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287 Cards in this Set
- Front
- Back
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Purpose of Neurologic Exam |
-Determine if the neurologic system is involved
-Figure out where the problem is coming from --Anatomic Diagnosis/localization --guides diagnostic plan and treatment |
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Anatomic diagnoses
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-Prosencephalon:
--telencephalon (cerebral hemispheres) C1-C5 --Diencephalon: C6-T2 -Caudal Fossa: --Pons and medulla: T3-L3 --Cerebellum: L4-S1/3 |
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Functional Spinal Cord Divisions
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-A: Cranial cervical spinal cord, C1-C5
-B: C6-T2 -C: T3-L3 -D: L4-S1 -E: S1-S3 |
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Peripheral Nervous System Disorders
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-Segments of spinal cord nerve roots form nerve, neuromuscular junction, and connection to muscle
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Parts of the Neurologic Exam
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-Sensorium: how the patient is responding to the environment |
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Tools for the Neurologic Exam |
-Transilluminator
-Lens -Hemostat -Taylor or Tomahawk reflex hammer |
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Sensorium during neurologic exam
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-How patient is responding to the environment
-Continuum from dullness, lethargy to obtundation, to semicoma, to coma -Dull/lethargic is a sick animal but still responsive -Obtunded takes some extra effort to make animal pay attention -Srupor/semicoma is painfully responsive -Coma is non responsive, animal seems anesthetized |
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Gait during neurologic exam
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-Normal gait
-Paresis (weakness) --lower motor neuron --upper motor neuron -Ataxia (3 types) -Orthopedic issue |
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Lower Motor neuron (LMN) Disease
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-Animal has a problem supporting its weight
-Saggy in the back -Short stride length, choppy steps -Can look like a lameness, cruciate disease -Localized to more peripheral area of spinal cord --could be spinal cord disease or peripheral nerve disease --issue with segments, nerves, roots, or neuromuscular junction -Front legs will function normally, back legs will be problematic |
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Upper motor Neuron (UMN) paresis
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-Looks like a stiff gait
-Limbs are fully extended, may have more tone -Long, elongated, floating gait -Excessive flexion, adduction or abduction, scuffing, knuckling, crossing limbs over -Delay in onset of protraction, long strided |
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Ataxia
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-Incoordination |
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Postural Reactions
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-Palpation of musculature, feel for atrophy, orthopedic changes
-Paw placing, should right the paw when knuckled -Hopping response, put all weight onto one limb --should adjust before past midline -Hemiwalk, pick up both limbs on one side and push to the other side --dog should catch before falling --front limbs correct before back legs -Wheelbarrow: good for cats -Extensor postural thrust: lift animal up completely and put back down, animal should backup to catch themselves |
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Spinal Reflexes on Thoracic limb
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-Appreciate muscle tone
-Biceps reflex -Triceps reflex -Extensor carpi reflex -Withdrawal (more reliable) -All but withdrawl can be “not present” in normal animals -Withdrawal assesses all muscles in the limb |
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Spinal Reflexes on Pelvic Limb
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-Appreciate muscle tone
--look for cruciate disease or hip disease -Gastrocnemius reflex -Cranial tibial reflex -Patellar reflex: hit patellar tendon and look to see if there is a jerk in the limb -Withdrawl reflex: --test is for a reflex, not a test for motor ability of the animal or sensation -Not a way to tell if the animal can feel the limb or can move limb on own |
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Nociception assessment
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-Ability to feel painful stimulus
-Provide a noxious stimuls to elicit a conscious response -Want to see limb withdrawal and ALSO see a response that shows animal is bothered by the stimulus -Manifestation of the patient’s pain -Superficial pain vs. deep pain can be hard to assess |
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Cutaneous Trunci Reflex
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-Pinch skin, nerve transmits signal to spinal cord
--goes bilaterally, signal ascends spinal cord to C8-T1 region -Synapses on LMN, becomes lateral thoracic nerve that innervates cutaneous trunci muscle -Get a bilateral flinch |
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Perineal Reflex
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-Mild digital pressure on the anus or adjacent perineal skin
-Look for contraction of the sphincter and tail flexion -Depends on sacral segments and spinal nerves and pudendal nerves -Can also check tail tone, tail response depends on caudal segments and nerves -Perineal reflex allows localization |
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Cranial nerve assessment
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-Position of the eye: 3,4,6, Stabismus |
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Neurologic Exam basic principles
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-Make a problem list and find anatomic diagnosis |
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Cranial nerves
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-Come off the base of the brain
-12 total -All control a different part of the head -Help brain allow body to move, eyesight, sensory -Need to know what is normal and what is abnormal |
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Neurologic exam for cranial nerves
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-Perform full neurological exam
-List dysfunctions that are present -Localize the lesion -Generate list of differential diagnoses --Degenerative, anomalous, metabolic, neoplastic, infectious/inflammatory/infarct/immune-mediated/idiopathic, trauma/toxin -Perform tests to confirm or rule out DDx |
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CN I: Olfactory Nerve
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-Sense of smell
-May not have any clinical signs -Test via response to food, alcohol, cloves --test with something the animal is used to, not something new -Electro-olfaction -Damage can be due to tumors, inflammatory disease |
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CN II: Optic nerve
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-Vision, sensory portion of PLR
-Clinical signs: blindness, mydriasis -Test with menace response, obstacle course, visual placing, electroretinogram |
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Lack of a menace response |
-Cannot see (CN II) |
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Tests for CN II (optic nerve)
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-Walk placing limbs too far in front
--long stride length --stumbling, problems with balance -Throw a noiseless object, should be able to respond to sight -Obstacle course -Visual placing -ALWAYS look at the back of the eye, look for disease in the retina |
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Visual pathway
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1. Retina
2. Optic nerve, through optic chiasm 3. Lateral geniculate Body 4. Occipital lobe in the back of the head, visual cortex |
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CN III: Oculomotor nerve
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-Responsible for eye movement
-Constricts pupil -Moves globe -Elevates eyelid -Clinical signs: ventrolateral strabismus, dilated, non-responsive pupil, ptosis -Testing: PLR, physiological nystagmus, look at eye position, pilocaprine response testing of eye |
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Cranial nerves responsible for eye movement and position
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-CN III: oculomotor
--eye drifts to the side and down, ventrolateral stabismus -CN IV: Trochlear --rotational srabismus -CN VI: Abducens --medial strabismus |
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Ventrolateral Stabismus |
-Eyes look down and to the side
-Due to CN III oculomotor nerve deficit --pulls eye up and medial |
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Pupillary Light Reflex PLR
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-Shine a light in the eye, both pupils should constrict
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PLR
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1. Retina
2. Optic Nerve (skips lateral geniculate body) 3. Pre-tectal nucleus in mid-brain 4. Oculomotor nucleus 5. Sends fibers to opposite oculomotor nucleus, allows for bilateral response |
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Pre-chiasmatic blindness vs. post-chiasmatic blindness
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-If Pre-chiasmatic, will not have PLR in both eyes
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Physiological Nystagmus
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-spin or move animal from side to side, eyes should move in cacitic way
-Slow phase and fast phase to maintain balance |
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CN IV: Trochlear nerve
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-Rotates dorsal part of the globe medially
-Responsible for eye position and movement -Clinical signs: rotational strabismus -Testing: physiologic nystagmus, observation of the eye or retina |
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CN VI: Abducent nerve
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-Moves globe laterally, retracts globe
-Clinical signs: medial strabismus, inability to retract the globe -Testing: physiologic nystagmus, observation of the eye, globe retraction |
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CN V: Trigeminal nerve
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-Sensation over the face
-Motor innervation to muscles of mastication -Clinical signs: loss of sensation over the face, inability to close the mouth -Testing: corneal reflex, palpebral blink reflex, stimulation over the face, muscle palpation and jaw tone, electromyography --test sensation over the head and ability to close the jaw |
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Unilateral trigeminal nerve deficits
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-Will see a caved in side of the head
-Lose muscle mass over one side of the head |
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CN VII: Facial nerve
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-Motor innervation to muscles of facial expression
-Allows blinking, smiling, talking -Sensory innervation to palate and tongue -Motor innervation to salivary and lacrimal glands, responsible for tears and salivation -Clinical signs: inability to blink, drooping of the face, deviation of the nose towards side (“tragic facial expression: -Testing: palpebral and corneal blink reflex, lip withdeawal, Schirmer tear test |
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Stapedius Muscle
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-Blunts sound, modulates sound in the middle ear
-Decreases stimulus of loud noises to the ear, decreases damage to ear |
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CN VIII: Vestibulocochlear nerve
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-Responsible for balance and equilibrium
-Responsible for hearing -Clinical signs: deafness, loss of balance --ataxia, head tilt, falling or rolling to one side, nystagmus, strabismus -Testing: behavioral testing, BAER, physiological nystagmus, post-rotatory nystagmus, vestibular righting |
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Hearing Test
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-Make clicking sound in the ear
-Waves 1 and 2 indicate cochlear function -Waves 3, 4, and 5 indicate brainstem function -If cochlea is not functioning, get a flat wave |
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Cochlea
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-In inner ear, within the petrous temporal bone
-Connects to CN VIII |
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Bulla
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-Filled with air
-Contains hammer, anvil, stapes -Middle ear |
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Bone conduction vs Air conduction in the ear
