Neurology Exam 1

Front 1

Differentiate between white matter and grey matter.

Back 1

White matter-ascending and descending tracts of axons of UMNs.
Grey matter-neuronal cell bodies and synapses of UMNs and LMNs.

Front 2

What are intumescences? Where are they located?

Back 2

Enlargements of the spinal cord that contain LMNs to the limbs.
Cervicothoracic-C6 to T2
Lumbosacral-L4 to S3

Front 3

What are the four segments of the spinal cord?

Back 3

Cervical: C1-C5
Cervicothoracic: C6-T2
Thoracolumbar: T3-L3
Lumbosacral: L4-S3

Front 4

At what levels does a focal spinal cord lesion cause LMN deficits, UMN deficits, and sensory deficits?

Back 4

LMN deficits are seen at the level of the lesion. UMN deficits are seen caudal to the lesion. Sensory deficits are seen at the level of and caudal to the lesion.

Front 5

What are signs of lesions affecting UMNs?

Back 5

1. paresis/paralysis
2. normal/exaggerated reflexes
3. normal/increased muscle tone with spasticity
4. muscle atrophy if lesion is chronic

Front 6

What are signs of lesions affecting LMNs?

Back 6

1. paresis/paralysis
2. weak/absent reflexes
3. decreased muscle tone
4. marked, rapid muscle atrophy

Front 7

What is ataxia, what are the symptoms of ataxia?

Back 7

Ataxia is inappropriate gait/posture caused by loss of proprioception. Symptoms include: swaying, staggering gait, scuffing paws, inappropriate limb placement while walking, and change in stride length.

Front 8

How does an UMN lesion affect stride length vs a LMN lesion?

Back 8

UMN lesion will increase stride length.
LMN lesion will decrease stride length.

Front 9

What is paresis/plegia? What differentiates paraparesis/plegia from tetraparesis/plegia?

Back 9

Paresis is decreased voluntary movement in the limbs, plegia is absence of voluntary movement in the limbs. This can be caused by UMN or LMN lesions. Para- only involves the pelvic limbs; tetra- involves all 4 limbs. Animals with paresis/plegia will also exhibit ataxia.

Front 10

What is Schiff-Sherrington posture? Explain it's cause, and clinical significance.

Back 10

S-S posture is increased extensor tone in the thoracic limbs. Border cells in the lumbosacral intumescence synapse in the craniothoracic intumescence to inhibit LMN to the extensor muscles. When a lesion between the two disrupts this inhibition, extensor tone is increased. Typically occurs with acute, severe lesions in the TL spinal cord. Does not indicate irreversibility of the lesion.

Front 11

How is proprioceptive positioning tested? What is the benefit of this test, and what might be confounding factors?

Back 11

Proprioception is tested turning the paw so it is weight bearing on the dorsal surface and allowing the animal to replace the paw in a normal position. This test is good for differentiating between neurologic ataxia and orthopedic ataxia. Because a paralyzed animal cannot replace the paw in a correct orientation, this will mask the presence or absence of proprioception.

Front 12

How is hopping performed to assess neurologic function? What is this test useful for evaluating?

Back 12

Support all limbs but one, with as much weight as possible on the remaining limb. Move the animal to get them to hop on the one limb. This test can be useful for detecting subtle weakness in a limb that might not be seen while weight is evenly distributed, and for comparing right and left sides to detect asymmetric deficits.

Front 13

How is "placing reaction" tested? What might confound this exam?

Back 13

Move the animal forward so that the front paws touch the edge of a table. The animal should place their paws on the table. This is done with eyes open (tests vision), and covered (tests tactile sense). Small dogs that are used to being carried everywhere may not elicit an appropriate reaction even when there are no neurological deficits.

Front 14

Patellar reflexes and other myotatic reflexes are performed how? What information can be gathered from this type of examination?

Back 14

The animal is placed in lateral recumbency, and the appropriate tendon is slightly stretched/tensed, the tendon is then tapped to elicit a normal reflex response. The various myotatic reflexes can be used to assess LMN function as well as the integrity of associated spinal cord segments. The patellar reflex is the only reliable reflex test in cats and dogs. Exaggerated reflex, or clonus, is indicative of UMN lesions; absence of reflex is indicative of LMN lesions.

