Yonsei Medical Journal Vol. 37, No. 1, 1996 Pure Motor Hemiplegia with Conjugate Lateral Gaze Palsy in Pontine Lacunar Infarction Ji Hoe Heo, Oh Young Bang, and Sun Ah Choi The combination of pure motor hemiplegia and horizontal gaze palsy is a rave but identifiable la- cunar syndrome. Among horizontal gaze palsies, one-and-a-half syndrome and abducens nerve palsy are reported to be associated with pure motor hemiplegia in pontine lacunar infarction. Although conjugate lateral gaze palsy is also hypothesized, pure motor hemiplegia with conjugate lateral gaze balsy has never been reported. We present a 75-year-old man who showed right hemiparesis and im- aired left horizontal conjugate eyeball movement. Both the findings of the brain CT scan and those of the MRI study were consistent with a small infarction in the left midpontine tegmentum. Mag- netic resonance angiography revealed no stenotic narrowing of the vertebrobasilar artery. Radiological Findings suggested that pure motor hemiplegia with conjugate lateral gaze palsy, in our patient, might have been produced by the occlusion of a single penetrating branch of the basilar artery. Key Words: Cerebrovascular disorders, cerebral infarction, hemiplegia, oculomotor palsy, pons Since the concept of lacunar syndromes was established in the 1960s by Fisher and his col- leagues, many new syndromes have been iden- tified (Fisher, 1991). Pure motor hemiplegia (PMH), in pontine lacunar infarction, is de- scribed as being associated with such oculo- motor disturbances as abducens nerve palsy and one-and-a-half syndrome (Fisher and Caplan, 1971; Hommel e al. 1990; Besson and Hommel, 1993). However, to the best of our knowledge, the combination of PMH and con- jugate lateral gaze palsy has never been re- ported. We present a patient who showed PMH and transient conjugate lateral gaze palsy from pontine lacunar infarction. The Received January 4, 1996 Accepted February 17, 1996 Department of Neurology and Brain Research Insti- tute, Yonsei University College of Medicine, Seoul, Korea Address redprint requests to Ji Hoe Heo, M.D. Depart- ment of Neurology and Brain Research Institute, Yonsei University College of Medicine, C.P.O. Box 8044, Seoul, Korea 86 probable pathogenic mechanism is also dis- cussed. CASE REPORT A 75 year-old right-handed diabetic man with a history of cigarette smoking and alco- hol drinking suddenly developed weakness in his right extremities, along with dysarthria. Three days later, on admission, his blood pres- sure was 120/80 mmHg, and his pulse was reg- ular at 72 beats per minute. The general physical examination was normal. He was alert, well oriented, and dysarthric. The pupils were isocoric and reactive to light. Horizontal conjugate eyeball movement was impaired. He was unable to move his eyes to the left past the midline. However, both right lateral conju- gate and vertical eyeball movements were normal and no nystagmus was observed. Mod- erate weakness was present in his right upper and lower extremities. There were no additional neurological abnormalities. His hori- Volume 37 PMH with Conjugate Lateral Gaze Palsy Fig. 1. Axial T.-weighted magnetic resonance imag- ing of the brain shows a lesion of small high signal intensity in the left midpontine teg- mentum, consistent with an infarction. zontal gaze palsy improved after a two week follow-up, when no gaze palsy was observed. The brain CT scan obtained immediately after admission and the follow-up MRI per- formed with a 1.5-T Signa (General Electrics) after 1.5 months showed a finding consistent with a small infarction in the left midpontine tegmentum (Fig. 1). Magnetic resonance angi- ography revealed no stenotic narrowing of the vertebrobasilar artery (Fig. 2). DISCUSSION The association of PMH and oculomotor palsy has rarely been reported in pontine la- cunar infarction. Since Fisher and Caplan (1971) reported a pathologically proven patient who showed PMH with one-and-a-half syndrome in pontine lacunar infarction, the association of PMH and horizontal gaze palsy has been recognized as a form of lacunar syndrome (Fisher, 1982). However, few pa- Number 1 Fig. 2. Magnetic resonance angiography shows neither occlusion nor stenotic narrowing of the ver- tebrobasilar artery. tients afflicted with PMH and abducens nerve palsy, and few with PMH and one-and-a-half syndrome were described (Fisher and Caplan, 1971; Hommel et al. 1990; Besson and Hommel, 1993), Although it is suggested that PMH with conjugate lateral gaze palsy is a possible form of lacunar syndrome in pontine infarction (Fisher, 1991), this exact combination has never been reported. Our patient is the first case to present as PMH with conjugate lateral gaze palsy from pontine lacunar infarction as demonstrated by CT scan and MRI. An infarct affecting the pontine gaze center as well as the pyramidal tract may produce a combination of PMH and conjugate lateral gaze palsy. A lesion, demonstrated by MRI in our patient, was in the left midpontine teg- mental area involving part of the pyramidal tract. The lesion was presumed to be just ventral to the nucleus reticularis tegmenti pontis to where efferent fibers from the corti- cal eye field project (Leichnetz et al. 1984). The transient nature of conjugate left lateral gaze palsy in our patient may be explained by bilateral cortical projections to the nucleus reticularis tegmenti pontis, or by an indirect 87 Ji Hoe Heo, et ai. involvement of the nucleus reticularis tegmenti pontis, or both. Besson and Hommel (1993) suggest that an infarct involving the pontine gaze center as well as the pyramidal tract is usually larger than a lacune and is usually caused by an oc- clusion either of the basilar artery or of the ostia of several paramedian arteries. However, in our patient, the size of the lesion was less than lcm in diameter, and located in the ter- ritory of an anterolateral penetrating pontine artery (Pullicino, 1993). Neither an occlusion nor a stenotic narrowing of the basilar artery was found. These radiological findings suggest that PMH with conjugate lateral gaze palsy in our patient was due to the occlusion of a sin- gle penetrating branch of the basilar artery, and this is consistent with the findings in the only pathologically proven case. with PMH and one-and-a-half syndrome (Fisher and Caplan, 1971). In conclusion, we demonstrate that pontine lacunar infarction may manifest with PMH with conjugate lateral gaze palsy by an occlu- sion of a single penetrating branch of the bas- - ilar artery. REFERENCES Besson G, Hommel M: Lacunar syndromes. Adv Neurol 62: 141-160, 1993 Fisher CM: Lacunar strokes and infarcts: a review. Neurology 32: 87 1-876, 1982 Fisher CM: Lacunar infarcts -a review. Cerebrovasc Dis 1: 311-320, 1991 Fisher CM, Caplan LR: Basilar artery branch oc- clusion: a case of pontine infarction. Neurology 21; 900-905, 1971 Hommel M, Besson G, Le Bas JF, Gaio JM, Pollak P, Borgel F, Perret J: Prospective study of la- cunar infarction using magnetic resonance im- aging. Stroke 21: 546-554, 1990 Leichnetz GR, Smith DJ, Spencer RF: Cortical pro- jections to the paramedian tegmental and basi- lar pons in the monkey. J Comp Neurol 228: 388-408, 1984 Pullicino PM: The course and territories of cere- bral small arteries. Adv Neural 62: 11-39, 1993 88 Volume 37