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-Air conduction causes bones to move, which hit round window and conducts signal
-Bone conduction occurs when there is conductive deafness, clogged ears --Can do bone conduction test --cannot tell which way the sound is coming from, but can tell that there is sound |
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CN XI: Glossopharyngeal Nerve
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-Motor innervation to the muscles of the pharynx and palate
-Innervation of zygomatic and parotid salivary glands -Taste sensation to the posterior 1/3 of the tongue -Clinical signs: difficulty swallowing -Testing: gag reflex, carotid sinus pressure |
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CN X: Vagus
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-Allows for normal swallowing and laryngeal dunction
-Parasympathetic innervation to the heart -Clinical signs: difficulty swallowing, regurgitation, altered vocalization, laryngeal paralysis -Testing: gag reflex, laryngeal reflex, oculo-cardiac reflex |
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Gag reflex
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-Put finger in back of throat, dog should gag and push finger out
-Tests CN IX, X, and XII |
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CN XI: Spinal accessory
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-Helps to swing the forelimb forward |
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CN XII: Hypoglossal
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-Innervation to the tongue |
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Vestibular System
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-Sensory system
-Sensory information that allows organism to maintain balance ad orientation -Involves balance, positioning, coordination between eyes and body, accommodation of fine body movements |
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Balance
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-Vestibular System
-Vision and visual system -Proprioceptive system -2 out of 3 are needed to maintain balance -Loss of 2 results in balance loss |
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Function of the Vestibular System
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-Allows us to maintain balance
-Orients head with respect to gravity -Maintains position of the eyes, trunk, and limbs with respect to the position of the head --Body reads how the head moves and responds -Maintains vestibule-ocular reflexes -Keeps eyes fixed on a point in space even when the body is moving |
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Normal vestibular function tests
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1. Raise head up, eyes should stay lined up with head
2. Push animal to the side, should put a leg out to catch 3. Put animal on the table, animal should not let top of the head hit the table 4. Move head side to side |
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Dysfunction of the Vestibular System
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-One of 3 most common causes of neurologic diseases
-Abnormal orientation of the head with respect to gravity (head tilt) --head tilt is towards the side of the lesion -Abnormal position of the eyes, trunk, and limbs --positional strabismus --leaning --vestibular ataxia and loss of balance -Abnormal vestibule-ocular reflexes --nystagmus at rest, abnormal movement at rest -Inability to keep eyes fixed on a point in space when the body is moving |
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Most common neurologic diseases seen in general practice
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-Vestibular disease
-Back disease, discs -Seizures |
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Phases of Nystagmus
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-Fast phase away from side of the lesion
-Slow phase towards the side with the lesion |
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Accentuating dysfunction of the vestibular system
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-Enhance the loss of balance by taking away vision, proprioception, or spinning
-Lift the patient off the floor -Blindfold the patient -Spin the patient, look at post-rotatory nystagmus --should have less than 20 beats after spinning --age-dependent, young and old have more beats of nystagmus after spinning |
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Vestibular system in space
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-Cannot tell which direction is up
-Proprioception is gone, you are just floating -All stars look the same, vision is not relevant anymore -Astronauts will feel like they are flipping around |
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Approach a patient with vestibular disease
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-Gait and posture signs
--Loss of balance, vestibular ataxia, head tilt towards the side of the lesion -Cranial nerve signs: --positional strabismus --nystagmus -Vomition -Localize the site of the dysfunction -Generate a list of DDx -Determine diagnostic options -Determine treatment options |
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Localizing vestibular disease
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-Peripheral nervous system
--inner ear and vestibular nerve --fixable! Animal will probably be fine in a few weeks -Central nervous system --vestibular nuclei of the medulla --cerebellum --much more serious, animal may not be OK |
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Inner ear damage
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-Mostly due to infection
--generally curable, antibiotics -Neoplasia -Aminoglycoside toxicity -Idiopathic inner ear disease, “old rolling dog” disease |
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Central nervous system and vestibular system
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-Brainstem or cerebellar involvement
-Usually really detrimental, not a good prognosis |
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Signs of Peripheral Vestibular Disease
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-Vestibular ataxia
-Head tilt -Positional strabismus -Nystagmus -Vomition -May have middle ear involvement --facial nerve paralysis, horner syndrome |
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Nerves in the middle ear
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-Run through the Bullae
-CN VII (facial): muscles of facial expression -Sympathetic nerve, associated with horner’s syndrome |
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Horner Syndrome
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-Sympathetic nervous system to the eye is dysfunctional
-Sympathetic nerve runs through middle ear, middle ear infection can affect nerve fiber -Miosis, small pupil --pupil constricts, but does not dilate -Ptosis, drooping of the lids -Enophthalmosis, dropped eye -Raised 3rd eyelid |
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DDx for Peripheral Vestibular Disease
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-Congenital vestibular syndromes
-Hypothyroidism -Fibrosarcoma, osteosarcoma, lymphosarcoma, -Otitis interna -Polyneuropathy -Idiopathic -Trauma -Toxins |
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Diagnostics for Vestibular disease
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-CBC/Chem/Thyroid panel
-Otic examination -Brainstem auditory evoked response testing -Bulla and inner ear imaging --CT, MRI, skull radiographs |
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Bullae radiographs
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-Go down the mouth
-Need a lot of anesthesia |
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Treatment for Peripheral vestibular disease
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-Antibiotics
-Bulla osteotomy -Time -Thyroid hormone supplementation -Supportive care |
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Central nervous system vestibular dysfunction
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-Damage to brainstem or cerebellum
-May see damage to other cranial nerves, CN IX, X -May damage reticular activating system -May damage pathways for proprioception and ataxia, can result in paralysis -Vestibular ataxia -Head tilt -Positional strabismus -Nystagmus, vertical nystagmus -Vomition -Mental depression, disorientation, stupor -Postural deficits -Menace deficits, damage to cerebellum -Paradoxical central vestibular disease |
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Vertical nystagmus
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-Present with central vestibular disease
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DDx for Central vestibular disease
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-Storage diseases, neuronopathies
-Meningiomas, choroid plexus papilloma, other tumors -Viral, funcal, protozoal, rickettsial, bacterial, parasitic migration -Infarct -Thiamine deficiency -heavy metal toxicity -Metronidazole intoxication |
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Diagnostic options for Central Vestibular Disease
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-CBC/Chem, thyroid panel
-Otic examination -Brainstem auditory evoked response testing -MRI or CT -CSF analysis |
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Metronidazole Intoxication
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-Wipes out central vestibular nucleus |
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Lumbosacral Diseases
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-Affects upper motor neuron if synapse is in region of lesion
-Mainly affects lower motor neuron |
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Clinical signs of lumbosacral Diseases
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-Pelvic limb paresis
--short choppy motion in hind limb --can look like an orthopedic problem -Paralysis -Reflexes are decreased or absent -Muscle hypotonia, floppy muscle --may cause collapse -Sensory innervation may be affected if lesion is severe and bilateral |
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Lower Motor Neuron Bladder Dysfunction
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-Pelvic nerve (parasympathetic) innervation to the bladder from S1-S3
-Hypogastric nerve (sympathetic) innervation from L1-L4 -Pudendal nerve is volumtary from S1-S3 -Bladder will be flaccid and easy to express -Loss of inhibition to sphincters in bladder -Urine is leaking out, flows out of the body |
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DDx for lumbosacral disease
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-Degenerative disc disease
-Degenerative myelopathy -Lumbosacral stenosis -Congenital vertebral or spinal cord malformation -Primary or metastatic neoplasia -Infectious myelitis -Diskospondylitis -Granulomatous meningoencephalitis -Trauma -Fibrocartilagenous emboli (vascular issue) |
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Diskospondylitis
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-Infection of the intervertebral disc and vertebral bodies
-Commonly hematogenous spread from UTI or other infection -Direct infection can occur from surgery, penetrating wounds, abscess, or foreign body migration -Dogs: usually staph bacteria --need to be aware of strep and brucella canis -Fungal infection is also possible, rare but can happen |
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Diskospondylitis Location
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-L7-S1 disc space
-Due to capillary beds of endplate and pores in endplate --leads to infection -Poor blood supply in disc leads to stagnant flow |
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Diskospondylitis on Radiographs
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-Tipped vertebrae
-Joints -Spinal channel -Disc spaces --endplate next to the disc should be very regular -Dorsal portion of vertebral body |
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Clinical signs of Discospondylitis
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-Fever, depression, anorexia
-Patient will be painful -Signs depend on the location of the lesion in the spine -L7-S1 may cause pain alone, or may have pelvic limb paresis or ataxia |
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Diagnosis of Discospondylitis
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-Can get a definitive diagnosis with radiograph
-Changes on radiographs can lag behind clinical signs by 2-3 weeks -Need to image the entire spine once a lesion is found -Lysis of adjacent vertebral end plates, may see bony proliferation and narrowed disc space -Can do MRI also -CBC should show leukocytosis -Urine culture may be positive in 25-50% of cases -Blood culture will be positive in 45-75% of cases -Brucellosis testing in intact males -Aspiration of lesions under fluoroscopy may give culture medium --hard to get fluid from a disc -Can do surgical biopsy |
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Treatment for Discospondylitis
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-Antibiotics!
