neurologic examination

What is the BEST tool in neurology?

Okay, perhaps you'd want to stop and have a cry if you were stranded on an island with 100 neurologic examinations to do. Hear me out...
Imagine this scenario instead: 2-year-old MC Labrador, with a history of 2 seizures in the last month. The owner is coming to see you and wants to know what is going on!? What do you do first?
Hopefully your answer is a...

THOROUGH NEUROLOGIC EXAMINATION!


What if you don't have the time, staff or patient patience to do a complete exam? If you focus on a few specific parts of the neurologic examination, you can get a good picture of what that pesky forebrain is up to. (The part of the brain that causes seizures.)

Okay, grab your pen (or what ever writing implement you use these days), here are the 4 things to focus on when you perform a neurologic examination on a patient with a history of seizures:

  • Assess mentation: Signs of obtundation or stupor can indicate a lesion in the forebrain (but also the brainstem, so don't be narrow minded if the pet is mentally inappropriate. Do a full exam!)

  • Menace response, paired with pupillary light reflex (PLR): A unilateral absent menace, with a normal PLR and blink reflex, indicates a CONTRA lateral forebrain lesion. 

  • Gait assessment: Specifically, do you see circling? Unusual compulsion? If so, animals generally circle TOWARDS their lesion. E.g., circling left, I’d worry about a left forebrain lesion.

  • Postural reactions:  Deficits will be CONTRA lateral to a lesion causing seizures. E.g. an animal with a left pelvic limb paw replacement deficit may have a deficit on the right forebrain. Note: the new name for CP is paw replacement deficit. Also, remember that those tracts for paw replacement can be abnormal with anticonvulsants, or from other neurologic diseases. When in doubt... do a full exam!

Beware! The neurologic examination may be abnormal after IV administration of anti-convulsant drugs, during the post ictal phase, or if the pet has received long-term anti-convulsant drugs.

Did you know that 90-95% of dogs with idiopathic epilepsy will have a normal inter-ictal neurologic examination??

Furthermore, dogs with an abnormal exam are 16x more likely to have structural brain disease than their normal counterparts! Seriously. The neurologic examination is one of the biggest tools used to predict a diagnosis in an epileptic dog (and I might add, cat). 

Statistics never predict an individual’s condition but by focusing the neurologic examination on these areas you can gain important insight into the health of your patient’s forebrain. Please note: if you find an abnormality, the entire neurologic exam should be performed to make sure that you're not missing multifocal disease. Ultimately guiding owners, helping dogs, and improving everyone’s quality of life is what we’re after, right?

Not feeling confident on the neurologic examination? I'd love to help. The vast majority of my business is identifying IF neurologic disease is present in a given pet so that we can build a reasonable differential diagnoses list.  

Some of you very astutely noted that my schedule went a bit wonky this week. For some reason, the calendar program decided that I didn't need to work until the end of January. (Perhaps AI is more advanced than we know??) As much as I'd love to hibernate, please note that the schedule is now fixed and appointments are now available on the schedule for the end of December and January. Thank you to the vets that reached out!! The only way I knew that something was amiss was because of you so please, please don't hesitate to reach out if you cannot find a suitable time for a consult. It might be because I'm super busy, but, lit might be for other, fixable, reasons, too! 

Have a great week and please fill up the schedule! :)

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 in 2019, 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). 

Thanks for reading! This was an oldie, but a goodie and I hope you enjoyed revisiting it along with me. Please reach out if you have any questions. Have a great week

Age, The Neurologic Examination and Seizures


Age isn't a disease, right? No, it isn't but disease is associated with age. The older pet with seizures 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 differentiate disease in 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 were more likely to have a forebrain disease detected by MRI if they had 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.
What's the take-away message here? If you have an older pet with seizures, and the neurologic examination is NORMAL, you might miss underlying structural brain disease if you do an MRI but, then again, you might now. If you have an older pet with seizures and a menace or proprioceptive deficit is noted you'll LIKELY MISS a structural brain disease if you skip the MRI. 

Although this TidBit is a repeat from 2020, I liked this study and thought it was worth repeating...again. 

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.

Thanks for reading! I look forward to working with you soon. 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

To Seize is to Grab, to Seizure is to Convulse

Seizures and Deficits...What to Do?

Today, we have, back by popular request, another lesion localization practice case! Enjoy!!

Signalment: 7 year old MC Pitbull-X (maybe Boxer dog?)
History: The dog presented with a history of 2 seizures, 1 day apart. Since the seizures, the dog has been walking compulsively to the left, and appears to bump into objects. Although a decreased appetite has been appreciated, the dog is still eating when hand fed. 

Physical Examination: unremarkable

Neurologic Examination:
Mentation: Obtunded
Cranial nerves: Absent menace OD, intact PLR OU, mild head turn left, remainder normal. 
Gait: Ambulatory with intermittent compulsive circling to the left. He is able to walk to the right when asked but will not continue the circles without inspiration. 
Postural reactions: normal all limbs.
Reflexes: Normal all limbs.
Palpation: no spinal pain and normal cervical ROM  and tail jack. 

Neuroanatomic lesion localization (NALL) Practice

Let's look at the examination is sequence as it is listed above. If you wish to use the table format that I prefer, please look at the tables provided in the Small Animal Neuroanatomic Lesion Localization Practice Book (publisher CABI, date 2022 by yours truly). We'll discuss it in conversation format for this TidBit Tuesday. 

Seizures: Seizures ALWAYS localize to the forebrain and are not readily lateralized (left or right side). 

Obtunded: reduced mentation is noted with lesions in the forebrain and brainstem. This is NOT a clinical sign of cerebellar, spinal cord or neuromuscular disease, nor a non-neurologic finding. This narrows our lesion localization to forebrain or brainstem.

Cranial nerves: The menace pathway, in it's most basic sense, involves CN 2, the forebrain and CN 7. PLR involves CN 2, midbrain and CN 3. The blink reflex is not states as being abnormal above (blink reflex: CN 5 and CN 7) therefore by process of elimination, the menace deficit OD is most likely due to a forebrain lesion. The second part of the story is lateralization. Only the right eye is affected. This is a crossing tract (mostly) which means that the lesion should be on the left side of the forebrain.

Gait: The compulsive circling to the left is localized to the forebrain and, rarely, vestibular system. Localization to the vestibular system is most likely when a head tilt is present. Without a head tilt, I would consider a forebrain lesion most likely and they circle TOWARDS their lesion. This would further support a left forebrain lesion. 

NALL: Left forebrain

How'd you do? Did anything surprise you with the NALL? If you enjoyed this case, thank your colleagues for suggesting a seizure NALL case for practice. :)

As a reminder, I will be out of the country starting next week through November 14th. I will be available by email ONLY (no cell phone service) and will be doing my best to keep up on emails. Please expect minor delays in my response because I will be lecturing and we'll be on different time zones but I will do my best to be as responsive as possible. 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.