Neuro signs and neuro exam

Question 1

Explain “bunny-hopping”

Answer 1

simultaneous bilateral flexor responses at the onset of protraction and when both limbs respond when the withdrawal reflex is stimulated in one limb (instead of normal gait where the initial flexor muscle activation at the onset of protraction in one limb is accompanied by extension in the opposite limb and inhibition of the flexors of that opposite limb). Could be due to an alteration of the functional connections in the commissural interneurons (disorder of the central pattern generator network of the pelvic limbs).

Question 2

Name 3 abnormalities detected on the hands-on neuro exam of patients with prosencephalic disease

Answer 2

1) reduced menace response
2) slow postural reactions
3) reduced nasal septal nociception

(all contralateral in a unilateral disease)

Question 3

Name 3 abnormalities detected on the hands-off neuro exam of patients with prosencephalic disease

Answer 3

• behavioural changes
• seizures
• pleurototonus (adversive syndrome)

Question 4

Explain the pathway and how to perform the patellar tendon reflex

Answer 4

The patellar reflex is a tendon reflex that is composed of only two neurons.
- monosynaptic reflex arc (two neurons). Both the sensory and motor components are in the femoral nerve.
- the only reliable tendon reflex. The femoral nerve is formed from the spinal nerves of the L4, L5, and L6 spinal cord segments. The L5 segment makes the largest contribution to this nerve. The L6 segment may not contribute to this nerve in some dogs.
- The patient should ideally be held in lateral recumbency and must be relaxed. This reflex cannot be tested in a struggling patient. With the limb relaxed and flexed at the stifle, lightly strike the patellar tendon with a blunt instrument.

Question 5

Explain the pathway and performance of the withdrawal reflex of the pelvic limb?

Answer 5

The withdrawal reflex (also called the flexor reflex) in the pelvic limb is a test primarily for the sciatic nerve and its spinal cord segments L6, L7, and S1. Within the sciatic nerve, the neurons that are associated with the fibular nerve tend to be components of the L6 and L7 spinal cord segments, and those associated with the tibial nerve are components of the L7 and S1 segments. The S2 components primarily innervate muscles in the pelvis that do not participate in this test or in the animal’s posture or gait. The sensory component of the reflex depends on the area of skin that is stimulated. In a routine examination, the skin at the base of the claw of the fifth digit is compressed by using a pair of forceps. Finger pressure may be used but is not always sufficient, in our experience. In addition, hemostats apply a more consistent pressure between different patients. This area of skin is innervated by cutaneous branches of the fibular nerve dorsally and by the tibial nerve on the plantar surface. The motor response is a flexion of all the joints in the limb to withdraw the limb from the stimulus.

Question 6

Explan which musscles and nerves are involved in the flexion of the hip

Answer 6

Except for the hip, flexion of the pelvic limb is a function of the GSE components of the sciatic nerve. The major flexor muscle of the hip is the iliopsoas, which is innervated by all the lumbar spinal nerve ventral branches, with a contribution caudally from the femoral nerve. The latter also innervates the rectus femoris, which is the one component of the quadriceps muscle that also flexes the hip. Because of this anatomy, a patient with complete sciatic nerve dysfunction will have no reflex (or nociception) if the fifth digit is stimulated using a noxious stimulus, but if the first digit is compressed, the hip will flex to pull the limb away from the stimulus, but the rest of the joints will not flex. The first digit usually receives its cutaneous innervation from the saphenous nerve branch of the femoral nerve. It is important to look for this disparity. The same strong hip flexion in the absence of any flexion in the other joints will occur with severe but not complete sciatic nerve dysfunction when the fifth digit is compressed. As a rule, there is more clinical evidence of loss of motor function with some preservation of sensory function in a partially compressed nerve

Question 7

Which nerve innervates the first and which the fifth digit of the pelvic limb?

Answer 7

1st - saphenous nerve branch of the femoral nerve.

5th - cutaneous branches of the fibular nerve dorsally and by the tibial nerve on the plantar surface.

Question 8

Name the reflexes of the pelvic limbs, the nerves involved in them, spinal cord segments and level in the vertebral canal where the SCS reside:

Answer 8

Question 9

Name the reflexes of the thoracic limbs, the nerves involved in them, spinal cord segments and level in the vertebral canal where the SCS reside:

Answer 9

Question 10

Name the nerves and muscles innervated by these nerves:

Answer 10

Question 11

Which nerve is tested with the perineal reflex?

