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Year : 2020  |  Volume : 23  |  Issue : 1  |  Page : 3-4

Disease specific seasonal influence- geography and economy maters

Department of Neurology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttra Pradesh, India

Date of Submission18-Dec-2019
Date of Acceptance23-Dec-2019
Date of Web Publication20-Jan-2020

Correspondence Address:
Dr. Jayantee Kalita
Department of Neurology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow - 226 014, Uttra Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aian.AIAN_633_19

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How to cite this article:
Kalita J, Misra UK. Disease specific seasonal influence- geography and economy maters. Ann Indian Acad Neurol 2020;23:3-4

How to cite this URL:
Kalita J, Misra UK. Disease specific seasonal influence- geography and economy maters. Ann Indian Acad Neurol [serial online] 2020 [cited 2020 Feb 28];23:3-4. Available from:

Seasonal clustering of various neurological and non-neurological diseases has been reported in medical literature, especially in diseases with environmental, biological, and meteorological influences. Immune-mediated diseases such as Guillain–Barre syndrome (GBS), acute disseminated encephalo-myelitis, and acute transverse myelitis are affected by seasonal occurrence of various triggering infections. In a study from north India, seasonal influence of GBS was evaluated in 324 patients; acute inflammatory demyelinating polyradiculoneuropathy (AIDP) was more frequent in rainy season (25.7%) compared to acute motor axonal neuropathy (AMAN, 11.1%), whereas AMAN occurred during summer (42.2% vs 22.5%).[1] In Western countries, clustering of GBS during winter has been reported.[2] This difference in clustering may be attributed to seasonal prevalence of infection in different countries. In Asian or resource-poor countries, water and arthropod-born infections are common; whereas in temperate and developed countries influenza-like illnesses are more common. Myasthenia gravis and migraine precipitate during extremes of summer and winter. Intracerebral hemorrhage occurs more frequently in winter and ischemic stroke in summer.[3],[4] Ambient temperature may affect blood pressure and blood coagulability. Healthy volunteers exposed to 40°C for 6 hours had increased hematocrit by 9%, blood viscosity by 24%, platelets by 18%, and plasma cholesterol by 14%. Their core temperature raised to 0.84°C, heart rate by 32/minute, and reduction in body weight by 1.83 kg due to sweating despite accessibility to water and fall in blood pressure.[5] Platelet adhesion increased by five folds when hematocrit increased from 10% to 40%.[6] Red blood cell can also generate some particles, which can result in platelet aggregation and enhance coagulation.[7] Hypothermia also enhances fibrin formation and increase platelet activation.[8],[9] Increase in incidence of intracerebral hemorrhage during winter may be due to increase in blood pressure as a result of increased sympathetic activities, reduced fluid loss, and sodium. Cerebral venous sinus thrombosis (CVST) is a rare stroke-like illness. In South-East Asia, CVST has been reported more frequently during puerperium in earlier studies, but this notion has been blurring in recent studies, and may be due to availability of investigative facilities of underlying prothrombotic conditions.[10] In the present issue, Aaronet al. have reported seasonal influence in the occurrence of CVST. The frequency of CVST was the highest during summer (42.3%), followed by autumn (32.7%) and winter (25%). Females and younger patients were more vulnerable during summer, although CVST was independent of humidity and cloud.[11] Ferro et al. reported the highest frequency of CVST during autumn and winter.[12] Stolz et al. found higher frequency of CVST in summer and winter.[13] Winter peak has been attributed to thrombogenicity triggered by viral and bacterial infection, and summer incidence to dehydration. Salehi et al. found correlation of CVST occurrence with ambient temperature. They reported the highest incidence of CVST during July to September (1.69/month/year) and the lowest during December to April (0.83/month/year).[14] Seasonal influence, however, was not related to clinical severity and outcome in most studies. There is a limitation in deciding the exact onset of CVST unlike intracerebral hemorrhage and thrombotic or embolic stroke. The onset in CVST is mainly subacute (3–30 days) on chronic (>30 days).[10],[12] In an individual with inherent prothrombotic conditions, various infections, environmental, or dietary factors may enhance thrombosis, which needs further studies. Identification of such factors may go a long way in the prevent CVST.


We thank Mr. Shakti Kumar for secretarial help.

   References Top

Kalita J, Misra UK, Goyal G, Das M. Guillain-Barré syndrome: Subtypes and predictors of outcome from India. J Peripher Nerv Syst 2014;19:36-43.  Back to cited text no. 1
Webb AJ, Brain SA, Wood R, Rinaldi S, Turner MR. Seasonal variation in Guillain-Barré syndrome: A systematic review, meta-analysis and Oxfordshire cohort study. J Neurol Neurosurg Psychiatry 2015;86:1196-201.  Back to cited text no. 2
Biller J, Jones MP, Bruno A, Adams HP Jr, Banwart K. Seasonal variation of stroke--Does it exist? Neuroepidemiology 1988;7:89-98.  Back to cited text no. 3
Ogata T, Kimura K, Minematsu K, Kazui S, Yamaguchi T. Japan multicenter stroke investigators' collaboration. Variation in ischemic stroke frequency in Japan by season and by other variables. J Neurol Sci 2004;225:85-9.  Back to cited text no. 4
Keatinge WR, Coleshaw SR, Cotter F, Mattock M, Murphy M, Chelliah R. Increases in platelet and red cell counts, blood viscosity, and arterial pressure during mild surface cooling: Factors in mortality from coronary and cerebral thrombosis in winter. Br Med J (Clin Res Ed) 1984;289:1405-8.  Back to cited text no. 5
Turitto VT, Weiss HJ. Red blood cells: Their dual role in thrombus formation. Science 1980;207:541-3.  Back to cited text no. 6
Jy W, Johansen ME, Bidot C Jr, Horstman LL, Ahn YS. Red cell-derived microparticles (RMP) as haemostatic agent. Thromb Haemost 2013;110:751-60.  Back to cited text no. 7
Pivalizza EG, Koch SM, Mehlhorn U, Berry JM, Bull. The effects of intentional hyperthermia on the Thrombelastograph and the Sonoclot analyser. Int J Hyperthermia 1999;15:217-23.  Back to cited text no. 8
Vance Strother S, Bull JMC, Branham SA. Activation of coagulation during therapeutic whole body hyperthermia. Thromb Res 1986;43:353-60.  Back to cited text no. 9
Kalita J, Misra UK, Singh RK. Do the risk factors determine the severity and outcome of cerebral venous sinus thrombosis? Transl Stroke Res 2018;9:575-81.  Back to cited text no. 10
Aaron S, Lakshmanan J, Sudarsanam TD, Benjamin K, Durairaj J, Mathew V, et al. Cerebral venous thrombosis, seasonal trends, and climatic influence: A regionspecific study. Ann Ind Acad Neurol 2019. DOI: 10.4103/aian.AIAN_409_19.  Back to cited text no. 11
Ferro JM, Lopes GC, Rosas MJ, Araújo C, Henriques I; Venoport Investigators. Chronobiology of cerebral vein and dural sinus thrombosis. Cerebrovasc Dis 2002;14:265.  Back to cited text no. 12
Stolz E, Klotzsch C, Rahimi A, Schlachetzki F, Kaps M. Seasonal variations in the incidence of cerebral venous thrombosis. Cerebrovasc Dis 2003;16:455-6.  Back to cited text no. 13
Salehi G, Sarraf P, Fatehi F. Cerebral venous sinus thrombosis may follow a seasonal pattern. J Stroke Cerebrovasc Dis 2016;25:2838-43.  Back to cited text no. 14


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