The neurological examination consists of five parts:
- gait and posture
- postural reactions
- muscle tone, size and spinal reflexes
- cranial nerves.
How does the patient respond to you? A normal dog is alert and responsive but the degree of this varies between individual patients. The progressive loss of sensorium is described as depression, lethargy, obtundation, semicoma (stupor) and coma. The owner is the best judge of subtle changes in the behavior of their pet. Other descriptive terms for abnormal behavior include disoriented, hyperactive, aggressive and propulsive.
Gait and Posture
Evaluate the gait and posture in a quiet enclosed area with a carpet or some form of non-skid surface. If the patient is able to walk it is critical to evaluate the quality of the gait and the patient's posture. Do not miss a subtle head tilt, a lowered head and neck or overflexed tarsus or a mild tremor. Observe the patient walking from multiple directions. Look for short stiff strides suggesting a neuromuscular disorder. Look for a delay in the onset of protraction (the swing phase), an increased stride length with stiffness and lack of direction and scuffing of the digits or resting the paw on its dorsal surface with disorders of the upper motor neuron (UMN) and general proprioceptive (GP) systems.
If a patient exhibits a short stride in one or more limbs, ask yourself if this is because the patient is unwilling or unable to support weight normally. The former suggests a musculoskeletal disorder. The latter suggests a neuromuscular or LMN disorder. Loss of support due to a radial or femoral nerve dysfunction will cause a lame gait that mimics an orthopedic disorder.
Paresis is defined as weakness but in neurology it means a deficiency in the generation of the gait or the ability to support weight. There are two qualities of this paresis: LMN and UMN.
- LMN paresis is represented by varying degrees of loss of the ability to support weight. A patient with partial LMN paresis will have a short stride and appear to be “lame” but without any discomfort. A patient with UMN paresis will exhibit a delay in the onset of protraction which is the swing phase of the gait. The stride will usually be longer than normal. This overextension of the thoracic limbs will appear like a floating motion of the limbs. Stiffness in the stride represents spasticity. At the same time, the stride will be misdirected causing the limbs to swing wide due to excessive abduction or swing under the trunk due to excessive adduction and a paw will occasionally be placed on its dorsal surface. All of these latter clinical signs are those of ataxia due to interference with the general proprioceptive (GP) system.
- Clinical signs of UMN and GP dysfunction occur together in the gait and postural reactions because the pathways of these two systems are adjacent to each other in the spinal cord and brainstem. A lesion in one pathway usually also affects the other pathway. It is not important to differentiate between the UMN and GP clinical signs. It is sufficient to just recognize their collective presence to make the appropriate anatomic diagnosis.
Ataxia is incoordination and has three qualities: general proprioceptive (GP), vestibular and cerebellar.
- GP ataxia reflects the lack of information reaching the CNS that informs it of where the neck, trunk and limbs are located in space and the state of muscle contraction at any time. When this system is interfered with, the onset of protraction may be delayed and the stride lengthened. During protraction the limb may swing wide to the side from excessive abduction or under the body from excessive adduction. The limb may overflex on protraction. The dorsal surface of the paws may scuff along the ground surface or the paw may be placed on its dorsal surface. Remember that these clinical signs overlap with the signs of UMN paresis due to the adjacent location of their pathways.
- Vestibular ataxia results from loss of orientation of the head with the eyes, neck, trunk and limbs causing a loss of balance. Unilateral lesions in this system cause a patient to lean, drift or fall to one side, exhibit a head tilt and show an abnormal nystagmus.
- Cerebellar ataxia usually causes a hypermetric gait with sudden bursts of limb and trunk activity with marked overflexion of the limbs and often misdirected protraction. Clinical signs of vestibular ataxia often accompany these signs of a cerebellar disorder because the vestibular system has anatomic components in the cerebellum.
