Small Animal Neurology Continued

Question 1

a sudden loss of muscle tone

Answer 1

atonic seizures

Question 2

a seizure lasting more than 5 minutes

Answer 2

Status epilepticus

Question 3

two or more seizures within a 24 hour period

Answer 3

Cluster seizure

Question 4

sudden brief involuntary contraction of a muscle or group of muscles

Answer 4

myoclonic seizure

Question 5

sustained increase in muscle contraction followed by repetitively involuntary muscle contractions at a frequency of 2-3 seconds

Answer 5

Tonic Clonic seizures

Question 6

tonic clonic seizures are

Answer 6

sustained increase in muscle contraction followed by repetitively involuntary muscle contractions at a frequency of 2-3 seconds

Question 7

Ketamine can be considered for seizure control after 30 minutes of sustained seizure activity.

Q. True or False. This is because NMDA receptors are down regulated at this point.

Answer 7

False-

After 30 minutes of seizure activity, an alteration in the GABA A receptor subunit expression occurs with NMDA receptor ACTIVATION (which is the major mediator of excitotoxicity).

Question 8

A 10 year old female entire Labrador presents with a history of 2 seizures within the last 2 weeks. The owners report that the patient is normal between the seizures. On examination you note the following:

Clinical examination was unremarkable

Neurological examination:

Cranial nerve examination

Menace - absent on the right, normal on the left
Nasal mucosal stimulation - absent on the right, normal on the left
Conscious proprioception

Reduced on the right thoracic and pelvic limbs, normal on the left
Segmental spinal reflexes were within normal limits

Q. What is your neurolocalisation?

Answer 8

Left forebrain - likely neoplasia

Question 9

A 4 month old Boston Terrier presents with a history of circling to the left, difficulties learning commands and pacing. These signs had been present since the patient had been in the owners possession, without progression.

Clinical examination revealed a domed shaped skull but was otherwise normal.

Neurological examination revealed a tendency to pace and circle to the left.

Cranial nerve examination:

Bilaterally reduced menace response
Bilateral lateral/ventrolateral strabismus
Proprioception and segmental spinal reflexes were within normal limits

Q. What is your most likely differential diagnosis?

Answer 9

Hydrocephalus

Question 10

Your patient has lumbosacral stenosis due to a disc herniation at L7-S1, causing paraparesis and urinary dysfunction. On your examination, you palpate a very large, flaccid bladder.

Damage to which nerve is responsible for the large, flaccid bladder?

Answer 10

Pelvic Nerve

Question 11

You diagnosed Andrew’s dog, Charlie, with an L4-S3 myelopathy. You just performed decompressive surgery for his LS stenosis. Charlie has a huge flaccid bladder, and dribbles urine constantly.

Which medication would you consider most?

Answer 11

Bethanechol

Bethanechol is a great choice for a LMN bladder, to provide tone and strength to the detrusor muscle, and promote bladder emptying. For safety, you also need prazosin to relax outflow sphincters.

Question 12

Mary’s dachshund, Rose, just had a hemilaminectomy to decompress a T12-T13 disc herniation. Rose is ready to go home otherwise, but her bladder is very difficult to express.

What do you recommend?

Answer 12

Prazosin/Phenoxybenzamine

This is our mainstay of UMN bladder management, to relax internal sphincters. Where expression is extremely difficult, it can be combined with diazepam to also relax the external urethral sphincter.

Question 13

Which component of the autonomic nervous system is predominantly responsible for the filling phase of micturition?

Answer 13

Sympathetic system

Question 14

In a patient with a T3-L3 lesion, what would you expect to find in terms of detrusor and urethral sphincter tone?

Answer 14

Increase tone to detrusor muscle and increase to urethral sphincters

Question 15

A 6 year old Pug presents with a 2 week history of tonic-clonic seizures. On presentation, clinical examination is normal. Neurological examination reveals the following:

Head tilt to the left. Tendency to circle to the right.

Cranial nerves:

Menace response - absent on the left, normal on right
Nasal mucosal stimulation - absent on the left, normal on the right
Proprioception

Reduced on left thoracic and pelvic limbs, normal on the right
Segmental spinal reflexes within normal limits.

Q. What are your TWO most likely diagnoses?

Answer 15

Meningoencephalitis of unknown origin

Lymphoma

Question 16

In the 6 year old Pug described above. You perform blood work which was essentially unremarkable, and advanced imaging and CSF analysis which lead to a diagnosis of Meningoencephalitis of unknown origin.

