Neurol Sci DOI 10.1007/s10072-014-1636-5
LETTER TO THE EDITOR
Lateral medullary infarction with ipsilateral hemiparesis, lemniscal sensation loss and hypoglossal nerve palsy Xiaodi Li • Yuzhou Wang
Received: 26 October 2013 / Accepted: 12 January 2014 Ó Springer-Verlag Italia 2014
Abstract Here, we present a rare case of a lateral medullary infarction with ipsilateral hemiparesis, lemniscal sensation loss and hypoglossal nerve palsy. In this case, we proved Opalski’s hypothesis by diffusion tensor tractography that ipsilateral hemiparesis in a medullary infarction is due to the involvement of the decussated corticospinal tract. We found that the clinical triad of ipsilateral hemiparesis, lemniscal sensation loss and hypoglossal nerve palsy, which had been regarded as a variant of medial medullary syndrome, turned out to be caused by lateral lower medullary infarction. Therefore, this clinical triad does not imply the involvement of the anteromedial part of medulla oblongata, when it is hard to distinguish a massive lateral medullary infarction from a hemimedullary infarction merely from MR images. At last, we suggest that hyperreflexia and Babinski’s sign may not be indispensable to the diagnosis of Opalski’s syndrome and we propose that ‘‘hemimedullary infarction with ipsilateral hemiparesis’’ is intrinsically a variant of lateral medullary infarction. Keywords Stroke
Ipsilateral hemiparesis Medulla oblongata
Dear Sir, Ipsilateral hemiparesis as a part of lateral medullary infarction (LMI) is rare, and is known as Opalski’s syndrome [1]. LMI presenting with ipsilateral hemiparesis, lemniscal sensation loss and hypoglossal nerve palsy has never been reported.
X. Li Y. Wang (&) Department of Neurology, Guangdong 999 Brain Hospital, Shatai Road, 578, Guangzhou 510510, China e-mail: [email protected]
A 35-year-old housewife suffered sudden onset of vertigo, nausea, gait disturbance and left facial numbness at home. She could still cope with daily housework, but 15 days later she developed dysarthria, dysphagia, hoarseness and left limbs weakness. Neurological examination after admission revealed left Horner syndrome, clockwise rotary nystagmus on horizontal gaze, right supranuclear facial weakness, and paralysis of left soft palate, left tongue, and left limbs (MRC grade:upper/lower, III/III). Pinprick and temperature sensations were decreased on her entire face and right hemibody. Position and vibration senses were also decreased on both feet and left hand. It was hard to evaluate coordination on the left side at that time, but it was found to be abnormal 1 month later. Deep tendon reflexes were decreased on the left side, but plantar responses were equivocal. MR imaging showed an acute infarction at left lateral medulla oblongata (Fig. 1a, b). An injury to the ipsilateral corticospinal tract caudal to the pyramidal decussation was responsible for ipsilesional hemiparesis and was detected by diffusion tensor tractography (Fig. 1c). Left vertebral artery was not visualized on MR angiography (Fig. 1d). The involvement of ipsilateral dorsal column or decussating lemniscal fibers may be responsible for ipsilateral lemniscal sensation loss. She received low-dose aspirin therapy and rehabilitation training for over 3 months, and her neurological deficits gradually resolved. She was able to walk at discharge. The ipsilateral hemiparesis in our case was demonstrated to be result of injuries to pyramidal tract below the decussation, which was characteristic for Opalski’s syndrome [1]. Kim [2] argued that pure limbs weakness without concomitant hyperreflexia and Babinski’s sign may represent a spinocerebellar hypotonic hemisyndrome. Hermann et al. [3] reviewed eleven cases and came to the same conclusion. As hyperreflexia and Babinski’s sign
123
Neurol Sci
Fig. 1 a, b T2-weighted MR imaging demonstrated acute infarction in the left lateral and posterior territory of the medulla, with the anteromedial territory spared. c Diffusion tensor tractography. The
lesion was located caudally to the decussation of the corticospinal tract. d MRA revealed the absence of signal in the left VA on day 13