Front 15

How is a flexor reflex test performed? What does it indicate, not indicate, and what other test can often be performed simultaneously?

Back 15

While in lateral recumbency, the limb is extended, then the toe is pinched to elicit withdrawal of the limb. Appropriate response indicates the integrity of the associated spinal segment (C6-T2 thoracic limb, L6-S2 pelvic limb). Withdrawal alone does not indicate that the animal can perceive pain. However, if whining, biting, or other behavior reaction is elicited during this test it can indicate pain perception.

Front 16

What is a crossed extensor reflex?

Back 16

A crossed extensor reflex is an abnormal response in which the contralateral limb is extended when a withdrawal reflex is elicited. This indicates an UMN lesion.

Front 17

How is the cutaneous trunci reflex tested? What does it indicate?

Back 17

The cutaneous trunci reflex is elicited by pinching the skin on the dorsal surface of the thoracolumbar region (T3-L3) to observe twitching of the cutaneous trunci muscle. This reflex is useful for localizing lesions in this region. Response will be absent caudal to the lesion, possibly exaggerated at the level of the lesion, and normal above the lesion.

Front 18

What are the steps of appropriate spinal palpation?

Back 18

The entire spine, including the neck and joint of the tail should be palpated gently on the spinous processes, articular processes, and transverse process or ribs. While palpating the neck, a hand should be placed on the cervical muscle to detect tensing of the muscles; while palpating the thoracolumbar spine, a hand should be placed on the abdomen to detect tensing of the abdomen. If light palpation does not elicit pain, the neck may be gently flexed side to side and up and down, the spine may be manipulated ventrally and laterally, and the tail should be extended and flexed. Based on the animal's history, it is best to leave the painful portion for last to prevent continued reaction in non-painful locations (eg. if neck is painful, start at the tail).

Front 19

Why does intervertebral disk herniation rarely occur at T2-T10?

Back 19

The intercapital ligament connecting the left and right rib heads at these joints stretches across the dorsal aspect of the disk, preventing it from rupturing.

Front 20

What are the two types of intervertebral disk degeneration?

Back 20

Type I-cartilageous degeneration: occurs in chondrodystrophic breeds, and causes acute extrusion typically at a young(er) age.
Type 2-fibrous degeneration: occurs in large breed dogs, causes chronic (and smaller) protrusions that occur at an older age.

Front 21

What changes occur within the spinal cord during intervertebral disk disease?

Back 21

Mechanic derangement of tissue
Ischemia
Edema
Hemorrhage (hematomyelia)
Release of free radicals
Damage may ascend and descend from original location.

Front 22

What three factors determine the severity of neurological deficits seen with IVDD?

Back 22

Amount of disk extruded
Rate of extrusion
Duration of compression

Front 23

What are the two most common sites of IVDD?

Back 23

Cervical: C2-3
Thoracolumbar: T11-12

Front 24

What are the stages of neurologic signs caused by IVDD?

Back 24

1. Pain
2. Paresis
3. Paralysis
4. Loss of pain perception
5. Ascending/descending myelomalacia

Front 25

What are common signs of thoracolumbar disk disease?

Back 25

Pain
Kyphosis
Paraparesis/paraplegia
Spreading myelomalacia

Front 26

What are common signs of cervical disk disease?

Back 26

Pain
Neck flexion
Thoracic limb lameness
Tetraparesis/tetraplegia
Respiratory arrest

Front 27

What radiographic findings are diagnostic for IVDD?

Back 27

Narrowed disk space, intervertebral foramina, and space between the articular facets
Wedged-shaped disk space
Opacity within the IV foramina
Calcified disk within the IV space indicates disk degeneration but not extrusion.
*Positioning is imperative to get diagnostically useful radiographs.

Front 28

What additional diagnostic step (after radiographs) should be pursued before surgery to correct IVDD?

Back 28

Myelography, CT, or MRI should be used to confirm location of the lesion.