Normal postural reactions require normal function of the UMN, GP and LMN systems. There is no one postural reaction that will test just one of these systems. They are most valuable in detecting prosencephalic lesions where the patient’s gait is normal but the postural reactions are abnormal. There is no need to perform the postural reactions in a tetraplegic patient. However in a paraplegic patient they are valuable to evaluate in the thoracic limbs when an abnormality may indicate a mulifocal disorder or a focal cranial thoracic spinal cord lesion. Of the various postural reactions the hopping responses are the most reliable.
Before testing the postural reactions, it is convenient to evaluate the standing patient’s muscle size and tone. Stand over the standing patient facing in the same direction and simultaneously palpate the muscles in both thoracic limbs to assess their size. Flex and extend the thoracic limbs for range of motion and muscle tone. After flexing the limb, when you place the limb on the ground surface, place it on the dorsal surface of the paw and observe how rapidly it is replaced on its palmar surface. A significant and repeatable delay is abnormal. This is NOT a test limited to GP function. The normal response requires normal activity of the UMN, GP and LMN systems. This is the paw replacement postural reaction test. It is not a test limited to conscious proprioception referred to as the CP test. This is a misnomer. Repeat these assessments of muscle size, tone and range of limb motion in the pelvic limbs along with pelvic limb paw replacement. Assess the tone in the tail and anus.
Return to the thoracic limbs to test the hopping responses. With one hand elevate the abdomen to lift the pelvic limbs off the ground surface. With the other hand hold one thoracic limb off the ground surface and push the patient laterally towards the supporting limb forcing it to hop. This should occur as soon as the shoulder passes over the position of the paw. It should be a rapid and smooth response. Elicit three or four hops then switch hands and hop the patient back on the other thoracic limb. Keep repeating this until you are comfortable that these responses are normal or abnormal. Any delay, stiffness or exaggerated response is abnormal. Occasionally a dog will refuse to hop on a thoracic limb and just roll over on its side. In this case, lift the dog up to the level of your waist. Hold one thoracic limb against the dog’s trunk so only the thoracic limb to be tested is free. Then, quickly bring the dog with its free thoracic limb to the ground surface and push it laterally as it strikes the surface. This will usually elicit three or four hops before the dog rolls over again. Repeat these lateral hopping movements in each pelvic limb with one hand under the thorax elevating the thoracic limbs off the ground surface. Only evaluate the hopping response in the lateral direction. Pick the dog up by its thoracic limbs and quickly bring the pelvic limbs back to the ground surface and as they meet this surface back the dog up. This should be a smooth rapid response. Any delay is abnormal and usually correlates with abnormal hopping responses in that limb. It is helpful to compare these hopping responses in one limb with the opposite limb. In prosencephalic lesions the postural reaction deficit will be present in the contralateral limbs.
If you are not sure of an abnormality in the postural reactions that you have tested, you can do the placing postural reaction. Hold the dog with one hand under the abdomen and the other hand holding the head and neck in extension. Bring the dog to the edge of a table or chair until the dorsal surface of the forepaws touches the edge of this supporting surface. As soon as this contact is made the normal car will briskly place the paws on to the supporting surface. Repeat this test while holding the dog from each side. Similar to the hopping responses this placing response requires all three systems – UMN, GP LMN- to be intact. With LMN disorders, the postural reactions will be performed rapidly and smoothly but with the more severe lesions support will be decreased. Repeat the same placing responses with the pelvic limbs.
These postural reactions are most useful in diagnosing prosencephalic lesions where the gait is normal or as an indication of a more subtle caudal brainstem or spinal cord lesion or in determining a multifocal disorder. In addition, abnormal postural reactions may be the first indication of a developing progressive disorder in any part of th CNS or PNS involved with limb movements.
