Thank You!

In this week of Thanksgiving, I am remembering you and your staff.

• Thank you for trusting your patient's care to me. I am humbled by the kindness, consideration and feeling of welcome that I receive when I enter your clinic to help care for your patients.

• Thank you for having a room ready for me.

• Thank you for having kind, knowledgeable staff to assist me.

• Thank you for giving up valuable floor space (rooms, hallways, office space or even bathrooms!) to allow me to fully examine the pet.

• Thank you for the insight, nuance and personal touch you add when talking about a client or patient. I love being a part of your team.

• Thank you for being an advocate for your patient and for including me in their health care needs.

• Thank you for following up with me, giving me feedback, patient updates and answering my emails when I check in.

Most of all, thank you for being you!

Many of you I now call friends. I look forward to seeing you and your staff when I get that "ping" on my phone that signals a consult was scheduled. Keep up the good work. You are valuable and important.

Happy Thanksgiving! May you have many of things to be thankful for in life. Thanks for reading. :)

PS - in case you're confused by the photo, it is an image of Turkey. Here is your TidBit of knowledge: Istanbul (which is not the capitol), spans two continents. It spans Asia and Europe, but only about 5% of the city is on the Europe side. What is the Capital of Turkey?

(Ankara) Now you can quiz your know-it-all Uncle on Thanksgiving.

Paroxysmal Movement Disorders

Welcome to another "what-if" TidBit Tuesday! Here we go...

It's Wednesday morning and on your schedule is a 6 month old MC Cavalier King Charles Spaniel to see you for a complaint of "seizures". Upon examination, you find the pet to be normal both physically and neurologically. The client proceeds to describe the events that they've noticed as follows:

"When she goes to jump up on me to greet me she will sometimes fall into a praying position with all four legs stiff. It lasts 2-3 minutes and then she gradually relaxes and is able to walk normally."

Upon further questioning you discover that the dog appears mentally appropriate without signs of drooling, urinating, defecating or vomiting before or after the event. The client provides you a video of the event and at the conclusion, the dog resumes wiggling and excited behavior without obvious change in mentation. Hmmm....no preictal phase, no postictal phase and a relatively long ictal phase. Maybe it isn't an ictus at all???

Hopefully by now you're starting to think this may not be a seizure at all, but in fact one of those "movement disorders" you've been hearing about. What are they, and what can we do?

Movement disorders are a large group of diseases that are non-epileptic changes in muscle tone that happen episodically. They can be triggered by environment, or not. The most common classification that we see in veterinary medicine is a paroxysmal dyskinesia (PD), with or without dystonia. (I'm sorry...say what?? Okay, sorry. Paroxysmal = sudden violent or periodic event; dyskinesia = involuntary, erratic movements of muscles, usually face or limbs; dystonia = sudden muscle contracture, usually of opposing muscle groups which results in a writhing or twisting movement.) There are breed-specific PD which can be found here (https://www.frontiersin.org/files/Articles/163467/fvets-02-00065-HTML/image_m/fvets-02-00065-t005.jpg). Many of these are known to be inherited and some form of genetic mutation has been identified but in some cases we aren't clear on the cause. In humans there are inherited and acquired causes and entire books written about the different forms of movement disorders and their appearance. We don't have that...yet.

Pathophysiology

What happens to cause this, if it isn't a seizure? That is a complex question that I will try to answer simply. Most movement disorders originate from the brain in an area of the basal nuclei. This is where one of the most famous movement disorders, Parkinson's disease, originates from. Pathophysiology is largely unknown for animal movement disorders but there is definitely something going on in the basal ganglia. Diagnostic testing including brain MRI/CSF and at times muscle/nerve biopsies are recommended to pursue an acquired cause. These tests are often negative because inherited causes are more common.

Treatment

Effecting the basal ganglia through the use of benzodiazepine drugs (clonazepam 0.5 mg/kg) or even acetazolamide has shown some improvement. Some dyskinesia respond favorably to zonisamide and potassium bromide as well which further complicates our ability to decide cage-side if this is a seizure disorder, or not. An EEG is valuable here to identify the lack of brain changes consistent with seizures. However interpretation and acquisition of an EEG is challenging making this less available and useful for veterinary patients.

Sometimes it is plain ol' not clear if this is a seizure disorder or a movement disorder and we must do a trial and error with medications. In either case, breeding pets with known or suspected movement disorder OR epilepsy is discouraged due to the likelihood of inheritance.

Do you have a case in which you suspect a movement disorder? Let me know if you want to work through the case together! (Group frustration is much more tolerable than beating your head against the wall - metaphorically speaking - alone!).

Thanks for reading and have a great week! Stay safe, stay well and let me know how I can help you.

Brachial Plexus Injury and Recovery

Brachial Plexus Injury and Recovery

Nerve injury can take 3 different forms, from least to most severe:
1) Neurapraxia: transient function loss (ex: conduction block) with no loss of nerve anatomy.
2) Axonotmesis: disruption of axons with some (mild) degree of myelin loss. Importantly the surrounding perineurium and epineurium are intact.
3) Neurotmesis: complete rupture of the nerve (axon, myelin and all surrounding structures).This injury does not lend itself well to recovery.
**Important, but trivial sounding, note: Nerve root avulsion is irreversible.