Front 29

Principles of non-surgical management of IVDD

Back 29

Indications: pain only, or mild neurological deficits
Exercise restriction, in a crate just large enough to stand up, lay down, and turn around, is the most important aspect of non-surgical management. Analgesics and anti-inflammatories may be used, but do not "cure" the problem.
Cage rest for 2 weeks, if returning to normal, slowly reintroduce activity over 2-4 weeks.

Front 30

Principles of surgical management of IVDD

Back 30

Indications: Substantial neurological deficits, cases unresponsive to cage rest, or recurrent episodes.
Hemilaminectomy: Used for thoracolumbar lesions. Pedicles, articular facets, and lamina are removed on one side to expose the vertebral canal and extruded disk material is removed. Landmark is the rib of T13.
Ventral slot: Used for cervical lesions. Ventral side of the vertebral bodies is approached by incising on midline and moving all other structures to the side. Slot is made in through the vertebral body to expose the vertebral canal. The sharp ventral process of C1 and the wide transverse processes of C6 are used as landmarks.
Fenestration: Combined with hemilaminectomy or ventral slot. Disc space is incised and the nucleus removed, to prevent further extrusion. May also be done on adjacent discs to prevent rupture at other "hot spots".

Front 31

Prognosis of IVDD

Back 31

Pain only: 80-90% recover with cage rest, 30% recurrence.
Paresis: Similar to pain only.
Paralysis: 80-90% recover with surgical correction, 20-30% recover with cage rest.
Loss of deep pain: 50% recover if surgery is performed in the first 24 hours, less than 5% if more than 24 hours.
Ascending-descending myelomalacia: Almost no chance for survival, death due to respiratory paralysis.

Front 32

Spondylosis deformans

Back 32

Formation of body spurs or bridges across the intervertebral disc space.
Pathogenesis: non-inflammatory degenerative disease secondary to breakdown of the outer annulus fibrosis fibers.
Incidence: Most common in large breed dogs and older cats.
Diganosis: Radiographs-lateral and ventral osteophytes at the edge of the vertebral body (below/around disc space, not in it!)
Clinical significance: None. Often an incidental finding, and does not cause any clinical signs. In rare cases, may cause stiffness or mild pain.

Front 33

Degenerative myelopathy

Back 33

Degeneration of the axons and myelin in the white matter of the thoracolumbar spinal cord.
Pathogenesis: caused by a mutation in the superoxide dismutatse 1 gene.
Incidence: occurs in older dogs; German shepherds (and crosses), corgis, and boxers are predisposed.
Clinical signs: Insidious onset of pelvic limb ataxia-paresis. Postural deficits, UMN signs in rear limbs, later in disease forelimbs may be affected too. This is not a painful disease.
Diagnosis: Based on signalment, history and neuro findings. Often differentiated from disc protrusion and neoplasia by the lack of pain. Genetic testing is available.
Treatment: No effective treatment is currently available.
Prognosis: Prognosis for recovery is poor; depending on the level of care provided, average survival time is 6-12 months.

Front 34

Degenerative lumbosacral stenosis

Back 34

Compression of the cauda equina due to narrowing of the vertebral canal and intervertebral foramen in the lumbosacral area.
Pathogenesis: 1. Typic II degeneration of the L7-S1 disc, leading to protrusion. 2. Collapse of the disc space leading to nerve root compression. 3. Thickening of the interarcurate ligament, compressing the cauda equina from above.
Incidence: common in middle-aged, medium to large breed dogs. Working/military dogs are over-represented.
Clinical signs: lumbosacral pain, unilateral or bilateral pelvic limb lameness, incontinence, tail weakness, weak flexor reflex, weak perineal reflex.
Diagnosis: History and PE findings. Imaging-MRI is best, other forms of imaging often non-specific.
Treatment: similar to IVDD, mild cases may respond to rest and anti-inflammatories; surgery is a dorsal laminectomy (ileum prevents hemilaminectomy).
Prognosis: Good if pain/ataxia only. Poor in dogs with incontinence, but surgery still typically worth trying. Working dogs have a more reserved prognosis, and my not be able to resume work even if clinical signs resolve.

