A New Study Evaluates a Seizure Questionnaire

                 A large multicenter European group recently published data regarding a new survey designed to help more closely evaluate seizure semiology (appearance) to help us better classify seizures vs dyskinesias (abnormal movements that aren’t seizures). Over 600 dogs were included in the initial survey. You can view the survey here: https://dogepilepsyresearch.org/us/. The owners were instructed to proceed through 7 steps during episode description.

Step 1: report the seizure appearance in their own words

Step 2: Read a description of one of 4 episodes and see which one best fits their pet. These included 1) generalized seizures 2) non-generalized motor events 3) sudden falls without movement and 4) episodic impaired awareness (stare into space with behavioral arrest). The survey provides verbal descriptions of the categories as well as videos.

Step 3: Owners answer specific questions about the seizures include pre/post ictal signs, signs at first onset, description of the position, muscle tone, responsiveness during the event, age at onset, triggers and a few other questions.

Step 4: Historical questions about familial history, a history of head trauma or puppyhood diseases are asked.

Step 5: Veterinary exam results

Step 6: Medications and medication history

Step 7: Interictal changes in behavior

Results

The most common breeds were Labrador retrievers, Siberian Huskies and Border collies. Median age at onset was 2 years (IQR 1-5 yrs) with 80% experiencing their first episode between 6 months and 6 years old. Only about 50% of the dogs has neurologic examinations (what??!). Interestingly, owners described generalized seizures in about 58% of dogs, non-generalized motor activity in 58% of dogs, sudden falls in 6% and episodic impaired awareness in 15% of dogs. Over 25% had multiple types reported. Overall, reviewers agreed with owner classification about 90% of the time. Similarly, for dogs with multiple different types of seizures, reviewers agreed with classification about 86% of the time. The questionnaire was considered usable and/or easy to complete by about 70% of owners.

Interestingly, Labrador retrievers were more likely to have one classification, and it was the non-generalized motor event. This was compared to Huskies and Border Collies who were more likely to have generalized type seizures. Within the Labrador group, the majority of cases were consistent with dyskinesias NOT seizures (70%) and focal motor seizures in 24%. The remainder were undefined in classification.

Key Points
This questionnaire is a great tool for those researching seizures (um…me) but might be worthwhile for all of us to look at to make sure we are asking the right questions. While they did not set out to differentiate between dyskinesias and seizures, they state that this questionnaire might be the right tool to do so. My goal in showing you this article was to make you aware of the existence of this seizure questionnaire. Your clients can contribute to the ongoing data collection (by completing the form), and you can become familiar with the types of questions that might be helpful when faced with a dog with a possible seizure disorder.

If you’d like to watch the videos linked to the survey please see the article: https://doi.org/10.1111/jvim.70077

Thanks for reading! I hope you are finding time to enjoy this wonderful fall weather!

Phosphate concentrations and Seizures vs. Syncope?

Seizures Vs. Syncope

We've all been there, right? An elderly small breed patient with a grade II or III heart murmur presents to you with a history of "passing out". Clients aren't more descriptive than that, and they didn't catch a video. Is this syncope or was this a seizure?

You have several things to ask and look for (see prior TidBit Tuesday on syncope) but recent research has given us one more tool in our belt to help differentiate between these two diseases. 

Human patients with generalized tonic-clonic seizures demonstrate a reduced phosphate level within several hours of the event and patients with syncope do not. A study from Israel published data in January 2023 that strongly suggested a link between hypophosphatemia and seizures in dogs, as well. According to this study, 87 dogs with seizures and 26 dogs with syncope were included. Phosphate was evaluated within 3 hours of the "event" in question and noted to be decreased in 28 (32%) of dogs with seizures. None of the dogs with syncope had a low phosphate level. Dogs were excluded from the study if their creatinine was above the normal range to eliminate those cases with hypophosphatemia from renal causes. Median phosphate levels were significantly different between the two groups!

Key point: With an optimum cutoff value of 0.97 mmol/L (about equal to 3.0 mg/dl), evidence of hypophosphatemia has a 100% specificity and 44% sensitivity to diagnose seizures. 

Importantly, this tool should not be used as a stand alone finding to differentiate between seizures and syncope! However, identification of hypophosphatemia, within 3 hours of the witnessed event, could suggest a generalized seizure was more likely than a syncopal event if all other historical, physical examination and biochemical findings are concurrently evaluated. Important note: This has not been verified in dogs with focal seizures or complex partial seizures OR cats! 

This week's TidBit Tuesday is short and sweet. Have a wonderful week!

Reference: https://doi.org/10.1016/j.tvjl.2022.105914

Are Vertebral Malformations in French Bulldogs Painful?

Many of us have evaluated a spinal radiograph on a French Bulldog and thought “is this dog painful”? A recent study out of UW-Madison tried to evaluate this question in a prospective study.

Methods

Twenty-five client owned French Bulldogs, and 12 non-French Bulldog breed dogs were included as case and control animals, respectively. All dogs were perceived to be neurologically normal and non-painful by the owners. It is unclear if the researchers performed a neurologic examination to confirm this suspicion, but I assume that they did. All dogs had full spinal radiographs performed and mechanical sensory threshold (MST) testing was performed at 3 separate vertebral sites. The maximal force was 11 lbs. – which seems adequately weighted to assess for pain.

Results

What do you think they found? This study found no significant difference in MST testing between dogs with vertebral malformations and those without. This means dogs with only radiographic vertebral malformations do not need pain management. If you palpate a patient and elicit spinal pain, do not assume the pain is due to the underlying vertebral malformation. Keep digging! This pet may have a disc herniation, or articular cyst, or even meningitis causing its pain.