A recent study evaluated traumatic nerve injury and outlined their findings. The most clinically applicable key points are listed below:

• 226 animals were included (175 dogs, 51 cats)

• 46% were injured before age 2

• Horner's syndrome was seen in 68 animals (42%of dogs and 38% of cats) with miosis ipsilateral to the affected thoracic limb. Note: It should always be ipsilateral unless there is spinal cord damage.

• Cutaneous trunci reflex (which has it's motor origin between C8-T2) was lost in 81% of dogs, again ipsilateral to the affected limb. This reflex doesn't count in cats. :)

Prognostic factors in this study were largely related to electrodiagnostic studies, which are not clinically useful markers in practice. (Unless you have access to electrodiagnostic testing...which I don't, anymore!) That said, we know that animals with neurotmesis do not recover and prior studies have identified that animals with axonotmesis can recover but it may take awhile. Nerves may regrow 1 inch per month for a total of 8 inches. Therefore distal injuries resulting in axonotmesis may result in some functional recovery of the limb.
In the study referenced below, the only important clinical prognostic indicator from this study was the absence of cutaneous trunci reflex. When, absent, it was linked to a lesser chance of recovery, but no statistical analysis was performed to assess this trend. This study also reinforced the finding that electrodiagnostic testing is a valuable testing tool for providing a prognosis for dogs and cats following brachial plexus injury.

Do you have a patient with a traumatic limb injury with possible neurologic involvement? A neurologic examination may be able to better identify chances of recovery and direct treatment towards appropriate physical therapy, acupuncture and other management during the recovery phase. Reach out if I can help!

Have a great week and stay warm in this chilly turn towards fall!

Referenced article: https://doi.org/10.1111/jvim.16254

CBD, THC and Neurology

It doesn't matter how hard I try to avoid this question, it always comes up with clients. Perhaps you feel similarly? A group from Ontario, Canada recently published a study evaluating safety profiles of several CBD-oil, CBD/THC-oil and THC-oil containing products in a dose escalation study. The study evaluated 20 dogs in a blinded, placebo controlled (sunflower oil or MCT oil) multidose parallel study.

The following comparisons were made:
1. CBD oil or THC oil compared to MCT placebo
2. CBD/THC combined oil (ratio: 1.5) to sunflower oil

Results

This study contained a lot of data about adverse effects (AE: the new fancy word for side effects) that you might find interesting. The article is linked below. I will focus on the neurological and hepatic side effects.

Overall, they had mostly (n =401/505) mild adverse effects but a few moderate and severe adverse effects were seen. The oils containing THC had the most AE and were also the only groups to show severe AE. Neurologic AE that were noted included tremors and ataxia but AE categorized as "constitutional" included lethargy and hyperesthesia. I did not include the "constitutional" numbers below but could be persuaded that indeed those should have been considered neurological AE as well. Liver values were considered abnormal when they exceeded a 2-fold increase from normal.

1. CBD oil (80 AE): 13 were neurologic; 1 dog had elevated ALP (2.9-fold)
2. THC oil (206 AE): 89 were neurologic*
3. THC/CBD oil (115 AE): 56 were neurologic*; 1 dog had an elevated ALP (3.6-fold)
4. Placebo: 27 AE, 13 were neurologic (!)
* The proportion of GI to neurologic side effects were higher in the groups containing THC compared to placebo or CBD oil only groups.

Moderate side effects were not noted in the CBD oil group and accounted for 22 or 505 AE in the THC and CBD/THC group with also a few dogs in the placebo group.

Severe side effects were noted in 3 dogs - one in the THC only group and 2 dogs in the CBD/THC group. Signs were transient and resolved in 9-28 hours.

A reminder about hepatic metabolism

The elevation of ALP due to CBD results from activation of the p-450 system in the liver. This should sound familiar because it is the workhorse for drug metabolism for drugs such as phenobarbital or zonisamide. Co-administration of CBD and phenobarbital (and probably zonisamide but not in published data for dogs) can affect the metabolism of phenobarbital.

Take away message: What is the big picture here?

My take away from this article was that THC containing products have more neurological side effects compared to CBD containing products and CBD containing products affect liver metabolism. You may be thinking "but I wouldn't recommend THC products for my patients!" and I would support that. And yet, remember production oversight and regulation of these products, especially for animal consumption, isn't robust therefore contamination of THC may be possible. Please note that the State of Wisconsin continues to prohibit prescribing CBD products by vets with clients unless under specific situations. (https://datcp.wi.gov/Documents/VEBCannabis.pdf) therefore this TidBit Tuesday in no way supports or advocates for the use of CBD oil containing products for veterinary patients.

Article link: https://www.frontiersin.org/articles/10.3389/fvets.2020.00051/full#B21

Thanks for reading! Have a great day, and keep those consults coming!

