Syndromes of posttraumatic neurological deterioration in children with no focal lesions revealed by cerebral imaging: evidence for a trigeminovascular pathophysiology.
Palavras-chave
Resumo
OBJECTIVE
To explain the pathophysiology of the neurological deterioration that occurs after trivial head injuries in children and that is not caused by focal structural brain damage. Symptoms and/or signs include headache, confusion, drowsiness, vomiting, hemiparesis, cortical blindness, and seizures.
METHODS
We propose that children who are susceptible to such neurological attacks have an unstable "trigeminovascular reflex," which is activated by craniofacial trauma.
BACKGROUND
After posttraumatic mechanical stimulation and activation of a defective or immature "excitable" trigeminovascular system, release of perivascular vasodilatory peptides causes cerebral hyperemia, which underlies the neurological deterioration.
CONCLUSIONS
The original assumption that underlying cerebral edema was responsible for these phenomena has been proven incorrect by computed tomography. Subsequent proposed pathophysiological mechanisms include cortical spreading depression and trauma-triggered migraine. Recent research has implicated the trigeminovascular pathways in both these conditions and documented that head trauma can be associated with noncongestive cerebral hyperemia (i.e., not causing swelling). Thus, we propose that head trauma activates trigeminal nerve endings in face, scalp, dura, or cortex and, via a reflex, causes intracranial vasodilation and cerebral hyperemia. Drugs that block trigeminovascular activation might offer a benefit.
