Neurolocalization Notes PDF
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Virginia–Maryland College of Veterinary Medicine
Richard Shinn
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These notes cover neurolocalization, focusing on neurological examination techniques, lesion localization (central vs. peripheral nervous system), and various neurological conditions. The document also includes information on different types of lesions and their associated symptoms, like circling or altered mentation.
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Neurolocalization Part 1 Richard Shinn, DVM, MS, DACVIM (Neurology) What you need to know for practicing veterinary medicine How to perform a neurological examination How to interpret the neurological examiation How to localize the lesion(s) Neurological Examiation Consist of two majory aspects Obse...
Neurolocalization Part 1 Richard Shinn, DVM, MS, DACVIM (Neurology) What you need to know for practicing veterinary medicine How to perform a neurological examination How to interpret the neurological examiation How to localize the lesion(s) Neurological Examiation Consist of two majory aspects Observation – what you see and hear Behavior Mentation Gait Posture Loading… Hands On Cranial nerves Proprioception Segmental spinal cord reflexes Hyperpathia Nociception Neurological Examiation Form Observation Loading… Hands-On Localization - Terminology In terms of localization, an initial way to try and localize is to differentiate if the lesion is: Central Nervous System Brain Spinal Cord Peripheral Nervous System Nerves Muscles Localization - Terminology In terms of localization, an initial way to try and localize is to differentiate if the lesion is: Central Nervous System Brain Spinal Cord Peripheral Nervous System Nerves Muscles Analology – Efferent System Think of the nervous system as an electrical system The Brain is the lightswitch The Nerves are the wires The Effector Organ (gland, muscle) is the lightbulb The signal has to travel from the lightswitch to the lightbulb through the wires, there is no secondary pathway for the signal to take If there is a break in the wire, the signal will no longer cause the lightbulb to turn on Analogy – Afferent System The same analology works for the afferent where sensation has to travel from the point of origin to the brain, there is no alternative route for it to take Loading… Localization When an intracranial lesion is suspected, you can localize to four different areas Forebrain Cerebellum Brainstem Vestibular Localization When a spinal cord lesion is suspected, you can localize to four different areas C1-C5 S3 C6-T2 T3-L3 L4- This localization does not equal the vertebrae, but rather spinal cord segments Neurolocalization Review 4 areas of the brain to localize Forebrain – Prosencephalon 4 areas to localize the spinal cord Cerebrum - Telencephalon (Blue) Thalamus – Diencephalon (Red) Brainstem Midbrain – Mesencephalon (Green) Pons – Ventral Metencephalon (Orange) Medulla – Myelencephalon (Purple) Cerebellum Dorsal Metencephalon (Pink) Vestibular Central – Cerebellum, Myelencephalon Peripheral – Vestibular apparatus and CNVIII C1-C5 – Cranial Cervical Spinal Cord C6-T2 – Cervicothoracic Intumescense T3-L3 – Thoracolumbar L4-S3 – Lumbosacral Intumescense Decusation As a general rule, everything in the forebrain crosses over, or decusates, before making its way to the rest of the body. The right side of the brain controls the contralateral side of the body (the left side) and vice versa. The brainstem and spinal cord is ipsilateral. A lesion on the left side will cause neurological signs on the left side of the body. The same is true for sensory information. Central versus Peripheral Nervous System Lesions within the central nervous system often have mixed motor and sensory (meaning proprioception and/or nociception) deficits Lesions to the peripheral nervous system are often sensor or, more commonly, motor This is a general rule to help with understanding the concept of how to localize central versus peripheral as peripheral lesions can also be mixed Example – A cat with diffuse weakness in all legs but no propriocepive deficits most likely has a lesion to the PNS Example – A cat with diffuse weakness in all legs with severe proprioceptive deficits most likely has a lesion to the CNS Summary Central Nervous System – Motor and Sensory Systems Affected Brain – Forebrain, Brainstem, Cerebellum, Vestibular Spinal Cord – C1-C5, C6-T2, T3-L3, L4-S3 Peripheral Nervous System – Can Be Sensory and/or Motor System Motor Unit Disease Sensory Neuropathy Mixed Neuropathy Lesions of the brain are called encephalopathy Lesions of the spinal cord are called myelopathies Lesions localized to the PNS can be classed as a radiculopathy, neuropathy, myelinopathy, juctionopathy, or myopathy (this is not Autonomic Nervous System The ANS originates in the hypothalamus (red), a ventral portion of the diencephalon (blue). Autonomic Nervous System There are two main division of the ANS The sympathetic nervous system Norepinephrine is the main neurotransmitter Affector organ receptors are either α or β The parasympathetic nervous system Acetylcholine is the main neurotransmitter Affector organ receptors are either muscarinic (PNS) or nicotinic (CNS) The confusion with the ANS is that the nerves only come out at certain locations For sympathetic, the nerves arise from C8-L4 For parasympathetic, the nerves arise from cranial nerves III, VII, IX & X, along with the sacral spinal cord segments (S1-S3 in the dog and cat) Autonomic Nervous System Sympathetic innervation to the head comes from the C8-T2 spinal cord segments. Sympathetic innervation to the caudal abdomen and sacrum come from the L1-L4 spinal cord segments (in the dog). Parasympathetic innervation to the thoracic and most of the abdominal cavity comes from the Vagus nerve (Cranial Nerve X). Autonomic Nervous System Sympathetic – Thoracolumbar (C7-L4) Parasympathetic – Cranial Nerves III, VII, IX, X & Sacral Plexus (S1S3) Vagosympathetic Trunk Vagus Nerve Autonomic Nervous System Horner Syndrome Lack of sympathetic innervation to the head and neck Lesion Location Hypothalamus Cervical Myelopathy Cranial Thoracic Cavity Lesion Trauma to the neck Middle Ear or Guttural Pouch Localization - Terminology Intracranial Localization Forebrain, brainstem, cerebellum, vestibular Spinal Cord Localization C1-C5, C6-T2, T3-L3, L4-S3 Peripheral Nervous System Motor Unit Disease – Nerve, myelin, neuromuscular junction, muscle Sensory Neurolopathy Mixed Neuropathy Autonomic nervous system Localization Terminology The next terms to become familiar with are: Upper Motor Neuron Cells that arise from the forebrain, brainstem, or cerebellum Lower Motor Neuron Cells that arise from the spinal cord segment Ventral nerve roots are formed by the axons of the LMN Nerve roots combine with other nerve roots to form the named nerves (such as the radial nerve) To differentiate an UMN lesion from a LMN, we have to assess reflexes and tone of the limbs Reflexes Reflexes do not involve concious perception meaning the brain is not involved. In other words, if you cut the cranial cervical spinal cord in two, reflexes would still work. It is also important to understand that neurons are excitable tissue, and lower motor neurons are spastic, or hyperexcitable, in the abscense of upper motor neuron influence. One purpose of the upper motor neuron is to decrease this spasticity of the lower motor neurons. Without this influence, lower motor neurons become spastic. Reflexes If reflexes are intact, then the lower motor neuron (area in red) is not affected. If the reflexes are decreased or absent, then the lower motor neuron is affected. Upper versus Lower Motor Neuron If a spinal cord lesions is suspected, the next step is to decide which limbs are affected, and if there are upper or lower motor neuron signs to thoses limbs. Upper motor neuron lesion Normal to increased reflexes in the affected limbs Normal to increased tone in the affected limbs Lower motor neuron lesion Decreased to absent reflexes in the affected limbs Decreased to absent tone in the