Is Age a Disease?

Age, The Neurologic Examination and Prediction of Disease

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

Can the Neurologic Examination Help Vets with Older Patients?

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

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

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

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

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


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

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

How to Diagnose Idiopathic Epilepsy in the Exam Room

In 2015, the International Veterinary Epilepsy Task Force (IVETF) published a list of criteria to diagnose idiopathic epilepsy in dogs (not cats). The IVETF consisted of a group of veterinary neurologists, neuropathologists, and epileptologists. If you wish to see all of the resulting publications, just let me know! (They are available open access.)

The IVETF listed several ways to make a diagnosis of idiopathic epilepsy, starting with the lowest level of confidence (Tier I) and rising to the top with the most confidence in the diagnosis (Tier III). When using this information in your daily practice, consider writing "diagnosis: idiopathic epilepsy with Tier 1 confidence" in the medical record when a patient meets the criteria for a Tier I diagnosis of idiopathic epilepsy.

Please note, idiopathic epilepsy does not mean, any seizure disorder. Idiopathic epilepsy is a specific disease, that causes repeated seizures. ANY animal with repeated seizures can be diagnosed with epilepsy, but idiopathic epilepsy is ONE form of epilepsy. Make sense?

Tier I:

A dog must have:

• A history of 2 or more seizures at least 24 hours apart

• Have the age at onset between 6 months and 6 years

• Demonstrate a normal inter-ictal physical and neurologic examination

• A normal CBC, and serum biochemistry (the IVETF lists what they consider to be standard in a serum biochemistry analysis. Let me know if you want/need this list.)

• A normal fasting bile acids and/or ammonia

• A normal urinalysis

• A familial history of IE is supportive, but not required

Tier II:

To diagnose idiopathic epilepsy with Tier II level confidence a dog must have:

• All of Tier I plus...

• A normal brain MRI

• A normal CSF analysis

• Normal fasting and post-prandial bile acids

Tier III:

• All of Tier II plus...
  

• Identification of ictal or inter-ictal EEG abnormalities suggestive of seizure disorders.

So, if a patient meets Tier I level confidence, when should MRI be performed?

• Anytime a client wishes to confirm a diagnosis of intracranial disease. (This includes idiopathic epilepsy which is diagnosed by exclusion of other causes)

• If a dog has a seizure onset of < 1 year or > 7 years of age (according to the IVETF)

• If neurologic abnormalities reflective of the prosencephalon/forebrain are identified on the neurologic examination regardless of age, breed or a familial history of seizures.

In summary, it is always worthwhile to inform clients of the option of MRI when their dog (or cat) has seizures however, if the Tier I criteria are met and MRI has a high likelihood of normal results, it is very reasonable to skip this test and begin treatment for idiopathic epilepsy.

I try to remember that MRI abnormalities were identified in 22% of dogs with a normal neurologic exam and 90% of dogs with an abnormal neurologic examination in one study.

What about CSF analysis, you ask? I'm glad you asked! Some dogs with meningitis will have a normal MRI, therefore an MRI PLUS CSF tap is often my recommendation to ensure we don't overlook those patients inappropriately by just performing an MRI.

What about cats? The IVETF recommendations do not specifically apply to cats however many neurologists, including me, extrapolate this information to cats in practice. My fingers and toes are crossed for science driven cat-specific recommendations in the near future.

Have a great week! As always stay safe, and let me know how I can help you, help your patients, with neurologic disease.

Rabies Awareness

Etiology

Rabies is neurotropic rhabdovirus that causes fatal infection in dogs, cats and humans. Usually infection is transmitted by inoculation with saliva by means of a bite. The virus then spreads into the CNS via peripheral nerves. Once the brain is infected, the virus spreads out through peripheral nerves to the salivary glands among other targets – at this point, the animal can transmit rabies.

Signalment
Any dog, cat, horse, cow, HUMAN

Clinical Signs

Two syndromes are described:

• Furious syndrome (forebrain signs)

• Paralytic syndrome (lower motor neuron signs ascending from the site of the bite).

Once neurologic signs are present, progression is rapid, and most animals will be dead within several days. Rabies should be considered as a differential diagnosis in any animal with acute onset, rapidly progressive neurologic disease especially if there is a poor vaccination history or exposure to other rabid animals.

Diagnostic Tests

Key point: Definitive diagnosis can only be achieved postmortem, and requires fluorescent antibody staining of brain tissue to demonstrate rabies antigen. A serum RFFIT (Rapid fluorescent foci inhibition test) can be performed to evaluate for evidence of previous vaccination however it should NOT be used to make a diagnosis of active rabies infection. Due to the neurotropic nature of rabies it can remain undetected by the immune system and therefore cause a negative (false negative) RFFIT antibiotic result.

Further reading
If you're interested in reading about a real case of Rabies virus infection please check out this article. https://doi.org/10.5326/0390547 I saw this case a number of years ago, but the disease hasn't changed much in 20 years! Furthermore, a rabies positive bat was identified on a sidewalk in Dane county just this week. Although fewer Rabies positive bats have apparently been identified this year (so far) the virus is still around and therefore still something we should be talking about!