This week’s Tidbit Tuesday is short and sweet…just like summer! Enjoy the last few weeks of summer with those you love, and I look forward to working with you soon!

Reference: Pinal K, Zidan N, et al. Mechanical Sensory Threshold in Neurologically Normal French Bulldogs with Vertebral Malformations. ACVIM abstract 2025.

Epidural Steroids for Disc Herniation in Dogs?

Epidural Steroids for Disc Herniation in Dogs?

Epidural steroid administration has been a common therapeutic option for humans with low back pain secondary to intervertebral disc herniation (IVDH) but is rarely employed for veterinary patients. This option was recently evaluated in a double blind evaluation in 41 dogs.

Methods
The dogs were randomly assigned to either the control group (given epidural saline) or treatment group (1 mg/kg epidural methylprednisolone sodium succinate: MPSS). All dogs underwent surgical intervention (decompression) and the saline or MPSS was applied in the epidural space at surgical closure. Post operative care was similar between both groups.

Results

The dogs that received MPSS walked at a median of 3 days (range 1-8 days) and control dogs walked in a median of 7 days (range 1-17 days). This was a significant (P=0.01) difference between groups. Bodyweight did not affect recovery, however age did influence recovery. Younger dogs walked faster than older dogs, but both groups contained similar age ranges nullifying this finding as a cause for the significant difference.

One dog in the treatment group became non-ambulatory after regaining the ability to walk. This dog developed discospondylitis secondary to Staphylococcus aureus and dygalactidae which was ssumed to be seconcary to MPSS application, however an N=1 makes this association challenging to make. The dog was treated with antibiotics and subsequently regained ambulation.

Key Points

Although this isn’t the first report of intrathecal MPSS use in dogs, it contained the biggest case count. The significant difference in ambulation leads me to wonder about using this as another treatment option for dogs unable to undergo surgical intervention. Given the sufficient safety data from this and prior studies, it appears safe to administer with a less than 10% chance of serious adverse effects (discospondylitis). If you have a patient that is non-ambulatory but cannot go forward with surgery, and we have a high index of suspicion for IVDH, let’s talk about intrathecal MPSS. If you are a general surgeon performing spinal surgeries, or a neurosurgeon, I’d love to know if you give epidural MPSS or if you’re inclined to do so after reading this report. In case you’d like to read the full study you can find it here: DOI: 10.1002/vetr.4962

Thanks for reading!  Have a wonderful week!

Sleep and Neuropathic Pain in Cavalier King Charles Spaniels

A study was presented at ACVIM this year (2025) by Drs. Parker et al that evaluated sleep scores, neuropathic pain scores and perceived QOL by owners in a cohort of Cavalier King Charles Spaniels. The premise for this study was that poor sleep might exacerbate chronic pain in humans. They enrolled 68 CKCS, 37 of whom were diagnosed with caudal occipital malformation syndrome (COMs). Of these 37 dogs, 19 of them were considered to be clinical for the diagnosis and 18 were not clinically affected. Interestingly, dogs with clinical COMS also had greater difficulty falling asleep, ability to stay asleep for long periods of time, and overall poorer sleep quality. It was noted that more dogs slept with their heads propped up than not in the clinically affected group.

Why are they sleeping more poorly?

The authors propose that dogs with COMs may have chronic pain, which results in greater sleep disturbances. Additionally, part of the COMs complex is kinking of the brainstem which is where respiratory centers and the reticular activating system (RAS) are housed. The authors proposed that disrupted sleep could be due to alterations of these systems as well. Lastly, these dogs are brachycephalic which can result in snoring while sleeping, which is also linked to poorer sleep scores.

What do we do about it?

Owners can purchase a “fit bark” or other activity monitor that tracks their dog’s sleeping patterns. If frequent sleep disturbances are noted, initiation of pain management, investigation into brachycephalic airway surgery, or allowing for a “propped” head position might be indicated to improve sleep. The pain management medication I suggest in these cases is gabapentin or pregabalin, however excessive sedation should be monitored.

Although not exactly in line with our summer of cranial nerves, I thought this study was interesting and worth sharing. Stay tuned for more Tidbits gleaned from the national meeting this year!

Thanks for reading. I hope you have a wonderful week and enjoy these dog days of summer with those you love.

Time For a Tongue Twister!

For my "old-timers" this is a repeat TidBit Tuesday from 2021 (wow! time flies!). This is a really cool case about a cranial nerve deficit that we don't see very often. Enjoy this week's installment of our Cranial Nerve Summer Bonanza!

Signalment: 12 year old MC Mixed breed dog, 45 kg
History: 1 month history of change in bark, with a 1-2 week history of difficulty eating and drinking. The owners also identified difficulty walking in the last few days and a decrease in the dog's interaction with them. 
Physical Examination: Grade II/VI left heart murmur, previously noted and not progressed. The remainder of the exam was unremarkable.

Neurologic Examination

Mentation: Mildly obtunded. The pet interacted when asked, but otherwise seemed content to stare at the floor. 
Cranial nerves: Decreased to absent gag reflex, tongue atrophy (see the photo above), all remaining cranial nerves were normal. 
Gait: Ambulatory mild proprioceptive ataxia in all four legs
Reflexes: Normal spinal reflexes including c. trunci and perineal. 
Palpation: Non painful spinal palpation however pain elicited with cervical ventroflexion
Postural reactions: absent right thoracic and right pelvic limb paw replacement test, normal left paw replacement thoracic and pelvic.

Neuroanatomic Lesion Localization??