Q. What medication would you advise initially?

Answer 16

1) Prednisolone +/- cytarabine

2) Phenobarbitone

Question 17

Q. True or False. Steroid Responsive Meningitis Arteritis (SRMA), is commonly associated with neurological deficits in its acute form.

Answer 17

False

Although SRMA can be associated with neurological deficits, this is in its chronic form. In acute SRMA (which is most common), clinical signs are usually limited to neck pain, pyrexia and lethargy.

Question 18

Which of the tests likely offer the greatest predictor for survival following head trauma?

Answer 18

Modified Glasgow Coma Score (MGCS)

The MGCS predicts the probability of survival in the first 48 hrs after head trauma with 50% probability in a patient with a score of 8.

MRI and CT do not have a lot of prognostic value. They should not be the primary decider for when to euthanize. MRI requires general anesthesia and should only be performed when clinically warranted in head trauma (i.e. declining neurologic status, signs not explained on CT, and/or no improvement after 48-72 hours).

CSF collection has little prognostic value, requires general anesthesia, significant manipulation of the head/neck/spine, and usually has no diagnostic value (the diagnosis was made on history, exam, etc.). Increased ICP is also a risk factor for brain herniation during CSF collection.

CBC and chemistry are important in decision making throughout head trauma management, but alone, they do not predict survival.

Question 19

A patient just presented to your hospital after being kicked in the head by a donkey. There are deep abrasions in the skin over the skull. Based on definitive evidence in the vital parameters and on your neurologic exam, you are very concerned about rising intracranial pressure (ICP). Resuscitative efforts, including fluid therapy, have already begun and a positive response is noted so far. However, the patient is hypovolemic, hypotensive, and hypothermic.

How would you like to address the rising ICP?

Answer 19

Give hypertonic saline 3 ml/kg IV

If you are worried about rising ICP, you must give either mannitol or hypertonic saline. In the patient of this example, hypertonic saline is the fluid of choice, since it would be contraindicated to give mannitol in the presence of hypotension and hypovolemia. A hemodynamically unstable patient – such as this guy – should not receive mannitol as this will exacerbate poor tissue perfusion.

Since there are already signs that ICP is rising, NOW is the time to intervene to avoid herniation of the brain. If the situation was different and you are questioning whether or not a patient is neurologic from primary CNS causes or if they are neurologic secondary to systemic derangements, waiting until the patient is resuscitated is advisable since most hypovolemic animals will have deficits that resolve once euhydrated. However, you are not questioning if this patient has a primary CNS problem. You know it does because there was witnessed trauma and you have definitive support for rising ICP. NOW is the time to intervene to avoid herniation of the brain.

Steroids are contraindicated in head trauma (and that is an outrageously high dose).

Steroids are contraindicated in head trauma.

Question 20

According to the Monroe-Kelly Doctrine (aka intracranial compliance) the skull only has enough room for three types of tissue: brain, CSF, and

Answer 20

blood

Question 21

A 2 y/o MN DSH presents to you 20 minutes after being bit on the head by a Golden Retriever puppy.

T: 98.1F, P: 100 bpm, R: 40 bpm; BP: 90 mmHg

There is marked anisocoria with normal PLRs; remaining cranial nerves are normal. He is non-ambulatory with severe vestibular ataxia seems very quiet and disoriented but has a normal sensorium otherwise. You feel bony crepitus on the dorsum of the skull consistent with bone fragments.

What do you want to do first?

Answer 21

Resuscitate and re-evaluate

Question 22

What is a contraindication for mannitol?

Answer 22

Hyponatremia

Any electrolyte abnormalities, hypovolemic, hypotension, dehydration and any derangement causing hypovolemic shock are clear contraindications for mannitol.

Cardiac and kidney insufficiency are not contraindications (unless there is heart or kidney failure). But these organ’s function should be monitored closely and/or the dose of mannitol titrated. Usually patients with mild or stable renal or cardiac disease tolerate mannitol well.

Mannitol was once thought to worsen hemorrhage and at one time was contraindicated. This has not been substantiated in more recent studies and is no longer a contraindication.

