Neuro - muscular Flashcards

Question

Describe the reciprocal sympathetic and parasympathetic innervation of the bladder

Answer 1

The external urinary sphincter is under voluntary control in adults The micturition reflex is controlled by the autonomic nervous system. When the bladder is filling, sympathetic from L1, L2, L3 predominates. This produces relaxation of the dextrusor by beta2 and constriction of the internal urethral sphincter via alpha1 (external by trained voluntary action). When the bladder is full, this is sensed by baroreceptors in the bladder, which communicate via afferent nerves to the spinal cord and brain. Micturition reflex is then triggered by the midbrain which upregulates parasympathetic control. Parasympathetic causes the dextrusor to contract (via M receptors) and relaxation of internal sphincter (this is just downregulation of alpha 1 as sympathetic tone is gone). Voluntary relaxation is needed by the external urethral sphincter to open

Answer 2

two mucles control pupil size; - pupillary dilator -> pupillary dialator (also known as radial) muscle -> sympatheric -> alpha1 receptors - Pupillary costrictor -> sphincter muscle -> parasympahteric -> muscarinic Activtion of sympathetic tone, thus alpha 1 receptor, causes constriction of the pupillary dilator muscle, which dilates the pupil. Parasympathetic tone on the other hand, thus activation of muscarinic receptors, will cause contricion of the pupillary costrictor which contsticts the pupil

Answer 3

bright light, hits the retina, this activates parasympathetic nerve fibers in the Edinger-Westphal nucleous -> contriction of the pupillary constrictor muscle. Concurrently the ciliary muscle contracts, causing the lens to round up, increasing reflective power

Answer 4

A1 -> STIMULATION of Pkc ->IP3 -> increased intracel Ca A2 -> INHIBITION of Ac decreasing cAMP ß1-> STIMULATION of Ac increasing cAMP ß2 ->STIMULATION of Ac increasing cAMP Nicotinic -> Openin Na and K channels -> depolarization Muscarinic; - All effector organs PNS -> M1, M3, M5 -> STIMULATION of IP3 -> increase Ca - Sweat gland and SNS -> INHIBITION of Ac and decrease cAMP

Answer 5

Vascualr smooth muscle skin, skeletal muscle, splachnic region, sphincters of the GIT and bladder, radial iris muscle ACTIVATION -> CONSTRICTION of ALL of these Transmembrane GPCR bound -> Gq detaches αq -> PKC -> IP3-> Ica

Answer 6

Inhibitory receptors, located both pre and post synaptically. Found on preganglionic and postganglionic (autoreceptors) adrenergic nerve terminals and in the GIT. Gi -> α1-> inhibit Ac -> decrease cAMP

Answer 7

these are α2 postganglionic receptors. Norepinepherine is released by the postganglionic nerve ending and feeds back on its self via α2 reducing the release of further norepinepherine These help conserve norepinepherine in periods of high sympathetic tone

Answer 8

The adrenal medulla. this means that adrenal glands can become depleted of norepinepherine during intense stress (hence you crash). Additionally, may help explain some pulsatile effects of phao where they run out of nora and then symptoms abate

Answer 9

Heart - ventricular myocardium, SA node and ?AV node. Small amount in atrial myocardium -> increase Hr, and contractility Kidney - promote renin secretion Salivary glands -> increase enzymatic component Adipose tissue -> increase lipolysis β1-> Gs -> αs-> PKA ->incease cAMP

Answer 10

α1; vascular smooth muscle, skin, renlan, splachnic, GIT, sphinters, bladder, radial muscle, iris -> increase Ca entry α2; GIT, presynaptic adrenergic neurons -> inhibition of cAMP β1; Heart, salivary glands, adipose tissue, kidney -> stimulation of cAMP β2; vascular smooth muscle of skeletal muscle, GIT wall, bladde wall, bronchioles -> stimualtion of cAMP (with epi, not nora) β3; brown and white adipose tissue -> increase lipolis and thermogenesis

Answer 11

Vascular smooth muscle -> relaxation skeletal muscle -> contraction Heart -> increase HR and ionotropy

Answer 12

α1; nore and epi have the same effect with epi being slightly more potent (α1 are relatively insensitive to catecholamines though - with high concentrations needed for a response) β1; norepinepherine and epinepherine are equipotent, but much lower doses are needed to activate these β2; preferentially activated by epinepherine, so, as epinepherine is released from the adrenal medulla we expect a larger response while sympathetic nerve endings have little effect

Answer 13

This is an antagonist of Nictinic Nn receptor, which on the glial neuron but not endpalte. Because of this, it will inhibit BOTH the nicotinic receptors on the sympathetic and parasympathetic neurons. To predict, the actions of ganglionic blocking drugs you need to know what the preferential control is, sympathetic or parasympathetic. -> E.g. Vascular smooth muscle has only sympathetic innervation thus we get relaxation -> salivary gland; has both parasympathetic and sympathetic effect, you you will get less serous and less enzymatic secretion

Answer 14

Has two α, and one β, and one δ subunit which form a pore. When ACh binds, the conformation changes, and the pore opens allowing Na and K to enter raising the membrane potential up to 0mv which results in depolarisation.

Answer 15

Effector of the Parasympathetic nervous system in the bronchioles, GIT, bladdrr, male sex organ, heart Effecter of sympathetic nervous system of the seat glands

Answer 16

M1, M3 and M5 receptors have the same mechanism of action as α1. Ach -> Gq ->αq-> Pkc -> Ip3+DAG -> release of Ca from stores M4 -> Gi -> αi -> inhibit Ac-> reduce cAMP M2-> direct G-protiein function e.g. Sa node; ACh+ M2->Gi->αi->binds to K channel opening them slowing rate of depolarisation

Answer 17

Brain stem; - Medulla - Pons - Midbrain Diencephalon - thalamus - hypothalamus Cerebral hemispheres - white matter - basal ganglia - hippocampal formation - amygdala ## Footnote Spinal cord leads into brain stem, cerebellum is not associated with these and sits ontop of them, same with pituiitary

Answer 18

Ascending; spinal cord carries SENSORY information FROM the perifery TO the higher levels of the CNS Descending; Carries MOTOR information from the higher levels of the CNS to the motor nerves of the periphery

Answer 19

III= O = occlumotor IV= T= Trochlear V= T= Trigeminal VI= A= Abducens VII = F= facial VIII = V= vestibulocochlear IX= G= glossopharyngeal X= V= vagus XI = A = accessory XII = H = hypoglossal

Answer 20

Medulla; rostral extension of the spinal cord whichcontains autonomic centers that regulate breathing, blood pressure, as well as centers which coordinate coughing, swallowing and vomiting reflexes Pons; Rostral to the medulla, and with the medulla, participates in balance and mainanance of posture and helps regulate breathing Midbrain; rostroal to the pons and participates in the control of eye movement. It also contains relay nuclei of the auditory and visual systems

Answer 21

Medulla; rostral extension of the spinal cord whichcontains autonomic centers that regulate breathing, blood pressure, as well as centers which coordinate coughing, swallowing and vomiting reflexes

Answer 22

Pons; Rostral to the medulla, and with the medulla, participates in balance and mainanance of posture and helps regulate breathing

Answer 23

Midbrain; rostroal to the pons and participates in the control of eye movement. It also contains relay nuclei of the auditory and visual systems (eye movement too)

Answer 24

Thalamus; processes all sensory information GOING TO the celebral cortex and almost all motor information COMING FROM the cerebral cortex to the brain stem Hypothalamamus; Lies ventral to the thalamus and contains centers that regulate body temperature, food intake, water balance. It is also an endocrine gland that controls the hormone secretions of the pituitary. The hypothalamus secretes releasing hormones and release-inhibiting hormons into the hypophyseal portal blood that cause the release or inhibits the release of the anterior pituitary hormones.

Answer 25

Thalamus; processes all sensory information GOING TO the celebral cortex and almost all motor information COMING FROM the cerebral cortex to the brain stem

Answer 26

Hypothalamamus; Lies ventral to the thalamus and contains centers that regulate body temperature, food intake, water balance. It is also an endocrine gland that controls the hormone secretions of the pituitary. The hypothalamus secretes releasing hormones and release-inhibiting hormons into the hypophyseal portal blood that cause the release or inhibits the release of the anterior pituitary hormones.

Answer 27

C1->C5 for all limbs C6->T2 Forelegs T3->L3 Hindlegs L4-> caudal (usually lesion here will show anywhere between l4 and the tail) S1->S3 bladder/hindleg ## Footnote These are axons in the spinal cord which do not leave the spinal cord

Answer 28

C6->T2 for thoracic L4->caudal for hind limbs, urethral and anal sphinceters

Answer 29

1) enter and exit of neurons from the spnal cord are on the same side 2) The neurves injured in the spinal cord will be on the same side as the lesion 3) The nerve crosses in the midbrain and go to the controlateral side of the brain

Answer 30

They start brainstem at the medulla and pons level, bellow the decussation of the midbrain, so the lesions will be on the same side as the affected neurons

Answer 31

Only when you do not see any form of voluntary motor funciton (you do not see any flexin on the joins when they re walking around the room)

Answer 32

Dull is generally this is a disease outside of the brain that is causing an affect on the brain. Abnormal mentation; there is a ether a problem in the pro-encephalon or the caudal fossa Prosencephalon: Telencephalon + diencephalon

Answer 33

Define; Obtunded; decreased response to stimuli Stuporous; no response to non-painful stimuli Comatose; no reponse to any stimuli Demented; exagerated response to stimuli

Answer 34

Global hypoxic anaesthetic event or a prolonged arrest

Answer 35

Thsi is the region that contains the brainstem (ie midbrain, pons and medulla)

Answer 36

The reticular activating system (RAS) travels through these regions to keep the cerebrum awake. Lesions in the caudal fossa can lead to obtundation, stupor or coma

Answer 37

Ambulatory: able to get across the room independently (using all limbs) Non-ambulatory; unable to get accross the room using all limbs

Answer 38

Lameness; - muscoloskelateal - Nerve root signature Paressis - LMN paresis - UMN paresis Ataxia - General proprioceptive - Vestibular - Cerebellar

Answer 39

Both are decreased voluntary motor function - LMN -> Short, choppy steps; Crouched stance; look weak - UMN-> Long, lopey steps; exagerated; look stiff ## Footnote when describing a patient you then have to add mono (one limb), para (two limbs), hemi (two limbs on one side), tetra (all four limbs) - paresis

Answer 40

Anywhere from the cell body in the spinal cord, all the way down the axons that innervate the effector tissue. ## Footnote tick paralysis

Answer 41

Anywhere from the midbrain down to the axon in spine where they comunicate with the LMN ## Footnote disk

Answer 42

Their cell bodies are in the spinal cord and their axons travel town to the effect tissue via nerves. One exception being the craniam nerves, where the cell bodies are in the brain stem or brain and their axons navigate out within the cranial nerves

Answer 43

The cell bodies are in the brain and the axons travel down the spinal cord.

