Artificial Intelligence in Neurology

Artificial Intelligence (AI) has really taken off in the last few years and, as such, has driven us as veterinarians to critically evaluate where and how we would like to utilize this new technology. Last year I reported to you about a lecture I listened to at ACVIM about the use of AI for writing radiology reports. It was eye opening, to say the least! Recently (October 2023), a group of mostly veterinary neurologists took on AI in a new way. Abani et al challenged 13 boarded neurologists from Europe and North America to distinguish between AI-generated abstracts and human-generated abstracts. The results are chilling...

Materials and Methods

There were 3 test topics provided in this study. The purpose of providing 3 was to discriminate between "highly familiar" topics and the less familiar topics to see if there was a difference in detection of AI by the reviewers. 
Topic 1: SARS-CoV2 scent detection in dogs (considered low familiarity)
Topic 2: Biomarkers for SRMA (considered high familiarity)
Topic 3: Staining of cannabinoid receptor type 1 (medium familiarity)
An abstract, reference and introduction paragraph were written by humans on these 3 topics. ChatGPT was then used to generate 3 additional abstracts, with references and an introduction paragraph on the 3 topics. It was interesting that the authors noted ChatGPT was prompted as such: " Write an academic abstract with a focus on (subject) in the style of (author characteristics such as position, gender and age) at (University name), for publication in (journal name)." I mean...wow. ChatGPT is able to provide gender, age and position sensitivity. 

Results

• Topic 1 and 3: 4/13 (31%) correctly identified the AI generated abstract when only provided the abstract without references and introduction paper. This increased to 9/13 (69%) when all parts were provided. 

• Topic 2: 7/13 (54%) correctly identified the AI-generated abstract (provided alone), which increased to 10/13 (77%) when all parts were provided. 

Two separate plagiarism detectors were studied in this study as well. All of the original published manuscripts were noted to have 58%-100% similarity to available work which indicated this had been published elsewhere (it had). Test 1, 2, and 3 with the AI-generated papers had similarity indexes of 0-18%. This suggests that the plagiarism detectors could identify what had been previously published (the human-generated papers) and which hadn't (the AI-generated papers). Furthermore, they then evaluated all of the abstracts with an AI-detector. All original manuscripts were noted to have 0% AI-writing. Test 2 was noted to have 100% AI generation, and Tests 1 and 3 were noted to have 0% content written by AI. Gulp. 

Where does this leave us? My heightened sense of anxiety about AI-generated content was further heightened when realizing that many of my well respected, high academic achieving colleagues struggled to distinguish between AI-generated abstracts and human-generated abstracts in an area of our specialty. This further reinforced my commitment to reading the entire paper, whenever possible, before considering the data valid. We were taught to do this in school but alas, with our busy schedules, it can be missed. AI is not all bad, however. It can be quite helpful for correcting grammar, editing, summarizing references or papers and even performing statistics. I would encourage all of us to move through published literature with our eyes fully focused and with awareness of the use of AI in modern veterinary medicine. Except yesterday...hopefully you kept your eyes partially closed and didn't look directly at the sun!! 

I hope you enjoyed this little TidBit. It is a little bit off topic, but I hope you will find it useful, nonetheless. Please know that my TidBit Tuesdays are (to date) fully human-generated, as are my patient reports! Let me know if you have any topics that you'd like me to cover. Have a great week!

Which Reflexes Should I Do?

Have you ever looked down at the patient, laying calmly and quietly in lateral recumbence, and thought “okay, which reflexes do I do?” There are several choices for each limb, but the most commonly assessed reflexes are as follows:

• Thoracic limb (I was trained by Dr. DeLahunta and was taught to never call this the front limb, but you are welcome to do so!): Biceps, triceps, extensor carpi radialis and withdrawal.

• Pelvic limb (same story as above): patellar reflex, cranial tibialis, gastrocnemius and withdrawal.

Some of these reflexes are harder than others to observe and obtain. The purpose of performing the spinal reflexes is to assess the sensory and motor pathways associated with that specific peripheral nerve and the spinal cord segment. For example, the patella reflex evaluates the femoral nerve and the L4-6 spinal cord segment. A present reflex suggests this pathway is intact. An absent reflex suggests that the peripheral nerve (femoral nerve) and/or the L4-6 spinal cord segments are NOT intact. A recent study (Chiang B, Garia G, et al 2024) evaluated each of these reflexes in 101 dogs and asked 1 neurologist and 1 resident to determine if they were obtained, or not (simple binary question).
Several of the reflexes had high intraobserver agreement, which would suggest that these are both easy to detect and possibly easier to obtain. The reflexes which high intraobserver agreement included the extensor carpi radialis, withdrawal reflexes in both thoracic and pelvic limbs, patellar reflex and cranial tibial reflex. Although all reflexes could (might I say should?) be attempted in the neurologic examination, sometimes we don't have this luxury. From this study, I would suggest that the 4 reflexes mentioned above should be reliably present. If you perform these reflex tests and do not observe a response, it is reasonable to consider them absent or delayed. 

Not sure how to perform these reflexes? I run personalized CE events, including live animal neurologic examination practice, in your clinic. Email me to learn more or to schedule. 
Does neurology make you nervous?? Please reach out to schedule your patient for a neurologic examination or reach me via email with any questions. My job is to help you decide if a patient has neurologic disease, or not, and the way we do this is to utilize the neurologic exam.