Thanks for reading! Rabies virus infection is something I think about daily, given the cases that I see, and is one of the more daunting diseases we are faced with. Please reach out if you have any questions!

Other good resources:
The Wisconsin Rabies Algorithm: (for exposure or sick animals) https://www.dhs.wisconsin.gov/rabies/algorithm/algorithmcategories.htm
Illinois Rabies information: https://www.ilga.gov/commission/jcar/admincode/008/00800030sections.html

Temporalis and Masseter Muscle Atrophy

It's Tuesday at 10 am and you're about to see a 7 year old dog with unilateral temporalis and/or masseter muscle atrophy. What parts of the neurologic system could be involved?

1. Muscle: A problem with muscle function, termed a myopathy, can result in muscle atrophy. The most common cause of temporalis and masseter muscle atrophy in dogs is masticatory muscle myositis (MMM), which is caused from an immune mediated attack against the muscle fiber. This is a UNIQUE form of muscle inflammation because the proteins on these muscles are embryologically unique (2M fiber type, if you must ask) from all other muscles in the body. We care about that because it means that we can have a an antibody (AB) test that we can run that is highly specific AND sensitive! The second myopathic disease of the head muscles, that I see commonly, is myositis due to neospora or toxoplasma infection. Simply put, the protozoa get into the muscle, set up a secondary inflammation (myositis) and sometimes you can see a mild positive on the aforementioned MMM AB titer test. However, if you concurrently test for neospora and toxoplasma (serum titers) you can catch this "false" positive, and treat the correct disease.

Treatment for MMM: Immunosuppressive steroids for 30+ days
Treatment for infectious myositis: clindamycin or sulfa antibiotics until negative or stable titers.

2. Cranial nerve 5: A dysfunction of CN 5 can result in denervation atrophy of one (or both) temporalis muscles. On the exam, look closely for concurrent signs of a sensory neuropathy to the face and if present, a CN 5 dysfunction should be suspected. The differential diagnoses list is much bigger but typically centers around a few common causes (neoplasia, neuritis, hypothyroidism, and trauma). To diagnose a CN 5 neuropathy the best approach is a brain MRI followed by a spinal tap, along with titers for infectious diseases, thyroid panel and routine CBC, serum biochemistry. Not all of those tests are needed for each patient so pick and choose as appropriate for your case.

Treatment for CN 5 deficits: this varies widely and is dependent on the underlying cause. It is a bit hard to summarize TidBit Tuesday-style. :) Stay tuned for another email detailing all of the possible causes and treatments for cranial neuropathies.

I hope this TidBit Tuesday helps you focus your exam, and thoughts, when faced with a case of unilateral atrophy of the muscles of the head. This report was stimulated from recent conversations about this presentation so please reach out if you have a case, or questions about a case, with unilateral muscle atrophy. The more we talk with each other, the more we learn from each other!

Have a great week!

Traumatic Brain Injury And Blood Glucose

We're approaching the month of October - known for scary costumes and sugar overload. Why not look at a recent study about glucose to kick up our adrenaline? Okay, so this is a study in dogs and cats, specifically about traumatic brain injury and relationship between glucose and prognosis but don't shame me for trying to make a link to "current events"!

Background

This was a retrospective study (Cameron S, et al. JVECCs, 2021) looking at 131 dogs and 81 cats that were presented to one of two teaching hospitals following trauma and were diagnosed with traumatic brain injury (TBI). (TBI is the new term for head trauma, in case you're wondering.) At admission, glucose and a modified Glasgow Coma Scale, among other tests, were evaluated from the record and correlated to outcome. The animals were termed "survivors" if they lived to be discharged from the hospital and they were termed "non-survivors" if they, well, didn't.

Results

Here are the key points, and the interesting bits!

Dogs:

• The MGCS was significantly lower in non-survivors compared to survivors.

• Blood glucose concentration was significantly higher in non-survivors compared to survivors.

• A cut off of 148 had a sensitivity of 73% and specificity of 76% for a poor outcome (non-survivor)

Cats:

• The MGCS was the ONLY significant predictor of outcome

• Glucose was not significantly related to outcome!

Take home message:
When presented with a post-traumatic patient, perform a serum blood glucose concentration and a neurologic examination (to get a MGCS). Both of those may be able to help you predict the outcome for a DOG (not cat) and guide the clients towards or away from referral if they are considering humane euthanasia. Naturally, we must account for co-morbidity, financial impact and prior medical conditions of the pet when faced with a post-traumatic patient but hopefully these two little points will further improve your ability to help the patient.

Thanks for reading! I hope you have a nice week and keep those consults coming!
New hours are in effect so please use the online scheduler whenever possible to schedule a consult or email/text me if you cannot find a suitable time. Thanks!

Cluster Seizure Management

What is a cluster seizure?

