Spinal Cord Neuroanatomic Lesion Localization

"DIR" Coming In

Does anyone else use the acronym "DIR" to represent "down in rear"? I dislike this phrase but it's a soapbox rather than scientific fallacy, I suppose. Anyway, today, let's imagine that you have a patient on your schedule coming to see you for signs of difficulty walking. Today is a lesion localization practice case, so grab a pencil and dig in!

History:
Gabby is a 4 year old FS Beagle-X. She is presenting with a 3 day history of difficulty walking in the pelvic limbs with swaying, falling, and occasional vocalization such as pain. No prior medical history and normal physical examination. 

Neurologic examination:
Mentation: BAR, anxious
Cranial nerves: normal
Gait: Ambulatory, paraparesis with moderate proprioceptive ataxia in pelvic limbs only. 
Reflexes: normal withdrawal in all four limbs, normal patellar reflexes bilaterally and normal anal reflex. The cutaneous trunci reflex stops at L2 bilaterally. 
Postural reactions: Absent paw replacement testing in both pelvic limbs, normal in both thoracic limbs. Normal hopping in both thoracic limbs, absent hopping in both pelvic limbs. 
Palpation: Spinal pain at TL junction, the remainder was non-painful. Normal cervical ROM and tail ROM. 

The first questions we ask ourselves is "is this dog normal or abnormal neurologically?"
The answer, of course, is abnormal, so let's break it down.

This dog has normal mentation, no cranial nerve deficits and no history of behavior changes or seizures so I think we can safely assume the lesion is NOT intracranial. This leaves spinal cord, peripheral nerve, neuromuscular junction, or muscle to choose from. Let's start by assuming it's spinal cord in origin but if the lesion doesn't localize to ONE spot on the spinal cord you should then move on to considering the neuromuscular system. When looking at the spinal cord, you have four localization segments to choose from:

C1-C5
C6-T2
T3-L3
L4-S3

The C6-T2 and L4-S3 segments are where the lower motor neuron cell bodies are housed and where the peripheral nerves that you test with limb reflexes originate. Look at the reflexes listed on the neurologic examination. No spinal reflex deficits are noted, except for c. trunci, correct? This means you can consider C6-T2 and L4-S3 "free" of disease, or normal. This leaves us C1-C5 and T3-L3 to evaluate. To do this, we must look at the gait description. 

What is paraparesis? Paraparesis is a weakness in the pelvic limbs. Monoparesis = one limb weakness, tetraparesis = all four limb weakness. Make sense? 

What is proprioceptive ataxia? There are 3 forms of ataxia, and proprioceptive ataxia is the most common one. This gait deficit occurs when the sensory nerves running from the toes --> peripheral nerve --> spinal cord --> brainstem --> forebrain become disrupted. When the nerves are disrupted, anything "downstream" or caudal to that disruption may show ataxia. In this case, it is just the pelvic limbs, therefore the lesion is caudal to the thoracic limbs. Caudal to the thoracic limbs is T3. We've already decided that we don't have reflex deficits therefore the lesion must be in front (cranial to) L4. Voila! The neuroanatomic lesion localization for this case is T3-L3 by process of elimination (and by doing a thorough neurologic examination). 

DDx: The most common differential diagnoses for this dog with spinal pain and acute, progressive T3-L3 myelopathic signs would be an intervertebral disc herniation, meningomyelitis, and trauma. I wouldn't exclude neoplasia or discospondylitis however they are less likely based on her history. 

Plan: Spinal radiographs would rule out discospondylitis but don't diagnose disc herniations, meningomyelitis and rarely will diagnose neoplasia. 3D imaging is needed to look at the spinal cord which would be a myelogram with CT, a CT alone or an MRI (my personal favorite). 

How did you do? Was this easy-peasy or more challenging? I'd love to know! Please feel free to email me your comfort with the localization on this case so I can introduce either more or less challenging localization practice in the future. 

Thanks for reading! Have a great week!

Autoimmune Feline Encephalitis

Autoimmune encephalitis is a unique pathology, identified in perhaps up to 50% of humans with encephalitis, and recently identified in a large cohort of cats. In a study published in Vet Journal (2023), Glantschnigg-Eisl et al described the clinical, laboratory, radiological and pathological findings in 32 cats diagnosed with this specific form of epilepsy. Human autoimmune epilepsy is caused by immune attack of the voltage-gated potassium channel (VGKC), generating specific antibodies to this protein complex and the secreted protein LGI1 as well. It is now proposed that the presence of these antibodies reflect a specific form of limbic epilepsy in cats, similar to the autoimmune epilepsy noted in humans. Most importantly to us (veterinarians), cats with this form of epilepsy have a normal MRI and CSF analysis! Therefore, calling it encephalitis based on our standard testing is challenging. Is it a form of idiopathic epilepsy, or an encephalitis? Time shall tell. The authors describe this as an encephalitis, similarly to the human counterpoint. Below is a small summary of their findings. For the full study, please refer to the article link at the bottom. 

Clinical Picture

All cats in the study had seizures as their presenting complaint. All cats had positive antibodies to VGKC, with 26 cats having LGI1 antibodies as well. No clinical findings distinguished cats with LGI1 antibodies from those without. Focal and generalized seizures were almost evenly divided as a presenting seizure type with cluster seiuzres in 27/32 cats. Similar to humans with limbic epilepsy, many of the cats (22/32) had interictal behavior changes with  a history of unprovoked aggression in 12/32 cats. This was identified as a common finding but not yet pathognomonic for this form of epilepsy. Median age at onset was 3.42 years.

Laboratory Findings

.No significant laboratory abnormalities were identified. As noted above, CSF analysis was normal for all but 1 cat and that cat had only a mildly elevated protein. 

Long-term Outcome

Phenobarbital was started in 26/28 cats that underwent treatment with about 1/2 of the cats having a second AED added throughout treatment. Prednisone was administered in 10/32 cats (most of which were the LGI1 positive cats).The cats that received steroids, often received prednisone. This medication was administered to the cats with the most severe neurologic signs, including seizure frequency or severity, and was linked to poorer survival. As the authors noted, it is unclear if the prednisone is linked with poorer outcome or if the survival is linked to more severe condition and therefore prognosis.  This was interesting because the human seizure disorder associated with LGI1 antibodies is typically rapidly and markedly responsive to steroids.

Two factors were associated with prognosis in this study. The first was number of seizures at presentation. Cats with a higher seizure frequency were more likely to be euthanized. The second was the association with hippocampal pathology. Higher MRI scores suggested a lower prognosis and higher likelihood of euthanasia. The overall survival rate was 70-80%, which was similar to survival rates for idiopathic epilepsy in cats. At 1 year, most cats had a marked decrease in seizure activity from a mean of 3.6  seizures daily to 1-2 per year. This suggests that if they survive the short term, their long-term prognosis is good. QoL scores were good to acceptable in the long-term follow-up group.

What are my take away points from this study for practice?
1. Be aware that this disease exists. If you see cats with seizures, especially severe onset seizures, VGKC autoantibodies could be an underlying cause. 
2. Treat with phenobarbital - it works terrifically for most cats, regardless of the underlying cause. 
3. Steroids may not be the answer. Then again, maybe they are if we catch the disease earlier?? I don't think we can make this a take away just yet; more information is needed. 

