II - Neuro Flashcards
Cranial Nerve I name, function, and assessment
Olfactory
Smell
Response to odor without visual cues - hidden treats!
Cranial Nerve II name, function, and assessment
Optic
Vision
Menace response, pupillary light reflex, obstacle course, dazzle reflex, ophthalmic cam including retinal evaluation
Cranial Nerve III name, function, and assessment
Oculomotor
Motor function to most of the extra-ocular muscles of the eye; motor to constrictor muscles of the pupil; motor to elevator palpebrae superior is (upper eyelid)
Pupillary light reflex, assessment of pupil size, eye position; lesion causes ventral lateral strabismus
Cranial Nerve IV name, function, and assessment
Trochlear
Motor function to dorsal oblique (extra-ocular) muscle.
Eye position; lesion causes dorsomedial strabismus.
Cranial Nerve V name, function, and assessment.
Trigeminal
Motor function to the major muscles of mastication and sensory function to most skin and mucous membranes of the head.
Response to tactile stimulation of palpebral area, ear, and nostril; assessment of masticatory muscle size and tone.
Cranial Nerve VI name, function, and assessment
Abducens
Motor function to the lateral recuts and retractor bulbs (extra-ocular) muscles of the eye.
Eye position, globe retraction, corneal reflex; lesion causes medial strabismus
Cranial Nerve VII name, function, and assessment
Facial
Motor function to most of the muscles of the head; parasympathetic to salivary and lacrimal glands
Facial symmetry (look for ear droop, muzzle deviation); response to tactile stimulation of palpebral area, ear, and nostril; decreased lacrimation and secondary corneal ulceration is common
Cranial Nerve VIII name, function, and assessment
Vestibulocochlear
Vestibular function (posture and balance) and hearing
Head and eye position; assessment for nystagmus, head tilt, balance; deficits exacerbated by blindfolding; evaluation of hearing by response to auditory stimuli or BAER testing.
Cranial Nerve IX name, function, and assessment
Glossopharyngeal
Motor function to muscles of the pharynx; sensory to pharynx
Evaluation of swallowing, laryngeal movement (observation, palpation, endoscopy); endoscopy to assess laryngeal function. Dysphagia often present.
Cranial Nerve X name, function, and assessment.
Vagus
Sensory and motor function to pharynx and larynx
Evaluation of swallowing, laryngeal movement (observation, palpation, endoscopy); endoscopy to assess laryngeal function. Dysphagia often present.
Cranial Nerve XI name, function, and assessment
Accessory
Motor function to cervical muscles
Muscle atrophy; not routinely assessed
Cranial Nerve XII name, function, and assessment
Hypoglossal
Motor function to tongue
Tongue strength, symmetry; tongue replacement response
Define paresis.
Decreased strength in the limbs.
Define ataxia.
Unconscious, general proprioceptive deficit causing poor coordination when moving the limbs and body
Define spasticity.
Stiff or spastic movement of the limbs with little flexion of the joints, increased extensor tone
Define dysmetria.
Abnormality in rate, range, or force of a movement; may seem both hypometric and hypermetric
Describe signs of paresis.
Dragging of toes
Knuckling at the fetlock
May be more easily observed when walking on hills
Describe signs of ataxia.
Swaying or weaving of the body or limb
Abducted or addicted foot placement
Crossing of the limbs
Stepping on a foot
Describe signs of spasticity.
Short-strided, stiff gait
Tin soldier appearance
Describe signs of dysmetria.