--based on susceptibility, cephalexin is best start -Prolonged therapy for at least 8 weeks -Surgery is not recommended unless there is severe spinal cord compression --do not want to risk spread of infection -Cage rest -NSAID treatment, pain control --no steroids, do not want immunosuppression -Fungal and Brucella cases have guarded prognosis |
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Complications of Discospondylitis
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-Infected, weakened vertebrae can easily fracture
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Degenerative Lumbosacral Stenosis Signalment
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-“Cauda equina” syndrome
-Middle aged to older large breed dogs -Degenerative process, takes time to appear -Large breed dog problem -Has been recognized in some older cats -Compression of the cauda equine causes syndrome, multiple problems |
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Intervertebral Discs
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-“Dried apricot”
--waxy, fibrous outer coat --juicy, spongy middle |
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Pathogenesis of Degenerative Lumbosacral Steonsis
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-Annulus fibrosis changes
-Intervertebral disc protrusion -Narrowing of the intervertebral disc space and foramen --potential for pinching -Osteophytes around the foramen to stabilize the area, stick into foramen or spinal canal -Ventral displacement of the sacrum -Soft tissue proliferation |
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Clinical Signs of Degenerative Lumbosacral Stenosis
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-Caudal lumbar pain
-Difficulty rising -Exercise exacerbates signs -Paraparesis is not as common -Plantigrade stance -Altered tail carriage, dropped tail -If sacral nerves are involved, may have urinary and fecal incontinence |
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Degenerative Lumbosacral Stenosis Diagnosis
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-Radiographs
--transitional vertebrae, spondylosis, subluxation, sclerosis of end plates, bony proliferation -Electromyography: evidence of denervation -CT and MRI: --MRI always gives more info --CT gives more bony detail, flexed and extended views are helpful |
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Treatment for Degenerative Lumbosacral Stenosis
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-Conservative treatment/management for first episode or if there is intermittent signs
--4-8 weeks confinement/cage rest and pain control (tramadol, gabapentin) -25-50% improve -Recurrence rate is high |
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Surgical management of Degenerative Lumbosacral Stenosis
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-Dorsal laminectomy
--remove portion of bone from L7-S1 on dorsal side of spinal cord -Discectomy, remove disc -Facetectomy, frameinotomy, fixation-fusion --all more advanced and carry a greater risk -Dogs with fecal and urinary incontinence for more than a few weeks have poor prognosis for return to control --long-term presence gives poor prognosis |
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Fibrocartilagenous Emboli
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-Occurs most often in lumbar region, but can occur anywhere in the spinal cord
-Fibrocartilagenous material plugs vessels around the meninges and spinal cord --found in arteries and veins -Results in ischemic change and necrotizing myelopathy -Nucleus pulposus material gets into meninges and vessels |
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Clinical signs of Fibrocartilagenous Emboli
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-Non-chondrodystrophic dogs
-large-breed dogs -Usually active dogs -German shepherds, Labradors, schnauzers -Acute onset -Non-progressive, non-painful -Can be para-paresis to para-plegia -Can be asymmetric or bilateral, usually asymmetric -Loss of nociception in both limbs |
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Fibrocartilagenous Emboli pathgenesis
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-Nucleus pulposus material is pushed out of the end plate of the vertebrae
-Gets into medullary cavity and dumped into the venous return system -Ends in the veins |
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Diagnosis of Fibrocartilagenous Emboli
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-History, clinical signs, diagnosis of exclusion
-Radiographs and myelography can be normal, not helpful --change is in the spinal cord, intramedullary lesion -Swelling noted on myelogram -MRI is best diagnostic tool --focal, intramedullary, hyperintense T2 images |
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Treatment of Fibrocartilagenous Emboli
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-Steroid treatment: controversial |
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Fibrocartilagenous Emboli Prognosis
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-Poor prognosis: |
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Thoracolumbar Diseases
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-T3-L3 myelopathies
-Lesions affect the upper motor neuron --change UMN input to the LMN --Loss of inhibition to LMN, LMN is extremely excitable |
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Clinical signs of Thoracolumbar Disease
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-Signs associated with loss of UMN inhibition of LMN
-Ataxia -Weakness or paralysis in hind limbs -Decreased or absent proprioception in hind legs -Reflexes are normal to exaggerated -Withdrawl reflex is present, may be increased due to increase in extensor tone -Pain sensation is only lost of the lesion is severe and bilateral (Worst case scenario) -Control of bladder may be lost -Schiff-Sherrington posture |
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Schiff-Sherrington posture
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-Increased extensor tone in thoracic limbs when an animal is on the side
-From lesion between T3 and L4 -Border cells in ventral horn of L1-L5 normally provide inhibition to the front limbs --loss of inhibitory fibers from L1-L5 gives increased tone in forelimbs --Alpha motor neurons in cervical intumescence are not inhibited |
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Spinal Shock
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-Occurs in patients with T3-L3 lesions
-Unknown cause -Flacid tone in back legs, limb hypotonia -Spinal reflexes are decreased to absent, takes away increased reflexes expected with T3-Le patient -Animal appears incontinent, bladder is flaccid -Loss of anal sphincter tone, anal sphincter hypotonia |
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Upper Motor Neuron UMN bladder dysfunction
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-Loss of inhibition to muscles and sphincters of the bladder
-Bladder feels like a firm water balloon -Will not be able to express the bladder -Will eventually overcome the tone of the bladder, but will happen rapidly and with force |
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DDx for T3-L3 lesions
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-Degenerative lesion: Intervertebral disc degeneration, degenerative myelopathy
-Congenital vertebral or spinal cord malformation -Primary neoplasia or metastatic neoplasia -Infectious myelitis, diskospondylitis -Trauma -Fibrocartilagenous emboli |
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Intervertebral Discs
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-Allow stable motion
-Accomodates some of the forces on the spine -Disc sits under the vertebrae -Annulus fibrosis: --around the edge of the disc --firmly adhered to the end-plates of each vertebrae --multi-layered ligament -Nucleus pulposus: hydrated central portion --should distribute forces well --remnant of the notochord |
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Intervertebral Disc Degeneration
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-Disc becomes “dehydrated” before it should
-Common on chondrodystrophic and small-breed dogs -Glycosaminoglycans in nucleus pulposus degenerate, causes decreased water content -Normal forces on the abnormal disc cannot be distributed evenly --disc is forced into the spinal canal |
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Disc Degeneration: Hansen Type I
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-Acute disc herniation
-Focal compressive myelopathy -Chondrodystrophic breeds --Dachsund, miniature poodle, beagle, cocker spaniel, Pekinese -Weakened annulus and degenerative nucleus -Extrusion of the nucleus pulposis -Abnormal material extrudes into spinal canal |
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Disc Degeneration: Hansen Type II
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-Chronic, slow, progressive focal myelopathy
-Annulus fibrosis metaplasia builds up and bulges into the spinal canal -Not an eruption, more of a protrusion -Non-chondrodystrophic, middle aged/older breeds --labs, german shepherds -Occurs over months/years |
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Type III disc
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-Acute, non-compressive extrusion of the nucleus pulposus
-Nucleus pulposus is of normal consistency, normal looking -Occurs with extreme and sudden force, nucleus is ejected through the disc via rent in annulus -Nucleus pulposus material Disperses in the spinal canal without causing compression -Hard to distinguish from fibrocartilagenous emboli -Can’t do anything about it surgically, no compression present |
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Progression of Functional loss
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1. loss of proprioception
--scuffing, knuckling, long-strided gait 2. loss of voluntary motor ability --dragging hind end, loss of bladder function 3. Loss of nociception (no pain perception) |
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Disc degeneration location
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-65% occur in T3-L3 region
--T11-T12 most common in small dogs --L1-L2 most common in large dogs -Intercaptial ligament prevents extrusion in cranial and mid-thoracic intervertebral disc spaces --Sits at head of the rib and holds down disc material |
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Ascending Descending Myelomalacia
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-Softening of the spinal cord, necrosis of the spinal cord