Question 23

Which of the following is not a feature of pure cerebellar disease?
A) Tetraparesis
B) Cranial nerve deficits
C) Vestibular ataxia
D) Spasticity

Answer 23

A) Tetraparesis

The cerebellum does not initiate motor. Therefore, a cerebellar disorder should not cause any deficit in motor initiation (i.e. no paresis/paralysis).

An ipsilateral menace deficit could be seen with cerebellar lesions.

Spasticity is characteristic of UMN dysfunction, in which the cerebellum plays a role. Often dysmetria and intention tremors would accompany the spacticity.

A portion of the cerebellum plays a pivotal role in the vestibular system & normal balance. In fact, an unambiguous collection of vestibular signs, called paradoxical vestibular, indicate that not only is there a problem with vestibular system, but more specifically, the problem is in the cerebellum.

Question 24

A 5 y/o MN mix breed dog presents with acute onset, slowly progressive chronic cerebellar signs. Which differential diagnosis would you eliminate from your list?

Answer 24

An infarct would have an acute onset but should improve over time. Thus, an infarct does not fit with the history provided, of slowly progressive signs. The others could stay on your differential list.

Question 25

You are presented a 4-week-old M Miniature Schnauzer with moderate cerebellar signs (intention tremors, truncal sway, dysmetria). These signs have been present since birth, though the breeder feels like they are more apparent now than before. You refer for an MRI and the only abnormal finding is a small cerebellum; CSF was normal. What’s your top differential?

Answer 25

Cerebellar hypoplasia This dog has cerebellar hypoplasia: abnormal at birth, overall non-progressive (as the animal starts to move around more with age, the signs will be more apparent, but not necessarily worse), and a small cerebellum on imaging all fit. Although cerebellar hypoplasia can be due to infectious agents or drugs/toxins, the infection/drug exposure usually occurred in-utero and would not be ongoing. Dogs with cerebellar abiotrophy are born normal, and like most degenerative disorders, their signs progress over time. Though toxicity is more common in younger animals, 4-weeks might be a little extreme – the dog can barely crawl around! Most toxins that would affect the cerebellum also cause generalized tremor syndromes (e.g. mycotoxins, pyrethrins). This dog has only intention tremors which are defined as tremors that only occur with initiation of an activity, i.e. intent to perform a task. They are confined to the head/neck regions. Metronidazole toxicity could cause cerebellar signs, but toxicity usually resolves within 24-48h of stopping this medication. This would not cause a small cerebellar size. Further the dog would have been born normal. Cerebellitis, or broadly inflammation of the cerebellum, can be secondary to infection (Neospora, Distemper virus, FIP, others) or idiopathic/autoimmune (GME, Idiopathic generalized tremor syndrome/White Shaker syndrome) causes. This would not cause a small cerebellum and typically these dogs are older than the dog in this example. Lastly, they are born normal and usually have a pleocytosis (increased WBC and protein) on CSF analysis.

Question 26

T/F: The cerebellum initiates movement; the cerebrum coordinates it.

Answer 26

False: The cerebellum is a regulator not initiator of movement The initiators of motor are the cerebrum and (mostly) brainstem.

Question 27

T/F: Tremors that occur with intent and are restricted to the head and neck region, localize to the cerebellum or its tracts.

Answer 27

True

Question 28

Which of the following is NOT a hallmark sign of dysfunction of the motor unit? A) Myalgia B) Reduced muscle tone C) Reduced spinal reflexes D) Muscle atrophy

Answer 28

A) Myalgia

Question 29

A patient with episodic weakness, improving with rest, is most likely to be suffering from which TYPE of neuromuscular disease? A) Myopathy B) Neuropathy C) Junctionopathy

Answer 29

Junctionopathy

Question 30

What is electromyography (EMG) used to test?

Answer 30

The electrical activity in MUSCLE

Question 31

A 4 year old cocker spaniel presents to you with right facial nerve paralysis, a right head tilt, and nystagmus, fast phase to the left. There are no other neurological signs (no cranial nerve deficits, and no proprioceptive deficits). The patient is otherwise normal. Q. True or False. The combination of right facial nerve paralysis and right vestibular signs, without other deficits, makes peripheral disease more likely.

Answer 31

True. Without other signs of brainstem disease, the combination of unilateral facial nerve and vestibulocochlear nerve signs, makes peripheral disease more likely.

