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Table of Contents    
Year : 2020  |  Volume : 68  |  Issue : 1  |  Page : 76-77

Blink and Don't Miss it: The Role of Blink Reflex in Neurodegenerative Disorders

1 Department of Neurology, All India Institute of Medical Sciences, New Delhi, India
2 Department of Neurology, Lady Hardinge Medical College, New Delhi, India

Date of Web Publication28-Feb-2020

Correspondence Address:
Prof. Achal K Srivastava
Room No. 60, Cardio Neuro Sciences Centre, All India Institute of Medical Sciences, New Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.279681

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How to cite this article:
Srivastava AK, Garg D. Blink and Don't Miss it: The Role of Blink Reflex in Neurodegenerative Disorders. Neurol India 2020;68:76-7

How to cite this URL:
Srivastava AK, Garg D. Blink and Don't Miss it: The Role of Blink Reflex in Neurodegenerative Disorders. Neurol India [serial online] 2020 [cited 2020 Apr 4];68:76-7. Available from:

The electrophysiological counterpart of the corneal reflex, the blink reflex, is often used in clinical practice as a surrogate marker for brainstem integrity in the absence of cranial nerve pathology. In the article published in this issue of the journal by XXXXXXX titled “Blink reflex is significantly altered in patients with multiple system atrophy compared to patients with progressive supranuclear palsy, Alzheimer's disease and frontotemporal dementia—A pilot study”, the authors have compared blink reflex among patients with two parkinsonian disorders, multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) which largely affect the brainstem, as well as Alzheimer's disease (AD) and frontotemporal dementia (FTD) wherein the pathology is cortical.[1] The study concludes that ipsilateral R1 and R2 latencies and ipsilateral R1 to contralateral R2 latencies were comparatively prolonged in patients with MSA than the remaining three groups, although the absolute values of the same were within the normal range.

The blink reflex is characterized by an early component, R1, which lies ipsilateral to the site of stimulation and is conducted via an oligosynaptic pontine pathway. It also has a bilateral component, R2, representing the medullary reticulum, which is mediated by a polysynaptic pathway via brainstem interneurons. As such, R1 and R2 represent conduction through brainstem circuits. The excitability of these circuits is reflected by R2 recovery time which can be assessed by specific stimulation techniques. However, it is also under supranuclear control. Unconditioned stimulus influence is via the inferior olive and cerebellar climbing fibers while conditioned stimulus occurs through pontine sensory nuclei, magnocellular red nucleus, and nucleus interpositus via the superior cerebellar peduncle.[2] Basal ganglia can also modulate the brainstem blink pathway through descending cortical influence or the tectoreticular projections to the superior colliculus.[3] Based on this anatomy, the authors posit that blink reflex may be impaired in disorders that affect the brainstem, such as Parkinson's disease (PD), MSA, and PSP. Over the last three decades, numerous neurophysiological studies in atypical parkinsonian disorders have shed light on the pathophysiology underlying these disorders.[4] Indeed, impairment of the R2 blink reflex latencies has been reported in almost one-fifth of patients with PD, MSA, and PSP in one study.[5]

In the present study, it would have been of additional value if patients with PD had also been studied because clinical differential often lies between MSA-parkinsonian type (MSA-P) and typical PD, apart from PSP-P.

Also, it is interesting to note that although both PSP and MSA affect the brainstem, only MSA patients demonstrated abnormal blink reflex. Previous studies have also consistently demonstrated normal R1 and R2 latencies in patients with PSP.[6] However, studies on both MSA and PD have demonstrated hyperexcitability of the blink reflex, which would also have been a useful parameter to see in this study.[3]

In addition, although cortical disorders such as AD and FTD have been included, dementia with Lewy bodies (DLB) has also been reported to have abnormalities on blink reflex evaluation. In a study including 26 patients with DLB, 26 with MSA, 26 with PD, 20 with AD, and 20 with PSP compared with 30 healthy controls, blink reflex values were significantly delayed (P< 0.001) only in DLB patients compared with all other groups including healthy controls; 53.8% of DLB patients had blink reflex latencies above two standard deviations of the control mean.[7] This suggests that not only the brainstem but also cortical dysfunction may exert an influence on the interpretation of blink reflex abnormalities or that there exists some brainstem dysfunction in these primarily cortical disorders.

Although these findings are interesting, larger studies inclusive of patients with PD and DLB are warranted. Also, the clinical correlation of abnormal electrophysiology in terms of disease severity and duration, as well as phenotype, needs to be addressed to imbue these preliminary observations with clinical meaning.

  References Top

Blink reflex is significantly altered in patients with multiple system atrophy compared to patients with Progressive Supranuclear Palsy, Alzheimer's disease and Frontotemporal dementia- A pilot study. Neurology India 2019.  Back to cited text no. 1
Bologna M, Marsili L, Khan N, Parvez AK, Paparella G, Modugno N, et al. Blinking in patients with clinically probable multiple system atrophy. Mov Disord 2014;29:415-20.  Back to cited text no. 2
Basso MA, Evinger C. An explanation for reflex blink hyperexcitability in Parkinson's disease. II. Nucleus raphe magnus. J Neurosci 1996;16:7318-30.  Back to cited text no. 3
Bologna M, Suppa A, Stasio FD, Conte A, Fabbrini G, Berardelli A. Neurophysiological studies on atypical parkinsonian syndromes. Parkinsonism Relat Disord 2017;42:12-21.  Back to cited text no. 4
Szmidt-Salkowska E, Gawel M, Jamrozik Z, Salkowska-Wanat J, Gawel D, Kaminska A. Diagnostic value of blink reflex in multisystem atrophy, progressive supranuclear palsy and Parkinson disease. Neurol Neurochir Pol 2016;50:336-41.  Back to cited text no. 5
Bologna M, Agostino R, Gregori B, Belvisi D, Ottaviani D, Colosimo C, et al. Voluntary, spontaneous and reflex blinking in patients with clinically probable progressive supranuclear palsy. Brain J Neurol 2009;132:502-10.  Back to cited text no. 6
Bonanni L, Anzellotti F, Varanese S, Thomas A, Manzoli L, Onofrj M. Delayed blink reflex in dementia with Lewy bodies. J Neurol Neurosurg Psychiatry 2007;78:1137-9.  Back to cited text no. 7


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