To do this, we need to break it down and identify all of the possible anatomic localizations each neurologic deficit could be noted. I prefer table form, but flow charts are also great.

DeficitWhere are ALL the places this abnormality could localize?Likely localization for THIS patient and whyObtundedCerebrum, diencephalon, midbrain, pons, medullaMedulla due to cranial nerve deficits noted.Gag reflexAbsent CN 9 and/or 10. This localizes to the medulla OR the peripheral nerves of 9 or 10Unable to determine if it has affected 9 or 10 however a central (not peripheral) lesion localization is suspected due to the concurrent paw replacement deficits and obtunded mentation.Tongue atrophy (right)Right CN 12 or right medullaSuspect medulla due to concurrent right sided paw replacement deficits and obtundationProprioceptive ataxia in all 4 legsC1-C5, medulla, pons, midbrain, prosencephalonSuspect medulla due to other findings but this does not localize all by itselfPain on cervical ventroflexionIncreased intracranial pressure (also called referred spinal pain), C1-C5, C6-T2 myelopathyLikely intracranial referred spinal pain due to concurrent cranial nerve deficitsAbsent right thoracic and pelvic paw replacementTo cause ataxia in both front and back legs, we need to assume the lesion is cranial to C6. Therefore, possible locations include C1-C5, medulla, pons, midbrain, prosencephalon.Likely medulla based on concurrent CN 9, 10 and 12 deficits noted above.

Do you see what I did here? I listed all  of the possible locations that the affected deficit might involve and then narrowed down the lesion localization two ways:

1. Find the common denominator. In this case, the medulla. OR

2. Find the cranial nerve(s) affected and determine if the pet also has: a) abnormal mentation, b) hemiparesis ipsilateral to the affected cranial nerve or c) paw replacement deficits ipsilateral to the affected cranial nerve. If they do, it is central. If not, it is a likely a peripheral neuropathy. 

Neuroanatomic Lesion Localization

Medulla, right side.

Differential Diagnoses

Neoplasia, meningoencephalitis (infectious or inflammatory)

Case Conclusion

This dog had normal CBC, serum biochemistry, UA, chest radiographs and abdominal ultrasound. Brain MRI identified a discrete contrast enhancing extra-axial mass in the right caudal fossa affecting the right side of the medulla. This finding was most consistent with a meningioma. A spinal tap was not performed due to the proximity of the mass to the cerebellomedullary cistern. Based on the working diagnosis surgical decompression, radiation therapy or supportive care were discussed with the owners and they elected supportive care.

Thanks for reading! I hope you have a great week. If you have a new colleague in your clinic please ask them if they'd like to sign up - the more the merrier!

Recurrence of Cervical Disc Herniation following Prophylactic Fenestration

Today we're going to take a small break from our cranial nerve evaluation to look at the recurrence rate of confirmed and suspected cervical intervertebral disc herniations in dogs with or without prophylactic fenestration. A study published in Veterinary Surgery by Berthome et al detailed the recurrence rate in a group of dogs that received prophylactic fenestration to those that did not.
What is fenestration? Fenestra means “window” in Latin, which is exactly what we’re cutting in the disc. This procedure is performed in dogs with a concurrent Type I disc herniation after removal of the herniated disc. This surgery is performed on the discs that did NOT herniate; thus, it is called prophylactic. During surgery, many neurologists, me included, cut a small window in the outer annulus fibrosis and “scoop” or attempt to remove the nucleus pulposus from the intervertebral disc. Fenestration is supposed to reduce the risk of herniation via three ways: 1) remove of the offending nucleus decrease the amount of material available to herniation. 2) provide a different path of least resistance for the disc to herniation (in the neck this will be ventrally away from the spinal cord) and 3) the scar tissue that forms after mechanical fenestration holds the remaining nucleus pulposus in place.
Results
The study by Berthome et al included 55 dogs, with weights less than 20 kg. Of these 55 dogs, 18 received prophylactic fenestration, and the remaining 37 did not. Neurologic grades were similar between groups, as were surgical sites for the herniated disc. Recurrence was defined as confirmed if advanced imaging was performed and a new disc herniation was noted. It was defined as suspected if clinical signs of new neck pain or worsening gait changes were documented by a veterinarian, but no advanced imaging was performed. A recurrence rate of 25% was noted (14/55) and all 14 dogs were in the non-fenestrated group. Only 1 dog had a confirmed new disc herniation, the remaining 13 were suspected. Surgical times were significantly shorter (p = 0.017) for dogs not undergoing fenestration compared to those that underwent prophylactic fenestration. Complication rates were similar (p=0.838), and no major perioperative complications were found in this study in either group.
Take Home:

• Prophylactic cervical disc fenestration may reduce the risk of disc herniation

• Srugical times may be longer if prophylactic fenestration is performed, leading to higher anesthetic costs (significance unknown)

• Recurrence was not confirmed in most of the cases so take this will a little grain of salt

Reference:DOI: 10.1111/vsu.14303. Vet Surgery J 2025

 
As I mentioned above, I do fenestration and have been an advocate for this for years. If you perform ventral slot surgeries and are unclear on the fenestration technique let me know; I’d be happy to teach you. Based on this data, hopefully we can reduce the risk of recurrent neck pain on our small dog population that is already over represented with cervical pain!Thanks for reading. I hope you’re staying cool in this summer heat.

Visual Fixation Test

In keeping with our cranial nerve summer theme, I thought you might enjoy this interesting study about visual fixation testing in dogs.  

What is Visual Fixation testing?