Muscle Size, Tone and Spinal Reflexes
To assess spinal reflexes, some restraint of the patient will be necessary. I have found it very useful, especially if working without assistance, to sit on the floor with my back against a wall and my knees flexed. I lay the dog between my thighs with its back resting on my thighs. Most dogs adapt to this very well. In this position I reassess muscle size and tone and perform the spinal reflexes. Tap the patellar ligament with a pleximeter or any blunt object and observe the reflex stifle extension. This patellar reflex requires normal function of the femoral nerve and spinal cord segments L4-L6. This is the only reliable tendon reflex. Others that are described may not be present in many normal animals.
Gently compress the digits at the base of the claw using your fingers or a pair of forceps to elicit the withdrawal-flexor reflex, The sensory component tested depends on the digit that is compressed. Using the fifth digit this tests both the sensory and motor components of the sciatic nerve (spinal cord segments L6,7 and S1). The hip flexion that is elicited is a function of the iliopsoas muscle and its innervation by most of the lumbar spinal cord segments and lumbar nerve ventral branches as well as the femoral nerve. Be aware that a patient with a complete sciatic nerve dysfunction will flex its hip when its second digit is compressed as the sensory nerve to the medial side of the second digit is the saphenous nerve, a branch of the femoral nerve. Hip flexion is a function of the iliopsoas muscle ad the lumbar nerves and the femoral nerve that innervate it.Do not mistake this hip flexion for a normal pelvic limb withdrawal reflex and therefore overlook a sciatic nerve lesion
The thoracic limb withdrawal reflex is a test of the brachial plexus and cervical intumescence (C5-T2) as many nerves are involved in the motor response. The nerve(s) involved with the sensory component of the reflex depends on the digit or cutaneous portion of the limb stimulated. There is no reliable tendon reflex in the thoracic limb.
Two assessments are made with the withdrawal reflex. One assessment is the reflex itself which only depends on the nerves tested in that limb and their spinal cord segment components. The other assessment is nociception which requires the sensory component of the reflex arc and a cranial projecting pathway from the involved spinal cord segments to the thalamus with projection to the frontoparietal cerebral cortex. Pain is not a sensory modality. Pain is the subjective response of the patient to a noxious stimulus. This response is nociception. Compression of the digit at the base of the claw is the noxious stimulus. The patient’s response that indicates awareness of this stimulus is nociception or an indication of pain.
At some point with the patient restrained between your thighs, evaluate the anus for its tone and reflex closure to a mild stimulus of the perineum (perineal reflex-sacral nerves and spinal cord segments).
In patients with a suspected thoracolumbar spinal cord lesion or disorder of the brachial plexus it is useful to perform the cutaneous trunci reflex. This is a long reflex arc. In the standing patient, compress the skin over the vertebral column with forceps and observe for movement of the skin caused by contraction of the cutaneous trunci muscle. Start this over the sacral vertebrae and repeat the stimulus in a cranial direction over the vertebral column. The normal reflex usually starts over the caudal lumbar vertebrae. This stimulus activates sensory neurons in the dorsal branches of the spinal nerves that innervate the portion of skin that is compressed. This is projected to their spinal cord segment of origin where synapse occurs in the dorsal grey column. The axon of this second neuron usually crosses to the fasciculus proprius of the opposite lateral funiculus where it projects cranially to the C8 and T1 spinal cord segments contralateral to the site of cutaneous stimulation. Here the axons of this projection pathway synapse on the LMN cell bodies of axons that leave the spinal cord, pass through the brachial plexus and enter the lateral thoracic nerve to innervate the cutaneous trunci muscle. This reflex is useful in paraplegic patients to estimate the level of the spinal cord lesion. With transverse spinal cord lesions this reflex and nociception will be absent caudal to the cranial margin of the lesion.
Cranial Nerves I - VIII
The cranial nerve exam requires a cooperative patient or one that is restrained so that you can relax and have time for a careful evaluation. The thigh restraint position described for testing spinal reflexes is very useful for this. If your patient is getting tired of this restraint or is down right uncooperative, you can gain considerable advantage by wrapping the patient in a towel so that the limbs are bound against the body and only the head is exposed. Place the bound patient between your thighs. With one hand you can control the head and the other hand is free to perform the tests.