I hope you have a wonderful week and thanks for reading! 

A gentle reminder: I've had an uptick in cancelations over the past few days. I know my schedule is getting booked out further than is typical, and I apologize for the resulting delay.  Please cancel your appointments with as much notice as possible, whenever possible. I have a waitlist and would LOVE to move folks forward if I have an opening. I am hopeful that the waitlist will diminish soon now that I able to open up a few more days for consults. Thank you!

Lastly, gut yantif to those of you celebrating! I hope you had a safe fast yesterday. 

Reference: https://www.sciencedirect.com/science/article/pii/S1090023323000254

Can You Help?

Hello fellow Veterinarians!

I am working with a company to possibly purchase a MOBILE MRI that would be small enough to literally fit into a Sprinter van. This would enable me to drive an MRI to your facility, evaluate pets and do the MRI right then for you and them. This is unique - no other small animal veterinary neurologist currently has this machine in the USA so the company has asked for my help. Consequently, I'm asking for yours.

The coil (the place the head goes when it goes into an MRI) is smaller than many other big machines and I need to make sure that the majority of my patients could fit. I'm only looking at skull size right now. 

What do I need? I need head measurements, please. Specifically, can your pet/patient/parent's dog/etc. fit inside of a 7" tall x 6" wide space? If you can measure and send me a YES or NO and the dog breed that would be terrific. The more data the merrier so don't limit yourself to just one dog. :) We know cats fit, so no need to annoy them with a measurement of their head.

How to measure: The photo above is my simple calipers that I'm using when I travel to hospitals. You can make something similar or just use a ruler and a piece of string or paper. Measure across the top of the head putting a string at "0" and 6". If the head bends the string, it's too big. Then, measure the height  using a piece of paper or cardboard at the edges of the ruler to approximate 7". If you cannot fit the paper across the top and bottom, the head is too big. Although science is precise, this doesn't need to be at this stage.

Thank you!!

Thank you for reading, and for your help!
Sincerely,
Heidi

Geriatric Vestibular Disease

Geriatric Vestibular Disease of Dogs and Cats

Geriatric vestibular disease (GVD) is characterized by an acute onset, unilateral failure of the peripheral vestibular system. The cause remains unknown, but causes such as inflammation (viral or immune mediated) or atrophy have been hypothesized. A study back in 2021 (DOI: 10.1111/vru.12893) by Sungjun Won and Junghee Yoon out of South Korea identified a significant size difference in the utricle, one of the parts of the bony labyrinth in the ear, in dogs with GVD compared older dogs without GVD. Necropsy evaluation has shown a reduction in the size of the peripheral CN 8 and the affected ganglion, further supporting atrophy as a cause. And yet, it is difficult to explain the recovery that most dogs and cats experience 1-6 weeks after onset of signs.

Common Clinical Signs

Animals with GVD are middle age to older dogs and cats that demonstrate peracute onset of signs, often proceeded by vomiting with no clinical worsening after 24 hours. These dogs and cats usually have very severe vestibular signs such as head tilt, nystagmus, ataxia (if ambulatory), positional strabismus and rolling/nonambulatory vestibular ataxia. IF you are able to have the animal stand you should not find paw replacement deficits, hemiparesis or obtunded mentation. If you do, the lesion localization is central and a different set of differential diagnoses should be considered. 

Differential Diagnoses for Peripheral Vestibular Disease
Not accounting for history, a general list of differential diagnoses for peripheral vestibular disease would be as follows:
Degenerative: none
Anomalous: none
Metabolic: hypothyroidism
Neoplasia/nutritional: Yes (lymphoma, nerve sheath tumor)
Infectious/Inflammatory/Idiopathic: Yes (neuritis and geriatric vestibular disease)
Trauma/Toxin: Topical antibiotics (Oral metronidazole SHOULD be central, but it may be difficult to tell in a recumbent animal.) Trauma - less common in dogs and cats.
Vascular: none. 

Geriatric vestibular disease is diagnosed by exclusion at this time. Although the report referenced above does provide measurements for the utricle on MRI, it is not yet a diagnostic marker for GVD. Exclude all other causes using chest x-rays, blood work including T4, brain MRI and spinal tap, if indicated. 

Treatment?

This is a self-resolving disease. The head tilt is commonly permanent, but all other signs of vestibular disease should resolve over several weeks. Signs begin to improve 24-48 hours after onset of signs but may take up to 1 week to start improving. Full resolution of clinical signs should be by 6 weeks. If signs wax and wane, or progressively worsen, GVD is not the proper diagnosis. Supportive care such anti-emetics. diazepam or meclizine for anti-vertigo effects, and nutritional support such as hand feeding (only when sternal!) , may be used. IV fluids may be needed for severe or prolonged nausea. 

Prognosis

Don't euthanize these pets in the first 24 hours! They look miserable...but they can recover with time and supportive care. This can be very difficult for clients to witness and, because the pets are elderly, may result in a triggered response to consider euthanasia. If you can, please hang in there for a few days even if that means hospitalization. Also, please note that signs may reoccur multiple times over the animals' life. 

Thanks for reading! I'd love to hear if you have any suggested topics for TidBit Tuesdays. If you have a question, chances are that other readers are interested in the topic too! I tend to pick things that I think are timely or interesting (or both!) but then again, I find everything interesting in neurology so help me narrow this down! :)

Have a great week!

IVDH Consensus Statement – Medical Management Data

In July 2022, the ACVIM Consensus Statement on the diagnosis and management of acute canine thoracolumbar intervertebral (IVD) disc extrusion was published. This is the first of two installments about this consensus statement as a TidBit Tuesday. For this one, we will discuss the expected outcomes from medical vs. surgical management and what entails medical management. Enjoy!

The recommendations by the committee were graded as being supported by high, medium and low levels of evidence. Recommendations with high level of confidence include multiple randomized controlled trials with concordant findings. The evidence strongly supports the conclusions. Medium level of confidence includes retrospective studies with concordant findings, or small placebo-controlled trials. The evidence suggest that the findings are likely to be real. Lastly, low levels of confidence include isolated or small retrospective studies or single non-controlled trials. The evidence suggests that the findings might be real.

Medical vs. Surgical IVD extrusion management

A very helpful table was presented to help guide appropriate treatment for dogs presenting with signs consistent with TL IVD extrusion. The “%” represent the % of dogs that respond favorably to medical (M) or surgical (S) treatment.

·         Pain only: M 80%, S 98.5% à lateral extrusion may lead to reduced response to medical management.

·         Non-ambulatory paraparesis: M 81%, S 93% à level of recovery was less with medical management.

·         Paraplegia with deep pain: M 60%, S 93% à medical recovery is prolonged and less complete.

·         Paraplegia loss of deep pain: M 21%, S 61%

This is based on moderate level of evidence.  The statement here is “In paraplegic deep pain negative dogs, success with medical management is largely poor with an increased frequency of progressive myelomalacia. Surgical management is recommended.” – moderate to high level evidence.