Answer 11

Pudendal nerve (S1-3)

The perineal reflex is a test of the branches from the sacral plexus that is located in the pelvic canal. These branches supply the external sphincter muscle of the anus; the striated muscles of the penis, vulva, and vestibule; the urethralis muscle; and the skin of the anus, perineum, and caudal thigh. It is not necessary to learn the names of the specific nerve branches or their individual areas of innervation. Mild compression of the skin of the perineum or anus with forceps elicits an immediate contraction of the external anal sphincter and flexion of the tail. The latter response requires that the caudal spinal cord segments and nerves be intact.

Question 12

Which nerves are involved in the flexor reflex of the thoracic limbs?

Answer 12

• shoulder flexion -> axillary, radial, and thoracodorsal nerves;
• elbow flexion -> musculocutaneous nerve;
• carpal and digital flexion -> median and ulnar nerves.

Question 13

Which nerves innervate the autonomous skin zones of the thoracic limb paws (afferents for the withdrawal reflex)?

Answer 13

1st toe - radial nerve
5th toe - ulnar nerve
dorsal aspect of toes - radial
ventral aspect of paw - median + ulnar

Question 14

Which SCS are tested with the m. cut. trunci reflex?

Answer 14

C8-T1

Question 15

Pathway of the m.cut.trunci reflex?

Answer 15

cutaneous nerves -> dorsal branches of the lumbar and thoracic spinal nerves -> dorsal rootlets –> dorsal grey column –> synapse on the long interneurons -> fasciculus proprous bilaterally to C8-T1 -> synapse on GSE neurons -> ventral grey matter -> ventral rootlets -> ventral branches -> lateral thoracic nerve -> m. cut. trunci bilateral

Question 16

How do you explain an assymmetric m.cut.trunci reaction?

Answer 16

In dogs with asymmetric spinal cord lesions, the cutaneous trunci reflex is absent caudal to the lesion on the ipsilateral side of the body. The cutaneous trunci muscle reaction (skin twitch) on the side contralateral to the lesion remains intact, providing evidence of the bilateral projection of this pathway.

This is particularly helpful in cases such as brachial plexus injuries, asymmetric spinal cord lesions in the thoracolumbar spinal cord, or unilateral fibrocartilaginous embolic myelopathy of the cervical intumescence.

Question 17

Name the nerves and muscles innervated by these nerves if the cervical intumescence

Answer 17

Question 18

Explain “skipping gait”

Answer 18

the skipping-­type gait in the pelvic limbs, which is related to the brisk overflexion of the hips. This has sometimes been confused with a cerebellar hypermetria. It represents the loss of tone in the antagonistic caudal thigh hip extensor muscles that are innervated by the sciatic nerve.

Question 18

Describe the gait in LMN paresis

Answer 18

The lack of ability to support weight characterizes LMN paresis. If the patient is ambulatory, the gait will include short strides and will appear as a lameness. The gait in LMN disease is identical to that of an animal that has discomfort when the diseased limb attempts to support weight. The inability to support weight looks the same as when an animal expresses pain whenever weight is supported. Animals with LMN disease walk as you would with a stone in your shoe. The stride is shortened. Consequently, it is important to rule out any orthopedic disorder in the evaluation of an animal with LMN disease by doing a complete orthopedic examination.

Question 19

For the thoracic limb, which nerve is important for waight bearing, which for advancing the limb by extending the shoulder, which to flex the elbow and which to flex the carpus?

Answer 19

The inability to support weight is caused by the loss of function of the radial nerve (C7, C8, T1).

Extending the shoulder (suprascapular nerve, C6, C7; nerve to brachiocephalicus muscle, C6)

To lift the limb off the floor by flexing the elbow (musculocutaneous nerve, C6, C7).

Flexion of the carpus: median nerve (C8, T1)

Question 20

Explain Horner syndrome with brachial plexus avulsion

Answer 20

Avulsion of the ventral roots of T1 or of the T1 spinal nerve causes a miosis because of the interruption of the GVE preganglionic neuronal axons located there that provide sympathetic innervation to the eye. An elevated third eyelid and ptosis require interruption of the ventral roots of the T2 and T3 spinal cord segments.

Question 21

In which domestic animal does the radial nerve have no autonomous zone for the branches that provide cutaneous innervation

Answer 21

Horse

Question 22

Dysfunction of which nerve causes lateral deviation of the lip and nose in the horse?

Answer 22

CN VII, buccal branches

Question 23

Which muscles are medial and which lateral rotators of the shoulder joint?

Answer 23

• medial rotators (subscapularis and teres major muscles)
• lateral rotators (infraspinatus and teres minor muscles).

Question 24

Neuroanatomic diagnosis?