Cranial nerves can be examined in their order from I to XII or by regions of the head. I much prefer the latter. Testing olfaction is difficult, rarely reliable or necessary. I do not do it. I start with the evaluation of the eyes and orbital structures.
Test vision with the menace response. Using your hand that is supporting the head, cover one eye. Tap the eyelids of the exposed eye to be sure the facial nerve is functional for eyelid closure and to alert the dog that it is about to be threatened. Menace the exposed eye with your free hand and observe eyelid closure in the normal patient. Cover the opposite eye and repeat the menace response in the eye now exposed. Be sure you do not touch the eyelids with the menacing hand or get close enough so that a breeze is felt. When the menace response is absent be sure that the dog is able to close its eyelids (normal facial nerve function). An absent menace response indicates an abnormality in the visual pathway from the eyeball to the occipital cerebral cortex.,
Uncover the eyes and continue to hold the head so that both eyes can be observed. Assess the size of the pupils in room light. They should be moderately constricted and of equal or nearly equal size. If the pupils are difficult to see, hold a pen light or other bright light source a few inches from the dog’s nose. Then, rapidly bring the light source as close to the eye as you can get without touching the dog and so you can still see the pupil. The normal pupil will rapidly constrict. Quickly move the light source to the other eye. Its pupil should still be constricted from the light placed in the first eye and should stay constricted. As you swing the light from one eye to the other, the normal pupils will stay constricted. The normal pupillary light reflex pathway requires an uninterrupted pathway from the eyes, through the optic nerves, optic chiasm, optic tracts, over the lateral geniculate nuclei to the pretectal nuclei and both oculomotor nuclei. The oculomotor neurons of the rostral mesencephalon that are stimulated in this light reflex pathway are preganglionic parasympathetic neurons. Their axons project in the oculomotor nerve through the orbital fissure to the ciliary ganglion located within the periorbita adjacent to the optic nerve. The postganglionic axons of these second neurons innervate the pupillary constrictor muscle of the iris. A majority of the axons involved in the pupillary light reflex cross at the optic chiasm and cross back at the pretectal nuclei so that more response may occur in the eye that is stimulated but enough uncrossed axons allow enough activation of both oculomotor nuclei so that both pupils respond the same degree with light directed into either eye.
To avoid confusion always record the response of both eyes from the light directed into each eye separately. Avoid the use of direct, indirect and consensual responses.
Although absent vision (no menace response) with intact pupillary light reflexes supports a prosencephalic lesion and absent pupillary light reflexes supports an ocular or brainstem lesion, it is rarely that simple. Progressive retinal and optic nerve lesions often clinically cause visual loss (no menace response) with normal pupillary light reflexes as the latter pathway appears to be more resistant and the last to be clinically affected. As a rule the resting pupillary size in these patients is larger than normal in room light.
Lesions of the somatic components of the oculomotor nerve, the trochlear nerve and the abducent nerve will cause a strabismus of the eye with the denervated extraocular muscles. This should be apparent as you evaluate the position of the eyes. A cranial nerve III (oculomotor) lesion causes a ventrolateral strabismus. A cranial nerve VI (abducent) lesion causes a medial strabismus. A cranial nerve IV (trochlear) lesion causes extorsion of the eye seen as a lateral deviation of the superior end of the vertical pupil. The function of the third and sixth cranial nerves can be evaluated by moving the dog’s head from one side to the other and observing the normal physiologic nystagmus that occurs. When the head is moved to the right, the right eye will jerk laterally (lateral rectus-abducent nerve) and the left eye will jerk medially (medial rectus-oculomotor nerve). The reverse occurs when the head is moved back to the left side. The vestibular system is involved in normal eye posture and occasionally with vestibular system dysfunction a strabismus will be seen in some head positions but normal physiologic nystagmus as just described will still be normal.