Cluster seizures are defined as 2 or more discrete seizures within a 24 hour period.1 Cluster seizures are different than status epilepticus (any one seizure lasting for an extended period of time, or 2 seizures in which poor recovery occurred between seizures). Cluster seizures pose a special concern for seizure patients because of they have been linked with poorer outcomes compared to dogs without a history of cluster seizures.

The goal with cluster seizure management is to minimize the number and duration of seizures. A secondary goal is to reduce the need for hospital visit or stay thus reducing the financial burden to the client.

When should I provide a cluster seizure plan to a client?

• If a patient has a history of 2 or more times when they had cluster seizures

• If the patient has a history of status epilepticus

What drug choices, routes of administration and doses can I offer?

Levetiracetam

1. Rectal administration – 40 mg/kg PR at the time of seizure, repeated once if needed within 24 hours. Results suggest an improvement in seizure management in the medium term using rectal levetiracetam AND standard anticonvulsant therapy in one stud

2. Oral administration – start 20-30 mg/kg PO q8hr (NOT Extended release) levetiracetam after a pet experiences the first seizure and has recovered enough to eat and continue q8hr dosing for 2 days beyond the pet’s last seizure. The levetiracetam is then stopped, and standard anticonvulsant therapy is continued long-term. Clinical experience suggests this approach will reduce clinic visits, number of seizures during the cluster event. However, clinical side effects such as sedation or ataxia may be present during the dosing period. Note: This approach should NOT be used if levetiracetam is part of a patient’s standard oral therapy for long-term seizure control. Suddenly discontinuing an anticonvulsant medication can lead to breakthrough seizures or status epilepticus.

Benzodiazepine
Diazepam has been the main acute anticonvulsant treatment for veterinary patients.4–7

1. Rectal - Be sure to target the rectum, not colon, to avoid hepatic metabolism. Start 1-2 mg/kg per rectum.10 Compounded suppository formulations of diazepam have not demonstrated reliable serum diazepam concentrations in dogs therefore compounded suppositories are not currently recommended.9

2. Intranasal – preferred by some due to the ease of administration, and avoidance of the first pass effect of metabolism. Start with 0.5 mg/kg intranasal.

Midazolam

1. Intranasal – this is my preferred route and drug for at home benzodiazepine administration. Additionally, it was reported to be favorable compared to intravenous midazolam in 44 dogs. 11 Start with 0.2 mg/kg intranasal.

2. Intramuscular – this route is favored by some but is not my recommended route of administration for clients at home in emergency situations. In a clinical situation, intramuscular administration can be effective when intravenous access is limited. Starting dose of 0.2 mg/kg is recommended.

3. Rectal – do not use midazolam rectally due to erratic and unpredictable plasma concentrations at standard doses.

Phenobarbital
Patients receiving daily phenobarbital administration can benefit from an increase, or pulse, of phenobarbital therapy during a cluster event.

1. Oral increase – in my clinical practice we regularly recommend increasing a dog from q12h dosing to q8h dosing for 2 days beyond the last seizure. An example of this would be if a dog had a seizure Saturday morning. Upon recovery from the seizure an additional oral dose of phenobarbital (at the same oral dose administered) is recommended followed by q8hr dosing Sunday and Monday. Tuesday the dog would return to the standard twice daily dosing interval. This approach provides a slight increase of serum phenobarbital concentrations which may protect against further cluster seizures. Clinical adverse effects such as increased sedation, ataxia, polyuria, polydipsia, and polyphagia may become evident during the increased dosing period.

Summary
Providing options at home for cluster seizure care can reduce the need for hospitalization, or clinic visits. Additionally, any of the above treatments can be provided in hospital during seizure observation should that be needed. All the treatment choices discussed above are targeted for dogs and are rarely used in cats. Although the medications discussed have been evaluated for safety for use in cats, the specific protocols do not have clinical trial data, and minimal clinical experience.

This week I spoke to a wonderful group of vets at IVECCs about cluster buster protocols and it reminded me that we haven't read about this in awhile on our TidBit Tuesdays. We're all learning together!
(references available upon request)

Canine Cognitive Dysfunction

Cognitive Dysfunction Syndrome in Dogs

Canine cognitive dysfunction syndrome (CDS) is reported to be a progressive disorder with specific characteristics. Many authors group canine CDS signs into specific categories such as:

• disorientation

• social interactions

• sleep-wake cycles

• house soiling, learning and memory

• activity and anxiety

There is a scoring system called the DISHAA Cognitive Dysfunction Evaluation Tool that utilizes these categories in forming a score, that has been shown by some to correlate to the level of impairment of the dog.

A recent study out of The Ohio State University by Dr. O'Brian et al, published in JAVMA (Sept 15, 2021), described the use of an educational 50 minute weekly class, as a means to controlling clinical progression of CDS. This is a case-control study with about 20 owner/dog pairs completing the class and 66 owner/dog pairs used as control. Scoring was performed at entrance to the study, as well as at 3, 6 and 12 months. During class the instructor spent part of the time informing the clients about a specific aspect of CDS, and the remainder of the time working on an interactive activity with the dog/owner pair geared towards cognitive enrichment and new learned tasks. The owners were asked to practice outside of class as well as in class. The most notable finding was a significant progression of clinical score, using the DISHAA scoring system, in the control group and a lack of progression in the class group. The only exception to this was the disorientation scores. These appeared to increase in the class group which, as the authors suggested, may be due to increased owner awareness by attending the class. The authors suggest that owner information, and structured interaction with the dog, is what slowed progression of all of the other markers of CDS.