Front 35

Canine cervical Spondylomyelopathy

Back 35

Compression of the cervical spinal cord secondary to malformation or misarticulation of the vertebra.
Pathophysiology: Hereditary factors and/or over nutrition (large breed dogs) lead to orthopedic developmental defects. Ultimate results are: stenosis of the vertebral canal, malformation of the articular processes, disc protrusion, and hypertrophy of the ligamentum flavum and joint capsule.
Incidence: Great danes/giant breed dogs less than 1 year of age due to severe malformations. Dobermans older than 6 years of age due to secondary changes.
C5-6 and C6-7 are most often involved.
Clinical signs: Onset of signs may be acute or chronic. Ataxia, abnormal proprioception, cervical pain.
Diagnostics: Radiographic findings are non-specific but good for ruling out other differentials. Myelogram or MRI suggested for definitive diagnosis.
Treatment: Medical management of less severe cases. Surgical treatment is best and based on type of lesion and location of lesion.
Prognosis: Variable, prediction is difficult. Long-standing signs or multiple compression sites worsen prognosis.
It is important to screen for other diseases that may impair healing ability such as hypothyroidism, van Willebrand's disease, or cardiomyopathy.

Front 36

Hemivertebrae

Back 36

Malformation in which a portion of the vertebra does not develop. Typically results in a triangular shaped vertebra.
Incidence: Common in brachycephalic breeds with "screw" tails.
Clinical signs: Frequently of no clinical significance, but can cause instability and compression of the spinal cord. Problems typically occur at 6-12 months of age.
Most often occurs in the thoracolumbar region.
Diagnosis: Myelogram, CT, or MRI.
Treatment: decompression and stabilization.

Front 37

Block vertebrae

Back 37

Pathophysiology: Congenital defect results in partial or complete fusion of two (or more) vertebral bodies.
Signs: Usually of no clinical significance. May make adjacent discs more prone to extrusion, but not proven.

Front 38

Spina bifida

Back 38

Developmental failure of fusion of the vertebral arches.
Three types: Occulta-no protrusion of meninges or spinal cord, meningocele-protrusion of just the meninges (with pocket full of CSF), myelomeningocele-protrusion of the meninges and spinal cord.
Pathophysiology: failure of the neural tube to close or cleft formation after closure. May be genetic or due to teratogenic toxins.
Incidence: common in bulldogs and manx cats. Lumbosacral area is most commonly affected.
Clinical signs: may be insignificant (occulta); meningitis common with meningiocele; neuro deficits with myelomeningocele, degree is variable but paraparesis and incontinence most common.
Diagnosis: Radiographs and myelogram
Treatment: surgical closure of meningocele is possible; treatment not often necessary for occulta; nothing to be done for myelomeningocele.

Front 39

Sacrocaudal dysgenesis

Back 39

Malformation of agenesis of the sacral and caudal vertebra
Pathophysiology: autosomal dominant trait, often lethal in homozygotes.
Incidence: Manx cats and other tail-less breeds.
Clinical signs: Tail-less, often with no other signs; incontinence, absent anal and urinary sphincter tone, paraparesis, "bunny hop" gait, weak flexor reflexes.
Diagnosis: radiographs/myelogram
Treatment: symptomatic therapy.

Front 40

Myelodysplasia

Back 40

Malformation of the spinal cord itself.
Pathophysiology: inherited neural tube defect.
Incidence: congenital lesion of Weimeraners. Leads to hydromyelia/syringomyelia, spinal cord dysplasia or hypoplasia. Most severe in lumbar segments.
Clinical signs: Nonprogressive paraparesis, "bunny hop" gait. Onset at 4-6 weeks of age.
Diagnosis: clinical findings.
Treatment: none
Prognosis: since deficits do not progress, prognosis depends on the severity of the deficits.

Front 41

Atlantoaxial Subluxation

Back 41

Subluxation of the C1-C2 joint, typically due to congenital malformation
Pathophysiology: Agenesis or hypoplasia of the dens, fracture of the dens, agenesis or hypoplasia of connecting ligaments, traumatic rupture of the ligaments.
Incidence: Most common in toy breed dogs, at less than one year of age.
Clinical signs: Neck pain, gait deficits, tetraparesis, spinal reflexes normal to exaggerated (UMN), respiratory paresis/paralysis in severe cases.
Diagnosis: radiographs-inc space between C1 arch and C2 spinous process, dorsal displacement of C2, absence of dens.
Treatment: Neck brace works well for traumatic rupture of ligaments. Surgical correction-dorsal fixation (wire loop between arch of C1 and spine of C2), or ventral fixation (pins, screws, or plate, often accompanied by bone graft fusion).
Prognosis: Depends on severity of neuro signs. High rate of complications and failure of surgical correction, but prognosis is good if surgical correction holds for the first 6-8 weeks.

