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Compared with other neurological deficits in patients with stroke, clinicians often overlook taste disorders, even though more than 30% of patients with acute stroke have taste disturbances.1 Some authors have reported cases with bilateral taste disorders induced by a unilateral lesion in the brainstem, putamen, insular cortex or the parietal lobe. We present the first case of a bilateral taste disorder due to a unilateral paramedian thalamic infarction.
Case report
A 40s healthy person suddenly developed double vision on downward gaze and transient weakness of the right limbs. After 5 days, the patient became aware of paraesthesia and dullness of taste on both sides of the tongue. On the next day, the patient consulted our hospital and was admitted with a diagnosis of cerebral infarction.
The admission physical examination showed a blood pressure of 110/54 mm Hg, with a regular pulse of 60 beats/min. No abnormal sounds were heard on chest auscultation. On neurological examination, the patient was alert, and the visual fields were full. On downward gaze, the patient complained of double vision due to limitation of the left eye's downward movement. The pupils were isocoric, and both had prompt and complete light reflexes. The patient complained of paraesthesia and dullness of taste on both sides of the tongue. No abnormal findings were noted in the sensory and motor systems, including the deep tendon reflexes. Simple gait was stable and not ataxic.
The patient had a normal sinus rhythm; no atrial fibrillation was detected on either 12-lead electrocardiogram or 24 h Holter electrocardiogram monitoring. Transthoracic echocardiography was normal, and transesophageal echocardiography did not reveal an intracardiac right-to-left shunt or atherosclerotic lesions in the aortic arch. On electroencephalography, there were no epileptic discharges. Laboratory and haematological data were normal, including fibrinolytic and coagulation markers. Both lupus anticoagulant and antiphospholipid antibodies were negative. On brain diffusion-weighted MRI, there was evidence of an acute infarction in the paramedian region of the left thalamus (figure 1). Intra-arterial digital subtraction angiography (DSA) showed that the left posterior cerebral artery (PCA) had an irregular wall, and there was fenestration of the right PCA. On 3D-rotational DSA, an intimal flap was detected in the left PCA. Thus, a left perforating thalamic artery occluded by spontaneous dissection of the left PCA was diagnosed.
MRI fluid-attenuated inversion recovery image. A hyperintensity lesion can be seen in the paramedian lesion of the left thalamus.
Oral aspirin 100 mg/day was prescribed on the day of admission. The patient's sense of taste was evaluated using the filter paper disc method of a commercial assay kit (Taste Disk, Sanwa Chemicals, Nagoya, Japan). This kit can be used to distinguish each fundamental taste (sweet, salty, sour and bitter) in the various regions corresponding to the appropriate nerves. A severe taste disturbance was seen on both sides 11 days postinfarction. In chorda tympani nerve area, hypogeusia was seen only in the left side, while severe hypogeusia was seen in both sides of glossopharyngeal nerve and greater petrosal nerve area. The taste disturbance partially improved by the 20th postinfarction day; the patient's subjective taste perceptions and paraesthesia of tongue had almost completely recovered by then. No ischaemic events occurred during the patient's hospital stay, and the patient's visual disturbance also improved gradually.
Discussion
While hypogeusia caused by bilateral thalamic lesions was previously reported,2 this is the first case of bilateral hypogeusia caused by a unilateral thalamic infarction. The lesion included the ventral posteromedial nucleus, which was found to have a strong association with the sense of taste in cat experiments.
In previous reports, unilateral supratentorial lesions tend to cause both bilateral and unilateral dysgeusia, while unilateral brainstem lesions under the midbrain or the pons tend to cause unilateral dysgeusia. This is probably due to the anatomy of the gustatory pathways. Gustatory pathways from the facial nerve, the glossopharyngeal nerve and vagus nerve connect to the ipsilateral solitary nucleus. Then, the tract ascends via the medial lemniscus to the contralateral parietal operculum (Brodmann's 43rd field), through the contralateral ventral posterior medial nucleus of the thalamus. However, controversy exists about this aspect.3 The exact crossing area has also not yet been clarified.4 Some authors suggest that the crossing occurs in the upper pons or midbrain.
In our case, a unilateral thalamic lesion caused bilateral taste dysfunction. We propose three possible mechanisms for this patient's dysgeusia. First, there may be a gustatory tract located both on the ipsilateral side and on the contralateral side of the gustatory receptor.5 Second, the crossing site may be adjacent to the ventral posterior medial nucleus of the thalamus. Third, taste information from both sides of the tongue may be projected to the left insular cortex before ascending to the higher-order taste areas. However, the last hypothesis does not explain the cases reported with hemilateral dysgeusia due to supratentorial lesions on the left side.1
One of our patient's main symptoms was hypogeusia. Our patient was young and alert enough to complain of this subtle stroke symptom. The patient's dysgeusia improved over a short period of time, perhaps because of incomplete involvement of the unilateral gustatory tract. On the other hand, some authors have reported cases that lost weight over a period of years due to dysgeusia.
Our patient complained paraesthesia of tongue on admission. However, no objective trigeminal disorder was seen in sensory testing, and the symptoms decreased with improvement of taste disturbance. We speculated that severe taste disturbance might cause the subjective paraesthesia.
In conclusion, we report a case with left paramedian thalamic infarction who presented with bilateral hypogeusia. This case suggests the existence of a gustatory tract that ascends on the ipsilateral side from the solitary nucleus to the thalamus, or crosses near the level of the thalamus. To clarify the central gustatory pathway, patients' symptoms should be carefully elicited and the sense of taste examined, even in patients with stroke who do not complain of hypogeusia.
Footnotes
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.