Answer 24

Lateral rotation of the shoulder, Medial displacement of the elbow. --> infraspinatus contracture A 2-­year-­old doberman pinscher that was struck by a vehicle and 1 month later was presented for a persistent abnormality in the use of the left thoracic limb. This dog sits with the characteristic posture of a dog with excessive lateral rotation of the shoulder, which results in medial displacement of the elbow. This is an example of the infraspinatus contracture that follows an injury to the muscle and the healing by fibrosis. Could also arise from a lesion in the spinal cord contained within the foramen of the C5 vertebra. This was likely the C6 spinal cord segment; the suprascapular nerve arises from the C6 and C7 spinal cord segments.

Question 25

What could cause a significant carpal overextension (palmigrade posture)

Answer 25

loss of the integrity of the palmar carpal ligaments. If all the nerves and muscles are removed from a thoracic limb specimen, the carpus cannot be manually forced into a palmigrade position as long as the palmar carpal ligaments are intact. These ligaments become stretched when the thoracic limb must bear more weight than usual, as when a young dog has a fracture in one thoracic limb and bears all its weight on the normal limb for a period of weeks. That normal limb slowly assumes a more palmigrade posture. Older dogs that are overweight often assume this carpal posture. Chronic neuromyopathies cause dogs that have lost the normal muscle strength necessary to support weight to assume a palmigrade posture. This clinical sign reflects the secondary loss of integrity of the palmar carpal ligaments and is not a sign of a specific neuromuscular disorder. A plantigrade posture in a pelvic limb has a very different pathogenesis;

Question 26

Which nerves are involved in the sensory innervation of the penis?

Answer 26

Skin of the penis: dorsal penis nerve (branch of pudendal n., S1-3) Skin of the prepuce: genitofemoral n. (ventral branches of L3-4) The distinction between sensation of the skin of the penis and the skin of the prepuce may be helpful in making a correct anatomic diagnosis in male dogs with diseases affecting the lumbar spinal cord.

Question 27

Which nerve deficit could cause a hyperflexion of the tarsus?

Answer 27

Tibial nerve (part of sciatic nerve). Neuronal cell bodies are in L7-S1 SCS.

Question 28

Which nerve is involved if there is an overflexion of the tarsus?

Answer 28

Tibial nerve (inability to flex it)

Question 29

Which nerve is involved if a dog is standing on the dorsum of his pelvic limb paw?

Answer 29

Fibular nerve

Question 30

Which nerve and muscle are involved in hip flexion?

Answer 30

Lumbar spinal nerves (ventral branches) -> psoas major muscle

Question 31

What causes the limb defomities contractures/arthrogryposis?

Answer 31

These joint abnormalities are the result of denervation atrophy in a young dog whose bones are growing in length. These limb deformities (contractures, arthrogryposis) result from the disparity in the normal growth of bones in the limbs and the abnormal shortening of the associated muscles. Denervation atrophy does not cause this in the adult dog.

Question 32

Which nerves provide cutaneous sensory innervation of the proximal medial thigh (1) and which to the craniolateral thigh (2)?

Answer 32

1) genitofemoral (L3, L4) 2) lateral cutaneous femoral (L3, L4)

Question 33

Which nerves are commonly damaged with pelvic fracture?

Answer 33

The sciatic nerve is commonly injured in pelvic trauma because it is formed by the L6 and L7 spinal nerve ventral branches that pass across the ventral surface of the sacroiliac joint, where they are at risk for injury by luxations. These two branches are joined by the ventral branch of S1 to form the sciatic nerve, which then courses across the dorsal surface of the body of the ilium where fractures are common. The obturator nerve courses on the medial surface of the ilium and is at risk for injury by these iliac fractures, but the slight sliding-­out of the limb laterally during weight bearing when the dog is walking on a slippery surface is probably not recognized. The femoral nerve is rarely affected by these pelvic fractures because it is never directly associated with bones of the pelvis in its course from the psoas major muscle, where it is formed primarily by the ventral branches of the L4 and L5 spinal nerves and enters the quadriceps femoris.

Question 34

Which nerve is affected? The limb is protracted by hip flexion and the ability to support weight, but the paw is often placed on its dorsal surface. The stifle flexors and the tarsal flexors and extensors are hypotonic.

Answer 34

Sciatic (predominantly fibular nerve) L6-S1

Question 35

Dysfunction of which nerve causes this stance in cows?

Answer 35

Tibial nerve (S1,2) The overflexed tarsus is the result of loss of the innervation to the tarsal extensors (gastrocnemius and superficial digital flexor muscles). The basis for the dorsal buckling of the metatarsophalangeal joints is not clearly understood but presumably represents the loss of the function of the digital flexors.