Thanks for reading. This article can be found here:DOI: 10.1111/jvim.16999

Heat Tilt, Turn or Neck Turn...so what?

Does a head tilt help with neurolocalization?
 

A recent study by Nagendran et al (The value of a head turn in neurolocalization, JVIM 2023) described 4 distinct areas of neuroanatomic lesion localization for head turn, head tilt and neck turn and looked at head and body position in each of these localizations. If you see a patient with their head deviated to one side yet parallel to the floor, that would be a head turn. If a patient has their head deviated to one side NOT parallel to the floor, we would consider this a head tilt. The head tilt can be anything from 1-90% from the x axis! If the neck is turned to one direction it would be called torticollis and may be (and often is) associated with either head tilt, head turn, or both. This recent article looked at these three signs, in reference to the neuroanatomic lesion localization, with the goal of trying to sort out the underlying neuropathology (totally cool but not "light reading" and therefore saved for another conversation).
Key Points:

• Forebrain disease – The majority or patients had an ipsilateral head turn, with less than ½ of the dogs demonstrating ipsilateral body/neck turn.

• Brainstem disease – All dogs had an ipsilateral head turn, and 5/9 had an ipsilateral head tilt, with a rare dog demonstrating a neck turn.

• Cerebellar disease – All dogs had an ipsilateral head turn and the majority had a contralateral head tilt with a rare neck/body turn noted showing a contralateral neck/body turn.
  

• Cervical spinal cord disease – all dogs had a contralateral head turn along with a majority (6/7) showing a ontralateral head tilt.

Summary:

• Head turn ONLY – consider forebrain disease

• Head turn with neck turn (ipsilateral) – consider forebrain disease, but the neck turn is an inconsistent finding in many dogs with foreain disease.

• Head turn, neck turn AND head tilt – most likely cervical spinal cord disease but cannot rule out cerebellar disease.

• Head tilt only – likely brainstem disease (or peripheral vestibular disease!)

Take Home Points:
A head tilt, head turn, or neck turn is a useful physical examination finding to point you at neurologic disease however they aren’t discretely localizing on their own. Using the information above, you may be able to support a localization noted in concurrence with your other neurologic findings.

Thanks for reading! I made the difficult decision to increase my consultation fees this year so if you didn’t get an announcement please reach out and I can send you the updated fee schedule. Lastly, it’s winter!! That means sometimes travel can be hazardous and cancelations can happen. I don’t charge if we cancel due to inclement weather and will do my best to work your patient into the schedule as quickly as possible afterwards. I appreciate your business very much and do my best to meet your expectations. Have a great week!

When is Lameness not Orthopedic?

Lameness is typically orthopedic, as we know, but there are times when this isn’t true. How do we know when this is true? To answer this question, I’d love to go through a case with you today.

Signalment: 11 year old FS Labrador

History: She has a 4 week history of right thoracic limb lameness. She is a hunting dog, and signs were noted after a busy weekend in the field. On initial evaluation, mild discomfort was appreciated in her elbow therefore carprofen was started. Clinical signs did not improve; they worsened. She became intermittently non-weightbearing lame in the right limb. All other limbs appeared normal. Additionally, she started helping when laying down or rising from laying. At this point, I stepped into the game. What am I looking for to suggest this might be neurologic in origin?

Neurologic Examination:

Mentation: BAR

Cranial nerves: miosis OD, did not dilate in a dark space. Remaining CN normal.

Gait: Ambulatory, moderate right thoracic limb lameness. When toe touching, the limb was touching on tiptoe only.

Reflexes: Reduced withdrawal distal to the elbow on the right (unable to flex the carpus or elbow completely during withdrawal but able to mechanically flex both joints when I flex them), unable to detect triceps reflex on either side, remainder normal. Absent cutaneous trunci reflex on right, normal on left. Normal reflexes both pelvic limbs.

Postural reactions: Normal paw replacement in left thoracic limb and both pelvic limbs. Unable to assess paw replacement in the right thoracic limb due to non-weightbearing status. Reduced hopping on right thoracic limb compared to left thoracic limb.

Palpation: No spinal pain, normal cervical ROM.

What is the neuroanatomic lesion localization?

The first question is always, is the problem neurologic in origin? She has evidence of reduced reflexes so I would suggest, yes, it is. Essentially, our abnormalities are focused on that right thoracic limb with the addition of miosis OD and absent c. trunci right side.

Reduced withdrawal in the thoracic limb suggests a radial nerve injury/damage. Even though signs are distal to the elbow, the lesion could still be proximal, and neurodegeneration has occurred distally. Is the damage inside the spinal canal (central) or in the peripheral nerves (brachial plexus)? To answer this question, look at the right pelvic limb. Do you see any paw replacement deficits or weakness in the right pelvic limb? These are the long tracts going from the limb to the brain and the must pass right through C6-T2 and C1-C5 as they do so. If the lesion is in the canal, we should see paw replacement deficits in the right pelvic limb. We don’t, so the lesion is more likely in the radial nerves after they have exited from the canal.

What do we do with the miosis? The sympathetic pathway to the eye is as follows: thalamus à brainstem à cervical spinal cord à exit T1-T3 à join vagosympathetic trunk and ascend to the head à ganglion  à go through bulla to jump on CN 5 (trigeminal) à end in the iris for dilation. The radial nerve exits from segments C6-T2, which would cross over with T1-T3 and therefore we could make an argument that the miosis is secondary to involvement of this segment of the radial nerve.