affected limbs C1-C5 Myelopathy C6-T2 Myelopathy T3-L3 Myelopathy L4-S3 Myelopathy Thoracic Limb Reflexes Normal to increased Decreased to absent Normal Normal Thoracic Limb Tone Normal to increased Decreased to absent Normal to increased Normal Pelvic Limb Reflexes Normal to increased Normal to increased Normal to increased Decreased to absent Pelvic Limb Tone Normal to increased Normal to increased Normal to increased Decreased to absent C1-C5 – Upper motor neuron x 4 C6-T2 – Lower motor neuron thoracic, upper motor neuron pelvic limbs T3-L3 – Normal to increased pelvic, thoracic limbs are normal with the exception of Schiff Sherrington L4-S3 – Decreased to absent pelvic, thoracic limbs are normal Localization - Terminology Intracranial Localization Forebrain, brainstem, cerebellum, vestibular Spinal Cord Localization Loading… C1-C5, C6-T2, T3-L3, L4-S3 Peripheral Nervous System Motor Unit Disease – Nerve root, nerve, axon, myelin, neuromuscular junction, muscle Sensory Neurolopathy Mixed Neuropathy Has nothing to do with Autonomic nervous system Upper & Lower Motor Neuron sensory (meaning proprioception and nociception) Spinal Cord Segments versus Vertebra There are 8 cervical spinal cord segments and only 7 cervical vertebrea therefore when we localized C6-T2 this does not corelate to the C6-T2 vertebrea, but the spinal cord segments. Where ever there is a nerve root, there is a spinal cord segment. In the cervical region, the nerve roots exit cranial to the respective vertebrea. In the thoracic and lumbar region, it is caudal. Within the thoracic and cranial lumber region, the spinal cord segment lines up with the vertebrea. Within the caudal lumbar and sacral region, the spinal cord segments are generally cranial to the vertebrea, but the nerve roots still exit caudal to the numbered vertebra. Neurological Examination Observation Behavior Mentation Gait Posture Tools Needed Surface with traction Plexor (reflex hammer) Hemostats Transilluminator (adjustable light source) Fundic exam lens Cotton Ball Behavior Changes Pacing Head Pressing Circling Aggressive Blind Obsessive Incontinence Distant Seizures Head pressing The red nucleus within the midbrain is the main gait generator in four legged animals. With a forebrain lesion, the inhibitory effects of the forebrain are no longer present on the red nucleus (termed disinhibition). Therefore the red nulceus takes over and since its main goal is to walk, that is what the animal will do. Because there is lack of higher cognition from the forebrain, when an animal gets to a wall it does not know what to do and will therefore press its head into the wall trying to continue to go because of the input from the red nucleus. Circling An animal with a forebrain lesion will circle towards the side of the lesion due to a phenomenon known as hemineglect. Hemineglect means an animal will “ignore” one side of their world because it no longer exists. The patient circles towards the lesion because of decussation from the forebrain. Think of vision. If an animal has a right forebrain lesion, then they may be blind on the left eye. Therefore the left side of their world no longer exists. Since there is no longer input from the left side of the body, the animal will circle right because that side of their world still exists, thus circling towards the side of the lesion. Mentation Change Mentation is the level of conciousness a patient is. There are 3 degrees of abnormal mentation commonly discussed. Obtunded – Abnormal response to stimulus and not fully aroused Stuporous – Patient only reponsive to strong or noxious stimulus Comatose – Patient has a heart beat, may or may not be breathing, and is not responsive to any stimulus Dull, depressed or lethargic are similar terms that can describe a patient that is not fully alert but is able to be fully aroused when interacted with. This is a depressed level of conciousness that could be secondary to an intracranial or systemic disease. Mentation Change The ascending reticular activating systemt (ARAS) is resonponsible for keeping a patient alert and is located within the brainstem. Obtunded – could be secondary to a diffuse forebrain lesion or from a brainstem lesion. Stuporous and Comatose – secondary to a brainstem lesion affecting the ARAS. A forebrain lesion can lead to stupor or coma but only if it directly effects the brainstem, such as with brain herniation. Delirium could be toxin related or from a forebrain lesion but is not commonly recognized in veterinary medicine. Modified Glasgow Coma Scale This is a scale that is used for animals with encephalopathy, especially when secondary to head trauma. It is based on 3 different categories, and each category is added together to give a total score. Motor Activity Brainstem Reflexes Level of conciousness It is useful to help look at trends and determine prognosis in animals with head trauma. You do not need to memorize this, it is just a clinical example of how helpful knowing different levels of conciousness is. Modified Glasgow Coma Scale Motor Activity Normal gait and reflexes 6 Hemi/tetraparesis or decerebrate activity 5 Recumbent, intermittent ext. rigidity 4 Recumbent, constant ext. rigidity 3 Recumbent, constant ext. rigidity & opisthotonus 2 Recumbent, hypotonic muscles or decreased 1 to absent reflexes Brain-stem reflexes Normal PLR & Oculocephalic reflex (OCR) 6 Slow PLR, normal to decreased OCR 5 Miosis OU, normal to decreased OCR 4 Pinpoint pupils, decreased to absent OCR 3 Unilateral, unresponsive mydriasis, decreased to absent OCR 2 Bilateral, unresponsive mydriasis, decreased 1 to absent OCR Level of consciousness Alert, responsive to environment 6 Mildly obtunded, inappropriately responsive 5 Mod/severely obtunded 4 3 MSCS Score Prognosis 3-8 Grave Stuporous, responsive to auditory, visual stimuli, and/or tactile 9-14 Guarded Stuporous, responsive to noxious stimuli 2 15-18 Good Comatose 1 Behavior and Mentation Summary Abnormal behavior from a neurological abnormality are the result of a forebrain (prosencephalon) lesion. Depending on the behavior abnormality, it could be possible to localize the lesion as a left or right sided forebrain. Abnormal behaviors such as seizures and narcolepsy localize to the forebrain as well. Mentation changes could be the result of a forebrain or brainstem (mesencephalon and rhombencephalon) lesion. Systemic disease could also lead to mentation change and needs to be ruled out. Gait Ataxia a – without taxia – order Paresis Difficulty initiating a movement Often used synonymously with weakness Paralysis (or plegia) Absence of movement Ambulatory versus nonambulatory Able to take 50 unassisted steps Tetra (or quadra) All four limbs Para Implies pelvic limbs only Hemi Implies only one side of the body Mono Implies only one limb Gait When describing the movement, we want to know: Is the patient nonambulatory or ambulatory? Is the patient paretic or plegic? Is there ataxia, and if so what type of ataxia? Which limbs are affected? An example to describe gait is: The patient is ambulatory with paraparesis and proprioceptive ataxia. An example to describe gait is: The patient is nonambulatory with tetraparesis (since the animal is nonambulatory, they cannot be ataxic). Ataxia There are 3 types of ataxia Proprioceptive Often called spinal or sensory ataxia With this type of ataxia patients will cross their limbs, and scuff and knuckle the paws (or hoves or claws) There is often an upper motor neuron component with proprioceptive ataxia Vestibular Patients will drift towards one side with vestibular ataxia There are usually other signs of vestibular disfuction such as a head tilt and nystagmus Cerbellar ataxia This type of ataxia results in dismetria, often described as a hypermetria. Hypermetria is an over flexion and over extension of the limb. It is not uncommon for a patient to have more than one type of ataxia Lameness versus Ataxia Both lameness and ataxia describe gait abnormalities. Therefore an animal must be able to walk to have a lameness or ataxia. If an animal presents with an abnormal gait, one of the first steps is to decide if the abnormality is orthopedic or