めまいを主訴とした交通外傷後低髄液圧症候群 (脳脊髄液減少症) の2症例

抄録

We herein describe two patients with cerebrospinal fluid (CSF) leakage after whiplash injuries, mainly complaining of dizziness and vertigo. After automobile rear-end collisions with whiplash injuries but without head trauma, both patients immediately suffered from headache, vertigo, dizziness, nausea, neck pain and cervico-brachialgia. Neurological examinations were normal in both patients, except for neck tenderness. The RI cisternographies revealed the early filling of bladders within 2 hours and definite CSF leakages at the cervicothoracic junction in one of the patients and at the lumbar portion in the other. The magnetic resonance (MR) images depicted downward displacement of the cerebellar tonsils and the brain stem, and narrowing of the lateral ventricles, presenting an acquired Arnold-Chiari malformation. The patients were consequently diagnosed as having the intracranial hypotension (or CSF hypovolemia) syndrome and underwent several epidural blood patch (EBP) therapies. Transiently their various symptoms improved, but were soon exacerbated once more and have continued until the present. In the electronystagmography (ENG) studies, spontaneous downward nystagmus was observed in a patient in the dark. In the eye-tracking test (ETT), the smooth pursuit was relatively preserved with a saccade superimposed. The most striking finding was that of optokinetic nystagmus (OKN). In both patients, the slow phase velocity was saturated below 60 degrees and could not hold the steady state level in response to a higher stimulus velocity. The frequency of slow phase nystagmus was remarkably reduced. In Cohen & Raphan's model, the slow phase of OKN is supposed to be composed of two components; one is the "direct pathway" which is responsible for a rapid rise. The other is the "indirect pathway" which contains the velocity storage integrator and is responsible for a slower rise and maintaining the slow phase velocity to the steady state level. Our findings suggested the deterioration of both pathways in the slow phase velocity of OKN, that is dysfunctions of the vestibulo-cerebellar interactions. In conclusion, the dizziness and vertigo in the currently reported CSF hypovolemic patients were presumed to be derived from the severe damage especially to the cerebellum and the brain stem, caused by the downward sagging of the brain structures.