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VTS ECC 2024 > Neuro/Ophtho > Flashcards

Neuro/Ophtho Flashcards

1
Q

Neurotransmitters

A

nervous system’s chemical messengers and produced only by neurons
– travel only very short distances, across spaces between nerve cells called synapses.

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2
Q

Nervous System structure

A

central nervous system (CNS) = brain and spinal cord
peripheral nervous system (PNS) = cordlike nerves that link the CNS with the rest of the body

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3
Q

Functions of the Nervous system

x3

A

(1) sensory functions
(2) integrating functions
(3) motor functions

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4
Q

Neurons

A

– can be divided roughly into the central cell body, also called the soma or perikaryon
– very high requirement for O2
– extensions) from the cell body, called dendrites and axons

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5
Q

Neuroglia or Glial cells

A

– structurally and functionally support and protect the neurons
– not directly involved in the transmission of information or impulses through the nervous system

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6
Q

Dendrites

A

– receive stimuli, or impulses, from other neurons and conduct this stimulation to the cell body. They can be referred to as afferent processes, because they conduct impulses toward the cell body
– sensory receptors that receive, or sense, stimuli such as heat, cold, touch etc

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7
Q

Axon

A

– conduct nerve impulses away from the cell body toward another neuron or an effector cell (a cell that does something when stimulated, such as a muscle or gland cell)
– axons are sometimes referred to by another name, nerve fibers
– Axons are often covered by a sheath of a fatty substance called myelin that appears white
– AKA white matter
– Myelinated axons conduct nerve impulses faster than unmyelinated axons

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8
Q

Myelin sheath

x3 structures

A

– made of the cell membranes of specialized glial cells called oligodendrocytes in the brain and spinal cord and Schwann cells in the nerves outside of the brain and spinal cord.
– myelin sheath and nodes of Ranvier work together to enhance the speed of conduction of nerve impulses along the axon

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9
Q

Cranial vs peripheral nerves

A

– Cranial nerves are those few nerves of the PNS that originate directly from the brain.
– Most PNS nerves are spinal nerves that emerge from the spinal cord.

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10
Q

Afferent nerve fibers

A

conduct nerve impulses toward the CNS
– usually called sensory nerve fibers

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11
Q

Efferent nerve fibers

A

conduct nerve impulses away from the CNS out toward muscles and other organs
– cause skeletal muscle contraction and movement, efferent nerve fibers are usually called motor nerve fibers.

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12
Q

Somatic nervous system

A

voluntary initiation of efferent impulses
– Impulses being sent to the CNS from receptors in the muscles, skin, eyes, or ears would be classified as somatic sensory functions, because they are consciously perceived by the brain.

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13
Q

Autonomic nervous system

A

the self-regulating system
– autonomic motor nerves send impulses to smooth muscle, cardiac muscle, and glands to regulate a wide variety of automatic body functions.
– Autonomic sensory nerves receive the afferent sensory impulses from sensory receptors that are used automatically to regulate these body functions
– sympathetic nervous system and the parasympathetic nervous system

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14
Q

Somatic afferent fibers

A

responsible for sensing pain, temperature, and pressure.

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15
Q

Somatic efferent fibers

A

are responsible for motor function and terminate at the neuromuscular junction of skeletal muscle.

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16
Q

Autonomic afferent fibers

A

are involved in the sensations of smell and taste as well as identification of distension or ischemia within the tissue of organs.

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17
Q

Autonomic efferent fibers

A

help to innervate cardiac muscle, muscles of the pharynx and larynx, and play many other roles throughout the body.

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18
Q

Neuron: Resting state

A

even when the neuron is resting, it is still working to maintain its resting state.
– cell membranes of neurons are electrically polarized at rest, like tiny charged batteries.
— Specialized molecules located in the neuron’s cell membrane pump sodium ions (Na+) from the inside of the neuron to the outside and pump potassium ions (K+) from the outside to the inside.
— called the sodium–potassium pump

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19
Q

Sodium diffusion

A

(Na+) cannot readily diffuse or leak through the cell membrane on its own. the action of the Na+/K+ pump causes a higher concentration of sodium to accumulate outside the cell.
– action of Na+/K+ pump and the negative charges inside the cell cause a higher concentration of potassium to accumulate inside the cell.
— By keeping the Na+ on one side of the membrane (outside) and K+ on the other (inside), the cellular membrane separating the two is said to be polarized (because it has two distinct poles of ions on either side of the membrane).

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20
Q

Resting membrane potential

A

– This electrical difference in charges across the membrane
– distribution of positive and negative charges from sodium, potassium, proteins, and other charged ions on either side of the neuronal membrane creates a difference in electrical charge across the membrane, with the inside of the neuron being more negatively charged than the outside.

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21
Q

Depolarization

A

– impulse from an adjoining neuron or from a specific type of external stimulus (e.g.,heat, touch, or taste) stimulates a neuron, a set of specific steps occurs, resulting in the nerve “firing” or depolarizing.
– At the point where the stimulus occurs on the neuron, a specialized molecular structure on the neuron cell membrane called a Na+ channel opens
– Na+ channel allows only Na+ ions to pass through it.
– Because a higher concentration of Na+ ions exists outside the cell than inside the cell, the sodium ions readily flow through the open sodium channels from the outside to the inside by passive diffusion
– positive Na+ ions are attracted into the cell by the net negative charge inside the cell

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22
Q

Action potential

A

If we hooked an electric meter to the neuron, we would see the inside of the neuron go from a negatively charged resting membrane potential to a net positive charge during depolarization.
– shift inside the cell from negative to positive makes sense when we consider the positive sodium ions flooding into the neuron.
– the significant change in electric charge from negative to positive is also referred to as an action potential.

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23
Q

Repolarization

A

Within a fraction of a second after sodium begins to flood into the cell during depolarization, the sodium channels snap shut, halting the influx.
Almost simultaneously, specialized potassium channels open in the cellular membrane Analogous to the sodium channels, the potassium channels allow only potassium ions to pass through them
– outflow of potassium ions continues until these specialized potassium channels snap shut a split second after they have opened
– Because the potassium ions (K+) are positive, the exodus of potassium ions from the neuron causes the charge inside the cell to swing back in the negative direction
– change of the cell’s charge back toward the net negative resting membrane potential is called repolarization

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24
Q

Threshold and Threshold stimulus

A

– stimulus is strong enough to cause complete depolarization, it is said to have reached the threshold, and this causes the cell to depolarize or “fire.”
– A stimulus of sufficient intensity to generate a nerve impulse is called a threshold stimulus.

