Introduction: Opalski Syndrome is a rare type of stroke variant presenting with signs of lateral medullary syndrome plus ipsilateral hemiparesis. A confirmed myocardial infarction simultaneously occurring with this acute ischemic stroke syndrome makes this an even more challenging case of Cardiocerebral infarction. Case: The patient is a 48-year-old female, a known diabetic and asthmatic, and was seen due to a 3-day history of sudden onset of non-rotatory dizziness associated with diplopia, non-projectile vomiting, numbness of the left side of the face and lingual dysarthria. She was initially admitted in a primary hospital wherein she developed chest pain, dyspnea and diaphoresis. She was transferred and was received with findings of miosis of the left eye, rotational nystagmus, left dysmetria, decreased pain and temperature sensation on the right extremities, left central facial palsy, tongue deviation to the left side, left hemiparesis and upward Babinski on the left. We localize this lesion on the left lateral medullary area with involvement of the caudal left corticospinal tract. Hence, a clinical impression of Opalski Syndrome was made. This was confirmed with cranial MRI findings of T2/FLAIR hyperintense focus involving the left lateral aspect of the medulla. The patient’s Troponin I was also elevated and she was managed as a case of acute coronary syndrome - NSTEMI. Hence, a diagnosis of Type III Cardiocerebral infarction was made. Medical intervention was started with dual antiplatelet therapy and anticoagulation with noted clinical improvement. Conclusion This case report highlights the diagnosis of Opalski Syndrome in a patient also presenting with Cardiocerebral infarction. There should be prompt recognition of the following disease entities to have an effective treatment, avoid cardiac and neurologic sequelae, and achieve an overall favorable prognosis.
Lateral Medullary Syndrome

The Wallenberg's syndrome is produced by infarction of lateral medulla. Isolated ipsilateral axial lateropulsion without other common symptoms of Wallenberg syndrome has rarely been reported as manifestation of lateral medullary infarction. The responsible anatomical structure of ipsilateral axial lateropulsion is still uncertain. We describe a patient with lateral medullary infarction who present with isolated ipsilateral axial lateropulsion without other symptoms of Wallenberg syndrome.
Humans ; Infarction* ; Lateral Medullary Syndrome

OBJECTIVE: To evaluate quiet standing balance of patients with Wallenberg syndrome before and after rehabilitation. METHOD: Six patients with Wallenberg syndrome were enrolled within one month after being affected by an infarct of the lateral medulla. Quiet standing balance was assessed using posturography with eyes open and closed. The assessment was repeated after the patients had undergone rehabilitation treatment for three to nine months, and the results of the two assessments were compared. RESULTS: The quiet standing balance evaluation was performed by measurement of center of pressure (CoP) movement. In the initial test, the mean scores of mediolateral and anteroposterior speed, velocity movement, mediolateral and anteroposterior extent of CoP were all high, indicating impairments of quiet standing balance in the patients. After rehabilitation treatment, the anteroposterior speed and extent, the mediolateral speed and extent, and velocity moment of CoP showed statistically significant reductions in the eyes open condition (p<0.05), and the anteroposterior speed and extent and velocity moment of CoP had decreased in the eyes closed condition (p<0.05). Mediolateral speed and extent of CoP in the eyes closed condition had also decreased, but the reduction was not statistically significant. CONCLUSION: This study demonstrated improvements of quiet standing balance, especially anteroposterior balance, in patients with Wallenberg syndrome following rehabilitation. We suggest that balance training is important in the rehabilitation of Wallenberg syndrome and that, as an objective measure of balance status, posturography is useful in the assessment of quiet standing balance.
Eye ; Humans ; Lateral Medullary Syndrome