--neurons, motor fibers, and sensory fibers -Occurs in first few days after an injury -Occurs uncommonly, usually less than 10% -Animal will not be able to feel limbs -Can occur over periods of time -Always a concern for paralyzed dogs -Hind limbs become flaccid, “line of sense” moves forward and more of body becomes non-sensory --Cranial migration of CT reflex --loss of intercostal muscle function --Loss of thoracic limb function -Caudal migration causes loss of patellar reflex and tone in pelvic limbs -No treatment! Once signs develop, tends to continue -Can stop on its own, most often progresses to a point where respiratory function is affected -Painful process! |
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Diagnosis of disc degeneration
|
-Radiographs can provide some evidence of disc herniation, but is not a definitive diagnosis
-MRI (gold standard) |
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Radiographic changes with disc degeneration
|
-Narrowing or wedging of the disc space and articular processes
-Smaller intervertebral foramen -T10-T11 is normally narrowed -Mineralized disc material |
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MRI for disc degeneration
|
-Gold standard for diagnosis
-Gives cross-sectional view, important for localization -Can look at meninges and changes in spinal cord parenchyma --helps determine prognosis? |
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Medical management of disc degeneration
|
-Can medically manage if lesion is not severe and animal can still walk
-Strict rest for 4-6 weeks -Anti-inflammatory drugs (steroids or NSAIDS) -Analgesia, pain medication (Tramadol, gabapentin) -Muscle relaxant (methocarbamol) -Physical rehab, weight control, avoid jumping -30-50% recurrence rate |
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Surgical management of Ascending descending myelomalacia
|
-Dorsal laminectomy
-Hemilaminectomy (most common) -Pediculectomy -Surgery within 12-24 hours gives best chance for functional outcome -Durotomy at time of surgery done to inspect spinal cord parenchyma does not change prognosis -Fenestration can help prevent recurrence --debated efficacy, clinician dependent |
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Durotomy
|
-Cut meninges, gives spinal cord more room to swell
-Does not change prognosis |
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Plegia with no pain perception
|
-Treat within 24-48 hours via surgical decompression
-Prognosis with medical management is less than 5% success -Prognosis with surgery is 50% |
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Plegia with pain perception
|
-Surgical decompression is best treatment
-Prognosis with medical management is 50% recovery -Prognosis with surgery is 80-95% |
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Non-ambulatory paraparesis
|
-Recommended treatment is surgical decompression
-Prognosis with medical management is 55-85% resolution -Prognosis with surgery is 85-95% resolution |
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Ambulatory paraparesis
|
-Medical management is recommended treatment
-Medical management gives 55-85% resolution -Prognosis with surgery is 85-95% resolution |
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Hyperesthesia
|
-Medical management is recommended treatment
-55-85% of cases will resolve with medical management -85-95% of cases will resolve with surgical treatment |
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Degenerative Myelopathy
|
-Insidious, progressive UMN ataxia in hind limbs
-Slowly progressing disease that starts it T3-L3 region -Not painful -Degeneration of the axon and loss of myelin around the axon -Occurs most commonly and first in thoracic region of the spinal cord -Progresses from thoracic region to cervical and lumbar regions -Some changes in LMN and muscles occur -Can also have cranial nerve issues |
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Degenerative Myelopathy genetics
|
-Mutation in SOD1 gene
--Same mutation as ALS in people -Missense mutation in superoxide dismutase -Genetic test exists, 2 copies of mutant gene indicate dog is likely to develop signs at some point -New genetic variations are likely to be discovered |
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Clinical signs of Degenerative myelopathy
|
-Specific breeds affected
-Usually in animals 5 years or older, usually over 8 years -Progressive, asymmetric, UMN paraparesis -Non-painful, lack of spinal pain -Animal will be non-ambulatory in 6-9 months from initial signs -Initially may have reflexes with UMN localization --brisk patellar reflex -If lesion progresses, patellar reflex is lost, becomes more flaccid paralysis -Thoracic limbs may also show signs -Urinary and fecal incontinence may develop |
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Breeds affected by Degenerative Myelopathy
|
-German Shepherds
-Boxer -Burnese Mountain Dogs -Chesapeake bay retrievers -Retrievers -Corgi -Rhodesian Ridgeback |
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Diagnosis of Degenerative Myelopathy
|
-Rule out other issues
-MRI: rules out compressive disease --often intervertebral disc protrusions are present, can confound diagnosis -CSF tap to look for inflammation -Genetic testing is available --2 copies on mutation indicate dog will be likely to develop signs at some time |
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Management for Degenerative Myelopathy
|
-No treatment exists
-intensive physical therapy may give longer survival times, study is biased -endpoint is usually elected euthanasia -Therapy may improve quality of life -Overall prognosis is poor |
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Spinal cord trauma
|
-Fracture/luxation is most common
-Put patient on a backboard until you are certain there is no fracture --immobilize -Stabilize cardiovascular and respiratory function -Assess neurological function as much as possible while maintaining restraint -Pain perception is most important prognostic indicator --do before giving pain medication --back legs is most important |
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Radiographs for spinal trauma
|
-Lateral views, attempt orthogonal view
--horizontal beam with animal on the backboard -Great for bony changes -Can be subtle changes with severe damage -Complete transection of the spinal cord may be present, will not see on radiograph |
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CT and MRI for spinal trauma
|
-CT first to look at bony changes
--CT is more important, do first -MRI to assess soft tissue damage and spinal cord investigation |
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Compartment Model for spinal injuries
|
-Used to determine if animal should be stabilized or not
-If 2-3 compartments are affected, consider patient unstable and need to stabilize for surgery |
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Conservative management of spinal injuries
|
-If stable, can confine for 6-8 weeks
-External coaptation can be helpful -NO coaptation for ventral compartment failure |
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Surgical intervention for spinal injuries
|
-Helpful in compressive lesions or to create stability |
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Prognosis for animals with spinal injuries |
-Little difference between surgical and medical management |
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Caudal Cervical Diseases
|
-C6-T2
-UMN is inhibitory to LMN and proprioceptive tracts -LMN in front and back limbs |
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Neuro exam findings in caudal cervical diseases
|
-Normal mentation
-cranial nerves may show Horner Syndrome -- disruption to sympathetic innervation to the eye, no sympathetic tone --ptosis, meiosis, enophthalmos, raised 3rd eyelid |
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Sympathetic Innervation to the eye
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1. Sympathetic innervation from the diencephalon runs down spinal cord in tectotegmental tracts
2. Synapses in T1-T3 region intermediate gray matter -leaves with roots of brachial plexus via ramus communicans -forms cranial sympathetic trunk 3. 2nd order neuron, runs outside of the spinal cord and synapses in cranial cervical ganglion 4. Takes varied pathway back out to tissues of the eye |
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2 engine gait
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-Lesion location affects both LMN (forelimbs) and UMN (hindlimbs)
-Short choppy strides in front legs -HUGE strides in the back legs, long and lopey -Head can be held a little low -Indicates caudal cervical lesion |
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Proprioception in caudal cervical lesion
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-Animal may be able to place limbs normally if it is held up
--only interrupting LMN, not proprioceptive tracts -Can have normal to decreased proprioception in front -Decreased placing and hopping in the hindlimbs |
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Reflexes in caudal cervical lesion
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-Affecting LMN in front
--decreased reflexes in front, will not see robust withdrawal -Inreased reflexes in the hindlimb, increased withdrawal --may have crossed-extensor reflex -Low reflexes in front, Big in the hind |
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Cutaneous Trunci muscle and cranial cervical lesion
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-LMN portion of the reflex arc may be affected
-If lesion is lateralized, there may be no cutaneous trunci reflex on the ipsilateral side --bilateral reflex |
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DDx for Caudal cervical lesion
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-Intervertebral disc degeneration
-Syringomyelia, cervical Spondylomyelopathy (wobbler’s), synovial cysts -Peripheral nerve sheath tumors -Meningomyelitis -Brachial plexus avulsion -Fibrocartilagenous emboli |
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Cervical Spondylomyelopathy
|
-Wobbler’s syndrome
-Signs develop due to progressive spinal cord compression from vertebrae and soft tissue structures -Progressive disease, comes on over time -degenerative disease -Mostly affects large breed dogs --great danes, Dobermans, burnese mountain dogs |
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Doberman Cervical Spondylomyelopathy
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-Show signs at 4-8 years old
-Hypertrophy of the interarcuate ligament and dorsal longitudinal ligament -Disc protrusion in caudal vertebrae --unique to Dobermans, causes disc-associated Wobbler’s -Abnormal remodeling and rotation of C6 |
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Cervical Spondylomyelopathy in Great Danes, Burnese Mountain Dogs
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-Occurs at 2 years old
-No disc-associated Wobbler’s -Ligamentous hypertrophy causes dorsal and dorsolateral compression from articular processes -Joint capsules can be thickened and have extra fluid -Tends to occur lower down in spinal cord, C5-6 or C6-7 |
