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Central Nervous System


Hi All,

Here is a supplementary video screencast of Neurodegenerative Diseases and CNS Effects of Alcohol.

To change the video speed, please refer to the Web Resource Survey page.

If you can't play the video, watch it here on YouTube:

Here is the PDF of the lecture. This is also in your notes in MedSPACE, but slightly more detailed here.

CNS Neurodeg and Alcohol Lecture notes PDF

Click below for an excellent resource on Anatomy, which includes Neuroanatomy – made simple and practical (best to use Chrome):


The mindmaps below provide a summarised overview of the main pathologies involving the CNS.

These are not comprehensive, but, rather provide a big picture view.

MINDMAP: CNS Pathology I - Raised ICP and Intracranial Haemorrhage

If you can't play the video, watch it here on YouTube:

MINDMAP: CNS Pathology II - CNS Tumours and Infections

If you can't play the video, watch it on YouTube:


  1. NUS Student on 7th February 2018 at 11:46 pm

    Hi Dr Nga!

    Could I find out why a venous thrombus in the CNS would result in pale/bland infarct, when elsewhere in the body it usually results in congestion (red)? Thank you! 🙂

    • on 11th February 2018 at 8:47 pm


      Venous thrombosis in the brain certainly can lead to haemorrhage, but still in the context of obstruction and ischaemia, i.e. the primary pathology is an occlusive one rather than cerebral haemorrhage. Ischaemia due to vascular occlusion can result in either bland or haemorrhagic infarcts. The arterial imflow is also compromised when there is a venous occlusion, hence the ischaemia. According to the literature, about half of venous thrombosis cases show evidence of haemorrhage.
      I hope this helps clarify!

      • NUS Student on 6th February 2019 at 11:00 pm

        Hi Dr Nga! Do you mind explaining why then, do embolic causes tend to result in haemorrhagic infarcts then?

        • on 7th February 2019 at 2:42 pm

          Hello, the embolic infarcts tend to have a higher change of dissolution of the embolus and hence recanalisation (vessel reopening) and this is thought to bring about the risk of reperfusion injury – with bleeding through vessels damaged by ischaemia. There may be other mechanisms as well, but this is the most generally documented cause. It is briefly described in Robbins. You can read on this and other suggested mechanisms of haemorrhage here:

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