Front 42

Multiple Cartilagenous exostoses

Back 42

Benign proliferation of the epiphyseal region.
Pathophysiology: Any bone with endochondral ossification can be involved. Vertebral involvement causes compression of the spinal cord. Growth of lesions stops at skeletal maturity.
Incidence: uncommon; occurs in dogs, cats, and horses.
Clinical signs: progressive, asymmetrical, focal spinal cord lesions in immature animals.
Diagnosis: Radiographs-lesions will be circular, smooth, and normal density. Myelogram required to identify cord compression.
Treatment: surgical removal
Prognosis: Good. Lesion may recur if remove is required before skeletal maturity is reached.

Front 43

Syringomyelia/hydromyelia

Back 43

Hydromyelia: accumulation of fluid in an enlarged central canal. Syringomyelia: fluid filled cavities within the spinal cord (involves tissue outside the central canal).
Pathophysiology: Caused by trauma, neoplasia, inflamation, and developmental malformations. Most common malformation is the Chiari I malformation-underdevelopment of the occipital bone overcrowds the caudal fossa and prevents correct circulation of spinal fluid.
Incidence: Chiari I malformation is common in Cavalier King Charles spaniels.
Clinical Signs: Progressive ataxia and paresis, scoliosis, spinal pain and neck pain, persistent scratching at the base of the head or shoulders.
Diagnosis: MRI
Treatment: Directed at the underlying cause if not congenital. Medical treatment-corticosteroids, gabapentin, and omeprazole will slow progression but not cure it. Surgical decompression of the caudal fossa for Chiari I malformations.
Prognosis: 80% success with surgical correction.

Front 44

Dermoid sinus

Back 44

Invagination of skin over the spine extending partially or completely to the dura mater.
Pathophysiology: failure of separation of the neural groove from the epidermis.
Incidence: most common in Rhodesian ridgebacks.
Clinical signs: If tract is not patent may be asymptomatic. If patent, meningitis, focal or generalized spinal pain, and gait deficits.
Diagnosis: palpation of fibrous tract, CSF analysis, radiographs-tract between spinous processes will be visible.
Treatment: Surgical correction (must get all the way down to the dura mater) of patent tract, antibiotics. Non-patent tracts typically do not require any treatment.

Front 45

Hypervitaminosis A of cats

Back 45

Exostosis of the spine caused by excess dietary vitamin A. Most severe in the cervical vetebra.
Pathophysiology: Caused by feeding mostly liver, or oversupplementation.
Incidence: Cats
Clinical signs: Insidious onset of neck rigidity and pain, paresis.
Diagnosis: Dietary history paired with radiographic findings.
Treatment: Changing diet will stop progression, but does not reverse condition.

Front 46

Spinal Tumors

Back 46

Three types: Extradural (50%), Subdural/Subarachnoid (35%), and Intramedullary (15%).
Incidence: Any aged animal. Neuroepitheliomas most common in large breed dogs less than 3 yrs of age. Spinal lymphoma is most common in cats.
Clinical signs: Rate of progression varies by tumor type. Acute or chronic. Spinal pain is usually the first sign, although intramedullary tumors may be nonpainful. Specific neurologic deficits depending on location.
Diagnosis:
1. Radiographs-lysis associated with vertebral tumors.
2. Myelography-extradural, lines diverge away from mass; intradural-extramedullary, filling defect will be circular on one view, and a break in the column on the other; Intramedullary, lines diverge away from the cord in all views.
3. CT-more sensitive than radiographs for vertebral lysis.
4. MRI-intramedullary tumors.
Treatment: Surgical excision can be done for some intradural-extramedullary tumors; chemotherapy or radiation therapy.
Prognosis: generally poor, but varies depending on tumor type and degree of cord damage.

