Comment on: A 57‐Year‐Old Woman With Progressive Left Hand Clumsiness and Falls

We read with great interest the article from Paramanandam and colleagues.1 The researchers report on a case about a patient clinically presenting with a corticobasal syndrome (CBS). However, the postmortem autopsy‐confirmed diagnosis was a synucleinopathy that was consistent with MSA as the underlying neuropathology. We agree with the researchers about the difficulties to discriminate between atypical parkinsonian syndromes (aPS) in clinical practice, including the diagnosis of MSA. As mentioned recently, the diagnosis of MSA is difficult, and the current consensus criteria will be modified soon.2 This is because various clinical syndromes can mimic MSA, and clinical features of MSA often have a wider range than previously assumed.1, 3 Apart from the clinical presentation, there is also a lack of biomarkers who can sufficiently discriminate the different aPS, and the clinicopathological correlation often is not satisfying.3 Because of the distinctive patterns of iron disposition in various parkinsonian syndromes, the use of specialized MRI has been shown to be a helpful tool for the diagnosis of MSA. In the present case report, however, neither the MRI examination of the brain nor nuclear medicine analyses were helpful for the diagnostic workup.1

Our group has been working in the field of transcranial sonography (TCS) and considers this method as a still underestimated tool. TCS has been shown to be very valuable in the diagnostics for parkinsonian and other movement disorders.

Most recently, Alonso‐Canovas and colleagues4 confirmed the high specificity for TCS in the diagnostic workup of aPS. Concerning MSA, they found a sensitivity of 41% and specificity of 95% for the combination of different echo features (third ventricle, nucleus lentiformis, and SN). Especially for MSA and PSP, hyperechogenic alterations of the nucleus lentiformis (LN) are a common finding, which was also demonstrated by our group in a recent meta‐analysis.5 As an example, Figure 1 demonstrates a hyperechogenic LN in TCS in a patient with MSA, which is usually accompanied with a normal echogenicity of the SN. Concerning corticobasal degeneration, the typical TCS pattern includes hyperechogenicities of SN, but an unimpaired isoechogenic LN, and thus helps to differentiate from MSA and PSP.4 The typical TCS pattern of PSP syndromes usually involves a normal echogenicity of SN, a hyperechogenic LN,5 and an enlarged third ventricle.4

Figure 1.

TCS examination of a patient with MSA. Large arrow marks the hyperechogenicity of the right nucleus lentiformis. Small arrow = pineal gland; small crosses mark = third ventricle diameter.

In summary, TCS is a rapid, low‐cost, and noninvasive tool for the differential diagnosis of aPS. The etiology of brain parenchyma echogenic changes in aPS disorders is still incompletely understood, but its analysis with TCS can help to more precisely define parkinsonian syndromes in addition to the more cost‐intensive and time‐consuming methods of specialized MRI and nuclear medicine imaging. A more extensive clinicopathological and desirably TCS‐pathological correlation analysis is still lacking and would be of high value to strengthen the use of TCS in our daily practice.

Author Roles

(1) Research Project: A. Conception, B. Organization, C. Execution; (2) Manuscript Preparation: A. Writing of the First Draft, B. Review and Critique.

D.R.: 1A, 1B, 1C, 2A

L.T.: 1B, 1C, 2B

C.K.: 1A, 1B, 1C, 2B

Ethical Compliance Statement: The authors confirm that the approval of an institutional review board or patient consent was not required for this work. 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.

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

Financial Disclosures for previous 12 months: L.T. has received travel funding and/or speaker honoraria from AbbVie, Bayer, Bial, Desitin, GE, UCB, and Zambon and consulted for AbbVie, Bayer, Bial, Desitin, UCB, and Zambon, none related to this article. C.K. received honoraria for oral presentations or travel grants for scientific meetings from Bayer Vital, Bristol‐Myers Squibb, and Boehringer Ingelheim, none related to this article.