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|LETTERS TO EDITOR
|Year : 2015 | Volume
| Issue : 6 | Page : 972-975
Ipsilateral hemisensory syndrome in a patient with lateral medullary infarction: A new sensory pattern
Rohan Mahale, Anish Mehta, R Srinivasa
Department of Neurology, MS Ramaiah Medical College and Hospital, Bengaluru - 560 054, Karnataka, India
|Date of Web Publication||20-Nov-2015|
Department of Neurology, MS Ramaiah Medical College and Hospital, Bengaluru - 560 054, Karnataka
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Mahale R, Mehta A, Srinivasa R. Ipsilateral hemisensory syndrome in a patient with lateral medullary infarction: A new sensory pattern. Neurol India 2015;63:972-5
|How to cite this URL:|
Mahale R, Mehta A, Srinivasa R. Ipsilateral hemisensory syndrome in a patient with lateral medullary infarction: A new sensory pattern. Neurol India [serial online] 2015 [cited 2020 Sep 29];63:972-5. Available from: http://www.neurologyindia.com/text.asp?2015/63/6/972/170070
Lateral medullary infarct (LMI) is the most common type of brain stem stroke and has been widely discussed in the literature. The sensory hallmarks of lateral medullary syndrome include a loss of spinothalamic sensation of the ipsilateral face and the contralateral hemi-body, usually seen in Wallenberg's syndrome. Magnetic resonance imaging (MRI) or clinical correlation studies have described different topographic patterns of the sensory abnormality in lateral medullary syndrome. Here, we report the case history of an elderly man who presented with acute onset vertigo with left hemi-ataxia. During his hospital stay, the patient developed left hemi-facial and hemi-body hypesthesia. Brain MRI revealed an infarct involving the left dorso-lateral aspect of the medulla oblongata, thus confirming the case to be a lateral medullary syndrome. The ipsilateral hemi-body sensory involvement in lateral medullary syndrome is uncommon and represents a distinct variant.
A 64-year-old man presented with a history of sudden onset giddiness of rotatory type and gait unsteadiness with a tendency to fall towards the left side for 1-day. The giddiness was continuous and was accompanied by multiple episodes of vomiting. There was no hearing loss, tinnitus, or speech disturbance. He had tremulousness of the left upper limb on target-oriented activities. On the second day of admission, he developed dysesthesia initially involving the left lower limb that gradually ascended to involve the upper limb and eventually the left-half of his face. Gradually, the dysesthesia turned into numbness. There was no dysphagia, dysphonia, or nasal regurgitation. He was a known hypertensive on medications but had no history of diabetes mellitus. General examination, vital parameters, and other system examination were unremarkable. On neurological examination, he was conscious and oriented. Speech was normal. Fundus examination and extraocular movements were normal. Horner's syndrome was absent. The pupils were equal and reactive. The touch and pain sensations over the left-half of the face were decreased. A fine, gaze-evoked jerky nonfatigable horizontal nystagmus to the left was also seen. There was no facial weakness, and soft palate and tongue moved normally. Motor examination revealed a normal tone, preserved muscle power, and normal deep tendon reflexes in all 4 limbs. Sensory examination showed hypoesthesia of the left hemi-trunk and left upper and lower limbs to touch and pain. Vibration and joint position sense were relatively preserved. Left sided finger-nose incoordination and impaired tandem gait with a tendency to sway towards the left were seen. Plantar response was flexor bilaterally. Brain MRI showed an infarct in the left dorso-lateral medulla with caudal extension. Magnetic resonance angiogram showed nonvisualization of the left vertebral artery [Figure 1]. The complete hemogram, blood sugar, lipid profile, renal, liver, and thyroid functions as well as echocardiogram were normal. He was treated with anti-platelet medication and received physiotherapy. The condition of the patient improved within a few days. He had mild numbness in the left extremities and mild ataxia at follow-up after 1 month.