Visual fixation testing (VFT) is performed in humans with vestibular disease to help differentiate between central and peripheral lesions. For this test, patients are asked to fix their gaze on a target and then a bright penlight is shone into one eye while the other is covered. Patients with peripheral disease can suppress spontaneous nystagmus during testing, while those with central disease cannot. Exceptions were described such as those with focal cerebellar lesions, however the majority of humans with central lesions fail this test.

Visual fixation testing in dogs?

We clearly cannot ask dogs to focus their gaze, so would this work in veterinary patients? A recent study from the UK asked this question. They omitted the request to fixate and simply covered one eye while shining a bright focal light into the other eye. The slow phase of nystagmus was expected to increase in velocity with peripheral vestibular disease, therefore increasing the number of beats counted in 10 seconds compared to prior to VFT. Dogs with central disease were expected to have no change in beat frequency.

Results

·         Almost ½ of the dogs had spontaneous nystagmus in both the peripheral and central group (48% and 44% respectively).

·         During the VFT, an increase in beat frequency occurred in 33% of the peripheral group

·         Only 1 case (6%) had an increase in beat frequency in the central group.

·         The change in frequency was significantly different between central and peripheral vestibular disease, with more dogs showing an increase in beat frequency in the peripheral group.

·         An increase in slow phase velocity was significantly associated with a peripheral diagnosis and this was significant even after the dogs with idiopathic disease were removed.

·         Dogs with peripheral vestibular lesion localization had a 95% of having peripheral diagnosis with a neurologic examination alone. When accounting for the VFT, this probability increased to 99% (1% of central disease).

·         Dogs with central lesion localization based on neurologic examination alone, had a 17% chance of peripheral disease. If they demonstrated an increase in beat frequency this increased their likelihood of peripheral disease to 52%.

Take away message

While only 1/3 of dogs with peripheral vestibular disease had an increase in beat frequency with the VFT in this study, this tool is one more easy option to attempt to localize vestibular disease more specifically. Central vestibular disease is frequently correctly localized based on the neurologic examination. On the contrary, 20% of dogs with central disease are diagnosed with peripheral vestibular disease. If a dog with suspected peripheral lesion localization has an increase in beat frequency during VFT, this can further support our lesion localization.

Reference: https://onlinelibrary.wiley.com/doi/epdf/10.1111/jvim.70182

Thanks for reading! I hope you enjoyed this “bright” TidBit Tuesday during this sunny summer day! Have a great rest of your week.

The Facial Nerve

The Facial Nerve 

The facial nerve is a large motor nerve, originating from the medulla, that causes the muscles of the face to contract. These are often called the "muscles of facial expression". What happens when this important nerve malfunctions?

What does paralysis look like?
The facial nerve innervates the muscles of facial expression in dogs and cats as well as innervation to the lacrimal eye glands. Clinical signs are typically unilateral and, result in an inability to move the eyelids (inability to blink), inability to move the lips (dogs may accidentally chew on their lips and look "droopy" ), lack of ear movement (especially noticeable in cats), and a dry, red eye with possible ocular ulceration. They look bored because they cannot make a facial expression. 

What causes facial nerve paralysis?
Facial nerve paralysis can be caused by peripheral or central dysfunction. Diseases affecting the peripheral nerve might include hypothyroidism, neoplasia, otitis media, polyps, rarely neuritis and everybody's favorite - idiopathic. Idiopathic facial nerve paralysis is actually the most common cause of peripheral facial nerve paralysis in dogs. Central facial nerve paralysis occurs when something dysrupts the nerve function at the level of the brainstem. In additional to facial nerve paralysis, dogs will show ipsilateral paw replacement deficits, changes in mentation, and occasionally hemiparesis with central dysruption. The causes of brainstem facial nerve paralysis are often neoplasia, meningoencephalitis or vascular. 

The Diagnostic Challenge
After localizing the lesion, the next step is to make the diagnosis. Animals with central disease are best diagnosed with MRI +/- spinal tap. Animals with peripheral disease would benefit from a T4, neospora IFA, toxoplasma IgG/IgM (and other geographically specific infectious disease testing), and an MRI. Idiopathic facial nerve paralysis is diagnosed when all causes have been ruled out. 

Treatment for facial nerve paralysis is clearly based on the diagnosis. All animals with facial nerve paralysis benefit from eye lube at night (they cannot blink or close their eyelids) and eye drops during the day until the blinking returns. 

I hope this TidBit was useful.  This summer I'm going to spend some time looking at the cranial nerves in TidBit fashion so buckle your seatbelts! Have a great week and I look forward to working with you soon!

Sedating Dogs with Intracranial Disease

Frequently I am asked if a specific sedation protocol should be used for a pet with known, or suspected, intracranial disease. The biggest concern with anesthesia is a shift in the intracranial pressure (ICP), which is directly linked with the mean arterial blood pressure. Therefore, it is commonly recommended that medications are chosen which have minimal effect on blood pressure. Butorphanol is a commonly used premedication for dogs and often part of the recommended protocol for “safe” sedation. A study performed in the UK, and published in Veterinary Anesthesia and Analgesia, evaluated the effect of intravenous butorphanol on dogs with and without intracranial disease.

Study Design

Fifty-three dogs, presenting for brain MRI, were enrolled in the study. Each dog was sedated with 0.2 mg/kg IV butorphanol and the time to recumbency as well as the sedation score were recorded for each dog.  The sedation score was adapted from a prior publication (Grint et al 2009) and was scored 0-4 for six separate categories with a maximum score of 19.