High stepping gait with limited movement of distal joints
Paresis lesion Iocations
- Can be UMN or LMN but generally have more severe muscle atrophy with LMN
- Peripheral nerves
- Musculoskeletal
Ataxia lesion locations
- General proprioceptive sensory pathways (spinal cord white matter)
- Vestibular
- Cerebellar
- Peripheral disease
Dysmetria lesion locations
- Cerebellum
- Spinocerebellar tracts
Clinical evidence for lesion in the brain, cranial to the foramen magnum
Abnormal behavior, seizures, abnormal mental status, aimless wandering or circling, head pressing, sleep alterations, central blindness
Clinical evidence for a brain stem lesion
Cranial nerve deficits, weakness, ataxia, altered mental status (obtunded, stuporous, comatose)
Clinical evidence for a cerebellar lesion
Intention tremors, hypermetria of limbs, ataxia, possible menace deficits
Clinical evidence of cervical (C1-C7) lesion
Gait and proprioceptive deficits in all four limbs with no sign of brain, brain stem, or cranial nerve deficits; generally UMN deficits of thoracic and pelvic limbs; often pelvic limbs show more severe deficits than thoracic limbs
Clinical evidence of C6-T2 lesion
LMN signs (weakness, paresis, decreased to absent muscle tone and reflexes) to thoracic limbs with UMN of pelvic limbs
Clinical evidence for lesion of the thoracolumbar spine (T2-L3)
Gait deficits confined to the pelvic limbs with normal thoracic limbs
Clinical evidence for lesion in L4-S1 region
Normal thoracic limbs with LMN signs to pelvic limbs
Clinical evidence for lesion at the sacral and coccygeal spine
Normal thoracic limbs; pelvic limbs normal or LMN; cauda equina signs including deficits in perineal sensation, poor tone, poor anal tone
Clinical evidence for peripheral nerve lesion
Neurogenic atrophy, loss of sensation in affected areas, weakness, loss of muscle tone
Clinical evidence for multifocal/disseminated disease
Signs of lesions in more than one neuroanatomical location
Clinical evidence for lesion of the sympathetic nervous system
Horner’s syndrome: miosis, ptosis, prolapsed third eyelid, enophthalmos, unilateral sweating
Normal mentation
Normal cranial nerves
Normal sacral nerve segments
Ataxia, proprioceptive deficits in all limbs
Lesion localization:
Cervical spinal cord
Treatment for head trauma
Osmotic diuretics for edema - Mannitol, hypertonic saline
Anti-inflammatories, analgesics - NSAIDs
Anti-convulsants if indicated - diazepam
Supportive care
Advanced critical care
Corticosteroids controversial
Three-week-old Arabian colt
Normal parturition
Physically normal since birth
Normal baseline physical exam
Excellent farm management
Acute onset of “falling over”
Possible DFDX:
Juvenile idiopathic epilepsy
- seizures stop between 1-2 years
- excellent long-term prognosis
Seizures can be difficult to distinguish from: (5)
- syncope due to heart disease
- electrolyte disorders, muscle fasciculations
- muscle diseases (e.g. HYPP)
- anaphylaxis
- sleep deprivation
What are the most common causes of seizures in horses?
Intracarotid injection
Hepatoencephalopathy
Trauma
Infectious diseases - viruses
Toxins
Neonates are most susceptible to what conditions that can cause seizures?
Hypoxia-ischemic damage
Metabolic derangement
Inherited/congenital abnormalities
Treatment for seizures
Treat underlying disease
Anti-convulsants
- acute: diazepam
- maintenance: phenobarbital
Other anti-convulsants: potassium bromide, phenytoin, primidone
Neuro non-infectious DFDX
- Trauma
- Seizure disorders
- Leukoencephalomalacia
- Nigropallidalencephalomalacia
- Sleep disorders
- Neoplasia, mass lesion
- EDM
Neuro infectious DFDX
- Encephalitis viruses (Eastern, Venezuelan)
- West Nile virus
- Rabies
- EPM
- Migrating parasites
- Meningitis (primarily foals)
- Other viruses
Twelve-year-old warmblood mare
- Kicked by another horse, laceration, swelling, pain
- Flunixin meglumin and enroflaxin administered IV
- Immediate seizure episode
- Unresponsive, recumbent
- HR 20-24 beats/min
- RR 4-6 breaths/min
- No PLR
- Hypothermic
Possible DFDX:
Intracarotid injection
Jugular vein and common carotid artery are right next to each other at the distal portion of the neck. The further up the neck you go, the thicker the omohyoideus muscle becomes, separating the two vessels.
- Cortical blindness may improve with time
- Self-trauma during seizure activity
- Brain trauma
What causes equine leukoencephalomalacia?
“Moldy corn disease”
Corn contaminated with Fusarium moniliforme while growing; toxin fumonisin B1 produced
What are the clinical signs of equine leukoencephalomalacia?
Acute onset (3-4 weeks post ingestion)
Anorexia, depression, ataxia, circling, blindness, head pressing
Recumbency, seizures, death in 2-3 days
Ante-mortem diagnosis of equine leukoencephalomalacia
Clinical signs, history
Fumonisin in feed
CSF - xanthochromia, increased protein, pleocytosis
Postmortem diagnosis of equine leukoencephalomalacia
Necropsy - focal liquefactive necrosis; sometimes hepatic involvement
Treatment of equine leukoencephalomalacia
Symptomatic, supportive
Check other horses
Remove from feed as soon as suspected
Etiologic agent for nigropallidal encephalomalacia
Yellow star thistle (Centaurea soltitialis)
Russian knapweed (Acroptilon repens)
Ingestion of large amounts over weeks to months
Premortem diagnosis of nigropallidal encephalomalacia
Clinical signs and confirmed access to plants
Clinical signs of nigropallidal encephalomalacia
Sudden onset
Retracted lips, continuous chewing movements
Aimless walking, circling, ataxic, tetra-acetic
Impaired eating and drinking
Unable to chew and propel food to larynx
Usually able to swallow
Treatment of nigropallidal encephalomalacia
No treatment
No recovery
Factors limiting recumbent sleep / contributing to sleep deprivation
Pain associated with recumbency
Don’t feel safe: environmental, social-behavioral factors