Question 36

How would the posture of a cow with fibular nerve dysfunction look like?

Answer 36

A ruminant with fibular nerve paralysis stands on the dorsal aspect of the digits because of loss of the function of the digital extensor muscles, but the posture of the metatarsophalangeal joints is normal.

Question 37

How can you differentiate a loss of sensation to the face (CN V) from loss of motor function (CN VII) clinically?

Answer 37

No palpebral reflex exists, but note the spontaneous blinking of the eyelids, which indicates normal facial nerve function. Stimulating the skin of the external ear canal tests multiple cranial and cervical spinal nerves and is not reliable for cranial nerve V. The ear movement supports normal facial nerve function.

Question 38

Describe the menace response, resting pupil size and PLR with a lesion affecting the R optic nerve?

Answer 38

OS menace normal, resting pupil normal, light in OS both constrict OD menace absent, resting pupile normal or mildly dilated, light in OD neither constricts

Question 39

Describe the menace response, resting pupil size and PLR with a lesion affecting the R CN III lesion?

Answer 39

OS: menace normal, resting pupil normal, light in OS only OS constricts OD: menace normal, resting pupil markedly dilated, light in OD only OS constricts

Question 40

Describe the menace response, resting pupil size and PLR with a lesion affecting the R retrobulbar space?

Answer 40

OS: menace normal, resting pupil normal, light in OS only OS constricts OD: menace absent, resting pupil dilated, light in OD neither constricts

Question 41

Describe the menace response, resting pupil size and PLR with a lesion affecting the R optic tract?

Answer 41

OS: menace reduced, normal pupil size, light in OS both constricts OD: mostly normal menace, normal pupil size, light in OD both constrict

Question 42

Describe the menace response, resting pupil size and PLR with a lesion affecting the R visual cortex?

Answer 42

OS: menace absent/reduced, normal pupil size and PLR (direct and indirect) OD: normal menace, normal pupil size and PLR

Question 43

Dysfunction of which CN is seen here. Menace response OU was normal.

Answer 43

CN III left. we see mydriasis OS, mild ptosis OS. Also to be expected, reduced adduction of the OS during physiologic nystagmus testing or resting latero-ventral strabism of OS complete GVE CN III deficit, and partial GSE (no strabism is seen)

Question 44

Why is the enophtalmos in Horner syndrome not strong/easily appreciated?

Answer 44

a marked enophthalmos is most commonly associated with atrophy of the muscles of mastication that form a significant portion of the border of the periorbita, and has nothing to do with Horner syndrome. With masticatory muscle atrophy, the eyeball sinks into the orbit, and as a result, the palpebral fissure is smaller and the third eyelid passively protrudes. These clinical signs may be mistaken for sympathetic paralysis, except that no miosis exists.

Question 45

What is seen here? This dog also exibited L ptosis, miosis and enophtalmos.

Answer 45

loss of their sympathetic innervation to the nasal mucosa resulting in a decreased airflow caused by vasodilation, causing increased tissue rigidity of the nasal mucosa and increased nasal gland secretion from disinhibition. The net effect may result in an accumulation of dried secretion, called crusts, within the naris

Question 46

What is seen here? This patient also has a drooped lip on the L side of the face.

Answer 46

A 9-year-old Cavalier King Charles spaniel with facial paralysis. There also is keratoconjunctivitis sicca and hyperkeratosis of the nasal planum secondary to a loss of parasympathetic general visceral efferent innervation to the lacrimal gland and nasal planum, respectively.

Question 47

Most reliable signs of Horner syndrome in cattle, sheep, and goats?

Answer 47

- Ptosis - palpable hyperthermia of the ear - (hypohydrosis/anhydrosis of planum nasolabiale)

Question 48

What is an unique clinical signs in horses with Horner syndrome?

Answer 48

sweating of the denervated area (usually in other animals it is hypo-/anhydrosis)

Question 49

Which signs of Horner syndrome are most easily recognised in horses?

Answer 49

sweating on the affected side (from tip of nose till 15 cm of the cervical region) ptosis decreased angle of eyelashes

Question 50

Which disease in horses causes bilateral Horner syndrome?

Answer 50

grass sickness

Question 51

What supplies the sympathetic ganglionic axons to the cervical spinal nerves from C2 through C6?

Answer 51

They are supplied by the vertebral nerve, which is a branch of the cervicothoracic ganglion that follows the vertebral artery into the transverse foramen of C6 and continues cranially through these foramina to C1

Question 52

Where is the lesion in horse with the following signs? smaller palpebral fissure, mild miosis, slightly elevated third eyelid, congested conjunctival vessels, decreased airflow from the ipsilateral naris, and sweating and hyperthermia in the head and cranial neck area plus sweating and hyperthermia of the entire ipsilateral side of the body.

