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The widespread use of MRI, allowing accurate localisation of brain lesions, particularly within the brainstem, tends to overshadow the usefulness of electrophysiology in evaluating functional loss. This is the case of the blink reflex which explores trigeminal and facial nerves, and the brainstem. Discrete lesions at sites along the structures involved in the reflex arc are associated with particular abnormalities of the blink reflex.1 Here we describe a patient with an isolated trigeminal sensory neuropathy in whom an abnormal blink reflex predicted the localisation of a brainstem lesion.
A 35 year old man reported acute onset of painless paraesthesiae in the ophthalmic territory of the left trigeminal nerve. Examination showed minimal hypaesthesia in the first division of the left trigeminal nerve, with preserved corneal reflex and with no other cranial nerve involvement, nor signs of long tract dysfunction. The blink reflex showed a consistent absence of RI response on the orbiculares oculi ipsilateral to the stimulated left supraorbital nerve. Stimulation of the right supraorbital nerve evoked normal R1 and R2 (ipsilateral and contralateral) responses. Brain MRI showed no supratentorial lesions. The only abnormality was a small hyperintense area in T2 weighted sequences in the left lateral upper pons, close to the entrance of the trigeminal nerve, slightly lateral to the principal sensory trigeminal nucleus (figure). Paraesthesiae resolved in 1 week, and there was full recovery of the R1 component of the blink reflex.
This case illustrates the anatomical and functional correlation between a focal demyelinating area next to the principal sensory trigeminal nucleus and the absence of the first component of the blink reflex. The R1, initially thought to be a myotatic response, is a cutaneous oligosynaptic reflex, the afferent arc of which travels in the supraorbital nerve and the efferent arc through the facial nerve. The central integration of this R1 component occurs at the level of the upper pons between the principal sensory nucleus of the trigeminal nerve and the nucleus of the facial nerve.2 Indeed, there is a correlation between the presence of a delayed (or absence) R1 response in patients with multiple sclerosis and clinical signs of pontine lesions.3 Studies of single pontine lesions demonstrated by MRI, or necropsy, and abnormal blink reflex have not been reported previously, although patients with isolated trigeminal sensory neuropathy and brainstem vascular lesions have been described.4 5 On the other hand, the R2 component of the blink reflex, a polysynaptic reflex, is integrated in the spinal nucleus of the trigeminal nerve establishing bilateral connections with facial nuclei in the pons. This is consistent with preserved ipsilateral and contralateral R2 responses in our patient. The present case further supports the concept that the absence of the first response of the blink reflex is highly suggestive of a pontine lesion, close to, or within, the principal sensory nucleus of the trigeminal nerve. It also illustrates the usefulness of a simple electrophysiological test in the evaluation of reversible dysfunction of the trigeminal nerve.
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