Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology), DECVN
Small Animal Medicine & Surgery, College of Veterinary Medicine, University of Georgia, Athens, GA, USA
A neurological examination is easily integrated into a routine physical examination. The objectives of the neurological examination are to confirm if there is a neurological abnormality and to specifically localize the abnormality within the nervous system. In conjunction with the history, signalment, presenting complaint and the physical examination, the neurological lesion localization is a piece of a jigsaw essential to creating a list of differential diagnoses for the disease. However, caution must be used as some manipulations necessary for the neurological examination could exacerbate problems such as spinal cord disease.
Observation of the dog or cat is essential as it allows evaluation of the mentation, posture, attitude, and gait. Changes in mentation (level and content of consciousness) are revealed by a history of personality change, change in awareness of surroundings, and inappropriate behavioural responses. Consciousness is a function of the brainstem (responsible for arousal) and the cerebral cortex (responsible for content and regulation). The evaluation of the state of consciousness can classify the patient as depressed, demented or obtunded, delirious, stuporous and comatose.
Simplistically, cranial nerve dysfunction may indicate a central nervous system (CNS) lesion (brainstem disease) or a peripheral lesion (affecting the cranial nerves after they have exited the brainstem and course through the skull). Evaluation of the cranial nerves should follow observation and palpation, with particular attention paid to normal functions of eye movement, head movement, blinking, jaw and tongue movement, and general symmetry of the head. Initially, an ophthalmic exam should be performed, which will assist with the evaluation of the optic (CN II), oculomotor (CN Ill), trochlear (CN IV), and abducens (CN VI) nerves.
The Menace Response
1. How to perform - obscure the vision in one eye and make slow threatening hand gesture toward the other eye.
2. How to interpret - this is a learned response, not a reflex, to a perceived threat, which evaluates CNs II and VII (responsible for innervation of the orbicularis oculi muscle which closes the eyelids), as well as the central visual pathways and the cerebellum. Normal function is demonstrated by a blink or retraction of the globe in response to the threat. To localize the lesion, other cranial nerve tests would be required.
The Pupillary Light Reflex
1. How to perform - shine a bright light in each eye to evaluate the response of the pupil.
2. How to interpret - this is a reflex. Light is sensed by CN II; parasympathetic fibers of CN III cause contraction of the iris muscle with direct and indirect simulation. The pupil is also innervated by sympathetic fibres responsible for dilation, which have their origin in the thalamus and send fibres down the cervical spinal cord to the T1–T3 spinal nerve roots, before they ascend up the neck and through the middle ear. A resting inequality in pupil size is termed anisocoria; to determine which pupil is abnormal, the animal should be evaluated in the light and dark. In the dark, a sympathetic lesion will mean the affected pupil will not be able to fully dilate. In the light, a parasympathetic lesion will mean the affected pupil will not be able to fully constrict. Animals with sympathetic lesions will often demonstrate miosis in accompaniment to third eyelid protrusion and enophthalmus; a condition called Horner's syndrome.
The Palpebral Reflex
1. How to perform - touch the medial canthus of the normal eyelid and watch response.
2. How to interpret - the normal eyelid should close. Cranial nerve V (trigeminal nerve) is responsible for facial sensation, whereas the motor response to facial sensory stimulation is generally provided by the facial nerve (CN VII). Facial paresis presents as a drooping of the facial muscles, most notably the lips and the eyelids. It may also be detected as a reduction or absence in the blink response.
Evaluation of Jaw Tone
1. How to perform - observe patient for a dropped lower jaw and/or an inability to eat. Assess the strength of the jaw safely by manually opening the mouth and evaluating the resistance to opening.
2. How to interpret - the mandibular branch of CN V provides motor function to the jaw. A dropped lower jaw or the inability to chew can indicate damage to CN V.
1. How to perform - a leg is placed in an abnormal position and a correcting response by the animal is observed. Knuckling the toes over whilst supporting the body can be done to evaluate how long it takes for the animal to correct. Alternatively, a piece of paper may be placed under each foot and slowly moved sideways, to see if the animal returns its foot to the standing position. Other postural reactions include wheelbarrowing, hopping, hemistanding, and extensor postural thrust.