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25
Q

Refractory Period

A

– a very brief period during and after a neuron has generated a nerve impulse, it cannot generate another impulse. This is called the neuron’s refractory period
– absolute vs relative

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26
Q

Synapse

A

junction between two neurons or a neuron and a target cell

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27
Q

Synaptic transmission

A

perpetuation of the nerve impulse from one neuron to the next cell

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28
Q

presynaptic neuron

A

The neuron bringing the nerve impulse to the synapse and releasing the chemical to stimulate the next cell

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29
Q

postsynaptic neuron

A

the neuron that contains the receptors that receive the neurotransmitter

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30
Q

Excitatory neurotransmitters

A

– excitatory effect on the postsynaptic membrane when they combine with their specific receptors
– cause an influx of sodium so that the postsynaptic membrane moves toward threshold.
– If the postsynaptic membrane is stimulated sufficiently by enough excitatory neurotransmitters, threshold will be reached and depolarization of the postsynaptic membrane will occur, beginning a new nerve impulse.

ex: Acetylcholines

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31
Q

Inhibitory neurotransmitters

A

tend to hyperpolarize the postsynaptic membrane, making the inside of the cell more negative instead of positive and moving the charge within the postsynaptic cell farther away from threshold.
– negatively charged (Cl − ) ions to enter the postsynaptic cell and allows (K+) ions to leave the cell
– makes it more difficult for the postsynaptic membrane to begin a new impulse

Ex: Gamma-aminobutyric acid (GABA) and glycine

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32
Q

Acetylcholine

Can be either this or that?

A

– It can be either an excitatory or inhibitory neurotransmitter depending on its location in the body
– At the junction between somatic motor neurons and the muscles they supply, acetylcholine is an excitatory neurotransmitter that stimulates muscle fibers to contract
– at the site where parasympathetic nerves synapse with the heart, acetylcholine has an inhibitory effect that slows the heart rate

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33
Q

Excitatory Neurotransmitters : Catecholamines

A

– Norepinephrine is associated with arousal and fight-or-flight reactions of the sympathetic nervous system
– Epinephrine is released from adrenal medulla (center of the adrenal gland) and plays more of a role as a hormone in the fight-or-flight reactions of the SANS
– Dopamine is found in the brain, where it is involved with autonomic functions and muscle control

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34
Q

Inhibitory neurotransmitters

A

GABA is found in the brain
glycine is found in the spinal cord
– tranquilizers, diazepam (Valium), work by increasing the GABA effect on the brain, thus inhibiting activity in the brain and producing tranquilization (reduced anxiety) with sedation (drowsiness).

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35
Q

Gray matter

A

contains most of the neuron cell bodies and grossly appears a dark brownish-gray. It is usually thought of as the “thinking” part of the CNS

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36
Q

White matter

A

contains most of the myelinated nerve fibers and appears white because of all the myelin. It is the “wiring” that connects the various components of the brain.

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37
Q

4

Sections of the Brain

A
  1. cerebrum,
  2. cerebellum,
  3. diencephalon
  4. brainstem
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38
Q

Cerebrum

A

–largest part of the brain
– made up of gray matter in the cerebral cortex (the outermost superficial layer of the brain)
– white matter beneath the cortex, including the corpus callosum (a set of fibers that connects the two halves of the cerebral cortex)
– responsible for functions associated with higher-order behaviors, such as learning, reasoning, and intelligence
– receives and interprets sensory information, initiates conscious (voluntary) nerve impulses to skeletal muscles

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39
Q

Longitudinal fissure

A

most prominent groove in the cerebrum is the longitudinal fissure, which divides the cerebrum into right and left cerebral hemispheres

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40
Q

Cerebellum

A

– located just caudal to the cerebrum, is the second largest component of the brain, wrinkled with grey and white matter
– allows the body to have coordinated movement, balance, posture, and complex reflexes
– also uses this same sensory feedback from the muscles to maintain posture and balance

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41
Q

Cerebellar Hypoplasia in Kittens

what causes this?

A

– born with an underdeveloped cerebellum
– One known cause of CH in kittens is infection of the dam with feline panleukopenia virus during pregnancy

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42
Q

Diencephalon

A

– serves as a nervous system passageway between the primitive brainstem and the cerebrum
1. thalamus acts as a relay station for regulating sensory inputs to the cerebrum.
2. hypothalamus is an interface between the nervous system and the endocrine system.
3. pituitary is the endocrine “master gland” that regulates production and release of hormones throughout the body

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43
Q

Brainstem

A

the connection between the rest of the brain and the spinal cord.
– most primitive part of the brain and is composed of the medulla oblongata, the pons, and the midbrain
– heavily involved in autonomic control functions related to the heart, respiration (including coughing, sneezing, and hiccupping), blood vessel diameter (vasomotor control), swallowing, and vomiting

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44
Q

Meninges

A

set of connective tissue layers that surround the brain and spinal cord
– fibrous dura mater, the delicate, spiderweb-like arachnoid, and the very thin pia mater, which lies directly on the surface of the brain and spinal cord
– contain a rich network of blood vessels that supply nutrients and oxygen to the superficial tissues of the brain and spinal cord

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45
Q

Cerebrospinal Fluid

A

brain and spinal cord are bathed and protected from the hard inner surfaces of the skull and spinal column by a fluid
–CSF’s chemical composition may be involved in the regulation of certain autonomic functions, such as respiration and vomiting
– Ex: pH of the CSF becomes more acidic, the respiratory center in the brainstem will increase the respiratory rate.

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46
Q

CSF Tap

A

– Since CSF circulates throughout the CNS, infection, inflammation, or cancer in the brain or spinal cord can cause changes in the amount of protein contained in the CSF; they can also cause changes in the composition of the CSF cells, including white blood cells or cancer cells.
– certain nervous system diseases or cancers by doing a CSF tap and examining it for particular types of cells or for specific changes in composition.

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47
Q

Blood–Brain Barrier

A

functional barrier separating the capillaries in the brain from the nervous tissue itself
– tightly constructed capillary wall and the additional glial cell membranes result in a cellular barrier that prevents many drugs, proteins, ions, and other molecules from readily passing from the blood into the brain
– protects the brain from many poisons circulating in the bloodstream.

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48
Q

Cranial Nerves

A

set of 12 nerve pairs in the peripheral nervous system that originate directly from the brain.
–identified as I through XII (1 through 12)
– contains axons of motor neurons, axons of sensory neurons, or combinations of both.

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49
Q

Cranial Nerves I - IV

A

I Olfactory; Sensory; Smell
II Optic; Sensory; Vision
III Oculomotor; Motor; Eye movement, pupil size, focusing lens
IV Trochlear; Motor; Eye movement

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50
Q

Cranial Nerves V - VIII

A

V Trigeminal; Both sensory and motor; Sensations from the head and teeth, chewing
VI Abducent; Motor; Eye movement
VII Facial; Both sensory and motor; Face and scalp movement, salivation, tears, taste
VIII Vestibulocochlear; Sensory; Balance, hearing

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51
Q

Cranial Nerves IX - XII

Name; Type; function

A

IX Glossopharyngeal; Both sensory and motor; Tongue movement, swallowing, salivation, taste
X Vagus (wanderer); Both sensory and motor; Sensory from gastrointestinal tract and respiratory tree; motor to the larynx, pharynx, parasympathetic; motor to the abdominal and thoracic organs
XI Accessory; Motor; Head movement, accessory motor with vagus
XII Hypoglossal; Motor; Tongue movement

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52
Q

Spinal Cord

A

caudal continuation of the brainstem outside the skull that continues down the bony spinal canal formed by the vertebrae.
– conducts sensory information and motor instructions between the brain and the periphery of the body
– contains many neuron cell bodies (in the gray matter) and extensive synapses (connections) between ascending nerve fibers conducting sensory information toward the brain and descending nerve fibers conducting motor information to muscles and other organs