were intermittent in such patients (including ours) [3], it seems that we have no alternatives but to exclude the involvement of spinocerebellar tracts to qualify for Opalski’s syndrome. Unfortunately mild hemiataxia was always accompanied by ipsilateral hemiparesis in them [3], making it fairly difficult. Besides, both the posterior and anterior spinocerebellar tracts were located adjacent to the pyramidal tracts in lateral caudal medulla. So we suggest that hyperreflexia and Babinski’s sign may not be indispensable to the diagnosis of Opalski’s syndrome. In our case we also found that the clinical triad of ipsilateral hemiparesis, lemniscal sensation loss and hypoglossal nerve palsy was intrinsically caused by infarction of the dorsomedial part, instead of the medial part of caudal medulla oblongata. Previously, these symptoms were thought to be characteristic for medial medullary infarction (MMI) and prompted a diagnosis of hemimedullary infarction (HMI) when present in massive LMIs [4]. Interestingly neither ipsilateral lemniscal sensation loss nor ipsilateral hemiparesis has ever been reported in MMIs before [5]. But they were reported in LMIs [2] now and then. So it is plausible to raise the hypothesis that when a LMI extended caudally, the major part or roughly the hemi half of the lower medulla would be involved and resulted in ipsilateral hemiparesis, lemniscal sensation loss,
and hypoglossal nerve palsy, namely ‘‘HMI with ipsilateral hemiparesis’’ [4]. In other words, ‘‘HMI with ipsilateral hemiparesis’’ may be essentially a variant of LMI. In conclusion, here we present a patient of LMI with alternating and dissociating sensorimotor deficits both on face and in limbs. The clinical triad of ipsilateral hemiparesis, lemniscal sensation loss and hypoglossal nerve palsy do not necessarily imply that the infarction extends beyond the lateral medulla oblongata.
123
References 1. Opalski A (1946) Un nouveau syndrome sous-bulbaire partiell’arte´re verte´bro-spinale poste´rieure. Paris Med 1:214–220 2. Kim JS (2001) Sensory symptoms in ipsilateral limbs/body due to lateral medullary infarction. Neurology 57:1230–1234 3. Hermann DM, Jung HH, Bassetti CL (2009) Lateral medullary infarct with alternating and dissociated sensorimotor deficits: Opalski’s syndrome revisited. Eur J Neurol 16(4):e72–e74 4. Porto FH, da Silva SP, Orsini M et al (2009) Hemimedullary infarct with ipsilateral hemiplegia: a vertebral artery dissection syndrome? J Neurol Sci 278:135–137 5. Kim JS, Han YS (2009) Medial medullary infarction: clinical, imaging, and outcome study in 86 consecutive patients. Stroke 40:3221–3225
LETTER TO THE EDITOR
Lateral medullary infarction with ipsilateral hemiparesis, lemniscal sensation loss and hypoglossal nerve palsy Xiaodi Li • Yuzhou Wang
Received: 26 October 2013 / Accepted: 12 January 2014 Ó Springer-Verlag Italia 2014
Abstract Here, we present a rare case of a lateral medullary infarction with ipsilateral hemiparesis, lemniscal sensation loss and hypoglossal nerve palsy. In this case, we proved Opalski’s hypothesis by diffusion tensor tractography that ipsilateral hemiparesis in a medullary infarction is due to the involvement of the decussated corticospinal tract. We found that the clinical triad of ipsilateral hemiparesis, lemniscal sensation loss and hypoglossal nerve palsy, which had been regarded as a variant of medial medullary syndrome, turned out to be caused by lateral lower medullary infarction. Therefore, this clinical triad does not imply the involvement of the anteromedial part of medulla oblongata, when it is hard to distinguish a massive lateral medullary infarction from a hemimedullary infarction merely from MR images. At last, we suggest that hyperreflexia and Babinski’s sign may not be indispensable to the diagnosis of Opalski’s syndrome and we propose that ‘‘hemimedullary infarction with ipsilateral hemiparesis’’ is intrinsically a variant of lateral medullary infarction. Keywords Stroke
Ipsilateral hemiparesis Medulla oblongata
Dear Sir, Ipsilateral hemiparesis as a part of lateral medullary infarction (LMI) is rare, and is known as Opalski’s syndrome [1]. LMI presenting with ipsilateral hemiparesis, lemniscal sensation loss and hypoglossal nerve palsy has never been reported.
