Prevalence of clinical manifestations and neuroimaging features in cerebral small vessel disease.

BACKGROUND AND PURPOSE: Cerebral small vessel disease (CSVD) may present with gradual onset, chronic parkinsonism and/or dementia. In this study, we aimed to identify the prevalence and clinical characteristics of apathy, dementia and parkinsonism in a cohort of patients with CSVD and to determine the neuroimaging features in these patients. METHODS: We included all patients with CSVD, who were admitted to the stroke outpatient clinic between February 2018 and February 2019. All patients were over 18 years of age. Demographic, clinical and neuoimaging findings were noted. Detailed neurological examination and neuropsychiatric assessments were done in each patient. The types and anatomical sites of lesions in neuroimaging were also determined. RESULTS: Among all stroke patients in the study period, CSVD constituted 23.3%. The etiologies were possible arteriosclerotic, amyloid angiopathy and CADASIL in 85.0%, 3.3% and 11.7% of these patients, respectively. The most common clinical feature was apathy followed by dementia, parkinsonism, and parkinsonism plus dementia. In regression analysis, apathy and parkinsonism was associated with lesions in caudate or in other basal ganglia structures whereas lesions of corpus callosum increased the risk of dementia. Hypertension was also associated with the presence of dementia. There was no specific association between the type of lesion in neuroimaging and clinical findings. CONCLUSIONS: The risk of clinical manifestations such as apathy, dementia and parkinsonism is high in CSVD. Involvement of basal ganglia increased the risk of parkinsonism and apathy whereas involvement of corpus callosum increased the risk of dementia. A detailed assessment for apathy is necessary along with parkinsonism and cognitive findings since apathy is the most common finding in CSVD.

Fear leads to a deficit of prepulse inhibition of blink reflex in healthy humans.

OBJECTIVE: We aimed to analyze whether or not fear conditioning exerts an effect on prepulse inhibition (PPI) of blink reflex (BR). To create fear conditioning, we used fearful faces. Since fearful faces lead to a specific set of fear conditioning, we hypothesized PPI of BR would change under the observation of fearful faces. METHOD: We included 17 healthy subjects with a mean age of 30.8 ± 6.9 years and seven healthy subjects with a mean age of 57.7 ± 7.3 years between January 2018 and June 2018 and recorded PPI of BR. The recordings were done before observation of any image, during observation of images, and immediately after observation of images. Observation of images included observation of fearful faces for 30 s and a neutral image of a white screen for 30 s (in a randomized order). RESULTS: There was a R2-PPI deficit during observation of fearful faces in each group whereas R2-PPI fully developed at other time points. R1 amplitude and R2 magnitude were lower during observation of any image compared with baseline and post-observation time points. CONCLUSION: In conclusion, a deficit of R2-PPI develops during observation of fearful faces in humans which is probably related to activation of the amygdala.

THE DIAGNOSTIC AND MANAGEMENT CHALLENGES FOR POSTERIOR REVERSIBLE LEUCOENCEPHALOPATHY SYNDROME.

Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiological entity characterized by epileptic seizures, headaches, altered mental status and focal neurological signs. Hypertension is the second most common condition associated with PRES. The 50-year-old-male patient with, right-sided hemiparesis and speech disturbances admitted to our clinic. His blood pressure at the emergency service was 220/140 mmHg. A left putaminal hematoma was seen in his CT and MRI. In his brain MRI, FLAIR and T2 -weighted sequences showed bilateral symmetric diffuse hyperintensities in the brain stem, basal ganglia, and occipital, parietal, frontal, and temporal lobes. After the intense antihypertensive drug treatment, his blood pressure came to normal limits within a week. During his hospitalisation he had a recurrent speech disturbance lasting an hour. His electroencephalography was normal. In his repeated diffusion weighted MRI, an acute lacunary infarct was seen on right centrum semiovale. Two months later, the control MRI showed only the previous lacuner infarcts and the chronic putaminal hematoma. We presented a case developping either a cerebral hemorrhage or a lacunar infarction due to PRES. The main reason of the following complications of the disease was delayed diagnosis. Uncontrolled hypertension was guilted for the events.