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53
Q

divisions of the spinal cord

A
  1. cervical region (C1–C5)
  2. cervical intumescence region (C6–T2)
  3. thoracolumbar region (T3–L3)
  4. lumbar intumescence region with the cauda equina region (L3–cauda equina)
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54
Q

Spinal cord anatomy

A

– surrounded by meninges which support and protect it
– most superficial to most deep → dura mater, arachnoid mater, and pia mater.
– spinal cord is segmental in that it has paired spinal nerves that enter and leave at each intervertebral space
– Afferent fibers enter the cord via the dorsal root while efferent fibers leave at the ventral motor root

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55
Q

Myasthenia gravis

A

MG is an immune-mediated disease characterized by antibody inactivation of the neuromuscular end plate, often manifesting as muscle weakness.
– can occur as a focal or generalized disease and can lead to life-threatening complications, such as respiratory depression and aspiration pneumonia secondary to megaesophagus.

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56
Q

Optho

Exophthalmos

A

– Orbital fractures, retrobulbar space‐occupying lesions (e.g. neoplasia, abscess, zygomatic mucocele), traumatic proptosis

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57
Q

Ophtho

Enophthalmos

A

Horner’s syndrome, loss of retrobulbar fat, orbital fracture, temporal muscle atrophy

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58
Q

Ophtho

Small globe

A

Globe rupture, microphthalmos

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59
Q

Ophtho

Enlarged globe

A

Glaucoma, neoplasia

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60
Q

Ophtho

Anterior chamber: Turbidity

A

Lipid‐laden aqueous, uveitis (hypopyon, hyphema)

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61
Q

Ophtho

Hyphema

A

– Chronic glaucoma, congenital, hypertension, neoplasia, retinal detachment, trauma, uveitis

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62
Q

Optho

Dialated pupils

A

– Coloboma, dysautonomia, glaucoma, iris atrophy, oculomotor nerve lesion, optic nerve lesion, retinopathy, drugs, anxiety, pain

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63
Q

Optho

Constricted pupils

A

– Uveitis, Horner’s syndrome, drugs

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64
Q

Ophtho Anatomy

The Globe

A

– composed of three layers
1. fibrous tunic
2. nervous tunic
3. vascular tunic (uvea)

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65
Q

Ophtho

fibrous tunic

A

– includes the sclera, cornea, limbus, and area cribosa

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66
Q

Ophtho

nervous tunic

A

– photoreceptor layers and the fundus, which can be viewed with an ophthalmoscope

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67
Q

Ophtho

vascular tunic (uvea)

A

– composed of the choroid, ciliary body, and iris.

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68
Q

Ophtho

Which cranial nerves control movement of the globe?

A

– The third, fourth, and sixth cranial nerves, along with the extraocular muscles, control movement of the globe within the orbit, allowing nearly 240° of vision in the dog and cat versus the 200° degrees of human vision

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69
Q

Ophtho

Ciliary Body

A

caudal portion of the iris in which aqueous humor is produced by the ciliary epithelium

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70
Q

Ophtho

What is the fluid called that is produced in the Ciliary Body

A

– Passive ultrafiltration and active secretion of carbonic anhydrase within the ciliary epithelium produce a fluid known as the aqueous humor
– helps to distend the eye and is directly affected by mean arterial pressure.

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71
Q

What influences IOP

A

– inflammation, or lack thereof, in the anterior uvea
– obstruction of this outflow tract through the trabecular meshwork will increase IOP

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72
Q

The Iris and pupil

A

– Iris lies within the pupil
– divides the anterior and posterior portions of the eye
– keeps aqueous‐filled anterior portion separated from the posterior (between lens and iris) portions
– controls size of pupil allowing more or less light
– Contriction controlled by PANS
– Dilation controlled by SANS

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73
Q

Ophtho

Choroid

A

– most posterior portion of the vascular tunic (uvea) is the choroid

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74
Q

Ophtho

Lens

A

– fixed and anchored by zonules, small fibers connecting to the ciliary body
– lens luxation, the lens can become detached from the zonules and move either forward or backward in the eye

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75
Q

Ophtho

Retina

A

– photoreceptor of the eye
– onnect to bipolar cells which then connect to ganglion cells within the inner plexiform
– Axons of the ganglion form the nerve fiber layer joining to the optic nerve

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76
Q

Cornea

3 layers

A

– is collagenous, clear, smooth, and avascular, and is the most anterior portion of the fibrous tunic and eye
– has three layers, consisting of surface epithelium, collagenous stroma, and Descemet’s membrane

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77
Q

Ophtho

descemetocele

A

– Descemet’s membrane is relatively elastic, resisting damage in trauma
– If a laceration or wound reaches this membrane and is full thickness is it considered a descemetocele

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78
Q

Ophtho

Schirmer tear test

A

– measure the adequacy of tear production
– Inadequacy of tear production is suggestive of chronic keratoconjunctivitis sicca or a temporary cause of decreased tear production such as concurrent drug therapy

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79
Q

Ophtho

Tonometry

A

– measure intraocular pressure
– Pressures below 10 mmHg are often seen with uveitis
– Pressures greater than 25 mmHg are consistent with glaucoma

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80
Q

Ophtho

Hyphema

A

– blood collecting in the anterior chamber of the globe
– causes include coagulopathy, hypertension, trauma, and neoplasia
– can lead to glaucoma due to fibrin collection not allowing drainage of aqueous humor.

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81
Q

Ophtho

Anterior Uveitis

A

– inflammation of the iris and ciliary body
can be acute or chronic
– more advanced cases may result in the eye appearing cloudy or red due to inflammatory cells accumulating within the anterior chamber
– IOP will be low (opposite of glaucoma)
– can be caused by a variety of systemic dz’s

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82
Q

Ophtho

anterior flare

A

– used when the anterior chamber looks hazy (e.g. like a snow globe) when a bright light is shone into the eye

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83
Q

Ocular causes of uveitis

A
  1. trauma
  2. lens lux
  3. neoplasia
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84
Q

Fungal causes of uveitis

A
  1. Blasto
  2. Crypto
  3. Coccidio
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85
Q

Rickettsial causes of uveitis

A
  1. Rickettsia rickettsii
  2. Ehrlichiosis
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86
Q

Bacterial causes of uveitis

x4

A
  1. Sepsis
  2. Brucellosis
  3. Lepto
  4. Lyme dz
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87
Q

Viral causes of Uveitis

A
  1. Feline: feline infectious peritonitis, feline leukemia virus, feline immudodeficiency virus, herpesvirus, rabies
  2. Canine: adenovirus, distemper, rabies
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88
Q

Acute Glaucoma

A

– defined as an IOP greater than 25 mmHg in one or both eyes with associated clinical signs
– can be congenital or acquired

English and American cocker spaniels, Siberian husky, toy poodles, and basset hounds

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89
Q

Acquired causes of glaucoma

A

related to disease processes such as neoplasia, trauma, foreign bodies, anterior lens luxation, cataracts, severe uveitis, iris bombé, preiridial fibrovascular membrane, large number of iridial cysts, or high cellular debris