Results

Nineteen of the 53 dogs had intracranial disease, the remaining 34 did not. Ten of the 19 dogs also had signs of intracranial hypertension. The overall median sedation score time 0 was 1 (range 0-10) , and 6 (range 0-15) at 15 minutes. Dogs with intracranial disease had a significantly higher sedation score at both 0 and 15 minutes. This was especially notable at 15 minutes when the dogs with intracranial disease had a median sedation score of 12, compared to dogs without intracranial disease who had a median sedation score of 4. A greater number of dogs with intracranial hypertension achieved recumbency than those without intracranial hypertension.

Clinical application

If you sedate a dog with butorphanol for a procedure (dental, radiographs, other) and the dog becomes recumbent at 15 minutes, it would be wise to continue the anesthetic protocol under the assumption that the dog may have intracranial disease. For example, use propofol instead of dexdomitor so that the intracranial blood pressure (and flow) is less likely to be affected. As the authors point out, it is helpful to remember to account for other sedation medications on board and note any recent seizures that could play a role in the level of sedation that an animal achieves. Nothing will replace an MRI diagnosis of the presence of intracranial disease, however keeping the “butorphanol test” in mind might help reduce the risk of undesirable consequences in patients with undiagnosed intracranial disease.

Thought provoking, right? I hope you found this TidBit useful and look forward to working with you soon!

Acute, Progressive Tetraparesis in a Large Breed Dog

It is time again for a lesion localization practice case. This one is brought to you by springtime: the giver of all dormant insects, infectious diseases and allergies. 

Signalment: 4 year old  MC German Shorthaired Pointer 
History: The dog was noted to have weakness in the left back leg yesterday morning when the owners let him out. By noontime he was weak in both pelvic limbs, and this morning he is struggling to stand on all four limbs. He continues to urinate, defecate and wag his little nub tail. The dog is used as a fall hunting dog (it’s springtime now) and is a house pet for the remainder of the year.
Physical examination: He is a well-muscled, well behaved (for a pointer) dog without evidence of abnormalities on his physical examination. TPR is normal.
Neurologic examination:
Mentation: BAR
Cranial nerves: normal
Gait: Nonambulatory tetraparesis. When he tries to stand, he cannot rise on his pelvic limbs at all, and trembles when supporting weight on his front limbs before collapsing.
Postural reactions: with support, he does have paw replacement deficits in both pelvic limbs and the left thoracic limb. The right thoracic limb is slow, but intact.
Reflexes: Absent patellar reflexes bilaterally, absent withdrawal reflexes both pelvic limbs, reduced withdrawal both thoracic limbs (worse on the left thoracic compared to the right thoracic limb). Absent c. trunci reflex both sides. Normal anal tone and reflex.
Palpation: non-painful spinal palpation with normal cervical ROM and no pain on tail jack.
Neuroanatomic lesion localization
Whew. This is a toughie! Let us start from the top.

1. Does this animal have evidence of neurologic disease?

2. Does the dog have a seizure history, show evidence of mentation changes or have any cranial nerve deficits?

3. Does the dog have weaknesses in 1, 2 or more legs?

4. Does the dog have reflex deficits?

5. Does the dog present or absent reflexes?

Draw out a stick figure of a dog and follow along as we go through the answers. Answers:

1. Yes

2. No. This means the lesion shouldn’t be intracranial. Cross off the head on your stick figure.

3. Yes. The dog is weak on all four limbs. The pelvic limbs are weakest, followed by the left thoracic limb and least affected is the right thoracic limb. This means that the lesion is expected to be in the muscles, peripheral nerves, C1-C5 spinal cord or C6-T2 spinal cord. Circle these areas on your stick figure or cross off T3-L3 and L4-S3.

4. Yes! The reflex arcs for the limbs at C6-T2 (thoracic limbs) and L4-S3 (pelvic limbs). Animals with a spinal cord lesion in these areas will have reduced reflexes in the limbs. It is very rare to have two spinal cord lesions, one in each plexus, therefore when an animal has deficits in both thoracic and pelvic limbs it is reasonable to assume the lesion is in the peripheral nervous system rather than the central nervous system (spinal cord) until proven otherwise.

5. This answer is a little bit subjective, but the question is trying to make us think about the peripheral nervous system. If an animal has a myopathy, we expect them to have normal reflexes. Animals with neuromuscular junctionopathy are expected to have absent reflexes and lastly those with peripheral neuropathies are expected to have reduced reflexes. There are exceptions (myasthenia gravis is a junctionopathy but often animals have intact reflexes!). The dog has absent reflexes in both pelvic limbs, but it also has reduced reflexes in the thoracic limbs. This likely reflects progression of the disease rather than two different diseases so I would consider this most likely to be junctionopathy or a severe neuropathy.

Neuroanatomic lesion localization: Peripheral nervous system (PNS), specifically junctionopathy or neuropathy.
Differential diagnoses: common causes of junctionopathy include tick paralysis, botulism, polyradiculoneuropathy (coonhound paralysis), organophosphate toxicity and fulminant myasthenia gravis.

What do you do now?
Myasthenia gravis: acetylcholine receptor antibody titer (https://vetneuromuscular.ucsd.edu/)
Botulism: evacuating the stomach, supportive care such as IV fluids, nutrition, physical therapy, and nursing care
Tick paralysis: apply an anti-tick medication such as Frontline (no, I do not get kickbacks for saying this).  Provide supportive care and monitor.
Organophosphate toxicity: evacuating the stomach and supportive care like with botulism.
Polyradiculoneuropathy (Coonhound paralysis): supportive care. Some universities will use immunoglobulin. Electrodiagnostic testing and CSF can suggest this is the diagnosis, but we do not have a singular diagnostic test available.

