ABSTRACT Lateral medullary (or Wallenberg&apos;s) syndrome is characterized by vertigo, diplopia, dysarthria, Horner`s syndrome, numbness (ipsilateral face and contralateral limb) and traditionally it is not associated with any limb weakness. Localization in this syndrome is easy because of characteristic presentation, exclusive blood supply and very small area of involvement. In our case patient had features of lateral medullary syndrome with ipsilateral hemiparesis .In Opalski syndrome hemiplegia is ipsilateral due to the extension of the infarct caudally to involve the corticospinal fibers after the pyramidal decussation. Opalski syndrome is a rare variant of Wallenberg&apos;s syndrome with ipsilateral hemiparesis. It should not be diagnosed in the absence of hyperreflexia or Babinski sign. Excessive alcohol intake may play a role in the etiopathogenesis of posterior circulation stroke

Abhishek Ramakrishnan

Aravind R

C Ameen

Chitradatwant Manikandan

Kasha

Noorul Kh

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ISSN: 0975-8585 
May – June  2015  RJPBCS   6(3)  Page No. 1637 
Research Journal of Pharmaceutical, Biological and Chemical 
Sciences 
 
 
Interesting Case of Opalski Syndrome a Variant of Lateral Medullary 
Syndrome. 
 
 
KH Noorul Ameen, C Ramakrishnan, Abhishek Kasha*, V Chitradatwant Manikandan, and 
Aravind R. 
 
 
Department of General Medicine, Sree Balaji Medical College & Hospital, Bharath University, Chrompet, Chennai 600044, 
Tamil Nadu, India.  
 
 
ABSTRACT 
 
Lateral medullary (or Wallenberg's) syndrome is characterized by vertigo, diplopia, dysarthria, 
Horner`s syndrome, numbness (ipsilateral face and contralateral limb) and traditionally it is not associated 
with any limb weakness. Localization in this syndrome is easy because of characteristic presentation, exclusive 
blood supply and very small area of involvement. In our case patient had features of lateral medullary 
syndrome with ipsilateral hemiparesis .In Opalski syndrome hemiplegia is ipsilateral due to the extension of 
the infarct caudally to involve the corticospinal fibers after the pyramidal decussation. Opalski syndrome is a 
rare variant of Wallenberg’s syndrome with ipsilateral hemiparesis. It should not be diagnosed in the absence 
of hyperreflexia or Babinski sign. Excessive alcohol intake may play a role in the etiopathogenesis of posterior 
circulation stroke. 
Keywords: Hemiparesis, Lateral Medullary Syndrome, Opalski syndrome, Wallenberg’s syndrome, Babinski-
Nageotte syndrome , horners syndrome , nystagmus ,  
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
*Corresponding author 
 
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INTRODUCTION 
 
Lateral medullary (or Wallenberg's) syndrome is characterized by vertigo, diplopia, dysarthria, 
Horner`s syndrome, numbness (ipsilateral face and contralateral limb) and traditionally it is not associated 
with any limb weakness. Localization in this syndrome is easy because of characteristic presentation, exclusive 
blood supply and very small area of involvement. However in Opalski syndrome [1] and Babinski-Nageotte 
syndrome [2], lateral medullary syndrome is associated with hemiplegia. In Opalski syndrome hemiplegia is 
ipsilateral due to the extension of the infarct caudally to involve the corticospinal fibers after the pyramidal 
decussation [1]. In Babinski-Nageotte syndrome [2] there is contralateral hemiparesis because pyramidal tract 
is affected before decussation. 
    
We report a case of 50 yr old gentleman diabetic and hypertensive, presented to opd with complaints 
of giddiness three days, slight weakness of left upper and lower limb 3days. Numbness over left side of face 
and  right upper limbs & lower limbs 3days.patient was apparently normal 3days before , he developed 
giddiness which is acute in onset associated  with tinnitus , mild dysphagia to solids ,dysarthria which lasted for 
a day but vertigo was persistent in nature patient gives history of mild weakness of  left upper and lower limbs .
, unsteadiness while walking , decreased perception of sensation over right upper limbs and lower limbs , 
spillage of  water while drinking more on left side ,  slight deviation of angle of mouth to  right,  numbness over 
left side of face . No history of cough, hoarseness of voice, neck pain, no evidence of headache or vomiting and 
no fever during the period of illness. No bowel and bladder disturbance, no h/o trauma, seizures. Diabetic for 
the past 5yrs on OHA’s, hypertensive for the past 4yrs on tab.amlodipine 5mg once a day. No other significant 
past history. Family history not significant. Alcoholic and smoker for the past 20 yrs . Consumes  approximately 
360 ml of brandy per day thrice or more in week and a bundle of beedi per day.  On examination moderately 
built and nourished  pulse 84bpm , regular  BP 130/80 mm hg left upper limb in sitting position   130/80 mm hg 
right upper limb in sitting position . Patient is not pale / icteric ,no clubbing no cyanosis no edema no 
lymphadenopathy no neuro-cutaneous markers  ,HMF – conscious , oriented ,right handed , memory intact , 
dysarthria ,  cranial nerves - loss of pain and temperature over left half of the face , left side umn 7
th
  cranial 
nerve palsy  ,left horners syndrome (ptosis,miosis, decreased sweating) , nystagmus seen  rotatory left side , 
gag reflux diminished on left side , uvula deviated to right side. 
 