What about the c. trunci? This one is pretty simple to understand once we refresh our memory of anatomy. Cutaneous trunci reflex is a simple spinal cord reflex that uses the dorsal sensory spinal nerves as afferent (sensory), and lateral thoracic nerve as efferent (motor). The lateral thoracic nerve arises from C8-T1. This fits with our assumption of a C6-T2 right sided neuropathy because loss of the lateral thoracic nerve on one side would cause an absent cutaneous trunci reflex.

Neuroanatomic lesion localization: Peripheral C6-T2 neuropathy/radiculopathy.

The differential diagnoses for this case were a lateralized intervertebral disc herniation, neoplasia, much less likely neuritis (infectious or inflammatory) and hypothyroidism. As it turns out this dog was diagnosed via MRI with a mass in the right brachial plexus. The owners elected amputation and it was determined to be a nerve sheath tumor. Why did the signs appear acutely? It’s not completely clear but my guess is that the dog was already decompensated slightly, and the heavy work caused inflammation or maybe even hemorrhage around the mass that resulted in an acute exacerbation.

That’s it for now! Reach out if you have any questions about this case, or any other case! I look forward to working with you soon. Have a great week!

Neuroanatomic Lesion Localization Practice book!

It's Here! The Small Animal Neuroanatomic Lesion Localization Practice Book by yours truly!

It's always hard to self promote, so instead I wish to draw your attention to the many neurologists that contributed cases that made this little workbook the workhorse that it is.
1. Dr. Helena Rylander (UW-VC neurologist)
2. Dr. Joy Delamaide-Gasper (MVS neurologist)
3. Dr. Kari Foss (U of I neurologist, and former student)
4. Dr. Devon Hague (U of I neurologist)
5. Dr. Julien Guevar (Swiss neurologist and former UW-VC Neurologist)
6. Dr. Susan Arnold (U of Minnesota Neurologist and UW- VC graduate)
7. Dr. Sam Long (Australian neurologist and all around amazing guy)
8. Dr. Simon Platt (Forum UGA neurologist and ACVIM-Neurology past president)

The Small Animal Neuroanatomic Lesion Localization Practice Book is just that - a practice book - geared for general practitioners, students, and interns who are interested in brushing up or dusting off their neuroanatomic lesion localization skills. This little ditty has 7 chapters, with many cases in each chapter for you to try your hand at neuroanatomic lesion localization.

Not enticed enough?? If you get stuck - you know the author of the book and can email me directly for help! (yay for connections!)

Still not enticed?? Check out this link to see more: https://www.cabidigitallibrary.org/doi/10.1079/9781789247947.0000
Cost $65 USD

Note: I don't get any notifications of who buys a book, but if you suddenly stop consulting I'll assume you bought the book and learned it all and no longer need me. I really should stop trying to teach myself out of a job.... :)

That's it for this week. Not a typical TidBit per se, but hopefully you don't mind so much. Thanks for reading!
Have a great week!

Masticatory Muscle Myositis: That's a mouthful!

We are seeing more cases of masticatory muscle myositis lately so I thought we'd look into this interesting diagnosis together. Let's start by defining it.
Masticatory Muscle Myositis (MMM) is an inflammatory, autoimmune myopathy affecting the muscles of mastication (temporalis, masseter, pterygoid and rostral digastricus). All of these muscles are innervated by CN 5, specifically the mandibular branch.

Why only these muscles?
The muscles listed above have a specific myofiber type (type 2M), which is only present in these muscles and some fetal muscles. All other muscles in the body are 1A and 2A fiber types! Therefore, these muscles present a unique antigen for the immune system to target.

What does the clinical picture look like?
There is an acute phase, and a chronic phase. The acute phase occurs first and often includes signs such as jaw pain, swollen muscles, and difficulty chewing. (Note NOT drop jaw or difficulty closing the jaw....that is a different disease.)
If left untreated, patients will then progress into the chronic phase, which includes signs such as muscle atrophy and an inability to open the jaw. Muscle fibers are replaced with scar tissue during the chronic phase making the dog unable to open their mouth more than a few centimeters over time.

Must we take a chunk of muscle to make this diagnosis?
No, you don't! Although you will obtain a diagnosis in both the acute and chronic phase, there is an easier, and less invasive, way. The serum 2M antibody test is both highly sensitive (85-90%) and highly specific (100%) and is the preferred diagnostic test for MMM. Send it to the Comparative Neuromuscular Lab in La Jolla CA (https://vetneuromuscular.ucsd.edu/) if you live in the states. I think there are other choices worldwide but I'm not as aware of those.

Steroids are the best, and most effective treatment.
Immunosuppressive steroids are the most effective treatment for this disease and are strongly recommended in the acute phase. Your goal is to stop that inflammation in its tracks so that the patient doesn't progress to the chronic phase. Once they replace the muscle fibers with connective tissue, the game is over. The dog cannot open its mouth, chew, or be safely intubated or vomit. The chronic stage results in poor quality of life. Steroid protocols vary by neurologist. My protocol starts with 1 mg/kg PO q12h prednisone for 30 days, and then tapers slowly from there. Repeat 2M antibody titers every 1-2 months is recommended. Once the numbers return to normal, it is generally safe to stop the steroid administration.