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90
Q

Glaucoma treatment

A

– inhibiting the enzyme carbonic anhydrase

dorzolomide 2% and brinzolamide 1%

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91
Q

Sudden acquired retinal degeneration syndrome (SARDS)

A

– leading causes of currently incurable canine vision loss
– acute onset of blindness due to loss of photoreceptor function, extinguished electroretinogram with an initially normal‐appearing ocular fundus, and mydriatic pupils which are slowly responsive to bright white light, unresponsive to red light, but responsive to blue light.
– Both neuroendocrine and autoimmune mechanisms

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92
Q

Progressive retinal atrophy

A

– congenital inherited photoreceptor dysplasia seen in many dogs
– early‐onset form called retinal dysplasia vs late‐onset form detected in adult dogs

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93
Q

Retinal Detachment

A

– often caused by systemic hypertension
– hypertensive crisis, agents such as nitroprusside, hydralazine, and clevidipine may be selected to rapidly lower arterial blood pressure

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94
Q

Cerebral metabolic oxygen consumption (CMRO2)

A

– high degree of oxygen delivery to meet brain’s metabolic demands
– accomplished by maintaining a consistent cerebral blood flow (CBF)
– can be reduced (e.g. propofol administration) or increased (e.g. ketamine administration) through many modalities

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95
Q

cerebral autoregulation

A

– maintains balance in cerebral blood flow
– MAP between 60 and 160 mmHg= blood flow to the brain remains constant

96
Q

What does CBF depend on?

A

dependent on cerebral perfusion pressure (CPP) and cerebral vascular resistance (CVR).

CBF = CPP/CVR

97
Q

contents of the intracranial space (everything within the skull)

x4

A

– four distinct compartments:
1. blood,
1. cerebrospinal fluid,
1. intracellular fluid,
1. extracellular fluid

98
Q

Physiology of Intracranial Pressure

A

– If the contents or volume of one compartment in intracranial space increases, then the contents or volume of the other compartments must decrease.

99
Q

Elastance

A

– relationship between intracranial volume and intracranial pressure
– Ex: If CBF increases, then cerebral blood volume increases and there will also be an accompanying increase in ICP
– in healthy patients, changes to intracranial volume have minimal effect on ICP

100
Q

Effect of hyperventilation on ICP

A

– hyperventilation to cause cerebral vasoconstriction, thereby reducing CBF and ICP

101
Q

Neurolocalization

A

– concept of identifying which part of the neurological system is dysfunctioning
– lesions are often classified as being central within the brain itself, within a specific section of the spinal cord, or within the motor unit consisting of lower motor neurons, the neuromuscular junction, and the skeletal muscle fibers (e.g. myasthenia gravis)

102
Q

upper motor neuron signs

A

– disease occurring between C1 and C5
– front and hindlimbs

103
Q

lesions between C6 and T2

A

– lower motor neuron signs to the front limbs but upper motor neuron deficits to the hindlimbs.

104
Q

Disease between T3 and L3 will show

A

– normal thoracic limbs with upper motor neuron deficits to the rear limbs

105
Q

Disease of the L4–S3 region of the spine will show

A

no deficits to the thoracic limbs but lower motor neuron deficits to the pelvic limbs.

106
Q

Traumatic brain injury (TBI): Primary brain injury

A

direct tissue and vasculature injury from trauma.
– Damage to the tissue can be in the form of contusions, lacerations, or axonal damage.
– vasculature can be affected, causing hemorrhage, edema, and a decrease in perfusion to the brain.
– brain contusion occur directly under site of impact and direct opposite (coup/couter coup) lesion) from brain displacement

107
Q

Traumatic brain injury (TBI): secondary brain injury,

A

occurs when biochemical pathways, set off by direct tissue primary brain injury, hypoxia, and decreased perfusion, act together to perpetuate further brain damage.
– inflammatory mediators and excitatory neurotransmitters, and changes in cellular membrane permeability
– ultimatel result in neuronal cell death
– Secondary brain injury further contributes to increased ICP.

can occur hours to days later

108
Q

What occurs immediately after brain injury?

A

– massive release of excitatory neurotransmitters that causes influx of sodium and calcium into neurons, resulting in depolarization and further release of excitatory neurotransmitters.
– Increased influx of calcium overwhelms mechanisms for removal, causing severe intracellular damage and ultimately neuronal cell death

109
Q

production of reactive oxygen species after TBI

x4 mechanisms

A

– hypoperfusion and local tissue acidosis favors ROS production
– Hemorrhage provides a source of iron for hydroxyl radicals.
– Catecholamines may also contribute to the production of free radicals by direct and indirect mechanisms.
– Because the brain provides a lipid-rich environment, it is particularly susceptible to oxidative injury

110
Q

production of inflammatory mediators after TBI

x3

A

nitric oxide production,
triggering influx of inflammatory cells,
activating the arachidonic acid and coagulation cascades, and disrupting the blood–brain barrier.

111
Q

What can cause neuronal damage?

x6

A
  1. adenosine triphosphate (ATP) depletion,
  2. intracellular sodium and calcium accumulation,
  3. elevated excitatory neurotransmitters,
  4. oxygen free radical production,
  5. unregulated inflammatory mediators,
  6. lactic acidosis.
112
Q

Pulmonary gas changes: elevated PaCO2 levels (hypercarbia) effect on ICP

A

cause vasodilation, leading to increased ICP

113
Q

Pulmonary gas changes: decreased PaCO2 levels (hypocarbia) effect on ICP

A

can result in vasoconstriction of the brain’s vasculature and decreases to ICP

114
Q

Cushing’s reflex

A

– elevated ICP or intracranial hypertension
–in the face of elevated ICP, the body attempts to raise MAP in an effort to maintain CPP.
– reflex baroreceptor‐mediated bradycardia then occurs

115
Q

Cerebrovascular Accident

A

– “stroke”
– an alteration of blood supply within the brain
– ischemic (obstructive) and hemorrhagic (rupture) forms

116
Q

ischemic CVA

A

consequence of an arterial or venous obstruction secondary to a thromboembolism or occlusion of the blood vessels from abnormalities such as neoplasia or vasculitis
– produces necrosis of neurons and glial elements, results in a focal area of dead tissue called an infarct.

117
Q

Diseases associated with ischemic CVA infarction

A

hypothyroidism,
idiopathic hyperlipoproteinemia (schnauzers), protein‐losing enteropathy and nephropathy, hyperadrenocorticism,
diabetes mellitus,
sepsis,
neoplasia,
heartworm infections.

118
Q

hemorrhagic CVA

A

– result of the rupture of blood vessels within or around the brain.
– classified as epidural, subdural, subarachnoid, intraparenchymal, and intraventricular
– presence of a hematoma initiates edema and neuronal damage in surrounding parenchyma

119
Q

Seizure definition

A

– sudden alteration of behavior due to a temporary change in the electrical functioning of the brain, in particular the outside rim of the brain called the cortex
– most commonly thought of as being tonic‐clonic; body is unconscious and undergoes spastic muscle contraction
– intracranial vs extracranial causes

120
Q

Reactive seizure:

A

normal brain’s natural response to a transient disturbance in function, usually metabolic or toxic in nature. This is usually reversible when the inciting cause is removed or corrected

Ex: hypoglycemia

121
Q

Epileptic seizure:

A

manifestation of excessive synchronous epileptic activity of neurons in the brain.
Epilepsy is recurrent seizures of at least two unprovoked epileptic seizures (of any type) in a 24-hour period, resulting from a disease in the brain causing a predisposition to generate epileptic seizures.

