Article Text

Hemiageusia from an ipsilateral multiple sclerosis plaque at the midpontine tegmentum
  1. ONOFRE COMBARROS,
  2. PASCUAL SÁNCHEZ-JUAN,
  3. JOSÉ BERCIANO
  1. Service of Neurology, University Hospital “Marqués de Valdecilla”, 39008 Santander, Spain
  2. Service of Clinical Neurophysiology
  1. Dr Onofre Combarros neuro{at}humv.es
  1. CARMEN DE PABLOS
  1. Service of Neurology, University Hospital “Marqués de Valdecilla”, 39008 Santander, Spain
  2. Service of Clinical Neurophysiology
  1. Dr Onofre Combarros neuro{at}humv.es

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The exact location of the pontine gustatory pathway has not yet been clarified, probably because there are so few studies of taste in patients with well localised brainstem lesions.1-3 Here we report on a patient with isolated hemiageusia and trigeminal sensory neuropathy from a single small pontine lesion.

A 46 year old woman experienced a burning sensation on the left side of the tongue. The next day she discovered a loss of taste on the entire left half of her tongue and numbness on the left side of her face. Neurological examination was normal except for hypaesthesia to pain, touch, and temperature sensation in all three divisions of the left trigeminal nerve, with decreased left corneal reflex and no weakness of masseters. Taste sensation was tested using separate solutions of 1.2 M NaCl, 0.47 M glucose, 0.17 M citric acid, and 2.52 mM quinine HCl. Marked disturbance on the left side involving the anterior two thirds and posterior one third of the tongue was noted with all four substances. Routine laboratory tests were normal. Analysis of CSF showed 8 lymphocytes/mm3, 46 mg/dl protein, increased quantitative intrathecal IgG, and oligoclonal bands. Visual evoked potentials, brainstem auditory evoked potentials, and somatosensory evoked potentials after both median and posterior tibial nerve stimulation were normal. The blink reflex was normal on stimulation on the right, and when stimulated on the left, there was no R1 component and R2 responses were elicited normally. Masseter reflex was absent on the left side. Brain MRI demonstrated multiple bilateral hyperintense white matter signals in periventricular distribution on T2 weighted images, and a hyperintense small lesion in the lateral part of the left midpontine tegmentum that showed enhancement after gadolinium injection (figure A and B). After intravenous high dose methylprednisolone therapy there was no immediate improvement of the patient′s neurological symptoms. In the follow up MRI after 3 months, the gadolinium enhanced pontine image had disappeared, the blink and masseter reflexes were normal, and trigeminal neuropathy and the taste disturbance had gradually reduced.

Gadolinium enhanced T1 weighted MRI of coronal (A) and axial (B) sections showing a high intensity lesion in the lateral portion of the left midpontine tegmentum. Diagram (C) showing the area clinically affected (shaded area). ML=medial lemniscus; CTT=central tegmental tract; Vs=trigeminal principal sensory nucleus; Vm=trigeminal motor nucleus.

The present case supports the finding that unilateral pontine lesions result in ipsilateral gustatory deficits, suggesting that gustatory fibres ascend from the solitary nucleus in the medulla up to the homolateral pontine tegmentum without decussating.1-3Lower midbrain level decussation is supported by a recent report.3 Topography of gustatory pontine fibres has been discussed in cases with taste disturbance,1 3 and, as found here, the absence of limb sensory involvement with normal somatosensory evoked responses contradicts the widely accepted notion that the pontine medial lemniscus conveys taste. On the other hand, Uesaka et al 2 described a patient who presented with ageusia and ipsilateral truncal ataxia presumably due to brachium conjunctivum involvement, and, therefore, it was suggested that the adjacent parabrachial nucleus might constitute a pontine taste area. Our patient developed left sided hemiageusia and trigeminal sensory disturbance, and electrical stimulation on the left elicited no R1 response and absence of masseter reflex. These electrophysiological abnormalities imply ipsilateral brainstem lesions at the trigeminal principal sensory and motor nuclei, respectively.4 Moreover, MRI confirmed the existence of a new gadolinium-enhanced demyelinating lesion in the left midpontine tegmentum. The precise correlation between our patient′s symptoms and the electrophysiological and MRI abnormalities indicates that the involvement of the central tegmental tract, which is the anatomical structure adjacent to the sensory and motor trigeminal nuclei at the midpontine level (figure C), is probably important in causing taste disturbance. According to this hypothesis, Norgren5 showed in primates that axons of neurons located in the solitary nucleus ascend in the central tegmental tract to the ventroposteromedial nucleus of the thalamus without terminating first in the pontine parabrachial nucleus.

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