What is medical management?

“At least 4 weeks of restricted activity is recommended, putatively to promote the healing of the annulus fibrosus. This period should include confinement to a restricted area 9crate, ideally, or small room without furniture) except when performing rehabilitation exercises or outdoor toileting. There should be no off-leash walking, no jumping on or off furniture and no access to stairs during this time”. This statement was supported by low level evidence. Corticosteroids are NOT recommended (moderate level evidence). Dogs with NSAIDs had a higher quality of life score than those on corticosteroids but NO STUDIES specifically address the use (or no use) of NSAIDS. Pain management is discussed, but no recommendations were made because of the lack of studies evaluating different medication protocols. Acupuncture was noted to be good adjunctive treatment for medical management but is not a recommended substitution for surgical management. What are my typical recommendations? For an uncomplicated T3-L3 myelopathy without MRI, with a strong suspicion of IVDH, I recommend NSAIDs, muscle relaxants and most importantly, cage rest for at least 3 weeks.

I hope this was enlightening. Please reach out with questions and stay tuned for the next update on the consensus statement. I hope you have a wonderful week. I am enjoying our tiptoe into fall and hope you are too!

Limber Tail?

Limber tail, or cold tail, is known medically as coccygeal myopathy and is a poorly characterized condition associated with acute onset tail flaccidity and pain. Working dogs are more commonly associated with the disease, especially hunting breed dogs. I recently evaluated a patient with suspected "limber tail" and thought it might be fun for us all to review this unusual disease. The most recent study published was 2016, so I'll reference data from that study in this TidBit Tuesday. Reference at the end. 

What is the pathology associated with limber tail?

Limber tail is a self-resolving disease, usually within 10 days of the onset of signs, therefore very little pathology has been described for the problem. One study from Norway in 1999 identified inflammatory cells in the coccygeal muscles along with evidence of myofiber damage and elevated CK in dogs with clinical evidence of limber tail, compared to breed matched control (nonclinical) dogs. 

What are common triggers?

In a questionnaire to dog owners in the UK (2016) the following triggers were queried and the responses are as follows:

• Swimming (29 yes, 9 no)

• Exposure to cold weather ( 19 yes, 19 no)

• Exposure to wet weather (11 yes, 26 no, 1 unsure)

• Vigorous exercise (18 yes, 18 no, 2 unsure)

• Confinement (5 crate, 1 car, 31 no, 1 unsure)

Some triggers appeared to be dual, such as swimming on a cold day. Increasing latitude has been identified as a risk factor, which is assumed to be linked to colder temperatures. They determined that while swimming was not a necessary precursor to the development of limber tail, it appeared to be a risk factor. The odds ratio of a swimming case compared to control was 4.7. Furthermore, cases were more related (had common ancestors) compared to controls and this was more than is expected for random selection. Otherwise, a similar distribution between cases and controls was noted for neuter status, coat color, height, weight, exercise levels, household type, and smoking vs non-smoking in the home. 

Do you need to treat it?

The self-resolving nature has made treatment protocols difficult to evaluate. Pain management in the early phases, as needed, is appropriate. This could include anti-inflammatory medications such as NSAIDs, but probably doesn't need to rise to the level of steroids in most dogs. Pain modulation with gabapentin, narcotics if severe pain is noted, or muscle relaxants could be utilized. If clinical signs have not resolved by day 10, additional diagnostic testing such as MRI of the lumbo-coccygeal region, electrodiagnostic testing or both may be indicated. 

I hope you enjoyed Labor Day holiday and weekend and have a great week! I am in town this week but leaving for a few days over next weekend to speak at IVECCs in beautiful Denver Colorado. I will have limited email and telephone access Monday-Tuesday September 11-12th due to travel and speaking hours. Please pardon my delay in response if you reach out on those days. Thanks for reading!

Reference: https://bvajournals.onlinelibrary.wiley.com/doi/epdf/10.1136/vr.103729

Prevalence of Idiopathic Epilepsy and Structural Epilepsy in Boxer Dogs

We have another interesting article to review this week! A group from Germany published a retrospective study of 74 Boxer dogs with epilepsy and, although the results aren’t surprising, I felt these were good statistics for us to have in our “conversation belt” when discussing seizures with owners of Boxer dogs. 
 
Before we dive into the results, a little refresher. Idiopathic epilepsy in the general (not exclusive to the Boxer dog) population occurs in about 53% of dogs with structural epilepsy occurring in about 45% of dogs. These numbers change a little bit with age qualifiers. Dogs between 6 months and 6 years of age were diagnosed with idiopathic epilepsy 75% of the time and structural epilepsy 45% of the time. Dogs greater than 6 years of age were diagnosed with idiopathic epilepsy only 34% of the time, with structural epilepsy taking a bigger chunk of the diagnoses at 64%. 

• 
  Now, let's compare these data to Boxer dogs. A recent retrospective study by Loncarica (August 2022...okay, recent is relative), looked at the prevalence of idiopathic epilepsy and structural epilepsy in Boxer dogs. They divided the groups into < 6 months old, 7 months and 6 years and > 6 years old. 
  Results
  < 6 months old - 2/74 dogs diagnosed with seizures: 1 had idiopathic epilepsy, 1 had a meningoencephalocele
  6 mo-6 years - 12/74 dogs diagnosed with seizures: 8/12 (66%) had neoplasia. Of these 8, 2 had a NORMAL neurologic examination. 
  > 6 years old - 60/74 dogs diagnosed with seizures. 58/60 (97%) were diagnosed with neoplasia. Of these 13.58 had a normal neurologic examination. 
  It is notable that only 11 of the dogs in the study had a histologic confirmation of neoplasia, the remainder were based on MRI characteristics. 
  
  Summary
  Is finding seizures in Boxer dogs earth shattering? No. It is noteworthy, I think, that boxer dogs had a MUCH higher prevalence of structural epilepsy, and probable neoplasia, than the average dog population. Is this novel? No, but now we have data to show what we have all been suspecting all these years. :)
  The other key point is that about 25% of dogs over 6 months of age had a normal neurologic examination with structural epilepsy. If a dog has an abnormal neurologic examination, with a seizure history, structural epilepsy is more common. A normal neurologic examination doesn't eliminate the possibility, however. 
  
  Thanks for reading! Please reach out if you have any questions. My schedule is quite limited over the next two weeks as I take a little vacation time with my family over the long Holiday weekend and then spend a few days at IVECCs speaking to an awesome bunch of criticalists, generalists and emergency docs. If you're planning to be there please stop in and say HI! (And come swim with me and my daughter in the water park!) If you have a case that should be seen sooner than later, and cannot find a suitable time on the scheduler, PLEASE REACH OUT. Thanks!
  

Global brain ischemia

A recent article by Dr. Harper Crawford and colleagues from the UK caught my attention. Global brain ischemia can be seen following minutes of poor blood flow including during cardiopulmonary arrest during general anesthesia, severe bite injuries and strangulation. It has also been associated with the use of mouth gags during dental procedures in cats. (Yikes! You probably knew this, but I was surprised by this!) This article was an enlightening review of global brain ischemia as well as a retrospective look at several cases with a focus on treatment, survival and prognosis. 