Answer 52

Ipsilateral mesencephalon, pons, and medulla, C1 to T1 lateral funiculus: lateral tectotegmentospinal tract (upper motor neuron for sympathetic lower motor neuron)

Question 53

DDs for a mydriatic pupil

Answer 53

1) ispilateral CN III lesion 2) ipilateral marked retina/CN II lesion 3) iris atrophy (age related) 4) glaucoma 5) topical mydriatics 6) ingestion of atropine (belladona plant) 7) lesion of cerebellar nuclei (ipsi or contralateral)

Question 54

DDs for a miotic pupil?

Answer 54

1) GVE sympathetic ipsilateral 2) ipsilateral swelling of the iris (with iritis) 3) oculopuppilary reflex (discomfort activates CN V ophtalmic branch sensory fibers and CN III efferents cause miosis) 4) opioids

Question 55

Why do we see a protrusion of the 3. eyelid in animals with Horner syndrome?

Answer 55

loss of the GVE sympathetic innervation of the orbitalis smooth muscle (that normally keeps the 3rd eyelid retracted)

Question 56

DDs for protrusion of the 3rd eyelid

Answer 56

1) Horner syndrome 2) tetanus (horses) - brief rapid protrusions 3) with facial paralysis when menacing the animal 4) dehydration (common in cats w/ systemic disease) 5) cachexia (bilateral) 6) dysautonomia (bilateral) 7) severe atrophy of muscles of mastication

Question 57

Which neuro signs are expected with a lesion of the pyramidal system in domestic animals

Answer 57

No gait changes on level surface contralateral GP deficits (postural reactions) Visual deficits (in primates contralateral paralysis of the voluntary muscles)

Question 58

The role of the cross extensor reflex in neuro-localisation?

Answer 58

The crossed extensor reflex is another form of release from inhibition caused by a UMN disorder. The crossed extensor reflex is normal in a standing animal and is used to support weight when the weight is taken off the opposite limb. It is abnormal when present in a recumbent animal but is easily confused with voluntary movement if the animal is able to struggle to move away from a noxious stimulus. It is best observed in a patient that has a serious enough UMN lesion to result in the absence of any voluntary movement. This abnormal reflex is seen when a mild noxious stimulus causes flexion of the limb stimulated and extension of the opposite limb or crossed extension.

Question 59

What is a mass reflex?

Answer 59

In severely disinhibited LMNs of the lumbar intumescence and of the sacral and caudal spinal cord segments, a single noxious stimulus may induce what is referred to as a mass reflex. After a single noxious stimulus is applied to a digit, that limb or both pelvic limbs repeatedly flex three or four times, and the tail may flex without further stimuli. A single noxious stimulus to the tail may elicit repeated tail and pelvic limb flexion and even urination and defecation.

Question 60

Explain why the clinical signs with decerebrate rigidity occur

Answer 60

When the brainstem is transected between the rostral and caudal colliculi of the midbrain, an uninhibited extensor tonus of the antigravity muscles is produced. The head and neck are markedly extended dorsally, which is known as opisthotonos, and all four limbs in the quadruped are rigidly extended. This is explained as a release mechanism. The myotatic reflexes involving the extensor muscle LMNs have been released from the effects of the descending inhibitory UMN pathways. The facilitatory centers in the pontomedullary reticular formation and the vestibular system can function autonomously, whereas the inhibitory centers in the pontomedullary reticular formation require continual input from the cerebral cortex, basal nuclei, and cerebellum to function. This experimental midbrain transection removes all the prosencephalic input, causing the imbalance that is observed as a release phenomenon or decerebrate rigidity. The alpha and gamma LMNs that innervate extensor muscles have been released from the influence of the caudally projecting UMN spinal cord tracts. The vestibulospinal tracts also contribute their facilitatory influence to that of the reticulospinal tracts.

Question 61

What is "overreaching" or "floating" thoracic limb gait?

Answer 61

A common clinical sign of dysfunction of the UMN and GP systems in the cervical spinal cord is a longer thoracic limb stride that hesitates slightly before the paw or hoof lands on the ground surface --> reflects a cervical SC white matter lesion

Question 62

Difference between dermatome, cutaneous area and autonomous area?

Answer 62

Dermatome: the area of skin innervated by a spinal nerve Cutaneous area: the portion of the surface of the body innervated by one GSA specific (named) nerve Autonomous zone: the portion of the body surface that is innervated purely by only one specific spinal or named nerve

Question 63

Why are vestibular signs possible with high cervical lesions?

