Nervous System Pathology 2 Flashcards
Disease causes of the nervous system.
(VITAMIN D).
Vascular related (circulatory) disease.
Inflammation/infection.
Trauma and compressive injury.
Anomalies and malformation.
Metabolic and toxic disorders.
Idiopathic.
Neoplasia.
Degenerative disease.
Vascular-related (circulatory) disease.
Often present as haemorrhage and/or malacia (necrosis) e.g. due to ischaemia.
Neurones in cerebral cortex have highest metabolic rate and can die w/in a few minutes of cessation of blood flow.
Most sensitive regions to hypoxic-ischaemic injury:
- cerebral cortex (results in laminar cerebrocortical necrosis).
- hippocampus and various nuclei.
- cerebellar Purkinje cells.
Possible causes of brain haemorrhage.
Vascular injury, altered vascular integrity (incl. rupture) or vascular degeneration associated with:
- trauma.
- inflammatory disease, vasculitis.
- infarction or ischaemic injury.
- toxic/metabolic disease.
- neoplastic disease (primary or secondary).
Coagulopathies.
Possible causes of ischaemia?
Localised:
- vascular disease:
– loss of vascular integrity.
– vascular obstruction.
–> e.g. thrombosis from localised vascular injury; embolic disease (neoplastic or non-neoplastic).
Global:
- globally reduced CNS perfusion or global hypoxia.
– cardiac arrest, HV shock, hypotension.
– severe anaemia.
– asphyxiation (incl. during parturition).
- anaesthetic accidents (loss of O2 supply, airway obstruction).
NOT SEEN HISTOLOGICALLY FOR ~6-8HRS
What does the distribution pattern of haemorrhagic/ischaemic lesions tell you about potential causes of the disease?
Focal:
- trauma.
- focal infarction or inflammation.
- spontaneous blood vessel rupture.
- neoplastic disease.
Multifocal (non-symmetrical):
- trauma.
- inflammatory disease e.g. infectious, immune-mediated.
- vascular disease e.g. vasculitis, infarctions, coagulopathy.
- neoplastic disease.
Multifocal (symmetrical):
- metabolic/toxic.
- global hypoxia.
- What is the most common cause of NS inflammation?
- Important information to consider in NS inflammation cases.
- Infectious agents.
*BUT also consider non-infectious causes e.g. immune-mediated conditions. - Signalment - e.g. spp, breed, age.
Epidemiology - single or multiple animals affected.
Distribution/anatomical location of inflammatory lesions.
Type of inflammation.
Routes of infectious agents into the CNS.
Haematogenous (most common):
- septic thromboemboli.
- infection of endothelial cells or blood monocytes.
- through choroid plexus (may gain entry to CSF).
Via CSF.
Direct extension from surrounding tissues or (rarely) penetrating injury.
- e.g. nasal cavity and sinuses (through cribriform plate), middle ear, bone (skull, vertebrae).
– meninges often good at preventing infection into brain so may be looking at things in the epidural space.
Intraneural extension:
- along peripheral nerves.
– e.g. listeria, rabies.
Bacterial infections of NS?
Any spp., but farm most common.
Often suppurative inflammation, but are some exceptions.
Distribution patterns can range from widespread meningitis and/or encephalitis to localised infection e.g. abscess.
Neonatal bacterial suppurative meningitis.
Haematogenous e.g. E.coli, Streptococci.
Neonatal/juvenile FAs.
Predisposed by lack colostrum, poor hygiene.
Meninges = cloudy, opaque, hyperaemia.
Purulent or fibrinopurulent exudate may pool in sulci, and on ventral aspect of brain.
Variable brain swelling.
May have concurrent infections at other sites e.g. joints (polyarthritis) and, in calves, eyes
(endophthalmitis).
What is the collective name for the arachnoid mater and pia mater?
How do these structures look histologically when there is meningitis?
Leptomeninges.
Expanded by suppurative material, lots of neutrophils, hyperaemia.
A secondary reaction of the brain under the meninges can occur as a result on the overlying infectious meningitis.
Some possible complications of suppurative meningitis?
Involvement of the choroid plexus (choroiditis) and ependyma (cells lining ventricular system - ependymitis) can lead to pus accumulation in ventricles (suppurative ventriculitis) and abscess formation.
Brain swelling and herniation.
Abscesses in CNS tissues.
