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Different locations but common associations in subcortical hypodensities of presumed vascular origin: cross-sectional study on clinical and neurosonologic correlates

João Sargento-Freitas12*, Ricardo Felix-Morais3, Joana Ribeiro4, Ana Gouveia2, César Nunes3, Cristina Duque2, João Madaleno5, Fernando Silva12, Cristina Machado2, Gustavo Cordeiro2 and Luís Cunha2

Author Affiliations

1 Neurosonology Laboratory, Coimbra University and Hospital Centre, Coimbra 3000-075, Portugal

2 Neurology Department, Coimbra University and Hospital Centre, Coimbra, Portugal

3 Neuroradiology Department, Coimbra University and Hospital Centre, Coimbra, Portugal

4 Medicine Faculty of Coimbra University, Coimbra, Portugal

5 Internal Medicine Department, Coimbra University and Hospital Centre, Coimbra, Portugal

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BMC Neurology 2014, 14:24  doi:10.1186/1471-2377-14-24

Published: 5 February 2014



Subcortical hypodensities of presumed vascular etiology (SHPVO) are a clinical, radiological and neuropathological syndrome with a still largely unexplained pathophysiology. Parallel to the clinical heterogeneity, there is also recognised cerebral topographical diversity with undetermined etiological implications. Our aim is to assess clinical and neurosonological predictors of SHPVO according to their location.


Cross sectional analysis of consecutive patients that underwent neurosonologic evaluation and head CT within one month, during a one year period. We excluded patients with absent temporal sonographic window, any pathology with a possible confounding effect on cerebral arterial pulsatility, atrial fibrillation and other etiologies of white matter diseases. The mean pulsatility index (PI) of both middle cerebral arteries was measured in the middle third of the M1 segment; intima media thickness was evaluated in the far wall of both common carotid arteries. SHPVO were rated by analysis of head CT in deep white matter (DWMH), periventricular white matter (PVWMH) and basal ganglia (BGH). We conducted a multivariate ordinal logistic regression model including all clinical, demographic and ultrasonographic characteristics to determine independent associations with SHPVO.


We included 439 patients, mean age 63.47 (SD: 14.94) years, 294 (67.0%) male. The independent predictors of SHPVO were age (OR = 1.067, 95% CI: 1.047-1.088, p < 0.001 for DWMH; OR = 1.068, 95% CI: 1.049-1.088, p < 0.001 for PVWMH; OR = 1.05, 95% CI: 1.03-1.071, p < 0.001 for BGH), hypertension (OR = 1.909, 95% CI: 1.222-2.981, p = 0.004 for DWMH; OR = 1.907, 95% CI: 1.238-2.938, p = 0.003 for PVWMH; OR = 1.775, 95% CI: 1.109-2.843, p = 0.017 for BGH) and PI (OR = 17.994, 95% CI: 6.875-47.1, p < 0.001 for DWMH; OR = 5.739, 95%CI: 2.288-14.397, p < 0.001 for PVWMH; OR = 11.844, 95% CI: 4.486-31.268, p < 0.001 for BGH) for all locations of SHPVO.


Age, hypertension and intracranial pulsatility are the main independent predictors of SHPVO across different topographic involvement and irrespective of extracranial atherosclerotic involvement.

White matter lesions; Ischemic leukoencephalopathy; Small vessel disease; Transcranial doppler; Neurosonology; Stroke; Atherosclerosis