What is the consequence of failure?

The authors suggest that cerebral perfusion failure can simply be defined as failing to meet the energy demands of the brain and failure of adequate waste removal products. Simple, yes? Irreversible failure can start within minutes of ischemia through loss of ATP. After ATP is depleted, Na+ and K+ will influx intracellular dragging water with it and the neuron will depolarize. This is the start of cytotoxic edema. From there, a secondary release of excitatory neurotransmitters, particularly glutamate will be released which results in eventual mitochondrial dysfunction, lipid peroxidation and vascular injury. The final nail in the proverbial coffin is rising intracellular Ca++ which triggers cell death. The most sensitive cells are in the cerebral cortex, hippocampus and Purkinje neurons in the cerebellum.

Materials and Methods

Short term outcome was defined as survival (or not) for the first 72 hours. Long-erm was defined as the neurologic examination at the last follow-up examination available for review.
The study utilized an outcome scale as follows:
0: dead or euthanized due to severe neurologic deficits
1: poor recovery with severe persistent neurologic deficits
2: good recovery with mild persistent deficits
3: excellent recovery with normal function.

Results

10 animals were included: 8 dogs and cats with in hospital cardiopulmonary arrest and 2 dogs with out of hospital arrest (1 vehicular trauma, 1 asphyxiation from food). The duration of suspected arrest ranged from 1-5 minutes (median 3 minutes) for animals with in-hospital cardiopulmonary arrest and 10-22 minutes for the 2 animals with out of hospital cardiopulmonary arrest. The neurologic exam for the animals with in hospital cardiopulmonary arrest was reported at a median of 9 hours post insult. Median hospital duration was 7 days. Short term survival occurred in 8/10 cases including 1 case that did not survive to long-term. Seven animals survived to discharge and were re-evaluated at a median of 67 days. Outcome scale results:
Grade 0: 3
Grade 1: 1
Grade 2: 2
Grade 3: 4
The patients with an outcome score of 2 or 3 all showed consistent neurologic improvement in the first 48-72 hours. For the animals that experienced seizures during hospitalization (3), anti-epileptic medication was continued for between 2-8 months after starting. Levetiracetam was used in 1 cat and 1 dog, and phenobarbital was used in 1 dog. No additional seizures were reported in any pet following discharge.
This report demonstrated that although global ischemia can cause severe neurologic deficits, successful long-term outcomes are possible. Furthermore, they noted that an association with duration from onset of cardiopulmonary arrest to spontaneous breathing is a factor in recovery in rodent models and human studies, but this study was too small to draw those conclusions.

References: DOI: 10.1111/jvim.16790 Harper Crawford A, Beltran E, Danciu CG, Yaffy D. Clinical presentation, diagnosis, treatment and outcome in 8 dogs and 2 cats with global hypoxic-ischemic brain injury (2010-2022). JVIM 2023.
Thanks for reading! I hope you have a great week and I look forward to working with you soon!

Feline Hyperesthesia Syndrome

What is it?

Appropriately termed a ‘mystery disease’, feline hyperesthesia syndrome (FHS) has an unknown etiology to date. Clinical signs often include skin rippling over the dorsum, tail chasing and self-trauma, sudden jumping and running for no obvious reason and occasionally vocalization during episodes. Interestingly most cats are young (less than 1 year of age). The etiology has been proposed to be behavioral (due to the lack of identifiable organic disease), seizure disorder (due to the paroxysmal type clinical signs and directed motor activity), or a collection of multiple factors including behavioral and environmental.

How is it Diagnosed?

Obtaining a diagnosis is complex because as of yet, we don’t understand the etiology. <Groan> Therefore, as a neurologist I attempt to rule out organic CNS disease. This includes MRI, spinal tap, sometimes muscle biopsies and electrodiagnostic evaluation for peripheral neuropathy/myopathy. A recent retrospective study evaluated 7 cats with this clinical picture and did not identify any neurologic cause in these cats.1 Treatment with gabapentin, meloxicam, antibiotics, phenobarbital, prednisolone, and topiramate were tried in multiple cats. Clinical improvement was noted in 6 of 7 cats using gabapentin alone (2 cats), gabapentin, cyclosporine, and amitriptyline (1 cat), gabapentin, prednisolone, phenobarbital (1 cat) or gabapentin, topiramate and meloxicam (1 cat). Treatment in my practice consists of anticonvulsants to rule out/in epileptic activity, followed by pain management with gabapentin.  Referral to a behaviorist, dermatologist and/or internist is often made as well because of the complex and unknown nature of this mystery disease.

That's it for this week. Short and sweet because, honestly, I thought you could use a little less to read during summer!

Have a terrific week. Keep those consults coming! We've worked through some really interesting cases lately.

The Gut and The Brain

The gastrointestinal microbiota (GIM) is the new hot topic in neurology. This contractile organ, far distant from the brain is now considered a a possible source for drug resistant epilepsy in canine epilepsy research as well as a potential cause for behavioral disease in epileptic and non-epileptic dogs alike. A recent article by Watanangura et al highlighted the importance of the GIM in epilepsy.
The aim of their study was to investigate the effect of phenobarbital (monotherapy) on the composition of the GIM and to determine if it resulted in a change to behavior in a select group of dogs. To be included in this study, all dogs had to meet Tier II level of confidence for epilepsy (normal brain MRI, spinal tap, normal blood work and neurologic examination) and be naive on any anticonvulsant treatment. They had 12 dogs who meet these inclusion criteria. On day 1, they started phenobarbital at 2.5 mg/kg PO q12h and took fecal samples. The drug was continued without dose adjustment for 90 days at which time another fecal sample was taken. Behavioral questionnaires were submitted on day 1 and day 90 as well.

The results:

• Serum phenobarbital concentrations ranged from 19.8-18.1 mg/L (day 30 and day 90)

• Seven of 12 dogs were seizure free throughout the study and called responders.

• Five of 12 dogs were not seizure free and were called non-responders.

• Short chain fatty acids (SCFA) did increase significantly in the study, specifically propionate and butyrate.

• Butyrate was significantly higher in the responder group compared to the non-responder group. Butyrate is an anti-inflammatory fatty acid which may  benefit epileptic dogs, yielding better response to treatment. Perhaps this is due to the neuroprotective effects, or by providing an alternative energy source for the brain.

• The behavior survey showed a significant decrease in stranger-directed fear, and non-social fear with an increase in trainability! Phenobarbital has been used as an anxiolytic for humans and veterinary patients, supporting this finding. An idiosyncratic hyperexcitability and aggression has been reported with phenobarbital however it is rare. (More commonly seen with levetiracetam.)

• There was no difference in the bacterial taxa in this study except for a significant decrease in Clostridiales on day 90. The significance of this remains to be seen, however it may affect the distribution of MCFA and other products.