Answer 44

Generally UMN are inhibitory for LMN

Answer 45

Ataxia is the sensory parallel to paresis which is the motor dysfunction. You have; - General proprioceptive -> cross midline - knuckel - circumduct - Vestibular -> fall to one side - circle to one side (defined as circling but they are actually persistently falling to one side and catching themselves) - Cerebellar -> truncal sway - dysmetria - intention tremor

Answer 46

The patient can get across the room using all limbs but has hypermetria of the left limbs

Answer 47

Tilt -> eyes are not parallel to the floor -> vestibular localization Turn -> entire head facing one direction and eyes paralell to the floor -> procencephalon localisation

Answer 48

- vestibular or celebellar lesions - (arhed back) back pain - neck pain

Answer 49

Decerebrate rigidity; - Severe brainstem lesion -> cerebrum is disconnected from brainstem - > extensor rigidity x4, opisthotonus, coma Decerebellate rigidity; - Severe cerebellar lesion - > extensor rigidity EXCEPT may see flexion at hips, opisthotonus, normal mentation Schiff-Sherrington - Severe thoracolumber spinal cord injury - ASCENDING UMNs from PL to TL arre lost - Extensor rigidity in the thoracic limbs when in lateral recumbency

Answer 50

Spinal lesion at T3-L3 that damage AFFERENT UMN projections to their thoracic limbs, so they cannot coordinate their gaint. These will have extensor rigidity in the front legs when laying in lateral recumbency but a T3-L3 lesion.

Answer 51

LMN paresis -> neurogeny atrophy and decreased tone UMN paresis -> disuse atrophy and increased tone

Answer 52

These are tests of kinesthesia: does the animal know where its limbs are in space. These are SENSORY tests PAthway; 1 Sensory nerve -> spinal cord 2 Projection travels cranially through ipsilateral spinal cord, contines rostrally throguh ipsilateral medulla, pons, midbrain 3 Decussates in the midbrain 4 Travels through controlateral thalamus to controlateral prosencephalon

Answer 53

1) Peripheral sensory component 2) Ipsilateral spinal cord component 3) Peripheral LMN component A lesion anywhere in the reflex arch will lead to DECREASED reflexes. A spinal cord lesion cranial to the reflex arc CAN leato to INCREASED reflexes Testing reflex lets you evaluate; 1) spinal nerve functions 2) allows you to evaluate the function of the spinal cord segment

Answer 54

Withrawl fore; C6-T2, all TL nerves, flexors Patellar; L4-L6. femoral nv, extensor Withdral Hl; L6-S1, sciatic, flexors Cutaneous trunci; C8-T1, sensory spinal nerves and motor lateral thoracic nerves - mutaneous trunci muscle Perineal; S1-S3, pudental, ext anal sphincter

Answer 55

Sensory; ispilateral CN V (trigeminal) Brain region; Ipsilateral pons and medulla Motor; Ipsilateral VII (Facial nerve)

Answer 56

Reflexes -> test a reflex arc Responses -> involve the controlateral prosencephalon

Answer 57

Sensory; Ipsilateral CN II (optic) -> most fibers cross at the chiasm Brain region; CONTROLATERAL Procencephalon processes this information, and interacts with the IPSILATERAL facial nucleous in the medulla Motor; Ipsilateral CN VII (Facial)

Answer 58

Sensory; Ipsilateral CN V (trigeminal) Brain region; controlateral sensory cortex in proencepalon Motor; Ipsilateral CN 5

Answer 59

1) CN V dysfunction 2) controlateral prosencephalon dysfunction

Answer 60

Menace response -> responses involve controlateral procencephalon which reflex ars are local.

Answer 61

Ipsilateral. For our purpoises CN nerves enter the brain ipsilaterally and as they are reflexes they are local responses that do not invovle the procencephalon.

Answer 62

Procencephalon- CN I and II Midbrain - CN III and IV Pons - CN V Medulla - CN VI-> XII

Answer 63

1) if you have ONE cranial nerve affected -> prioritise localizing to the CN 2) If ultiple CN affected + other exam abnormalities-> prioritise central lesions affecting regions of brain associated with the cranial nerve Exception is when you have a problem with CN VII, CN VIII +/- horner -> middle/inner ear

Answer 64

Test in plegic animals only. Remeber, withdrawl reflex does not men pain. They need to have a CONSCIOUS response to pain

Answer 65

Paraplegia -> T3-L3 myelopathy Reflex is positive, so we know L7-S1 segment is intact. There is no deep pain, which means there is a block in the afferent sensory nerve comunication past the lesion point in the T3-L3 region

Answer 66

White = Axons Grey = Cell bodies Sensory = dorsal spinal cord ( white matter) Motor = ventral part spinal cord (white matter) Grey mattter in the ventral horn are cell bodies of LMN - C6-T2-> LMN to thoracic limbs - L4->caudsal contains LMN to pelvic limbs, tail and bladder

Answer 67

LMN - lesion implies a lesion affecting LMNs - Loss of LMN -> decreased LMN activity resulting in; 1) LMN paresis or plegia 2) DECREASED tone 3) DECREASED/ABSCENT reflexes UMN - Lesion implies a lesion affecting the UMNs - UMNs are generally inhibitory to the LMN they synapse with - so loosing UMN you loose the inhibition on LMN 1) UMN paresis or plegia 2) INCREASED tone 3) HYPER-reflexia/INCREASED reflexes

Answer 68

One) rule out muscoloskeletal cause. If you have ruled this out; Two) Three possible neuroanatomuc localizations; 1) Femoral/sciatic neuropathy - lesion outside of spinal cord - LMN coalesceess into the final common pathways of the femoral and scietic nerves -> femoral; LMN to peripheral limb EXTENSOR muscle -> Sciatic ; LMN to peripheral limb FLEXOR muscles You need to look at the autonomous zones (quite academic) - LMN paresis or plegia - Decreased tone (weak flexors so they throw legs forward, gain plantigrade stance so that they can stand etc) - Decreased/abscent reflexes - often good awareness of where the limbs are in space 2) L4->caudal myelopathy - Entrance/exit ramp for the peripheral limb nerves - Contains cell bodies for the pelvic limbs/sphincteres - Final common pathways to all the muscles -> femoral; LMN to peripheral limb EXTENSOR muscle -> Sciatic ; LMN to peripheral limb FLEXOR muscles - LMN paresis or plegia, decreased tone, - decreased abscent/reflexes so YOU know L4-L6 is affected 3) T3-L3 myelopathy

Answer 69

You will have the same defecits to the effector muscles if it in the CNS (MYELOpathy ) vs PNS (Neuropathy). However, give aways are; Neuropathy; - peripherl neuron so 1 reflex is affected - Usually unilateral, can be bilateral Myelopathy; - Bilateral and - Multriple reflex archs affected - Decreased anal tone - LMN incontinence

Answer 70

UMN to pelvic limbs and sphincters and synapse with LMN in th eL4 caudal region. UMN are INHIBITORY to LMN so; - loss of initiation leads to INCREASED LMN activation ; - UMN paresis or plegia -> stiff, long, lopy steps in pelvilimbs - increased tone - Normal to incrwased reflexes - crossing while walking -> genrral prorpioceptive ataxia which leads to decreased postural reactions (eg hemiwalking he will cross midline before catching hithemselves)

Answer 71

1) identify the issue is affecting all 4 limbs 2) Confirm there is nno intracranial diseases. To do so you want; - Normal mentation - No head tilt or head turn - Normal cranial nerve exam 3) if lameness is observed, rule out muscoloskeletal cause 4) Three possible neuroanatic locations - C1-C5 MYELOpathy - C6-T2 MYELOpathy - Diffuse neuromuscular

Answer 72

C1-C5 MYELOpathy - Contains UMN for both thoraxic and pelvic limbs - UMN synapse with LMN in the C6-T2 (thoracic) and L4 caudalregion (pelvic - UMN are inhibitory to LMN -> loss of function = increased LMN activation knucle/look stiff on all 4 limbs with normal reflexes C6-T2 MYELOpathy - entrance/exit ramp for thoraci LMN - Expressway for pelvic lumns UMN - short choppy steps in the front legs - General propriceptive ataxia in the hingdlegs with long stiff steps and are discodinated and all over the place with thse limbs Diffuse neuromuscular - PNS problem - nerve issues - Weak in all 4 limbs with decreased tone and abscent reflexes in all 4 - LMN paresis or plegia x4 - Floppy all over

Answer 73

Brachial plexus lesions or unilateral neurotoxin exposure.

Answer 74

NEUROpathy, there is no impact on the UMN fibers traveling to the ipsilateral hindlegs as this lesion is peripheral. No changes usually seen with the controlateral thoracic. So all other limbs are normal when the lesion is outside of the spinal cord. C6-T2 myelopathy, the lesion is in the CNS, so the ispilateral hind limb will be affected, and the controlateral thoracic limb can also be affected .