What is the take away?

Well...maybe an information session (zoom or live) once monthly for all of your dogs over age 8 could increase awareness by clients and alert them to seek medical attention should signs arise. Or, maybe a senior class in your area (lead by a veterinarian or a trainer) might be the best answer for your clientele.

I hope you have a wonderful week! Please remember that I will be closed Monday-Thursday next week, with limited hours on Friday September 10th. Have a safe and happy Labor Day and Happy New Year, if you celebrate!

Canine Distemper

Etiology

Viral replication initially begins in lymphoid tissue and induces marked immunosuppression. Virus then reaches the CNS through the choroid plexus, ependymal cells and perivascular spaces 1-3 weeks after infection by virus infected lymphocytes and monocytes. What is the significance here? Neurologic signs often follow GI and respiratory signs.

Signalment

Distemper should be strongly suspected in an unvaccinated young dog with neurologic signs and with a history of recent GI and/or respiratory disease. Myoclonus, a repetitive twitching of muscles, is a common indication of current or previous distemper infection. Distemper can also be present – and a diagnostic challenge – in older, vaccinated dogs with no history of systemic disease prior to neurologic signs. Older dogs typically have a demyelination, with chronic, slowly progressive, signs of a myelopathy.

Clinical Signs

Respiratory and GI signs occur 1-3 weeks prior to CNS signs. The presence and pattern of illness depend primarily on the viral strain and the age and the immunocompetence of the patient. (Different strains but only one serotype means that exposure to one strain protects dogs against any subsequent strain.) There are 3 different scenarios:

• Dogs that develop an early, effective immunological response recover from mild or no neurological signs. Approximately 50% of dogs have a subclinical neurologic course

• Dogs that are unable to mount an immunological response suffer severe systemic illness, including acute encephalitis, leading to death within about 3 weeks of exposure. These dogs will have seizures, blindness, and other signs of grey matter disease.

• Dogs with delayed immunologic response don’t develop acute illness but may develop a chronic, persistent infection, characterized by chronic encephalitis or myelitis.

In acute disease, infection of neurons and microglia and astrocytes leads to mostly grey matter damage. In chronic infection, the immune response to persistent viral infection leads to inflammation and demyelination. Vaccine induced distemper is associated with a mild encephalitis in dogs vaccinated with modified live vaccines.

Diagnostic Tests

• Active or inactive chorioretinitis may be evident on ophthalmoscopic examination.

• CSF varies from normal to having increased protein and lymphocytic pleocytosis during active infection

• Distemper antibody titers or PCR in CSF, blood and urine can be helpful. False positive urine and blood PCR results may occur within 3 weeks of vaccination.

• PCR on CSF is the most diagnostic test for active infection, however myoclonus, demyelination and seizures can be residual neurologic signs after the acute infection has been cleared. Therefore, a negative PCR on CSF does not suggest that the pet NEVER had distemper, it merely suggests that there isn't detectable virus at that point in time. CSF titers (IgG/IgM) can be quite useful in this situation when compared to the serum titers. That said...what do we do with this information?
  

• Immuno-histochemistry on hyperkeratotic foot pad, conjunctiva, respiratory epithelium or CSF WBC can be diagnostic.

Treatment

Supportive care is important. Anticonvulsant drugs should be employed if seizures are present. Quality of life may be limited and poor if seizures are present and progressive. Myoclonus does not necessitate euthanasia (and should be differentiated from seizures) but it may negatively affect the quality of life depending on the muscles involved. I have personally seen distemper cause myoclonus of the jaw with repeated opening and closing (it looks like a pet gasping for air), flexion of the lips (with resultant wear of the teeth due to grinding) and abdominal contraction (like a hyperactive cutaneous trunci reflex) in dogs with confirmed distemper. No treatment resolves myoclonus at this time.

Although this is a rare disease due to vaccination, we have had a resurgence in our area due, I suspect, to an increase in pet adoptions from endemic areas such as the southeastern USA. Vaccination can prevent infection for most pets!

Have you treated distemper? How did it go? Reach out and let me know if you have any questions or comments on this disease.

For those of you in my referral zone - please note that I will be closed and not responsive to email or telephone Monday-Thursday September 6-9th as we celebrate Rosh Hashanah (Jewish New Year). I apologize for any delayed responses during this time and, as always, appreciate your patience!

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 idiopathic, but causes such as neuritis (viral or immune mediated) or atrophy have been hypothesized. A recent study (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 and demonstrate peracute onset of signs, often proceeded by vomiting with no progression 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: 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 needed.