If any dog has painful muscles of mastication, struggles to open its jaw without pain, and has an elevated CK on lab work a 2M antibody titer is recommended. Don't forget: neospora caninum and toxoplasma gondii can cause myositis and do attack the muscles of mastication. Concurrent testing for these two diseases in all dogs is strongly encouraged before starting immunosuppressive prednisone. I have been taken by surprise how often these tests are positive when I suspect this is "just" MMM.

Hopefully this helps you address muscle pain in your patients. If you have a question about a patient, please contact me via email or schedule a consultation online! Have a great week!

Trazodone and the Neurologic Exam

Finally!! Trazodone and gabapentin are frquently recommended medications used for anxiolysis in the veterinary clinic but it has long been suspected that they have an impactful effect on the neurologic examination. We now have data! In this month's JVIM (https://doi.org/10.1111/jvim.16536), Drs. Lueck, Cameron and Zidan (from the University of Wisconsin-Madison!) evaluated 32 apparently healthy dogs pre and post trazodone administration and documented their findings.
Here are the key points:

1. The dose of trazodone in this study was 6.25-8.60 mg/kg PO single dose.
2. Neurologic examinations were performed before and 2.5 hours after trazodone administration
3. Decreased mentation changes were noted in about 25% of dogs (BAR going to QAR). Oddly enough, 7 dogs were noted to be QAR on initial exam and 3 were graded as BAR on post dosing exam. Not sure what to do with that except to say that we're obviously quite subjective on this assessment and BOTH are considered normal so should it matter?
4. Paw replacement deficits changed with identification of new, or worsened deficits in 22% of dogs. This finding isn't surprising but it bothers me. The neurologic examination is perhaps the most important tool to localize as well as determine differential diagnoses. We could misguide a client if we acted on the deficits identified while under the influence of trazodone!
5. Not a single dog had a worsening evaluation of their cranial nerves or reflexes in this study. Even 1 dog with reduced reflexes on the pre-trazodone assessment had similarly graded reflexes following trazodone administration.

What should we do with this information?

First, don't extrapolate to cats. Second, I strongly urge you not to have a client give trazodone to a pet prior to a neurologic examination based on this data. This recommendation has been previously based on my clinical suspicion so I'm thankful the authors went through the effort to perform and publish this data for the rest of us! Lastly, if you happen to do a neurologic examination on a pet ON trazodone and find deficits, consider repeating the examination without administration of trazodone to document consistence in the findings prior to recommending extensive work up. If that isn't possible, acknowledgement to the client of the possibility of a confounding factor, is recommended.

I look forward to hearing from you and working with you again soon! Have a great week and stay safe.

Walk This Way: Describing Ataxia and Paresis in the Clinical Patient

Perhaps you’ve wondered what the difference is between ataxia and paresis? Perhaps you already know, in which case you can grab that cup of coffee and move on to your next email!

Still with me? Okay, here we go. Ataxia is the failure of coordination. This suggests a sensory abnormality and when noted, it is a hallmark for neurologic disease. As you’ll see in the next section, paresis can be noted with neurologic, orthopedic, neuromuscular or muscular conditions, making it much less specific. Ataxia, however, is a failure of neurologic sensory information which means it can only be noted with dysfunction of the neurologic system. There are three forms of ataxia: 1) proprioceptive, 2) vestibular and 3) cerebellar.

• Proprioceptive ataxia is an indication of a spinal cord, brainstem or forebrain disease. Ataxia is not noted with neuromuscular disease.  Signs of proprioceptive ataxia include a crossing of the limbs when walking down a straight pathway, or placing the limbs narrow and wide of the midline of the body without regularity.

• Vestibular ataxia indicates dysfunction of the vestibular apparatus.  When observing a patient with vestibular ataxia, the observer can appreciate a falling or drifting towards one side when walking. This can be especially magnified when the patient is turned in a circle. 

• Cerebellar ataxia occurs with disease or injury to the cerebellum. Signs of hypermetria, truncal sway, and a wide based stance with, or without intention tremor are indications of cerebellar ataxia.

Paresis, on the other hand, is a weak movement or incomplete paralysis. This involves most commonly UMN or LMN, but remember the neuromuscular junction, muscle and bones or joints can be a source of paresis also. A patient with mild paresis will exhibit a reduced joint range of motion when walking giving the appearance of shuffling. Severe paresis may be more profound so that an animal is unable to support weight even with purposeful limb movements.
Common terminology when describing paresis:

• Mono: one limb (any)

• Para: pelvic limbs (both)

• Tetra: four limbs

How can you write the gait abnormality in the record?

• If the pet has only a proprioceptive ataxia: Pet is exhibiting crossing of pelvic limbs, consistent with proprioceptive ataxia.

• If the pet has proprioceptive ataxia AND paresis: Pet shows crossing of pelvic limbs and reduced joint ROM (or weakness /unable to rise/collapsing frequently) consistent with proprioceptive ataxia and paraparesis.

• If the pet is non-ambulatory in the pelvic limbs (cannot walk without support): non-ambulatory paraparesis*

• If the pet does not have any observable motor, even with support, in the pelvic limbs: paraplegia. *

*Comments about ataxia cannot be made once the pet is non-ambulatory or plegic.
 

Hopefully this helps clarify when to use paresis and ataxia when describing the gait. Enjoy your week and stay safe!

Is Age a Disease?

Age, The Neurologic Examination and Prediction of Disease

Age isn't a disease, right? No, it isn't but disease is associated with age. The older pet is more likely to have structural disease (i.e. neoplasia instead of idiopathic epilepsy), compared to the younger pet. That said, none of us want to diagnose a terminal disease in an older patient simply because the patient is older!