Answer 75

Dorsal paw -> radial nerve Medial antebrachium -> musculocutaneous nerve Caudal antebrachium -> ulnar nerve

Answer 76

Procencephalon

Answer 77

Lesions will always be ipsilateral; - Cranial nerve deficites III-> XII - *UMN hemiparesis - General proprioceptive ataxia - Postural reaction deficits *It is uncommon to see unilateral lesions due to the small size of thr canine brainstem. If you do have unilateral leasions, then the ipsilateral side of the lesion will be affected postural reaction and ataxia wise. Again, it is usually bilateral due to the small size of a dogs brain stem

Answer 78

- Reticular activating system - Ascending sensory projections - Descending motor projections - Nuclei for CN III-XII

Answer 79

Ipsilatoreal if lesion is small, or controlateral if larfe effects to CN III->XII - reduced eye movements - myadrasis - hyp/analgesia - facial paresis - abdnormal gag - Possibly vestibular dysfunction

Answer 80

If you have a unilateral lesion, you will see CONTROLATERAL deficits. This is a big area, so it is common to see unilaterla lesions They will have contorlateral postural reaction deficits Sensory information of the face will present as controlateral nasal hypalgesia visual information will present as a controlateral menace deficit In dogs and cats it is NOT involved in gaint generation. They will not have paresis or ataxia, but they may walk propulsevely TOWARD the affected side. As the procencephalon processes outside world information and is involved with consciousness and personality we may see; - Obtundation/dementia - controlateral postural reaction deficits - Controlateral menace deficit - Controlateral nasal hypalgesia - normal gaint, but circle towards the lesion - not necessarily just circuling, even when walking around, they will always turn to the side of the lesion, even if turning the otherway will be easier. Its like if the controlateral side does not exist

Answer 81

it is hypoalgesia -> experience LESS pain to a painful response

Answer 82

Right procencephalic lesion The controlateral menace and nasal sensation are affected, his gaint is normal, but he truns in the direction of the lesion. Mentation is normal (can be abnormal in procencephalic lesions)

Answer 83

The cerebellum is a DOWNER of the CNS - Fine tunes movements - inhibitor of the vestibular system and flexors Cerebella r pathways are caudal to the decussation of th midbrain so they are IPSIlateral. Receives a large amount of sensory projections Hallmark signs are; - Cerebellar ataxia; large compensatory steps (like if they are stopping a stumble) - Intention tremmor - Truncal sway (best seen when standing still) - Ipsilateral postural reaction deficits - +/- paradoxical vestimbular sings (in unilateral cerebellar dysfunction as the cerebellum inhibits the vestibular system) - occasionally ipsilateral menace defecit (because the menace response does include the cerebellul) - Posteral reactions are delayed and then exagerated (e.g. hemiwalking, they wont do anything initially and then suddenly make a large step)

Answer 84

Oftnen used interchangiably but this is incorrect, as postuaral reactions include cerebellar input while CP do not. Most of the time we mean postural reactions when we say CP

Answer 85

The ipsilateral side of the cerebellum. the menace pathway includes the cerebellum, and a defecit in this pathway in a patient with cerebellar disease has a lesion in the cerebellum affecting the menace, not a peripheral neuropathy or a brainstem lesion. If the menace was controlateral, then it could be due to a neuropathy/brain stem lesion as well

Answer 86

1) peripheral vestibular system (CN VIII an inner ear) 2) Central vestibular system (vestibular nuclei in rostral medulla) 3) Flocculonodular lobe of cerebellum which comunicatess with the brainstem by the caudal cerebellar peduncle

Answer 87

Maintain balance coordinate head and eye movements

Answer 88

1) Head tilt 2) Vestibular ataxia 3) Spontaneous or inducible nystagmus 4) Positional strabismus

Answer 89

Cerebellar ataxia results from damage to the cerebellum, which is responsible for coordinating movements, while vestibular ataxia is caused by a problem with the inner ear, which plays a role in balance and spatial orientation. Cerebellar ataxia often presents with dysmetria (inability to control the rate and range of movements) and hypermetria (exaggerated steps), while vestibular ataxia is characterized by head tilt, leaning, falling, and nystagmus

Answer 90

Strabismus is a condition where the eyes don't align properly, while nystagmus involves involuntary, rhythmic eye movements.

Answer 91

You confirm there is a vestibular lesion with the 4 hallmark sings 1) head tilt 2) Vestibular ataxia 3) Spontaneous or inducible nystagmus 4) positional strabismus These do not help localise though. You then have to use non vestibular sings to localise the lesion to one of the 3 leasions 1) peripheral vestibular system (CN VIII an inner ear) 2) Central vestibular system (vestibular nuclei in rostral medulla) 3) Flocculonodular lobe of cerebellum + caudal cerebellar peduncle If there are the following, then we have a central vestibular lesion (ie other stuff in the brainstem is affected); - decreased bentation - general proprioceptive ataxia - ispilateral postural reaction - UMN tetraparesis - Ipsilaterl CN defecits V-XII If you have the following, then you have a lesion affecting the ear/CN VIII? KEY -> NORMAL MENTATION, NORMAL POSTURAL REACTIONS (brainstem and midbrain are not affected) Others; - Hallmark signs of vestibular disease (nystagmus always horizontal/rotary) - Mayhave ipsilateral CN VII defecits - May see psilateral horners

Answer 92

Ie brain stem - where CNVIII comes into from the vestibular system - decreased bentation - general proprioceptive ataxia - ispilateral postural reaction - UMN tetraparesis - Ipsilaterl CN defecits V-XII

Answer 93

KEY -> NORMAL MENTATION, NORMAL POSTURAL REACTIONS (brainstem and midbrain are not affected) Others; - Hallmark signs of vestibular disease (nystagmus always horizontal/rotary) - May have ipsilateral CN VII defecits - May see psilateral horners

Answer 94

Vestibular disease quad sings; 1) head tilt 2) Vestibular ataxia 3) Spontaneous or inducible nystagmus 4) positional strabismus IS Mentation NORMAL (Key)? - No -> CENTRAL! - Yes -> peripheral or central Are postural reactions NORMAL? - No -> central - Yes -> peripheral or central Are other CN nerves affected ? - I and II not helpful - III->VI and XI->XII affected -> CENTRAL - None affected or VII/VIII -> most likely peripheral (cannot 100% rule out central) Vertical nystagmus (key) -> NOT PERIPHERAL -> LESION IS CENTRAL vs PENDUCLE/FLOCCULONODULAR Horizontal nystagmus or rotary -> Most likely peripheral IPSIlateral postural reaction defecits (key) -> CENTRAL -> NOT PERIPHERAL

Answer 95

Hallmarks -> nystagmus can be horrizontal, rotary or vertical Dysmetria on OPPOSITE side of head tilt Postural reactions defecits on OPPOSITE side of the head tilt

Answer 96

Cerebellum modulates the vestibular system. If you lose cerebellar modulation -> increased IPSIlateral vestibular activity Cerebelum also modulates the limb flexors. If you lose cerebellar modulation -> inceased IPSIlateral flexor actvitivity

Answer 97

Sensory; Ipsilateral CN II (optic nerve) -> most fibers cross at chiasm Brain; Controlateral procencephalon processes this informaion an then interacts with ipsilateral facial nucleous Motor; Ipsilateral CN VII (facial nerve) To determine the cause of deficit, you need two other cranial nerve exams; 1) PLR; Ipsilateral CNII (Optic)-> procencephalon -> ipsilateral CNIII (Occulomotor) 2) Palpebral-> ispilateral CN V (trigeminal) -> procencephalon -> Ipsilateral CN VII (facial) Menace deficit; Pupillary light reflex; -> Normal CN II -> abscent direct and consensual PLR; Retina or CNII dysfunction is the cause Palpebral reflex; -> normal; CN VII is ok -> abnormal; CN VII dysfucntion

Answer 98

Normal CNII -> most fibers cross contralaterally at the chiasm, but not all, with others going to the controlateral eye -> cross chiasm to the pretectal nucleus -> most (but not all) fibers cross to parasympathetic CNIII -> CNIII to pupil - contriction (because of the chiasm both pupils contrict Lesion of CNII Affected eye PLR - No constriction in ether eye Non affected eye PLR - PLR in both eye - Signal gets through to parasympathetic nucleous of CN III Lesion of CNIII - Light shown in the eye innervated by damaged CNIII will not respond, but the controlateral will constrict (chiasm and pretectal nucleous are intact so CNIII to the which is unafected will cause contriction) - Light shown in eye innervated by intact CNIII will contrict, while the one with damaged CNIII will not do anything - normal light, there will be myadrasis as the normal CNIII eye can contrict while the other is dilated

Answer 99

Trigeminal (V) -> Ipsilateral pons and medulla -> Facial (VII)

Answer 100

V; Absent palpebral, normal menace, ipsilateral hypalgesia VII; Abscent palpebralm abscent menace (VII is motor), ipsilateral lip drop, may have ipsilateral KCS

Answer 101

Sensory; Ipsilateral VIII (vestibulochlear nerve) Brain; ipsilateral midbranin, pons, medulla Motor; ipsilateral CN III (occlumotor), IV (trochlear), VI (abducens)

Answer 102

- Bilateral peripheral vestibular disease (VIII vestibulochlear KO) - Severe lesion in brainstem: Absent physiologic nystagmus OU Coma, absent PLR, absent corneal reflex

Answer 103

Fixed strabismus: Abnormal eye alignment all the time Positional strabismus: Abnormal eye alignment with change in head position

Answer 104

- paralysis of CN III (oclumotor) -> ventrolateral strabismus (up and down) due to loss of innervation of medial, dorsal and ventral rectus and levator palpabre superioris - Paralysis of IV (trochlear nerve) -> creates extortion nystagmus due to loss of innervation to the dorsal oblique - Paralysis of VI (abduscent) -> medial nystagmus from loss of lateral rectus and retractor bulbi