Thankfully, this lovely dog had tick paralysis and was back up and running 48 hours after applying the anti-tick treatment topically.
Tick paralysis is NOT caused by an infection (e.g. Lymes disease) carried by the ticks. This is caused by an autoimmune reaction against the tick “saliva” when it bites the animal. Minimizing tick bites is the best prevention. Removing the tick is the treatment. It does not appear that a dog will develop immunity after developing tick paralysis so keep applying the topical preventative all through tick season!
 
I hope you have enjoyed this week’s TidBit Tuesday. Please reach out with any topics you would like to see covered. Have a wonderful week!

Acute Seizure Monitoring Devices

Recording the number and duration of seizures is the best way for owners to help us manage seizures long-term. Should we start anticonvulsant medications? Should we increase medications? Should we stop medications or try something different? These questions are all dependent on the seizure frequency and duration. If the seizure frequency is acceptable but each seizure is 15 minutes long, adjustments are needed. If the pet is not showing adverse clinical effects, and the serum drug concentration is good, but the pet has 1 seizure per week, we need to make a change. If the pet continues to have cluster seizures, despite adequate drug concentrations, we need to make a change.
There are many data recording options available to owners.

1. Keep a paper log with date, duration and number of seizures (this doesn’t need to be a diary!)

2. Keep a spreadsheet record

3. Use a smartphone app. There are many available and some can even connect to the vet clinic. (RVC Pet Epilepsy Tracker; PetPace; Safetail; SeizAlarm)

What if the owner cannot be with their pet 100% of the time? (This is everyone.) How will we know if we missed a seizure? Here are some options that I provide for owners:

1. Consider a video camera and keep the pet in the room with the camera when you are gone. This works well to document seizures but can increase anxiety in an owner if they witness the seizure but aren’t there to intervene or comfort the pet.

2. Consider using a FitBark monitor. FitBark is like the human FitBit. It detects gyroscopic movements and is an activity monitor. It has also been evaluated as  a “scratch-o-meter” by dermatologists. I have played with it as a seizure monitor but do not have official data to support its use as a seizure alert tool. If a pet has partial seizures (head shaking, jaw chomping, other) it likely will not trigger the FitBark. Generalized seizures are likely to be identified as an increase in activity but the monitor cannot distinguish between running around the house after a housemate or having a generalized seizure.

3. Observe for signs of a seizure upon your return. This is our typical recommendation for owners. If a pet voids during a seizure, they may see urine or feces unexpected. If a pet has profound ptyalism, there may be evidence of drooling on the pet or surroundings. This is the least objective measure and probably has a high false negative result.

Recently a report was published out of Japan (https://doi.org/10.3389/fvets.2025.1558274) detailing a patented seizure-detection system (SDS) that they developed for dogs. This is not yet commercially available but, based on the results, it may be available in the near future. The device was previously tested in laboratory dogs.

Study Design and Outcome
One research Beagle and 12 client-owned dogs were enrolled in the study. The dogs were hospitalized with 24-hour staff who were available for intervention for seizure management. A video system was placed and the SDS was  placed into a custom designed jacket worn by the pet during the observation period. The device was connected to an application on a smartphone.  The SDS detected 25 of 34 seizures during the observation period, providing a sensitivity of 74.3%. The median sensitivity for detection was calculated to be 37.5% for each dog (range 0-91.7%). Three false positives were noted in only 1 dog, one of which was excluded because the jacket fell off. The authors calculated the positive predictive value to be 92.6%. Median latency from onset to detection was 11 seconds (range 6-75 seconds). During the observation period 35 focal seizures, which did not develop into generalized seizures, were observed and none of them triggered the SDS.

Discussion
This device performed more poorly than previously reported data for human SDS. Human SDS have a sensitivity between 79-91% and this device had a sensitivity of about 74%. That said, this is a very positive step toward canine SDS. The time from the onset of the seizure to detection by the SDS was a respectable 11 seconds. This latency is well within the acceptable window of observation expected in a hospitalization scenario or it would allow an owner to address the seizure if they are in the area but not directly observing the dog. This tool may soon be one more option for us to accurately record seizures for pets at home. As with all tools, knowing the limitations (partial seizures) and the expected outcome (low false positive results) will help us guide owners to the best monitoring for their pet.

 
Thanks for reading! Have a wonderful week and I look forward to working with you soon!

MRI changes in dogs with Neosporosis vs Meningoencephalitis of Unknown Origin (MUO)

Well folks, we’re back to talking about Neospora caninum infections this week. BOY have I been seeing a lot of these! Are you holding them special for me or are we seeing a global increase in neosporosis in dogs?

This week, I reviewed an article that was published in the Frontiers Journal (doi.org/10.3389/fvets.2024.1517256) in January 2025. The purpose was to describe the MRI and biochemical findings in dogs diagnosed with Neospora caninum and compare them to those diagnosed with meningoencephalitis of unknown origin (MUO). Quick refresher:

MUO: non-infectious, inflammatory (suspected auto-immune) inflammation in the brain, spinal cord and nerves that can affect dogs or cats. Diagnosis is obtained via a combination of MRI, CSF and clinical history findings in conjunction with negative infectious disease testing.  Treatment is immunosuppression. Not curable.
Neospora caninum: a protozoal parasite that can affect brain, spinal cord, nerves or muscles. Diagnosis is obtained via positive serum titers and/or histopathologic observation of the encysted organism. Treatment is clindamycin or sulfa antibiotics, in most cases. Maybe curable?