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Clinical signs of Cervical Spondylomyelopathy
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-More severe in pelvic limbs, recognized in pelvic limbs first
--loss of proprioception, scuffing -Usually not a painful problem unless disc rupture is involved -UMN ataxia that eventually becomes tetraparesis -Compression is happening laterally/dorsally, pushing down on spinal cord --presses on tracts and fibers that go to back legs initially --progresses as there is more compression over time |
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Diagnosis of Spondylomyelopathy
|
-Radiographs
-Myelography is better for dynamic visualization --need to be careful with injecting dye around spinal column --can measure stenosis -MRI is best for soft tissue compression -CT in cases where compression is dynamic |
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Radiographic changes associated with Spondylomyelopathy
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-Changes in disc space, narrowing
-Articular facets -Vertebral displacement -Stenosis of the vertebral canal -Malformed vertebrae -Misshapen spinous processes -Vertebral bodies are “tipped” and out of alignment -Need orthogonal views to assess dorsal and lateral compression |
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Spondylomyelopathy treatment
|
-No consensus on treatment
-Conservative management is pretty effective -Restriction of activity -Steroids may or may not be used -Surgical options for ventral or dorsal decompression -Distraction techniques and stabilization are also common -If there is one easily identifiable site of compression, surgery is recommended -If there are no easily identifiable sites, medical management is recommended |
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Spondylomyelopathy Prognosis
|
-Poor for tetraplegic dogs
-Guarded for all dogs -No difference in outcome or survival time in conservative vs. surgical management -33-80% success rate with surgery --no one knows best method or approach -24-40 month expected lifespan |
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Caudal Cervical Spinal Cord Trauma
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-Usually the result of a hit by car, major fall
-70% of fractures occur at C1-C2, 10% between C3-C7 --Can present with caudal cervical cord signs as result of brachial plexus injury -Check for nociception and proprioception in feet before giving pain meds! -Ttetraplegia with loss of pain perception is rare but concerning --usually occurs due to concurrent respiratory failure |
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Traction Injury to brachial plexus
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-Often related to trauma
-Force that abducts and caudally displaces thoracic limb --can sever nerves in brachial plexus -Trauma most often occurs at roots, as they arise from spinal cord -May also cause damage to spinal cord, can have signs associated with hind limbs -Can be complete or may have some nerves intact |
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Clinical signs of Traction Injury/Brachial plexus avulsion
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-Related to affected roots
-Cranial roots (C6, C7) vs caudal roots (C8-T1) -Complete and caudal avulsion: triceps are mostly affected --cannot extend elbow or bear weight -Cranial avulsion: can bear weight but cannot flex elbow or bring elbow forward -Neurogenic atrophy will occur within 1 week, best to treat early! |
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Horner Syndrome and Cutaneous Trunci
|
-Traumatic case
--Horner syndrome and cutaneous trunci as clinical signs -Easy to localize, know injury must have happened to T1 at least -Injury to T1 ventral spinal nerves |
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Prognosis for Caudal cervical spinal nerve avulsion/Brachial plexus injury
|
-Sensory loss gives best prognosis
-Pattern loss of sensation can help localize lesion also -Best prognostic indicator for return of function is pain perception -Complete avulsion results in no pain perception --does not mean it will never come back -EMG and nerve conduction studies are useful for localization --if nerves going to muscle are disrupted, muscle will make lots of noise on EMG --can see if nerves are innervating the muscle normally -Can do nerve conduction tests |
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Treatment for Caudal cervical spinal nerve avulsion/Brachial plexus injury
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-Short-term corticosteroid therapy to reduce inflammation
-Gabapentin to address neuropathic pain -Physical therapy -Prevent trauma to distal limb -1-2 weeks to 3-4 months for recovery -Severed nerves can regenerate if nerve sheath is intact --grows about 1mm per day -After 6 months of supportive care, may opt for amputation |
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Caudal Cervical neoplasia
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-Peripheral nerve sheath tumor is most common neoplasia
-Lymphoma and meningioma can also occur -Older dogs -Ipsilateral horner syndrome and no cutaneous trunci -Ipsilateral Severe atrophy -May be able to palpate the nerve sheath tumor -Are extremely painful! |
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Peripheral nerve Sheath Tumors
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-Can be in brachial plexus area of the spinal canal
-Most originate peripherally and slowly extend proximally to involve spinal cord -Cause monoparesis, only one side is affected -Root signature: dog limps on whole leg, does not put weight on leg --thinks pain is coming from the leg when it is actually coming from the nerve roots -Pronounced atrophy -May be able to palpate tumor |
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Diagnosis of Peripheral nerve sheath tumor
|
-EMG to provide evidence of denervation
--epaxial muscles indicates invasion of the spinal canal, gives idea for prognosis -MRI is gold standard for diagnosis --Soft tissue neoplasia |
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Treatment for Peripheral nerve sheath tumor
|
-Resection is ideal, local resection or limb amputation |
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Cranial Cervical Anatomy
|
-7 cervical vertebrae
-Atlanto-axial joint does not have a disc space -Rest of vertebrae are separated by intervertebral disc space |
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Atlanto-Axial Anatomy
|
-Axis has a dens that sits in ring of Atlas
-Dens is held in place by ligaments --transverse ligament is thickest, holds down |
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Cranial Cervical Lesions
|
-Motor pathways from brainstem centers to LMN
-Release or disinhibition of LMN -Affects proprioceptive tracts, results in ataxia |
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C1-C5 myelopathy Cranial cervical injury
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-hypermetria, lifting feet far off of the ground
--“floating gait” -Long strides -Not lame -UMN general proprioceptive ataxia (gait) -normal mentation -Loss or deficiency in placing/hopping -Increased stretch reflexes -Normal or increased withdrawl reflex -Crossed extensor reflex -Normal cranial nerves -Horner syndrome is possible, but not common |
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Lesion localization in Cranial cervical spine
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-Not all dogs that cannot stand or walk have neurologic disease
-If are neurologic, are not always a C1-C6 problem -Tetraparesis must be differentiated from generalized weakness, orthopedic disease, and obtundation |
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Neurologic localizations that can cause tetraparesis
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-Brainstem
-Cervical spinal cord -LMN |
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DDx for cranial cervical lesions
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-Intervertebral disc degeneration, neuraxonal dystrophy
-Atlanto-axial subluxation, syringomyelia, cervical spondylomyelopathy, synovial cysts -Neoplasia -Meningomyelitis -Traumatic injury -Fibrocartilagenous emboli |
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Cervical Intervertebral Disc Disease
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-14% of all disc herniations occur in cervical region
-Small breed dogs: C2-3, C3-4 -Large breed dogs: C6-7 -Less commonly results in paresis or paralysis --spinal canal is wider, more room for compression --less myelomalacia, very rare |
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Clinical signs of Intervertebral disc degeneration in cranial cervical region
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-Cervical pain is most common, “neck pain”
-Low head and neck carriage -Muscle spasms, can look like seizures -Tetraparesis or tetraplegia -Ataxia -Root sign |
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Cranial cervical Intervertebral Disc degeneration diagnosis
|
-Radiographs
-Myelography: attenuation and displacement of contrast -CT and MRI --MRI is modality of choice --CT can be challenging in neck region -CSF to rule out sphingomyelitis |
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Radiographs for cranial cervical intervertebral disc degeneration
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-Rule out bony lesions
-Show narrowed disc spaces -Show evidence of disc mineralization -Cannot be used for definitive diagnosis |
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Intervertebral Disc mineralization in cranial cervical region
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-Gives very severe neck pain
-Normal gait -Lots of muscle spasms -Can see mineralized discs on radiographs |
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Cranial cervical Intervertebral disc degeneration medical management
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-Medical vs. surgical treatment
-Depends on clinical signs and severity -Medical management: strict confinement --use harness, no collars or leashes --opioid analgesics, corticosteroids, NSAIDs, gabapentin -If medical management fails in 1-2 weeks, reassess |
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Cranial cervical Intervertebral Disc degeneration surgical management
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-Dorsal laminectomy or ventral slot
-80-99% success rate for ventral slot surgery -Small breeds do better, especially if recover within 96 hours -Large breed dogs have slower recovery, requires physical rehab --66% success rate -Recurrence rate is 10-33% --usually from a second site |