Can the Neurologic Examination Help Vets with Older Patients?

Let's look at the two most commonly performed parts of the neurologic examination and see how they related to disease. The menace response and paw replacement testing (previously called conscious proprioception) both assess the forebrain and are some of the most commonly performed parts of the neurologic examination. Here is what a recent group from Australia found in reference to finding evidence of forebrain disease on MRI:

Menace response
Sensitivity: 72%
Specificity: 47%
Odds ratio: 2.26

Proprioception
Sensitivity: 54%
Specificity: 72%
Odds ratio: 3.08

If age is then factored into the analysis, dogs greater than or equal to 6 years of age are more likely to have a forebrain disease detected by MRI if they have a menace or proprioceptive deficit.

As a "field" neurologist (without a pocket MRI...yet) this tells me that I should encourage diagnostic imaging in patients with menace deficits, and possibly for those with proprioceptive deficits depending on concurrent findings. The chances (or Odds) of a patient having underlying forebrain disease is higher if they have these deficits than if they don't. Seems intuitive, but proprioceptive testing isn't as sensitive as assessing the menace response.


Although this TidBit is a repeat from 2020, I liked this study and thought it was worth repeating.
Chan MK, Jull P. Accuracy of selected neurological clinical tests in diagnosing MRI-detectable forebrain lesion in dogs [published online ahead of print, 2020 Jul 15]. Aust Vet J. 2020;10.

Keep those consults coming! It has been a hectic week (for all of us, I think!) so remember to breathe, eat and hydrate. Have a great week!

The Neurology Checklist

The Checklist

Odds are high that you have probably heard about surgical or operative checklists and, perhaps, some of you employ them in your clinic. This week I wanted to revisit this idea because a recent article reminded me of the benefit of checklist so I thought I'd share it with you!

How Does it Work?

You and your team devise a list of important things to remember for a given procedure and create a checklist. This list then hangs in your OR, or outside of a lab, or wherever it will be used. Ten years ago I read a book called The Checklist Manifesto (https://www.amazon.com/Checklist-Manifesto-How-Things-Right/dp/0312430000). One of the simplest ways to save a life is to know the name of your anesthetist and lead surgeon. Yep, that's it. Instead of bumbling around and saying "hey you...anesthesia..." you can address them by their name and shorten communication time in a crisis. Perhaps you work very closely with your staff everyday and it seems inconceivable that you wouldn't know someone's name! However for new staff members, or in large clinics, this may not be the case.

What is the evidence?

A study published in the Journal of Veterinary Surgery this month identified that surgical times were significantly shorter (p= .005) , antibiotic administration (when appropriate) was given as intended more often (p=.01), and fewer dogs had an unplanned return to the OR (p=.006) when a perioperative checklist was employed. (Reference below.) It takes less than 1 minute to run through the checklist and it may change the course of you or your patient's day!

What is the Take Home Message?

If you don't already have one, consider making a checklist for any procedure in which patient care could be compromised if something was forgotten. This doesn't need to apply ONLY to surgical situations! I make an effort to know the name of my assistant during each and every neurologic examination for this exact reason. I don't expect a crisis during a neurologic examination but everyone feels more committed to the team when we ARE a team! (And I like to be friendly, too!) I also had a checklist hanging in the neurology room when I was at UW and at VCA Aurora to remind trainees of the parts of the neurologic examination.

Neuro Checklist:
Mentation
Cranial nerves
Gait assessment
Postural reactions
Reflexes
Palpation
Ask about a seizure history.

Having this list in your work space ensures that you don't accidentally forget to perform part of the neurologic examination and yet, it isn't so overwhelming that you hesitate to read it. (A checklist MUST be short or people hate to do them!)

I hope you enjoyed this not-fully-totally-neurology-related TidBit Tuesday. Please let me know if you have any comments, questions, or requests for topics. Have a great week and keep those consults coming!

Reference: Thieman Mankin, KM, Jeffery ND, Kerwin SC. The impact of a surgical checklist on surgical outcomes in an academic institution. https://doi.org/10.1111/vsu.13629

Are we any good at a neurologic exam when pets are vestibular?

How reliable is the neurologic exam for patients with vestibular disease?

We (neurologists) like to think that the neurologic examination is the ultimate-be-all-end-all tool. But in dark corners, we talk about how incredibly hard it can be to do on patients with vestibular disease.
First, there are three parts that we need to consider for the lesion localization, correct?
1) Brainstem
2) Cerebellum
3) Peripheral CN 8
My rule of thumb is this: If the pet has ipsilateral hemiparesis/monoparesis, ipsilateral paw replacement deficits or decreased mentation (obtunded, stupor, coma) it is a brainstem lesion. If the pet has hypermetria, or intention tremors along with the vestibular signs, it is cerebellar in origin. Finally, in absence of those findings the lesion is localized peripherally.

An article out of Europe, dispelled our fears of the neurologic examination failing us and (thankfully) helped us sleep better at night when it was published that the neurologic examination correctly predicted if the vestibular signs were central (brainstem or cerebellum) or peripheral (cranial nerve 8) over 90% of the time.

Interestingly, central disease was more common in this study and, it was localized correctly MORE often than peripheral disease was localized correctly. In other words, dogs with central disease were more likely to be localized on the exam as having central disease compared to dogs with peripheral disease which were occasionally incorrectly localized with central disease.

