Small Animal Neurology Continued Flashcards
a sudden loss of muscle tone
atonic seizures
a seizure lasting more than 5 minutes
Status epilepticus
two or more seizures within a 24 hour period
Cluster seizure
sudden brief involuntary contraction of a muscle or group of muscles
myoclonic seizure
sustained increase in muscle contraction followed by repetitively involuntary muscle contractions at a frequency of 2-3 seconds
Tonic Clonic seizures
tonic clonic seizures are
sustained increase in muscle contraction followed by repetitively involuntary muscle contractions at a frequency of 2-3 seconds
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.
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).
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?
Left forebrain - likely neoplasia
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?
Hydrocephalus
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?
Pelvic Nerve
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?
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.
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?
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.
Which component of the autonomic nervous system is predominantly responsible for the filling phase of micturition?
Sympathetic system
In a patient with a T3-L3 lesion, what would you expect to find in terms of detrusor and urethral sphincter tone?
Increase tone to detrusor muscle and increase to urethral sphincters
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?
Meningoencephalitis of unknown origin
Lymphoma
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?
1) Prednisolone +/- cytarabine
2) Phenobarbitone
Q. True or False. Steroid Responsive Meningitis Arteritis (SRMA), is commonly associated with neurological deficits in its acute form.
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.
Which of the tests likely offer the greatest predictor for survival following head trauma?
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.
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?
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.
According to the Monroe-Kelly Doctrine (aka intracranial compliance) the skull only has enough room for three types of tissue: brain, CSF, and
blood
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?
Resuscitate and re-evaluate
What is a contraindication for mannitol?
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.
Which of the following is not a feature of pure cerebellar disease?
A) Tetraparesis
B) Cranial nerve deficits
C) Vestibular ataxia
D) Spasticity
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.
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?
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.
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?
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.
T/F: The cerebellum initiates movement; the cerebrum coordinates it.
False:
The cerebellum is a regulator not initiator of movement
The initiators of motor are the cerebrum and (mostly) brainstem.
T/F: Tremors that occur with intent and are restricted to the head and neck region, localize to the cerebellum or its tracts.
True
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
A) Myalgia
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
Junctionopathy
What is electromyography (EMG) used to test?
The electrical activity in MUSCLE
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.
True. Without other signs of brainstem disease, the combination of unilateral facial nerve and vestibulocochlear nerve signs, makes peripheral disease more likely.
Results in bilateral paresis and atrophy of masticatory muscles and bilateral dropped jaw
Idiopathic trigeminal neuropathy
Results in acute onset muscle weakness and cervical ventroflexion
more common in cats than in dogs
Hypokalemic neuromyopathy
results in bilateral masticatory muscle atrophy and trismus (inability to open the jaw)
Masticatory Muscle Atrophy
Results in acute onset tetraparesis with concurrent GI signs
Botulism
Results in acute onset flaccid paralysis
patients retain their tail wag
more common in dogs than cats
Acute Polyradiculoneuritis
What are the 3 parts of the brainstem
1) Midbrain
2) Pons
3) Medulla
What are the clinical signs of damage to the brainstem
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
What is the peripheral vestibular system
the vestibulocochlear nerve (CN VIII)
What is in the central vestibular system
1) Vestibular nuclei (8) and the axonal projections to the cerebellum
2) Extraocular nuclei
3) Spinal cord
T/F: there might be mentation change with brainstem diseases
True- ARAS (ascending reticular activating system) runs through the brainstem, thalamus, and to cerebral hemispheres