122
Q

Cluster seizures

A

two or more seizures within a 24-hour period.

123
Q

Status epilepticus

A

“continuous seizures, or two or more discrete seizures between which there is incomplete recovery of consciousness, lasting at least 5 minutes.”

124
Q

Idiopathic epilepsy:

A

– no underlying cause can be found, with no evidence of a physical cause
– underlying cause of the epilepsy may be genetically determined,

125
Q

Structural epilepsy:

A

– caused by underlying physical intracranial disorder

126
Q

Focal seizures

A

originate from a focus in one cerebral hemisphere and usually manifest localized or regional clinical signs, which may include involuntary or compulsive actions such as chewing, licking, and defensive or aggressive behavior.

127
Q

Generalized seizures

A

– most common type is the tonic-clonic seizure.
– tonic, clonic, or myoclonic seizures

128
Q

tonic phase

A

increased muscle tone results in limb and head extension, causing the animal to fall to the side.

129
Q

clonic phase

A

alternating extension and flexion of the limbs, and exaggerated chewing movements may occur. The animal usually urinates, defecates, and salivates.

130
Q

epileptic seizure arises from

A

hypersynchronous neuronal electrical activity in the cerebral cortex.

131
Q

What contributes to Status Epilepticus

A

– excess of excitatory neurotransmitters such as glutamate, aspartate, or acetylcholine, or antagonists of γ-aminobutyric acid (GABA) (an inhibitory neurotransmitter)

132
Q

Extracranial Sz causes

A

metabolic disorders (i.e. hypoglycemia, hypocalcemia, and hypoxia), toxicities and environmental disturbances (i.e. lead, organophosphates, metronidazole, ethylene glycol, heat prostration, and snake envenomation), and nutritional disorders (late‐stage thiamine deficiency in cats)

133
Q

Intracranial Sz causes

x7

A

– neoplasia, idiopathic epilepsy, congenital, infectious, immune mediated, traumatic, and vascular disorders.

134
Q

Consquences of prolonged sz activity

A

– cerebral edema and disseminated intravascular coagulation (DIC) are two of the most serious sequelae to unrelenting seizures

135
Q

Benzos

A

– Diazepam is lipid soluble and enters the brain rapidly when given intravenously, intranasally (IN), or per rectum (PR). Midazolam is water soluble.
– Benzodiazepines bind to the GABA receptors and enhance neuronal hyperpolarization, reducing neuronal firing. Short acting.

136
Q

Barbiturates

A

– potentiate the action of GABA by interfering with sodium and potassium transmission in the neuronal membrane.
– maintenance anticonvulsant

137
Q

Levetiracetam (Keppra)

A

– binding of the synaptic vesicular protein (SV2A), which inhibits neurotransmitter release
– inhibition of voltage gated calcium channels

138
Q

second‐line anticonvulsants

A

levetiracetam, phenobarbital

139
Q

third‐line drugs for refractory sz

x4

A

– ketamine, lidocaine, thiopental, propofol

140
Q

Propofol’s use for sz

A

Propofol has been shown to control the muscular manifestations of the brain’s seizure activity
– but does little to affect the electrical activity within the brain
– also decreases ICP and brain metabolic activity
– anticonvulsant effect of propofol is likely because of its GABA agonist activity.

141
Q

Intervertebral Disk Disease

A

– function of the disk is to act as a cushion and absorb shock along the spinal column
– disk itself is composed of an outer fibrous material, known as the annulus fibrosus, and a jelly‐like inner material called the nucleus pulposus
– If annulus fibrosus ruptures, the nucleus pulposus takes the path of least resistance and moves dorsally to impinge on the spinal cord.

142
Q

evaluating spinal cord function

x3

A

– Criteria used to evaluate cord function include:
1. conscious proprioception → patient’s capacity to recognize the location of the limbs in relation to the rest of the body.
2. voluntary motor function → conscious purposeful movement of the limbs.
3. pain sensation → When pain is absent, the lesion is more severe and carries a poorer prognosis.

143
Q

Prognosis for IVDD

A

– varies depending on the patient’s neurological status
– patients that have absent deep pain sensation for less than 24‐48 hours, many surgeons give a 50:50 prognosis for return of neurological function
– In severe cases, even following surgery, ascending myelomalacia can occur, resulting in ascending spinal cord death that is ultimately fatal

144
Q

Fibrocartilagenous emboli (FCE)

A

acute neurological disease that occurs when a piece of fibrocartilage intervertebral disk material suddenly breaks off and enters the spinal artery or vein, causing a local infarction and obstruction of blood flow.
– infarction results in necrosis in the spinal cord region affected
– CS: acute, usually non‐painful, and often follow exercise with some mild trauma

145
Q

Tx for FCE

A

– therapy for FCE is centered around providing pain control and supportive care.
– There is no surgical procedure to repair the infarcted portion of the spinal cord and healing of the area will take time
– PE beneficial

146
Q

Electrocution

Neurogenic edema

A

– form of non‐cardiogenic pulmonary edema
– damage to the central nervous system (CNS), causes a massive sympathetic outflow from the CNS results in vasoconstriction and subsequent hypertension
– leads to an increase in left ventricular afterload, which will result in a decreased stroke volume of the left ventricle
– pulmonary edema can arise from an increase in pulmonary capillary pressure, due to blood backing up into pulmonary circulation

147
Q

CNS injury from electrocution

A

– arises from direct stimulation from electrical energy as opposed to electroporation, but the latter may still play a part in CNS hypoxia.
– altered mental status, muscle tremors, seizure activity, or paresis

148
Q

Autonomic Nervous system response to Hypothermia

A

– sympathetic nervous system’s activity increases to conserve metabolic function.
– Heart rate, cardiac output, and mean arterial pressure increase.
– as temperature decreases, responsiveness to catecholamines results in a blunted and eventually decreased sympathetic response.
– Vasodilation, CNS depression, decreased cardiac output, hypotension, and respiratory depression may result.

149
Q

CNS effects of hypothermia

A

– some hypothermia may be neuroprotective
– however cerebral blood flow reduces significantly for every 1 °C drop in temperature.