Answer 63

interruption of the spinovestibular tracts that carry GP impulses from the first three cervical spinal nerves, which are important in the orientation of the head to the neck (first 2-3 SCS)

Question 64

Neuro basis of Schiff-Sherrington

Answer 64

The disinhibition of the thoracic limbs is the result of a sudden loss of the axons in a long interneuronal pathway that originates from neuronal cell bodies primarily in the gray matter of the L1 to L5 spinal cord segments. These interneurons are referred to as border cells because they are located in the dorsolateral border of the ventral gray column of the lumbar spinal cord segments. Their axons course cranially in the fasciculus proprius and terminate by synapsing on thoracic limb extensor LMNs in the cervical intumescence. Their normal function is to inhibit these extensor motor neurons. The purpose of this pathway is to synchronize extension of the pelvic limbs with flexion of the thoracic limbs while walking or running. Without this synchronization the patient may extend both thoracic and pelvic limbs on one side while running and fall over. This extensor release phenomenon is observed only with peracute severe lesions, and it spontaneously resolves in about 10 to 14 days. The presence of Schiff-Sherrington syndrome indicates a severe lesion and a guarded prognosis but does not indicate that recovery cannot occur. Occasionally Schiff-Sherrington syndrome is seen in patients with lesions involving the cranial component of the lumbar intumescence, but this is far less common than disorders involving the T3–L3 spinal cord segments. This likely represents the greater frequency of these severe lesions in the TL region rather than in the cranial lumbar region of the spinal cord.

Question 65

Neuro basis of spinal shock

Answer 65

in severe peracute transverse thoracolumbar spinal cord lesions in which Schiff-Sherrington syndrome is present, severe pelvic limb hypotonia usually is present. If the patient is examined within a few hours of the onset of the paraplegia, pelvic limb tone and spinal reflexes may be absent or very depressed. These paradoxic LMN-like pelvic limb signs in a patient with a UMN pathway interruption represent what is called spinal shock. n primates spinal shock causes areflexia and atonia for 2 to 3 weeks. In domestic animals the areflexia (primarily the patellar reflex) is observed for only a few hours after the onset of the lesion, but the hypotonia and a depressed withdrawal reflex may persist for 10 to 14 days, when it is replaced by normal tone at first and then by hypertonia. The reason a UMN lesion causes LMN signs is poorly understood. One explanation is that the sudden loss of the UMN synapses, indirectly via interneurons or directly on the dendritic zones or the cell bodies of the alpha motor neurons, causes such a disruption to that LMN cell body that it cannot function for a variable period. In primates more of these UMN pyramidal system synapses are directly on the LMN, which may explain the difference in reaction among species that is observed here. Some studies have found an excessive accumulation of the inhibitory neurotransmitter glycine in the lumbar intumescence in these patients.The basis for the release of glycine is unknown.

Question 66

Which cranial nerve innervates the cutaneus colli muscle? (equine neuro exam, cervicofacial reflex)

Answer 66

CN VII

Question 67

Sensory and motor component of the withdrawal reflex in large animals

Answer 67

Pelvic limbs - sensory: sciatic nerve, L6, S1, S1 SCS - motor: sciatic nerve, L6, S1, S1 SCS + flexion of the hip (femoral nerve + all lumbar SCS) Thoracic limbs: - sensory: median and ulnar nerve (horse), median, ulnar and radial nerve (other large animals), C6-T2 SCS - motor: radial, axillary, musculocutanous, median and ulnar nerves, SCS C6-T2

Question 68

Lesion localisation based on the area of sweating in the horse

Answer 68

1) Unilateral head and body: ispilateral lateral funiculus of the cervical spinal cord (causes UMN paralysis of the sympathetic innervation) 2) focal area of sweating: ipsilateral focal lesion between T1-L4 SCS intermediate grey horn

Question 69

Mayhew grading system for horses with cervical SC disease

Answer 69

- Grade 0: Normal strength and coordination - Grade 1: Normal gait when walking straight; slight deficit on walking in tight circles or walking with the neck and head extended or when pulled by the tail (sway) - Grade 2: Mild spastic tetraparesis and ataxia at all times and especially during the manipulations described for grade 1 - Grade 3: Marked spastic tetraparesis and ataxia with a tendency to buckle and fall on vigorous circling, backing, or swaying - Grade 4: Spontaneous stumbling, tripping, and falling - Grade 5: Recumbent, unable to stand

Question 70

What is the “stair test”?