The lateral medullary syndrome, I. E. Wallenberg syndrome, presents with several forms of sensory deficits. However, the correlation between the sensory deficits and the MRI findings of the medulla has been rarely attempted. We studied 16 patients with lateral medullary infarction who showed appropriate MRI lesions and correlated their sensory findings with the MRI results. In order to examine the extent of lesion of medulla in the MRI, we divided the medulla into three parts, namely upper, middle, and lower parts. The patients exhibited six types of sensory manifestation. In brain MRI, five patients with uncrossed sensory deficit; three patients with contralateral sensory deficit involving only body; and one patient with contralateral sensory level on trunk showed a diagonal band, lateral, or combined lesion in the medulla. Four patients with crossed sensory deficit and one patient with ipsilateral sensory deficit involving only face showed a large, laterodorsal lesion in the medulla. Two patients without sensory deficit exhibited a dorsal lesion in the medulla. In conclusion, lateral medullary syndrome usually has a characteristic lesion in the MRI according to the sensory deficits.
Brain ; Humans ; Infarction ; Lateral Medullary Syndrome* ; Magnetic Resonance Imaging*

No abstract available.
Humans ; Infarction* ; Ischemic Attack, Transient* ; Lateral Medullary Syndrome ; Trigeminal Neuralgia*

Opalski syndrome is a rare lateral medullary infarction variant presenting with ipsilateral motor deficits known to be caused by involvement of the post-decussating pyramidal tract. Here, we report two rare cases of Opalski syndrome presenting as ipsilateral sensorimotor deficits in cerebral infarction.
Cerebral Infarction ; Infarction ; Lateral Medullary Syndrome ; Pyramidal Tracts

We studied three patients who developed left unilateral punctate keratitis after suffering left-sided Wallenberg Syndrome. A complex evolution occurred in two of them. In all cases, neurophysiological studies showed damage in the trigeminal sensory component at the bulbar level. Corneal involvement secondary to Wallenberg syndrome is a rare cause of unilateral superficial punctate keratitis. The loss of corneal sensitivity caused by trigeminal neuropathy leads to epithelial erosions that are frequently unobserved by the patient, resulting in a high risk of corneal-ulcer development with the possibility of superinfection. Neurophysiological studies can help to locate the anatomical level of damage at the ophthalmic branch of the trigeminal nerve, confirming the suspected etiology of stroke, and demonstrating that prior vascular involvement coincides with the location of trigeminal nerve damage. In some of these patients, oculofacial pain is a distinctive feature.
Aged ; Cornea/*pathology ; Diagnosis, Differential ; Female ; Humans ; Keratitis/diagnosis/*etiology ; Lateral Medullary Syndrome/*complications ; Middle Aged

No abstract available.
Hearing Loss ; Vestibular Neuronitis ; Vertigo ; Lateral Medullary Syndrome ; Cochlea ; Ear, Inner

Pure limb ataxia without other common symptoms of Wallenberg syndrome has rarely been reported as manifestation of lateral medullary infarction. We describe a patient with lateral medullary infarction who presented with almost isolated right limb(mainly lower limb) ataxia without usual symptoms such as hemibody sensory changes, dysphagia, hoarseness, hiccup, and Horner sign. The brain magnetic resonance image showed small ischemic lesion involving the dorsolateral portion of the medulla oblongata.
Ataxia ; Brain ; Deglutition Disorders ; Extremities ; Hiccup ; Hoarseness ; Humans ; Infarction ; Lateral Medullary Syndrome ; Magnetic Resonance Spectroscopy

Lateral medullary syndrome is famous for its unique symptom complex such as crossed sensory change or Homer syndrome, and thus hardly can be misdiagnosed. Though this syndrome has been reported to be able to accompany ipsilateral motor weakness, the sensory change of extremities is known to be almost always contralateral to the lesion. We recently experienced one case presented with weakness and dysmetria on the right associated with ipsilateral sensory change. But few days later, he showed additional neurologic signs compatible with right lateral medullary syndrome. Brain MRI showed rostro-caudally elongated lesion extending from right lateral medulla to the upper cervical cord. Here we suggest the probable neuroanatomical substrate for this symptom and clinico-radiologic relationship with previous literature.
Brain ; Cerebellar Ataxia ; Extremities ; Lateral Medullary Syndrome* ; Magnetic Resonance Imaging ; Neurologic Manifestations ; Stroke*