Test 2- Neuro Flashcards
1
Q
Ectodermal Origin
A
Ectodermal Origin (sensitive to hypoxia)
- Neurons
- Astrocytes
- Oligodendrocytes
2
Q
Mesodermal Origin
A
Mesodermal Origin (not as sensitive to hypoxia)
- Microglia
- Vascular endothelium
3
Q
nuclei
A
Arranged in nuclei
– CNS
4
Q
ganglia
A
• Arranged in ganglia
– PNS
5
Q
A
Neuron with nissl substance
6
Q
A
Chromatolysis in a neuron
7
Q
Chromatolysis
A
- Swelling of cell body and dissolution of nissl granules with margination of nucleus
- Degenerative change (reversible)
- Non-specific cause (eg injuries to axons, overstimulation/deficiencies)
- Seen in EMN, dysautonomias, copper def,
8
Q
A
Acidophilia
Ischemic change, permanent
Cell death
Cell is shrunken, acidophilic, angular
Nucleus pyknotic-absent
Depending on cause may be regional
Occurs in trauma, hypoglycaemia, thiamine deficiency
9
Q
A
Cytoplasmic vacuolation
• Lipid
Intracytoplasmic oedema
Lysosomal storage (accumulation of products) eg GM1 gangliosidosis
Transmissible Spongiform Encephalopathies (TSE eg BSE)
10
Q
A
Rabies inclusions (in cytoplasm)
11
Q
A
Herpes inclusion body (in nucleus)
12
Q
Neuronophagia
A
Neuronophagia “eating neurons”
- Phagocytosis of neurons by microglia/monocytes
- Hallmark in some viral infections
13
Q
oligodendrocytes
A
sythesized myelin in the CNS
14
Q
Schwann cells
A
synthesize myelin in the PNS
15
Q
gliosis
A
Proliferation of astrocytes
16
Q
gemistocytes
A
Swelling of astrocytes
17
Q
Gitter Cell
A
Following brain trauma microglial cells will replicate and activate to clear up debris
18
Q
Myelophages
A
Microglial cells, when they mop up myelin are called myelophages
19
Q
Ependymal Cells
A
- Ciliated cubodial cells lining neural canal, ventricles, choroid plexus
- Formation of CSF
20
Q
A
Cerbellar coning
21
Q
A
Vasculitis (inflammation of a blood vessel)
22
Q
A
Area of malacia(softening) within a portion of brain
23
Q
Encephalo
A
involving brain
24
Q
A
GM1 Gangliosidosis of
Friesian Calves
25
Parasitic cysts in various portions of brain
26
Coenuris cerebalis
Common in sheep
T. Multiceps (dog faeces)- ingestion by sheep- migration to CNS
Acute Gid: 3-4 weeks following ingestion, multiple parasites & malacia
Chronic Gid: 6 months PI, cysts large, compression, oedema, hydrocephalus, bone softening.
– Cerebrum most common location
27
Toxoplasmosis
* Sheep: abortion, multifocal encephalitis in foetus
* Dogs: rare, as complication of CDV immunosuppression
* Cats: rare
28
Typical cotyledon necrosis seen in toxoplasmosis abortions
29
Neospora Caninum
* Dog is definitive host, excretes oocysts in faeces
* Similar to T gondii
• Vertical (transplacental) transmission – Myositis/ meningoencephalomyelitis
– Hindlimb paralysis
- CAN CAUSE ABORTIONS IN CATTLE!
30
Neospora caninum Myelitis / Myositis
Seen in spinal cord in this case leading to paralysis
31
Equine protozoal encephalomyelitis
Most common disease in horses with multifocal or asymmetric neurologic deficits.
Sudden or gradual onset of pelvic limb paresis and ataxia
Caused by infection with Sarcocystis neurona
32
In the horse the organism replicates in the CNS rather than in muscle.
Asymmetry of clinical signs help to differentiate this disease from wobbler syndrome and herpesvirus myeloencephalitis (usually symmetric or mildly asymmetric).
