Neuroanatomic Lesion Localization for Busy Vets

Here is the case: A 5 year old cat that cannot blink one eye. What cranial nerve is affected?
To answer this question, of course you must do a cranial nerve exam. At its most basic level, it is a process of elimination. If you touch the medial and lateral canthus and the cat does not blink what cranial nerves are you testing? (CN 5 and CN 7)

How can you isolate these two nerves from each other to see which is the affected nerve? If you do corneal reflex you're testing CN 5 (sensory) and 6 (motor). Voila! So, if the cat does not blink when you touch the medial or lateral canthus, but DOES retract the globe when you do corneal reflex which nerve is affected? Think you know... scroll (or read!) to the bottom to see the answer. 

Need a little refresher on the cranial nerves and their jobs? The table below has all nerves, and their main jobs, for quick easy reference. 

Cranial nerveFunctionNeurologic examination CN I: OlfactorySmellWatch the dog sniff, ask about eating habits. * Difficult to objectively evaluateCN II: OpticSightMenace, PLR, Cotton ball test, trackingCN III: OculomotorSomatic: eye movement.
Innervates all extraocular muscles except lateral rectus and dorsal obliqueAutonomic: Parasympathetic function to the pupilPhysiologic nystagmus (medial movement), Strabismus (if present this indicates an abnormalities of CN)
 
PLRCN IV: TrochlearEye positionStrabismusCN V: Trigeminal

• Ophthalmic

• Maxillary

• Mandibular

Sensory to the face, cornea
 
Close the jaw (muscles of mastication)Sensory: Corneal reflex, blink reflex, sensory assessment of the nares and lips
Motor: ability to CLOSE the jawCN VI: AbducentSomatic eye movementPhysiologic nystagmus (lateral movement), StrabismusCN VII: FacialSomatic: muscles of facial expression
Autonomic: parasympathetic innervation to the lacrimal gland, 3rd eyelid gland, palatine and nasal glands, taste rostral tongueMenace, blink reflex, lip and ear twitchCN VIII: vestibulocochlearSensory: balance and hearing
Innervates: vestibulospinal tracts, MLF (eye movement), reticular formation, cerebrum and cerebellumPhysiologic nystagmus, pathologic nystagmus,  positional strabismus, head position (tilt), ataxia, hearing test (BAER)CN IX: GlossopharyngealSensory to pharynx
Motor to pharynx
Autonomic: parasympathetic function – taste from the caudal tongueGag reflexCN X: VagusMotor to pharynx
Parasympathetic: taste to pharynx, larynx, heart rate, GI motility, otherGag reflex
CN XI: Spinal accessoryMotor: trapezius, sternocephalicus, brachiocephalicusPalpation of associated musclesCN XII: HypoglossalMotor: tongueMove tongue left and right, visually assess for symmetry and movement.

Answer: Cranial nerve 7 is affected. (5 is normal in corneal reflex therefore it is not the problem in the blink reflex either.)

Thanks for reading and have a great week!

 Do you have a case that is puzzling you? Please reach out - I'd love to help. Did you know I also do onsite or virtual private CE for hospitals? Reach out for more details, if you're interested.

Cognitive Dysfunction Syndrome in Cats

What is Cognitive Dysfunction in Cats?

Sixteen years ago when I left my residency and started out as a newly minted neurologist, feline cognitive dysfunction syndrome (CDS) was not on my radar. That has changed. As we learn more about aging in cats, it has become a more widely recognized disease by yours truly, as well as many of you in practice. If you're like me and need a Tidbit-Tuesday style refresher...read on!

What is cognitive dysfunction syndrome?
Cognitive dysfunction syndrome (CDS) is a term used to describe deterioration of mental capabilities associated with age.  Clinical signs referred to cognitive dysfunction can also be associated with other age-related illnesses (e.g. osteoarthritis, structural intracranial disease such as neoplasia, or cardiovascular disease). See table 1 for an outline of behavior changes seen in cats with CDS.
The underlying etiology of CDS is yet unknown. Causes such as oxidative stress/damage, neurodegeneration  and vascular changes are among the leading hypothesis for human and canine CDS, and therefore suspected to be similar in feline CDS.  Deposits of extracellular B-amyloid and intracellular accumulation of microtubule-associated protein tau have been seen in human patients with cognitive dysfunction. Similarly,  B-amyloid deposits and increased tau have been detected in aged cats with cognitive decline, however the significance remains unclear. 

What are the clinical signs of cognitive dysfunction in cats?
There is a handy article, recently published in the Veterinary Clinics of North America by Dr. Miele and associates that echos what others have been reporting in a very concise little table. (See reference at bottom) I have replicated this table, with a few modifications, here. Note: There are other signs such as decreased appetite or thirst, that don't usually drive an owner or veterinarian to seek consultation from a neurologist so I haven't included them here. 

Table 1: Clinical behavioral changes associated with CDS in cats.Increased vocalization, especially at nightAltered social interaction and relationships, either with other or other pet. Altered sleep/wake patterHouse soilingSpatial Disorientation or confusion (i.e. forgetting the location of the litter box)Temporal disorientation (i.e. forgetting if they have been fed)Altered activity (i.e. aimless wandering)AnxietyLearning and memory dysfunction
How is CDS in cats diagnosed?
Oh, this is as tangled of a web as the tau proteins we chase. (A little CDS humor here...you see the tau proteins can cause the "tangles" seen in human CDS.). Currently, the diagnosis is made by ruling out structural brain disease and systemic causes for disease. This may include complete blood count, full biochemistry panel including thyroid screening, urinalysis, chest radiographs, blood pressure assessment, brain MRI and possibly spinal tap. Imaging changes associated with canine CDS include increased depth of the sulci, dilation of ventricles secondary to neuronal loss (called ex vacuo hydrocephalus) and a measurably small interthalamic adhesion. Exclude everything else, and it's probably CDS.

How can we help these cats age easier?
Currently, there are no proven treatments for feline CDS.  The addition of antioxidants (B vitamins, vitamin C, other) as well as fish oil were evaluated for use in cats in one study and showed promise. The use of S-adenosyl-L-methionine (SAMe) has been recommended for cats based on a study that identified improved performance on cognitive testing. This study only found significant improvement in cognitive function testing in the least affected cats. In addition to medical management, environmental management with ready access to food, water, litter box and areas of comfort (beds, hiding spots) is recommended. Environmental stimulation with low impact toys, or bird feeders in which the cat can choose to ignore any activity if they do not feel inclined to engage, are recommended. Finally, focused veterinary visits can be important for cat owners to feel supported through the aging process. Focus your exam specifically evaluating body weight, urine production (to assess for signs of dehydration), behavior changes and mobility.This may help detect signs earlier in the course of disease and to identify concurrent morbidity that may contribute to, or be confused with, cognitive dysfunction.

Did I forget anything? Most of you treat and see this more than I do. What do you see in practice? What have you used (successfully, or not) for treatment? Please reach out - I want to hear your perspective!

Reference:
Miele A, Sordo L, Gunn-Moore DA. Feline Aging: Promoting Physiologic and Emotional Well-Being. Vet Clin North Am - Small Anim Pract. 2020;50(4):719-748.