Front 47

Discospondylitis

Back 47

Infection of the vertebral body and disk space.
Pathophysiology: Hematogenous spread, foreign body migration, or penetrating wounds. Staph. intermedius is the most common organism; Brucella canis must be considered. Osteomyelitis of L2-L4 with sparing of disc spaces is most commonly Actinomyces secondary to grass awn migration.
Incidence: Large breed dogs are most common.
Clinical Signs: Focal spinal pain is most consistent sign. Systemic illness, neurologic deficits.
Diagnosis: Radiographs-lysis of adjacent vertebral end plates. Follow radiographs with: blood cultures, urine cultures, and brucella screening.
Treatment: Abx for at least 8 weeks, based on culture/sensitivity; however, if nothing cultures, treat for staph. If no improvement, and treating presumptively, consider fluoroscopic guided needle aspirate.
Prognosis: Usually pretty good if causative agent can be identified. Guarded if marked spinal cord compression has already occurred.

Front 48

Meningomyelitis

Back 48

Inflammation of the meninges and spinal cord.
INFECTIVE TYPE:
Pathophysiology: routes of infection include hematogenous, direct extension from adjacent tissue, and trauma.
Clinical signs: Hyperpathia, fever, ataxia or paresis, depression, seizures.
Diagnosis: CSF analysis, +/- culture.
Treatment: Abx, do not withhold treatment if CSF cannot be collected immediately. Mannitol, anticonvulsants.
STEROID RESPONSIVE MENINGITIS-ARTERITIS
Pathophysiology: Idiopathic, immune mediated component suggested.
Incidence: breed disposition in boxers, bernese mountain dogs, and beagles (lab colonies).
Clinical signs: Neck/back pain, fever, ataxia or paresis, depression, seizures. Clinical signs may wax and wane.
Diagnosis: CSF analysis, non-degenerative neutrophilic pleocytosis is suggestive.
Treatment: Prenisone 4mg/kg/day for 1-2 weeks, taper to 0.5 mg/kg every other day, and continue for 6 months.
Prognosis: Good with prompt treatment, may recur if therapy is discontinued early.

Front 49

Spinal Cord Trauma

Back 49

Concussion, compression, or secondary injury that causes traumatic damage to the spinal cord.
Incidence: Common causes include motor vehicle trauma, falls, bite wounds, and gunshot wounds.
Clinical signs: Neurologic deficits, focal hyperesthesia, other injuries may also be present.
Diagnosis: Limit to voluntary movement in non-ambulatory patients; most important assessment is deep pain perception, but shock patients may not respond. Radiographs should be taken after the patient is stabilized. Myelography and CT can further diagnose spinal cord compression and fractures.
Biomechanics: 2 categories-dorsal compartment (vertebral arch, articular facets, associated ligaments), and ventral compartment (vertebral body, disc, associated ligaments). Dorsal only is very stable, ventral only is fairly stable, both is unstable.
Treatment: Manage life-threatening injuries first. Immobilize the patient. Medical treatment with methylprednisilone(solu-medrol) or prednisolone (solu-delta-cortef).
Conservative management may be used for stable injuries with mild neurologic deficits; cage rest and splint. Surgical management recommended for unstable injuries, or spinal cord compression. Variety of techniques involving dorsal or ventral stabilization.
Prognosis: similar to IVDD.

Front 50

Fibrocartilagenous Embolism

Back 50

Ischemic necrosis of the spinal cord cause by fibrocartilage embolism in the spinal cord vessels.
Pathophysiology: poorly understood, but fibrocartilage (most likely from the disc) enters the vessels resulting in ischemia and infarction.
Incidence: Common in large and giant breed dogs; Schnauzers and Shetland sheepdogs.
Clinical Signs: Sudden onset, often associated with exercise, non-progressive, often asymmetrical. May be painful at onset, but no identifiable focal pain.
Diagnosis: Clinical signs (sudden, non-painful, focal), rule out other causes, MRI is usually diagnostic.
Treatment: supportive care and physical therapy.
Prognosis: If intact pain perception, usually improves within 2-3 weeks. Development of collateral circulation and alternative neural pathways.