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Ventral Slot procedure
|
-Treatment for cranial cervical intervertebral disc degeneration
-Drill and burr through the bone and disc material -Bleeding from venous plexus is a major complication |
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Dorsal Laminectomy Procedure
|
-remove “roof” of the vertebrae
--includes part or all of the spinous process to remove compression |
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Cervical Meningomyelitis
|
-Inflammation of the meninges
-Can be bacterial, viral, rickettsial, fungal infections -Idiopathic -Auto-immune version --steroid responsive meningitis arteritis --Granumomatous meningoencephalitis --meningoencephalitis of unknown etiology |
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Steroid Responsive Meningitis Arteritis
|
-Large breed dogs over 2 years old
-Young dog, terrible neck pain, fever -Boxers, beagles -Bernese mtn dogs, weimaraners -Walk stiffly and do not turn head, turn whole body -90% of dogs show severe pain -Neutrophilic leukocytosis and fever in 2/3 of dogs -50% of dogs with joint inflammation have steroid-responsive meningitis arteritis also |
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Steroid responsive meningitis arteritis Pathology
|
-Unknown cause
-Something sets immune system to create inflammation of leptomeninges -Mostly neutrophilic inflammation -Causes vasculitis at the same time --vessels can be obliterated by neutrophil inflammatory cells |
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Steroid Responsive meningitis arteritis diagnosis
|
-CSF tap
-Imaging is not as helpful as imaging -LOTS of neutrophils and protein in spinal tap -bacterial culture will be negative -IgA concentration is high in CSF and plasma --can stay high for a long period of ime -CRP reduction in spinal fluid indicates treatment is working |
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MRI as diagnostic for Steroid Responsive meningitis arteritis
|
-Only do if there are also proprioceptive deficits
-Get contrast uptake in meninges, should not happen if animal is healthy |
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Treatment for steroid-responsive meningitis arteritis
|
-Immunosuppressive dose of steroids (Prednisone)
-LONG treatment, at least 6 months -Prognosis is good with immunosuppressive treatment -Azathioprine can be used for recurrent chronic cases --can remove prednisone |
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Atlantoaxial Anatomy
|
-Joint is responsible for Rotational and lateral movement
-Held in place by ligaments, transverse ligament is most important -Dens hypoplasia or aplasia causes failure of the ligaments --ligaments cannot hold onto anything, cannot prevent movement -Trauma can rupture the ligaments |
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Atlantoaxial Luxation
|
-Most commonly in small breed dogs with malformation
-Pain, ataxia, UMN tetraparesis -Can be acute or chronic, may be asymmetric -Check for respiration! Ventilator support can be required -Avoid flexion of the neck, will drive the dens into the spinal cord -Sedation or anesthesia can destabilize the musculature -If luxation or fracture is suspected maintain extension, neutral position |
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Atlantoaxial luxation diagnosis
|
-Spinal radiographs to show C1-C2 malalignment
-Fluroscopy can be used to see dynamic lesion -CT provides more information of bony lesion -MRI may show additional spinal cord injury --not best modality |
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Atlantoaxial luxation treatment
|
-Joint stabilization and fusion is the goal
-Surgical treatment is preferred method of therapy -Conservative therapy can be useful --restrict exercise, use external coaptation |
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Conservative treatment for Atlantoaxial lucation
|
-External copatation: incorporate head and forelimbs
--all the way up on the head, all the way down on the chin, down back to mid-thorax --need to ensure neutral position! -Use soft padded bandage or splint, leave on for 6-8 weeks -Complications: --failure to promote fibrous tissue --decubital ulcers and dermatitis --otitis externa -Prognosis is fairly good |
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Surgical stabilization of atlantoaxial luxation
|
-Ventral fusion is most common
-Chronic history, relapse of signs -Need to fix the articulation in place -Transarticular fixation vs. multiple implants secured with PMMA |
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Complications of surgical stabilization of atlantoaxial luxation
|
-Most complications occur during the surgery
-Death -Implant failure -May need to repeat surgery in 8-20% of cases -Migration or breakage of implant -Gagging, laryngeal paralysis, tracheal collapse, pneumonia -30% risk of serious complication or death! |
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Caudal Occipital malformation Syndrome
|
-Chiari-like malformation, syringohydromylea, syringomyelia
-Common disease in small-breed dogs --dogs with shortened noses and rounded skulls -Rounding the skull makes back of the skull very small --not enough room for development of cerebellum and brainstem --skull squishes into the cerebellum -Small caudal fossa, results in secondary herniation through foramen magnum -Fluid gets pinched, flows to any available space at high pressure --forms syringomyelia -Cavalier King Charles Spaniels are most common (80-90%) |
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Clinical signs of Caudal Occipital Malformation Syndrome
|
-Cervical pain, radiating pain
-Excessive scratching, vocalizing, facial rubbing --neuropathic pain -Ataxia, UMN tetraparesis -Central vestibular or cerebellar signs -Scoliosis -Seizures (rare) -Commonly are treated for skin disease or otitis before coming in for neuro exam |
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Syringomyelia
|
-Fluid-filled cavity within the spinal cord
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Caudal Occipital Malformation Syndrome diagnosis
|
-MRI mid-saggital image of the brain and cervical spinal cord
-Can see pinching of cerebellum and fluid in the spinal cord --looks like a giant pocket of fluid -40% of clinically normal animals have syrix on MRI |
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Caudal occipital Malformation Syndrome treatment
|
-Medical treatment is tried first |
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Caudal occipital Malformation Syndrome surgical treatment
|
-only if medical management fails |
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Causes of LMN disorders
|
-Neuropathy: only affects nerve
-Myopathy: only affects muscle -Junctionopathy: junction between muscle and nerves -Spinal cord intumescences --C6-T2, L4-S3 --mimics LMN disorders |
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LMN disease clinical characteristics
|
-Decreased or absent sensation
-Poor muscle tone (main diagnostic that differentiates UMN from LMN) -Weakness -Depressed reflexes (also differentiates peripheral from spinal cord injury) -Decreased or absent motor function |
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LMN
|
-Axon of the ventral horn and muscle it innervates
-Motor unit -Any part of motor unit can be affected and give LMN disorder signs |
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Peripheral nerve
|
-Motor and sensory axon, travel in the same nerve
-Associated myelin sheath -Cell bodies of each axon in peripheral nerve -Axons are VERY long! -Distal aspect of the nerve is most susceptible to diseases, furthest from the cell body |
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Myelin Sheath
|
-Associated with the speed of electrical conduction
-Myelin = speed -Often affected by immune mediated or genetic disease, can also be affected by trauma |
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Axon and Schwan Cell Interactions
|
-Proteins maintain connection between schwann cell and axon
-“glue” schwann cell to the axon -Proteins are responsible for nodes of Ranvier, leaving space open for nerve conduction |
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|
Axonal size and fiber types
|
-Type A: contain a lot of myelin, conduct impulses faster
--can be sensory or motor -Type AB: -Type C: Slow fibers --deep, slow, dull pain |
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Classification of Peripheral nerve Disease
|
-Generalized vs. Focal
-Acute vs. Chronic -Axonal vs. demyelinating |
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DDx for General Peripheral neuropathies
|
-Hereditary disease
-Hypothyroid, hypoglycemia, diabetes mellitus, uremia --CBC/chem -Panthothenic acid deficiency, pyridoxine toxicity -Lymphosarcoma -Acute polyradiculoneuritis (Coon hound toxicity) -Immune mediated disease -Paraneoplastic syndromes -Idiopathic cause -Toxoplasmosis -Neospora caninum -Organophosphates, lead, vincristine -Tetracyclines, sulfonamides, polymixin B |
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Polyradiculoneuritis
|
-Coon hound toxicity
-Inflammation in many nerve roots -Inflammatory cell infiltration into axons -Can be immune-mediated -Can be caused by raccoons but not common |
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DDx for Focal peripheral neuropathies
|
-Vertebral canal stenosis
-Intervertebral disc disease -Foramen stenosis -Nerve sheath tumor (neurofibroma, schwannoma, sarcoma) -Lymphosarcoma (usually general, not focal, but can happen) -Injection neuritis -Ischemia -Contusion, laceration, fracture -Brachial or lumbar plexus avulsion |
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Focal peripheral neuropathies
|
-Easy to localize the lesion
- |
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History of patient with peripheral neuropathy
|
-Acute vs. chronic
-Duration -Progression -Current medications -Toxic exposures -Tick exposure and tick paralysis -Vaccination history |
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CBC/Chem for patient with peripheral neuropathy
|
-Creatinine phosphokinase (CPK)
--muscle enzymes, indicates muscle disease -Lactate dehydrogenase (LDH) -Aspartate transferase (AST) -Cholesterol --high indicates problem with thyroid, damages myelin -Potassium |
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Endocrine tests for patients with peripheral neuropathy
|
-Thyroid profile
-Resting cortisol level (Addison’s) -ACTH stimulation (Cushing’s) |
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Infectious disease testing for patients with peripheral neuropathy
|
-Toxoplasmosis in cats
-Neospora caninum in dogs |
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CSF analysis for patients with peripheral neuropathy
|
-Nerve root diseases
--inflammatory processes --neoplasia, esp. lymphoma -Not an essential test, but available test |