neurologic. Orthopedic disease is more common than neurologic disease, especially in large animals and horses. Orthopedic disease results in lameness. Lameness is predictable with every step, or regullary irregular. Ataxia is secondary to neurological disease and the gait is not predictable, or irregularly irregular. Be sure to use the entire exam to help differntiate the two. Lameness will often have localized pain to the limb. Ataxia will often have other neurological deficits found on the exam. Lameness: Looking at where the horse places the hooves, there is less weight placed on the affected limb, but the limb placement is predictable. Ataxia: Looking at where the horse places the limbs, it is unpredictable, there is crossing of the limbs, wide placement of the limbs, and scuffing of the hooves (black lines). Posture There are several types of postures secondary to neurological disease which can help with neurolocalization. Decerebrate Decerebellate Head Turn Head Tilt Torticollis Opisthotonus Schiff Sherrington Risus Sardonicus Spasticity Flaccid Neck Guarded Kyphosis Posture Continued Decerebrate Patient is rigid in all limbs, often with opisthotonus (star gazing) Lesion is within the brainstem (more specifically midbrain) Patient is generally stuporous to comatose Decerebellate Patient is rigid in the thoracic limbs, may have opisthotonus, but has flexed pelvic limbs There is a lesion to the cerebellum or cerebellar peduncles Patient is generally alert to obtunded Posture Continued Head Turn Secondary to a forebrain lesion Head is no longer along the longitudinal axis Head Tilt Secondary to vestibular disease Head is no longer level along the horizontal axis Torticollis Secondary to a cervical lesion causing flexion of neck or malformation Contracture or flexion of cervical muscles Posture Continued Opisthotonus Head in dorsoextension, often referred to as star gazing Secondary to an intracranial lesion or cranial cervical lesion Risus Sardonicus Due to lack of inhibition to the facial nerve causing contracture of the facial muscles Secondary to Tetanus Infection Schiff Sherrington Secondary to a T3-L3 myelopathy Thoracic limbs have increased extensor tone (spacticity), pelvic limbs are paretic to plegic Posture Continued Spacticity Secondary to an upper motor neuron lesion (except in the case of Schiff Sherrington) If all 4 limbs are spactic, then a C1-C5 myelopathy is suspected, if just the pelvic limbs then a T3-L3 lesion is suspected Flaccid Secondary to a lower motor neuron lesion Lesion can either be diffuse, or at the intumescense of the spinal cord Neck Guarded – Secondary to cervical pain Kyphosis – Secondary to thoracolumbar pain, abdominal pain, or malformation Final Comments on Myelopathies At each spinal cord segment localization, such as C1-C5, unique neurological abnormalties might be seen depending on the severity and location of the lesion C1-C5 T3-L3 Respiratory depression C6-T2 Horner syndrome Nerve root signature Absent Cutaneous Trunci Schiff Sherrington Spinal Shock Cuteous Trunci Cutoff L4-S3 Abnormal anal tone Flaccid tail Summary The nervous system is on a closed circuit, meaning if you are familiar with the function and pathway, you can predict what the deficit means There are 9 places to localize: cerebrum, brainstem, cerebellum, vestibular, C1-C5, C6-T2, T3-L3, L4-S3, PNS Understand the difference between UMN and LMN Obervation is extremely helpful for the neurological examination and should not be “overlooked” Neurolocalization Part 2 Richard Shinn, DVM, MS, DACVIM Neurology Objectives Discuss the hands on portion of the neurological examination Cranial Nerves Proprioception Segmental Spinal Cord Reflexes Hyperesthesia Nociception Bowel and Bladder Function Observe a neurological exam Cranial Nerves I – Olfactory II – Optic III – Oculomotor IV – Trochlear V – Trigeminal VI - Abducens VII – Facial VIII – Vestibulocochlear IX – Glossopharyngeal X – Vagus XI – Accessory XII - Hypoglossal Loading… Loading… Components of the CN’s Efferent Somatic: III, IV, VI, XI, XII Visceral It gets far more complicated as you can see below, but for the purpose of clinics and therefore this class, you do not need to know this degreee of detail. Just understand I am only telling you part of the story, the part most clinically important. In other words, you don’t need to memorize this slide. Special: V, VII, Nucleus ambiguus (IX, X) and XI General: III, VII, IX, X Afferent Somatic General: V, VII, X Special: II, VIII Visceral General: VII, IX, X Special: I, VII, IX, X Olfactory Nerve (I, Sensory) Olfactory Nerve The olfactory nerve is responsible for the sense of smell. It is difficult to assess this nerve and therefore we typically don’t. Avoid irritating substances Nociception 5th nerve If an animal sniffs, they likely smelt a scent and therefore at least part of the olfactory nerve is working. However if they do not sniff, it could be behavior where a patient is just nervous. Food can be hidden in a hand or under a cup to see if the animal can find it however again, if they don’t actively seek out the food, it could be behavioral or stress. Optic Nerve (II, Sensory) Optic Nerve The optic nerve is responsible for transmittion information from the retina to the brain. It is impossible to talk about the optic nerve without discussion vision and the visual pathway and will be discussed here. The visual pathway starts at the retina, then the axons from the rods and cones form the optic nerve. From there fibers may or may not cross at the optic chiasm (varies between species), after which the optic tract is formed. From here the fibers synapse on the lateral geniculate nucleus, the relay center of vision in the thalamus. Neurons from the thalamus then send ascending projections to the occiptital cortex through the optic radiations. Communication occurs between different areas of the brain, such as the frontal cortex and occiptial Assessing Vision There are several ways to assess vision, these are the most common Menace response Watching a patient navigate an unfamiliar environment, such as an exam room or an obstacle course Blindfold one eye at a time Table test Cotton ball test Loading… Menace Response –II afferent, VII efferent This is a learned response, and not a reflex. In the dog and cat, most animals learn this by 12 weeks of age, but some a little later. The afferent (sensory) pathway for the menace response is the same for vision. The efferent (motor) pathway begins at the motor cortex, travels down to the pons where it synapses on the pontine nucleus. The pontine axons then travel to the cerebellum where another synapse occurs. From here the signal is relayed from the cerebellum to the cranial nerve VII nucleus, before it finally travels down the axon to the Orbicularis Oculi muscle to cause the eyelid to blink. Menace Response When doing the menace, the hand is moved quickly towards the patient’s eye and stopped just before touching the whiskers or hairs around the eye. We will generally cover one eye at a time so each eye is assessed individually. It is a common misconception that if you move your hand too quickly, it will move a lot of air creating wind which will then cause the eyelid to close due to stimulation of the ophthalmic branch of the trigeminal nerve from the cornea. This does not appear to occur clinically as an animal’s corneal sensation is nowhere near as sensitive as people. I find that students are often not “menacing” enough and therefore the animal does not menace because one goes to slow. In other words, like most things, performing the menace response is a skill that has to be worked on to get a reliable response. Placing or Table Test Reaction The table test is performed with and without the eyes covered, and is only performed on animals small enough to lift with one are. To assess vission bring the animal close to the edge of a table and see if they lift their paw prior to hitting the table. This is another way to assess vision but is not commonly performed. With the eyes closed (as shown in the image) proprioception is assessed. Cotton Ball Test This is another way to assess vision, but is not 100% reliable