II - Neuro Flashcards by Jessica Hanaumi

Cranial Nerve I name, function, and assessment

Olfactory
Smell
Response to odor without visual cues - hidden treats!

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Cranial Nerve II name, function, and assessment

Optic
Vision
Menace response, pupillary light reflex, obstacle course, dazzle reflex, ophthalmic cam including retinal evaluation

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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

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Cranial Nerve IV name, function, and assessment

Trochlear

Motor function to dorsal oblique (extra-ocular) muscle.

Eye position; lesion causes dorsomedial strabismus.

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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.

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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

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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

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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.

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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.

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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.

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Cranial Nerve XI name, function, and assessment

Accessory

Motor function to cervical muscles

Muscle atrophy; not routinely assessed

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Cranial Nerve XII name, function, and assessment

Hypoglossal

Motor function to tongue

Tongue strength, symmetry; tongue replacement response

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Define paresis.

Decreased strength in the limbs.

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Define ataxia.

Unconscious, general proprioceptive deficit causing poor coordination when moving the limbs and body

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Define spasticity.

Stiff or spastic movement of the limbs with little flexion of the joints, increased extensor tone

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Define dysmetria.

Abnormality in rate, range, or force of a movement; may seem both hypometric and hypermetric

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Describe signs of paresis.

Dragging of toes
Knuckling at the fetlock
May be more easily observed when walking on hills

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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

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Describe signs of spasticity.

Short-strided, stiff gait
Tin soldier appearance

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Describe signs of dysmetria.

High stepping gait with limited movement of distal joints

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Paresis lesion Iocations

Can be UMN or LMN but generally have more severe muscle atrophy with LMN
Peripheral nerves
Musculoskeletal

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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