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|
Electrophysiology for peripheral nerve disease
|
-Electromyelogram
-Nerve conduction velocity - |
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Electromyelogram
|
-Test for spontaneous activity in the muscle
-Normal muscle should be silent -Adding a needle should make noise, disturb things, then will be silent -With peripheral nerve disease, muscle can be over-stimulated --hypersensitive to stimuli -Will record abnormal noise and electrical activity -Will also be abnormal with diseased muscle -Indicates neuromuscular disorder, not peripheral nerve disease specifically --do nerve conduction velocity testing to confirm peripheral nerve disease |
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|
Nerve Conduction Velocity test
|
-Differentiates between neuropathy and myopathy
-Indicates demyelination -Can tell if damage is sensory vs. motor |
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Muscle and nerve biopsies for peripheral nerve disease
|
-Take sample of affected muscle
-Look at via pathology and histochemistry -Can tell if there is inflammation or fibrosis and scarring via pathology -Histochemistry can tell what kind of fibers are diseased and do antibody studies |
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|
Pathology diagnostics for peripheral nerve disease
|
-Sample Peronial and ulnar nerve
--fascicular biopsy -Formaldehyde and gluteraldehyde preservation -Can look for demelination, axonal disease, or inflammation in nerve |
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|
Treatment for peripheral nerve diseases
|
-Do not need to restore function to all axons
--preserving function to some of the fibers will allow function |
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Myelin incisures
|
-Myelin fibers start to become “unrolled”
-Need molecules that allow transport of substances into and out of myelin sheath -No transport, sheath becomes diseased |
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|
DDx for Generalized Polyneuropathy
|
-hypothyroidism
-Diabetes and hypoglycemia -Hypoadrenocorticism (addison’s) -Lymphoma -Paraneoplastic syndrome -Toxoplasmosis and neosporosis -Polyneuritis -Polyradiculoneuritis -Botulism -Tick paralysis |
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|
Generalized Polyneuropathy Diagnostics
|
1. Look for ticks!
-T4 and tree T4 testing -Blood glucose -Toxoplasmosis and neosporosis -Cortisol levels 2. Electrodiagnostics -Lumbar CSF tap 3. Muscle and nerve biopsy or MRI |
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|
Treating metabolic disease causing generalized polyneuropathy
|
-Hypothyroidism: levothyroxine
-Diabetes and hypoglycemia: insulin or glucose -Hypoadrenocorticism |
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|
Treating Immune mediated or infectious disease causing generalized polyneuropathy
|
-Clindamycin or TMS for toxo or neospora
-Steroids and supportive care |
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|
Focal peripheral nerve disorders
|
-Injection neuritis
-Compression ischemia -Contusion or laceration -Brachial plexus avulsion -Nerve trauma with fractures -Ischemic neuromyopathy -Peripheral nerve sheath tumors |
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|
Brachial Plexus or pelvic plexus injury
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-Nerve roots can be pulled from spinal cord
-Radial nerve is often involved -Animal will not be able to feel the limb -Horner syndrome may be present -Ulnar, radial, musculocutaneous nerves also involved -No cutaneous trunci reflex -Flacid paralysis of one of the legs -EMG and NCV |
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Neuromuscular Junction Diseases
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-Disease between peripheral nerve and muscle
-Motor unit is affected -Intermittent weakness, generalized severe weakness --exercise intolerance -Facial weakness -Voice changes -Megaesophagus is common -Botulism, tick paralysis, and myasthenia gravis are common disease processes |
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Botulism
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-Disease that relates to release of ACh
-Not enough ACh is released into the synaptic cleft --Do not get muscle contraction -Vesicles with NT are not able to fuse with the pre-synaptic membrane and be released into synaptic cleft -LOTS of botulinum toxins that can affect synaptobrevin, Syntaxin, or SNAP-25 -Tick paralysis works via similar mechanism |
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Myasthenia gravis
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-ACh receptors on post-synaptic membrane are destroyed by immune-mediated process
-No receptors available to receive ACh -Easy to diagnose --serology: antibody to ACH receptor in serum --electrodiagnostic repetitive nerve stimulation, nerve tires easily --Tensilon test, momentarily increases amount of ACh in synaptic cleft, allows for short period of normal motor function --Muscle biopsy and look for ACh receptors in immunohistochemistry |
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ACH-esterase agents
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-Treatment for Myasthenia gravis
-Pyridostigmine bromide (Mestinon) is long-term treatment -Edrophonium Chloride (tensilon) for short-term -Provide substrate for ACh-Esterase or increase ACH at neuromuscular synapse |
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Steroids for Myasthenia gravis
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-Will reduce immune-mediated disease
-Also causes muscle atrophy over the long term --do not want more muscle weakness! -Dogs are also already predisposed to aspiration pneumonia, do not want immunosuppression in lungs |
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Electrophysiology
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-Zap an animal with 20-100V discharge right onto the nerve
-Will have insertional activity right when needle is inserted -Animal needs to be anesthetized! -normally at rest, should be silent -If abnormal, will have spontaneous discharges -Does not differentiate between myopathy and neuropathy, just indicates issue with motor endplate |
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Spontaneous discharges with Electromyography
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-Fibrillation potentials: crackling
-Positive sharp waves: thumping -Complex repetitive discharges: machine gun -Myotonic discharges: airplane noise |
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Peripheral nerve studies
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-Assesses motor and sensory function |
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Factors Affecting Motor Nerve conduction
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-Temperature |
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Anatomical Divisions of the Brain
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-Cerebral hemispheres
-Brainstem -Cerebellum |
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Functional Divisions of the brain
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-Cerebral hemispheres and diencephalon
-Brainstem: pons, medulla, midbrain -Cerebellum |
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Neurologic exam assesses 6 categories of brain function
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-Mental status
-Gait -Postural ability -Segmental reflexes -Sensation -Cranial nerves |
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Questions to ask with neurologic brain issues
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-Is neurological dysfunction present?
-If yes, what part of the nervous system is malfunctioning -What diseases may be responsible for malfunction of this region? |
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What part of the nervous system is malfunctioning?
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-Gait abnormalities: behind the cerebrum/diencephalon
--in midbrain, pons, medulla, cerebellum -Ipsilateral deficits are behind the cerebrum/diencephalon -Seizures: above the midbrain, in cerebrum/diencephalon -Contralateral defects: above the midbrain in cerebrum/diencephalon |
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Cerebral hemisphere disease
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-Altered mental status
-Normal gait --circling and pacing is possible, may walk towards side of lesion -Contralateral deficits in posture --ability to hop, wheelbarrow, hemi-walk is altered -Contralateral deficits in sensation -Normal segmental reflexes -Cranial nerves: olfactory and visual system may have abnormalities -Seizures may be present |
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Midbrain disease
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-Altered mental status
-Gait abnormalities --ataxia, spastic tetraparesis or paralysis due to increase in tone (UMN issue), sloppy in-coordinated gait --weakness -Contralateral or ipsilateral postural deficits -Contralateral hyper-reflexia -Pupillary abnormalities and strabismus due to CN III (oculomotor) and CN IV (trochlear) --thiamin deficiency in cats |
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Pons/Medulla Disease
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-Altered mental status
-Ataxia, spastic tetraparesis, paralysis -Ipsilateral deficits (caudal to mid-brain) -Ipsilateral hyperreflexia, increased reflexes -CN V, VI, VII, VIII, IX, X, XI, and XII are affected |
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Cerebellum disease
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-Normal mental status, acute damage to cerebellum does not affect mental status
-Ataxia with dysmetric gait --make bigger or smaller motions than they should -Ipsilateral deficits in posture -Normal sensation -Normal segmental reflexes -No cranial nerve deficits -Menace deficits and intention tremors may be present |
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Intention tremors
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-Present with cerebellar disease
-At rest there is no tremor, but increases with activity |
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What diseases may be responsible for damage to brain in specific regions? Asymmetric vs. symmetrical
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-Degenerative diseases: always symmetrical, both sides affected
-Anomalous diseases: focal and usually asymmetric -Metabolic disease: diffuse and symmetrical -Neoplastic: focal, asymmetric -Inflammatory: can be anything -Infarcts: focal, asymmetric -Trauma: focal, can be asymmetric or symmetric -Toxins: act like metabolic disease, diffuse and symmetrical |
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What diseases may be responsible for malfunction of this region based on history?