Nystagmus is an involuntary oscillation of the eyeballs. It is a normal feature when the head is moved from one side to the other or in an up and down direction. Lesions of the vestibular portion of the vestibulocochlear nerve or its central connections in the brainstem will cause an abnormal nystagmus. In acute disorders this will be present at all times and in all head positions and is referred to as a resting nystagmus. In many vestibular system disorders it is only seen when the head is held in an extended or laterally flexed position or with the patient placed on its back with the head and neck extended. This is a positional nystagmus and is abnormal. The nystagmus associated with disorders of the vestibular system is a jerk nystagmus with a fast phase and a slow phase. A pendular nystagmus consists of movements of equal speed in each direction and may be associated with congenital ocular disorders or as a genetic disorder with no interference with vision.
I do not routinely test for the cochlear division of the vestibulocochlear nerve (cranial nerve VIII) unless hearing loss is part of the owner’s complaint or it is apparent that the patient is not responding to my voice. Hand clapping that can not be seen by the patient during the neurologic examination or banging metal feed dishes together when the patient is sleeping in its cage may indicate a hearing deficit. The use of brainstem auditory response testing is the most reliable way to assess hearing in animals. Most all recognizable hearing loss occurs with lesions of the spiral organ in the inner ear.
Palpebral fissure - third eyelid
Observe the palpebral fissures and their symmetry. Evaluate closure of the fissure by touching the eyelids. This palpebral reflex is a function of the sensory branches of the trigeminal nerve and the somatic motor branches of the facial nerve to the orbicularis oculi muscle.
A ptosis is failure of elevation of the superior eyelid, a 'dropped eyelid', and is due to an oculomotor nerve lesion that denervates the levator palpebrae superioris muscle. A narrow palpebral fissure which has a similar appearance occurs with loss of sympathetic innervation of the orbitalis muscle. This is the smooth muscle that extends into the eyelids to keep them retracted. Loss of the sympathetic innervation of the components of this muscle in the periorbita results in enophthalmos. Be aware that atrophy of the muscles of mastication will cause the eye to sink into the orbit (enophthalmos) and result in a smaller palpebral fissure.
A persistent elevation of the third eyelid also occurs with sympathetic neuronal denervation of this orbitalis muscle which normally keeps the third eyelid retracted. This will also occur secondary to atrophy of the masticatory muscles. In a dog with normal vision but facial paralysis you will often see the third eyelid elevate when you menace the patient as the eyelids will not close and the eyeball will retract causing physical elevation of the third eyelid.
Facial and trigeminal neurons
Up to this point, all of your evaluations have been involved with the eye and adjacent orbital structures. Some of these assessments have involved components of the facial and trigeminal nerves. Now evaluate all of the functions of the facial (cranial nerve VII) and trigeminal (cranial nerve V) nerves. Repeat the palpebral reflex (sensory V and motor VII) by touching both the medial and lateral eyelid commissures and observe for reflex eyelid closure of the palpebral fissure. Blowing in the ear or palpation of the external acoustic meatus with a blunt instrument will stimulate the sensory receptors of a plethora of nerves but the only nerve that is motor to the ear muscles is the facial nerve. In facial paralysis there will be no response to this stimulation other than the dog may move its head away from the stimulus. Observe the corner of the lips for laxity and possible drooling caused by loss of facial nerve innervation of the lip muscles. The philtrum usually does not deviate in dogs with facial paralysis. Stimulating the skin of the muzzle or oral mucosa will not elicit any lip or nose movements on the side of the facial paralysis. The sensory component of these responses is all dependent on normal trigeminal nerve function.
Open the mouth and assess the degree of tone in the muscles of mastication. Loss of tone or inability to close the mouth requires a bilateral deficit of the neurons in the mandibular nerve portion of the trigeminal nerve. Unilateral loss of these neurons can only be recognized by palpating atrophy of the muscles of mastication on the affected side.
