Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 
  • Users Online: 477
  • Home
  • Print this page
  • Email this page
Cover page of the Journal of Health Sciences

 Table of Contents  
Year : 2017  |  Volume : 10  |  Issue : 3  |  Page : 340-342

Concurrent infarction in bilateral middle cerebellar peduncles: Rare presentation of stroke

Department of Neurology, SMS Medical College, Jaipur, Rajasthan, India

Date of Web Publication5-Sep-2017

Correspondence Address:
Ankur Garg
Department of Neurology, SMS Medical College, Jaipur, Rajasthan
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/kleuhsj.kleuhsj_50_17

Rights and Permissions

Although some pathologies like demyelination have predilection for middle cerebellar peduncles (MCPs), infarction of bilateral MCP simultaneously is an exceedingly rare presentation of stroke. Patient was a 70-year-old smoker and hypertensive male presented with acute onset vertigo, imbalance while walking and slurred speech for 2 days and examination revealed horizontal nystagmus bilaterally, scanning speech with cerebellar signs and Modified Rankin Score (MRS) of 3. Magnetic resonance imaging brain showed symmetrical areas of diffusion restriction in both MCP, and there was occlusion of bilateral vertebral arteries (partial occlusion of right and complete occlusion of left) and basilar artery in computed tomography angiography. Oral antiplatelet with antihypertensive medication was started along with gait training and speech therapy. Patient had gradual and significant recovery and his MRS improved to 2 after 3 months' follow-up. Hypoperfusion along with atherothrombotic occlusion of vessels can be probable explanation to the bilateral infarction in MCPs which forms important watershed zone in posterior circulation of the brain.

Keywords: Bilateral infarction, hypoperfusion, middle cerebellar peduncles, watershed

How to cite this article:
Sharma CM, Kumawat BL, Garg A, Sharma V. Concurrent infarction in bilateral middle cerebellar peduncles: Rare presentation of stroke. Indian J Health Sci Biomed Res 2017;10:340-2

How to cite this URL:
Sharma CM, Kumawat BL, Garg A, Sharma V. Concurrent infarction in bilateral middle cerebellar peduncles: Rare presentation of stroke. Indian J Health Sci Biomed Res [serial online] 2017 [cited 2020 Jun 4];10:340-2. Available from: http://www.ijournalhs.org/text.asp?2017/10/3/340/214005

  Introduction Top

The aphorism of neuroradiology that differential diagnosis is narrowed down when the specific sites are involved is truly applicable to involvement of the bilateral middle cerebellar peduncles (MCPs).[1],[2] The MCPs carry main afferents to cerebellum, and being the white matter tracts, they have predilection for demyelinating or neurodegenerative disorders, but ischemic cerebrovascular diseases can also involve bilateral MCPs rarely, which can be explained by some intriguing abnormalities of posterior circulation of the brain.[1],[2] This syndrome of concurrent bilateral MCP infarction is exceedingly rare, reported in only few case reports [3],[4],[5] in the literature, which will be further enriched through the present case in which stroke is apparently caused by involvement of bilateral vertebral arteries and basilar artery simultaneously.

  Case Report Top

A 70-year-old male, a known hypertensive and chronic smoker, presented with acute onset vertigo accompanied by imbalance while walking and slurring of speech for 2 days. Vertigo was persistent, not related to change in posture and associated with two episodes of vomiting. He was unable to maintain the balance while walking with swaying to both sides, and according to his relative, his gait resembled a drunken person. On examination, pulse rate was 88/min, with regular rhythm and normal force and volume. Blood pressure was 168 mmHg systolic and 96 mmHg diastolic. There was no evidence of systemic atherosclerosis other than arcus senilis. Neurological examination revealed scanning speech with bilateral horizontal grade one nystagmus without any other cranial nerve involvement. Cerebellar signs were evident symmetrically on both sides with truncal ataxia. The National Institutes of Health Stroke Scale was 4 on presentation while Modified Rankin Score (MRS) was 3.