MRI brain with MRA features suggestive of acute infarct in left lateral medulla 
 
 
 
Spino motor system( reveled left hemiparesis ) bulk was normal on both sides , tone appears normal 
on both sides , power of 4/5 in both upper and lower limbs on left side with normal power on right side , 
reflexes brisk on left side upper and lower limbs with normal reflexes on right side , plantar extensor on left 
side .No involuntary movements, ataxic gait. 
 
Sensory loss over right half of body which included loss of pain and temperature sensation.  No 
sensory loss on left half of body, vibration and joint position sense were intact on both sides. Cortical sensation 
intact on both sides .cerebellar signs are present on left side.  Spine and cranium normal, no signs of meningeal 
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May – June  2015  RJPBCS   6(3)  Page No. 1639 
irritation, no trophic changes. Lungs were clear and heart sounds were normal .abdomen was soft, non-tender, 
no hepatomegaly no splenomegaly, bowel sounds were heard normally.  
 
Laboratory investigations revealed normal complete blood counts, esr with in normal limits, normal 
renal function, normal serum electrolytes. Urine routine analysis was normal, Liver function test revealed mild 
elevation of GAMA GGT, SGOT, SGPT.  USG abdomen revealed fatty liver. Blood sugars were within limits. Lipid 
profile was impaired. 
 
ECG was normal, 2d echo normal study , doppler study of carotids and vertebral artery was normal.  
 
This patient presented with all features of lateral medullary syndrome. In addition patient had 
ipsilateral hemiparesis (corticospinal tract involved) it is a variant of lateral medullary syndrome – opalski 
syndrome type 1 sensory variant. 
 
He was reassured  started on tab.aspirin 150mg once a day , tab.rosuvastatin 10mg hs, Tab.citicoline 
500mg twice a day , tab.enalapril 2.5mg twice a day ,continued oral hypoglycemic drugs ,physiotherapy  and 
diet management. Neurologist consultation was done. His general condition gradually improved and is in 
follow up with us. 
DISCUSSION 
 
Lateral Medullary Syndrome (LMS) was described by Wallenberg [3]. It is a relatively uncommon 
stroke with slight male sex preponderance [3,4]. The classical presentation consists of crossed sensory deficits, 
specifically loss of pain and temperature sensation affecting trunk and extremities contralateral to the infarct 
along with ipsilateral facial numbness. Other features of the syndrome include vertigo, nystagmus, hoarseness, 
dysphagia, ipsilateral cerebellar signs and Horner’s syndrome [4]. 
 
In most cases the diagnosis of LMS is made on the basis of classical clinical features and some authors 
even recommend delaying the MRI scan when the presentation is classical [5]. However, a wide variation has 
been recognised in the clinical presentation [5,6] and studies have demonstrated that the classical 
presentation is not seen most of the time. Hence, efforts have been made to classify LMS on the basis of 
pattern of sensory involvement [7], anatomical localisation [8] and radiological pattern of involvement [3]. 
 
The wide variation in sensory involvement has long been recognised and Zhang et al., described five 
patterns of sensory impairment [7]. 
 
Type 1: Ipsilateral face and contralateral trunk and limbs 
Type 2: Ipsilateral face and contralateral face, trunk and limbs 
Type 3: Contralateral face and body 
Type 4: Ipsilateral face and contralateral trunk and leg 
Type 5: Contralateral face, arm and upper trunk 
 
Our patient would come under classical or type 1 sensory involvement, as he presented with left 
sided face and right sided trunk and limb involvement. In clinico radiological correlation studies by Kim et al., 
only 26% of the patients presenting with the classical crossed sensory pattern or Zhang type 1 and 25% 
presented with Zhang type 2.This variation has been attributed to the different patterns of involvement of 
medulla classified horizontally as dorsal, ventral and lateral and vertically as rostral and caudal [4]. The more 
rostral lesions which tend to be more ventral presented with contralateral trigeminal nerve involvement while 
the more caudal and dorsolateral lesions tend to present classically as seen in our case [3]. 
 