Question 32

Results in bilateral paresis and atrophy of masticatory muscles and bilateral dropped jaw

Answer 32

Idiopathic trigeminal neuropathy

Question 33

Results in acute onset muscle weakness and cervical ventroflexion more common in cats than in dogs

Answer 33

Hypokalemic neuromyopathy

Question 34

results in bilateral masticatory muscle atrophy and trismus (inability to open the jaw)

Answer 34

Masticatory Muscle Atrophy

Question 35

Results in acute onset tetraparesis with concurrent GI signs

Answer 35

Botulism

Question 36

Results in acute onset flaccid paralysis patients retain their tail wag more common in dogs than cats

Answer 36

Acute Polyradiculoneuritis

Question 37

What are the 3 parts of the brainstem

Answer 37

1) Midbrain 2) Pons 3) Medulla

Question 38

What are the clinical signs of damage to the brainstem

Answer 38

1) General proprioceptive ataxia 2) Postural reaction deficits (ipsilateral) 3) UMN paresis (hemi or tetra) 4) Change in mentation if ARAS affected 5) +/- vestibular signs *Looks like cervical myelopathy +/- cranial nerve deficits

Question 39

What is the peripheral vestibular system

Answer 39

the vestibulocochlear nerve (CN VIII)

Question 40

What is in the central vestibular system

Answer 40

1) Vestibular nuclei (8) and the axonal projections to the cerebellum 2) Extraocular nuclei 3) Spinal cord

Question 41

T/F: there might be mentation change with brainstem diseases

Answer 41

True- ARAS (ascending reticular activating system) runs through the brainstem, thalamus, and to cerebral hemispheres

Question 42

What are the signs of vestibular disease

Answer 42

1) Ataxia- lean, list, fall or roll, loss of balance 2) Head tilt 3) Circle 4) Hemiparesis/postural reaction deficits- with central disease ONLY 5) Nystagmus 6) Strabismus "forced" usually ventral or ventrolateral 7) Horner syndrome- sympathetic trunk runs near bulla 8) Facial paresis of CN VII - can be seen with peripheral or central

Question 43

How do you distinguish central vestibular disease from peripheral vestibular disease

Answer 43

Central has hemiparesis/postural reaction deficits Central disease can have a vertical nystagmus

Question 44

From the input from the haircells in the ear, where is that sensory information integrated?

Answer 44

1) Sensory information travels up the vestibulocochlear nerve 2) Travels to vestibular nuclei 3) Information is processed and sent to a) Forebrain b) Cerebellum c) Extraocular Muscles- physiological nystagmus d) Spinal Cord - extensor and flexor muscles

Question 45

What are the 4 places that information from the vestibulocochlear nerve can travel to once it is at the vestibular nuclei

Answer 45

1) Forebrain 2) Cerebellum 3) Extraocular muscles 4) Spinal cord

Question 46

The fast phase of the nystagmus is always **

Answer 46

away from the lesion

Question 47

What is seen with nystagmus in peripheral vestibular disease

Answer 47

-Horizontal or rotary -Fast phase always away from the lesion -Does not change fast phase direction with position changes

Question 48

What is seen with nystagmus in central vestibular disease

Answer 48

-Horizontal, rotary, or vertical -May change +/- with position changes

Question 49

What kind of nystagmus is seen with peripheral vestibular disease

Answer 49

Horizontal or rotary with fast phase always away from the lesion

Question 50

What kind of nystagmus is seen with central vestibular disease

Answer 50

a horizontal, rotary, or VERTICAL nystagmus that may change with position changes

Question 51

T/F: With peripheral vestibular disease, the fast phase is changed with position changes

Answer 51

False- it does not change fast phase direction with positional changes

Question 52

a vision disorder that causes the eyes to be misaligned when looking at an object.

Answer 52

strabismus

Question 53

What strabismus is usually seen with vestibular disease

Answer 53

usually ventral or ventrolateral forced because of the head tilt

Question 54

what syndrome might be seen with vestibular disease

Answer 54

Horner Syndrome -Sympathetic trunk runs near bulla -Can be seen with peripheral vestibular disease

Question 55

Why is horner's syndrome seen sometimes with vestibular disease

Answer 55

sympathetic trunk runs near the bulla can be seen with peripheral vestibular disease

Question 56

What cranial nerve deficits can also been seen with peripheral or central vestibular disease

Answer 56

Facial paresis/paralysis (CN VII)