Answer 70

Make a patient walk up and down stairs. - an excellent way to observe the effect of mild clinical signs of cerebellar dysfunction in dogs. - when the cerebellar ataxia is mild or difficult to recognize in a short-limbed breed such as the Scottish terrier, examining the gait as the patient ascends or descends stairs is helpful. This action will markedly exacerbate the clinical signs of cerebellar dysfunction and frequently cause patients to fall, which often makes them reluctant to go up or down stairs

Question 71

Explain decerebellate posture

Answer 71

The rostral lobe of the cerebellum is especially inhibitory to the stretch reflex mechanism of antigravity muscles (extensor muscle tone). Lesions in this area may result in opisthotonos with rigidly extended thoracic limbs. In some instances the pelvic limbs may be flexed cranially ventral to the trunk by hypertonia of the hypaxial muscles that flex the hips. The combination of extended neck and thoracic limbs with flexed hips is called a decerebellate posture. If the rostral lobe lesion involves the ventral lobules, the pelvic limbs may be extended away from the trunk, similar to the thoracic limbs, as is seen in a decerebrate posture.

Question 72

Neurological signs with thalamic disease

Answer 72

* Lateral geniculate nucleus: contralateral loss of vision, hemianopsia * Medial geniculate nucleus: possibly vestibular ataxia. Occasionally, thalamic lesions result in various combinations of vestibular ataxia, head tilt, and abnormal nystagmus, which are most often, but not always, contralateral to the side of the lesion. The most common lesion to do this in our experience is a vascular compromise leading to ischemia or infarction. * Ventral caudal lateral nucleus: contralateral hypalgesia of the neck, trunk, and limbs and contralateral loss of proprioception in the limbs (delayed to absent postural reactions) * Ventral caudal medial nucleus: contralateral hypalgesia of the head (typically observed as a reduced or absent response to stimulating the mucosa of the nasal septum with the closed end of a hemostat) * Ventral lateral nucleus: possibly hypermetric ataxia, cerebellar ataxia * Ventral rostral nucleus: possible contralateral delayed to absent postural reactions from loss of upper motor neuron (UMN) circuitry * limbic system: behavioural changes like pacing, circling, aggression, unresponsiveness to the owner, and loss of trained habits * reticular system: reduced level of consciousness (obtundation to coma) * seizures * pleurotothonus (adversive syndrome) ispilateral to lesion * thalamic pain syndrome

Question 73

Breathing irregularities seen with different brain diseases?

Answer 73

- Cheyne-Stokes respirations may occur with severe bilateral cerebral disease, diencephalic disease, or both. This abnormal breathing pattern is characterized by gradually increasing and decreasing tidal volume interspersed with periods of apnea and is an indication of increasing intracranial pressure. - central neurogenic hyperventilation - mesencephalic lesions may cause a regular sustained hyperventilation. - ataxic breathing - more caudal brainstem lesions produce bizarre abnormal breathing patterns, which usually precedes cardiac arrest.

Question 74

How can different ataxias be accentuated?

Answer 74

GP tetra-ataxia: by holding the head and neck extended as the patient is led, especially in horses Vestibular ataxia: by blindfolding the patient Cerebellar ataxia: staircase test

Question 75

How can you use the hopping postural test to differentiate subtle changes between LMN and UMN paresis of the limbs?

Answer 75

- patients with LMN disease that still have some voluntary movements hop or circle rapidly if their weight is supported because their GP is unaffected. This observation may help distinguish between subtle UMN and LMN paresis. When presented with a patient with suspected LMN paresis, we hop the patient with and without supporting all the weight on the affected limb or limbs. - The patient with LMN paresis should know exactly where the limb is located during these postural reactions. de Lahunta

Question 76

A patient has normal menace responses. Anisocoria is present with the pupil in OD widely dilated. Light directed into OD causes the pupil to constrict only in OS. Light directed into OS causes only the OS pupil to constrict. NAL?

Answer 76

Anatomic diagnosis: Right oculomotor nerve general visceral efferent (GVE) component, ciliary ganglion, ciliary nerves Be aware that this reaction may be the first clinical sign of an extraparenchymal mass lesion ventral to the diencephalon compressing the oculomotor nerve and causing a loss of function of the GVE preganglionic neurons, which may precede the loss of function in the GSE neurons with extraparenchymal lesions at this location. This disparity between the altered pupil size without ptosis or strabismus is useful in making an anatomic diagnosis of the different components of the oculomotor nerve.