33
Halicephalobus gingivalis (H. deletrix) and Strongylus vulgaris larvae migration are the most common cause of verminous encephalomyelitis in the horse
Cerebrospinal nematodiasis, horse,
34
Cat, Cryptoccocus neoformans (cryptococcal meningo- encephalitis)
Viscous mucoid exudate–mucopolysaccharide capsule of the yeasts
35
Swayback
• Newborn or young lambs
Copper deficiency during periods of myelination
Deficiency can be primary or secondary (competing with sulfates)
• Forms
– Congenital
– Delayed
– Acute delayed
36
Congenital Swayback
From birth, blind, unable to suckle
Cavitation/gelatinous subcortical white matter
Hydranencephaly/hydrocephalus
See wallerian degeneration of spinal cord
Bilateral, symmetrical in dorsolateral and
ventromedial columns
37
Congenital Swayback / Lamb
Marked loss of white matter making ventricles look big
38
Delayed swayback
• At 1-2 months show ataxia
No gross brain lesions
Chromatolysis of neurons in red nucleus and brainstem nuclei
Spinal cord lesions similar to congenital form
39
Pathogenesis of Swayback
* Not sure
* Cu needed for myelin stability, for cytochrome oxidase and superoxide dismutase
* Accumulation of toxic superoxides
Large neurons rich in cytochrome oxidase
Get neuronal damage (mitochondrial)
Axonal degeneration then secondary demyelination
Loss of support for myelin
* Congenital form observed when Cu deficiency occurs during 100-120 days of gestation
* Period of marked myelination in cerebrum and cord
* Mild winters
* Less hand feeding
* Soil intakes (rich in molybdenum/sulphates)
• Admin Cu injections to ewes mid- pregnancy
40
Cerebrocortical Necrosis
• Laminar cortical necrosis, polioencephalomalacia
• Young ruminants (cattle/sheep)
– Cattle 4-6 mts, june-august
– Sheep, no age or seasonal predisposition
* Sudden onset 5-10days after change in pasture/management
* Blindness, opisthotonus (star-gazing), nystagmus, convulsion, death
41
CCN
Gross Pathology
* Brain swelling & herniation in acute cases
* Reduction in brain size and narrowing of gyri in chronic cases
* Affected areas yellow-tan coloured with autofluorescence under UV light
42
Since the lesions of CCN are hard to see what do you do?
43
CCN aetiology
Thiamine deficiency
Animals respond to thiamine within hours
Thiamine critical for carbohydrate metabolism
Low in young ruminants (ruminal microbes)
Diet changes lead to proliferation of thiaminase producing bacteria (Cl sporogenes)
44
Thiamine deficiency
Thiamine deficiency is also reported in cats, dogs and farmed wild carnivores (mink and foxes).
Diets containing fish as the primary ingredient contain high levels of thiaminase (destroys thiamine).
Diets based entirely in cooked meat are thiamine deficient and also produce the disease
45
Hound Ataxia
* Ireland, UK
* Foxhounds, Beagles, Harriers
* Packs fed on paunches (rumen/intestines)
• No access to carase meats
* Ataxia
* No pain
* Sluggish reflexes
• No gross lesions
Degenerative myelopathy
Myelin vacuolation of descending motor tracts
Axons preserved
Disappeared when carcase diet restored
Suggested methionine deficiency
46
Salt Poisoning
* Common in pigs, occasional in ruminants
* Direct- excessive salt in diet & restricted water (rare, no swill feeding)
* Indirect- water supply restricted (frozen pipes, or relative if animals have diarrhoea)
* Acute onset convulsions, opisthotonus, blindness, recumbency, paddling
* High mortality
* Gross lesions – brain swelling (congestion/oedema)
47
Histo of salt poisioning
Histopathology
Oedema/laminar necrosis of cerebral cortex
Eosinophils in perivascular spaces (first 48 hours)- pathognomonic in pigs
Neuronal changes (degeneration- death)
48
Laminar Necrosis in salt poisoning
49
Salt Posioning Pathogenesis
* High intracellular Na, reduced ATP for Na/K pump --- intracellular oedema
* Increased vascular permeability ---- extracellular oedema
* Neurons synthesize small mol. Wt proteins, chemotactic for eosinophils
* Return water slowly or else get excessive oedema
50
Lead Poisoning
* Occurs in all species, but mainly cattle/calves
* Batteries, old paint, fishing weights, contaminated feeds
