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Table of Contents    
Year : 2021  |  Volume : 69  |  Issue : 4  |  Page : 1072-1073

Bihemispheric Anterior Cerebral Artery Infarction Imitating an Akinetic Crisis in a Patient with Parkinson's Disease

1 Department of Neurology and Neuroscience, University of Freiburg, Breisacher Straße 64, D-79106 Freiburg, Germany
2 Department of Radiology, University of Wuerzburg, Oberduerrbacher Straße 6, 97080 Würzburg, Germany

Date of Submission03-Nov-2018
Date of Decision06-May-2019
Date of Acceptance04-Dec-2019
Date of Web Publication2-Sep-2021

Correspondence Address:
Konrad Whittaker
Department of Neurology and Neuroscience, University of Freiburg, Breisacher Straße 64, 79106 Freiburg
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.325301

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How to cite this article:
Whittaker K, Guggenberger K, Rijntjes M, Bardutzky J. Bihemispheric Anterior Cerebral Artery Infarction Imitating an Akinetic Crisis in a Patient with Parkinson's Disease. Neurol India 2021;69:1072-3

How to cite this URL:
Whittaker K, Guggenberger K, Rijntjes M, Bardutzky J. Bihemispheric Anterior Cerebral Artery Infarction Imitating an Akinetic Crisis in a Patient with Parkinson's Disease. Neurol India [serial online] 2021 [cited 2021 Dec 9];69:1072-3. Available from:


The patient was a 74-year-old, right-handed male who had been suffering from clinically diagnosed akinetic-rigid Parkinson's disease (PD) for about six years. Shortly before admission, his motoric symptoms consisted of moderate rigidity, mild resting tremor, and moderate gait disturbance. The patient was living with his wife, able to walk with the help of a wheeled walker, and mostly independent in his day-to-day tasks. The initial dopaminergic medication with levodopa (L-DOPA) was supplemented with dopamine agonists during disease progression and to date consisted of L-DOPA/benserazide in a cumulative dose of 562.5 mg/112.5 mg, respectively and pramipexol 0.52 mg. The patient reported no adverse effects under this medication.

The day before admission, the patient had gone on an extensive walk with his wife. The following morning, he did not respond to his wife's attempts to wake him up. Upon admission, the patient was found to be somnolent with psychomotor retardation, severe hypokinesia, and a nearly complete lack of speech. Furthermore, he was not able to lift his legs against gravity, which was interpreted as a severe rigidity of the legs by the consulting neurologist. There was pronounced rigidity, yet there was no paresis of the upper extremities and abnormalities of the cranial nerves. Besides a subcortical arteriosclerotic encephalopathy (SAE) and mild global brain atrophy, a computed tomography (CT) scan of the brain did not reveal any abnormalities. Sonography (USG) of the extra and intracranial vessels remained normal. Laboratory testing revealed a moderate leukocytosis (16.0 × 103/μl) and chest X-ray and urine analysis were normal.

The symptoms were interpreted as an akinetic crisis in PD, triggered by dehydration and infection. After substituting fluids, the patient showed a modest improvement in alertness, yet continued to exhibit severe hypokinesia and near anarthria. Therefore, the dopaminergic medication was gradually increased to a cumulative dose of 1,000 mg L-DOPA, transdermal rotigotine (8 mg/24 h), and supplemented with 3 × 200 mg intravenous (IV) amantadine, which did not lead to a significant improvement of symptoms. Likewise, an administration of subcutaneous apomorphine (4 mg) did not noticeably affect the symptoms. During the course of the next 2 weeks, the patient continued to show a nearly complete lack of speech and developed severe flexor contractions in his arms and legs. He was transferred to our clinic for further diagnostics.

We initiated a continuous subcutaneous application of apomorphine (10 mg over 24 h), which was not able to ameliorate the symptoms either. We, therefore, conducted a magnetic resonance imaging (MRI) scan [Figure 1], which revealed an occlusion of the A2-segment of the bihemispheric right anterior cerebral artery (ACA), with bilateral ischemic lesions in the rostral corpus callosum, cingulate gyrus, and superior frontal gyrus, leading to the paresis of the lower extremities and akinetic mutism. We diagnosed an embolic stroke of undetermined source (ESUS) after ischemic stroke workup (24-h-ECG, transthoracic echocardiogram [TTE]) did not reveal a source. In the short-term follow-up, the patient did not benefit significantly from conservative treatment and remained severely hypokinetic.
Figure 1: Time of flight angiography (a) reveals occlusion of the A2-segment of the bihemispheric right anterior cerebral artery, with a corresponding thrombus signal in SWI (b) as well as diffusion restriction in diffusion-weighted image (DWI; corpus callosum, cingulate gyrus, and superior frontal gyrus) (c), slight signal decrease in ADC (d) with hyperintense FLAIR correlates (e and f) in the ACA territory on both sides, indicating a subacute infarction

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  Discussion Top

The present case illustrates two important aspects of clinical practice. One, our patient mainly showed akinetic mutism because of bilateral ischemia of the A2-segment. Typical lateralized symptoms of acute stroke were not present. Ischemia in the territory of the ACA typically involves either the superior frontal gyrus, corpus callosum, or cingulate gyrus.[1],[2],[3] In patients with a bihemispheric ACA (e.g., hypoplasia of one A2 segment, with the contralateral A2 segment providing the major arterial supply bilaterally to the ACA territories, prevalence 0.2–8%), bilateral ischemia manifests itself as motor deficits of the lower extremities and can present itself as akinetic mutism, as reported in earlier case reports[4] because of the ischemic dysfunction of the limbic system, especially the bilateral cingulate gyrus.[5],[6] As in our patient, a classical disconnection syndrome is not seen if the genu of the corpus callosum remains intact. Two, in patients with PD and presumed akinetic crisis, which do not respond to adequate parenteral dopaminergic medication within hours, another differential diagnosis, such as cerebral ischemia, should be taken into account early.

Physicians should be aware of this rare clinical manifestation of acute stroke and perform MRI or CT angiography on the admission of patients, where an acute onset of neurological symptoms cannot be ruled out as there might be an indication for thrombolysis or thrombectomy.


The authors thank their patient for participating in this report.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Kumral E, Bayulkem G, Evyapan D, Yunten N. Spectrum of anterior cerebral artery territory infarction: Clinical and MRI findings. Eur J Neurol 2002;9:615-24.  Back to cited text no. 1
Arboix A, García-Eroles L, Sellarés N, Raga A, Oliveres M, Massons J. Infarction in the territory of the anterior cerebral artery: Clinical study of 51 patients. BMC Neurol 2009;9:1-7.  Back to cited text no. 2
Alonso A, Gass A, Rossmanith C, Kern R, Griebe M, Binder J, et al. Clinical and MRI patterns of pericallosal artery infarctions: The significance of supplementary motor area lesions. J Neurol 2012;259:944-51.  Back to cited text no. 3
Oomman A, Madhusudhanan M. A case of unpaired anterior cerebral artery occlusion producing akinetic mutism. Neurol India 1999;47:157-8.  Back to cited text no. 4
[PUBMED]  [Full text]  
Cilliers K, Page BJ. Review of the anatomy of the distal anterior cerebral artery and its anomalies. Turk Neurosurg 2016;26:653-61.  Back to cited text no. 5
Cruz-Culebras A, Vera R, JSM. Bilateral infarction of the corpus callosum in a patient with a single pericallosal artery. JAMA Neurol 2016;73:1246-7.  Back to cited text no. 6


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