LAUSR

Pure sensory stroke (PSS) is one of the well-defined classic or typical lacunar syndromes described by Fisher [1]. The complete hemisensory syndrome (with a facio-brachio-crural distribution of the sensitive deficit) is the most frequent clinical presentation of PSS (more than 80% of the cases) [1, 2]. A lacunar infarction in the thalamic ventroposterior lateral nucleus is the most common cause of PSS [1–3]. We describe two patients presenting with unusual incomplete pure hemisensory symptoms due to medial lemniscus pontine lacune in whom MRI identified appropriate lesions. None of 19 consecutive incomplete pure sensory stroke patients from a total of 99 patients with pure sensory stroke included in our stroke registry over a 19-year period showed the pons as the brain lesion lacunar site. The present cases are the unique ones in our stroke registry that present incomplete pure sensory stroke related to pontine lacunar cerebral infarction, which may result in isolated pure sensory loss. Table 1 shows the demographic and clinical characteristics of the two patients of the study: patient case #1 was a 64-year old man with a history of arterial hypertension referred to our department because of a 24 h history of hemiparesthesia in his distal right arm and leg. Patient case #2 was a 61-year-old man with a past medical history of arterial hypertension and hyperlipidemia referred to our Department because of a 24-h history of numbness and tingling in his distal right arm. In both cases, symptoms developed without headache, nausea, vomiting, limb weakness or speech disturbances. They had no sensory disturbances in their facial or in ipsilateral leg or thoraco-abdominal anatomy (mRS = 1, NIHSS = 1). They had neither nuchal rigidity nor semiology of meningeal syndrome. The following investigations were normal or unremarkable: chest roentgenography, 12-lead electrocardiography, brain CT scan, two-dimensional echocardiography, and Doppler ultrasonography of the supra-aortic trunks, complete hematological screening, routine biochemical profile, urinalysis, serology for syphilis (VDRL), immunologic blood test (including ANA, ENA, lupus anticoagulant, IgG and IgM anticardiolipin antibodies, rheumatoid factor), basic hemostasis study and hypercoagulable panel (including protein C and S, antithrombin III, factor V Leiden mutation and homocysteine). The use of cocaine or other substances with vasoconstrictive properties as amphetamines was ruled out. Brain MRI on day 3 (case #1) and day 2 (case #2) after the stroke onset showed increased signal on FLAIR, and T2-weighted sequences and diffusion images involving the left medial lemniscus in dorsal paramedian pontine region compatible with an acute lacunar infarct (Fig. 1). Antiplatelet therapy with acetylsalicylic acid at doses of 100 mg/24 h was prescribed as secondary prevention of cerebral ischemia, together with strict control and treatment of cerebral vascular risk factors. The clinical course was favorable. A gradual regression of symptomatology was observed and, 1 month after onset in case #1 and 2 months after onset in case #2, focal neurological deficit was completely recovered (mRS = 0, NIHSS = 0). The pure sensory syndrome usually has a characteristic facio-brachio-crural distribution and a contralateral thalamic topography [1]. The presence of an incomplete sensory deficit is less frequent [2]. In a recent hospital series that analyzed patients admitted with a pure sensory syndrome, the incomplete distribution was observed only in 19% of the cases, [3] the partial lesion of the ventroposterior lateral thalamic nucleus being the most common lesion topography, and no patient had a contralateral brainstem lacunar infarct (LI) topography. Infrequently, it can * Adrià Arboix [email protected]