Uncommon within spinal cord , more commonly in epidural space..
Origins:
- haematogenous – septic embolism.
–> sources of thromboembolism e.g. endocarditis.
–> bacterial emboli occurring during septicaemia.
- local extension.
– choroid plexus infections.
– meningitis (rare).
– extension from inner or middle ear infections.
– extension of infection from cribriform plate, paranasal sinuses or pituitary fossa.
– penetrating wounds, FBs (rare).
Abscesses in epidural space, especially in the spine.
Origins:
- haematogenous – septic embolism e.g. endocarditis.
- local extension.
– paranasal sinuses (into cranium).
– penetrating / traumatic wounds incl. bites or contaminated spinal needles.
- tail biting in pigs.
- tail docking in lambs.
- vertebral osteomyelitis.
- FBs e.g. migrating grass awns in dogs.
Listerial encephalitis (listeriosis).
Ruminants.
Caused by Listeria monocytogenes.
Sporadic cases or outbreaks may be associated w/ spoiled silage (pH >5.5).
Invades oral mucosa, infects cranial nerve(s) e.g. trigeminal and spreads to brainstem.
(Meningo)encephalitis in brainstem +/- spinal cord.
Clinical signs typically incl. head tilt and circling bhvr.
Gross changes often not evident.
- usually requires culture (of brainstem) and/or histopathology to diagnose.
Microscopically:
- “microabscesses” – aggregations of neutrophils and mononuclear inflammatory cells.
- perivascular cuffing by inflammatory cells.
Main viral infections affecting the NS.
Louping ill.
Equine herpesvirus-1.
Malignant catarrhal fever.
Canine distemper virus.
FIP.
Manifestations of viral infection of NS.
Viral encephalitis:
- may have no gross changes.
- additional dx tests often required to identify or confirm agent.
- typically non-suppurative inflammation w/ perivascular cuffing..
- may have neuronal necrosis.
- some viruses produce inclusion bodies e.g. rabies (Negri bodies).
- some viruses cause vasculitis e.g. FIP, EHV1.
Pre/peri-natal infections.
- some viruses can cause congenital malformations.
Fungal infections of the NS.
Generally uncommon.
Often opportunistic infection (consider immunocompromised animals).
Haematogenous spread or occasionally local extension to the brain.
Agents - Aspergillus, Candida, Cryptococcus spp. (rare in UK).
Inflammatory response typically pyogranulomatous or granulomatous.
Fungal hyphae often cause vasculitis w/ thrombosis and infarction.
May be some non-specific gross changes and culture would confirm fungal.
Parasitic - helminth - infection of the NS – Coenurus cerebralis.
Coenurus cerebralis in brain of sheep (coenurosis).
- Progressive clinical signs e.g. circling, depression, head-pressing.
Sheep is an intermediate host.
- taenia multiceps.
Dog in definitive host.
- adult T. multiceps in dog intestine.
- proglottids passed out onto pasture.
– sheep eats proglottids.
– scolex erupts out through wall of intestine into bloodstream.
– haematogenous spread to brain.
– forms cysts in brain over period of months.
Prevention:
- stop dogs eating sheep carcase.
- administer worming treatment to dogs.
Parasites affecting the NS - Protozoa and microsporidia.
Protozoa:
- Neospora caninum.
- Toxoplasma gondii.
Older animals:
- CNS inflammation.
Puppies/juveniles:
- myositis, CNS and peripheral nerve inflammation.
– predilection for lumbosacral nerves (polyradiculoneuritis).
– progressive HL paralysis w/ atrophy of HL muscles.
Cysts in brain, perivascular cuffing w/ mononuclear inflammatory cells (non-suppurative).
- Encephalitozoon cuniculi.
– in rabbits.
– primarily affects CNS and kidneys.
–> cause foci of granulomatous inflammation w/in brain.
Non-infectious, immune-mediated neurological inflammatory disease.
Group of poorly understood idiopathic and sporadic conditions.
Inflammation +/- malacia.
Dogs:
- necrotising meningoencephalitis (NME).
- necrotising encephalitis (NE).
- eosinophilic meningoencephalitis (EME).
- steroid-responsive meningitis-arteritis (SRMA).
- granulomatous meningoencephalitis (GME).
- can be disseminated, or focal discrete mass lesion.
Horse - poly neuritis (cauda equina neuritis).
Definitive dx may only be poss. on PME.
