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CASE REPORT |
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Year : 2015 | Volume
: 8
| Issue : 5 | Page : 633-635 |
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Bilateral acute cerebellar infarcts in a young patient
Chandrashekhar A Sohoni
Department of Radiology, NM Medical, Pune, Maharashtra, India
Date of Web Publication | 10-Sep-2015 |
Correspondence Address: Chandrashekhar A Sohoni B-5, Common Wealth Hsg. Soc., Opp. Bund Garden, Pune - 411 001 India
Source of Support: Nil., Conflict of Interest: None declared. | Check |
DOI: 10.4103/0975-2870.164943
Stroke in the young population though unusual is being reported with increasing frequency. A very interesting case of posterior circulation stroke in young male is reported here. Multiple focal acute infarcts in bilateral cerebellar hemispheres were seen. Magnetic resonance angiography revealed an unpaired left posterior inferior cerebellar artery supplying both cerebellar hemispheres, which explained the bilateral involvement. The only positive finding on further investigation was presence of hyperhomocyteinemia, which suggested underlying hypercoagulable status and thromboembolism as the possible mechanism of stroke. Keywords: Bilateral acute cerebellar infarcts, hyperhomocysteinemia, unpaired posterior inferior cerebellar artery
How to cite this article: Sohoni CA. Bilateral acute cerebellar infarcts in a young patient. Med J DY Patil Univ 2015;8:633-5 |
Introduction | | |
Acute bilateral cerebellar infarcts with involvement of the medial as well as lateral posterior inferior cerebellar artery (PICA) territories is very rare.[1] In young individuals with posterior circulation stroke, the developmental variations in PICA can sometimes explain the unusual vascular territorial involvement. Hypercoagulability is considered a risk factor for stroke in young individuals.[2] With the availability of magnetic resonance imaging, the diagnosis of stroke in young is being made with increasing frequency.
Case Report | | |
A 29-year-old nondiabetic, normotensive male patient presented with complaints of headache and dizziness since past 8 h. There was no history of fever, vomiting, convulsions or transient loss of consciousness. The patient was not on any anticoagulant or antiplatelet drugs. Family history was negative for any vascular events. On examination, the patient was conscious and well oriented with a Glasgow coma scale score of 15/15. Neurological examination revealed presence of bilateral cerebellar signs in the form of nystagmus on bilateral gaze, dysdiadocokinesia and dysmetria, in addition to truncal and gait ataxia. The motor and sensory examination was normal. The stretch reflexes were normal, and Babinski sign was not elicited. The cranial nerves examination was unremarkable. The general physical examination was normal with a pulse rate of 90/min and blood pressure of 120/80 mm Hg.
Magnetic resonance imaging of the brain revealed multiple focal areas of restricted diffusion suggestive of acute infarcts in bilateral cerebellar hemispheres [Figure 1]a and [Figure 1]b with involvement of the territories supplied by medial and lateral branches of PICA bilaterally. The magnetic resonance angiography showed presence of an unpaired prominent PICA on the left side arising from the vertebral artery and supplying both the cerebral hemispheres [Figure 2]. The right PICA was not visualized, suggesting either absence or severe hypoplasia. The bilateral vertebral arteries, rest of the posterior circulation and the carotid arterial system were normal. Electrocardiogram and two-dimensional echocardiography studies were also normal. | Figure 1: The diffusion weighted (a) axial and (b) coronal magnetic resonance images reveal multiple acute infarcts in bilateral cerebellar hemispheres with involvement of medial as well as lateral posterior inferior cerebellar artery territories
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| Figure 2: The intracranial magnetic resonance angiography image reveals a prominent unpaired posterior inferior cerebellar artery arising from the left vertebral artery
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Laboratory investigations revealed a normal haemogram, renal and liver function tests. The fasting and postprandial blood glucose levels were normal. The laboratory profile for hypercoagulable conditions revealed a high-plasma homocysteine level of 30 µmol/L. Serum antiphospholipid antibody, protein C and S, antithrombin III and factor V Leiden levels were normal. High-plasma homocysteine level suggested the possibility of arterial thromboembolism as the cause of cerebellar infarcts. The variant bihemispheric PICA explained bilateral involvement. Since the patient was clinically well preserved, he was managed conservatively with oral aspirin and supportive treatment. At the time of discharge from the hospital, the patient had considerably improved symptomatically with residual ataxic gait. The patient was advised neurologic rehabilitation and follow-up.
Discussion | | |
Acute bilateral cerebellar infarcts have been reported previously. Although PICA is the most variable cerebellar artery, the estimated incidence of the artery crossing the midline is only 0.1%.[3] In the case of an unpaired PICA, or bihemispheric PICA as it is also called, the artery usually supplies the ipsilateral complete PICA territory and the contralateral medial PICA territory.[4] The contralateral lateral PICA territory in that case is supplied by anterior inferior cerebellar artery. The peculiar topographic pattern of multiple acute infarcts in the medial as well as lateral PICA territory bilaterally is hence extremely unusual and not yet reported in young individuals to the best of our knowledge.
Conventional risk factors such as smoking, higher systolic blood pressure and fasting blood glucose, and lower high-density lipoprotein cholesterol still play an important role in the causation of stroke in young.[5] However, hypercoagulable conditions are increasingly gaining importance as independent risk factors for arterial stroke in young. The commonest hypercoagulable conditions are hyperhomocysteinemia, presence of antiphospholipid antibodies, deficiency of protein C, protein S and antithrombin, and elevated levels of factor V Leiden and prothrombin due to gene mutation.[2] Many prospective and retrospective studies have shown a strong, independent and dose-related association between moderately elevated homocysteine and atherosclerotic vascular disease, including stroke.[6] The absence of any other causative factor in our case suggests hyperhomocysteinemia as the cause of thromboembolic stroke.
In the absence of complications arising due to edema and brainstem compression, the clinical recovery of patients with bilateral acute cerebellar infarcts on conservative management is good, and the same was seen in our case.[4] Physicians should keep in mind the rare possibility of bilateral cerebellar infarcts, while evaluating patients with bilateral cerebellar signs as large infarcts may cause rapid deterioration due to edema and mass effect. Radiologists should always make an attempt to look for possible variations in vascular anatomy in case of bilateral cerebellar infarcts as it may give a clue to the possible etiology.
References | | |
1. | Gupta PK, Ramnath KP, Sudhakar PJ. Bilateral medial cerebellar infarction in a patient positive for lupus anticoagulant. J Thromb Thrombolysis 2007;23:241-4. |
2. | Verma R, Shukla R. Bilateral superior cerebellar artery infarcts: Unusual presentation in two patients of stroke in young. J Assoc Physicians India 2007;55:663-6. |
3. | Carlson AP, Alaraj A, Dashti R, Aletich VA. The bihemispheric posterior interior cerebellar artery: Anatomic variations and clinical relevance in 11 cases. J Neurointerv Surg 2013;5:601-4. |
4. | Umashankar G, Gupta V, Harik SI. Acute bilateral inferior cerebellar infarction in a patient with neurosyphilis. Arch Neurol 2004;61:953-6. |
5. | Lipska K, Sylaja PN, Sarma PS, Thankappan KR, Kutty VR, Vasan RS, et al. Risk factors for acute ischaemic stroke in young adults in South India. J Neurol Neurosurg Psychiatry 2007;78:959-63. |
6. | Hasan N, McColgan P, Bentley P, Edwards RJ, Sharma P. Towards the identification of blood biomarkers for acute stroke in humans: A comprehensive systematic review. Br J Clin Pharmacol 2012;74:230-40. |
[Figure 1], [Figure 2]
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