Herp Neurology Flashcards

1
Q

Describe the neuroanatomy of reptiles.

What is the general appearance of teh brain?

What are the three sections of the brain and what functions occur in each section?

What are the fnctions of the dorsal and ventral horns in the spinal cord?

Where do the visceral nerves of the ANS originate? How is this different from mammals?

What is the meningeal anatomy of reptiles like? How does this differ from mammals?

A
  1. Neuroanatomy
    1. Brain
      1. Lissencephalic: lacking gyri and sulci
      2. Forebrain = olfaction, taste, sensorimotor integration
      3. Midbrain = vision, neuroendocrine
      4. Hindbrain = hearing, balance, homeostasis
        1. Cerebellum (part of hindbrain) integrates sensory/motor input and postural equilibrium
      5. Most reptiles lack neocortex, but internal dorsal ventricular ridge is similar in chelonians
      6. Lots of room between brain and braincase in lizards, aquatic turtles, and tuataras
        1. Minimal space in snakes
  2. Spinal Cord
    1. Extends to the tip of tail with no cauda equina
    2. Locomotor centers exist within the spinal cord
    3. Laterally paired spinal nerves exit through the intervertebral foramen
      1. Dorsal horns = dorsal roots (sensory)
      2. Ventral horns = sensory & motor neurons (reflex arc)
    4. Visceral nerves of ANS arise along the length of the spinal cord with both sympathetic and parasympathetic components
      1. Not segregated into thoracolumbar sympathetic and craniosacral parasympathetic like in mammals
    5. Cranial nerves = 12-13 in most reptiles (11-12 in snakes)
  3. Meninges = dura mater (outer avascular layer) + pia-arachnoid (inner, vascularized layer)
    1. Space between meninges = subdural space
    2. Reptiles DO NOT have a subarachnoid space
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2
Q

Describe the neuro exam of reptiles.

How many cranial nerves do reptiles have? How are they assessed?

A
  1. Neurological Exam
    1. Pertinent History:
      1. Sudden hypothermia → neuro signs in chelonians
      2. Low calcium diet
      3. Thiamine deficiency
      4. Toxins: rhubarb, firefly, lead, ethylene glycol, antibiotics, ivermectin
    2. Things to assess:
      1. Mentation (abnormal mentation = forebrain disease)
      2. Head and spinal posture
    3. Gait evaluation and circling
    4. Ability to strike/constrict prey (snakes
    5. Cranial Nerves
    6. Reflexes (withdrawal, cloacal, panniculus, righting reflex)
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3
Q

Describe the infectious diseases of reptiles that produce neruologic disease.

What two protozoal infections may result in meningoenephalitis?

What bacterial infection may progress to meningoencephalitis?

What are two viruses may cause neurologic signs in snakes? What species are affected? What clinical signs may occur?

What virus causes neurologic signs in bearded dragons? What other signs are seen?

What virus causes encephalitis in crocodilians?

A
  • Neurologic Disease in Reptiles
    • Infectious Diseases
      • Protozoa
        • Acanthomoeba from contaminated water → meningoencephalitis
        • Toxoplasma spp. → brain abscess + meningoencephalitis
      • Bacteria
        • Gram - bacteria are most common isolates of nervous system
        • Spinal osteopathy/discospondylitis/osteomyelitis in snakes
          • Pseudomonas, Salmonella arizona, Staphylococcus
          • Bony proliferation → ankylosis and spinal cord compression
          • Blood or lesions cultures to identify bacteria
    • Viruses
      • Paramyxovirus (Ferlaviruses) in snakes
        • Transmitted vis respiratory secretions +/- snake mites
        • Respiratory, Gi, and neuro signs (opisthotonus, torticollis, reduced righting reflex)
        • Sunshine virus → respiratory and neuro disease
      • Inclusion body disease of boids (arenavirus)
        • Clinical signs = regurgitation, pneumonia → terminal CNS signs
          • Much worse in pythons than boas
        • Boas may be subclinical carriers (do not mix pythons and boas)
        • Transmitted via direct contact, venereal spread, and snake mites (Ophionyssus natricis)
        • Inclusion bodies are occasionally seen in white blood cells
        • Diagnose with PCR but no treatment
      • Agamid adenovirus
        • Endemic in pet bearded dragons
        • Neuro and Gi signs, reduced growth, hepatitis, death
        • Transmitted via fecal-oral
      • West Nile virus
        • Reptiles are reservoirs for western and Venezuelan equine encephalitis
        • WNV affect crocodilians (paresis, circling, head tremors, neck spasms, star-gazing, death)
        • Transmitted via insect or infected horse meat
        • WNV vaccine is approved for alligators
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4
Q