Riddle me this: What do you do when you see a dog with multifocal neurological signs, and you’ve identified inflammation on MRI and spinal tap but don’t have the infectious testing back yet? Statistically, about 98% of dogs have MUO… infectious meningoencephalitis is only about 2% of the population. Infectious meningoencephalitis could be caused by fungal, bacterial, protozoal or viral infections. Infectious serology/PCR takes 7-10 days to come back in many cases. So, what do you treat? This article attempted to identify markers of neosporosis on MRI to improve early identification BEFORE serology is available. Here is what they found:

• CSF analysis: no statistical difference between dogs with MUO and those with Neosporosis in WBC or protein.

• CK: Dogs with Neosporosis had significantly higher CK compared to those with MUO. (median 1423 U/L vs 161 U/L).

• MRI: Dogs with neosporosis had inflammation more frequently in the masticatory muscles compared to dogs with MUO. The presence of muscle changes had a sensitivity of 27% and specificity of 96% to predict a diagnosis of neosporosis. The odds ratio was 8.25 but not statistically significant.

Take home message:

• If you have a dog with multifocal neurologic lesion localization, run a CK on your routine biochemistry testing. If it’s pretty darn high, run a Neospora caninum titer on serum (IFA)!

• If I see masticatory muscle inflammation on MRI, I’m going to suggest we treat with clindamycin while awaiting serology results…just..in..case.

• Keep up the good referrals! We’ll keep trying to figure out why Neospora caninum has become so prevalent in Wisconsin.

Thanks for reading! I hope you have a great week!

"Doc, The Dog is Having A Seizure!"

No one likes to hear those words (not even neurologists). Upon hearing those words you rush into the exam room and are faced with a convulsing dog on the floor. Here is your preemptive stop and think moment (yay!):

Why do we want to stop seizures, anyway?

Prolonged seizures can result in hypertension, tachycardia, acidosis and hyperthermia with secondary neuronal cell death and hypoxia. These changes negatively affect the brain and may have systemic effects as well. The goals of acute seizure management are to stop the seizure as quickly as possible thereby limiting secondary brain and extra cranial organ damage.

Give me the "Go-To"!

Look no further than your Benzodiazepine class of drugs. Benzodiazepine drugs (Diazepam, Midazolam, Lorazepam) were introduced in the 1960s for human status epilepticus. A human meta-analysis identified that benzodiazepines are the “best” first line IV drugs and identified the therapeutic concentration to be between 150-300 ug/ml. To date, there have not been any veterinary studies identifying which drug is ‘best’ for acute seizure management. We’ve always used benzodiazepines so, we continue to do so.

• Rectal, at home care: Home care with liquid rectal diazepam is often recommended for patients at risk for cluster seizures. Compounded suppositories are not currently recommended. Rectal midazolam and lorazepam are not recommended! We also know that chronic phenobarbital use reduced plasma concentrations of diazepam. With this knowledge we recommend dosing rectal diazepam at 1-2 mg/kg if the patient is receiving chronic phenobarbital therapy.

• Intranasal diazepam and midazolam: Intranasal diazepam, using an atomizer, resulted in detectable levels in about 2.5 minutes which makes this drug a viable alternative for at home anticonvulsant care. Midazolam was even more rapid and had a better outcome than rectal diazepam in one study of epileptic dogs so it is currently my drug of choice for at home (or non-IV) care. 

All the "cool kids" are using levetiracetam. Should I?

Well, maybe yes, maybe no. Levetiracetam's use has been documented in veterinary medicine since 2004. It is considered a relatively safe drug, with few reported side effects. This drug is typically used as an add-on or alternative to intravenous benzodiazepine therapy for acute seizure management at doses ranging from 30-60 mg/kg IV. Adding diazepam and levetiracetam together resulted in improved seizure control in epileptic cats so this is currently my recommended way to give IV levetiracetam. (Unless diazepam is contra-indicated such as with hepatic failure.)
Rectal levetiracetam may be on the horizon according to one study in 2014. However the first sampling time was 10 minutes therefore it is unclear if this drug will be useful in acute seizure management.  

Is Propofol Still Used?

Yes, but I don't have any new information. We all like shiny, new things, but propofol may still have a place in acute seizure management. There are a small number of published studies addressing this use in veterinary medicine. This drug is only recommended for intravenous use. Care must be exercised when using propofol due to its respiratory suppressor effects. Occasionally, intubation may be required if apnea is encountered during bolus therapy. Propofol withdrawal may result in distal limb twitching which may be difficult to distinguish from seizure activity. Extended exposure in cats to propofol may result in Heinz body anemia therefore a CBC analysis is recommended every 24 hours during constant rate infusion of propofol with cats.

Thanks for reading! I hope you have a great week and look forward to working with you soon!!

Quiz Time! Test your Lesion Localization Skills!

It's Monday morning, and your first case is presenting for "not walking well". Let's review some neuroanatomic lesion localization so you can be awesome on a Monday morning!

Signalment: 4 year old FS Labrador X
History: The dog was outside playing in the backyard last night when suddenly she yelped and fell over. The owners use this dog for sport as well as for a pet, so she is known to be a very stoic dog. Right away they worried about pain because she vocalized. It was apparent that she couldn't walk back into the house, so they put her on a blanket and carried her inside. She was able to stand up but couldn't use her right front or right rear leg normally. They gave her dinner (which she ate) and allowed her to rest until the visit today. (Why didn't they take her to ER? I don't know...I'm just the neurologist!)

