Abstract: The nervous signs of torticollis and paralysis in chickens affected with velogenic viscerotropic strains of Newcastle Disease Virus (NDV) are most often preceded by other common signs associated with velogenic Newcastle Disease (ND). This study was carried out to investigate the time of detection of NDV in the brain of affected chickens compared with the time of detection in other organs. Velogenic NDV (VGF-1) was obtained from the National Veterinary Research Institute, Vom. Nigeria. A total of 120 white cockerels were used for the experiment. At 6 weeks of age, the birds were divided into two groups of 80 and 40, the first group of 80 served as the infected group, while the second group served as control. Birds in the infected group were challenged each with 0.2 mL of this isolate each containing embryo infective dose 50% end point (EID₅₀) of 10^6.36. Birds in the control group were inoculated with 0.2 mL of Phosphate Buffered Saline (PBS). Clinical signs and post mortem lesions were observed and recorded. Internal organs including the brain, proventriculus, spleen, thymus and bursa of Fabricius were collected at Post Mortem (PM) from the infected group and after sacrifice from the control group on days 5, 6, 7 8, 9, 10, 11, 12 and 21 Post Inoculation (PI). The organs collected on each day (five from infected and three from control) were pooled together on the basis of organs. Tissues extracts were prepared to constitute 80% suspension in PBS by homogenizing the pooled organs and using 4 gm of this with 1 mL of PBS. Each was centrifuged at 3000 rpm for 30 min and the supernatant collected. The supernatant was assayed for NDV using Haemagglutination (HA) and Haemagglutination Inhibition (HI) tests. Results showed typical clinical signs and PM lesions associated with velogenic ND. However, paralysis and torticollis appeared among few birds later in infection as compared to other signs of dullness, reduction in feed and water intake and greenish diarrhea. HA activity was seen in tissues extracts prepared from the brain by day 10 PI as compared to other organs, where it was detected earlier at day 5 PI. It was concluded that after viraemia, viruses multiplied first in non-nervous tissues and later in the nervous tissues. A possible explanation for this delay could be the role played by the blood-brain barrier in restricting the rate of infection of the nervous tissues. This may also explain why nervous signs appeared later in infection.