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CASE REPORT Table of Contents  
Ahead of print publication
Lateral medullary syndrome presenting as babinski–nageotte syndrome with ipsilateral upper motor neuron facial palsy

 Department of General Medicine, Government Medical College and Hospital, Chandigarh, India

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Date of Submission04-Jun-2022
Date of Decision20-Jul-2022
Date of Acceptance26-Jul-2022
Date of Web Publication12-Nov-2022


Babinski–Nageotte syndrome is one of the variants of lateral medullary syndrome (LMS) with contralateral hemiparesis along with classical LMS findings. The simultaneous occurrence of ipsilateral central facial nerve palsy and contralateral hemiparesis is an extremely rare occurrence in LMS. We report the case of a 46-year-old male who presented with complaints of acute onset of vertigo, right-sided (ipsilateral) Horner syndrome, facial sensory loss, upper motor neuron facial nerve palsy, ataxia, and left hemiparesis (contralateral). Magnetic resonance imaging brain suggested acute infarct of the right dorsal medulla and medial aspect of the right cerebellar tonsil with attenuation of the distal segment of the right vertebral artery and right posterior inferior cerebellar artery.

Keywords: Babinski–Nageotte syndrome, lateral medullary syndrome, posterior inferior cerebellar artery, supranuclear corticofacial fibers

How to cite this URL:
Dhir A, Gupta M, Aggarwal J. Lateral medullary syndrome presenting as babinski–nageotte syndrome with ipsilateral upper motor neuron facial palsy. APIK J Int Med [Epub ahead of print] [cited 2022 Dec 4]. Available from: https://www.ajim.in/preprintarticle.asp?id=361011

  Introduction Top

Lateral medullary syndrome (LMS) is a brainstem stroke syndrome associated with variable vascular pathology and clinical presentation. It occurs due to occlusion of the posterior inferior cerebellar artery (PICA) (10%), intracranial vertebral artery (67%), and rarely anterior inferior cerebellar artery,[1],[2] leading to acute infarct and damage to the lateral medulla and inferior part of the cerebellum.[3] The vascular causes include atherothrombotic or embolic occlusion, vertebral artery dissection, craniovertebral anomalies,[4] fibromuscular dysplasia, or Marfan's syndrome. The underlying risk factors may include hypertension, diabetes mellitus, smoking, and cocaine abuse.[1],[5],[6] Clinically, it is a triad consisting of Horner's syndrome, ataxia, and hypoalgesia of the ipsilateral face; however, it may present with an array of atypical manifestations[1] as highlighted in [Table 1].
Table 1: Clinical features in lateral medullary syndrome corresponding to the structures involved[1]

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The presence of ipsilateral upper motor neuron (UMN) facial palsy is unusual in LMS (23.5%)[1] and occurs due to the hypothetical facial nerve corticobulbar tract (CBT) fibers that descend till the ventromedial part of the upper medulla. These fibers decussate and ascend in the dorsolateral part of the medulla to synapse at the contralateral facial nucleus.[7] The presence of contralateral hemiparesis in LMS occurs in Babinski–Nageotte syndrome (BNS), another rare variant which involves the corticospinal tract before the decussation at the medulla. Here, we present the case of a 46-year-old male with uncharacteristic manifestations of LMS; notable being ipsilateral UMN facial palsy and left hemiparesis.

  Case Report Top

A 46-year-old male hypertensive and current smoker presented with sudden onset vertigo, inability to stand with a tendency to fall toward the right side, and left hemiparesis for the last 2 days. He had an episode of bilateral transient visual loss in the previous month which recovered spontaneously in minutes. On initial evaluation, the patient was conscious and oriented with Glasgow Coma Scale 15/15. His vital parameters were normal, pulse was regular at 88 beats/min, blood pressure – 140/80 mm Hg, respiratory rate – 16/min, oxygen saturation – 98% on room air and was afebrile.