Answer 105

Lesion affecting sensory input from vestibular system Mannually tilt the head towards the ceiling and the -> unaffected side reflexively focuses on ceiling, affected eye will have ventral nystagmus (this is ipsilateral to the side of the lesion) Lesion of CN VIII on the ipsilateral side of the eye that ventral nystagmus

Answer 106

this is circuitous pathway that provides sympathetic innervation to the head. - To the eye and periorbital (levator palpabre superioris, retrobulbar muscles) - To the arteires: facilitates alpha-andrenergic mediated vasocostriction Lateral tectotegmentospinal tract originates in the hypothalamus -> at T1-T4 synapses with sympathetic trunc and travels through the brachial plexus -> travels up the vagosympathetic trunc to the cranial cevical ganglion

Answer 107

- pupil dilation - eyes positioned rostrally in orbit - eyelids open

Answer 108

- Miosis - Enophtalmos -> raised third eyelid - Ptosis

Answer 109

T1W: characterised by bright fat and dark water T2W: bright water and dark fat - Oedema readily apparent increased signal Fluid attenuated inversion recovery (FLAIR) sequence suppressed signal from fluid with low or no protein (CSF) so that it is hypointense and allows improved id of pathologies (tissue oedema) and lesions near ventricles) Short-tau inversion recovery (STIR) sequences allow for fat suppression. Gradient echo T2W used to detect artefact from blood products formed in haemorrhage.

Answer 110

Advantage; Bone imaging, speed of scan, Attenuation of x-rays will be similar to that of gamma rays used in radiation therapy- hence CT can be used to calculate dose delivery. Disadvantage; fine parenchymal lesions often not visible, resolution limited by x-ray attenuation by the skull. Density of petrosal bones at base of skull limits CT image quality to the tentorium cerebelli.

Answer 111

Treatment: often based on gram stain initially or most likely pathogen. Need to be bactericidal, cross BBB and low-level protein binding. IV for first 3-5 days. - High dose ampicillin (22mg/kg q6h) appropriate for most cases. - If gram negative confirmed, then enrofloxacin 10mg/kg IV q12h in dogs or third gen cephalosporin cefotaxime 25-50mg/kg IV q8h good choices. - Metronidazole 10mg/kg IV q8h for anaerobes. If severe infection, broad spectrum while await lab results. Once positive response to IV abs then swap to oral. TMS (15m/kg PO q12h) penetrates BBB (fluconazole + fluorocytosine) able to cross BBB, amphoteracin B

Answer 112

- ischaemic strokes 66% - hemorrhagic strokes 33%

Answer 113

Systemic and occular sings, multifocal (occasionally focal) CNS signs, altered mentation, cranial nerve abnormaliteis and seizures DDX; - toxoplasma - FelV induced lymphoma

Answer 114

Fip - Non regenerative aneami, - Alb:glob <0.8, - CSF Fcov titer, - increased alpha-1 serum glycoprotein Toxo - Non-regenerative anemia - Increased neutrophols and lymphocytes - CSF antibody titers - head MRI FeLV induced lymphoma - Blood FeLV antigen or PCR - Lymphoma cells in CSF - Head and spine MRI

Answer 115

Bacterial meningioencephalitis Neutrophilia with left shift, CSF and/or blood culture, heat CT/MRI

Answer 116

Protozoal meningioencephalitis e.g. Toxoplasma Fungal meningioencephalitis e.g. cryptococcus

Answer 117

Behavioural and/or motor changes. Young-middle aged cats most commonly affected. DDx Borna disease virus, viral non-FIP encephalitides

Answer 118

- Lipid solubility: major limiting factor - Molecular size - Degree of protein binding - Drug efflux system: 70% of penicillin is effluxed!

Answer 119

- Aminoglycosides: poor BBB penetration even in presence of significant meningitis - Cephalosporins: 1nd/2nd gen poor bc not lipophilic, 3rd gen acceptable - Clindamycin: doesn’t cross readily, even with inflammation - Quinolones: good BBB penetration - Penicillins: low penetration. Exception is ampicillin. It can reach high CNS concentrations regardless of state of meninges - TMS readily crosses BBB at all times, is broad spectrum, and is bactericidal

Answer 120

Most common in dogs and cats: Staph, Strep, Pasteurella Most common in dogs: E. coli, Strep, Klebsiella Acute, progressive neurological dysfunction - Fever and neck pain reported, but relatively uncommon (only 40% have fevers, only 20% have neck pain) Diagnostic tests: - CBC is normal in 43% of cases - CSF/blood/urine culture only 20% positive - CSF shows degenerate/toxic neutrophils, elevated protein

Answer 121

Incubation period generally 1-3 months Coma and death within 7-10 days of onset of signs

Answer 122

- Intracytoplasmic, eosinophilic inclusion bodies (Negri bodies) - immunohistochemistry for rabies antigen

Answer 123

Family: Rhabdoviridae, Genus: Lissavirus Know the disease pathogenesis Incubation period generally 1-3 months Coma and death within 7-10 days of onset of signs Definitive diagnosis: Intracytoplasmic, eosinophilic inclusion bodies (Negri bodies) Immunohistochemistry for rabies antigen

Answer 124

In dogs and cats Herpesvirus suis causes pseudorabies (Aujesky’s disease). Become infected from eating uncooked pig meat. Clinical signs: hypersalivation, respiratory signs, pruritus, autonomic signs Histopath: Brainstem more affected than cerebrum Inclusion bodies are INTRANUCLEAR (whereas for rabies, in cytoplasm) | Pig virus which causes respiratory sings in pigs

Answer 125

Histopath Inclusion bodies are INTRANUCLEAR (whereas for rabies, in cytoplasm)

Answer 126

Canine distemper | enal hyperplasia and ocular signs are key !

Answer 127

Acute respiraoty and GIT signs; Ocular; Uveitis, chorioretinitis, KCS. Virus can also infect corneal cells Enamel and dentin hypoplasia due to infection of stratum intermedium of developing teeth

Answer 128

Can try to find inclusion bodies in circulating blood cells or in conjunctival scrape - low sensitivityIn CNS: Intranuclear, intracytoplasmic -> Most common in astrocytes (94.8% of cases) but can also occur in neurons (3% of cases) Immunostaining for the CDV antigen - More sensitive but can have a false positive in recently vaccinated dogs Antigen detection ELISA assays: - Sensitivity and specificity have not been validated Serology: - IgM antibodies appear one week before serum neutralization titers IgM and IgG -> can be confounded by recent vaccination - Four-fold increase in titer over 2-4 week period supports diagnosis - Dogs with delayed CDV encephalomyelitis have high levels of antibody in the CSF compared with serum, so if you suspect CDV in a dog, more likely to get positive result with CSF titers compared to serum titers

Answer 129

- Occurs in up to 10% of cats infected with FeCoV - 30% of cats with FIP have CNS signs Systemic pyogranulomatous to granulomatous disease -> develop pyogranulomatous meningoencephalitis from FIP have the dry form rather than the effusive form

Answer 130

38% of cats with noneffusive form develop CNS disease 5% of cats with effusive form develop CNS disease

Answer 131

Hyperproteinemia secondary to hyperglobulinemia, polyclonal gammopathy - 70% of dry - 50% of wet - Not as prominent in cats with CNS disease CSF tap - marked increase in total protein concentration and TNCC - High protein (30-1000mg/dL) - Neutrophilic pleocytosis is most common, but can also have lymphocytic or mixed pleocytosis MRI - /leptomeningeal and ependymal vasculitis with secondary venticulomegaly and mass effect

Answer 132

Cryptococcus neoformans and gatti most common in cats (and dogs) - cats, tends to cause mild signs, usually respiratory due to the involvement of the nasal cavity. Roman nose, chorioretinitis, papilledema. Cats can also develop Cryptococcal granulomas that result in peripheral vestibular disease - Neuro sings tend to develope due to direct extension of the rhinitis Diagnostics; - Latex agglutination test (>90% sensitivity and specificity)

Answer 133

Cryptococcus neoformans and gatti most common in dogs (and cats) Dogs are much more likely to develop severe, disseminated disease from Cryptococcus and neurological signs are present in up to 2/3 of affected dogs Diagnotstic test - Latex agglutination; >90% specificity and sensitivity

Answer 134

Cats Amphotericin B and 5-flucytosine is considered optimal treatment for cats because they are synergistic and 5-flucytosine effectively penetrates the BBB Sole Amphotericin B is aslo very effective for Cryptococcus in cats - Doesnt have good BBB penetration, but it does seem to matter suggesting BBB is distrupted by the disease Dogs Ideally, treat with liposomal amphotericin-B and fluconazole - Don’t use flucytosine in dogs because it can cause toxic epidermal necrolysis 10-14 days after starting therapy Both Glucocorticoid administration after diagnosis is associated with improved survival in the first 10 days: helps mitigate the inflammation that occurs as the organisms are dying

Answer 135

Glucocorticoid administration after diagnosis is associated with improved survival in the first 10 days: helps mitigate the inflammation that occurs as the organisms are dying

Answer 136

NEVER because it can cause toxic epidermal necrolysis 10-14 days after starting therapy

Answer 137

Toxoplasma gondii: both dogs and cats Neospora caninum in puppies and occasionally older dogs

Answer 138

Generally causes PL dysfunction in puppies - But can also lead to brain infection in older dogs - Generally, leads to cerebellitis and cerebellar atrophy, but can cause prosencephalic signs

Answer 139

Meningoencephalitis of unknown etiology Daft way of saying MUO

Answer 140

Any dog can be affected, but most commonly affects small, female dogs aged 3-7 Up to 25% of cases of MUO occur in large breed dogs

