Sural nerve presents great topographic variability and it is responsible for sensory innervation of the posterolateral side of the distal third of the leg and lateral aspect of the foot. Entrapment of the nerve could be caused by compression due to fascial thickening, while the symptomatology includes sensory alterations and deficits at the nerve distribution area. We report a cadaveric case of a variant sural nerve that presented a distinct entrapment site. A supernumerary sensory branch was encountered originating from the common peroneal nerve, while the peroneal component of the sural nerve was observed to take a course within a fibrous fascial tunnel 3.1 cm in length that caused nerve fixation and flattening. The tension applied to the aforementioned branch was shown to worsen during passive forcible foot plantaflexion and inversion. The etiology, diagnosis and the treatment options are discussed comprehensively.
Cadaver ; Diagnosis ; Fascia ; Foot ; Leg ; Peroneal Nerve ; Sural Nerve*

Sural nerve presents great topographic variability and it is responsible for sensory innervation of the posterolateral side of the distal third of the leg and lateral aspect of the foot. Entrapment of the nerve could be caused by compression due to fascial thickening, while the symptomatology includes sensory alterations and deficits at the nerve distribution area. We report a cadaveric case of a variant sural nerve that presented a distinct entrapment site. A supernumerary sensory branch was encountered originating from the common peroneal nerve, while the peroneal component of the sural nerve was observed to take a course within a fibrous fascial tunnel 3.1 cm in length that caused nerve fixation and flattening. The tension applied to the aforementioned branch was shown to worsen during passive forcible foot plantaflexion and inversion. The etiology, diagnosis and the treatment options are discussed comprehensively.
Cadaver ; Diagnosis ; Fascia ; Foot ; Leg ; Peroneal Nerve ; Sural Nerve*

Background: and Purpose Left ventricular hypertrophy (LVH) is associated with the risk of stroke and dementia independently of other vascular risk factors, but its association with cerebral small vessel disease (CSVD) remains unknown. Here, we employed a systematic review and meta-analysis to address this gap.
Methods: Following the MOOSE guidelines (PROSPERO protocol: CRD42018110305), we systematically searched the literature for studies exploring the association between LVH or left ventricular (LV) mass, with neuroimaging markers of CSVD (lacunes, white matter hyperintensities [WMHs], cerebral microbleeds [CMBs]). We evaluated risk of bias and pooled association estimates with random-effects meta-analyses.
Results: We identified 31 studies (n=25,562) meeting our eligibility criteria. In meta-analysis, LVH was associated with lacunes and extensive WMHs in studies of the general population (odds ratio [OR]lacunes, 1.49; 95% confidence interval [CI], 1.12 to 2.00) (ORWMH, 1.73; 95% CI, 1.38 to 2.17) and studies in highrisk populations (ORlacunes: 2.39; 95% CI, 1.32 to 4.32) (ORWMH, 2.01; 95% CI, 1.45 to 2.80). The results remained stable in general population studies adjusting for hypertension and other vascular risk factors, as well as in sub-analyses by LVH assessment method (echocardiography/electrocardiogram), study design (cross-sectional/cohort), and study quality. Across LV morphology patterns, we found gradually increasing ORs for concentric remodelling, eccentric hypertrophy, and concentric hypertrophy, as compared to normal LV geometry. LVH was further associated with CMBs in high-risk population studies.
Conclusions LVH is associated with neuroimaging markers of CSVD independently of hypertension and other vascular risk factors. Our findings suggest LVH as a novel risk factor for CSVD and highlight the link between subclinical heart and brain damage.