The sensory component of the trigeminal nerve was evaluated with the palpebral reflex and when assessing the movements of the lips and nose. Trigeminal nerve nociception is best evaluated by placing a blunt instrument such as the end of closed forceps on the mucosa of the nasal septum. This is a very sensitive area and normal animals will immediately pull their head away from the stimulus. Patients with prosencephalic lesions involving the nociceptive pathway of the trigeminal nerve somatic afferent neurons will show a reduced response (hypalgesia) when the nasal septum is stimulated. The same hypalgesia in the limbs is more difficult to appreciate. This is a very sensitive test for unilateral prosencephalic lesions where the nasal hypalgesia is contralateral to the prosencephalic lesion. Remember that a reduced nasal septum response may be explained by an ipsilateral lesion of the ethmoidal branch of the ophthalmic nerve (V) or a contralateral lesion in the nociceptive pathway in the brainstem to the frontoparietal cerebral cortex.
Cranial nerves IX, X and XII
Although these neurons have a widespread distribution, that which can be evaluated in the physical clinical exam involves the tongue and pharynx. Often there will be some complaint of dysphagia when these cranial nerves are affected. To test the innervation of these cranial nerves, perform the gag reflex. This is a very brief exam with multiple observations necessary. Open the mouth which assesses the tone in the muscles of mastication (cranial nerve V). Observe the size and movement of the tongue. Touch the surface of the tongue to stimulate movement. These are functions of cranial nerve XII (hypoglossal nerve). Quickly pass your index finger deep into the oropharynx and feel for pharyngeal muscle tone and observe for a gagging response as you remove your finger. These are functions of cranial nerves IX and X (glossopharyngeal and vagus nerves). This gag reflex is often difficult to evaluate and you may need to observe the patient as it is prehending and swallowing food.
There is no examination of cranial nerve XI (accessory nerve) as there are no obvious clinical signs of its dysfunction.
Summary of cranial nerve function
In order to test individual nerves, the following chart is usually followed to help isolate and test individual cranial nerve function.
Table 1. Cranial nerves and their function
|Cranial nerve||Function||Dysfunction / test|
|I||Olfactory||Smell||Hard to assess in dogs|
|II||Optic||Sight||Navigation around the room, cotton wool balls, menace response|
|III||Oculomotor||Innervates medial, ventral and lateral rectus muscles (extra-orbital muscles)||Ventrolateral strabismus, persistent pupillary dilation with absent constriction to light directed into either eye|
|IV||Trochlear||Innervates dorsal oblique extra-orbital muscle||extorsion- lateral deviation of the superior end of the pupil|
|V||Trigeminal||Ophthalmic branch||Sensory - mostly medial eyelids, cornea and nasal septum|
|Maxillary branch||Sensory - mostly lateral eyelids, superior lip and external muzzle|
|Mandibular branch||Tone in muscles of mastication on opening the mouth. Sensory- inferior lip and tongue|
|VI||Abducent||Lateral rectus and retractor bulbi extra-orbital muscles||Medial strabismus.|
|VII||Facial||Facial expression||Absent ear and eyelid movement, xerophthalmia, drooling,|
|Test - plapebral reflex, stimulation of ear canal for ear movement, lip movement|
|VIII||Vestibulocochlear||Hearing and balance, physiological nystagmus||Unilateral deficits cause head tilt, spontaneous resting or positional|
|nystagmus (fast phase away from the site of a peripheral lesion), falling, rolling if acute, circling (to the side of the lesion).|
|Bilateral deficits cause wide excursions of the head, low posture, panic when picked up.|
|IX||Glossopharyngeal||Pharyngeal and soft palate musculature||Deficits cause dysphagia|
|Test - gag reflex|