Answer 141

Large breed dogs are more like to be presented for decreased mentation compared to small breed dogs Prognosis is just as guarded in large breed dogs as in small breed dogs

Answer 142

Multifocal: acute onset and rapid progression of multifocal CNS signs - Some dogs have fever - Some dogs have cervical pain - Usually have both forebrain and brainstem localization Focal: more insidious onset than multifocal GME - Usually just forebrain localization Ocular: acute signs of visual dysfunction due to optic neuritis - Estimated 10% of dogs with GME have concurrent optic neuritis - Optic nerve head swelling - Can be optic neuritis exclusively or can be part of MUE complex - 50% of dogs do not regain vision, regardless of if they have isolated optic neuritis or if it is part of MUE - Partial or complete recovery in 30% of cases, again regardless of if they have isolated optic neuritis or if it is part of MUE

Answer 143

- Estimated 10% of dogs with GME have concurrent optic neuritis - 50% of dogs do not regain vision, regardless of if they have isolated optic neuritis or if it is part of MUE - Partial or complete recovery in 30% of cases

Answer 144

Necrotizing meningioencephalitis Originally reported as breed-specific disease in pugs but has now been described in many other dog breeds; Pugs, Maltese, chihuahua, Pekingese, Yorkshire terrier, Papillon, shih tzu, Coton de Tulier, Brussels Griffon

Answer 145

Pugs: median age 18 months and fawn females over represented followed by black males Chihuahuas: mediam age is 5 years Varies with other breeds

Answer 146

Hallmark clinical sign is extensive necrosis. Also leads to a lot of leptomeningitis

Answer 147

ot fully understood, but it is believed to be an immune-mediated disease, potentially with genetic factors playing a role

Answer 148

Described in Yorkshire terriers and French bulldogs, but with different lesion distributions - French bulldogs, has been observed in optic nerves and retina, also in spinal cord. Most common clinical signs are; vision loss, seizures, central vestibular signs - In Yorkshire terriers, have at least one of these clinical signs

Answer 149

mononuclear pleocytosis in which at least 50% of the cells are mononuclear However, there are reports of normal CSF in cases with histopathologically confirmed inflammatory disease

Answer 150

Immunosupression - Procarbazine->alkylating agent -> MST 425 days - Lomustine: Alkylating agent -> MST 150-740 days - Vincristine and cyclophosphamide -> Vinca alkaloid (tubule inhibitor) + Alkylating agent -> MST 198 days *and authors concluded came with unacceptable side effects and did not recommend using it for MUE* - Mycophenolate -> Purine metabolism (analogue = apoptosis) -> MST 250 days - Azathioprine -> Purine metabolism -> MST 1834 days -> Cytosar (Cytosine arabinoside) -> DNA polymerase and topoisomerase inhibitor -> MST wide range of 28-602 days - Cyclosporine -> Calcineurin inhibition -> wide range of 236-930 days

Answer 151

Novel neurotoxic rodenticide Mechanism of action: uncouple oxidative phosphorylation Primary metabolite, desmethylbromethalin, is an active metabolite that also uncouples oxidative phosphorylation Acute signs seen with ingestion >LD50: CNS excitation, muscle tremors, seizures More common, at least in dogs, to see neurological signs that develop 1-7 days after ingestion and include ataxia, seizures, paresis

Answer 152

- charcoal - Intralipid emusion - IVF

Answer 153

Leukoencephalomalacia -> mycotoxin called fumonisin Affects horses and pigs

Answer 154

Congenital - Most common cause is stenosis of mesencephalic aqueduct. Often, fused rostral colliculi is a concurrent abnormality. In many cases, cause of obstruction is not apparent (might be due to obstruction of arachnoid villi or due to abnormalities at the subarachnoid space, or, could be due to intraventricular obstruction during a critical stage of development) Other congenital causes include - Meningomyelocele - Chiari malformation - Dandy-walker syndrome (lack of a cerebellar vermis) - Cerebellar hypoplasia Acquired - Tumors that obstruct or overproduce CSF (some choroid plexus tumors) - Meningoencephalitis

Answer 155

Medical; - Acetazolamide: carbonic anhydrase inhibitor -> Decreases CSF production - Furosemide: loop diuretic Partially inhibits carbonic anhydrase, working to a lesser degree than acetazolamide - Omeprazole decreases CSF production in normal dogs - Glucocorticoids may decrease CSF production (data are conflicting) Surgery; - If there is a primary cause that can be addressed, address it - Ventriculoperitoneal shunts

Answer 156

blockage of CSF flow

Answer 157

Reduced or absent gyri. Can calso have pachygiria (abnromally thick cerebral cortex. Lhasa apso -> most common Clinical sings; Behavioural abrnormalities and seizures

Answer 158

- Mitochondrial encephalopathy - Thiamine deficiency - Vascular (deep cerebral vein thrombosis) - L-2 hydroxyglutaric aciduria - Hepatic encephalopathy - Myelinolysis from rapid correction of hyponatremia (symmetric lesions in thalamus) These cause symmetrical changes to the procencephalon

Answer 159

Ammonia builds up in the systemic circulation. This is uptaken by astrocytes, leading to increase glatamine synthesis which is uptaken by the mitocondria resulting in the priduction of ROS. Additionally, the NH4 disrupts the TCA cycle, which disrupts metabolism and leads to cell swellign. Also, Atrocytes which produce glatamine, secrete this and it is uptaken by neurons which break it down into NH4 and glutamate, increasing intracellular NH4 content

Answer 160

Thought to occur because the brain gets used to the abnormal metabolic environment preoperatively, and the sudden change caused by surgical attenuation favors an excitatory state - 12% of dogs with PSS treated with attenuation develop PANS - Do not have elevated ammonia - 12/28 had seizures in one study - 5/28 dogs with PANS died. All of the dogs that died had seizures, meaning that 5/12 dogs with seizures died...almost 50% (none of those that died receied pre-op leviteracetam while 4/7 dogs with seizures who survived DID receive perioperative levetiracetam)

Answer 161

Distinctly different from hepatic encephalopathy. Dogs with HE after attenuation (because the attenuation wasn’t sufficient) have persistently elevated ammonia levels, whereas dogs with PANS DO NOT have elevated ammoni

Answer 162

The recommended correction rate is generally to increase Na by no more than 10-12 mEq/L per 24 hours. If you correct it too quickly you can get central myelinolysis (sometimes called pontine myelonisis - not correct)

Answer 163

Lysis of the myelin shift that occurs when hypernatremia is corrected too quickly. causes a sudden osmotic shift, pulling water out of brain cells and leading to dehydration and damage to the myelin sheat

Answer 164

Hypocalcemia lowers the threshold for neuronal and muscular depolarization because it alters sodium flux and membrane potential Clinical signs: facial rubbing, muscle twitching, cramping, tetanic tremors, ataxia, seizures Diagnosis: ical <1mmol/L Management: only treat if the animal is clinical - Calcium gluconate 10% as slow IV bolus over 10-30 minutes (0.5-1.5ml/kg; 5-15 mg/kg) - Need to have continuous ECG on while doing this and stop infusion if bradycardia, increased P-R interval, prolonged QRS complex, shortened QT interval observed

Answer 165

Occurs due to reduction in thyroid hormone circulation (Usually there is a precipitating factor that overwhelms normal thyroid homeostasis) Doberman pinschers seem to be overrepresented Clinical signs: dull mentation, edema, obesity, hypothermia, bradycardia, hypotension, hypovolemia On bloodwork, look for hypercholesterolemia

Answer 166

Brain uses 25% of total body glucose Brain has very limited glycogen stores. When glycogen stores are depleted, neurons have to shift to glycolysis to form pyruvate, leading to lactic acidosis At some point, without getting glucose, they run out of energy → ATP depletion → sodium potassium pumps fail → cell swelling occurs, which leads to excitatory cascade that develops with the release of lots of glutamate and aspartate, which then leads to cell membrane damage, oxidative damage, which leads to cellular necrosis and irreversible brain injury (glatamate increases ROS in the mitroconfria - like in hyperammonea)

Answer 167

BG is closely monitored by glucose-sensing neurons in hypothalamic ventromedial nuclei

Answer 168

Insulin is not required for glucose uptake in the brain, glucose instead enters brain through non-insulin dependent facilitated transport diffusion. Diffusion doesn’t work very well when there isn’t a lot of glucose in the blood to create the gradient

Answer 169

Neuronal energy depletion (neuroglycopenia) associated with BG < 45mg/dL Neuronal glucose uptake is insulin INDIPENDENT and relies on a concentration gradient. Concentratio n gradients become less effective the lower the BG is

Answer 170

toy breed/hunting dog, endogenous/iatrogenic hyperinsulinemia, HAC, PSS, neoplasia (beta islet cell tumor, leiomyosarcoma, hepatoma, HCC)

Answer 171

Idiopathic epilepsy is the only idiopathic condition of the prosencephalon

Answer 172

- Dolichocephalic breeds more likely to get meningiomas - Brachycephalic breeds more likely to get gliomas Large breed dogs at increased risk for primary brain tumors compared to small breed dogs Decreased risk of brain tumors: Dobermans and Cocker spaniels

Answer 173

Glioma rad = 500 day Other tumour radiaion =350day Surgery 312 day

Answer 174

meningioma, then lymphoma

Answer 175

Surgery -> can be curative

Answer 176

Haemangiosarcoma

Answer 177

Ventricular tumors: choroid plexus papilloma/carcinoma, ependymoma Germ cell tumors Granular cell tumors Pituitary macroadenomas

Answer 178

Absorbed in the jejunum and ileum Thiamine pyrophosphate (also called thiamine diphosphate) is one of the four derivatives of thiamine and it is the most biologically active form of thiamine, acting as a cofactor in both the TCA cycle and the pentose phosphate pathway - In TCA cycle, it is a cofactor in the conversion of pyruvate to acetyl CoA - -thiamine deficiency = decrease thiamine pyrophosphate = buildup of pyruvate and lactate, (because if pyruvate cannot be used in the TCA cycle) then it is converted into lactate -> This can result in type B lactic acidosis