2. How to interpret - conscious proprioception is the patient's awareness of limb position and movement without visual information. When the knuckling test is performed, an abnormality is indicated by a delay or absence of the response. The sensory branch of proprioception is carried from the skin, muscle and joints of the leg through the spinal cord and brainstem to the sensory motor cortex, where the brain responds by sending messages back to the lower motor neuron for motor function, resulting in a rapid correcting foot placement. Ascending sensory pathways are located in the outermost regions of the spinal cord and are very sensitive to compression. With minor spinal cord injury, proprioceptive deficits may be present because of disrupted sensory pathways, while motor function persists because the deeper motor tracts are unaffected. Both visual and tactile placing reactions require an intact motor cortex and intact motor pathways to the involved limb. A cortical lesion may produce deficits in the contralateral limb, whereas lower lesion produces deficits in the ipsilateral limb.
It is rare to have any reflex abnormalities if the animal has no evidence of gait abnormality, muscle mass loss or conscious proprioceptive deficits. In these cases, a complete reflex examination is unlikely to be helpful. Completion of a reflex requires an intact sensory nerve that provides transmission to the spinal cord and an intact motor nerve that elicits function from the innervated muscle. The reflex arc itself does not involve the brain or the remainder of the spinal cord. Lesions in the motor arm of the reflex arc, termed lower motor neuron (LMN), may cause a decreased or absent reflex (hyporeflexia or areflexia). An exaggerated response (hyperreflexia) results from an interruption in proximal motor pathways that modulate the reflex, termed upper motor neuron (UMN); however, stress or anxiety may cause an apparent increased reflex response, so it should not be considered too important without other evidence of neurological disease. Lower motor neuron signs indicate damage to one or more components of the reflex arc. Upper motor neuron signs indicate damage anywhere between the reflex arc and the brain. The most reliable reflex is the flexor withdrawal in the thoracic and pelvic limbs. The other reflexes can appear to be present in small dogs just because the limbs will move when struck with a reflex hammer irrespective of reflex function.
The Anal Sphincter Reflex
1. How to perform - pinch the anal sphincter with haemostats and watch for a wink-like contraction of the external sphincter muscles and tail flexion.
2. How to interpret - this reflex reveals information regarding the pudendal nerve and caudal segments of the spinal cord. A flaccid unresponsive anus indicates LMN damage to the pudendal nerve or its spinal roots. A hypertonic, hyperresponsive anal sphincter indicates UMN damage at any point cranial to the pudendal nerve.
The Pedal Flexor Reflex
1. How to perform - apply a pinch stimulus to each foot and evaluate the response of the ipsilateral and contralateral limb.
2. How to interpret - this is a withdrawal reflex in which stimulation of sensory receptors in the toes elicits contraction of flexor muscle groups in the leg. Presence of a withdrawal reflex requires an intact sciatic nerve (sensory and motor) and an intact spinal segment at the lumbosacral plexus, but does not require transmission along the spinal cord to the brain. Absence of the withdrawal reflex in the pelvic limb denotes extensive lower motor neuron damage involving the lumbosacral spinal cord segments (L6-S2) as well as the nerve roots and the lumbosacral plexus; in the thoracic limb it denotes damage to the cervical spinal cord segments (C6-T2), the spinal nerve roots and the brachial plexus.
The Patella Reflex
1. How to perform - a tap stimulus should be applied to the straight patella tendon and the response of the limb should be evaluated. Reflex hammer size must be adapted to patient size for improved accuracy.
2. How to interpret - this is a myotactic (stretch) reflex that effectively stretches the quadriceps muscle. This stretch stimulates the femoral nerve (L4-L5), which generates muscular contraction to extend the stifle. Upper motor neuron lesions cause hyperreflexia and should be accompanied by weakness and poo r weight bearing. Disease in the L4-L5 spinal cord segments or nerves causes hyporeflexia.