The neurological examination is the most fundamental tool that neurologists use to identify and isolate problems in the central and peripheral nervous system (CNS & PNS). A thorough clinical examination should, however, also be performed, as many non-neurological diseases can provoke signs that are very similar to the presentation of neurological diseases.

First of all, the neurological examination serve to detect malfunctions of the CNS and PNS and to determine if the problem presented is of a neurological nature or not. The individual tests performed in the neurological examination targets specific structures of the CNS and PNS and thus abnormal findings indicate which neuro-anatomical structures are affected (neuro-anatomical lesion localization). Advanced neuro-diagnostic tests such as computed tomography (CT), magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) examination are commonly used to advance the diagnostic procedures to a level where a suspected lesion can be precisely localized and the disease process identified.

The present abstract highlights the components of the neurological examination concerned with the patient history, mental status and cranial nerve functions.

History

Always listen to the owner! Owners certainly know their animals’ normal behavior and reactions better than veterinarians, which are only observing the animal through a limited time-window. The benefit of taking up a detailed history can never be emphasized enough!

The history should include the animals breed, sex, age and medical history, including information of the events which have motivated the owner to seek veterinary advice.

Some clues to the disease process might already be indicated by the history, breed or age. Certain neurological diseases are for example more prevalent in certain breeds and at a certain age - e.g., disc disease in middle aged dachshunds or syringomyelia in Cavalier King Charles Spaniels. The debut of neurological signs at a very young age should alert the clinician to consider a congenital malformation. In the case of seizures, it is of importance to question the owner about any possible events which preceded seizures and to remember that seizures can be of intracranial origin as in epilepsy (idiopathic or symptomatic) or of extracranial origin (non­epileptic seizures), where the seizure activity is a reaction of the brain to external factors, such as e.g., intoxication or generalized metabolic disease.

It is equally important to retrieve information regarding the nature of the problems observed. Did they come on acutely or did they develop slowly? Are they of a stationary or progressive nature? Some diseases like, e.g., an ischaemic stroke will present with sudden and rather dramatic neurological signs which will not develop further after 48 hours. Other diseases, such as e.g., aseptic cerebral meningoencephalitis, might initially present with subtle and unspecific signs including moderately decreased appetite and retraction, which however, if not recognized, can progress to a stage causing fulminant neurological deficits with changes of mental status, seizures, blindness and paralyses. Other diseases, like e.g., degenerative myelopathy (a degenerative disease in middle-aged to older dogs with diffuse axonal necrosis, primarily affecting the thoracolumbar spinal cord lateral and ventral funiculi), will progress slowly over months or even years. A neuromuscular disease, such as myasthenia gravis, will be episodic in nature.

Mental Status

The normal animal is alert, responsive and attentive and reacts promptly to stimuli to vision, hearing and touch. In the normal brain, the ascending reticular activating system (ARAS), consisting of a complex of neuronal circuits situated in the brainstem and projecting to the brain, is a regulator of such responses. The main function of the ARAS is to regulate arousal and sleep­wake transitions by keeping the brain alerted. The ARAS responds to incoming input by sending stimulating impulses to nuclei in the thalamus, which then projects diffusely to activate higher cerebral cortical centers. Thus the ARAS acts as a “pacemaker” for the brain. Sleep is associated with decreased activity of the ARAS.

If the ARAS is com promised (as can be the case if, e.g., a tumor, ischaemic stroke or hemorrhage affects the brain stem) the animal will not be able to respond sufficiently to the environment. In that case, the owner might, if questioned thoroughly, report that the animal’s behavior is altered. Very commonly, the owner has observed that the animal is no longer coming to the door to greet the family members, sleeps more than before or do not respond to the mailman’s visit, events which would previously have alerted the animal or triggered a defensive reaction. Animals with lesions compromising the ARAS will show signs of affected consciousness. Such dysfunction is graded after severity into depressed (decreased responsiveness to the environment), stuporous (the animal is only responding if provoked by vigorous or unpleasant stimulation) and comatose (deep and prolonged state of unconsciousness where the patient is unable to respond to external stimuli).

Animals with lesions affecting the frontal cerebrum (e.g., space occupying lesions such as tumors or hemorrhage) or focal ischemia caused by embolic stroke will often also display and altered behavior which is dominated by signs such as difficulties to interpret the environment. Head pressing and circling in large circles toward the lesion are also common in such patients.

Table 1

Cranial Nerves

Twelve pairs of cranial nerves (CN) positioned symmetrically right and left emerge from various parts of the brain and brainstem. They are identified by numbers I–XII and by names which are inspired from Latin and Greek and give a hint to the function of the nerve. CN I is positioned most rostral and CN XII is positioned mos t caudal. CN I–XII are named as follows: CN I: N Olfactorius, CN II: N Opticus, CN Ill: N Oculomotorius, CN IV: N Trochlearis, CN V: N Trigeminus, C N VI: N Abducens, CN VII: N Facialis, CN VIII: N Vestibulocochlearis, CN IX: N Glossopharyngeus, CN X: N Vagus, CN XI: N Accessorius and CN XII: N Hypoglossus.

Each pair of CN is evaluated separately and by specific tests in order to determine if the right and the left CN is responding sufficiently and equally. A short review of the cranial nerves and the tests which can be used to evaluate CN structures and their function can be found in Table 2 below.

Table 2. Neurological examination function and tests of cranial nerves

References

1.  De Lahunta A, Glass EN, Kent M. Veterinary Neuroanatomy and Clinic IJI Neurology. 3rd ed. Saunders Elsevier; 2009:134–167,476–486,487–524.

2.  Garosi L, Lowrie M. The neurological examination. In: Platt SR, Olby NJ, eds. BSAVA Manual of Canine and Feline Neurology. 4th ed. BSAVA British Small Animal Veterinary Association. BSAVA; 2013:1–24.

3.  Garosi L. Lesion localization and differential diagnosis. In: Platt SR, Olby NJ, eds. BSAVA Manual of Canine and Feline Neurology. 4th ed. BSAVA British Small Animal Veterinary Association. BSAVA; 2013:25–35.

4.  The Free Dictionary/Medical Dictionary: www.dictionary.thefreedictionary.com.