The pathophysiology of stroke has several complex mechanisms. Understanding these mechanisms is essential to derive neuroprotective agents that limit neuronal damage after ischemia. Imaging and clinical strategies aimed at extending the therapeutic window for reperfusion treatment with mechanical and pharmacologic thrombolysis will add value to existing treatment strategies. Acute ischemic stroke is defined as abrupt neurologic dysfunction due to focal brain ischemia resulting in persistent neurologic deficit accompanied by characteristic abnormalities on brain imaging. Knowledge of the pathophysiologic mechanisms of neuronal injury in stroke is essential to target treatment. Neuroprotective and thrombolytic agents have been shown to improve clinical outcome. Physiologic imaging with diffusion-weighted imaging (DWI) and perfusion CT and MRI provide a pathophysiologic substrate of evolving ischemic stroke.

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Metronidazole is a very common antibacterial and antiprotozoal with wide usage across the globe, including the least developed countries. It is generally well-tolerated with a low incidence of serious side-effects. Neurological toxicity is fairly common with this drug, however majority of these are peripheral neuropathy with very few cases of central nervous toxicity reported. We report the imaging findings in two patients with cerebellar dysfunction after Metronidazole usage. Signal changes in the dentate and red nucleus were seen on magnetic resonance imaging in these patients. Most of the cases reported in literature reported similar findings, suggesting high predilection for the dentate nucleus in metronidazole induced encephalopathy.

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Background and Purpose Both diffusion tensor imaging (DTI) and R2* have shown promise in differentiating Parkinson’s disease (PD) from atypical parkinsonism [particularly multiple system atrophy (MSA) and progressive supranuclear palsy (PSP)]. We assessed DTI, R2*, and their combination for differentiating PD, MSA, PSP, and controls. Materials and Methods A total of 106 subjects (36 controls, 35 PD, 16 MSA, and 19 PSP) were included. DTI and R2* measures from striatal, midbrain, limbic, and cerebellar regions were obtained and compared between groups. The discrimination performance of DTI and R2* among groups was assessed using elastic-net machine learning and receiver operating characteristic analysis. Results Compared to controls, PD patients showed significant R2* differences in the red nucleus. Compared to PD, both MSA and PSP patients showed more widespread changes, extending from the midbrain to striatal and cerebellar structures. The pattern of changes, however, was different between the two groups. For instance, MSA patients showed decreased FA and increased R2* in the subthalamic nucleus, whereas PSP patients showed increased MD in the hippocampus. Combined DTI and R2* were significantly better than DTI or R2* alone in separating controls from PD/MSA-P/PSP, controls from PD, PD from MSA-P/PSP, and PD from MSA-P, but not PD from PSP or MSA-P from PSP. Conclusion DTI and R2* provide different but complementary information for different parkinsonisms. Combined DTI and R2* may be a superior marker for PD differential diagnosis.

The ingestion of ethylene glycol results in toxicity with characteristic chemical, pathological, and imaging findings. In the case presented, magnetic resonance imaging demonstrated bilateral symmetric hyperintensity within the basal ganglia, thalami, and brainstem. Ethylene glycol toxicity also resulted in restricted diffusion within the white matter tracts of the corona radiata, a finding not previously described in the literature. In the acute clinical setting, ethylene glycol toxicity is an important differential consideration of the pathologies involving the deep grey matter nuclei.

Olfactory impairment is associated with prodromal Alzheimer’s disease (AD) and is a risk factor for the development of dementia. AD pathology is known to disrupt brain regions instrumental in olfactory information processing, such as the primary olfactory cortex (POC), the hippocampus, and other temporal lobe structures. This selective vulnerability suggests that the functional connectivity (FC) between the olfactory network (ON), consisting of the POC, insula and orbital frontal cortex (OFC) (Tobia et al., 2016), and the hippocampus may be impaired in early stage AD. Yet, the development trajectory of this potential FC impairment remains unclear. Here, we used resting-state functional magnetic resonance imaging (rs-fMRI) data from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) to investigate FC changes between the ON and hippocampus in four groups: aged-matched cognitively normal (CN), early mild cognitive impairment (EMCI), late mild cognitive impairment (LMCI), and AD. FC was calculated using low frequency fMRI signal fluctuations in the ON and hippocampus (Tobia et al., 2016). We found that the FC between the ON and the right hippocampus became progressively disrupted across disease states, with significant differences between EMCI and LMCI groups. Additionally, there were no significant differences in gray matter hippocampal volumes between EMCI and LMCI groups. Lastly, the FC between the ON and hippocampus was significantly correlated with neuropsychological test scores, suggesting that it is related to cognition in a meaningful way. These findings provide the first in vivo evidence for the involvement of FC between the ON and hippocampus in AD pathology. Results suggest that functional connectivity (FC) between the olfactory network (ON) and hippocampus may be a sensitive marker for Alzheimer’s disease (AD) progression, preceding gray matter volume loss.

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