The Take Home Message
What do we do with this information? Well…we tuck it away in our heads and know that phenobarbital, or seizures themselves, might affect the GI microbiome and SCFA in the GI. Does this mean we should supplement? Not yet. I am not sure we know who, how and when to supplement based on this study. This was a critical step forward in our path towards understanding the GIM and I am excited to share additional information that comes forth in this area!
 
Have a wonderful week and enjoy what August has to offer us! I look forward to working with you soon.

The 5 Types of Disc Herniation (that we know of!)

The Five Types of Disc Herniation (that we know of!)

'Tis CE season so I thought it would be fun to pull up this old TidBit Tuesday from 2020 and refresh our memories about the different types of disc herniation that may be diagnosed in dogs. I hope you enjoy this light reading on your midsummers morning!

1. Dystrophic calcification secondary to chondroid degeneration of nucleus pulposus (NP), is called Hanson Type I. This causes mechanical stress on the outer annulus fibrosus (AF), leading to rupture of individual collagenous strands of AF and eventually full failure and extrusion.

2. Fibrous degeneration occurs when fibers of the disc split leading to accumulation of tissue fluid and plasma between the annular fibers. Over time the mechanical pressure exerted by NP causes thickening of the AF dorsally, causing protrusion. (Hanson Type II).

3. ANNPE (Acute noncompressive nucleus pulposus extrusion) - this is normal (probably) NP that is exploded into the canal, usually during high activity. Also called a traumatic disc herniation by some folks.

4. AHNPE (Acute hydrated nucleus pulposus extrusion) – An apparently normally hydrated NP that is compressive and often located ventral to the cord in the cervical spine.

   1. There may be significantly more neuro deficits and less signs of cervical pain with AHNPE compared to other causes of cervical myelopathy.

5. FCE (Fibrocartilaginous embolism): a piece of material histologically similar NP that becomes dislodged and finds its way into the vasculature surrounding the spinal cord. This can be into venous or arterial blood vessels. The end result is an acute shift in blood flow at the level of the spinal cord.

Match the clinical sign with the type of disc herniation

A. Chronic, progressive ataxia progressing to paresis
B. Acute, non-progressive unilateral weakness affecting one leg, or one side (hemiparesis)
C. Acute, progressive, painful ataxia progressing to paresis in a chondrodystrophic dog
D. Acute non-progressive ataxia and paresis affecting both sides of the body (paraparesis or tetraparesis)
E. Acute, rapidly progressive tetraparesis and ataxia of all four limbs with minimal cervical pain

If you answered...
Type I: C
Type II: A
ANNPE: D
AHNPE: E
FCE: B

you are correct!

Based on the clinical picture, it can be very difficult to distinguish Type I from ANNPE, and AHNPE. Typically, type I is painful (but not always), and the other two are minimally to non-painful. 

Which of these require surgery?

Any disc herniation that results in compression of the spinal cord with associated clinical signs could be considered for surgical correction. This statement would then suggest that Type I, Type II and AHNPE could be surgically corrected. Therefore, any patient with signs of a progressive or painful myelopathy should be evaluated for diagnostic imaging (typically MRI) for possible surgical intervention whenever possible.


Thanks for reading! I hope you have a wonderful week. As always, reach out if I can help you, help your patients, with neurologic disease. 

Brain Herniation in Cats

Brain herniation is diagnosed when one part of the brain shifts to another part of the cranial vault. The four most common types of herniation include: 1) Midline falx herniation (from left to right side of the forebrain), 2) caudal transtentorial herniation (cerebrum herniations under the tentori cerebelli onto the cerebellum and brainstem, 3) rostral transtentorial herniation (cerebellum herniates rostrally into forebain and 4) foramen magnum herniation (cerebellum exits out the foramen magnum). Brain herniation may be acute, secondary to a sudden shift in intracranial pressure or gradual secondary to a chronic or slow rising intracranial pressure.

The most common cause of acute herniation is trauma, resulting in cytotoxic and vasogenic edema or hemorrhage with a subsequent sudden increase in intracranial pressure. Brain tumors account for the majority of cases with a gradual increase in intracranial pressure.

The Cushing's Reflex, identified by Dr. Harvey Cushing, describes a reflexive bradycardia and hypertension with a reduced level of consciousness, induced by increased intracranial pressure. Increased pressure can result in poor cerebral perfusion, and ultimately brain herniation. 
A recent article evaluated cats with brain herniation noted on MRI to cats with intracranial disease WITHOUT brain herniation for signs of the Cushing's Reflex, and other clinical factors that might predict the presence of herniation. They evaluated: age, weight, heart rate, respiratory rate, temperature, blood pressure, level of mentation, Glasgow Coma Scale gait assessment and brainstem reflexes. Can you guess what they found?

There was no significant difference in any of these factors between the two groups except as related to level of consciousness and age. Cats with brain herniation were significantly older, and had a reduced level of consciousness compared to cats with intracranial disease without evidence of herniation. Wow!

Why didn't we see a Cushing's Reflex? Well, one option is that the majority of cats were diagnosed with intracranial neoplasia which we know is a slow growing process. This may have provided ample time for compensatory mechanisms so that a significant difference couldn't be determined in this study. Another option is that clinical evidence of brain herniation is simply less obvious or prevalent in cats. One prior study of cats with normal brains found incidental herniation in up to 40% of the cats! 

What's the take away? Cats with brain herniation may present very similarly to cats without brain herniation . Therefore, any cat with an intracranial neuroanatomic lesion localization undergoing general anesthesia should be managed as if they have increased intracranial pressures. Do not administer anesthetic drugs that are known to markedly increased or decrease blood pressure as this may negatively affect the cerebral perfusion pressure. When in doubt, assume they have increased intracranial pressure. 

Thanks for reading! This week is the 4H Dane County Fair so if you need me I'll be watching horse shows and eating cotton candy! Feel free to text or email anytime, however my live consult availability is very limited due to my kid's show schedules. Have a great week!

The use of AI In Veterinary Medicine

At the recent ACVIM Forum in Philadelphia, a radiologist gave a very enlightening presentation about AI, and specifically ChatGPT. Have any of you messed around with this technology yet? Is anyone using it for work flow support? Although this TidBit Tuesday isn’t specifically about a neurology topic, I was so blow away by the ChatGPT lecture I decided to include it as a TidBit Tuesday. We’ll be back to our regularly scheduled neurology topics next week… 😊

To get us all on the same page, ChatGPT is a new artificial intelligence (AI) software developed by Microsoft engineers. The presenter at ACVIM (Dr. Eli Cohen, provided an example during his talk of a “conversation” he had with ChatGPT that terrified me. While reviewing a radiograph ChatGPT suggested that one of the differentials for this pet with clear lytic bone lesions on each side of an intervertebral disc space could be “sterile discospondylitis”. Dr. Cohen, like all of us in the audience, instantly worried that we had missed this diagnosis in our years of practice experience. STERILE disco? Is this real? How could I have missed this?? So, he asked ChatGPT to provide references for this statement. AND IT DID. Dozens of references popped up on the screen. They were from reputable journals like JAVMA, JVIM, and Vet Rad and Ultrasound. By real, live people, practicing veterinary neurologists and radiologists. Some of us were in the audience. The catch? None of these references were real. NOT ONE of the references was actually a reference for this imaginary disease. ChatGPT had taken names of people that may have written about “sterile” and “discospondylitis” separately and combined this into believable reference points. My take away from this was to make sure if and when I use ChatGPT for any work-related item, that I personally double check (dare I say vet?) all of the data points. Here is a perfect example. I fed ChatGPT the following question:

What is the neuroanatomic lesion localization for a dog with seizures?