as some animals are not interested in the cotton ball. To perform this, have a cotton ball in hand out of the animal’s field of view. Then throw the cotton ball into the field of view of the animal, ideally assessing one eye at a time. If the animal sees the cotton ball, they will generally turn towards it or try and smell/eat it. A cotton ball is chosen because it is lite and makes little to no sound when it hits the ground thus you won’t be assess hearring. Pupillary light reflex Another way to assess the optic nerve is by the pupillary light reflex. Prior to performing the PLR, you must look at the pupil size in ambient light and ideally in dim light as well. For large animals, this can be difficult to perform in the daylight as no light is going to compete with the sun. Therefore you have to get a patient in a darker setting. The pathway for the PLR starts the same as the menace, with the signal starting at the retina, then to the optic nerve, optic chiasm, then optic tract. From there the signal travels to the pretectal nucleus within the midbrain. The signal then crosses over to the parasympathetic nucleus of the occulomotor nerve who’s axons then help form the occulomotor nerve. PLR Note the number of times the signal could cross depending on where the light hits the retina. The most important crossing occurs from the pretectal nucleus to the parasympathetic nucleus (Edinger-Westphal nucleus). That side, some of this information does not decussate and therefore both para-sympathetic nuclei will PLR To performed the PLR, again assess pupil size first in the ambient room light, then turn off the lights. If you shine a light at the bridge of the nose, this often causes a tapetal reflexion in both eyes making it easier to see pupil size (top image). Afterwards with the lights still off, shine the light in one eye close to the eye and see if constriction occurs in that eye (direct) and the other eye (consensual). Quickly move the light over to the other eye to ensure the eye remains constricted (swinging flashlight test). PLR abnormalities Assess for anisocoria. If present, determine if one eye is miotic (constricted) or mydriadic (dilated). If miosis is present, assess for Horner syndrome. If myosis is present, assess if it is secondary to the optic or occulomotor nerve. Example: If the right eye is mydriadic, and you shine a light in the right eye and the left eye constricts, then the lesion location is to the occulomotor nerve on the right. Example: If the right eye is mydriadic, and you shine a light in the right eye and neither eye constricts but when you shine it on the left and both eyes constrict, then the lesion location is to the pre-chiasmal on the right. Sympathetic (Horner syndrome) Miosis- small pupil Ptosis- drooping lid Enophthalmos- sunken Elevation third eyelid Vasodilation Schematic representation of the oculo-sympathetic pathway superimposed over a sagittal cervical and thoracic CT image. The central/first order neuron begins within the hypothalamus and travels through the lateral tectotegmental spinal tract (1). The preganglionic/second order neuron begins within the gray matter of the first 3 thoracic spinal cord segments (T1, T2, T3). Its axon continues through the ramus communicans and travels though the thorax within the sympathetic trunk (2a). Dazzle Reflex This is performed similar to the PLR, but the bright light is introduced very quickly to the eye. The dazzle reflex is an involuntary aversion response (blinking, globe retraction, third eyelid protrusion, and/or head movement) to intense illumination of the eye. This response involves the retina, cranial nerve II, the rostral colliculus, and cranial nerve VII. This does not assess vision, however if an animal is trying to move their head away from the light, that requires the cerebral cortex. Fundic Exam This is commonly performed during the neurological exam as the optic nerve is the only nerve that we can vizualize, but will be covered in other lectures in more detail. Sometimes the eye must be dilated to perform a thorough fundic exam and should be done after the PLR is assessed. Retinal artery and vein Tapetal Fundus Optic n. head Nontapetal Fundus Cranial Nerves III, IV & VI Red – Oculomotor Nerve (from midbrain) Blue – Trochlear Nerve (from dorsal midbrain) Green – Abducense Nerve (from medulla) Cranial Nerves III, IV & VI These nerves innervate the extraoccular muscle to the eye. In other words, CN I & II were purely sensory, CN III, IV & VI are purely motor. A lesion to the occulomotor nerve will cause a ventrolateral strabismus (B). A lesion to the trochlear nerve will cause a rotational strabismus (D). A lesion to the abducense nerve will Occulomotor Nerve The occulomotor nerve originates in the midbrain. The extra-occular muscles innervated are the dorsal, medial and lateral rectus mm., and the ventral oblique. In addition to the extra-occular muscles, the occulomotor nerve also provides parasympathetic innervation to the internal occular muscles, specifically the pupillary sphincter muscle. Thus it is responsible for constriction of the pupil. Trochlear Nerve This nerve also originates in the midbrain. This unique part of this nerve is that it originates from the dorsal aspect of the midbrain, and is the only nerve to do so. The only muscle the trochlear nerve innervates in the dorsal oblique. So the nerve that comes out dorsally innervates only a dorsal muscle. Abducense Nerve The abducense nerve originates from the medulla. Muscles innervated by the abducense nerve include the lateral rectus m. and the retractor bulbi. As a general rule, the afferent for the menace is the optic nerve and the efferent is the facial nerve. However if there is facial nerve paralysis an animal could still “raise” the third eyelid (nictitating membrane) as this occurs secondary to the function of the abducense nerve. When the globe is retracted by the retractor bulbi this causes the nictitating membrane to cover the eye. When the facial nerve is functioning correctly, we cannot evaluate this due to the eyelids. Assessing III, IV & VI Parasympathetic Occulomotor Nerve Evaluate for mydriasis Extra-occular muscles Loading… Evaluate for strabismus (abnormal eye position) Evaluate the occulocephalic reflex (discussed with vestibulochoclear nerve) Trigeminal Nerve (V) Aqua Color indicating the origin of cranial nerve V and the immediate branching that occurs. Trigeminal Nerve (V, Motor and Sensory) The trigeminal nerve originates at the pons then immediately splits into three components: mandibular branch, maxillary branch, and ophthalmic branch. The mandibular branch is motor to the majority of muscles of mastication. All 3 branches are sensory to the majority of the head and face. Ophthalmic – purple Maxillary – red Mandibular – green Additionally, the trigeminal nerve innervates the eustacian tube (connects Muscles of Mastication The masseter and temporalis mm. are broad responsible for closing the jaw, and is innervated by the mandibular branch of the trigeminal nerve. The pterygoid m. is resposible for protraction and Assessing muscle of mastication Due to the size of the temporalis and masseter mm., a lesion leading to unilateral atrophy is generally obvious. For more subtle lesions, you would need to put your hands on the animal’s head to assess for assymetry. If both mandibular branches of cranial nerve V are affected, then a dropped jaw results. When muscle atrophy is present, sensory to the head and the face may or may not be affected, depending on where the lesion is located and which branches of cranial nerve V are affected. Sensation to the head and face Ophthalmic branch—this branch of CN V can be evaluated via the corneal reflex and by specifically touching the medial canthus of the eyelid region during the palpebral reflex. The efferent part of this reflex is dependent on normal function of the facial nucleus and nerve (CN VII). Maxillary branch—the maxillary branch can be tested touching the lateral canthus during the palpebral reflex. Pinch the upper lip lateral to the canine tooth. A normal response is a wrinkling of the face and a blink, which also depends on motor supply by the facial nerve. Some animals also turn or withdraw their head, indicating a conscious response mediated at the level of the forebrain. Palpebral reflex Corneal reflex Afferent- trigeminal (5th) 5 Medial canthus or cornea = ophthalmic branch 5th Efferent- facial (7th) Retractor bulbi = 6th 3rd eyelid & passive eyelids The corneal reflex is performed the same way but with a soft object directly touching the cornea. Assess for a blink and behavioral response. 