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-Degenerative: insidious and progressive
-Anomalous: static, do not change over time -metabolic: waxes and wanes, tends to be episodic, can be progressive -Neoplasitc: insidious or acute, progressive -Inflammatory: insidious or acute, progressive -Infarct, trauma, and toxins are all acute and tend to improve over time |
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Degenerative Focal Brain Disease
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-Lysosomal storage diseases
-Neuronal abiotrophies -Canine cognitive dysfunction |
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Anomalous focal cerebral hemisphere disease
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-Arachnoid Cyst
-Meningoencephalocele -Cerebral Aplasia |
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Arachnoid Cyst
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-Fluid accumulation in meninges
-Occipital lobe is often compressed -Clinical signs: blindness, tremors, seizures, normal gait but circling -Disease does not make clinical signs, location makes clinical signs -Can remove cyst, will resolve clinical signs |
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Meningoencephalocele
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-Protrusion of meninges or meninges and brain through defect in the skull
-Commonly occurs in nose |
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Cerebral Aplasia
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-anencephaly, born without cerebral hemispheres
-Failure of neural tube to close, animal is born without top part of the brain |
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Hydranencephaly/porencephaly
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-not a true anomaly, more destructive disorder
-Due to infarct during development -Can be due to viral infections or vascular events -Cerebral hemispheres “died” in-utero -Porencephaly is just losing part of the cerebral hemisphere, other side is normal |
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Holoprosencephaly
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-Failure of right and left hemispheres to separate
--Form one big hemisphere -Communication between areas that should not connect -Seizures are most common clinical sign |
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Arhinencephaly
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-Born without the olfactory bulbs
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Agenesis of corpus callosum
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-Connection between right and left hemispheres does not form
-No connection between sides, brain falls apart when removed from skull |
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Abnormalities of neuronal migration
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-Heterotopias
-Hamartoma -Pachygria |
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Heterotopias
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-Gray matter exists where it should not belong, in white matter area
-Causes seizures and behavioral changes in dogs -Can be removed if there are just a few -If there are a lot, have to try to control the seizures medically |
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Hamartoma
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-Abnormal arrangements of neurons, oligodendrocytes, vessels
-Benign tumors that sit in the brain but do not grow or metastasize |
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Pachygyria
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-All gyri are lumped into big, large gyruses
-End up with 2 big gyruses -Failure of development of the cortex |
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Lissencephaly
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-No Gyri over brain
-No corona radiate -Smooth brain with no white matter -Normal gait, seizures, decreased mental status |
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Polymicrogyria
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-Too many small folds in the gray matter of the brain
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Hydrocephalus
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-“Water on the brain”
-Increase in spinal fluid volume that causes enlarged ventricles --ventriculomegaly -Can have obstruction to flow in ventricular system, causes buildup of water -treat with a shunt, prevents atrophy -Can be due to compensatory changes in the brain --fluid builds in spaces where brain went away -Can have over-secretion of spinal fluid -Common in Chihuahua, King Charles Spaniels, Bulldogs, Pugs, Boston terriers, boxers, Brachycephalic dogs! |
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Neoplasia of Cerebral hemispheres/diencephalon
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-Meningioma is most common
-Astrocytoma, oligodendroglioma, choroid plexus tumors are next common -Cats and people have benign meningiomas --dogs have malignant meningiomas |
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Tumors arising from tissue surrounding the brain
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-Extra-axial tumors, not from brain tissue
-Meningioma -Choroid plexus tumors |
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Choroid plexus tumors
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-Papillomas, carcinomas
-More common in 4th ventricle than in lateral and 3rd ventricles -Occur in dogs more often than cats -Associated with hydrocephalus, block flow of CSF -Can be benign |
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Meningiomas
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-Malignant in dog
-Benign in cats and humans -Come out easily in cats, hard to extract in dogs --have to do radiation and chemotherapy with dogs |
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Extra-axial tumors of the Sellar region
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-Suprasellar germ cell tumors
-Pituitary adenoma and pituitary carcinoma -Craniopharyngyoma -Meningiomas |
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Extra-axial tumors that impinge or extend into CNS
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-Nasal carcinoma
-Multilobular tumor of bone -Chondroma -Sarcomas and carcinomas -Lymphoma -Histiocytic sarcoma |
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Tumors arising from the brain
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-Intraaxial
-Glioma --astrocytoma --oligodendroglioma -Focal cerebral hemisphere or diencephalon disease |
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Tumors arising from neurons
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-Not very many!
-Neurons are differentiated, do not typically become tumors -If become neoplastic, are stem cell derivatives -Very rare! |
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Astrocytic tumors
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-Neuroepithelial cells, astrocytes
-Occurs in older animals, dogs more than cats -predilection for brachycephalic breeds -Most common glioma in dogs -Usually occurs in cerebrum and diencephalon --cerebellum and spinal cord location is less common |
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Oligodendroglial tumors
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-Neuroepithelial cells, oligodendrocytes
-Occurs in older animals, dogs more common -Predilection for brachycephalic dogs -Tends to localize in the white matter of cerebrum and diencephalon or frontal lobe adjacent to lateral ventricle |
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Ependymoma
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-Ependymal cells line surface of ventricles
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Intraaxial metastasis
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-Hemangiosarcoma is most common
-Go to brain with high incidence from heart -Mammary carcinoma is also a common metastasis -Different from humans --lung and breast tumor are most common metastasis |
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Infectious/inflammatory diseases in cerebrum in the dog
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-Viral: CDV, rabies
-Protosoa: toxoplasma, neospora -Rickettsial: RMSF and ehrlichia -Fungal: Cryptococcus -Parasitic migration: heartworm, cuterebta -Bacterial: hematogenous spread, ascending from ear -Non-infectious: granulomatous meningoencephalitis (GME), necrotizing encephalitis |
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Infectious/Inflammatory diseases in cerebrum in cats
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-Viral: FIV, FIP, rabies
-Protozoal: toxoplasma -Fungal: Cryptococcus -Parasitic migration: Cuterebra -bacterial: hematogenous spread, ascending from ear |
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Necrotizing Encephalitis
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-Pug encephalitis, “small dog encephalitis”
-Most common encephalitis in clinical situation -Unknown cause -Affects young dogs, 6 months-1 year old -Flattened gyri, loss of distinction between gray and white matter, cavitation -Necrotizing meningoencephalitis of the leptomeninges -Inflammation and necrosis of white matter in the brain --can no longer tell the difference between gray matter and white matter -Can suppress immune system and give dog a year to live -Body is attacking something in the brain |
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Infarcts in the brain
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-Not common
-Tend to occur in old dogs -Dog will be fine one minute, shows clinical signs the next minute |
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Focal disease of the Hypothalamus
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-Rathke’s cleft cyst/pituitary cyst
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Nerve sheath tumor
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-Schwanoma
-Nerve is not neoplastic, covering of the tumor is neoplastic -in dogs affect trigeminal nerve -in humans affects vestibulocochlear nerve -Does not occur significantly in cats -Affects mature/older animals -Cannot be removed! Sits right up against brain tissue -Tumor gets larger and larger --animal loses muscle of mastication on one side |
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Focal Cerebellar Disease
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-Degenerative: lysosomal storage disease, abiotrophies
-Anomalous: hypoplasia, arachnoid cyst, caudal occipital malformation -Neoplasia -Inflammatory: shaker dog disease -Infarct -Toxins: hexachlorophene, alcohol |
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Diffuse/multifocal symmetric disease in brain
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-Degenerative process:
--lysosomal storage diseases --leukodystrophies --neuronal abiotrophies --neuroaxonal dystrophy -metabolic process: --uremic encephalopathy --hepatic encephalopathy --hypothyroidism --glucose and electrolyte abnormalities -toxin -Clinical signs: ataxia, paresis, spastic tone, vertical nystagmus, postural reaction deficits, tremor |
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Multifocal asymmetric disease in brain
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-Neoplastic:
--lymphosarcoma, histiocytic sarcoma, metastatic neoplasia -infectious, inflammatory -Vascular |
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Metabolic processes that affect the brain
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-Uremic encephalopathy
-Hepatic encephalopathy -Hypothyroidism -Glucose and electrolyte abnormalities |
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Granulomatous Meningoencephalitis |
-Affects all parts of the brain |