Describe the noninfectious causes of neurologic disease in reptiles.

What are three nutritional deficiencies that can result in neurological signs?

How does neurologic trauma manifest differently?

What is xanthomatosis?

What species are prone to caudal coiling syndrome?

What concentration of chlorhexidine can be fatal to reptiles?

What is the mechanism of action of organophosphate and pyththrin toxicities?

What is the mechanism of ivermectin toxicity? What species are susceptible?

A
  • Nutritional Diseases
    • Thiamine deficiency
      • In piscivorous reptiles fed frozen-thawed fish
      • General neuro signs, except enophthalmos in chelonians
      • Treat with SC thiamin
    • Biotin deficiency
      • Avidin (found in eggs whites) has anti biotin activity
      • Too many unfertilized eggs may cause biotin deficiency
      • Treat with vitamin B complex
    • Hypocalcemia
      • Inadequate dietary calcium or vitamin D3, low UV lighting, or low temperatures
      • Treat with calcium
      • Seen in alligators fed exclusively red meat
    • Hypovitaminosis E
  • Trauma
    • Brain Trauma
      • Brain volume increases from edema and hemorrhage
      • Increased intracranial pressure → decreased CSF → decreased brain blood flow
    • Spinal Cord Injury
      • Reptiles may have better prognosis than mammals due to neurogenesis within spinal cord
      • Some reptiles okay with complete spinal transection
    • Peripheral Nerve Injury
      • Forelimb monoparesis after trauma is likely brachial plexus avulsion
  • Metabolic Diseases
    • Xanthomatosis = cholesterol-laden granules in organs
      • Brain xanthomas can cause hydrocephalus from obstruction and other CNS signs
      • Exacerbated by renal disease
    • Freeze Damage → crystal forming in neuro tissues +/- lenticular opacities and retinal lesions
    • Hypoglycemia
      • Can be stress induced in crocodilians
    • Hepatic Encephalopathy
  • Congenital Diseases
    • Caudal coiling syndrome = newborn boas with normal vertebrae but severe spinal bending
      • No treatment
  • Toxicities
    • Chlorhexidine
      • Bathing in 2% solution leads to death
    • Insecticides can be absorbed through many routes, including skin
      • Organophosphates, carbamates → inhibits acetylcholinesterase → ACh accumulation
      • Pyrethrin, pyrethroids → alter sodium channels in nerves
    • Ivermectin
      • Macrocyclic lactone that stimulates excess release of GABA
      • Binds irreversibly and takes > 7 days to clear
      • Can lead to paresis, paralysis, and respiratory arrest
      • Milbemycin is safe in chelonians
    • Antimicrobials (Metronidazole, Aminoglycosides)
    • Heavy Metal Intoxication (Lead, Zinc)
    • Bromethalin: neurotoxin that decouples oxidative phosphorylation
    • Wood Shavings with High Resin Content
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5
Q

Describe spinal oseopathy in snakes.

This condition is associated with what bacterial infection?

What are the typical clinical signs? How do they progress?

How is this diagnosed? When do bony lesions develop after infection?

How is this treated?

What is the general prognosis?