7 Facial Nerve (VII) The facial nerve originates from the medulla. This means that cranial nerves VI through XII originate from the medulla. In other words, have of them. Facial Nerve (VII, Motor and Sensory) The facial nerve is motor to muscle of facial expression (different from muscles of mastication), sensory to the inner ear pinnea, has parasympathetic innervation to glands on the face. CN VII also innervates the stapedius muscle which protects the tympanic membrane from loud noises but is not clinically important. The facial nerve also innervates the caudal belly of the digastricus muscle but is also not clinically relevant. The facial nerve is also sensory and taste to the rostral 2/3 of the tongue, but again this is not likely clinically relevant. Assessing Muscles of Facial Expression During the neurological exam, performing the palpebral and corneal reflex, along with the menace response are great for assessing cranial nerve VII. However, all of these use other cranial nerves are the afferent and could be abnormal if other nerves are affected. That said, it would be uncommon for both optic and trigeminal nerve to be affected at the same time. If both menace and palpebral are absent, a facial nerve lesion is more likely, especially if the retractory bulbi is still working Facial nerve: sensation & parasympathetic The facial nerve is sensory to the inner pinna (red) where the remainder of the ear is largely from the second cervical spinal cord segment. Parasympathetic innervation from the facial nerve supplies the: lacrimal gland, nasal & palatine glands, sublingual salivary and mandibular salivary glands. A lesion to cranial nerve VII can lead to Neurogenic Keratoconjunctivitis Sicca not only because of the inability to blink, but also because of the lack of tear production from the lacrimal gland. Vestibulocholear Nerve (VIII, Sensory) Originates from the medulla. The vestibular portion of CN VIII is part of the peripheral vestibular system and connects the inner ear to the medulla. Given the function of the vestibular function and it’s relationship to CN VIII, both will be discussed in the following slides. The chochlear portion of CN VIII is responsible for transmitting the signal from the chochlea to the medulla. Hearing is difficult to fully assess on a neurological exam but may be attempted. Vestibular Apparatus The vestibular system is responsible for maintaining tone to the muscles of the neck, trunk and limbs. The anatomy of the vestibular system is extremely complicated and we will only hit on the highlights. Like with the rest of the exam, I am only telling you part of the story, the part that is clinically relevant. Within the inner ear is the bony laberinth which houses the vestibular apparatus and chochlea. The Vestibular appratus is composed of the utricle & saccule (horizontal and verticle acceleration) along with the semicircular canals (see next slide). Semicircular Canal utricle saccule Middle Ear Semicircular Canals For the purpose of the exam we will focus on the semicircular canals which have an organ at each base called the ampulla. The ampulla has a basal rate of firing, like a pacemaker cell in the heart. When an animal is not moving, this basal rate from the ampulla sends signals from their axons, which make up part of the vestibular nerve, to the medulla. From the medulla, the signal is transferred to the muscles of the eyes, neck, trunk and limbs to maintain an upright posture. When the head is moved in a certain direction, the firing rate from the ampulla either increases or decreases (depending on the direction) which will increase or decrease the tone of the muscle on one side of the body preventing the animal from falling. This is how the occulocephalic reflex works. Occulocephalic reflex Oculocephalic reflex, vestibulo-ocular reflex, doll’s eye or physiologic nystagmus is elicited by moving the patient’s head side to side and up and down. Normal physiologic nystagmus has a fast phase in the direction of the head movement. This test evaluates cranial nerves VIII (sensory) and III, IV, VI (motor). In small dogs or cats, primarily those with significant cervical pain, the test can be performed moving the entire patient sideways. This test does not assess vision, and blind animals will still have an oculocephalic reflex. Pathological nystagmus and head tilt Going back to the basal rate of the vestibular appratus, if there is a lesion where this basal rate is no longer going to one side of the body, then the animal will feel as if though it is falling towards one side. Thus the animal feels like they are spinning which causes the pathological or spontaneous nystagmus (abnormal eye movement). This is the same reason why a strabismus could be present. Similar, because there is no input from one side of the vestibular system, the muscle tone to one side of the body will be lost leading to the animal having a head tilt and falling towards one side (vestibular ataxia). Cochlea The cochlea is within the ventral portion of the boney labyrinth and is responsible from turning sound waves into electrical impulses. It is not important clinically to understand how this occurs, but the shape of the cochlea is extremely important. Additionally the tympanic membrane and collection of 3 small bones (malleus conneted to the tympanic membrane, the incus, and the stapes connected to the cochlear window), play a role in this as well and a lesion at any point in this apparatus can lead to deafness. Testing Hearing Generally an animal has to be deaf in both ears for us to appreciate any form of hearing loss. It is common that an owner will pick up on hearing loss before we can on routine examination. A crude way to test for hearing (yes or no) is to clap once loudly out of the animal’s field of view. Avoid creating noises that will create vibrations on the floor or table, such as stomping on the ground. A more objective way to test hearing is with a brainstem auditory evoked response (BAER). This is performed using specialized equipment where electrodes are placed in specific areas on the head and a timelocked noise is created. The electrodes are able to measure electrcle impulses from cranial nerve VIII and the brainstem if hearing is present. Cranial Nerves IX, X & XI All originate from the caudal medulla and share a lot of functions. Glossopharyngeal and Vagus Nerves Cranial nerves IX and X have several of the same functions and are therefore hard to separate out clinically. Both nerves have motor and sensory, along with parasympathetic function. Both nerves have proprioception to the head, but this will not be discussed further as it is not clinically useful and adds to confusion. Both nerves arise from the caudal portion of the medulla. Both nerves are involved in the swallowing reflex. The vagus innervates the organs of the thoracic and abdominal cavities, both motor and sensory. Glossopharyngeal Nerve (IX, Motor & Sensory) Motor to the soft palate and pharyngeal muscles (shared with CN X). Sensory for the carotic body and carotid sinus, along with the pharyngeal mucosa and caudal 1/3 of the tongue (and taste). Parasympathetic to parotid and zygomatic salivary glands. Vagus Nerve IX, Motor & Sensory) Motor to the soft palate and pharyngeal muscles (shared with CN IX). Motor to the larynx and esophagus (shared with internal branch of accessory nerve). Sensory to the pharynx, larynx, trachea, esophagus, and thoracic and abdominal viscera. Parasympathetic to mucosal glands of pharynx, larynx, trachea, esophagus, and thoracic and abdominal viscera. Accessory Nerve (XI, Motor) Although there is evidence that CN XI does have a sensory component, clinically