The time course of acute Percheron artery ischemic coma on imaging: A retrospective cohort study.

We were to investigate the time course of lesions for awakening in acute Percheron artery ischemic coma (PAIC), which was previously unknown. Patients who had newly identified acute PAIC events in 2012-2015 and had not received thrombolytic therapy were enrolled retrospectively. The time course of lesions in PAIC was investigated by diffusion-weighted imaging (DWI). Ninety-three patients met the inclusion criteria, of whom 63 and 30 had transient PAIC and persistent PAIC, respectively. The time course of awakening events in persistent PAIC decreased over time, with large lesions in the bilateral paramedian thalamus/ rostral midbrain on DWI almost in all patients who was either plus or minus a "top of basilar artery" strokes. Whereas awakening events in transient PAIC increased over time, with small or lacunar lesions in the unilateral or bilateral thalamus/rostral midbrain about in 30.2 % cases, and the rest in naturally recanalization of infarcts or TIA. Lesion volumes were larger for persistent PAIC than for transient PAIC (median, 2.4 cm3 vs. 0.03 cm3, P < 0.0001). In Cox hazards ratio (HR) analysis, a lower GCS score was associated with mortality (HR, 5.5; 95 % confidence interval [CI],1.427-21.45). Multivaliate analysis shown that the predictors of higher risk of persistent PAIC were only increased NIHSS scores (HR,1.3; 95 % CI,1.109-1.640) and large lesions in bilateral thalamus/rostral midbrain (HR,15.0; 95 % CI,1.440-58.13). The time course of acute PAIC included transient and persistent. Most persistent PAIC was associated with large lesions in bilateral paramedian thalamus/ rostral midbrain, and with high mortality.

Hemorrhagic pure sensory strokes in the thalamus and striatocapsular area: causes, clinical features and long-term outcome.

BACKGROUND: Although there have been sporadic reports of patients with hemorrhagic pure sensory strokes (HPSS) in the thalamus and striatocapsular areas, the causes, clinical featuring and long-term outcome have not been adequately investigated. METHODS: We recruited 7 consecutive patients without hemiparetic stroke who had HPSS in the thalamic and striatocapsular areas. A CT scan was performed to verify brain imaging patterns, and their causes, clinical featuring and long-term outcome were observed. RESULTS: We studied 7 patients who had HPSS in the thalamic and striatocapsular areas as seen in CT scans. The 7 patients had hypertension, and small hemorrhages were found in the thalamus of 2 patients and in the posterior quarter of the posterior limb of the internal capsule in 4 patients; only 1 patient had a microhemorrhage in the thalamus. The volume of the hemorrhages ranged from 0.3 to 6.3 ml, with a mean of 2.3 ± 1.9 ml. Three patients showed a decreased sense of spinothalamic modality, and position and vibration senses were spared. Four patients showed a sensory deficit of both spinothalamic and medial lemniscal type. The outcomes were excellent and without post-stroke pain in all patients. CONCLUSION: HPSS in the thalamus and striatocapsular area are usually small hemorrhages or microhemorrhages from rupturing of the microvessels or the branches of small vessels. HPSS only have an impact on the adjacent sensory nucleus or pathway, and have a good outcome without post-stroke pain.