Answer 179

Dogs and cats cannot synthesize large quantities of thiamine. As a water soluble vitamin, doesn’t accumulate in the body (as opposed to fat soluble vitamins) so there isn’t a reserve supply. Thiamine is a relatively labile molecule and is easily destroyed by typical food processing techniques

Answer 180

Cats are more susceptible to thiamine deficiency than dogs: Cats have 3x higher requirement for thiamine compared to dogs

Answer 181

Systmeic disease - leading to alteration of absorption, retention, and metabolism of thiamine Medications; - Loop diuretics lead to increased excretion - Amprolium (coccidiostat) - Pyrimethamine (used to treat Hepatozoon Dietary related - Diets that are higher in carbs than in fats and proteins require more thiamine since more pyruvate is entering the TCA cycle rather than having fatty acids or proteins enter the cycle. - More likely to occur with canned foods than dry foods ( sterilizing process denatures thyamine, and presence of gels that alter pH and absorption availability of thiamine) - Loss during storage, worse in dry food - Diets that contain fish viscera, which are high in thiaminase - Thiaminase also found in plants, bacteria, fungi - Preserving meat with sulphur derivatives (sulphites) - All meat diet: cooking the meat will lead to destruction of 73-100% of the thiamine content in most meat

Answer 182

one of earliest signs is spastic cervical flexion - Anisocoria or mydriasis with decreased to absent PLR and absent menaces, normal fundic exam - Electrocardiographic abnormalities in end-stage disease (Bradycardia - tachycardia syndrome: brief period of tachycardia followed by severe bradycardia and rhythm irregularity. Flattening or inversion of T wave, QRS prolongation, prolongation of ST segment) Three progressive stages; Induction - begins one week after eating thiamine deficient diet - Hyporexia, vomiting Critical Terminal - Happens after thiamine deficiency of at least a month One terminal stage has started, animal will die in a few days if the deficiency is not corrected

Answer 183

- History and PE - MRI; look for bilateral T2 hyperintensities in brainstem nuclei as well as cerebral cortex (lot of nuclei can be affected - cerebla cortex, vermis and hippocampus can be affected) - Blood test for thiamine concentrations

Answer 184

Parenteral administration of thiamine for 3 to 5 days, followed by oral administration for 2-4 weeks Cats: 50-100mg every 12 hours in cats. Up to 600mg in dogs Response to treatment is observed in hours Don’t give it IV: can lead to neuromuscular paralysis and ganglionic blockade

Answer 185

Don’t give it IV: can lead to neuromuscular paralysis and ganglionic blockade

Answer 186

Anomalous; - quadrigeminal arachinoid like cyst - caudal occipital malformation syndrome - hydrocephalus Metabolic - Hypothyroidism +/- infarction Nutritional - Thiamine defficiency Neoplasia - Primary intracranial -> meningioma, glioma, medulloblastoma, chorid plexus tumour, lymphoma - Metastatic neoplasia (HSA most common ) Infectious/inflammatory - Viral -> canine distemper, FIP - Bacterial -> abscess, rocky mountain spotted fecer, erlichia, bartonellolos - Protozoal ->Toxo, neospora - Mycotic ->crypto, blasto - Non- infectious; granulpmatous meningioenceph, necrotizing meningionencep Trauma - Brainstem trauma Toxic - Metronidazole Vascular - Cerebrovascular diseases

Answer 187

- Highly lipophilic and crosses the BBB very readily (T1/2 4-6h) - Historically used to think that it only happened at really high doses but has now been reported in dogs that have been receiving 20mg/kg Q12 - Mechanism of neurotoxicity is unknown but suspected to be due to modulation of GABA receptors - Most common clinical sign of toxicity in dogs is vestibulocerebellar ataxia. They don’t always have other vestibular signs to go with the ataxia - Histopath findings: Purkinje cell loss and axonal degeneration of vestibular tracts - MRI findings: bilateral T2 hyperintensity in the lateral (dentate) cerebellar nuclei

Answer 188

Metronidazole toxicity

Answer 189

Metronidazole tox

Answer 190

Purkinje cell loss and axonal degeneration of vestibular tracts

Answer 191

Thiamine deficiency

Answer 192

Administering diazepam significantly reduces the time to recovery - GABA is the major inhibitory neurotransmitter of the cerebellum and the vestibular system - Benzodiazepene have major effects on GABA receptors, leading to increased chloride movement → hyperpolarization - Metronidazole might bind to the same region on the GABA receptor as benzodiazepene, but instead of leading to activation, lead to inhibition of chloride channel.

Answer 193

Gaba is the major inhibitor neurotransmitterr in cerebellum and vestimular systme. Benzodiazepene have major effects on GABA receptors, binding them, leading to increased chloride movement → hyperpolarization stops seizures

Answer 194

-Identifiable structural brain lesion present or prior history of brain disease or injury - Seizures > 5 minutes - 3 or more generalized seizures occur within a 24 hour period -2 or more seizures without recovery between seizures (more common per Patterson) ## Footnote goals Decrease freqency Decrease number Decrease severity (length)

Answer 195

GABA-A agonist, where they prolong opening of the associated chloride channel causig hyperpolarization and preventing depolaristion (or reducing rate of) and nerve action potential propagation. -sedation if leaded too quickly - PU/PD/polyphagia -Hepatotoxicity (up to 20% of dogs can occur but rare in cats) -Monitor liver values q2 weeks then q 3-6 months after steady state dose; monitor 2 weeks after dose change -Monitor trough serum levels after 2-3 weeks then q 3-6 months

Answer 196

Competes with cloride for entry via gabachannels hyperpolarising the cell -Pancreatitis (10% of dogs) -DO NOT USE IN CATS (asthma) -High salt intake makes renal elimination and makes less effective

Answer 197

Not entirely knownn. Tough to block SV2A synaptic vescicle glycoprotein preventing the release of neurotransmitters. May orevent selective hyperpolarisato=ion of epilepiform burst-firing and propragation of seizure activity -Safe (probably due to MOA) -Rarely sedation or stomach issues

Answer 198

Inhibits voltage gated sodium channel and T-gate Ca channels. Na channle inhibition prevents depolarisation, while the Ca prevents neurotrnasmitter release from the synapse. -Ataxia, lethargy, liver issues, dry eye, skin rashes? -More side effects noted in cats

Answer 199

The drug is metabolised into phenobarbitol (~85%) -DO NOT RECOMMEND USING because phenobarbitol is active form anyway -High incidence of hepatotoxicity

Answer 200

Partial agonist of GABA-A receptor allowing increased Cl- entry into the cell and increased hyperpolarization - ataxia - lethatgy - Polyphagia - hyperactivity - aggression - somnolence

Answer 201

I - olfactory II- Optic III- occlumotor IV - trochlear V- trigeminal VI- abduces VII - Facial VIII- vestibulocholear IX - glossopharingeal X- vagus XI- abducents XII- hypoglossal ## Footnote oh, oh, oh, to, touch, virgin, girls, vaginas, and, hymens, ah, heaven

Answer 202

Motor for eye Motor to dorsal, medial, ventral recus, ventral oblique, levator palpabre superioris Autonomic Cilliary ganglion, ciliary nerves to iridial sphincter mucles (control pupil costriction via parasympathetic innervtion )

Answer 203

the only cranial nerve that emerges from the brainstem dorsally, crosses to the other side and innervates contralateral structures Motor; - to dorsal oblique muscle (superior oblique m. ) [SO4 memory aid] - repsonsible for inward turning of the controlateral eyeball

Answer 204

Trigeminus = 3 fold (ie 3 branches and 3 roles) Branches into; 1) ophthalmic (V1) -> (Sesory) cornea, medial canthus, nasal planum, nasal septal mucosa 2) Maxillary (V2) -> (sensory) zygomatic n to lacrimal gland and lateral palpebrae + Pterygopalatine ganglion to lacrimal, nasal and palatine glands (splits into major nd minor palatine nn) + infraorbital to skin, upper lip and nose + superior alveolar branches to dental arcade and tooth roots 3) Mandibular (V3) -> (Sensory and Motor) branches into; bucaln which is sensory to mucosa and skin of cheek + lingual n which is sensorty to rostral 2/3 of tongue + inferior alveolar n which is sensory to lower arcade and sends mental branch to lower lip + auriculotemporal n which is sensoy to external ear/canal and temporal region. MOTOR is mylohyloid nerve branch to rostral digastricus Roles 1) motor 2) Sensory 3) prasympathetic

Answer 205

to abduct -> take away (e.g. child abduction) Motor to lateral rectus (LR6 like LRS - Laterarl Rectus cn6) and retractor bulbi

Answer 206

sensory AND motor AND parasympathetic * Sensory – taste to rostral 2/3 of tongue * Motor – muscles of facial expression, caudal digastricus, platysma * Parasympathetic – to lacrimal gland, and the mandibular and sublingual salivary glands Branches; * auriculopalpebral n (rostral auricular and palpebral - to o. oculi) * Buccal ns. (Dorsal and Ventral) ## Footnote If you eat something sour, you taste it at the back of your tongue, your grimace and hypersalivate

Answer 207

SENSORY * Vestibular n. – positional information, motion sense; to the semicircular canals * Cochlear n. – hearing; to hair cells in spiral organ of the cochlea ## Footnote “vestibulis” meaning courtyard; “kochlias” meaning snail

Answer 208

sensory AND motor AND parasympathetic Has complex branching. Large terminal branches: Pharyngeal and Lingual * Sensory – caudal tongue 1/3, pharyngeal mucosa * Motor - pharyngeal muscles, stylopharyngeus * Parasympathetic – parotid and zygomatic salivary glands