it is not important and likely overlaps with other nerves so will not be discussed further. There are two parts to the accessory nerve External branch: Motor to the trapezius, omotransversarius, sternocephalicus, and cleidocephalicus. Internal branch: Joins the recurrent laryngeal nerves to share motor function with the Vagus nerve as discussed on the previous slide. Assessing IX, X and internal XI Ask the client about any dysphagia, regurgitation, voice change, or inspiratory stridor. Touch the left or right side of the caudal pharyngeal wall with an applicator stick or finger and watch for elevation of the palate and contraction of the pharyngeal muscles, called the gag reflex. An asymmetrical response is more significant than a bilateral loss of the gag reflex, because this reflex is difficult to elicit in some normal animals. If the patient’s demeanor precludes stimulating the pharyngeal mucosa, a similar reflex can sometimes be elicited by externally palpating the pharyngeal region dorsal to the larynx. Assessing XI CN XI (spinal accessory branch) supplies motor innervation to the trapezius muscle. A lesion in this nerve results in atrophy of the trapezius muscle. However, this is difficult to detect in most patients, and lesions restricted to this nerve are rarely recognized. The internal branch of CN XI is structurally and functionally part of the Vagus nerve. Hypoglossal Nerve The most caudal nerve originating from the medulla Hypoglossal Nerve (XII, Motor) Inspect the tongue for atrophy, asymmetry, or deviation. Animals usually lick their nose immediately after the gag reflex is tested. Patients with unilateral loss of innervation may be able to lick only one side of the nose, with the tongue usually deviating toward the side of the lesion when actively protruded. Watching the patient drink water also helps assess tongue function. Cranial Nerve Summary Proprioception There are two tests for proprioception that should be performed on every animal unless tempermant precludes you from doing so. Paw Placement Hopping Other tests include: Wheelbarrowing Extensor postural thrust Hemiwalking Blind table test Paw (Foot, Hoof, Limb) Placement This reaction tests more than general proprioception: light touch and pressure are also evaluated. Although sensory functions are evaluated, the reactions described in this section also require motor responses. It is incorrect to assume that abnormalities observed are strictly due to proprioceptive dysfunction. The simplest method of evaluation entails flexing the foot so that the dorsal surface is on the floor. The animal should return the foot to a normal position immediately. Most animals do not allow weight bearing to occur in the abnormal position. Additionally, the foot or hoof is placed on a sheet of paper cardboard that is slowly pulled laterally. As the limb reaches an abnormal position, the animal should reposition it for normal weight bearing. The first test is the most sensitive for proprioception in the distal Paw Placement General proprioceptive information is carried from the tip of the to to the dorsal region of the spinal cord, to the brainstem where a synapse occurs then to the sensorimotor cortex. These are the longest cells in the body, reaching from the tip of the toe all the way to the brainstem. That means in a giraffe one cell is meters long! Because of how long they are, they are sensitive to injury. The motor response is initiated by the cerebral cortex and is transmitted to the LMN in the spinal cord. Because the proprioceptive pathways are sensitive to injury, abnormalities in proprioceptive positioning may occur before motor dysfunction (paresis) can be detected. The response is abnormal if significant paresis exists, but other postural reactions such as hopping are also affected. Proprioceptive positioning is less useful in large Hopping The hopping reaction is a reliable postural reaction test. It evaluates all components involved in voluntary limb movements. Normal hopping responses require intact sensory receptors, peripheral nerves, ascending long tracts in the spinal cord, cerebellum, and brainstem, sensory cortex, UMN systems, and integration with LMNs in the spinal cord. The hopping reaction of the thoracic limbs is tested with one thoracic limb lifted from the ground. Although it is easy to pick up three limbs in small dogs and cats, this is not necessary in Hopping With the animal facing away from the examiner, the patient’s weight is then shifted laterally (as on previous slide) over the limb being tested, and initiation, movement, and support during hopping are assessed. Hopping of the pelvic limbs is accomplished by supporting the thorax and lifting one pelvic limb. With the patient facing toward the examiner, weight is shifted laterally over the limb being evaluated and initiation, movement, and support are assessed. A large animal, such as a giant-breed dog, a horse, and a cow, can be tested by lifting one limb and shifting the weight of the animal so that it hops on the opposite limb. Alternatively, large animals can be pulled by the tail or pushed laterally (sway reaction) to elicit movements similar to the hopping reaction. The hopping reaction is more sensitive than other postural reactions Wheelbarrowing Reaction The animal is supported under the abdomen with all of the weight on the thoracic limbs. The normal animal can walk forward with coordinated movements of both thoracic limbs. The examiner should not lift the pelvic limbs so high that the animal’s posture is grossly abnormal. If movements appear normal, the maneuver is repeated with the head lifted and the neck extended. This position prevents visual compensation, making the animal mostly dependent on proprioceptive information. A tonic neck reaction, which causes slightly increased extensor tone in the thoracic limbs, is also elicited. When the neck is extended, subtle abnormalities of the thoracic limbs may be seen in animals that otherwise appear normal. This reaction is especially useful for detecting compressive lesions in Wheelbarrowing Reaction Weakness in the thoracic limbs may be detected when the wheelbarrowing reaction is tested because the animal is forced to carry most of its weight on two limbs while standing on only one limb while moving. Slow initiation of movement may be a sign of a proprioceptive deficit or of paresis that is caused by a lesion of the cervical spinal cord, the brainstem, or the cerebral Extensor Postural Thrust Reaction Extensor postural thrust is elicited by supporting the animal by the thorax caudal to the thoracic limb and lowering the pelvic limbs to the floor. When the limbs touch the floor, they should move caudally in a symmetric walking movement to achieve a position of support. As the animal is lowered to the floor, it extends its limbs, anticipating contact. This is a vestibular reaction and may be lacking or uncoordinated in animals with lesions of the vestibular system. Asymmetric weakness, lack of coordination, and dysmetria can be seen in the extensor postural Hemistanding and Hemiwalking The thoracic and pelvic limbs on one side are lifted from the ground so that all of the animal’s weight is supported by the opposite limbs. Forward and lateral walking movements are then evaluated. Abnormal signs may be seen in hemistanding and hemiwalking as in the other postural reactions. They are most useful in animals with forebrain lesions. These animals have relatively normal gaits but have deficits of postural reactions in both the thoracic and the pelvic limbs contralateral to the side of the lesion. This reaction should be performed with caution in large dogs with obvious weakness as they can easily fall and potentially exacerbate their clinical signs. Placing or Table Test Reaction Placing is evaluated first without vision (tactile placing) and then with vision (visual placing) as previously discussed. The examiner supports the animal under the thorax and covers its eyes with one hand or with a blindfold. The thoracic limbs are brought in contact with the edge of a table at or ventral to the carpus. The normal response is immediate placement of the feet