A few more good reminders:

• Nystagmus are not a localizing sign! (E.g. 8 dogs with peripheral and 5 dogs with central disease had horizontal nystagmus.)

• The onset of disease does not predict it's lesion localization. (E.g. Acute and chronic onset of signs were not statistically different between the central and the peripheral groups.)

• They had a lot of French Bulldogs in the study! Huh..I'm not sure I've noticed an over representation of French Bulldogs in my clinical work. It's good to learn something new everyday.

So, what does that mean for us?

It means if you do a thorough neurologic exam, you'll be correct about 90% of the time when you guide a client towards an MRI and spinal tap (for central disease) or treat for idiopathic or otitis (for peripheral disease). If you're unsure, err on the side of it being a central lesion and recommend a full work up. (Or contact me for a consult!) Oh, and 68% of dogs diagnosed with peripheral vestibular were idiopathic! Idiopathic disease means we have a lot more to learn...so let's get back to it!

(Bongartz U, et al. Vestibular Disease in dogs: association between neurological examination, MRI lesion localization and outcome. JSAP 2019).

My current work days are...well, all of them except Sundays. I'll post on FB or my website if I'm closed on a random day so feel free to check those spots if you're not sure. Otherwise, feel free to call, email or hop online to schedule a telephone, live or video consultation with me. Remember, all live consults are still curbside!

Steroid Responsive Meningitis-Arteritis

It's a cold Tuesday morning and your first patient today is a painful, 6 month old Boxer dog. You dutifully run through the differential diagnoses in your head as you walk into the room. What you see when you arrive is a depressed, febrile Boxer puppy trying really hard not to move their head or neck and wincing when doing so.
After examination you find the dog has the following neurologic examination findings:
Mentation: QAR, especially for this normally hyperactive puppy
Cranial nerves: normal
Gait: stiff, stilted gait but no evidence of paresis, ataxia or lameness. (Although lameness and paresis CAN happen with steroid responsive meningitis-arteritis, a.k.a. SRMA)
Postural reactions: normal paw replacement in all four limbs
Reflexes: normal in all four limbs, normal c. trunci and perineal (you did a great job!)
Palpation: Oh how the dog winces with cervical palpation! (Don't do cervical ROM on this dog, okay?)

Neuroanatomic lesion localization: Well...technically the neurologic examination is all normal, right? So all you can say is "cervical pain" on the record. No neuroanatomic lesion localization when they are neurologically normal.

Differential diagnoses: Trauma, fracture, subluxation, muscle strain, infection/polyarthritis, and yes, SRMA.

What is SRMA?

It is an immune mediated disease that affects the vasculature of the meningitis, and sometimes the joints and it typically affects dogs < 2 years of age, with large breed dogs and beagle dogs over represented.

How do you diagnose it?

First, rule out other causes (radiographs, spinal MRI). Next, perform a spinal tap and identify a neutrophilic pleocytosis (often with a SUBSTANCIALLY increased cell count!). Third, rule out infectious diseases that cause meningitis in your area of practice. For most of us in Wisconsin, this is Neospora (toxoplasma if cat), fungi, and bacterial causes.

What is the recommended treatment?

Steroids at 1-2 mg/kg PO q12h, depending on the literature. I start with 1 mg/kg PO q12h for 30 days and then reassess the CSF. Some studies suggest doing this dose, or a slightly tapered dose, for up to 3 months and then reassessing the CSF. When normal, a gradual taper over 3-6 months is common. Relapses can occur in up to 80% of the studies published but my experience has been a much lower recurrence rate.
A recent study by Giraud et al* found a lower relapse rate with the addition of azathioprine. They used 2 mg/kg PO q24h x 1 month and then tapered from there to an every other day dosing interval for 2 months for a total of 3 months of treatment. The authors suggested that the addition of azathioprine allowed them to reduce the prednisone dosage sooner and more rapidly, thus reducing long-term side effects. Over 80% of the dogs in this study were in clinical remission within the 2 year follow-up time without signs of relapse.
Azathioprine was also reported to have exceptionally long survival times when used in combination with steroids to treat meningitis of unknown etiology (MUE), another immune mediated CNS disease. So...perhaps we're on to something here! Interestingly, azathioprine was suspected not to cross the blood brain barrier initially. Hummm...

Key Points:

• SRMA is often treatable, but relapses do occur.

• A CSF tap is needed to confirm the diagnosis however MRI is often performed before CSF to rule out physical/structural abnormalities. This helps to decrease the risk of harm from a spinal tap.

• Steroids are the mainstay of treatment but azathioprine may be added to allow a more rapid reduction of steroids (thus reducing long-term side effects from steroids).

Have a great week and stay safe out there! It's been a snowy few weeks here in Wisconsin so drive safely if you're out and about!

Anisocoria

** Credit for the amazing hand-drawn image goes to my good friend, and veterinarian Dr. Pam Boutilier.

Anisocoria

Anisocoria is defined as pupil asymmetry and may be seen with ocular or neurologic dysfunction. Malfunction of the sympathetic, parasympathetic, or visual system may result in anisocoria.

Neuroanatomy

Visual Pathway
When light enters the eye, it activates the light receptors in the retina. That information then travels along CN II, crosses in the optic chiasm, and terminates in the thalamus. Optic radiations relay the visual information from the thalamus to the visual cortex in the brain. This pathway can be tested using the menace response test and/or cotton ball testing.