Here is the answer:

Seizures in dogs can arise from various neuroanatomic locations. The specific neuroanatomic lesion localization for seizures depends on the underlying cause and can vary between individual cases. Here are a few examples of potential lesion locations associated with seizures in dogs…

WRONG. What is the correct neuroanatomic lesion localization for a dog with seizures? That’s right, forebrain or prosencephalon. There is only one neuroanatomic lesion localization for pets with seizures. The etiology varies widely from hypoglycemia to brain tumors, but all seizures come from one part.

This was a wonderful reminder to me how important the grasp of words, terms and phrases is when we communicate in veterinary medicine. I, probably similar to you, will be using AI in my veterinary career in the future. I think it is probably inevitable. However, we must remember to double check what we put in is using the correct terminology, and that the produced answer is in line with our knowledge and understanding.

I’d love to hear if you use AI in your personal or professional life and how it has affected you. I hope you had a safe and happy 1st or 4th of July and I look forward to seeing you, without robots, in the future!

CBD Treatment for Resistant Epilepsy in Dogs

Use of CBD Oil for Refractory Epileptic Dogs

It's baaaack! At the ACVIM conference a few weeks ago I had the pleasure of listening to researchers from Colorado State University present data from a recent double blinded, placebo controlled prospective study evaluating CBD oil in resistant epileptic dogs. 

How the Study Worked

51 client owned dogs, taking at least 1 ACD (anticonvulsant drug) and continuing to have 2 or more seizures every month, were included. Resistant epileptics are already the hardest subset to manage so this was a really tough crowd for the researchers to target. The dogs were given either placebo or CBD oil for 3 months and then switched and given the other compound for 3 months. Initially, they dosed at 2.5 mg/kg PO q12h but no effect was noted so after 12 dogs the dose was increased to 4.5 mg/kg PO q12h. 

Key Points

• ALP and ALT were elevated in this study. This is the first study to document elevated ALT during CBD administration in dogs. The researchers aren't sure why this happened but hepatocellular damage of some sort was suspected. Bile acids were normal in all dogs except 2.

• No significant difference in response (response = a > 50% reduction in seizures) was noted between the placebo and CBD administrations group.

• Total number of seizures/month and seizure days/month was reduced in the CBD group compared to the placebo group BUT over all seizures went UP with both groups

Should we use CBD to manage seizures for resistant epilepsy?

Sorry, not based on this study. It's not compelling enough to suggest that we should be using this drug PLUS it showed evidence of liver enzyme changes that could be concerning AND phenobarbital serum concentration went by 11% when the dogs were on CBD. That said, they targeted resistant epileptic dogs so could this be effective in "easier" to control dogs? Maybe. Could this increased phenobarbital concentration mean that we could lower the dose of phenobarbital in these pets? Maybe. Do we need to check out different doses? Maybe - but at least with this question I am cautious because of the new elevation of ALT at this higher dose. Can we safely increase the CBD dose? Unknown. 

This is a good step forward but alas, we still don't have enough compelling evidence to say CBD should be a part of seizure therapy and at what dose.

Keep up the good work managing epileptic dogs! I'm available if you have questions about a case or need a second opinion. Have a great week!

What is Temporal Lobe Epilepsy?

Temporal lobe epilepsy (TLE) is a newly emerging term in feline seizure discussions and one worth becoming acquainted with. TLE is not an etiology, but rather a specific seizure phenotype (appearance) caused by epileptic seizures in a specific part of the brain (hippocampus) resulting from multitudes of causes.

What does TLE look like?

Cats with TLE have 6 specific stages or appearances. Not all cats go through all 6 stages, nor are all 6 stages apparent. The stages are:

Stage 1: looking around, sniffing, attention

Stage 2: Immobility and staring (arrest)

Stage 3:Orofacial automatism (lip smacking, facial twitching, swallowing, blinking) hypersalivation, mydraisis

Stage 4: Masticatory movement, facial twitching

Stage 5: Head turning, head nodding

Stage 6: Generalized convulsive tonic-clonic seizure

Most cats are observed in stage 2 or 3, and may progress to stage 4 and 5 but stage 6 is rarely observed.

What causes TLE?

Because TLE is not an etiology, but a description of a seizure syndrome located in one part of the brain, any cause of non-TLE seizures can cause TLE seizures as well. This list could include vascular causes, neoplasia, meningoencephalitis (infectious or non-infectious), or idiopathic.

How is TLE diagnosed?

When orofacial automatisms are observed, TLE should be suspected. To confirm TLE, an MRI with changes in the hippocampus is needed. There may be evidence of the seizure etiology such as neoplasia, or vascular disease as well, but the hippocampus must show specific MRI changes. Histopathology can reveal hippocampal sclerosis or necrosis. Some authors think sclerosis precedes necrosis but this sequence isn’t fully established. I won’t bore you with the detailed differences between sclerosis and necrosis, especially since the difference is detected on necropsy.

Can we treat TLE?

Yes! Treat seizures with antiepileptic drugs (AED) as you would any feline or canine seizure disorder. Any 1 seizure more than every 3 months, or longer than 3 minutes warrants a discussion of starting AEDs. Recently, hippocampectomy (removal of part of the hippocampus) has bene published in a cat as a treatment for TLE. This is a well-established treatment for human TLE (a common form of AED-resistant epilepsy in humans) and it carries an extremely high success rate for seizure elimination. Unfortunately, the procedure in cats needs a bit more work before we start considering it standard treatment. The hippocampus is the memory storehouse therefore loss of the hippocampus can cause difficulty with motivation, spatial memory, and learned behavior. Some researchers have described the effect to be similar to feline cognitive disorder in geriatric cats. Hippocampectomy was extensively performed in the 1960s during the time of rapid, although sometimes perhaps unethical, knowledge acquisition of how the brain works in animals and humans. We must acknowledge this work, even if we might find it ethically repulsive today.

Key Points

·         Temporal lobe epilepsy is a syndrome, resulting in damage to the hippocampus and a classic seizure presentation.

·         Temporal lobe epilepsy can be treated, but may be progressive and unresponsive to treatment once the necrosis stage has been reached. How do we know we reached this stage? No one knows antemortem….stay tuned!

·         Cats should take phenobarbital or levetiracetam. These are currently (2023) the only two drugs with enough literature to support their use and predict a reasonable efficacy. (Sorry my zonisamide-using friends.)

Intervertebral Disc Herniation in Yorkshire Terriers

Yorkies are a popular, and common dog breed in the USA and I (we?) see them quite a bit in neurology referral practice. That said, I had never read that they were officially considered a chondrodystrophic breed. Apparently, they are! 