on the table surface in a position that supports weight. Care must be taken not to restrict the movement of either limb. When one limb is consistently slower to respond, the animal should be held in the examiner’s other hand to ensure that its movements are not being restricted. Visual placing is tested by allowing the animal to see the table surface. Normal animals reach for the surface before the carpus touches the table. Peripheral visual fields can be tested by making a lateral Placing Reaction Tactile placing requires touch receptors in the skin, sensory pathways through the spinal cord, cerebellum, and the brainstem to the cerebral cortex, and motor pathways from the cerebral cortex to the LMN of the thoracic limbs. Visual placing requires normal visual pathways to the cerebral cortex, communication from the visual cortex to the motor cortex, and motor pathways to the LMN of the forelimbs. A lesion of any portion of the pathway may cause a deficit in the placing reaction. Segmental Spinal Cord Reflexes Thoracic Limbs Withdrawal or Flexor Reflex Biceps Reflex Triceps Reflex Extensor Carpi Reflex Pelvic Limbs Withdrawal or Flexor Reflex Patellar Reflex Sciatic Reflex Gastrocnemius Reflex Cranial Tibial Reflex Cutaneous Trunci Reflex Perineal Reflex Babinski Reflex Crossed Extensor Reflex A word on reflexes Reflexes are a vital part of the neurological examination however there must be other neurological abnormalities present in order for reflexes to be reliable. In other words, if an animal has an absent withdrawal reflex, then they should also have paresis in that limb as well. You will never say that an animal has a normal examination other than reflexes which lead you to your neurolocalization. Although the response is what we evaluate, the afferent portion of the reflex also has to be intact for a response. A word on reflexes continued Reflexes are graded as follows: a. Absent b. Weak (present but reduced) c. Normal d. Exaggerated e. Clonus(repetitive flexion and extension of the joint in response to a single stimulus). These grades are translated into numbers used to fill the neurologic examination form. A normal reflex is graded as “2,” whereas a decreased reflex is assigned “1,” an absent reflex “0,” an increased “3,” and a clonic reflex “4”. Causes of weak or absent reflexes are: A lesion affecting any part of the reflex arc, including the peripheral nerve, nerve roots, spinal segments, neuromuscular junction, and muscle. Other signs A word on reflexes continued Causes of exaggerated reflexes or clonus are: A lesion in the UMN pathways cranial to the spinal segment involved in the reflex. Other signs of UMN disease, such as paresis or paralysis, are also evident. Patients who are excited or anxious. In this case, other signs of a UMN lesion are absent. Again, never diagnose a UMN lesion in a patient with exaggerated reflexes but normal gait and postural reactions. A lesion of the L6–S1 spinal segments or sciatic nerve can cause an exaggerated patellar reflex (pseudohyperreflexia). This is due to decreased tone in the muscles that flex the stifle and normally dampen stifle extension when the patellar reflex is elicited. Such lesions also cause other abnormalities, such as a decreased flexor reflex. Order of spinal reflex testing—it is important to only perform tests that can be perceived as uncomfortable to the patient last, as it is important to have their cooperation to properly perform testing of spinal reflexes. Thoracic Limb Reflexes If reflexes are normal to increased in the thoracic limbs in an animal with tetraparesis, then the localization is a C1-C5 myelopathy. If reflexes are decreased to absent in the thoracic limbs in an animal with tetraparesis, then the localization is a C6-T2 myelopathy or lower motor neuron. The only reliable thoracic limb reflex is the withdrawal (flexor) reflex however other reflexes will be discussed for completeness. Withdrawal Reflex The animal is maintained in lateral recumbency. A noxious stimulus is applied to the foot. The normal response is a flexion of the entire limb, including the shoulder, elbow and carpus. The least noxious stimulus possible should be used. If an animal flexes the limb when the digit is touched, the digit need not be crushed. If a response is not easily elicited, a hemostat should be used to squeeze across a digit. Pressure should not be so great as to injure the skin. Both dorsal and ventral regions should be tested on each limb (see sensory zones on previous slide). The limb should be in a slightly extended position when the stimulus is applied to allow the limb to flex. The opposite limb also should be free to extend. The flexor reflex is more complex than the myotatic reflex (such as patellar reflex). The response involves all of the flexor muscles of the Withdrawal Reflex The flexor reflex is a spinal reflex and does not require any activation of the brain. If an animal steps on a sharp piece of glass, it immediately withdraws the foot before consciously perceiving pain. If the spinal cord is completely transected cranial to the segments that are responsible for the reflex, the reflex is present even though the animal has no conscious perception of pain. Absence (0) or depression (+1) of the reflex indicates a lesion of C6T1 segments or the peripheral nerves. Unilateral absence of the reflex is more likely the result of a peripheral nerve lesion, whereas bilateral absence or depression of the reflex is more likely the result of a spinal cord lesion. A normal (+2) flexor reflex indicates that the spinal cord segments and the nerves are functional. An exaggerated (+3) flexor reflex rarely is Extensor Carpi Radialis Reflex The animal is in lateral recumbency and the limb is supported under the elbow, with flexion of the elbow and the carpus maintained. The extensor carpi radialis muscle is struck with the plexor just distal to the elbow. The response is a slight extension of the carpus. The carpus must be flexed, and the digits must not touch the floor or the other limb or the reflex will be mechanically inhibited. The extensor tendons crossing the carpal joint are struck in large animals. The extensor carpi radialis muscle is an extensor of the carpus and is innervated by the radial nerve (with origin in the C7-T1 segments of the spinal cord in the dog). The extensor carpi radialis reflex is more difficult to elicit than the patellar reflex but usually can be recognized in dogs. Absent or Triceps Reflex The animal is held in the same position as that for the extensor carpi radialis reflex. The triceps brachii muscle is struck with the plexor just proximal to the olecranon. The response is a slight extension of the elbow or a visible contraction of the triceps muscle. The elbow must be maintained in flexion for a response to be elicited. The triceps brachii muscle extends the elbow and is essential for weight bearing in the forelimb. Innervation is through the radial nerve (with the origin from spinal cord segments C7-T1 in the dog). The triceps reflex is difficult to elicit in the normal animal. Absent or decreased reflexes should not be interpreted as abnormal. Lesions of the radial nerve can be recognized by a loss of muscle tone and an inability to support weight. Exaggerated reflexes are interpreted in the same way as for the extensor carpi radialis reflex. Biceps Reflex The index or middle finger of the examiner’s hand that is holding the animal’s elbow is placed on the biceps and the brachialis tendons cranial and proximal to the elbow. The elbow is slightly extended, and the finger is struck with the plexor. The response is a slight flexion of the elbow. Movement of the animal’s elbow must not be blocked by the examiner’s restraining hand. In this case, movement of the skin overlying the biceps brachii muscle may be observed. The biceps brachii and brachialis muscles are flexors of the elbow. They are innervated by the musculocutaneous nerve, which originates from spinal cord segments C6-8 in the dog. The biceps reflex is difficult to elicit in the normal animal. Absent or decreased reflexes should not be interpreted as abnormal. Flexion of the elbow on the