Question 57

If there is right vestibular dysfunction there is head tilt in what direction

Answer 57

toward the site of the lesion (right side) due to imbalance of the action potentials

Question 58

if there is left vestibular dysfunction, there is a head tilt in what direction

Answer 58

toward the site of the lesion (left side) due to imbalance of action potentials

Question 59

The cerebellum ______ the vestibular system

Answer 59

inhibits

Question 60

What is paradoxical vestibular disease

Answer 60

normally the cerebellum inhibits vestibular system so if there is a lesion in the cerebellum there are more action potentials on the lesion side *Inhibitory cerebellar efferent destroyed on left side -> leading to head tilt away from the lesion nystagmus towards the lesion ipsilateral UCP deficits Head tilt away falling/leaning away fast phase nystagmus towards postural reaction deficits on same side of lesion (only reliable way to localized)

Question 61

How do you distinguish vestibular disease from paradoxical vestibular disease

Answer 61

the only clue is your postural reactions Always will be on the same side of the lesion

Question 62

With Paradoxical Vestibular Disease there is: Head tilt ____ lesion Falling/Leaning ____ lesion fast phase nystagmus _____ Postural reaction deficits on ______ side of lesion

Answer 62

Head tilt away from lesion Falling/Leaning away from lesion fast phase nystagmus toward lesion Postural reaction deficits on same side of lesion

Question 63

What causes paradoxical vestibular disease

Answer 63

there is cerebellar involvement - lack of inhibition 1) Caudal cerebellar peduncle 2) Flocculonodular lobe

Question 64

What kinds of nystagmus are seen with paradoxical vestibular disease

Answer 64

Horizontal, rotary, vertical

Question 65

With paradoxical vestibular disease, the fast phase of the nystagmus is

Answer 65

towards the lesion

Question 66

With peripheral or central vestibular disease, the fast phase of the nystagmus is

Answer 66

away from the lesion

Question 67

With paradoxical vestibular disease, the head tilt is

Answer 67

away from the lesion

Question 68

With paradoxical vestibular disease, the are postural reaction deficits

Answer 68

on the same side of the lesion

Question 69

Are there postural reaction deficits with peripheral vestibular disease

Answer 69

NO

Question 70

Are there postural reaction deficits with central vestibular disease

Answer 70

yes- always on the side of the lesion

Question 71

What cranial nerve deficits is seen with peripheral vestibular disease

Answer 71

CN VIII +/- VII

Question 72

What cranial nerve deficits is seen with central vestibular disease

Answer 72

V-VIII, IX, X, XII

Question 73

With paradoxical vestibular disease, what cranial nerve deficits are seen

Answer 73

There are none

Question 74

With peripheral vestibular disease, the strabismus is _______ to the lesion

Answer 74

ipsilateral

Question 75

What might cause peripheral vestibular disease

Answer 75

-Otitis media/ interna -Idiopathic vestibular disease -Congenital vestibular diseases -Hypothyroidism -Feline inflammatory polyps -Aural neoplasia -Trauma -Toxic (aminoglycosides)

Question 76

How do you treat otitis interna

Answer 76

1) Prednisone for 3-4 days 2) Sysyemic antibiotics- Clavamox, Fluoroquinolones, Imipenem, Doxycycline 3) Myringotomy or bulla sx 4) Avoid flishing of bulla/middle ear

Question 77

What is most common cause of VII and VIII dysfunction

Answer 77

otitis interna -but could be central (medulla) *Can also see Horner's syndrome with sympathetic nerve involvement

Question 78

Idiopathic vestibular disease causes *

Answer 78

ACUTE peripheral vestibular signs no other cranial nerve deficits "Old dog vestibular disease"

Question 79

Hypothyroidism can cause ________*

Answer 79

peripheral vestibular disease

Question 80

Metronidazole Toxicity can cause signs of

Answer 80

central vestibular disease *Blocks GABA receptor

Question 81

What are disease of central vestibular system

Answer 81

-Inflammation -Infection -Neoplasia -Metronidazole toxicity -Vascular events -Congenital malformations -Thiamine deficiency -Trauma

Question 82

Is forced strabismus a sign of central vestibular disease or a non-specific vestibular sign