150
Q

Tetanus

A

– Clostridium tetani is a gram‐positive, anaerobic, spore‐forming bacillus
– spores are introduced into deep, penetrating wounds

151
Q

Neurologic effects of Tetanus

A

– organisms produce two exotoxins: tetanospasmin and tetanolysin
– Tetanospasmin marked effects on the gray matter of the brainstem and spinal cord
– Neurological deficits result because of alteration to inhibitory pathways within the central nervous system leading to unopposed excitatory action and excess acetylcholine
– may also lead to autonomic instability and respiratory failure

152
Q

Tetanus tx

A

– Antibiotic therapy with anaerobic spectrum
– infected wound explored and debrided
– Tetanus antitoxin
– Muscle relaxants

153
Q

Vestibular Disease

A

– vestibular system includes the parts of the inner ear and brain that process the sensory information involved with controlling balance and eye movements
– Dz categorized as either peripheral or central in origin
– classified into three major disease processes: idiopathic vestibular disease, inner ear disease, or central vestibular disease

154
Q

General vestibular dysfunction rules:

A
  • Head tilt, rolling, circling, leaning, falling: toward the lesion
  • Nystagmus: spontaneous, unchanging (nonpositional), horizontal/rotary, fast phase away from the lesion
  • Strabismus: positional, ventrolateral, ipsilateral to the lesion
  • Generalized ataxia
  • CN VII facial nerve: possible
155
Q

Peripheral vestibular disease

A

– problem is associated with the receptor organ in the inner ear or the vestibular nerve
– Peripheral vestibular disease obeys all the dysfunction rules (central does not)

156
Q

Central vestibular disease

A

disease in the part of the brain that controls balance (brainstem, vestibular nuclei, or cerebellum).
– central vestibular disease may obey the rules but also can break them (e.g., head tilt away from the lesion)

157
Q

Central vestibular disease: localize lesion based on nonvestibular deficits

A
  • Mentation changes (involvement of brainstem reticular activating system
  • Cranial nerves other than CN VII affected (ipsilateral to lesion)
  • Cerebellar signs (ipsilateral to lesion)
  • Proprioceptive placing deficits/paresis (ipsilateral
158
Q

Central: involving vestibular nuclei in brainstem, flocculonocular lobe of cerebellum, or caudal cerebellar peduncle (connection between vestibular nuclei and cerebellum)

A
  • Neoplasia (primary, metastatic)
  • Infectious (OMI with extension, infectious encephalitis)
  • Inflammatory/immune-mediated: granulomatous meningoencephalomyelitis, necrotizing meningoencephalitis, meningoencephalitis of unknown origin
  • Trauma
  • Toxic: metronidazole toxicity
  • Vascular: hemorrhage, infarct; vascular event may be secondary to underlying metabolic disease
159
Q

Clinical signs of vestibular disease

x3

A

head tilt (towards the side of the brain affected)
circling,
nystagmus (fast phase away from the side of the lesion)
strabismus, ataxia,
falling to one side (towards the side of the lesion)
and nausea from motion sickness.

160
Q

idiopathic vestibular disease

A

–sudden and dramatic clinical signs
– generally have a horizontal nystagmus and no other cranial nerve deficits or alterations in level of consciousness
– will resolve spontaneously over time

161
Q

inner ear vestibular disease

A

– usually slower in evolution and therefore cause less severe clinical signs
– varying degrees of facial nerve dysfunction and often Horner’s syndrome
– Inner ear infections are the most common cause

162
Q

central vestibular disease

A

– identified by observing changes to levels of consciousness, additional cranial nerve deficits, proprioceptive deficits, and motor deficits
– Vertical nystagmus also suggests a central lesion
– indication of brainstem damage affecting the vestibular nuclei and sensor and motor pathways which course through the vestibular region of the brainstem

163
Q

Common inflammatory and infectious causes for central vestibular diseases in dogs

A

canine distemper virus, granulomatous meningoencephalitis, toxoplasmosis, neosporidiosis, aspergillosis, cryptococcosis, steroid‐responsive meningoencephalitis, Lyme disease, Rocky Mountain spotted fever, and ehrlichiosis.

164
Q

Common inflammatory and infectious causes for central vestibular diseases in cats

x3

A

– Feline leukemia virus, feline infectious peritonitis, and cryptococcosis are the most common infectious diseases in the cat

165
Q

Normal Mentation evaluation

A

– Normal mentation requires a normal cerebrum (conscious reactions/interpretation of environment, personality) and a normal brainstem (contains the reticular activating system, which projects to activate cerebrum)

166
Q

Mentation abnormalities

A

– abnormal mentation implies either cerebrum or brainstem dysfunction;
– cranial nerve deficits are present with brain stem dysfunction
– if there are no cranial nerver deficits, abnormal mentation likely result from lesion in the cerebrum or thalamus

167
Q

Decerebellate posture

A

– secondary to an acute cerebellar lesion.
– Many times, pelvic limbs are flexed, but could be extended, depending on the somatotopic localization of the lesion.
– exhibit opisthotonus
– still has awareness

168
Q

Decerebrate posture

A

– secondary to a severe midbrain lesion, with extensor rigidity of all four limbs and a patient that is comatose.
– exhibit opisthotonus
– minor awareness

169
Q

Signs of cerebral/thalamic (forebrain) disease

A

Mentation/behavior changes
* Circling, compulsive movement (towards side of lesion, or both sides if diffuse disease)
* Seizures
* Central (cortical) blindness (contralateral to lesion or bilateral if diffuse disease)
* Head-pressing
* Placing deficits (contralateral to lesion, or all limbs if diffuse disease), with minimal gait abnormalities or paresis

170
Q

Signs of brainstem (midbrain-medulla) disease

A

Cranial nerve deficits III–XII (ipsilateral to lesion)
* Mentation changes (RAS: reticular activating system)
* Placing deficits, paresis (UMN signs ipsilateral to lesion), paresis usually moderate/severe
* Respiratory abnormalities
* Decerebrate posture: severe midbrain lesion, comatose

171
Q

Signs of cerebellar disease

A
  • Generalized ataxia
  • Dysmetria, hypermetria (ipsilateral to lesion)
  • Intention tremors
  • Truncal sway/ataxia
  • True vestibular signs (head tilt, nystagmus, etc.)
  • Normal mentation if no other structures involved
  • Decerebellate posture
172
Q
A
173
Q

Troubleshooting gait: thoracic and pelvic limbs affected

A

– lesion can involve the brain, C1–5 or C6–T2 spinal cord or generalized neuromuscular disease

174
Q

Troubleshooting gait: just pelvic limbs are affected

A

– lesion is caudal to T2 (T3–S2 spinal cord)

175
Q

Paresis vs. Weakness

A

– weakness implies pathology involving the motor unit in the lower motor neuron (LMN) cell body in the spinal cord, peripheral nerve axon and/or myelin, neuromuscular junction, or muscle
– paresis describes decreased voluntary movement, from either the upper motor neuron (UMN) or LMN lesion.

176
Q

Cranial nerves: Menace response

A

response because it involves recognition and processing in the cerebral cortex vs. reflexes that do not.

Afferent: ipsilateral CN II, contralateral thalamus and occipital cortex
Efferent: contralateral motor cortex, ipsilateral cerebellum, ipsilateral CN VII

177
Q

Cranial nerves: Pupillary light reflexes (PLRs)

where is the response? what CN?

A

midbrain

Afferent: CN II
Efferent: CN III parasympathetic

178
Q

Cranial nerves: Trigeminofacial reflexes

where is the response? CN?

A

(palpebral, vibrissae, lip pinch): PONS

Afferent: CN V
Efferent: CN VII

179
Q

Cranial nerves: Corneal reflex

Where is the response? What CN?