Answer 209

sensory AND motor AND parasympathetic Runs alongside sympathetic trunk to thorax/abdomen MOTOR * to larynx muscles via recurrent laryngeal and caudal laryngeal * Except cricothyroideus via cranial laryngeal * to pharynx and esophagus via pharyngeal, recurrent laryngeal, and vagal branches with help from CN 9 * SENSORY * Larynx, pharynx, thoracic and abdominal viscera * Distal (nodose) ganglion PARASYMPATHETIC * Thoracic and abdominal viscera (except pelvic) ## Footnote vagus means wanderer

Answer 210

Ventral and dorsal branches MOTOR * Ventral branch - to sternocephalicus * Dorsal branch - to brachiocephalicus, omotransversarius, and trapezius

Answer 211

MOTOR - muscles of the tongue (hyoglossus, styloglossus, genioglossus, geniohyoideus)

Answer 212

Exitatory neuron -> gluatamate -> binds NMDA or AMPA receptor -> depolarise Na into cell, K out -> synapse Ca into cell -> release neurotransmitter Inhibitory neurons -> release GABA - > bind GABR CL channels increasing CL - entry -> hyperpolarising cell

Answer 213

Potassium KCNQ2, KCNQ3, KCA1 Sodium SCN1A, SCN2A, SCN1 Chloride CLCN2

Answer 214

Helped some dogs already on phenobarbital or bromide. Evidence Grade = C Short elimination half life so many thinks its unlikely to help as monotherapy consistently. good for neuropathic pain? But not many studies to back up for seizures

Answer 215

Who – Labrador, Chesapeake, and curly-coated retrievers -> Highly pentrant autosomal recessive inheritance What – Weakness to temporary paralysis that starts in the hind legs. When - only after very intense exercise. Where – Labradors from US, Canada, England, Germany, Finland, Australia, and New Zealand. Why - A dynamin 1 gene mutation that slows neurotransmission during intense stimulation.

Answer 216

Flaccid, non-painful paralysis of rear legs after intense exercise and excitement. Usually resolves within 10-30 minutes. Sometimes progresses to front legs, and occassionally progresses even more to death. Diagnosis of exclusion – R/O myasthenia, cardiac, metabolic, and endocrine causes of collapse. Affected Dogs collapse after 5-15 minutes of strenuous exercise.Hind limbs become weak. Generally have high body temp. They are Normal at all other times. Usually Well muscled and very fit. Triggers – bumper training, upland hunting, running with ATV’s, and fun play with other dogs

Answer 217

strychnine

Answer 218

Blocks glycine receptors in the spinal cord. Strychnine blocks the binding of glycine to the glycine chloride channel within the spinal cord. Under normal circumstances, glycine binding to this channel causes increased inward flow of chloride, hyperpolarizing the cell, and inhibiting its ability to propagate nerve signals signs: Initial Nervousness; Hyperalert; Confusion Stiffness Later: Generalized rigidity Tetanic seizures Respiratory arrest my occur during spasm Muscle contraction may cause rhabdomyolysis

Answer 219

- Gastric lavage - Stiffness: Benzodiazepines; Barbiturates, methocarbamal - Rhabdomyolysis: Fluids; pH management - Prophylactic ventilation in severe cases

Answer 220

Clostridium tetani produces tetanospasmin tetanus neurotoxin. Inhibits (glycine and GABA release from interneuron nerve terminals, thereby causing excessive motor neuronal discharge -> increased extensor activity Predominantly at the spinal cord but the brainstem and autonomic nervous system can also be affected. Death may result from respiratory arrest.

Answer 221

Surgical debridement of the wound Antibiotic therapy (penicillins or metronidazole). Tetanus Antitoxin (Equine) - Controversial is given to neutralize any toxin that remains unbound to the CNS so may prevent progression of localized to generalized disease. Some patients may have an anaphylactic reaction to tetanus antitoxin (test dose first). Sedatives and muscle relaxants may be used to control spasms: Acepromazine, Diazepam, Midazolam. Supportive therapy, dark and quiet environment ,bladder care, feeding tube, tracheostomy if needed.

Answer 222

nicotinic receptors are ligand gated cation channels in postsynaptic membranes . These receptors are found in sympathetic ganglia and motor endplates of skeletal muscle. They are equally permeable to Na+ and K+. Na+ rushes in while K+ streams out, but, because the Na+ gradient across this membrane is steeper than that of K+, the Na+ influx greatly exceeds the K+ efflux. The influx of Na+ depolarizes the postsynaptic membrane, initiating an action potential in the adjacent membrane

Answer 223

e.g. botulism, tick paralysis Toxic LMN conditions

Answer 224

acute polyradiculoneuritis (CoonHound paralysis). This is a non-suppurative inflammation that primarily affects the ventral (motor) nerve roots

Answer 225

tick paralysis also involves a toxins that block the release of acetylcholine at the neuromuscular junction. Removal of any and all ticks is often curative with most dogs improving in 2-3 days. Supportive care until strength returns is essential as most dogs will need help eating, drinking and having bowel and bladder movements

Answer 226

The toxin works by Binding to ACH synaptic vesicle proteins and blocks release of acetylcholine, preventing muscles from contracting. resulting in flaccid paralysis of motor and respiratory muscles.

Answer 227

Canine anti type C botulism antitoxin: Antitoxin may be beneficial if absorption and circulation of toxins are still occurring. Often not readily available. It is not effective once toxin has penetrated the nerve endings but it could prevent further binding of toxin if absorption of toxin is still occurring. Otherwise supportive care

Answer 228

Equine antitoxin does not include subtype toxin C and is not useful for dogs.

Answer 229

autoantibodies - acetylcholine receptors (AchR) at the motor endplate

Answer 230

ACh antibody ->current Discontinued but in the lit; Tensilon (Edrophonium Chloride). Short acting acetylcholinesterase inhibitor (stops breakdown of acetylcoline so it remains in the synapse for longer). If this lead to a brief increase in muscle strength then the test was positive. Discontinued in humans due to false positives effects on skeletal muscle within one minute and effects may persist for up to 10 minutes No to limited availability generally.

Answer 231

- Immunosuppression - Pyridostigmine Bromide (Mestinon) Mechanism - inhibits the hydrolysis of acetylcholine by directly competing with acetylcholine for attachment to acetylcholinesterase Toxicity signs - (SLUD) Symptoms of cholinergic toxicity can include GI effects (nausea, vomiting, diarrhea), salivation, respiratory effects (increased bronchial secretions, bronchospasm, pulmonary edema, respiratory paralysis), cardiovascular effects (bradycardia or tachycardia, cardiospasm, hypotension, cardiac arrest), muscle cramps and weakness. ## Footnote Overdoses in myasthenic patients can be very difficult to distinguish from the effects associated with a myasthenic crisis. The time of onset of symptoms or an edrophonium challenge may help to distinguish between the two.

Answer 232

Nicotine & imidacloprid (Advantage) activate the nicotinic acetylcholine receptors -> hyperexcitation, convulsions, paralysis. OPs -acetylcholinesterase inhibitors-> hyperexcitation of the CNS occurs. restlessness, hyperexcitability, tremors, convulsions, and paralysis. Avermectins increase chloride conductance ->hyperexcitability, tremors, and incoordination, and later develops into ataxia and coma-like sedation

Answer 233

Hypersensitivity of the Ryanodine receptor (RYR) in the sarcoplasmic reticulum Ca++ release channel. -> excessive Ca release leading to Excessive muscular contraction. Autosomal dominant in people and dogs (rare) - Anesthetic induced only - Succinyl Choline and Inhalent Anesthetic agents

Answer 234

Muscle Chloride Channel (CLCN1) mutatio resulting in reduced or abscent Cl- conductance through the cahnnels Cl- conductance is necessary to stabilize membrane potential Slowed muscle relaxation No known treatment Genetic test in dogs. Over represented breed - > mini shcanuzer

Answer 235

may originate in subcortical structures, with preferential propagation patterns that can involve the contralateral hemisphere. With focal epileptic seizures, the abnormal electrical activity arises in a localized group of neurons or network within one hemisphere - Motor: facial twitching, head jerking, blinking - Autonomic (with parasympathetic and epigastric components): dilated pupils, hypersalivation, vomiting - Behavioral: humans - psychic and/or sensory seizure phenomena (in animals, may cause short lasting episodic change in behavior - anxious, restless, unexplainable fear)

Answer 236

animal will lose consciousness during convulsive epileptic seizures (myoclonic seizures excluded). types; Tonic lonic Tonic-clonic Myoclonic (rhythmic limb and/or head jerk movements, often with preservation of consciousness) Atonic (sudden and general loss of muscle tone) Absence (staring spells) - in Ettinger not task force consensus

Answer 237

Myoclonic -> rhythmic limb and/or head jerk movements, often with preservation of consciousness

Answer 238

phases of a generalised seizure. Prodrome: time period prior to onset of seizure activity -> Hours to days - change in disposition; restlessness, anxiety, irritable, attention-seeking behavior. Can represent a potential important therapeutic window for pulse therapy Aura: initial manifestation of a seizure; animals can exhibit stereotypic sensory or motor behavior (pacing, licking), autonomic patterns (salivating, vomiting) Ictal: actual seizure event; involuntary muscle tone or movement and/or abnormal behavior lasting seconds to minutes Postictal: completion of seizure; can last minutes to hours Brain restores its normal function; can be very short or last hours to days Disorientation, repetitive vocalization, compulsive locomotion, exhaustion, ataxic, hungry/thirsty, need to urinate/defecate, blindness, aggression

Answer 239

(i) Identifiable structural lesion present or prior history of brain disease or injury (ii) Acute repetitive seizures or, status epilepticus (ictal event ≥5 minutes or ≥3 or more generalized seizures within a 24-hour period) (iii) ≥2 or more seizure events within a 6-month period (iv) Prolonged, severe, or unusual postictal periods

Answer 240

Endogenous ACTH, ACTH stim, LDDST not affected Total and free T4 decreased

Answer 241

serum concs >35

Answer 242

If the diet is high in cloride, it may cause increased renal excretion of kBR and this diet may need to be changed.

