Search

We have created the immunodeficient SRG rat, a Sprague-Dawley Rag2/Il2rg double knockout that lacks mature B cells, T cells, and circulating NK cells. This model has been tested and validated for use in oncology (SRG OncoRat®). The SRG rat demonstrates efficient tumor take rates and growth kinetics with different human cancer cell lines and PDXs. Although multiple immunodeficient rodent strains are available, some important human cancer cell lines exhibit poor tumor growth and high variability in those models. The VCaP prostate cancer model is one such cell line that engrafts unreliably and grows irregularly in existing models but displays over 90% engraftment rate in the SRG rat with uniform growth kinetics. Since rats can support much larger tumors than mice, the SRG rat is an attractive host for PDX establishment. Surgically resected NSCLC tissue from nine patients were implanted in SRG rats, seven of which engrafted and grew for an overall success rate of 78%. These developed into a large tumor volume, over 20,000 mm3 in the first passage, which would provide an ample source of tissue for characterization and/or subsequent passage into NSG mice for drug efficacy studies. Molecular characterization and histological analyses were performed for three PDX lines and showed high concordance between passages 1, 2 and 3 (P1, P2, P3), and the original patient sample. Our data suggest the SRG OncoRat is a valuable tool for establishing PDX banks and thus serves as an alternative to current PDX mouse models hindered by low engraftment rates, slow tumor growth kinetics, and multiple passages to develop adequate tissue banks.

Cysticercosis, an infection caused by the larval stage of tapeworm Taenia solium, is the most common parasitic disease of the human nervous system and the single most common cause of acquired epileptic seizures in the developing world. Here, we describe the stormy course of a 67-year-old female with neurocysticercosis (NCC) having a recurrent encephalitic presentation. She went through the most severe spectrum of this disease, namely NCC encephalitis and disseminated cysticercosis and had a classical starry sky brain in neuroimaging. In contrary to the popular practice of avoiding antihelminthic drugs in such extreme presentation, as a desperate measure, we had to use albendazole in this case, which showed clinical and radiological improvement.

Acute neurovascular events, though rare, can complicate pregnancy and postpartum period. It is important to be aware of these clinical conditions for reducing maternal and fetal morbidity and mortality. In this review, we present a few important neurovascular emergencies and their imaging manifestations by various imaging modalities-computed tomography (CT), magnetic resonance imaging (MRI), and digital subtraction angiography (DSA)-which presented at our institution in the peripartum period.

Dentate nucleus is affected in a wide variety of conditions. Magnetic resonance imaging of the brain is the diagnostic modality of choice for delineating the signal characteristics, which helps in narrowing down a vast list of differentials for conditions affecting the dentate. Computed tomography plays an important role, especially for pathologies associated with calcification of dentate nucleus.

Neurotropism and infiltration by Mycobacterium leprae of peripheral nerves causing neuropathy are well established, but reports of central nervous system (CNS) damage are exceptional. We report CNS magnetic resonance imaging (MRI) abnormalities of the brain and spinal cord as well as lesions in nerve roots and plexus in leprosy patients. Eight patients aged between 17 and 41 years underwent detailed clinical, histopathological, and MRI evaluation. All had prominent sensory-motor deficits with hypopigmented and hypo/anesthetic skin patches and thickened peripheral nerves. All demonstrated M. Leprae DNA in affected peripheral nerve tissue. All received multidrug therapy (MDT). Two patients had brainstem lesions with enhancing facial nuclei and nerves, and one patient had a lesion in the nucleus ambiguus. Two patients had enhancing spinal cord lesions. Follow-up MRI performed in four cases showed resolution of brainstem and cord lesions after starting on MDT. Thickened brachial and lumbosacral plexus nerves were observed in six and two patients, respectively, which partially resolved on follow-up MRI in the two cases who had reimaging. The site and side of the MRI lesions corresponded with the location and side of neurological deficits. This precise clinico-radiological correlation of proximal lesions could be explained by an immune reaction in the gray matter corresponding to the involved peripheral nerves, retrograde axonal and gray matter changes, or infection of the CNS and plexus by lepra bacilli. Further study of the CNS in patients with leprous neuropathy is needed to establish the exact nature of these CNS MRI findings.

Hirayama disease is generally considered to be a sporadic disorder, except for a few reports of familial occurrence. In this study, we describe eight patients from four families with cervical flexion induced myelopathy (CFIM)/Hirayama disease (HD) and intra-familial phenotypic variations. All underwent clinical and electrophysiological evaluation, while seven of them had contrast MR imaging of cervical spine in flexion. There was significant intra-familial variability: distal bimelic form in four patients, classical monomelic form in three and proximo-distal form in one. Irrespective of the clinical phenotype, MRI showed characteristic dynamic changes of posterior dural detachment with prominent epidural enhancement extending variably from C3 vertebral level to dorsal spine in six patients. One patient with 28 years of illness, had only lower cervical cord atrophy without dynamic changes while another patient demonstrated forward dural displacement with epidural enhancement even after 38 years of disease duration.

Hirayama disease (HD)/cervical flexion-induced myelopathy (CFIM) is a lower motor neuron disease conventionally affecting a single upper extremity. We describe three men progressing after a long stable period to develop severe spastic paraparesis and bladder disturbances as a protracted implication of HD. The age at onset was 20, 24, and 15 years, while the age at presentation was 27, 41, and 57 years, respectively. The second phase of disease progression occurred after 4, 13, and 28 years of stationary period. All had CFIM with characteristic magnetic resonance imaging features as observed during progressive stages. The anterior dural shift extended variably from C4 to D4 levels with a median value of 5 mm and was maximum at C6 to C7 levels, pushing the cord anteriorly causing compression. This study emphasizes the need to recognize this unusual subgroup of HD and mandates long-term follow-up with timely intervention in arresting the progression/improving the deficits.