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 show improvement. Full resolution of clinical signs should be by 6 weeks. If signs wax and wane, or progressive 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. Signs may occur multiple times over the animals' life.

Thanks for reading! This TidBit Tuesday was prompted by one of you so keep those suggestions coming! If there is something you'd like to read about, chances are that someone else is also interested too.

My hours are changing the last week of August due to school starting. As always, please let me know if you cannot find an appointment time through the online scheduler.
Have a great week!

Time for a Tongue Twister!

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. Unfortunately the table does not copy to this blog very well so please email me or join our TidBit Tuesday mailing list to get all of the details.
What I did was list 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.

You may recognize this case if you have been a loyal TidBit Tuesday reader. This was repeated from February 2020 because I felt like it was a good time to review cranial nerve lesion localization with a very interesting cranial nerve deficit. Thanks for reading (again)!

I hope you have a great week!

Dysautonomia in Dogs and Cats

Dysautonomia in Dogs and Cats?

Before we dive into this topic, I wanted to report the diagnosis for the case from last week's TidBit Tuesday mailer. The cat with the C6-T2 myelopathy was diagnosed with an FCE and was managed successfully over about 2 months to an almost normal return to function.

Now, on to this week's TidBit Tuesday...

Several of us worked on an interesting case together this week that tickled my memory about a disease that we, in Wisconsin, do not see very often. I thought we could all refresh together.

Dysautonomia is (typically) caused by degeneration of the autonomic, and some somatic, nerve cell bodies throughout the spinal cord and some brainstem nuclei.
Common Clinical Signs

With this disease, you may see vomiting first, followed by dysuria (enlarged bladder that is easy to express but difficult to void by the patient). One of the hallmark signs is a loss of anal tone and THIS IS SOMATIC not autonomic. We can see a mix of lower motor neuron signs with autonomic loss in this disease! Absent PLR and elevated 3rd eyelid are common findings on physical examination. From there, you may diagnose megaesophagus and ileus on radiographs.

Diagnosis

A study by Dr. Berghaus et al in 2001 identified that dysautonomia was found more often in rural areas, with access to water or farm land. Additionally, all of the published US cases have been from Missouri/southern Illinois region.

This disease is diagnosed through pharmacological testing and elimination of other etiology. In Dr. Berghaus' study, the Schirmer tear test was below 5 mm/min in 50% (20) of dogs, between 5-10 mm/min in an 10 additional dogs. There was no response to an atropine response test in many dogs, and some response in a few cases. Finally, most dogs had a rapid response to dilute pilocarpine in the eye, but not all. All of these tests are looking at the autonomic system in different areas of the body. When a reduced response to one or more of these tests is noted, taking into account the clinical history, you may wish to consider dysautonomia as a diagnosis.

Unfortunately, there is no known treatment that will reverse clinical progression. A combined immune mediated dysautonomia, and myasthenia gravis has been reported but even these cases do not appear to respond adequately to immunosuppression. The final diagnosis is obtained on necropsy.

Although we are ending on a sour note, I hope you have enjoyed this review of dysautonomia. Please let me know if you have any questions on this case, or any other neurology case.

I love helping you, help your patients with neurologic disease!

Neurologic Cat?

Where is the Lesion?

History: Sarah is a 4 year old, indoor only FS DSH. She was obtained as a kitten and had been normal, per clients, her entire life thus far. She presented to me for acute onset (same day) weakness. No known trauma, toxin ingestion or medication exposure.

Physical examination: No abnormalities, normal TPR.

Neurologic examination:
•Mentation: BAR
•Gait: Ambulatory severe left hemiparesis with proprioceptive ataxia in all four limbs
•Cranial nerves: Normal
•Postural reactions: absent left thoracic and pelvic limbs only
•Reflexes: reduced withdrawal left thoracic limb, normal all other limbs. Cutaneous trunci absent left, normal right side.
•Palpation: Non-painful

Lesion localization? I do not see evidence of intracranial disease so automatically I localize caudal to C1. Both a front and rear leg are affect, so again, we can isolate cranial to T2. So...right away you can think left C1-C5 or C6-T2 myelopathy. Which is it? Well, the reflexes were reduced to the left thoracic limb, and the reflex arc is C6-T2, so our localization must involve C6-T2.
Up is differential diagnoses building. Here is what I came up with:
D: none, this is acute
A: None, the cat is too old for congenital disease onset signs
M: none
N: Lymphoma is possible however it is rarely acute in nature
I: Meningomyelitis (infectious or inflammatory) is possible
T: No known trauma, but cannot rule it out
V: Fibrocartilagenous embolism is highly likely due to the acute onset of signs.

Did you think of something else that I missed?
Unabashed plug for the CE August 2nd here - we will look more specifically at this case and do lesion localization in greater detail. Please consider joining us from 7-8PM. Details can be found at my website.

Diagnosis: I debated about giving this away before the talk and I have decided NOT to tell you the final diagnosis this week. I will share it on next week's TidBit Tuesday (August 3rd) so stay tuned!