All metabolic profiles including blood sugar, lipid profile, renal function tests, liver function tests as well as thyroid profile, and antinuclear antibodies were within normal range. Magnetic resonance imaging (MRI) of the brain done on day 2 revealed symmetrical hyperintensities in both MCPs on T2-weighted images with diffusion restriction and corresponding fall in apparent diffusion coefficient images without any contrast enhancement with gadolinium. In addition, a small right pontine lesion of similar signal characteristics was also seen [Figure 1]a and [Figure 1]b. No other signal abnormalities were evident on MRI. Computed tomography angiography (CTA) of the neck and brain vessels on day 5 revealed complete occlusion of the left vertebral and partial occlusion of the right vertebral arteries above V4 level. The basilar artery was partially occluded with beaded appearance and visualized through the collateral circulation proximal to the occlusion of the vertebral arteries [Figure 1]c and [Figure 1]d. Cardiology workup including electrocardiogram, two-dimensional and transesophageal echocardiography, and prolonged Holter monitoring was also normal. The patient was given option for digital subtraction angiography for further confirmation of angiographic findings but patient denied for same.
Figure 1: (a and b) Magnetic resonance imaging brain showing diffusion restriction in bilateral middle cerebellar peduncle with corresponding fall in apparent diffusion coefficient maps suggestive of infarction, (c and d) computed tomography angiography of neck and brain vessels showing occlusion of bilateral vertebral artery and beaded appearance of basilar artery

Click here to view

Patient received oral antiplatelets (aspirin 325 mg/day), antihypertensive, and other symptomatic medications. Furthermore, patient underwent gait training and enrolled for speech therapy. Patient had significant improvement in his symptoms in follow-up, and MRS was improved to 2 after 3 months of follow-up.

  Discussion Top

The MCP receives its blood supply from anterior inferior cerebellar artery (AICA) supported by superior cerebellar artery and forms a watershed zone.[1],[2] Hypoperfusion or alternation in AICA, vertebral arteries, basilar artery, or a combination of these arteries [3],[4],[5] may hamper this watershed area and lead to infarction in unilateral or rarely bilateral MCPs. Differential diagnosis for diffusion restriction in bilateral MCPs can include acute toxic leukoencephalopathy (e.g., heroin intoxication), acute osmotic demyelination syndrome, early stages of Wilson's disease or  Wallerian degeneration More Details of MCP after 3–4 weeks of acute pontine insult,[2] but these all conditions can be easily ruled out on basis of history and evidence of alternation in vessels of posterior circulation on CTA.

The mechanisms leading to simultaneous bilateral infarction of MCPs have been proposed previously in literature only as a few case reports.[3],[4],[5] Kataoka et al.[4] attributed this condition to acute occlusion of dominant vertebral artery while John et al.[3] showed alternation in bilateral vertebral arteries and basilar artery as a cause of bilateral MCP infarction and proposed hypoperfusion as a possible mechanism leading this watershed zone infarct. Akiyama et al.[5] reported a similar case, but traumatic vertebral artery dissection was the cause of MCP infarction in that case. In contrast to previous reports, mechanism of stroke in the present case can be attributed to both mechanisms, i.e., decreased flow in bilateral AICAs due to basilar artery occlusion and hypoperfusion due to bilateral vertebral artery disease leading to watershed zone infarct in the bilateral MCPs.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Okamoto K, Tokiguchi S, Furusawa T, Ishikawa K, Quardery AF, Shinbo S, et al. MR features of diseases involving bilateral middle cerebellar peduncles. AJNR Am J Neuroradiol 2003;24:1946-54.  Back to cited text no. 1
Morales H, Tomsick T. Middle cerebellar peduncles: Magnetic resonance imaging and pathophysiologic correlate. World J Radiol 2015;7:438-47.  Back to cited text no. 2
John S, Hegazy M, Cheng Ching E, Katzan I. Isolated bilateral middle cerebellar peduncle infarcts. J Stroke Cerebrovasc Dis 2013;22:e645-6.  Back to cited text no. 3
Kataoka H, Izumi T, Kinoshita S, Kawahara M, Sugie K, Ueno S. Infarction limited to both middle cerebellar peduncles. J Neuroimaging 2011;21:e171-2.  Back to cited text no. 4
Akiyama K, Takizawa S, Tokuoka K, Ohnuki Y, Kobayashi N, Shinohara Y. Bilateral middle cerebellar peduncle infarction caused by traumatic vertebral artery dissection. Neurology 2001;56:693-4.  Back to cited text no. 5


  [Figure 1]

This article has been cited by
1 The cerebellar peduncle as localization of a recurrent atypical plexus papilloma: A case report
Christian Saleh,Stefanie Wilmes,Kristine Ann Blackham,Dominik Cordier,Kerstin Hug,Margret Hund-Georgiadis
Surgical Neurology International. 2019; 10: 65
[Pubmed] | [DOI]


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
  Case Report
   Article Figures

 Article Access Statistics
    PDF Downloaded100    
    Comments [Add]    
    Cited by others 1    

Recommend this journal