|X||Vagus||Pharyngeal and soft palate musculature, larynx (via recurrent laryngeal nerve)||Dysphagia, laryngeal dysfunction|
|Test - gag reflex|
|XI||Accessory||Innervates trapezius, parts of sternocephalic and cleidocephalic muscles||Deficits can not be clinically appreciated|
|XII||Hypoglossal||Muscles of tongue||Dysphagia / prehension difficulties and unilateral tongue atrophy|
|Test - tongue pull|
Table 2. Clinical signs related to anatomical location
|Anatomical site||Concomitant signs|
|C1-C5||Not common site for lesions in the dog: neck pain, ataxia and spastic paresis in both pelvic and thoracic limbs but often worse in the pelvic limbs to tetraplegia with increased/normal spinal reflexes and muscle tone all limbs (UMN)|
|C6-T2||Thoracic limb lameness (LMN paresis), ataxia and spastic paresis in pelvic limbs to tetraplegia with decreased spinal reflexes and muscle tone in thoracic limbs (LMN), increased/normal spinal reflexes and muscle tone in pelvic limbs (UMN). Wiith unilateral lesion-ipsilateral signs.|
|T3-L3||Thoracolumbar pain, ataxia and spastic paresis (UMN) in pelvic limbs with normal to increased spinal reflexes and muscle tone in pelvic limbs|
|L4-S3||Lumbar/sacral pain, ataxia and LMN paresis to paraplegia in pelvic limbs with decreased spinal reflexes and muscle tone in pelvic limbs (LMN), normal thoracic limbs.|
Table 3. Clinical signs and prognostic indicators in sacrocaudal injuries
|Caudal segments/nerve roots||Flaccid analgesic tail, normal urination and defecation||75% regain tail function|
|Caudal segments/nerve roots and pelvic nerves||Flaccid, analgesic tail, postures to urinate, inability to void urine, normal defecation||75% regain tail function and most regain urinary function in 2-4 weeks|
|Caudal and partial sacral segments/nerve roots||Flaccid, analgesic tail, decreased anal tone and reflexes, absence of posturing to urinate, difficult to express bladder||Some regain urinary function over the next 1-2 months|
|Caudal and sacral segments/nerve roots||Flaccid, analgesic tail, absent anal tone and reflexes, absent of posturing to urinate, faecal incontinence, easy to express bladder||25% regain urinary function within 2-3 months|
Bladder function can be divided into 2 categories (see bladder physiology for further details):
- If the bladder is easy to express and overflows when full, the lesion is likely to be located at spinal cord segments S1-S3 as the pelvic and pudendal nerves originate from these segments and innervate the detrusor muscle and the skeletal muscle of the urethra respectively. Thus, damage here results in flaccid paralysis of these muscles. This is the so-called lower motor neurone bladder. This derives from the hypogastric nerve which originates from L2-L5 in dogs.
- If the bladder is difficult to express and does not overflow (or overflows only if the bladder is really distended) the lesion is likely to be located between T3-L3 (assuming the forelimbs are normal). A lesion here results in spastic paralysis of the bladder, the classic upper motor neuron bladder, because of the same loss of upper motor neuron pathways that affect the limbs. If an UMN bladder overfills, the tight junctions between the detrusor muscle can be irreparably damaged so that the bladder function will never be regained and bladder tone will decrease. In general, the UMN bladder will regain function at the same time and at the same rate as the limbs. However, the behavioral attributes of dogs may influence whether this truly happens in practice.
- Infectious disease - Infectious agents include bacteria, virus (Distemper), fungi (Cryptococcosis and other fungi), protozoa (Toxoplasma). Cryptococcus is the most commmn fungal cause of meningitis.
- de Lahunta, A. & Glass, E. (2008) Veterinary Neuroanatomy and Clinical Neurology, Elsevier, USA
- Nghiem, PP & Schatzberg, H (2009) The weak cat. Practical approach and common neurological differentials JFMS 11(5):373-383