Answer 243

Mucosal irritant - capsules may result in gastric irritation High doses (serum concs >3000): Intoxication to the point of stupor is rare, but pelvic limb ataxia, weakness, and altered behavior are more likely (renal insufficiency can make this more likely) asthma in cats (up to 50%)

Answer 244

Monitor phenobarbitone levels as 85% of this drug is metabolically converted to pheobarbitone

Answer 245

Imepitoin effective as phenobarbital in controlling generalized seizures in dogs, but the frequency of adverse events including somnolence or ataxia, polydipsia and increased appetite was significantly higher in the phenobarbital group.

Answer 246

Lack of hepatic metabolism (primarily excreted unchanged in the urine)

Answer 247

hepatic CYP3A4 coadmin w/phenobarb increases clearance of zonisamide by 50%, shortens half life

Answer 248

decreases total T4

Answer 249

IN HUMANS ketogenic diet ( high fat, low protein, low carbohydrate) diet designed to mimic the biochemical changes of fasting to potentiate mitochondrial-dependent energy metabolism in neurons and inhibition of glutamatergic metabolic pathways and synaptic transmission. RANDOMIZED DOUBLE BLINDED CONTROL IN DOGS SHOWE NO DIFFERENCE IN SEIZURE FREQUENCY

Answer 250

Most commonly presents with encephalitis (uncommon to see meningiomyelitis by its self) Canine distemper virus & protozoa - most common infectious causes SRMA - most frequent non-infectious cause Other: rickettsiae, fungi, bateria, helminths, & meningitides of unknown etiology (MUE) Most common clinical sings; Paraspinal hyperesthesia, general proprioceptive ataxia, limb paresis or paralysis

Answer 251

- Immune-mediated, leads to vasculitis - No triggers identified - High CD11a expression on polymorphonuclear cells appears to be important factor in PG of SRMA. May be involved in enhanced passage of neutrophils into subarachnoid space → meningitis - Matrix metalloproteinase (MMP)-2 also seems to be involved in neutrophil invasion of subarachnoid space - Progression → rupture and hemorrhage of weakened vasculature, thickened leptomeninges (with less severe inflammation)

Answer 252

- Usually febrile & hyperesthetic with cervical rigidity & anorexia - +/- neuro deficits in chronic form, rarely severe motor dysfunction (when hemorrhage into subarachnoid space) - Up to 46% of dogs with IMPA -> esp Berners, Boxers, and Akitas -> have concurrent meningitis

Answer 253

- +/- marked peripheral neutrophilia with left shift - CSF: often a marked neutrophilic pleocytosis & protein elevation, cell counts >100/mcL common - Nondegenerate neutrophils - Majority (acute or chronic) have IgA elevation in CSF & serum (nonspecific)-> CSF [IgA] significantly higher in SRMA than in other dz processes (except for inflammatory CNS disease)

Answer 254

- Immunosuppressive steroids - Long-term, over 2 years in some dogs - Monitoring of CSF cell count = sensitive indicator of treatment success Can add secondary agent if needed Prognosis good if treated early & aggressively < 80% go into long-term remission

Answer 255

Sites of disseminated infection include: bone, CNS, skin, peripheral lymph nodes, eyes, testes, prostate and pericardium Neurologic signs result from meningoencephalitis

Answer 256

Coccidiodes are dimorphic soil borne fungi that exist in the environment as mycelium and in the tissues as spherules The arhtospores remain viable in the soil for long periods of time, and typically fragment from each other and are inhaled by animal hosts. Leading to coccidiocomycosis, a localized pulmonary disease or multisystemic disease. The distribution of cocidio is mostly in the southwestern united states

Answer 257

AGID or ELISA (serum or CSF) - close to 100% sensitivity. Titers as high as 1:16 can exist in subclinically infected or previously exposed dogs, positive serology should be supported with other diagnostic tests. IgM - detectable 1-5 weeks post infection IgG - detectable after 4 to 12 weeks post infection If IgG positive, then this can support past infection or current CNS infection

Answer 258

guarded, but with appropriate treatment, many dogs can recover

Answer 259

- to reduce cerebral edema (mannitol, hypertonic saline, dexSP) - Fluconazole (median dose 9 mg/kg q12) ->indefinite tx bsed on ≥3 antibody titers - +/- anticonvulsants, denamarin, SAMe-LQ Coccidio we do NOT typically use steroids in - due to risk of dissemination

Answer 260

Most brain lesions in dogs with coccidioides manifest as single (occasionally multiple) intraparenchymal, well circumscribed, contrast enhancing lesions Hard to differentiate from malignancy - and the median age here was 7 years old A secondary form is characterized by bilaterally symmetrical T2 and FLAIR hyperintensity of the caudate nuclei and frontal lobes

Answer 261

Mortality rates without targeted antiviral therapy are 95% by 1 year

Answer 262

adenosine nucleoside analogue (active form of the remdesivir prodrug) and has greatly improved FIP outcomes Responses are fast (days) but relapses are common Most, but not all, cats who die do so within 48 hrs

Answer 263

Still somewhat poor overall but amazing relative to what it used to be without GS-441524 and potentially no different from non neurological cases

Answer 264

The low IgG is consistent with either past exposure or CNS infection.

Answer 265

a) >=50% response rate; improvement typically takes <1 week

Answer 266

It does not directly infect them. It relases Type C toxin which binds to presynaptic peripheral nerve terminals Bind neuronal cell surface receptors -> endosomal internalization of toxin -> membrane translocation -> modification of target SNARE proteins SNARE proteins required for exocytosis of acetylcholine at neuromuscular junction. Targeting of SNARE proteins by botulism toxin prevents presynaptic release of acetylcholine from neuromuscular junction = LOWER MOTOR NEURON (flaccid) paralysis, autonomic dysfunction.

Answer 267

Recovery depends on new axon terminals forming and reformation of functional neuromuscular endplates. Most dogs recover within 2-3 weeks

Answer 268

acute polyradiculoneuritis, tick paralysis, fulminant myasthenia gravis, acute polymyositis, coral snake envenomation, lasalocid poisoning, rabies poliomyelitis

Answer 269

Primarily based on history and CS CBC/chem/UA/CSF analysis usually normal Thx rads may show megaesophagus +/- secondary aspiration pneumonia ositive botulinum toxin in blood or intestinal contents via mouse protection assay Alternatives include ELISA, PCR to detect botulism toxin in food (not all have been validated) Culture of organism from feces or gastric content (only positive in ~60% of human patients with strict anaerobic handling) Electrodiagnostic evaluation of muscle/nerve function can be helpful, not definitive

Answer 270

Tetanospasmin light chain activated after internalization into inhibitory neurons (then no longer accessible for neutralization via antitoxin) Prevents neurotransmitter release by cleaving and inactivating synaptobrevin (membrane docking protein for release of neurotransmitter) Toxin predominantly affects inhibitory interneurons to inhibit release of glycine and gamma aminobutyric acid (GABA) -> motor neurons lose inhibitory control -> classic tetanus “sawhorse” stance i.e. disinhibitory effects Neuronal binding of toxin thought to be irreversible, recovery requires growth of new nerve terminals

Answer 271

CS can take up to 3 weeks post infection to manifest; most commonly CS within 5-12 days

Answer 272

CS: acute, ascending, flaccid tetraparesis Progress over several days, but may continue for up to 10 days Pelvic limbs usually affected first, followed by thoracic limbs, ssevere cases involve cranial nerves and respiratory musculature, hypoventilation Dx; history and PE (Segmental spinal reflexes: reduced to absent), intact to hyperaesthetic sensation. Electrophysiologic testing may help CSF: may have increased protein without pleocytosis Tx; Supportive care, if respiratory muscles involved mechanical ventilation may be necessary Corticosteroids not shown to be helpful Recent study showed human IV immunoglobulin may shorten recovery time in dogs Prog; most recover with time - complete recovery ca take a few weeks to 6 months

Answer 273

malfunction of the autonomic nervous system (ANS) - malfunction at the ganglia, PNS/CNS or the intersections betweenthes No known etiology. Risk factors exposure to cow pastures, farm ponds, eating wildlife Clinical presentation (CS ~2 weeks): dysuria, regurgitation, purulent nasal discharge, photophobia/mydriasis, anorexia, weight loss, aspiration pneumonia Exam findings usually show parasympathetic disruption: absent PLR, mydriatic pupils, distended urinary bladder, decreased anal tone, horner’s syndrome, dry eye, dry mucous membranes Neuro exam: withdrawal reflexes, sensory perception, postural reactions normal

Answer 274

Definitive via post-mortem exam: autonomic ganglia degeneration with minimal inflammation presumptive via testing autonomis nervous system; - Pilocarpine ophthalmic test: pilocarpine solution (1%) is diluted to 0.05% and 1-2 drops is applied to one eye, if no response in 90 minutes repeat using full strength (1%) solution Dysautonomia: rapid pupil constriction (secondary to denervation supersensitivity from postganglionic neuron loss) - Thoracic radiographs: +/- megaesophagus, aspiration pneumonia - Abdominal imaging: +/- distended urinary bladder - Atropine challenge: if no rise in HR, consistent with dysautonomia - Intradermal histamine: will not have appropriate wheal/flare response (due to lack of sympathetic function) - Blood pressure measurements: orthostatic hypotension (due to lack of sympathetic function)

Answer 275

Megaesophagus is theorized to be due to abnormalities of the afferent or efferent pathways involved in esophageal motility

Answer 276

diopathic Severe esophagitis Myasthenia gravis Systemic lupus erythematosus Polymyopathy Glycogen storage disease type II Dermatomyositis Dysautonomia Distemper Tetanus Lead poisoning Organophosphate toxicity Hypoadrenocorticism Hypothyroidism