A "Hot Cross Bun" sign on T2-weighted MRI was described as a result of selective loss of myelinated transverse pontocerebellar fibers and neurons in the pontine raphe with preservation of the pontine tegmentum and corticospinal tracts (CST). However, neuropathologic studies showed contradicting results with no sparing of the CST. This is a pictorial and quantitative demonstration of the sign on diffusion tensor imaging and tractography, which provides the imaging evidence that is consistent with neuropathologic findings.
A 20 year old male presented to the emergency department with generalized tonic clonic convulsions and up rolling of eye balls. He had history of seizure disorder for three years and on regular medical treatment and is compliant to medication. A non-contrast CT scan of the head was only done on 14th day of admission which showed hypodense areas in the right and left cerebellar hemisphere. MR imaging was performed four days later revealed high signal intensity in the both cerebellar hemispheres, both external capsules, both occipital and right parietal regions on fluid-attenuated inversion recovery (FLAIR). The post contrast MR imaging revealed diffuse cerebral and cerebellar hypervascularity in the similar region. This change of diffuse hypervascularity of both cerebral and cerebellar associated with seizure activity on post-contrast magnetic resonance imaging (MRI) has not been reported in any literature.
The present study aimed to investigate the behavior and neuronal morphological changes in the perihaemorrhagic tissue of the mouse intracerebellar haemorrhage experimental model. Adult male Swiss albino mice were stereotactically infused with collagenase type VII (0.4U/μl of saline) unilaterally in to the cerebellum, following anaesthesia. Motor deficits were assessed using open field and composite score for evaluating the mouse model of cerebellar ataxia at 1, 3, 7, 14 and 21 days after collagenase infusion. The animals were sacrificed at the same time interval for evaluation of perihaematomal neuronal degeneration using haematoxylin and eosin staining and Annexin V-FITC/Propidium iodide assay. At the end of the study, it was found that infusion of 0.4U collagenase produces significant locomotor and ataxic deficit in the mice especially within the first week post surgery, and that this gradually improved within three weeks. Neuronal degeneration evident by cytoplasmic shrinkage and nuclear pyknosis was observed at the perihaematomal area after one day; especially at 3 and 7 days post haemorrhage. By 21 days, both the haematoma and degenerating neurons in the perihaematomal area were phagocytosed and the remaining neuronal cells around the scar tissue appeared normal. Moreover, Annexin-V/propidium iodide-positive cells were observed at the perihaematomal area at 3 and 7 days implying that the neurons likely die via apoptosis. It was concluded that a population of potentially salvageable neurons exist in the perihaematomal area after cerebellar haemorrhage throughout a wide time window that could be amenable to treatment.
The underlying mechanisms of secondary neuronal damage following intracerebellar hemorrhage (ICbH) have not yet been clearly understood. Our previous study reported apoptotic neuronal damage in the perihematomal region (PH) in mice. However, the possible key factors causing secondary neuronal damage in ICbH are not yet known. Therefore, we aimed to study the vital factors in the mediation of secondary neuronal damage following ICbH induced by collagenase type VII (0.4 U/μL of saline) into the cerebellum of mice. The mice were grouped into four groups: (1) control group ( n = 12), (2) day-1 group ( n = 12), (3) day-3 group ( n = 12), and (4) day-7 group ( n = 12). All mice underwent behavior assessment following induction of ICbH and were subsequently sacrificed on days 1, 3, and 7. Perihaematoma samples were collected to study morphological changes, immunohistochemistry, nitric oxide (NO) estimation, and oxidative stress markers, respectively. Mouse behavior was disturbed following ICbH on days 3 and 7 compared to the control. In addition, neuronal damage was found in the PH region. Glial fibrillary acidic protein (GFAP) and excitatory amino acid transporter 1 (EAAT1) were highly expressed on day 7, while gamma-aminobutyric acid receptor subunit alpha-1 (GABA A α1)-containing receptor subunit was detected on days 1 and 3. NO increased on day 1 post-induction and decreased on days 3 and 7. The expressions of superoxide dismutase (SOD), catalase (CAT), neuronal nitric oxide synthases (nNOSs), glutathione peroxidase 1, and cyclooxygenase-2 (COX-2) were significantly increased on day 3. Morphological studies of the PH and tissue showed that neuronal damage occurred from day 1 onward and peaked on day 3, associated with alterations in NO, reactive astrocytes (GFAP), glutamate transport regulation (EAAT1), and GABA receptor. Briefly, significant changes in the key markers in the PH regions at different time points are possibly crucial factors facilitating secondary neuronal damage in the PH region. Identifying the time window of these vital changes could help prevent secondary damage and optimize the treatment to occur at proper time points.
Thymoquinone (TQ), a bioactive constituent of Nigella sativa Linn (N. sativa) has demonstrated several neuropharmacological attributes. In the present study, the neuroprotective properties of TQ were investigated by studying its anti-apoptotic potential to diminish β-amyloid peptide 1-40 sequence (Aβ1-40)-induced neuronal cell death in primary cultured cerebellar granule neurons (CGNs). The effects of TQ against Aβ1-40-induced neurotoxicity, morphological damages, DNA condensation, the generation of reactive oxygen species, and caspase-3, -8, and -9 activation were investigated. Pretreatment of CGNs with TQ (0.1 and 1 μM) and subsequent exposure to 10 μM Aβ1-40 protected the CGNs against the neurotoxic effects of the latter. In addition, the CGNs were better preserved with intact cell bodies, extensive neurite networks, a loss of condensed chromatin and less free radical generation than those exposed to Aβ1-40 alone. TQ pretreatment inhibited Aβ1-40-induced apoptosis of CGNs via both extrinsic and intrinsic caspase pathways. Thus, the findings of this study suggest that TQ may prevent neurotoxicity and Aβ1-40-induced apoptosis. TQ is, therefore, worth studying further for its potential to reduce the risks of developing Alzheimer's disease.