Question 77

A patient has no menace response in OS with a normal palpebral reflex. No anisocoria is observed. Light directed into OS causes no response OU. Light directed into OD causes a normal response OU. When swinging the light from OD where the pupil is constricted back to OS, the OS pupil that was constricted from the stimulation of OD is now dilating back to its original size. This asymmetry is repeated while swinging the light back and forth between the two eyes. When OD is covered with the hand, the OS pupil fully dilates. NAL?

Answer 77

Anatomic diagnosis: OS retina or left optic nerve In most cases with this anatomic diagnosis, room light entering the normal eye is sufficient to keep the pupil in the affected eye constricted. Occasionally in room light, the pupil on the affected side will be slightly larger than the pupil in the unaffected side.

Question 78

A patient has no menace response OD with a normal palpebral reflex. Anisocoria is present with the OD pupil widely dilated. Light directed into OD causes no response OU. Light directed into OS causes only the OS pupil to constrict. NAL?

Answer 78

Anatomic diagnosis: Eyeball OD, right optic nerve and the GVE neurons of the right oculomotor nerve, ciliary ganglion, ciliary nerves A retrobulbar neoplasm or abscess might produce this result. A decrease in the excursion of the OD may also be observed when testing physiologic nystagmus.

Question 79

A patient acts blind and has no menace response OU with normal palpebral reflexes. In room light, the pupils are mildly dilated. Light directed into OS causes the pupils to constrict OU. Light directed into OD causes the pupils to constrict OU. This dog’s sensorium is normal. NAL?

Answer 79

Anatomic diagnosis: Both eyeballs, optic nerves, optic chiasm, or optic tracts Patients with lesions in the retina (retinal degeneration, sudden acquired retinal degeneration) or optic nerves (optic neuritis) OU often lose their vision and are clinically blind but still have light-responsive pupils when a bright light is directed into the eyes. However, room light is insufficient to cause normal constriction, and the pupils appear mildly dilated. This response can be explained by the disease process sparing the retinal neurons involved with these light responses or, more likely, with progressive loss of function of retinal neurons, the threshold for loss of vision is lower than that for pupillary constriction to light. In other words, the pupillary light reflex neurons are the last to lose function when lesions disrupt the retina or optic nerve.

Question 80

Which nerve is responsible for the adduction and which for the abduction of the eyeball?

Answer 80

adduction (medial rectus, cranial nerve III) abduction (lateral rectus, cranial nerve VI)

Question 81

Sweating in horses to localise a sympathetic lesion

Answer 81

1. Lesions in the region of the guttural pouch and cranial cervical ganglion will result in sweating of the face (most prominent at the base of the ear) and the cranial neck down to the level of C2. 2. Lesions further down the neck involving the sympathetic trunk may result in sweating of the face and the neck extending down to the level of C3 to C4 3. Lesions in the thoracic inlet can result in this sweating extending down to the level of the shoulder. 4. Although extremely rare, lesions of the spinal cord involving the descending sympathetic pathway can result in Horner syndrome and sweating of the whole side of the body ipsilateral to the lesion. (VCNA)

Question 82

Tail pull test in horses to differentiate UMN from LMN paresis

Answer 82

1) standing tail pull: this initiates an extensor (patellar, quadriceps) reflex, and a poor response suggests a lower motor neuron lesion at the level of L3-5, and therefore, the patient will demonstrate weakness while standing still (hypotonia). A patient with paresis due to an UMN lesion, for example, cervical spinal cord disease, will not show paresis when the tail is pulled when standing. 2) walking tail pull: observe the placement of the limbs and whether you can pull the horse toward you—a horse with a cervical lesion and thus damage to UMN axons may be easily pulled to the side when walking, particularly if the lesion is acute.

Question 83

Tests to reveal ataxia in horses?

Answer 83

1) circling: wide circles, tight circles, serpentines; look for low foot flight or dragging of toes (hypometria, flexor paresis), overreaching (hypermetria), excessive circumduction of particularly the outside pelvic limb when turning, buckling of limbs. To detect milder degrees of ataxia, additional postural maneuvers may need to be performed, which include the following: 1. Elevating the head while walking the animal on a flat and on a sloping surface; ataxic horses can find this difficult, and the thoracic limbs often overreach, particularly when the head is elevated while walking down a slope 2. Turning tightly when stopping abruptly from a trot 3. Backing

Question 84

Where is the lesion likely located if a horse can adopt a "dog sitting" position?

Answer 84

Caudal to T2

Question 85

Autonomous zones for sensory branches of major spinal nerves of the horse limbs

Answer 85

Question 86

Which animals have a normally slightly weaker PLR?

Answer 86

Excited animals Farm animals, horses (also weaker indirect PLR due to more fibers crossing in optic chiasm)