Answer 82

Non-specific vestibular sign

Question 83

Some Features of general proprioceptive ataxia

Answer 83

-Scuffing dorsum of foot -Irregular gait tracking -Crossing over limbs

Question 84

6 year old MC pitbull mix with a 2-week history of "not walking right" (video below). His owners noticed he was falling occasionally in the pelvic limbs, which progressively worsened over the 2 week period. They also noticed in the last few days that his thoracic limbs seemed "off." Please watch video to observe gait and postural reactions. The remainder of your neurological exam showed decreased reflexes in the thoracic limbs and increased reflexes in the pelvic limbs. He showed some resistance to neck movement. The rest of his exam was within normal limits. Where do you localized

Answer 84

C6-T2 The correct answer is C6-T2 spinal cord segments. This dog exhibits a "two engine" gait. He is short-strided and stiff in the thoracic limbs, with decreased reflexes, and has a long, floating gait with crossing over, knuckling, and weakness in his pelvic limbs, consistent with upper motor neuron paresis and general proprioceptive ataxia - with increased reflexes. This discrepancy in gait (LMN signs in the thoracic limbs and UMN signs in the pelvic limbs) is characteristic of a C6-T2 myelopathy.

Question 85

What would be included on your list of differentials for a dog with progressive signs and possible pain associated with the C6-T2 myelopathy (no history of trauma)? Check all that apply. -FCEM -Discospondylitis -Intervertebral disc herniation -Spinal fracture/subluxation -Neoplasia -Degenerative myelopathy

Answer 85

-Discospondylitis -Intervertebral disc herniation -Neoplasia This case is progressive over a 2 week timeframe, which is not consistent with FCEM, and not typical for spinal fracture/subluxation. Degenerative myelopathy is progressive, but typically shows a T3-L3 localization, and tends to be very slowly progressive over months (not weeks).

Question 86

animal is dull and slow to respond but will respond appropriately

Answer 86

obtunded

Question 87

animal is unresponsive to normal stimuli can be aroused with strong stimuli

Answer 87

Stuporous

Question 88

posture in which the pelvic limbs are flexed normally and thoracic limbs are spastic, in rigid extension indicative of T3-L3 lesion caused by ascending inhibition from border cells in spinal cord to thoracic limbs

Answer 88

Schiff-Sherrington posture

Question 89

ataxia due to loss of proprioceptive pathways charactized by incoordination, crossing over of paws/limbs, knuckling/scuffing paws

Answer 89

General proprioceptive ataxia

Question 90

due to loss of vestibular pathways characterized by head tilt, leaning, falling to one side, wide based stance

Answer 90

vestibular ataxia bilateral = crouched, low stance and reluctance to walk

Question 91

due to loss of cerebellar mediation of motor function characterized by wide based stance, dysmetria, intention tremor no scuffing or knuckling

Answer 91

Cerebellar ataxia

Question 92

both of the pelvic limbs

Answer 92

Para-

Question 93

both limbs on one side (left or right)

Answer 93

hemi-

Question 94

a couarse tremor of low frequency worsens with movement, goal-direction typically occurs with cerebellar dysfunction

Answer 94

Intention tremor

Question 95

What is myotonia

Answer 95

delayed relaxation of muscle following voluntary contraction may occur with certain congenital and acquired myopathies

Question 96

What nerve does the perineal reflex test

Answer 96

Pudendal nerve (S1-S3 nerve root)

Question 97

neurons originate in the grey matter of the spinal cord in all segements function to have direct innervation of effector muscles or glands

Answer 97

Lower motor neuron system

Question 98

With LMN lesions, you get A) ______ of innervated muscles B) _______ reflexes C) ________ to muscles

Answer 98

Paresis/paralysis of innervated muscles Areflexia/hyporeflexia Severe muscle atrophy

Question 99

neurons that originate in various areas of the brain and function to initiate voluntary motor functions, maintain muscle tone, regulate posture

Answer 99

upper motor neuron system

Question 100

With UMN lesions you get _____ of innervated muscles ______ reflexes ______ muscle tone

Answer 100

paresis or paralysis of innervated muscles normal to hyperreflexia: because reflex arc remains intact but there is loss of inhibition from higher centers Normal to increase muscle tone Lack of noticeable muscle atrophy (perhaps disuse)

Question 101

Why is there normal to increased reflexes with UMNs

Answer 101

because reflex arc remains intact but there is loss of inhibition from higher centers

Question 102

What drugs might you use for physiologic tremors

Answer 102

metoclopramide, dephenhydramide