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Isolated hypesthesia in the right V2 and V3 dermatomes after a midpontine infarction localised at an ipsilateral principal sensory trigeminal nucleus
  1. T Kamitani1,
  2. Y Kuroiwa2,
  3. M Hidaka3
  1. 1Department of Neurology, Yokohama Miyazaki Hospital of Neurosurgery, Yokohama, Japan
  2. 2Department of Neurology, Yokohama City University Graduate School of Medicine, Yokohama, Japan
  3. 3Department of Neurosurgery, Yokohama Miyazaki Hospital of Neurosurgery, Yokohama, Japan
  1. Correspondence to:
 Dr T Kamitani
 Department of Neurology, Yokohama Miyazaki Hospital of Neurosurgery, 218-9 Kariba-cho, Hodogaya-ku, Yokohama, 240-0025 Japan; toshilhp.bias.ne.jp

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Isolated cranial nerve palsies are often attributed to lesions of the respective nerves along their extraaxial courses. However, ischaemic or haemorrhagic lesions of the brainstem also cause isolated cranial nerve palsies through involvement of the intraaxial segments of the respective nerves. Small lesions of the brainstem can affect the trigeminal nerve only, although isolated trigeminal nerve palsy occurs less frequently than third or sixth nerve palsy.1 A case of small medullary infarction was reported in this journal, involving the spinal trigeminal tract and nucleus and presenting as painful trigeminal sensory neuropathy. In this report, the patient presented with orofacial pain and abnormal sensation both of which were confined within ipsilateral maxillary (V2) and mandibular (V3) nerve distribution.2 A similar isolated sensory distribution in the V2 and V3 dermatomes was observed in our patient with a small dorsolateral midpontine infarction involving a principal sensory trigeminal nucleus. Our case was unique because light touch sensory deficit was restricted to the V2 and V3 dermatomes while the V1 dermatome remained intact. In a small number of previous reports, dorsolateral or entry zone infarction or bleeding at the midpons presented as isolated trigeminal nerve neuropathy which involved all trigeminal dermatomes, although some cases tended to show lesser involvement of the V1 dermatome and more marked involvement of the V2 and V3 areas.

Case report

A 51 year old man noticed a rubbing sensation on the right edge of his tongue. Then 9 days after onset, this abnormal sensation extended to the right half of his oral cavity including the tongue, gums, and buccal mucosa. The sensation gradually spread to the lower half of the face, from the mandibular nerve division (V3) to the maxillary nerve division (V2). When he woke up the next morning, he was aware of a slight diplopia lasting a few minutes.

At 2 weeks after onset, he visited our hospital because of hypesthesia in the right half of the oral cavity. He had no past history of stroke, hypertension, diabetes mellitus, or hyperlipidemia. A dental examination was normal. On neurological examination, light touch sensation was decreased in the V2 and V3 dermatomes of the right side of his face including the tongue, lips, upper and lower gums, and the hard palate. An evident boundary existed between the impaired sensory area (V2 and V3) and the intact sensory area (V1). Pinprick and temperature sensation were well preserved in the V2 and V3 areas. Slight weakness of the right masseter was detected. All modalities of sensation were preserved in the ophthalmic nerve division (V1). Corneal reflexes were normal. On examination of other cranial nerves we found no abnormalities, including eye movement and taste. Motor weakness of the trunk and the four extremities was not found. Jaw jerk and deep reflexes in the four limbs were normal. Truncal and limb ataxia was not seen. A blink reflex study showed no delayed latency of ipsilateral R1, R2, or contralateral R2 responses on stimulation of the left or right supraorbital nerve (V1). Brain magnetic resonance imaging (MRI) revealed a small T2 hyperintense lesion in the right dorsolateral pontine tegmentum (fig 1), but no additional lesions in the brain. By 3 weeks after onset, his sensory deficits to light touch and the slight weakness of the right masseter had disappeared, although paresthesia remained in the right V2 and V3 areas. Two months after onset, his subjective paresthesia was no longer present.

Figure 1

 (A) Axial T2* weighted image, (B) axial T2 weighted image, and (C) coronal T2 weighted image, taken 2 weeks after onset, showing a hyperintense lesion (arrow) in the right dorsolateral pontine tegmentum. Exrapontine trigeminal nerves are indicated by arrowheads. (D) A sketch of the intrapontine and extrapontine segments of trigeminal nerves and the trigeminal nuclei. The white thick line indicates the axial slice level used to obtain images (A) and (B). (E) A midsaggital view image with a white thick line indicating slices (A) and (B). (F) A neuroanatomical sketch corresponding to the MR imaging at slice “C”. 1, principal sensory trigeminal nucleus; 2, motor trigeminal nucleus; 3, middle cerebellar peduncle; 4, superior cerebellar peduncle.

A characteristic of our case was the restricted sensory impairment in the V2 and V3 dermatomes. The distribution of sensory deficits in our case, a dorsolateral pontine infarction, was very similar to that in a patient with a small medullary infarction reported by Nakamura et al.2 Our patient presented a rubbing sensation and decreased light touch sensation without pain, while the previous case presented orofacial pain and sensory deficit. Root fibres conveying impulses for tactile and pressure senses enter the principal sensory nucleus, while root fibres conveying impulses for pain and temperature senses enter the spinal trigeminal nucleus. The lesion in our case involved the principal sensory trigeminal nucleus and motor trigeminal nucleus, while the previous case involved the spinal trigeminal tract and nucleus. We assumed that the lesion in our case did not involve the tract or nucleus related to pain and temperature senses, because it was relatively small and located in a dorsolateral area of the midpons. For this reason, pain and temperature senses were preserved in our patient.

The size and location of the infarction in our case was very similar to that in a patient reported by Ishii et al.3 The sensory impairment in our case was restricted to the V2 and V3 dermatomes, while the previous case presented numbness and paresthesia over the left upper face, tongue, and buccal mucosa. The motor trigeminal nucleus was impaired in our case but not in the previous case. The lesion in our case was in a slightly dorsal location compared with the lesion of the previous case. The motor trigeminal nucleus was presumably affected in our case, since it is located on the dorsomedial side of the principal sensory trigeminal nucleus.

The most interesting finding of our case is that an evident boundary existed between the impaired sensory area (V2 and V3) and the intact sensory area (V1). As yet, it is not known whether or not a small lesion of the principal sensory nucleus can cause hypesthesia limited to the V2 and V3 areas based on “segmental distributions” of the face. Functional MRI activation was studied on brush or noxious stimulation of the V1, V2, and V3 areas of the face.4,5 However, somatotopic activation in the principal sensory trigeminal nucleus has been unsuccessful. According to Carpenter, neurons carrying sensation from the V1 area are localised in the most ventral part of the principal sensory nucleus, while the V2 and V3 areas are located more dorsally.6 The explanation for the deterioration of the tactical sense being limited to the V2 and V3 areas is that the lesion in our case involved the intermediate and dorsal portions of the principal sensory nucleus in which fibres of V2 and V3 terminate.

References

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