Intervertebral disc herniation (IVDH) occurs with high frequency in chondrodystrophic dogs, but how often do we see it in Yorkies? According to a recent article, about 10% of Yorkshire Terriers with neurologic disease are diagnosed with IVDH and undergo surgical intervention. 

How do Yorkies present with IVDH?

• Cervical hyperesthesia only 5/60 (8.3%)

• Ambulatory tetraparesis with or without neck pain (grade 2):  26/60 (43.3%)

• Non-ambulatory tetraparesis or plegia with or without neck pain: 29/60 (48.4%)

No association with recovery and presence or absence of ambulation was found in this study. This is inline with other studies that have not found voluntary motor to be a prognostic indicator. 

• Acute signs in 80% of dogs

• Chronic signs in the remaining 20%

Yorkies with IVDH instead of another neurologic disease were statistically heavier and older

How do Yorkies do with surgery?

Thankfully, quite well, according to this report. In this study, the majority (82%) had one IVDH, 15% had two and 3% had 3 IVDH site repaired. In my experience, Yorkies far exceed dachshunds for having multiple IVDH requiring surgery at the time of diagnosis. Could this be a difference in genetic pool (this study was conduced in Czechia, Slovakia and Hong Kong)? In this study, all dogs returned to ambulation at some point, post operative. Most were walking by hospital discharge, but not all. This is comparable to dachshunds. 

Key Points

• Yorkshire Terriers are chondrodystrophic and therefore predisposed to type I IVDH

• Surgical intervention is likely to improve ambulation

• Approximately 50% of Yorkies will be ambulatory, and 50% will not at the initial diagnosis. 

Thanks for reading! I am leaving for ACVIM today (Tuesday June 13th) and will be out for the remainder of the week. I'm so excited to collaborate with colleagues and bring new knowledge back to the patients we share! If you need me, email is preferred but texting is also fine. I will have limited ability to answer the phone but will do my best to return your call in a timely manner. Please excuse any unusual delays! Have a great week!
 

Immune-mediated Polyneuropathy in cats

Riddle me this: a 10 month old cat is brought into your exam room by a very concerned owner. They report that the cat has had a rapid, progressive weakness develop over the past 2 weeks. Being the astute veterinarian that you are, you notice that the cat takes 3-4 steps and then sits. There doesn't appear to be any ataxia...just paresis (weakness). 

Neurologic examination:
Mentation: BAR
Cranial nerves: all normal (about 11% of cats will have facial nerve paralysis with this disease)
Gait: Ambulatory tetraparesis, worse in the pelvic limbs
Reflexes: reduced withdrawal all limbs, absent patellar reflexes bilaterally. 
Postural reactions: reduced to absent tactile placing in both pelvic limbs, reduced tactile placing in both thoracic limbs. 
Palpation: non-painful

The remainder of the physical examination is unremarkable.

What is the neuroanatomic lesion localization?

Start at the very beginning. Are there any signs of seizures, mentation changes or cranial nerve deficits? No. Therefore this cannot be intracranial lesion localization. We have all four limbs affected therefore if this is a spinal neuroanatomic lesion localization it must be cranial to the front legs. This means C1-C5 or C6-T2 myelopathy. (If the lesion was T3-L3 or L4-S3, the thoracic limbs should be normal.) To narrow it down between C1-C5 or C6-T2, we look at reflexes. Reflexes are reduced in the thoracic limbs therefore this would suggest a C6-T2 myelopathy. BUT WAIT!! The reflexes in the pelvic limb are also reduced to absent and that cannot happen with a C6-T2 spinal cord lesion. The reflexes in the pelvic limbs should be normal with a C6-T2 spinal cord lesion. Is this a multifocal lesion, affecting two spinal cord segements (C6-T2 and L4-S3)? Although possible, you would expect a proprioceptive ataxia with a spinal cord lesion therefore this is very unlikely to be a spinal cord lesion at all, even a multifocal spinal cord lesion. There, we must assume this is not spinal cord or intracranial lesion. What does that leave us? Neuromuscular disease, that's right! Your options are: 1) peripheral nerve, 2) neuromuscular junction or 3) muscle. Animals with muscle disease should have normal reflexes (and do, except with myasthenia gravis), so it isn't that. This is either a neuromuscular or peripheral neuropathy localization. 

Our differential diagnosis would include diseases such as: toxoplasma or fungal neuropathy, myasthenia gravis (yes, I know this localizes to the muscle but clinical signs look like a junctionopathy at times!), and immune mediated neuropathy. 

Diagnostic testing for this patient

CBC, serum biochemistry (including CK!) is normal. Toxoplasma testing was negative, as is the myasthenia gravis titer. Occasionally we will see an elevated CSF WBC or protein count with this mystery disease, but it isn't common. 

Muscle and nerve biopsy results

Diffuse variability in muscle fiber size is expected on biopsy. Nerves are almost all missing from the muscle biopsy sections. The nerve biopsy is markedly abnormal, with inflammatory cells infiltrating the axon, nodes of Ranvier and Schwann cells. 

Diagnosis: Immune mediated polyneuropathy!

This is a very interesting disease for many reasons but most notably, most cats can achieve a complete recovery without any treatment at all. In a recent study (see below), 10/11 cats that received no treatment obtained full recovery with a median time of 4 weeks. Nine of 12 cats that received glucocorticoids and 18/20 cats that received L-carnitine supplementation recovered as well. Relapses are reported and can occur months or years after resolution of signs. Overall, all except 1 cat improved regardless of treatment in this study. This same study found a predominance in males but did not find a breed association. 

So there you go! A self resolving, relapsing remitting polyneuropathy of young cats. 

Article: DOI: 10.1111/jvim.16701

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

Long-term infection and monitoring of Brucella suis in dogs

B.suis, you say? Why do I need t know about a swine variant of Brucella?? Did you know that B. suis can be pathologic in dogs, as well as swine, and is also zoonotic? You're welcome :)

A recently published article detailed the clinical signs, blood work, imaging (when available), serologic progression over time, and body fluid levels of organism over an 18 month period in 27 dogs from 17 households. The study population was located in Australia where naturally occurring B. canis is not found. Exposure to feral pigs was considered an important source of disease acquisition and may be a stand alone reason to test. (1 in 10 pigs are positive in Australia.) Although B. suis is not as commonly noted in our US canine population, we are a global veterinary profession now with lots of dogs traveling or being adopted from international locations. I felt this article was a nice reminder that B. suis exists, and is pathologic in dogs as well as having zoonotic potential, like B. canis. 

Clinical Signs of B. suis

Ten dogs had clinical signs attributed to brucellosis. Clinical signs included pyrexia with orchitis and epididymitits (4/10), lymphadenopathy (1/10), spinal pain (3/10), abortion or dystocia ( 1/10), and athritis (2/10). The remaining 17 dogs were assymptomatic throughout the entire 18 month period!

