.

Radiation somnolence syndrome appears about three to eight weeks after cranial radiation: profound sleepiness, anorexia, irritability, and sometimes low-grade fever. It is usually self-limited over days to a few weeks. Support hydration and school absence. Distinguish it from recurrence, meningitis, and rising ICP. Morning vomiting plus a new pupil change or a falling GCS is not somnolence syndrome. Escalate those findings to the emergency ICP pathway rather than coaching a nap.

Assessment, safety, and neurocognitive late effects

Serial assessment is the intervention. Use the GCS (eye, verbal, motor, with pediatric verbal modifications for preverbal children), pupil size and reactivity, and a developmental baseline: what could this child do last clinic visit? A toddler who stops using two-word phrases is a neurologic change even if the GCS is still 15. Safety is falls (neuropathy, myopathy, ataxia) and aspiration (mutism, cranial-nerve weakness, encephalopathy). Seizure precautions belong whenever leukoencephalopathy, ifosfamide, or a fresh posterior fossa is in play.

Neurocognitive late effects after CNS-directed therapy—IT methotrexate, high-dose methotrexate, cranial radiation, especially at a young age—cluster on attention, processing speed, and working memory. Full-scale IQ can look acceptable while the child cannot finish a timed test. Arrange neuropsychological testing and school supports: a 504 plan or individualized education program (IEP) with extra time, reduced load, and seating that helps attention. Do not wait for the child to fail a grade. Cochlear hearing loss is an overlap, not the whole story; send audiology rather than blaming "not listening" solely on cognition.

A blown pupil, Cushing triad, or hypertensive encephalopathy with visual change is not an IEP meeting. Signpost ICP, seizures, and PRES to their emergency sections and keep this chapter on the chronic watch, the hold, and the school plan.