Our study found significantly higher proportion of headache as a presenting symptom and elevated DBP in CH patients. Moreover, white blood cells (WBC) ≥ 10,000 cells/mm3, obstructive hydrocephalus, and distortion of the fourth ventricle on initial brain scans were significantly more prevalent in CH as well. (Table 2) We propose that an abrupt and rapid increment of posterior cranial fossa pressure from cerebellar hematoma plus its later expansion possibly causes the anatomical distortions. Furthermore, acute physiological reaction to the acutely elevated intracranial pressure (ICP) probably results in leukocytosis. A study by Furlan showed that leukocytosis on admission was associated with poor outcome too.
Notably, we found no significant difference in NDDA between the two subtypes of cerebellar strokes. In addition, CH was not an independent risk factor of NDDA by logistic regression analysis in the current study. (Table 3) However, the time from onset to NDDA was significantly shorter in CH. (Table 2) This is explainable by more rapid rising of ICP in CH than in CI. Unlike a few previous studies,[6, 8] which included wider range of severe cerebellar stroke cases, the significant differences in characteristics between CH and CI were more obvious than ours. As we aimed to determine the predictors of NDDA in the patients initially without indication for neurosurgical interventions, we excluded all the cases with neurological deterioration at their first presentations. And, the limited number of cases enrolled in our study was likely to have fewer clinical parameters with statistically significant differences reported.
The shorter time from stroke onset to hospital arrival and hemispheric cerebellar signs at presentation were protective factors on multivariate analysis. (Table 3) We considered that the presence of cerebellar hemispheric signs was well realized by most physicians of having hemispheric cerebellar disorder, facilitating immediate neuro-imaging study and therapy. In contrast, in cases of cerebellar vermis stroke mostly are under evaluated, or missed as a peripheral vestibular disorder causing delayed diagnosis and also proper management. As found in our study, the presence of hemispheric cerebellar signs was a significant protective factor for NDDA in our study. (Table 3) Positive hemispheric cerebellar signs corresponding with the presence of hemispheric cerebellar lesions seen on the imaging studies were 51/74 (70%) cases in our study. 34/43 of them (79%) acquired favorable outcome eventually. A study by Erik, et al. supported our finding as they reported that cerebellar vermis hemorrhage was associated with higher rates of neurological deterioration. Direct compression of the hematoma against brainstem was attributed.
Our study revealed that DBP \(\ge\) 120 mmHg was an independent predictor of NDDA (adj. OR 15.39, 95% CI 1.58-149.59; p = 0.004). (Table 3) Elevation of blood pressure has been considered as a response to elevation of ICP at the stroke onset, however, it probably leads to neurological deterioration because of increased risk of massive cerebral edema and hematoma expansion as well.[12–17]
Hyperglycemia (Blood sugar \(\ge\) 140 mg/dL) was not an independent predictor of NDDA in the current study. (Table 3) Actually, we found that the median (IQR) Blood sugar (BS) level in our cases (117 (100, 133.7) mg/dL) was lower than some previous studies (> 150 mg/dL).[7, 8, 18] Therefore, lower BS levels would contribute to better cerebellar stroke outcomes in our study. To our knowledge, hyperglycemia worsens the overall stroke outcomes, because high blood sugar level has been known to exert adverse effects on the structures of cerebral vascular endothelial cells, and to induce acute oxidative stress along with vascular endothelial inflammation.[19, 20]
Koh concluded that hydrocephalus, brain stem deformity and basal cistern compression were associated with NDDA in cerebellar infarction. St. Louis also reported that patients with a cerebellar vermis hematoma and acute hydrocephalus were at high risk for NDDA. Furthermore, Ho reported that obliteration of basal cistern on the initial CT brain scans was associated with NDDA in cerebellar hemorrhages. Based on our available results, we found no neuro-imaging abnormality as a predictor of NDDA by multivariate analysis. (Table 3) Since most of the brain images done in our study were CT scans, demonstration of such mentioned imaging abnormalities in association with NDDA is possibly obscured.
Thirty-one (42%) of all cerebellar stroke patients developed NDDA, and 28 of the 31 (90%) patients acquired unfavorable neurological outcomes at hospital discharge. When compare with the overall cerebellar stroke outcomes, only 37.8% had favorable outcomes at discharge (2.4 folds higher in NDDA cases). Some previous studies reported a slightly higher percentage of unfavorable final outcomes (50%).[1, 6, 8] With the available information and based on our current findings, a worse neurological outcome is undoubtedly higher in NDDA cerebellar stroke patients.
Under limitation of accessibility of MRI brain, particularly under emergency service setting in our center and the similar others, we speculated that some clinical presentation characteristics could be practically useful to predict the occurrence of NDDA among the initially non-surgical-indicated patients. We hope that our findings could facilitate appropriate monitoring and timely starting of necessary neurosurgical interventions aiming at favorable cerebellar stroke outcomes.
The limitations of the current study are retrospective design and single-center study with limited sample size. Further prospective and multi-center studies, which include more study samples with variability of cerebellar stroke severity would be useful in providing an appropriate management decision on initiation of early neurosurgical interventions for cerebellar stroke patients.