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CASE REPORT
Year : 2017  |  Volume : 6  |  Issue : 4  |  Page : 259-261

An unusual case of posterior circulation stroke


1 Consultant Neurologist, Amaravathi Hospitals, Guntur, India
2 Consultant Neurologist, Sai Bhaskara Hospitals, Guntur, India
3 Consultant Radiologist, Kamaraju Diagnostic Centre, Guntur, India
4 Department of General Medicine, Katuri Medical College, Guntur, India

Date of Web Publication26-Dec-2017

Correspondence Address:
Dr. A Haritha Chowdary
c/o A. Prabhakar Rao, D No: 5-72-16, Pandaripuram, 1st line, Guntur, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JDRNTRUHS.JDRNTRUHS_8_17

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  Abstract 


Anterior circulation strokes are far more common than posterior circulation strokes. Approximately 80–85% of all strokes are ischemic, and 20% of lesions occur in the vertebrobasilar territory. Most common cause of lateral medullary syndrome is vertebral artery occlusion. Although vertebral artery also supplies the spinal cord, involvement of the spinal cord in a case of lateral medullary syndrome has not been reported before. Pyramidal tract involvement in lateral medullary syndrome can occur due to medial extension of infarct in the medulla or caudal extension into the spinal cord. Here, we report an interesting case of lateral medullary syndrome caused by vertebral artery occlusion with cervical cord infarct presenting as quadriparesis.

Keywords: Acute quadriparesis, lateral medullary syndrome, vertebral artery occlusion


How to cite this article:
Tharaknath V R, Chowdary A H, Kumar K S, Navya L. An unusual case of posterior circulation stroke. J NTR Univ Health Sci 2017;6:259-61

How to cite this URL:
Tharaknath V R, Chowdary A H, Kumar K S, Navya L. An unusual case of posterior circulation stroke. J NTR Univ Health Sci [serial online] 2017 [cited 2020 Jul 13];6:259-61. Available from: http://www.jdrntruhs.org/text.asp?2017/6/4/259/221534




  Introduction Top


The vertebral arteries are branches from the Subclavian arteries and merge to form a single basilar artery. As the vertebrobasillar system, they supply the brain stem, spinal cord, cerebellum and posterior part of cerebrum. The lateral medullary syndrome is a clinical constellation of symptoms due to occlusion of vertebral artery or posterior inferior cerebellar artery or superior middle and inferior cerebellar artery. Although the vertebral artery also supplies the spinal cord, simultaneous involvement of corticospinal tracts and the lateral part of medulla is unusual.


  Case Report Top


A 51-year-old patient, a fruit vendor by occupation who was apparently normal, complained of neck pain on the right side followed by headache in the occipital region, giddiness, with two episodes of vomiting followed by altered sensorium; 24 h later, he became alert and was found to have weakness of all four limbs, vertigo, as well as dysphagia and dysarthria.

There was no history of seizure, fever, trauma, and vaccination. Patient was a diabetic since 1 year, and a known smoker and alcoholic.

On general examination, he was moderately built and nourished. Blood pressure was 200/100 mmHg, pulse rate 90/min, afebrile. On examination, he was conscious and oriented with dysarthric speech. He had mild ptosis on the right side with small pupil reacting to light. There was skewing of eyes with the right eye lower than the left with horizontal jerky nystagmus and a rotatory component. The corneal reflex was lost on the right side with decreased sensation of touch, pain, and temperature. There was right Upper Motor Neuron (UMN) facial weakness and right-sided palatal palsy.

Motor system examination revealed normal bulk with hypotonia. The power was 4/5 on the left side and 3/5 on the right side limbs. There was no sensory impairment in the limbs or trunk. Plantar reflex was extensor bilaterally with loss of abdominal and cremasteric reflexes. Deep tendon reflexes were normal and symmetrical.

On investigating, hemogram is in normal range with blood sugar 223 mg/dl, hypertriglyceridemia. Rest of the blood parameters and echo, electrocardiogram, chest X-ray, and color Doppler were all normal. Magnetic resonance imaging (MRI) sagittal section of the brain, MRI diffusion weighted imaging (DWI) of spinal cord, and MR angiogram were obtained [Figure 1], [Figure 2], [Figure 3], [Figure 4].
Figure 1: MRI brain sagittal section showing acute infarct in the medulla, cerebellum, and cervical spinal cord

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Figure 2: MRI DWI showing acute infarct in the cervical spinal cord

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Figure 3: Neck angiogram showing absence of the right vertebral artery

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Figure 4: MRI brain showing chronic infarcts in the right posterolateral medulla and right cerebellum

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A provisional diagnosis of right lateral medullary syndrome with quadriparesis was made. On follow-up, patient had improved and was able to walk independently and was able to swallow. He was left with hoarse voice and mild gait ataxia, but is able to earn his livelihood.


  Discussion Top


Lateral medullary syndrome (Wallenberg syndrome) is often secondary to posterior inferior cerebellar artery or vertebral artery occlusion.

On side of lesion.[1] [Table 1]
Table 1: On Side of Lesion

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On opposite side of lesion [Table 2]
Table 2: Opposite to Side of Lesion

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Most cases result from ipsilateral verterbral artery occlusion; in the remaining cases, posterior inferior cerebellar artery occlusion is responsible. Occlusion of medullary penetrating branches may result in partial syndromes. Hemiparesis is not a feature of vertebral artery occlusion; however, quadriparesis may result from occlusion of anterior spinal artery.[2]

Fisher et al. reviewed pathological findings of 432 patients of lateral medullary infarction and found PICA disease, vetebral artery disease, and involvement of both in 14.3%, 38.1%, and 26.2% respectively.[3]

There are many case reports suggesting the various patterns of presentation of lateral medullary infarction. However, Oplaski syndrome,[4] Babinski–Nageotte syndrome,[5] and lateral medullary syndrome is associated with hemiplegia. In Oplaski syndrome, hemiplegia is ipsilateral due to the extension of infarct caudally to involve the corticospinal fibres after the pyramidal decussation.[4] In Babinsk–Nageotta syndrome,[5] there is contralateral hemiparesis because the pyramidal tract is affected before decussation.

There can be proximal quadriparesis which is explained by involvement of medial medullary reticular formation, supporting a hypothesis of reticulospinal tract.[6]

In our patient, the occlusion of vertebral artery produced infarct in lateral medulla and infarcts in cervical spinal cord resulting in quadriparesis. To our knowledge, simultaneous infarcts in the medulla and spinal cord in a patient has not been reported previously in literature.

Declaration of patient consent

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

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Harrison's principles of internal medicine volume 2: Page 2576.  Back to cited text no. 1
    
2.
Harrison's principles of internal medicine volume 2: Page 2577.  Back to cited text no. 2
    
3.
Fisher CM, Karnes WE, Kubik CS. Lateral medullary infarction, patterns of vascular occlusion, J Neuropathol Exp Neurol 1961;20:323-79.  Back to cited text no. 3
    
4.
Opalski A. A new sub-bulbar syndrome: Partial syndrome of the posterior verterbro-spinal artery. Paris Med 1964:214-20.  Back to cited text no. 4
    
5.
Babinski J, Nageotte J. Hemiaynergine, lateroplsion et myosisbulbaries avec hemianesthesia et hemiplegia croisees. Rev Neurol 1902;10:358-65.  Back to cited text no. 5
    
6.
Chen CN, Khor GT, Chen CH, Huang P, Wallenberg's syndrome with pronimal quadriparesis. The Neurologist, 2011;17:44-6.  Back to cited text no. 6
    


    Figures

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

  [Table 1], [Table 2]



 

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