A

PONS

Afferent: CN Vophthalmic branch
Efferent: CN VI (globe retraction), CN VII (blink)

180
Q

Cranial nerves: Physiologic nystagmus

where is the response? CN?

A

pons, midbrain

Afferent: CN VIII
Efferent: CN III, IV, VI

181
Q

Cranial nerves: Gag reflex

where is the response? CN?

A

medulla

Afferent: CN IX, X
Efferent: CN IX, X, XII

182
Q

Thoracic limb reflexes

A
  • Biceps: musculocutaneous nerve
  • Triceps: radial nerve (main weightbearing)
  • Flexion/withdrawal: mostly musculocutaneous nerve
183
Q

Pelvic limb reflexes

A
  • Patellar: femoral nerve (L4–L6 spinal cord segments) (main weightbearing)
  • Gastrocnemius: sciatic nerve (L6–S1)
  • Perineal: pudendal nerve (S1–S3)
  • Flexion/withdrawal: mostly sciatic with some femoral for hip flexion
184
Q

Cutaneous trunci muscle reflex

A
  • Afferent: T3–L3 spinal nerves/cord
  • Efferent: C8–T1 spinal nerves forming lateral thoracic nerve
185
Q

UMN system originates in

A

cerebrum and brainstem

186
Q

UMN Signs

A
  • Normal to increased reflexes
  • Normal to increased tone
  • Disuse atrophy (weeks/months)
  • Paresis/paralysis
  • Proprioceptive placing deficits
187
Q

LMN

A

in the brainstem (cranial nerves) and spinal cord to effect voluntary movement

188
Q

LMN Signs

A
  • Decreased to absent reflexes
  • Decreased to absent tone
  • Denervation atrophy (days/weeks)
  • Paresis/paralysis
  • Proprioceptive placing deficits
189
Q

C1–C5 myelopathy:

A

ipsilateral UMN signs to thoracic and pelvic limbs

190
Q

C6–T2 myelopathy:

A

ipsilateral LMN signs to thoracic limbs, UMN signs to pelvic limbs

191
Q

T3–L3 myelopathy:

A

normal thoracic limbs, ipsilateral UMN signs to pelvic limbs

192
Q

L4-caudal myelopathy:

A

normal thoracic limbs, ipsilateral LMN signs to pelvic limbs

193
Q

Spinal shock

A

– the transient loss of muscle tone and segmental reflexes caudal to an acute spinal cord injury.
– results from physiologic dysfunction of the LMN versus a true structural injury to the LMNs.
– appreciated on clinical examination by noting LMN signs (decreased/absent reflexes) in a patient with an otherwise UMN spinal cord localization.
– excessive inhibitory neurotransmitters secondary to the injury have a prominent role in the pathophysiology.

194
Q

Spinal shock vs. Myelomalacia

A

– LMN signs to the pelvic limbs are highly concerning for descending myelomalacia, with a grave to poor prognosis for any return to function.
–Spinal shock reflex deficits are often partial (i.e., absent flexion/withdrawal but present tendon reflexes) and may be asymmetric, while loss of reflexes with myelomalacia tends to be complete in both limbs.
–** myelomalacia will not have deep pain perception**
– spinal shock may also not have deep pain perception, depending on the severity of the lesion, but will have improvement of reflexes and tone to be more consistent with an UMN lesion, even if the spinal cord is functionally transected.

195
Q

Primary neuromuscular disease patients in ICU:

x4

A

polyradiculoneuritis, botulism, myasthenia gravis, Numerous metabolic diseases

196
Q

Determining brain death

A

– no standards to determine brain death in veterinary medicine,
– In humans; coma, absence of brainstem reflexes, and apnea listed as mandatory clinical findings
– functional assessment of the cerebrum (electroencephalogram [EEG]) and brainstem (brainstem auditory evoked response [BAER])

197
Q

BAER test

A

– hearing test, BAER evaluates brainstem function and may provide additional diagnostic support for severe brainstem injury.

198
Q

Diseases With Frequent Secondary Neurological Dysfunction

x9

A
  • Hepatic encephalopathy
  • Uremic encephalopathy
  • Heat stroke
  • Hypoxia/hypoxemia
  • Hypertension
  • Electrolyte disorders
  • Hypoglycemia
  • SIRS/MODS, sepsis
  • Endocrine dysfunction
199
Q

Intracranial hypertension (ICH)

A

– persistent elevation of intracranial pressure above the normal range of 5–12 mm Hg.

200
Q

Common Causes of Intracranial Hypertension

A

Traumatic brain injury
Intracranial mass
Inflammatory encephalopathy
Infectious, non-infectious
Status epilepticus
Obstructive hydrocephalus

201
Q

ICP: Pressure-volume curve

A

– Initially Compliance is high and compensatory mechanisms are functioning well, primarily due to expansion of the dura mater in the cranial and cervical spinal space, allowing for added volume with no or little increase in ICP.
– As volume is added to the system, displacement of CSF and blood allow for further volume additions with progressive changes in ICP.
– WIth higher pressure, low compliance situation that occurs when the volume buffering capacity is exhausted,
– Further displacement of intracranial fluids is not possible, and the addition of more volume causes an exponential rise in ICP = decompensation

202
Q

homeostatic mechanisms to maintain ICP: Volume buffering

A

– increase in one component must compensate with another
– occurs initially through displacement of CSF extracranially.
– As ICP increases and CSF displacement is exhausted, blood volume (flow) becomes compromised
– lack of blood to the brain = ischemia and neuronal damage, thus promoting further increase in volume and ICP
– process is depicted by the pressure-volume curve

203
Q

homeostatic mechanisms to maintain ICP: Pressure autoregulation

A

– Cerebral perfusion is largely maintained via arteriolar (myogenic) reflexes that alter vascular resistance in response to changes in transmural pressure
– mechanism normally functions at perfusion pressures between 50 and 150 mm Hg, preventing hypo- and hyper- perfusion of the brain

204
Q

homeostatic mechanisms to maintain ICP: Chemical autoregulation

A

– Chemical constituents of the brain’s environment function to control blood flow in the brain by altering cerebral vascular resistance, and by effect, ICP

205
Q

homeostatic responses with ICP: PaCO2

A

– cerebral vascular resistance or diameter is directly responsive to changes in global and local PaCO2 concentrations
– CO2 in water forms H2CO3 and subsequently dissociates to H+ and HCO3-, an increase in [H+] stimulates cerebral vasodilation, whereas a decrease in [H+] will lead to cerebral vascular constriction.

206
Q

homeostatic responses with ICP: PaO2

A

– affects cerebral vascular resistance
– Decreases in PaO2 lead to vasodilation, increased CBF, increased CBV, and elevated ICP.