Serology and PCR

Titers did not correlate with severity of signs. Postive results were deemed positive if a Rose Bengal rapid plate test (RBRPT) yielded a positive result along with a complement fixation test (CFT) greater than or equal to 8. Only 2 dogs had seronegative results after 18 months and both had low baseline serology. Brucella DNA was not detected by PCR in blood, urine, saliva or preputial swabs in any dog at any time in the study. Notably, they weren't swabbed weekly or daily, so it is possible that some shedding occurred without detection on the sporadic testing. Only 3 positive PCR tests were found and this occurred in 1 bitch post whelping (vaginal fluid), as well as milk at 3 and 7 weeks post whelping as well as a lymph node at necropsy on a puppy that died. Although culture may be the gold standard diagnostic test for some countries, the RBRPT and CFT were considered safter to personnel performing the test and were preferred in this study. 

Diagnostic Imaging Results

Fifteen dogs had some sort of radiograph taken during the study period. Two of 15 had joint siease, 3/15 had vertebral lesions and 2 of 15 had lymphadenopathy. The dogs with radiographic changes had spondylosis, which we know can be a normal finding, therefore I question the inclusion of this as a clinical sign of brucellosis. 

Treatment Response

Six dogs were treated with doxycycline and rifampicin (one dog relapsed and was treated twice. It was generally well tolerated with one case of marked hepatitis. There is no standardized treatment for brucella and many dogs are considered to harbor the bacteria long-term, with or without clinical signs, with intermittent bacteremia. The zoonotic risk to humans, therefore remains present with dogs with a current or historic positive Brucella test. Euthanasia is the recommended treatment for positive livestock, however this causes emotional conflict for veterinarians and owners of companion animals. Check with your local veterinary health directors to determine the legal requirements in your state or country. This is a reportable disease in the USA. 

If you'd like to read more about this study you can find it here: https://onlinelibrary.wiley.com/doi/epdf/10.1111/jvim.16678

In honor of Memorial Day yesterday, I wish to thank all of you that have served or have friends or family members that have been lost during military service. We honor you!

Have a wonderful week! My schedule has changed for summer so please reach out if you cannot find a suitable time for a consult online - I may have additional flexibility that isn't listed. 

Seizures, Quality of Life and Side Effects, oh my!

A study published in JAVMA (Gristina BR et al. JAVMA 2023)  just recently caught my eye and I thought, perhaps it might interest you as well. The study evaluated 100 dogs with , with Tier I or Tier II level confidence of idiopathic epilepsy and assessed owner satisfaction, seizure control and adverse effects (the fancy name for side effects) of various drugs. 
*Tier I = normal CBC, serum biochemistry, neurologic examination and bile acid test
* Tier II = all of tier I plus normal brain MRI and CSF analysis

How was the Seizure Control?

Improvement in seizure control was reported in 86% of dogs with phenobarbital, 76% in the levetiracetam and 65% in the zonisamide group. Treatment failure, due to inadequate seizure control, was 48% for phenobarbital, 32% for  levetiracetam and 35% for zonisamide. Importantly, they didn't corelate seizure control with serum drug concentrations because we don't have target serum concentrations for levetiracetam and zonisamide. HTerefore, some dogs could have been under medicated, and thus poorly controlled. Interestingly, 88% of dogs were still on their original antiepileptic drug (AED) at the time this study was performed. Mean daily doses for phenobarbital, levetiracetam and zonisamide were 4.9  mg/kg, 53.8 mg/kg and 12.4 mg/kg, respectively. 

What side effects made a splash?

Phenobarbital had the highest reported adverse effects at 77%, followed by levetiracetam at 59% and zonisamide at 39% of dogs. The most common adverse effects are listed below for each drug:

• Phenobarbital: polyphagia, polydipsia, ataxia, sedation and polyuria

• Zonisamide: sedation, ataxia, hyporexia

• Levetiracetam: Sedation, ataxia, hyporexia, diarrhea, behavioral changes.

What was the perceived Quality if Life?

Owners perceived a significant improvement in quality of life, regardless of the anticonvulsant used, between pre and post treatment assessment. This is important for us to realize: clients can tolerate adverse effects if they perceive improved seizure control and quality of life! Although this retrospective, owner-perception study has limitations (all studies do), I felt it was worth repeating a bit of the information for you to add to your knowledge when addressing seizure management with your clients. 

Have a wonderful week! Remember, early bird registration ends May 31st for the July CE event so register soon if you are planning to do so! Details are available on my website. 

Reference: doi.org/10.2460/javma.22.10.0469

How to Question an Owner

Careful questioning of the owner is required to determine if the episodes described ARE seizures. Syncope, vestibular signs, neck pain, and movement disorders (think Scottie cramp) have episodic presentations with similarities to seizures. Nothing is fool proof, even an EEG, but here are some tips to get you going in the right direction. 

Describe the event, please!

Discrete episodes, with a finite start and stop, combined with autonomic signs often indicate a seizure. Level of mentation can be confusing and difficult to determine (especially for those pesky night time seizures) so don't spend too much time grilling an owner on this one. Videos can be priceless. I have evaluated many dogs and cats for seizures that actually have something else after reviewing the video. Neck pain, movement disorders, and syncope are the most common pretenders that I've seen. Finally, ask how long the events are lasting. This question is subject to tremendous bias, but if the owner says "all day" I start wondering about other non-seizure events. 

How often have the events occurred?

Okay sorry, I need to harp on this one. My pet peeve is hearing "about once a month" as an answer! This is an easy one and something we should encourage ALL clients with seizure pets to do. Keep a calendar! Tell owners to write it down, put it in a spreadsheet, mark it on their phone, keep a list - the choices are as varied as the seizures they record! You will NEED this to be in place to help you direct treatment. The single biggest reason to change treatment is that the seizures do not meet the seizure goals for epileptic pets. What are the seizure goals? Animals should have 1 seizure or less every 3 months. 

Your second goal here is to learn about cluster seizures. If the animal has 2 or more seizures in 24 hours that is defined as cluster seizures. Cluster seizures need at home cluster seizure management (another topic for another day). Furthermore, some drugs work better for dogs with cluster seizures than those with single seizures. I personally believe that bromide is a terrific option for cluster seizures and will readily use it for patients with this type of pattern. 

How long is each seizure? 

This question is utilized to learn about status epilepticus. Any seizure longer than 3-5 minutes (people argue about what is the correct time) is considered status. Status warrants emergency management with injectable solutions (intranasal, intravenous, other). Untreated status can set an animal up for systemic side effects as well as increase the risk of permanent brain damage. 

What does the animal do after the event is finished?

Your goal here is to evaluate the post ictal phase so that you can decide if a change in treatment is needed. Based on the rules outlined by the International Veterinary Epilepsy Task Force, severe post ictal changes (such as aggression) warrant treatment even if the other parameters for treatment haven't been met. I also use this question to determine how the owner is feeling about the event. Answers such as "he was fine" or "he paced and paced and seemed really upset" give me a window into how they feel about as much as how the dog did. Helping owners cope with seizures is also part of our job!

Do you have a seizure case that isn't meeting your seizure goals? Let me know! My favorite part of neurology is long-term seizure management so I'd love to help you, help your patients!

I'm headed to Chicago Vet Conference on Friday for a few talks on seizures, the neuro exam and lesion localization. I'd love to see you if you're at the conference so stop by and say "hi" if you have time!