* Confirm with kidney lead
* Acute, subacute, chronic disease
Acute most common
Convulsions, bellowing, blindness, hyperaesthesia
PNS damage also eg oesophageal impaction, laryngeal paralysis
51
Lead poisoning- gross pathology and histo
• Gross pathology
– Cerebral oedema, congestion with brain swelling
• Histopathology
– Endothelial cell degeneration with astrocytic swelling
– Vasogenic oedema
– Neuronal ischemia & necrosis (laminar)
52
Focal Symmetrical Encephalomalacia
* Lambs (calves)
* Associated with Cl perfringens type D
enterotoxaemia
• Acute onset head pressing, paralysis, death
* Short course
* Gross pathology
– Brain swelling, bilateral symmetrical areas of malacia in midbrain, thalmus, hippocampus, frontal cerebral cortex, cerebellum
53
Focal Symmetrical Encephalomalacia
54
Focal symmetrical Encephalomacia HISTO
Histopathology
– Oedema, sometimes haemorrhage (perivascular), white and grey matter malacia, swelling of endothelial cells
55
Oedema Disease
Rapidly growing weaner pigs
• Haemolytic E Coli endotoxaemia
• Sudden changes in feeding systems
• Acute onset, convulsions, pigs die with 24 hours
Brain oedema
Fibrinoid Necrosis of small blood vessels
Oedema
Encephalomalacia (cerebrospinal angiopathy)
56
fribrinoid necrosis
57
MOULDY CORN TOXICITY
Ingestion of moldy feed, specially corn and corn by-products - contaminated by the fungus Fusarium verticillioides (F. moniliforme ) and/ or F. proliferatum (Fumonisin B1)
58
Leukoencephalomalacia in horse with mouldy corn toxicity
59
Bilaterally symetric foci of liquefactive necrosis within the
substantia nigra, Horse, UCDavis. Affected horses exhibit idle drowsiness and
are unable to grasp food or drink water. Purposeless chewing motions are apparent. Horses die of starvation, dehydration or aspiration pneumonia
60
Hepatic Encephalopathy
• Acute/chronic liver disease
* Cattle- ragworth poisoning
* Dogs- porto-systemic shunts
• Sheep- copper posioning
61
Some dramatic neurological disorders do not produce extensive neuropathology
Examples....
Some dramatic neurological disorders do not produce extensive neuropathology
* Strychnine
* Metaldehyde • Tetanus
* Botulism
62
Dysautonomias
Dysautonomias
• Degenerative changes in autonomic ganglia
– Key-Gaskell Syndrome in cats – Grass sickness in horses
– Chromatolysis, vacuolar degeneration in sympathetic and parasympathetic ganglia
63
Key-Gaskell Syndrome
Pupillary dilation
Megaoesophagus, constipation
Anorexia, dehydration •
Few survive
Was more common in early 1990s
UK mainly
64
Grass Sickness
Acute, subacute, chronic
Dyphagia, bowel stasis
Distended abdomen, constipation
Mortality almost 100%
Ileal biopsy (enteric ganglia) for antemortem diagnosis
65
Equine Motor Neuron Disease
Progressive weakness, muscle atrophy, weight loss
USA, UK & Ireland
Sporadic
Both sexes, all ages
(outbreaks in Brazil)
• No gross lesions
• Degeneration and loss
of motor neurons in ventral
horns of spinal cord
• Some degenration of neurons in brain nuclei
66
CNS neoplasia
* Primary CNS tumours rarely metastasise outside CNS
* Extracranial tumours can metastasis to CNS • Mammary carcinomas, lymphosarcoma
* Grow expansile, cause compression, hydrocephalus
* Prognosis poor
* Glial more common than neuronal • Most solid, firm, greyish
* Haemorrhagic if rapidly growing
67
Most common CNS tumors
Astrocytoma \*
Oligodendroglioma\*
Meningioma\*
Pituitary\*
68
Medullablastoma
* Undifferentiated cells of cerebellum
* Cells of external granular layer
* Rare in animals (children more common)
69
Astrocytoma
• Most common
70
Oligodendroglioma
71
Choroid Plexus Tumour
72
Meningioma
* Frontal, retrobulbar areas
* Most common in cats
* Histologically benign (shell-out)
73
Meningioma Dog
74
Meningioma Cat
75
Pituitary Tumours
• Chromophobe adenoma
Diabetes insipidus (pressure on pars nervosa, interference with ADH transport to nervosa)
Hyperadrenocorticism (ACTH producing chromophobes
• Dogs/horses
76
Pituitary Tumours (equine)
77
Canine, metastatic mammary tumour
78
Metastatic Hemangiosarcoma
79
Osteochondroma: tumor of calverium compressing on brain
