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. 2017 Mar 29;4(4):646. doi: 10.1002/mdc3.12482

Lentiform “Fork Sign” and Parkinsonism After Acute Myocardial Infarction and Cardiac Failure

Renata Fernandes Moreira 1, Orlando GP Barsottini 1,, José Luiz Pedroso 1
PMCID: PMC6353363  PMID: 30713979

A 78‐year‐old man presented with acute myocardial infarction, cardiac failure, and hypotension. Heparin, antiplatelet agents, and volume expansion were started. In the following days, he presented with bradykinesia, gait instability, global rigidity, and bradyphrenia. He had hypertension. Brain MRI performed 3 days later showed a hyperintense signal in basal ganglia, evolving lentiform nuclei, characterizing the lentiform “fork sign” (Fig. 1). EEG was normal. Glucose, electrolytes, creatinine, urea, ammonia, and metabolic tests were normal. Arterial gasometry did not show metabolic acidosis in the second day. Echocardiogram disclosed 46% ejection fraction (Normal: 55–70%) with global akinesia.

Figure 1.

Figure 1

A: Axial FLAIR‐weighted brain MRI shows bilateral symmetrical hyperintense signal in the basal ganglia surrounded by a more brightly hyperintense rim that delineates the lentiform nucleus. B: Axial FLAIR‐weighted brain MRI performed 1 month after the beginning of symptoms shows a marked reduction in the hyperintense signal after treatment of myocardial infarction, cardiac failure, and hypotension.

Although we had considered starting levodopa, the patient experienced a rapid neurological improvement that was coincidental with the clinical improvement—after 6 days (correction of hypotension and treatment of cardiac failure with inotropic drugs—digoxin). One month later, there was no parkinsonism, and brain MRI disclosed reduction of hyperintensity (Fig. 1).

The peculiar appearance of a reversible basal ganglia hyperintensity was called lentiform “fork sign,” described in metabolic acidosis and uremia.1 Although arterial gases can be normal, metabolic acidosis related with hemodynamic changes (hypotension and heart failure in this case but also in a myriad of clinical settings) is hypothesized as trigger in the pathogenesis of the vasogenic edema pattern evident in the imaging.1, 2

Author Roles

1. Case Report Project: A. Conception, B. Organization, C. Execution; 2. Imaging Project: A. Conception, B. Organization, C. Execution; 3. Manuscript: A. Writing of the first draft, B. Review and Critique.

R.F.M.: 1A, 1B, 1C, 2A, 2B, 2C, 3A, 3B

O.G.P.B.: 1C, 2A, 2B, 3A, 3B

J.L.P.: 1A, 1B, 1C, 2A, 2B, 2C, 3A, 3B

Disclosures

Ethical Compliance Statement: We confirm that we have read the Journal's position on issues involved in ethical publication and affirm that this work is consistent with those guidelines. Full consent was obtained from the patients for the case publication.

Funding Sources and Conflicts of Interest: The authors report no sources of funding and no conflicts of interest.

Financial Disclosures for the previous 12 months: The authors report no financial disclosures.

Relevant disclosures and conflicts of interest are listed at the end of this article.

References

  • 1. da Rocha AJ, Maia AC Jr, da Silva CJ, et al. Lentiform fork sign in a child with dialysis disequilibrium syndrome: a transient MRI pattern which emphasizes neurologic consequence of metabolic acidosis. Clin Neurol Neurosurg 2013;115:790–792. [DOI] [PubMed] [Google Scholar]
  • 2. Grasso D, Borreggine C, Perfetto F, et al. Lentiform fork sign: a magnetic resonance finding in a case of acute metabolic acidosis. Neuroradiol J 2014;27:288–292. [DOI] [PMC free article] [PubMed] [Google Scholar]

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