Neurology Lectures 3,4,5 Flashcards
i) State two causes of hepatic encephalopathy ii) State the pathogenesis of hepatic encephalopathy
i) Hyperammonemia from hepatic failure and hyper-uraemia from renal failure ii) 1. Excess ammonium is metabolised by astrocytes to glutamine 2. Osmotic changes w/development of cytotoxic oedema 3. Spongy vacuolation of myelin
What are the three main primary neoplasia’s of the CNS?
- Meningioma 2. Oligodendroglioma 3. Astrocytoma
Name the lesion and the cause of the pathology seen below and provide a possible pathogenesis:
Lesion: Polioencephalomalacia
Cause: Thiamine deficiency in herbivores - polioencephalomalicia. Main causes are ruminal acidosis + bracken fern (contains thiaminases)
Pathogenesis of condition:
- Acidosis kills thiamine producing bacteria
- Thiamine diphosphate is used in carbohydrate metabolism + neutrotransmitter release
- Disease occurs due to energy deprivation through Krebs cycle arrest + oxidative stress
- Results in free radical production (causing necrosis) + production of abnormal neutrotransmitter (excitotoxicity)
Name the lesion that is shown below and state a potential cause of it:
Clostridium enterotoxaemia - caused by overgrowth of clostridum perfringens type D
Name the condition that is shown in the image below:
CNS Oedema
Name the condition that is shown in the image below and provide an example of a condition that could cause it:
Cerebellar hypoplasia - cats, sheep and cattle - Feline panleukopenia virus, BVDV + Border disease virus
Name the condition that is shown below, state and cause and state how the presentation of this condition may vary in herbivores:
The cause of this lesion is deficient diets - diets high in thiaminase containing fish or destroyed by heating - leads to bilaterally symmetrical malacia (necrosis) of neurons in caudal colliculi of brainstem
Name the condition that is shown + provide a pathogenesis for it:
IVDD
Pathogenesis:
- In chondrodysplastic breeds the nucleus propulsis contains significiantly more collagen
- Gradually it almost completely becomes replaced by fibrocartilagenous material
- Eventually it becomes mineralised
- Degeneration of the inner portion of the annulus fibrosis
- Tearing of the annulus fibrosis
- Massive extrusion of degenerate nuclear material through annulus fibrosis + dorsal longitudinal ligament into spinal cord
- Compression on the spinal cord
- Wallerian degeneration
Type 2 = simmilar however it is not as severe - Dorsal longitudinal ligament remains intact
Briefly explain the pathogenesis of rabies and bat lyssaviruses:
Pathogenesis:
- Virus replicates in myocytes for a short period of time
- Enters local neuromuscular tissue
- Retrograde axonal transport
- Viral replication in CNS
- Spread to exit portals (nasal mucosa + salivary glands)
Name the condition that is shown below and provide a possible aetiological agent responsible for it:
Thrombotic Meningoencephalitis - caused by histophillus somni
Name the toxin that is responsible for tetanus and provide the pathogenesis of it:
a. The toxin is produced by Clostridium tetani
b. Pathogenesis:
- Tetanus bacterial toxin blocks the release of glycine (inhibitory) from Renshaw cells
- Unrestricted release of acetylcholine from motor neurons –> unrestricted stimulation + contraction of muscle –> spastic paralysis
Provide the pathogenesis of tick paralysis:
- Tick paralysis blocks axonal Na+ channels
- Inhibitis the release of acetylcholine
- Total neuromuscular blockade –> flaccid paralysis
Name the toxin that is responsible for botulism and provide the pathogenesis of it:
a. Clostridium Botulin
b. Clostridum Botulinum –> prevents release of acetylcholine –> lack of stimulation to muscles –> flaccid paralysis
Provide the a description of the pathogenesis of myasthenia gravis:
The antibodies directed toward the Ach receptor block ACh that is released from nerve a NMJ