Parasympathetic function: Pupil constriction
The parasympathetic pathway to the eye is a short, two neuron pathway which originates in the midbrain. The two, paired parasympathetic nuclei of CN III (PSNCNIII) send fibers along with the somatic nerves from CN III to the eye. The parasympathetic pathway is best assessed using PLR. When a bright light enters the eye, CN II activates and synapses on the PSNCNIII. The parasympathetic fibers transmit this information to the eye, using cranial nerve III as a conduit, resulting in pupillary constriction.

Sympathetic function: Pupil dilation
The opposing system is the sympathetic system, which causes pupillary dilation. The sympathetic pathway is a three neuron pathway and takes a longer course to the eye compared to the parasympathetic system. In general it goes from the thalamus, through the brainstem and cervical spinal cord to exit in the upper thoracic segments. Fibers then make a U turn and head back to the eye via the jugular groove (don't poke around too much when doing those jugular blood draws!), bulla (ear infection can = sympathetic dysfunction) and then hitches a ride with CN V to make the final leg to the eye. Malfunction anywhere along this pathway will result in a failure of iris dilation in a dark room and a comparatively miotic pupil, typically accompanied with enopthalmus and ptosis.

Putting it together

Let's put this new knowledge to work. If you see a case with anisocoria, how do you decide if it is a parasympathetic or sympathetic dysfunction?
1) Assess the pet in a dark room. Does the eye dilate? If yes --> The lesion is NOT due to sympathetic dysfunction.
2) Asses PLR. Does the eye constrict? If yes --> the lesion is NOT due to parasympathetic dysfunction.

To localize to the appropriate location beyond sympathetic or parasympathetic function requires a full neurologic examination. If you aren't comfortable performing or interpreting a neurologic examination please consider a neurology consultation! I am not comfortable doing a dental...we all have our limitations! :)
If you're interested in digging into anisocoria more deeply, or you have a case with anisocoria consider checking out the following article for a full discussion and more amazing images. Note: I do not receive any royalties or financial impact from this article.
* Barnes Heller H, Bentley E. The practitioner's guide to neurologic causes of canine anisocoria. Today's Veterinary Practice Jan/Feb 2016 pg. 77- 83.

Keep those consults coming; we all get to learn a little bit more with each consult. Have a great week!

Monoparesis following Vehicular Trauma

How do you sort out a cat or dog with thoracic limb monoparesis following trauma?

This is an important question. First, let's review the innervation to the front leg. (Get back here - it's not that bad!) There are two important nerves that guide weight bearing and movement in the front leg:
1) Musculocutaneous - exits spinal cord segments C6-8. Important innervation is biceps muscle but it does a few others. The important action is flexion of the elbow and extension of the shoulder
2) Radial - exits spinal cord segments C7-T1 +/- 2. Innervates triceps and the muscles on the cranial distal limb that extend the carpus. The important action is extension of the elbow and carpus for weight-bearing.

So, to weight bear there must be an intact radial nerve. To move the limb forward there must be an intact musculocutaneous nerve. The other nerves (supra and subscapular, axillary, median and ulnar) are important too, but not as important. If you want to remember only two nerves, remember radial and musculocutaneous.

Now that we have that over with, let's put this to practice. Here is the scenario: You are presented with a 1 year old cat with a history of vehicular trauma a few days ago. The cat is presented dragging the left thoracic limb, unable to bear weight. When you watch it walk you can see advancement of the shoulder and elbow but it is minimal.
Question: What nerve is affected MOST?
Answer: Radial
Question: What spinal cord segment does the radial nerve arise from?
Answer: C8-T1 or 2.

Really good question: What is this cat's lesion localization?
Answer: Let's do a neurologic examination! :)

Neurologic exam:
Mentation: BAR
Cranial nerves: normal (note Horner's can be seen with thoracic limb injuries but isn't seen in this cat).
Reflexes: Absent triceps, absent withdrawal of the left thoracic limb. Unable to detect bicep or extensor carpi reflex (hey, it's a cat, give me a break!). All other limbs have normal withdrawal and pelvic limbs have normal patellar reflexes.
Palpation: non painful
Proprioceptive testing: absent tactile placing left thoracic limb, absent tactile placing left PELVIC limb, normal entire right side.
Gait: left thoracic limb monoparesis as previously described.

Now you can properly answer the previous question.
With absent radial nerve and diminished musculocutaneous innervation to the left leg, we KNOW the lesion must involve C6-T2, correct? (It's absent because of the missing withdrawal reflex - mediated through largely the radial nerve but also musculocutaneous too.) The real question here is this: is the injury in the plexus only or is there evidence of spinal cord involvement? To answer that question, you must look downstream from the affected segment. This means, look at the left pelvic limb. This limb has absent tactile placement so there has been disruption to the spinal cord tract going from the brain to the left pelvic limb, and back again.
Answer: This cat has a C8-T2 spinal cord lesion.

The differential list must now include things that affect the spinal cord such as avulsion and a disc herniation, hematoma or hemorrhage. Your diagnostic plan would include advanced imaging of the spinal cord. If the lesion localization had been peripheral plexus (not spinal cord) you would consider a brachial plexus avulsion only and advanced imaging would not be indicated. Knowing the lesion localization can markedly change your differential diagnoses, diagnostic plan and ultimately treatment and recovery!