|Figure 1: Brain magnetic resonance imaging: (a and b) diffusion-weighted imaging shows restriction in the left dorso-lateral medulla with caudal extension and also involving the paravermian region (red arrow); (c and d) apparent diffusion coefficient shows the corresponding hypointensity suggesting an acute infarct (red arrow); (i) magnetic resonance angiogram shows nonvisualization of the left vertebral artery with vertebro-basilar arterial irregularities.|
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In patients with LMI, various patterns of sensory abnormalities have been described. These variations in sensory abnormality are due to the different patterns of involvement of the medulla that can be either horizontal (ventral, dorsal, and lateral) or vertical (rostral and caudal). The more rostral and more ventral the lesion, the incidence of contralateral trigeminal nerve involvement simultaneously increases. The most common pattern of sensory abnormality is the loss of pain and temperature sensation on the ipsilateral side of the face and the contralateral body. Sensory loss can also involve touch sensations. This classic pattern (Wallenberg syndrome) is due to the involvement of the ipsilateral descending spinal tract and nucleus of the trigeminal nerve, as well as the crossed lateral spinothalamic tract. The anatomic localization in this type of sensory pattern is a far lateral medullary lesion (Stopford Type I). When the lesion is medio-lateral, the hypoalgesia is only contralateral, affecting the face, arm, and trunk (Stopford Type II). The ipsilateral side of the face is spared due to preservation of the descending spinal tract and nucleus of the trigeminal nerve. If the lesion extends medially, the crossed trigeminothalamic tract (which carries the pain and temperature sensation from the contralateral side of the face) may be involved, leading to a bilateral facial hypesthesia (Stopford Type III). The crossed ventral trigeminothalamic tract ascends onto the medial part of the spinothalamic tract and carries the pain and temperature sensation from the contralateral side of the face. Based on the vascular supply, the medulla can be divided into anterior-medial territory, anterior-lateral territory, and lateral territory. Anterior spinal and vertebral arteries supply these areas. Vaudens and Bogousslavsky described two patients with LMI presenting with a sensory loss of contralateral face–arm–trunk–leg with sparing of ipsilateral face (pure sensory pattern), which they classified as Type IV pattern of sensory loss in lateral medullary infarction. Zhang et al. described five patterns of sensory abnormality. Type I: Ipsilateral face and contralateral trunk and limbs; Type II: Ipsilateral face and contralateral face, trunk, and limbs; Type III: Contralateral face and body; Type IV: Ipsilateral face and contralateral trunk and leg; and, Type V: Contralateral face, arm, and upper trunk. The classical crossed sensory pattern or Zhang Type I was seen in only 26% and Zhang Type II was seen in 25% of the patients in a clinico-radiological study by Kim et al.
Our patient presented with vertigo with left hemi-ataxia and left hemi-hypesthesia including the ipsilateral face. There was no evidence of Horner's syndrome, palatal, pharyngeal, or laryngeal palsy. The clinical localization in such a scenario would be the right thalamo-capsular area (ventro-posterior thalamus and posterior limb of the internal capsule). However, brain MRI showed an infarct in the left dorso-lateral medulla. The MRI findings very well explain the presence of vertigo with nystagmus, left hemi-ataxia, and left face hypesthesia. The absence of Horner's syndrome, palatal, pharyngeal, or laryngeal palsy can be explained by the dorso-lateral involvement of the medulla. Horner's syndrome is uncommon when only the dorsal part of the medulla is involved. Dorso-lateral lesions tend to be more superficial and hence do not involve nucleus ambiguus, which is situated more deeply. The lesion involved the inferior cerebellar peduncle, vestibular nucleus, spinal tract and nucleus of the trigeminal nerve. The occurrence of ipsilateral hemi-body hypalgesia cannot be explained. Kim et al., reported patients with LMI with ipsilateral hemi-body sensory symptoms as an uncommon and distinct variant due to dorso-medial extension of the infarct involving ipsilateral dorsal column or decussating lemniscal fibers.
Different topographic patterns of the sensory abnormality have been described in LMI. However, ipsilateral thalamic syndrome-like sensory abnormality in LMI is uncommon and represents a distinct variant.
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