Hopefully you enjoyed this case review this week. Do you have a suggestion for a TidBit Tuesday topic? If so - please send me an email. I would prefer to write about something you want to read. :)

I hope you have a great week!

How is Sleep Linked to Seizures?

I had the privilege to be involved in a prospective study regarding the effects of sleep and epilepsy. This study was published this week in the Journal of Veterinary Internal Medicine (see below for a link).

Disrupted sleep is common in human patients with epilepsy. Is the same true for dogs with epilepsy?

Dr. Starr Cameron spearheaded a study at the University of Wisconsin-Madison, and enrolled dogs with confirmed or suspected epilepsy, fit them with a FitBark(TM) the dog equivalent of a FitBit(TM) and watched their sleep patterns over 12 weeks. This study was one part of a multi-part study using the FitBark(TM) technology.

So, what is the answer?

Interestingly, a statistically significant change in sleep patterns was NOT noted. These were age and breed matched dogs, too. There was a trend toward poorer sleep for dogs receiving higher doses of bromide, but it was not noted at lower doses.

What is the relationship with sleep and seizures?

In human epileptic patients, seizures beget poor sleep and poor sleep can result in an increased frequency of seizures. This wasn't shown in our dog population, but that doesn't mean that it isn't a concern for some dogs. What do we take away from this? Keep an eye on the sleep pattern of your epileptic patients and consider sleep aids if they are restless. Oh, and stay tuned for more results looking at sleep and seizures in dogs - this is a hot area of research right now. :)
Article: https://onlinelibrary.wiley.com/share/JD24HPYCTIRKYTBVSJZA?target=10.1111/jvim.16205

I hope you have a great week! Let me know if you have an epileptic patient that needs a little extra assistance - I'd love to help!

Fibrocartilagenous Emboli

First...a Case (Details have been changed for anonymity!)

I evaluated a 3 year old MI Mixed breed dog with a history of acute onset paraparesis after chasing a ball. This dog is an athlete, and he competes at an international level. After acute onset signs, the dog was seen to gradually improve motor and coordination over about 7 days.
Neurologic Examination
Mentation: BAR
Cranial nerves: Normal
Gait: Ambulatory mild right monoparesis, remainder normal
Reflexes: normal including c. trunci and perineal
Postural reactions: absent right pelvic limb only.
Palpation: Non-painful, normal cervical ROM
Neuroanatomic lesion localization? ---> see below for the answer

Differential diagnoses: FCE, Acute non-compressive disc herniation, spinal trauma.
Due to the marked improvement, diagnostic testing such as MRI was not elected. Supportive care with physical therapy, acupuncture, and limiting jumping and other highly impactful activities was recommended. The dog continued to improve and returned to normal.

What are Fibrocartilagenous Emboli (FCE)?

As the name suggests, FCE are pieces of fibrocartilage that run amok, in this case, in the spinal cord vasculature. The material is thought to be part of the nucleus pulposus which somehow gains access to the blood supply around the spinal cord. This is very different from a typical type I disc herniation! How different, you ask? Let's compare...

—-> There is a table here but it wouldn’t copy to the website. Email me for a copy of a comparison between type I, Type II, ANNPE, AHNPE and FCE if you’re interested. (Barnes@barnesveterinaryservices.com)

Neuroanatomic Lesion Localization Answer: T3-L3, right sided.

We have had some really unusual cases this week...Keep them coming! I love working through these tough cases with you and look forward to doing so again. (The not-so-tough ones are also nice...and a nice break from the tough ones!)

Let me know how I can help you, help your patients.

Audiogenic Reflex Seizures, Anyone?

As I write this, the fireworks are blazing in my neighborhood and there is a general sense of noise in the nation. How can noise relate to seizures?

What are they?

Feline audiogenic reflex seizures (FARS) start in cats late in life (> 10 years of age) and are triggered by a sound or sounds. The seizure phenotype (appearance) has a myoclonic component, but may also have absence or generalized seizures, as well.

What causes FARS?
Any noise, but usually a high frequency sound such as clinking a spoon in a tea cup triggers the seizures. Some cats will have spontaneous seizures in addition to FARS and others will purely have FARS. If you are seeing an older cat with new onset seizures, consider having the client keep a "sound diary" for a few weeks to see if there is a correlation.

Why bother identifying this...you're going to tell me to give phenobarbital!
Au contraire mon frere! A sentinel study was published in 2017 by Lowrie, et al (https://doi.org/10.1177%2F1098612X15622806) that showed a marked improvement in cats on levetiracetam in a randomized, controlled, open-label study with phenobarbital. 100% of the cats in the levetiracetam group obtained seizure control compared to 3% in the phenobarbital group. So you're correct that I typically prefer phenobarbital for feline seizures...except for FARS!

What causes FARS?

Interestingly, the majority of cats diagnosed with FARS in the published studies have had idiopathic epilepsy with a small portion showing progressive signs suggestive of active forebrain disease (neoplasia, meningoencephalitis).

That's it for today, folks! I hope you have a safe, fun week and stay cool during this hot weather!