On neurological examination, higher mental functions were intact except for dysarthria and nasal intonation of voice. He had right-sided partial ptosis with miosis and bilateral horizontal nystagmus with a fast component to the right side. The right nasolabial fold was absent, bilateral forehead wrinkles were preserved, and the angle of the mouth deviated to the left on active movement. There was reduced pain and temperature sensation on the right side of the face. Uvula and soft palate were shifted to the left side, and gag reflex was impaired.

In the left upper and lower limb, muscle power was 2/5 accompanied by an increased muscle tone and exaggerated deep tendon reflexes (3+) with extensor plantar response. The right side was unremarkable. No abnormal sensory examination was observed over the trunk and limbs. No bowel and bladder abnormalities were present. Cerebellar signs such as intention tremors, positive finger–nose test, and dysdiadochokinesia were elicitable on the right side. The gait could not be assessed. No signs of meningeal irritation were present. The rest of the systemic examination was unremarkable. Based on the history and examination, the lesion was localized to the medulla and right-side cerebellum with a possible diagnosis of brainstem stroke. Fundus examination was normal.

The findings of contrast-enhanced magnetic resonance imaging (MRI) brain were suggestive of acute infarct in the right dorsal medulla and the medial aspect of the right cerebellar tonsil with the attenuated distal part of right vertebral artery and right PICA on magnetic resonance angiography [Figure 1] and [Figure 2]. The carotid artery and vertebral artery Doppler suggested of atherosclerotic changes in common carotid vessels, but normal flow in the vertebral arteries. Electrocardiography and transthoracic echocardiography were normal. The laboratory investigations done during the hospital stay are listed in [Table 2]. These were essentially within normal limits.
Figure 1: Magnetic resonance imaging of the brain. Avid diffusion restriction in DWI involving the dorsal medulla on the right suggesting acute infarct. DWI: Diffusion-weighted image

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Figure 2: Magnetic resonance imaging of the brain. Avid diffusion restriction in the DWI sequence involving the medial aspect of the right cerebellar tonsil suggesting acute infarct. DWI: Diffusion weighted image

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Table 2: Laboratory investigations during the hospital stay

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Initial management included insertion of a nasogastric tube, Foley's catheter, and intravenous fluids in fusion. The patient was initiated on 150-mg aspirin, 75-mg clopidogrel, and 40-mg atorvastatin. During the follow-up at 6 weeks, the patient could walk to the outpatient department with a walking aid and follow-up MRI brain showed resolution of lesions as shown in [Figure 3] and [Figure 4].
Figure 3: Magnetic resonance imaging of the brain. No diffusion restriction in the DWI sequence in the dorsal medulla on follow-up at 6 weeks. DWI: Diffusion-weighted image

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Figure 4: Magnetic resonance imaging of the brain. No diffusion restriction in the DWI sequence in the right cerebellar tonsil on follow-up at 6 weeks. DWI: Diffusion-weighted image

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  Discussion Top

Some of the atypical findings such as contralateral hemiparesis, UMN-type facial nerve palsy, and partial Horner's syndrome in our patient with dorsal medullary infarction question the diagnosis of LMS. Chakraborty et al.[6] observed similar atypical features in LMS such as contralateral hemiparesis, UMN facial palsy, and partial Horner syndrome.

The presence of hemiparesis can be explained by the two clinical variants of LMS reported in the literature.[8] Opalski's syndrome presents with classical LMS findings and ipsilateral hemiparesis due to caudal extension of dorsal medulla infarct, which involves the corticospinal tract fibers after decussation in pyramids.[9] Contralateral hemiparesis was clarified by BNS which is characterized by contralateral hemiparesis with accompanying classical LMS findings. In BNS, corticospinal tracts are involved before the pyramid decussation at the medulla due to the extension of the infarct caudally.[10]

Ipsilateral UMN facial nerve palsy is due to the interruption of hypothetical looping of CBT fibers.[11] The partial ptosis in Horner's syndrome as evident in our case too can be attributed to descending sympathetic tract fibers which may get spared in dorsal medullary lesions because of relatively deeper location.[12]

Although LMS is commonly known as PICA syndrome, the most common vascular pathology is vertebral artery occlusion by atherothrombosis and in BNS variant, medullary penetrating arteries are involved (supply corticospinal tract fibers), thereby leading to hemiparesis.[6] In our case, the MRI angiography suggested the involvement of the right PICA and distal segment of the right vertebral artery. The Doppler of the bilateral common carotid artery suggested the presence of atheromatous plaques. In literature, MRI brain revealed diffusion restriction at the level of the dorsal medulla in diffusion-weighted images suggestive of acute infarct[10] which was evident in our case as well.