X. Li Y. Wang (&) Department of Neurology, Guangdong 999 Brain Hospital, Shatai Road, 578, Guangzhou 510510, China e-mail: [email protected]
A 35-year-old housewife suffered sudden onset of vertigo, nausea, gait disturbance and left facial numbness at home. She could still cope with daily housework, but 15 days later she developed dysarthria, dysphagia, hoarseness and left limbs weakness. Neurological examination after admission revealed left Horner syndrome, clockwise rotary nystagmus on horizontal gaze, right supranuclear facial weakness, and paralysis of left soft palate, left tongue, and left limbs (MRC grade:upper/lower, III/III). Pinprick and temperature sensations were decreased on her entire face and right hemibody. Position and vibration senses were also decreased on both feet and left hand. It was hard to evaluate coordination on the left side at that time, but it was found to be abnormal 1 month later. Deep tendon reflexes were decreased on the left side, but plantar responses were equivocal. MR imaging showed an acute infarction at left lateral medulla oblongata (Fig. 1a, b). An injury to the ipsilateral corticospinal tract caudal to the pyramidal decussation was responsible for ipsilesional hemiparesis and was detected by diffusion tensor tractography (Fig. 1c). Left vertebral artery was not visualized on MR angiography (Fig. 1d). The involvement of ipsilateral dorsal column or decussating lemniscal fibers may be responsible for ipsilateral lemniscal sensation loss. She received low-dose aspirin therapy and rehabilitation training for over 3 months, and her neurological deficits gradually resolved. She was able to walk at discharge. The ipsilateral hemiparesis in our case was demonstrated to be result of injuries to pyramidal tract below the decussation, which was characteristic for Opalski’s syndrome [1]. Kim [2] argued that pure limbs weakness without concomitant hyperreflexia and Babinski’s sign may represent a spinocerebellar hypotonic hemisyndrome. Hermann et al. [3] reviewed eleven cases and came to the same conclusion. As hyperreflexia and Babinski’s sign
123
Neurol Sci
Fig. 1 a, b T2-weighted MR imaging demonstrated acute infarction in the left lateral and posterior territory of the medulla, with the anteromedial territory spared. c Diffusion tensor tractography. The
lesion was located caudally to the decussation of the corticospinal tract. d MRA revealed the absence of signal in the left VA on day 13
were intermittent in such patients (including ours) [3], it seems that we have no alternatives but to exclude the involvement of spinocerebellar tracts to qualify for Opalski’s syndrome. Unfortunately mild hemiataxia was always accompanied by ipsilateral hemiparesis in them [3], making it fairly difficult. Besides, both the posterior and anterior spinocerebellar tracts were located adjacent to the pyramidal tracts in lateral caudal medulla. So we suggest that hyperreflexia and Babinski’s sign may not be indispensable to the diagnosis of Opalski’s syndrome. In our case we also found that the clinical triad of ipsilateral hemiparesis, lemniscal sensation loss and hypoglossal nerve palsy was intrinsically caused by infarction of the dorsomedial part, instead of the medial part of caudal medulla oblongata. Previously, these symptoms were thought to be characteristic for medial medullary infarction (MMI) and prompted a diagnosis of hemimedullary infarction (HMI) when present in massive LMIs [4]. Interestingly neither ipsilateral lemniscal sensation loss nor ipsilateral hemiparesis has ever been reported in MMIs before [5]. But they were reported in LMIs [2] now and then. So it is plausible to raise the hypothesis that when a LMI extended caudally, the major part or roughly the hemi half of the lower medulla would be involved and resulted in ipsilateral hemiparesis, lemniscal sensation loss,
and hypoglossal nerve palsy, namely ‘‘HMI with ipsilateral hemiparesis’’ [4]. In other words, ‘‘HMI with ipsilateral hemiparesis’’ may be essentially a variant of LMI. In conclusion, here we present a patient of LMI with alternating and dissociating sensorimotor deficits both on face and in limbs. The clinical triad of ipsilateral hemiparesis, lemniscal sensation loss and hypoglossal nerve palsy do not necessarily imply that the infarction extends beyond the lateral medulla oblongata.
123
References 1. Opalski A (1946) Un nouveau syndrome sous-bulbaire partiell’arte´re verte´bro-spinale poste´rieure. Paris Med 1:214–220 2. Kim JS (2001) Sensory symptoms in ipsilateral limbs/body due to lateral medullary infarction. Neurology 57:1230–1234 3. Hermann DM, Jung HH, Bassetti CL (2009) Lateral medullary infarct with alternating and dissociated sensorimotor deficits: Opalski’s syndrome revisited. Eur J Neurol 16(4):e72–e74 4. Porto FH, da Silva SP, Orsini M et al (2009) Hemimedullary infarct with ipsilateral hemiplegia: a vertebral artery dissection syndrome? J Neurol Sci 278:135–137 5. Kim JS, Han YS (2009) Medial medullary infarction: clinical, imaging, and outcome study in 86 consecutive patients. Stroke 40:3221–3225