Front 51

Aortic thromboembolism

Back 51

Not neuropathic! Obstruction of distal aortic bifurcation.
Pathophysiology: Ischemia to the nerves and muscles of the pelvic limbs results in paraparesis/plegia.
Incidence: Cats! Often a sequela to hypertrophic cardiomyopathy. In dogs, due to hypercoaguable state.
Clinical signs: Acute, paraparesis/plegia, painful muscles, weak/absent femoral pulse, cold extremities.
Diagnosis: Clinical signs usually diagnostic, angiogram will show aortic obstruction, may be detected on ultrasound too.
Other differentials for paraparetic cats: spinal trauma, spinal lymphoma, FIP, infectious myelitis.
Treatment: Nursing care. Clot dissolution and heparin treatment have not proved to prevent recurrence or increase survival, but worth a try.
Prognosis: 50%, recurrence in common.

Front 52

CNS cell types: Neurons

Back 52

Transmit nervous impulses
Contain Nissl substance (RER) in the cell body.
Vary in size, shape, length, diameter of axon, type of neurotransmitter, and function.

Front 53

CNS cell types: Astrocytes

Back 53

Large, pale staining, round nucleus with no distinct cell body or nucleolus. Cytoplasm forms projections.
CNS equivalent of a fibroblast, but has other functions.
Requires special stain to see cytoplasm.

Front 54

CNS cell types: Oligodendrocytes

Back 54

In the white matter, CNS equivalent of a schwann cell. Produces myelin.
In the grey matter, small dense nucleus similar to a lymphocyte.

Front 55

CNS cell types: Microglial cells

Back 55

Monocyte/macrophage origin.
Nuclei shaped like rods and commas.

Front 56

CNS cell types: Ependymal cells

Back 56

Line the ventricles and central canal of the spinal cord.

Front 57

CNS cell types: Choroid plexus epithelial cells

Back 57

Modified ependymal cells that produce CSF.

Front 58

Why is the neuron especially vulnerable to injury?

Back 58

1. high metabolic rate
2. little stored energy
3. axon is very dependent on cell body
4. cannot regenerate

Front 59

Neural response to injury: acute necrosis

Back 59

Main causes: Ischemia, hypoxia, hypoglycemia, toxemia.
Cell body shrinks, cytoplasm is bright pink. Nuclear pyknosis and karyorrhexis.

Front 60

Neural response to injury: Chromatolysis

Back 60

Cell body's reaction to axonal insult. Cell body swells and Nissl substance disperses, leaving central clearing (helps cell body produce protein for rebuilding axon).

Front 61

What is Wallerian degeneration?

Back 61

Breakdown of the axon and myelin sheath distal to the point of injury.
Sequence of events.
1. insult to axon
2. axon swelling and fragmentation
3. myelin splitting and fragmentation->ellipsoid formation
4. Phagocytosis of axonal and myelin debris by macrophages.
5. If endoneurium is intact, an axon sprout will re-enter the endoneurial tube and regenerate slowly. If the severed ends are too far apart, a neuroma will form instead.

Front 62

How is Wallerian degeneration different in the CNS than the PNS

Back 62

Phagocytosis is slower.
Regen is less likely.

Front 63

What is distal axonopathy?

Back 63

"Dying back" neuropathy. Degeneration of the terminal or sub-terminal portion of the axon.
Follows neural cell body damage.

Front 64

What is neuronal vacuolation?

Back 64

Vacuolar degeneration.
Causes:
1. Can be normal occasionally.
2. Fixation artifact.
3. Occurs early in neuronal injury due to swelling of mitochondria.
4. Hallmark of transmissible spongiform encephalopathies.

Front 65

Response of glial cells to injury: Astrocytes

Back 65

Necrosis
Astrocytosis-hyperplasia
Astrogliosis-hypertrophy/hyperplasia
Gemistosis-enlargment
Gliosis-formation of glial fibers (CNS scarring)

Front 66

Response of glial cells to injury: Oligodendrocytes

Back 66

Degeneration due to hypoxia
Satellitosis-proliferation around damaged nucleus
Demyelination-oligodendrocyte death.