  Conclusion Top

In the abovementioned clinical scenario, because of the variations in the pathology of neuroanatomical structures, the atypical presentations and clinical variants of LMS can be evident. In our case, it was suggestive of BNS with UMN facial nerve palsy which is extremely rare. It is paramount to be aware of such neuroanatomical correlations for the identification of atypical variants of brainstem stroke for an early diagnosis and optimal management.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Venugopal K, Kushal DP, Shyamala G, Mohammed MZ, Naik S, Kumar DS. A stochastic variant of Wallenberg syndrome with ipsilateral central facial palsy. J Mahatma Gandhi Inst Med Sci 2016;21:140.  Back to cited text no. 1
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Sakai K, Hamaguchi T. Wallenberg's lateral medullary syndrome with facial palsy caused by anterior inferior cerebellar artery infarct. J Clin Neurosci 2014;2:122-3.  Back to cited text no. 2
Fisher CM, Tapia J. Lateral medullary infarction extending to the lower pons. J Neurol Neurosurg Psychiatry 1987;50:620-4.  Back to cited text no. 3
Ramaswamy S, Surendran D, Bammigatti C, Palamalai SR. A rare variant of the lateral medullary syndrome with craniovertebral junction and vascular anomalies. Neurol India 2020;68:934-6.  Back to cited text no. 4
[PUBMED]  [Full text]  
Srinivasan M, Bindu B, Gobinathan S, Balasubramanian S, Nithyanandam A, Shanbhogue KR. An unusual presentation of lateral medullary syndrome with Ipsilateral UMN facial palsy – An anatomical postulate. Ann Indian Acad Neurol 2005;8:37.  Back to cited text no. 5
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Chakraborty U, Banik B, Chandra A, Pal J. An atypical manifestation of lateral medullary syndrome. Oxf Med Case Reports 2019;2019:527-9.  Back to cited text no. 6
Park JH, Yoo HU, Shin HW. Peripheral type facial palsy in a patient with dorsolateral medullary infarction with infranuclear involvement of the caudal pons. J Stroke Cerebrovasc Dis 2008;17:263-5.  Back to cited text no. 7
Parathan KK, Kannan R, Chitrambalam P, Aiyappan SK, Deepthi N. A rare variant of Wallenberg's syndrome: Opalski syndrome. J Clin Diagn Res 2014;8:MD05-6.  Back to cited text no. 8
Pandey S, Batla A. Opalski's syndrome: A rare variant of lateral medullary syndrome. J Neurosci Rural Pract 2013;4:102-4.  Back to cited text no. 9
[PUBMED]  [Full text]  
Oruç S, Demirbaş H, Güzel A, Beker Acay M, Yaman M. Babinski-Nageotte syndrome diagnosed in postpartum period. Case Rep Neurol Med 2016;2016:5206430.  Back to cited text no. 10
Patten J. The brain stem. In: Patten J, editor. Neurological Differential Diagnosis. 2nd ed. London: Springer; 1996. p. 162-77.  Back to cited text no. 11
Kim JS. Pure lateral medullary infarction: Clinical-radiological correlation of 130 acute, consecutive patients. Brain 2003;126:1864-72.  Back to cited text no. 12

Correspondence Address:
Monica Gupta,
Department of General Medicine, Government Medical College and Hospital, Sector 32, Chandigarh - 160 030
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ajim.ajim_72_22


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

  [Table 1], [Table 2]


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