207
Q

homeostatic resposnses with ICP: Cerebral metabolic rate of oxygen of oxygen utilization

A

– pH alterations in perivascular environment, in regions of high cerebral metabolic activity, will have a direct influence on cerebral vascular tone
– Increased H+ concentration, as seen with lactic acidosis or other acids formed in the course of cerebral metabolism, will cause an increase in CBF
– situations of decreased CMRO2, low levels of H+ concentration will result in decreased CBF locally due to arteriolar constriction

208
Q

homeostatic resposnses with ICP: Cushing response

A

– ICP causing global ischemia, a physiological nervous system response, the Cushing response results in a triad of clinical signs: systemic hypertension, bradycardia, and irregular respirations
– MAP must overcome the pressure (ICP) present in the brain to maintain adequate tissue perfusion
– systemic hypertension results from sympathetic activation, and this can lead to bradycardia subsequent to a baroreceptor response

209
Q

Irregular respiratory patterns observed in the Cushing triad result from;

A

brainstem compression secondary to an increased in ICP

210
Q

Cushing triad represents

A

late stage of ICH and, in conjunction with a markedly reduced mental state, signifies impending brain herniation and death.

211
Q

most commonly reported electrolyte abnormalities following traumatic brain injury (TBI)

A

– hypo- or hypernatremia and hypokalemia
– result of a combination of intravenous fluid therapy, administration of hyperosmotic agent or diuretics, blood loss, and intracranial pathology

212
Q

mechanisms responsible for consciousness are located

A

rostral brainstem, the ascending reticular activation system, and diffusely throughout the cerebrum.

213
Q

Ocular and cranial nerve reflexes assess:

A

brainstem function
– MGCS assesses brainstem reflexes using pupillary light reflexes (PLR), oculocephalic reflexes, and pupil size to allow for easy, subjective scoring

214
Q

Assessing brainstem reflexes: Size and reactivity of pupils

A

– midbrain and efferent parasympathetic fibers of the third cranial nerve are responsible for pupillary constriction
– w/ absence of ophthalmic injury, abnormalities in pupil size or reactivity indicate brainstem dysfunction and/or oculomotor nerve injury

215
Q

Assessing brainstem reflexes: Mydriasis

A

usually denotes a lesion (ipsilateral or bilateral) of the midbrain or the third cranial nerve.

216
Q

Assessing brainstem reflexes: Miosis

A

occur ipsilateral to severe brainstem injury or as part of Horner syndrome (ptosis, enophthalmus, third eyelid protrusion) indicating a lesion along the sympathetic pathway.

217
Q

Assessing brainstem reflexes: Severe bilateral miosis

A

sign of acute, extensive brain disturbance and probably occurs due to functional disturbance of higher centers, with release of oculomotor efferent from their inhibition.

218
Q

Assessing brainstem reflexes: Severe unresponsive bilateral mydriasis

A

indicates a grave prognosis and often accompanies brain herniation. The return of pupils to normal size and response to light is a favorable prognostic sign.

219
Q

Assessing brainstem reflexes: Resting eye position

A

– presence of spontaneous nystagmus should be noted.
– Eye abduction is caused by paresis of the medial rectus muscle due to CN III damage
– Adduction of the globe is caused by lateral rectus muscle paresis due to injury of CN VI or damage to the rostral medulla oblongata or pons.

220
Q

Assessing brainstem reflexes: Oculocephalic reflexes

A

– elicited by moving the head from side to side or vertically
– convenient method for the examination of the functional integrity of a large segment of brainstem segmental pathways and the cranial nerves involved in eye movements.

221
Q

Assessing brainstem reflexes: Corneal reflexes

A

– findings may corroborate eye movement abnormalities
– Touching the cornea with a cotton tip should cause globe retraction and bilateral eyelid closure. The corneal reflex may be absent when the afferent fifth cranial nerve, the efferent sixth and/or seventh cranial nerve, or their reflex connections within the pons and medulla oblongata are damaged

222
Q

When ICP measuring not possible, what is the target MAP?

A

When it is not possible to monitor ICP, mean arterial blood pressure should be maintained at or above 80 mm Hg.

223
Q

ICH Tx: Control PaCO2

A

Controlled ventilation, used judiciously, can lower ICH by vasoconstriction and reduced CBF.
– Normal ventilation, with a target range of PaCO2 of 35–45 mm Hg, in mild to moderate TBI is recommended
– However, in severe cases of head injury, hyperventilation with a target PaCO2 of 30–35 mm Hg is still recommended as a temporary measure

224
Q

ICH Tx: Hyperosmolar fluid therapy

A

– mainstay of all current treatment protocols for acute brain injury
– create an osmotic gradient that moves water out of the interstitium and into the circulating blood volume, resulting in overall reduction of ICP and promoting CBF
– An osmotic increase of at least 10 mOsm is thought to be required for this effect to be seen
-

225
Q

Hypertonic Saline vs Mannitol

A

– sodium does not freely cross the blood–brain barrier, hypertonic saline has similar rheologic and osmotic effects to mannitol.
- Mannitol may also possess free radical scavenging properties.
- Because sodium is redistributed within the body and reabsorbed in the kidneys, hypotension is a less likely sequela than with mannitol, making it a better choice for patients with increased ICP and systemic hypotension.

226
Q

ICH Tx: Corticosteriods

A

– is not routinely recommended
– vasogenic edema associated with primary inflammatory diseases, tumor-associated edema and acute ischemia are valid indications for considering the use of corticosteroids to treat ICH

227
Q

Tetanus is the result of a bacterial infection

A

by Clostridium tetani
– Gram-positive, nonencapsulated, anaerobic, spore-forming bacterium

228
Q

Where is Clostridium tetani found?

A

– toxin is produced during vegetative growth of the organism in a suitable environment
- natural habitat in moist, fertile soil
- spores are resistant to boiling water and an autoclave temperature of 120°C for up to 20 minutes.

229
Q

How are cats and dogs resistant to tetanus?

A

– due in part to the inability of the toxin to penetrate and bind to nervous tissue.
– young large breed dogs typically affected
– very rare in cats

230
Q

How is tetanus infection acquired?

A

– develop after contamination of skin wounds with the spores, but infection can follow teething, parturition, or ovariohysterectomy

231
Q

tetanus bacillus secretes two exotoxins:

A

tetanospasmin and tetanolysin.

232
Q

tetanospasmin

A

– leads to the clinical syndrome of tetanus after binding to the membranes of the local motor nerve terminals.
– toxin is internalized and transported intraaxonally and in a retrograde fashion, first in motor and later in sensory and autonomic nerves, potentially spreading to the brainstem in a bilateral fashion up the spinal cord.
– neurotranmitter release is prevented by toxins
– predominantly affects inhibitory interneurons, inhibiting release of glycine and γ-aminobutyric acid (GABA)
– motor neurons are the first affected and lose control

233
Q

Tetanus affect on ANS

A

– Disinhibited autonomic discharge leads to disturbances in autonomic control, with sympathetic overactivity and excessive plasma catecholamine levels
– Neuronal binding of the toxin is thought to be irreversible.
– Recovery requires the growth of new nerve terminals, which explains the long duration of tetanus

234
Q

Tetanolysin

A

capable of locally damaging otherwise viable tissue surrounding the infected area and optimizing the conditions for bacterial multiplication.

235
Q

How long can it take for Tetanus CS to be seen?

A

– within 5 to 12 days
– but can take up to 4 weeks

236
Q
A

VTS ECC 2024 (17 decks)

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