Physical examination on presentation was unremarkable. (Yes, you examined her stifles, and they appear stable). 
Neurologic examination:
Mentation: BAR, very excited to see you (she's very excited to see EVERYONE)
Cranial nerves: all normal (high five for doing a full cranial nerve exam!)
Gait: She has an ambulatory right hemiparesis, with frequent falling to the right. She is able to walk 5-6 steps, unassisted, before falling or having her right limbs slide out. Note, the definition of ambulatory is the ability to walk a minimum of 5 unassisted steps IN ALL LIMBS. 
Reflexes: No withdrawal reflex in the right front leg, absent bicep and triceps reflexes right front leg. The reflexes are normal in all other limbs
Postural reactions: Absent paw replacement right front leg a right rear leg. Normal paw replacement in both left front and left pelvic limb. 
Palpation: No signs of pain on palpation or cervical ROM. 
Nociception: She has motor in all four limbs, so you do NOT need to test nociception (deep pain)

Neuroanatomic lesion localization: Right C6-T2 myelopathy (spinal cord)

Why? We know the dog is mentally normal and has normal cranial nerves. She does not have a seizure history therefore there is no evidence of intracranial disease. You can cross that body part off. Therefore, the lesion must be caudal to the foramen magnum. A forelimb AND pelvic limb are affected which means this lesion must be cranial to T3. If the lesion was caudal to T3, only a pelvic limb, or limbs, should be affected. That narrows our window of concern to C1-T2, correct? From there, you need to evaluate the reflexes. If they are normal, the lesion is likely C1-C5 but in rare situations it is C6-T2. Normal reflexes aren't super useful to narrow this window further. However, she has reduced to absent reflexes in the right front leg. Reduced to absent reflexes suggest a lesion in the reflex arc itself, which is located C6-T2 in most dogs. Why did I say this was a spinal cord, not a peripheral nerve injury? If you guessed it was because the pelvic limb on the same side was affected you'd be correct! The long tracts (paw replacement testing, upper motor control) going to or from the pelvic limb must travel through the C6-T2 part of the spinal cord. If the dog has sustained damage to the spinal cord, the tracts to the pelvic limb should be affected. If the nerves to the front leg are damaged peripherally (i.e. with brachial plexus injury) the pelvic limb should be normal. You did it!

Differential diagnoses: This dog has an acute onset, non-painful spinal cord disease. I would include an FCE, AHNPE (acute hydrated nucleus pulposus extrusion) and possibly at Type I disc herniation on the top of my list. As we learned last week, we cannot ever take meningomyelitis off the list so that goes on the list, but lower. Lastly, although trauma wasn't witnessed, this was an acute onset disease, so trauma goes on the bottom of my list until proven absent. 

We performed an MRI and diagnosed her with a suspected FCE. She entered rehab and supportive care and is doing well! With mobility and deep pain present, she is likely to make a good recovery but may not have completely normal mobility in the front right limb because the plexus was involved. 

Did you enjoy this case? Did you find it difficult? Please let me know if have any topics or a lesion localization case that you wish I'd cover on a TidBit Tuesday. Have a great week!

Vaccination and Seasonality in the Development of MUO

A study was published this Month in JVIM entitled “Vaccination and Seasonality as Risk Factors for Development of Meningoencephalitis of Unknown Origin in 172 Dogs”. I don’t know about you, but this is a super-hot topic in my world, so I immediately thought we needed to get this into a TidBit Tuesday!

Overview

MUO (meningoencephalitis of unknown origin) is a clinical diagnosis based on MRI findings, identification of a mononuclear pleocytosis and negative infectious disease testing. The authors proposed to investigate the association between vaccination WINDOW and the development of MUO. What is a vaccination window? A vaccination window is a categorization of the time from most recent vaccination to onset of clinical signs (that were later diagnosed as MUO) that was placed in 45 or 90 day intervals for analysis. For example, there was a window of 0-45 days and 46-90 days. Additionally, the authors evaluated the presentation season.

Results

172 dogs were included in the 2 year prospective study. The median age at onset of clinical signs was 5 years (range 0.18-15.3 years). Interestingly, Labrador and Labrador-X dogs were most common (13/172) followed by French Bulldogs and then Chihuahua/Chihuahua X. This should be a reminder that MUO can affect anyone, regardless of breed, age, sex, and size. It should always be on your differential diagnoses list for dogs with neurologic disease!
More dogs received vaccinations within 450 days of the onset of signs, so >450 days was considered “referential” for analysis. Looking specifically at dogs vaccinated within 450 days of the development of MUO, the highest risk for development of MUO was associated with vaccination in the first 45 days after vaccination (9x higher). This was not a case-control study, so we don’t know what the incidence of development in a breed or time. All that the authors are stating is that of the dogs with MUO that had received vaccination within 450 days of the development of signs, being vaccinated within 45 days resulted a 9x higher risk of developing of MUO.
The type and number of the most recent vaccinations administered was also evaluated. The number of vaccinations administered ranged from 1-7, median 4, in all dogs with MUO.  NO association with the type (Bordetella vs distemper, etc.) or number of vaccinations administered at one time was associated with the development of MUO.
Lastly, there was no associated with the season and the development of MUO.

Take home message:

• Dogs get MUO frequently so keep it on your differential diagnoses list

• Dogs who develop MUO have a 9x higher chance of developing it within 45 days of vaccination. (This doesn’t mean that dogs have a 9x higher chance of developing MUO overall!)

• MUO is not apparently linked to season

• We need to learn a lot more about MUO but likely there is a genetic risk that is triggered by something and that something might be vaccination.

 
If you found this article interesting and would like to read the entire thing it can be found at https://onlinelibrary.wiley.com/doi/10.1111/jvim.70013.  

Thanks for reading! I hope you have a great week and look forward to working with you very soon.