Not sure about this case? Feel free to email me! This TidBit Tuesday is a slightly altered version of a real case seen recently. Keep those consults coming so we can share the knowledge folks! Please email/call/text me to schedule a consult or hop on my website and utilize the online scheduler to find the best time.

Have a good week!

Can the neurologic examination predict disease?

Age, the Neurologic Examination and Prediction of Disease

Age isn't a disease, right? But, disease is associated with age. The older pet, is more likely to have structural disease (i.e. idiopathic epilepsy vs CNS neoplasia), compared to the younger pet. But, none of us want to diagnose a terminal disease in an older patient simply because the patient is older!

How can the Neurologic Examination Help Vets with Old Patients?

Can we look at two of the most commonly performed tests on the neurologic examination and determine the sensitivity and specificity for the detection of a forebrain lesion? Actually, yes we can.  The menace response and paw replacement (previously called conscious proprioception) testing both assess the forebrain and are some of the most commonly performed parts of the neurologic examination. Here is what a recent group from Australia found:

Menace response
Sensitivity: 72%
Specificity: 47%
Odds ratio:  2.26

Proprioception
Sensitivity: 54%
Specificity: 72%
Odds ratio: 3.08
If age is then factored into the analysis, dogs greater than or equal to 6 years of age are more likely to have a forebrain disease detected if they have a menace or proprioceptive deficit. 

As a "field" neurologist (without a pocket MRI...yet) this tells me that I should encourage diagnostic imaging in patients with menace deficits and proprioceptive deficits. The chances (or Odds) of a patient having underlying forebrain disease is higher if they have these deficits than if they don't. Seems intuitive, but proprioceptive testing isn't as sensitive as assessing the menace response so by all means don't forget to do that on an older patient! :)

Hope this little study was insightful for you too.
Chan MK, Jull P. Accuracy of selected neurological clinical tests in diagnosing MRI-detectable forebrain lesion in dogs [published online ahead of print, 2020 Jul 15]. Aust Vet J. 2020;10.

Keep those consults coming! I'm continuing to answer email consults in the evenings but do my best to be available during working hours should you have a questions and wish to call or text me. On site consultation is available Monday through Saturday at variable times throughout the week.

Have a good week! 

Neuroanatomic Lesion Localization Practice Case

Lesion Localization and Case Building Practice

Lesion localization is one of those things that can be lost, if not practiced. Don't lose it! You're welcome! :)

Maria, is a 13 year old FS Lab
History: Presented to me with a 24 hour history of acute onset difficulty walking. 

Neurologic examination:
Mentation: BAR
Cranial nerves: right head tilt, rotary nystagmus, remainder normal.
Gait: Moderate vestibular ataxia, falling right. No hypermetria or intention tremors noted. 
Postural reactions: absent right thoracic and right pelvic limbs, normal other limbs
Spinal reflexes: Normal all limbs, normal c. trunci and perineal
Palpation: non painful, normal cervical ROM

You know what you've got to do now, right?

What is the Neuroanatomic Lesion Localization?

There are several ways to go through lesion localization.

OPTION 1:
I like to make lists. Start by listing all of the abnormalities and ALL possible locations that could result in an abnormal finding. For example:
1) Right head tilt - peripheral CN 8 (right), medulla (right), cerebellum (right or left)
2) Rotary nystagmus - same as above
3) Vestibular ataxia - same as above
4) Reduced paw replacement right side - right C6-T2, right C-C5, right medulla, right pons, right or left midbrain, left prosencephalon.

Now, we start to eliminate some things. How do to differentiate peripheral vs. brainstem vs cerebellar disease? Well, for starters any animal with cerebellar disease is expected to have hypermetria and/or intention tremors and Maria did not. We can cross out cerebellar disease. What else? Animals with brainstem disease should have a) change in mentation and/or b)ipsilateral  paw replacement deficits and/or c) hemiparesis. Maria has paw replacement deficits ipsilateral to the head tilt so she most likely has brainstem disease. 

OPTION 2:
The other way to work through this is to identify the cranial nerve affected on the exam (in this case, cranial nerve 8), identify the brainstem segment associated with this cranial nerve (in this case, medulla) and then ask yourself if you can identify a,b, or c from above. If not, it is peripheral and if so, it is brainstem. 

Differential Diagnoses

Brain stem vestibular disease in an elderly dog without an important prior medical history would suggest the following differential diagnoses:
Degenerative: none
Anomalous: none
Metabolic: Hypothyroidism
Neoplastic/nutritional: Neoplasia of the brainstem
Infectious/inflammatory/idiopathic: meningoencephalitis (infectious or inflammatory)
Trauma: no supportive history
Vascular: Cerebrovascular accident (stroke)

Diagnostic plan

CBC, serum biochemistry, T4, blood pressure, urinalysis. (Screen for causes of stroke and hypothyroidism). Brain MRI +/- CSF tap. 

Final diagnosis: Cerebrovascular disease! She was lucky. We didn't find any underlying cause of disease therefore this was considered idiopathic vascular disease. She showed gradual improvement with the addition of meclizine over 3-4 days with a residual head tilt after 7 days. The head tilt is expected to be permanent but isn't always the case. 

How did you do? The neurologic examination, when done thoroughly, can be your best diagnostic tool for patients with neurologic disease! Keep practicing. 

I hope you are well, and taking care of yourself. If you have a dog or cat with neurologic disease please reach out - I'd love to help. 

Happy September 1st!