Front 67

Response of glial cells to injury: Microglial cells

Back 67

Gitter cells-cell becomes large with foamy cytoplasm due to phagocytosis of debris
Glial nodules-clusters of microglial cells, usually occurs with viral infection.

Front 68

Three main types of CNS edema

Back 68

Vasogenic-fluid gathers outside the cells.
Cytotoxic-fluid gathers inside the cells.
Interstitial-associated with hydrocephalus.
Consequences: Herniation, typically through the foramen magnum. Leads to compression of the respiratory centers.

Front 69

Primary vs. Secondary demilination. Be able to discuss the pathogenesis of demylination due to distemper virus.

Back 69

Primary demyelination-selective destrucion of normal myelin when the axon remains intact.
Secondary demyelination-loss of myelin following damage to the axon (wallerian degeneration).
Distemper virus: Virus systemically invades lymphoid tissues->viremia spreads to epithelial tissues->perivascular lymphoplasmacytic inflammation of the CNS and neural necrosis-> Myelin ballooning and astrocyte swelling in white matter->oligodendrocytes decrease in number (primary demyelination)->neuronal necrosis leads to further demyelination (secondary).

Front 70

Malacia of the CNS

Back 70

Aka. CNS necrosis.
Occurs following vascular blockage or reduced bloodflow, leading to ischemia.
Can lead to neuronal necrosis, vasogenic edema, and infarct.

Front 71

Laminar cortical necrosis

Back 71

Selective distruction of neurons in the deeper cerebral cortex. Distinctive pattern.
Involved in polioencephalomalacia (thiamine deficiency).
Gross appearance: brain swelling, flattened gyri, herniation.
Microscopic appearance: Cortical neuronal necrosis.

Front 72

Generalized causes of each type of leptomeingial inflammation: suppurative, eosinophilic, lymphocytic, granulomatous.

Back 72

Suppurative-bacterial. Neutrophils predominate. Most common.
Eosinophilic-Salt poisoning in pigs. Perivascular eosinophilic cuffing.
Lymphocytic-viral origin.
Granulomatous-Fungal disease and mycobacteria. FIP may cause granulomatous lesions as well.

Front 73

Concussion

Back 73

Temporary loss of consciousness following head trauma.
Causes diffuse brain injury with little or no visible lesion.
Causes: shear, tensile or compressive strains.

Front 74

Contussion

Back 74

Focal brain injury, usually indicates hemorrhage.
Brain strikes the inside of the skull at the point of impact (coup); the vessels and nerves on the opposite side of the brain stretch and tear (contracoup).
Coup lesion will be more focal, contracoup lesion will be more diffuse.

Front 75

Laceration

Back 75

CNS tissue is torn by bone within the skull or by a penetrating object.
Most severe of the traumatic injuries.

Front 76

Anencephaly

Back 76

Congenital absence of brain

Front 77

Lissencephaly

Back 77

Lack of gyri or sulci.
Normal in rats, mice, rabbits and birds.
Congenital anomaly common in Lhasas and Shih Tzus

Front 78

Meningoencephalocele

Back 78

Protrusion of brain and meninges through a defect in the cranium. Inherited in pigs and cats.

Front 79

Hydrocephalus

Back 79

Increased accumulation of CSF in the cranial cavity.
Internal-within the ventricles
External-within the arachnoid space
Communicating-within both spaces
Internal hydrocephalus is most common; is congenital in brachycephalic dogs, due to a malformed mesencephalic aqueduct.

Front 80

Cerebellar hypoplasia

Back 80

Decreased development of the cerebellum.
Can be genetically inherited, or due to gestational toxins/infections (eg. feline parvovirus, BVD)

Front 81

Spinal cord malformations: Spina bifida, hydromyelia, syringomyelia, scoliosis.

Back 81

Spina bifida-cleft in the dorsal vertebral column, +/- herniation of meningies and CNS tissue.
Hydromyelia-distended spinal canal.
Syringomyelia-cavitation of the spinal cord tissue.
Scoliosis-curvature of the vertebral canal, +/- neurologic defects.

Front 82

Compression of the spinal cord

Back 82

Caused by: Abscess, fracture, neoplasia, IVDD, or malformations.
Typically leads to neurologic deficits.