A

MARMS – 166. Spinal Osteopathy

  • Proliferative spinal osteopathy (PSO)
    • Most common in snakes, but described in turtles and lizards as well
    • Proliferative and progressive spinal lesions associated with chronic bacterial infections such as Salmonella sp
    • Excessive bone resorption followed by deformity and then excessive bone formation
  • Osteoarthritis - a disorder of moveable joints characterized by deterioration of articular cartilage, osteophyte formation, bone remodeling, and low-grade non purulent inflammation
    • Caused by trauma, diet, viral, inactivity, neoplasia, association with bacterial infection or septicemia
  • Clinical signs
    • Limited to no movement in affected areas/vertebral column stiffness
    • Affected vertebral regions can be extensive (30 cm)
    • Kyphosis, scoliosis, ankylosis, lordosis, occasional pathologic fractures
    • Focal nodular swellings/bulges
    • Hyperreflexia cranial to lesion
    • Motor deficits
    • Torticollis, trembling, spinal kinking
    • Severe luxation or vertebral rotation - corkscrew posture
    • Advances to prevent animals from moving, striking or swallowing prey
  • Diagnostics
    • Histopathology - close to gold standard, but not always practical
    • Radiographic/CT changes
    • Vertebral fusion by foci of irregular proliferative bone
    • Sclerosis of vertebral end plates with lysis
    • Advanced -periarticular bony proliferation involves dorsolateral and costovertebral joints (osseous metaplasia), ankylosis, pathologic fractures
    • Nuclear bone scan - identify site of active disease
    • Bone biopsy and culture may be helpful or not
    • Bony lesions may not develop until 22-26 months after infection
    • Blood culture is recommended
    • Bone/rib biopsy - risk of fracture
  • Treatment - Early diagnosis helpful for success
    • Appropriate antibiotic selection
    • Surgical debridement of granulomatous/lytic areas
    • Anti-inflammatories
    • Isolate from unaffected individuals
  • Prognosis - poor to grave
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6
Q

Describe the nuerological surgeries of reptiles.

How are mandibular fractures repaired? What species are susceptible?

When is spinal surgical repair not indicated?

What lizards species is prone to cervical sponylomyelopathy?

A

MARMS – 110. Spinal Sx

  1. Skull Fractures
    1. HIgh energy lizards (e.g. Chinese water dragons, sail-fin lizards) may break mandible with repeated concussive force against cage walls
    2. Treat mandibular symphyseal fractures with circumferential wiring
      1. External fixators for oral mandibular fractures
  2. Spinal Fractures
    1. Common sequelae of metabolic bone disease
      1. Surgical repair not as helpful
    2. Can perform spinal surgery, decompression, fracture stabilization
    3. Cervical spondylomyelopathy has been seen in komodo dragons → euthanasia
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7
Q

Describe the management of repitle mental health.

What are the principles of behavioral modification?

Describe the extrapolation of behavior drugs from mammalian or avian sources.

A

MARMS – 121. Mental Health Treatment

Chapter 121. Mental Health Treatment (Psychological Well-Being)

Clinical Presentation and Diagnostic Confirmation

●Diagnosis of exclusion

●Most common behavior clinical signs presenting

○Aggression

○Stereotypic (including self-injurious)

○Stress/fear based

Preferred Medical Therapy (decrease neuroendocrine response)

●Environmental enrichment and management

●Behavior therapy

●Medication

●Client education is super important

Behavior Modification- to any procedure that modifies behavior (brain surgery or shock therapy)

  • Cognitive Behavior Therapy- Treatments that change cognitions
  • *Behavior Therapy- systemic use of learning procedures to treat psychological problems and change behavior*

Desensitization and Counterconditioning Therapy

● Based on classical conditioning; (positive)

○Fears learned and phobias develop

○Plan- gradual exposure to fear-inducing stimulus

○Desensitization should be paired with counterconditioning, creating a positive association with the stimulus

Environmental Enrichment and Management

●Crucial

●Proper cage set-up

Psychopharmacology and Endocrine Therapy

●No safety or efficacy studies with use of psychoactive drugs for behavior treatments

●Most used for chemical restraint, sedation, anesthesia, and pain management

Be careful with extrapolation of doses from birds and mammals

●Sig differences to neurophysiology, neuroendicrinology, and general metabolism

Patient Follow-up important

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