The absence of the classical component of Wallenberg’s syndrome – Horner’s syndrome is also 
explained by this differential involvement. Kim et al., have demonstrated that Horner’s syndrome is 
uncommon when the dorsal part of medulla is involved, as seen in our patient [4]. It was also observed that 
dorsolateral lesions tend to be more superficial and hence do not involve nucleus ambiguous, which is situated 
more deeply [3]. This explains the absence of dysphagia and signs of palatal paralysis in our patient. The 
spontaneous facial pain experienced by our patient is part of some of the original descriptions of Wallenberg 
syndrome. It has been described as a burning type of pain which usually comes with the onset of symptoms. It 
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May – June  2015  RJPBCS   6(3)  Page No. 1640 
has been attributed to involvement of phylogenetically older pain pathway which receives fibres from both the 
spinothalamic tract and the trigeminal nerve [8]. 
 
The other additional feature in our patient was the presence of ipsilateral hemiparesis. This variant of 
Wallenberg’s syndrome was first described by Opalski in 1949[1]. Wallenberg’s syndrome with contralateral 
hemiplegia is called as Babinski Nageotte syndrome [2]. Some authors question the existence of hemiparesis as 
they attribute the weakness to represent a spinocerebellar hypotonic syndrome rather than represent a 
pyramidal tract involvement[3]. But the presence of Babinski sign in our patient suggests pyramidal tract 
involvement. In fact Hermann et al., have suggested that the eponym Opalski syndrome should be reserved 
only for those cases with ipsilateral hemiparesis with Babinski positivity and contralateral numbness [10]. 
 
The cause of hemiparesis remains controversial. Opalski attributed it to caudal extension of the 
infarct to involve corticospinal fibres after the decussation. But recent studies suggest that involvement of 
medullary penetrating arteries which supply the pyramidal fibres post decussation may be responsible. These 
arteries are a branch of the vertebral artery, which has been identified as being most common artery to be 
involved in Wallenberg’s syndrome [9]. 
 
Alcohol is not an established risk factor for stroke, specifically posterior circulation stroke. But, a study 
from China has suggested that incidence of posterior circulation stroke is twice as high in alcoholics when 
compared to general population [11]. More detailed studies are needed before we can establish the role of 
alcohol in posterior circulation stroke, but it is reasonable to say that it might have played a role in our patient. 
 
CONCLUSION 
 
LMS can have a diverse clinical presentation and the absence of the classical pattern should not defer 
one from diagnosing Wallenberg syndrome. Radiology helps in understanding how vascular lesion localisation 
can lead to changed presentation. Opalski syndrome is a rare variant of Wallenberg’s syndrome with ipsilateral 
hemiparesis. It should not be diagnosed in the absence of hyperreflexia or Babinski sign. Excessive alcohol 
intake may play a role in the etiopathogenesis of posterior circulation stroke. 
 
REFERENCES 
 
[1] Opalski A. Paris Med 1946:214–20. 
[2] Babinski J, Nageotte J. Rev Neurol (Paris) 1902;10:358–65. 
[3] Kim JS. Brain 2003;126:1864–72. 
[4] RL Sacco, L Freddo, JA Bello, et al. Arch Neurol 1993;50(6):609–14.  
[5] A Vrettos, K Fiotaki, E Galati, et al. BMJ Case Reports 2013 doi:10.1136/bcr-2012-006709.  
[6] P Cerrato, D Imperiale, M Bergui, et al. Stroke 2000;31(12):3064–66 
[7] SQ Zhang, MY Liu, B Wan, HM Zheng. Eur Neurol 2008;59(3-4):211–15.  
[8] RD Currier, CL Giles, RN Dejong. Neurology 1961;11:778–91. 
[9] S Pandey, A Batla. J Neurosci Rural Pract 2013;4(1):102–04.  
[10] DM Hermann, HH Jung, CL Bassetti. Eur J Neurol 2009;16(9):e72–4.  
[11] SS Yang, JP Jia. Zhonghua Yi Xue Za Zhi 2013;93(5):348–51.  
 


Interesting Case of Opalski Syndrome a Variant of Lateral Medullary Syndrome

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Interesting Case of Opalski Syndrome a Variant of Lateral Medullary Syndrome

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