flexor reflex provides a better assessment of the Pelvic Limb Reflexes If reflexes are normal to increased in the pelvic limbs in an animal with paraparesis, then the localization is a T3-L3 myelopathy. If reflexes are decreased to absent in the pelvic limbs in an animal with paraparesis, then the localization is a L4-S3 myelopathy or lower motor neuron. The only reliable pelvic limb reflexes are the withdrawal (flexor) reflex and patellar reflex, however other reflexes will be discussed for completeness. Saphenous Sciati c Fibula r Tibia l Fibula r Withdrawal Reflex The animal is maintained in lateral recumbency. Again a noxious stimulus is applied to the foot. The normal response is a flexion of the entire limb, including the hip, stifle, and hock. The least noxious stimulus possible should be used. If an animal flexes the limb when the digit is touched, the digit need not be crushed. If a response is not easily elicited, a hemostat should be used to squeeze across a digit. Pressure should not be so great as to injure the skin. Both medial and lateral digits should be tested on each limb. The limb should be in a slightly extended position when the stimulus is applied to allow the limb to flex. The opposite limb also should be free to extend. The response involves all of the flexor muscles of the limb and thus requires activation of motor neurons in several spinal cord segments. Withdrawal Reflex Absence (0) or depression (+1) of the reflex indicates a lesion of L6S1 segments or the branches of the sciatic nerve. Unilateral absence of the reflex is more likely the result of a peripheral nerve lesion, whereas bilateral absence or depression of the reflex is more likely the result of a spinal cord lesion. A normal (+2) flexor reflex indicates that the spinal cord segments and the nerves are functional. An exaggerated (+3) flexor reflex rarely is seen with acute lesions of descending pathways. Chronic and severe descending pathway lesions may cause exaggeration of the reflex. This exaggeration is manifested as a sustained withdrawal after release of the stimulus. A mass reflex (+4) occasionally is seen as a sustained flexion of both pelvic limbs, with Loading… Patellar reflex With the animal in lateral recumbency, the limb is supported under the femur with the left hand (by a right-handed examiner) and the stifle is flexed slightly. The patellar ligament is struck crisply with the plexor. The response is a single, quick extension of the stifle. The plexor is recommended for performing myotatic reflex testing, but other instruments such as bandage scissors may be used. Nose tongs or similar heavy instruments are useful for testing large animals. The examiner should use the same type of instruments in each examination to obtain consistent results. The myotatic or stretch reflexes are basic to the regulation of posture and movement. The reflex arc is a simple two-neuron (monosynaptic) pathway, versus the withdrawal which is polysynaptic. The sensory Patellar reflex continued The muscle spindle is the stretch receptor of the muscle and are located in the belly of the skeletal muscle (extrafusal muscle fibers). Stretching a muscle depolarizes the nerve endings of the spindle, producing a burst of impulses in the sensory fibers that travels up the nerve through then dorsal root, then, the sensory fibers directly activate the large (alpha) motor neuron in the spinal cord. The alpha motor neuron discharges impulses through its axon, causing a contraction of the extrafusal muscle fibers of the same muscle. Thus a sudden stretch of the muscle causes a reflex muscle contraction, as seen in the patellar reflex. A more tonic stretch of the muscle causes a slower discharge of sensory activity and a slower, steadier muscle contraction. Patellar reflex continued Alpha (and gamma but don’t worry about these) motor neurons are facilitated or inhibited by a variety of segmental and long spinal pathways. The output of the motor neurons is a summation of their facilitatory and inhibitory inputs. For example, the motor neuron that innervates the quadriceps responds to a sudden stretch by a quick contraction (patellar reflex), but the reaction can be modulated by voluntary inhibition. This occurs in animals that are nervous and maintain a pronounced tone in the limb as the examiner is performing the test. In such cases, the patellar reflex may appear blunted. The spindle sensory fibers also facilitate interneurons in the spinal cord, which in turn inhibit motor neurons of antagonistic muscles. This activity is called reciprocal innervation. For example, spindle Patellar reflex continued The patellar reflex is the most reliably interpreted myotatic reflex. The reflex should be recorded as absent (0), depressed (+1), normal (+2), exaggerated (+3), or exaggerated with clonus (+4). Normal responses vary widely among species and among breeds within a species. In large dogs the response is less brisk than in small dogs. The examiner should become familiar with these natural variations. Absence (0) of a myotatic reflex indicates a lesion of the sensory and/or motor component of the reflex arc—an LMN or segmental sign. In general, loss of the reflex in one muscle group suggests a peripheral nerve lesion; for example, a lesion of the femoral nerve. Bilateral loss of the reflex suggests a segmental spinal cord lesion affecting the motor neurons to both limbs located in spinal cord Patellar reflex continued Depression (+1) of the reflex has the same significance as absence of the reflex, except the lesion is incomplete. Depression of the reflex is more common with spinal cord lesions in cases in which some, but not all, of the segments (L4-6) are affected. Other reflexes also must be tested because generalized depression of reflexes may be seen in polyneuropathies or in abnormalities of the neuromuscular junction (botulism, tick paralysis). Animals that are tense and keep the limb in extension commonly have depressed or absent reflexes. Sometimes the reflex is hard to elicit in normal dogs in the recumbent or nonrecumbent limb. You only have to elicit the normal reflex one time to be sure the reflex arc is intact. Patellar reflex continued Normal (+2) or exaggerated reflexes (+3, +4) and increased tone result from loss of descending inhibitory pathways. The voluntary motor pathways are facilitatory to flexor muscles and inhibitory to extensor muscles. Damage to these pathways releases the myotatic reflex, causing an exaggerated reflex and increased extensor tone. Clonus (+4) is a repetitive contraction and relaxation of the muscle in response to a single stimulus. Clonus often is seen with chronic (weeks to months) loss of descending inhibitory pathways. Clonus has the same localizing significance as exaggerated reflexes. Bilateral exaggerated reflexes most often are associated with damage to descending inhibitory pathways cranial to the level of the reflex. UMN injury causing exaggerated myotatic reflexes also causes paresis. If gait and postural reactions are normal, the “exaggerated reflex” is then likely to be an examiner error or normal for the animal being tested. Exaggerated Cranial Tibial Reflex With the animal in lateral recumbency, the examiner tests the cranial tibial reflex. The belly of the cranial tibial muscle is struck with the plexor just distal to the proximal end of the tibia. The response is flexion of the hock. The cranial tibial muscle is a flexor of the hock and is innervated by the fibular branch of the sciatic nerve (with origin in the L6-7 segments of the spinal cord in the dog). The cranial tibial reflex is more difficult to elicit in a normal animal than is the patellar reflex. Absent or decreased reflexes should be interpreted with caution. Exaggerated reflexes indicate a lesion cranial to the spinal cord segments L6-7. Gastrocnemius Reflex The gastrocnemius reflex is tested after the cranial tibial reflex. The tendon of the gastrocnemius muscle is struck with the plexor just dorsal to the tibial tarsal bone. Slight flexion of the hock is necessary for some tension of the muscle to be maintained. The response is extension of the hock. Contraction of the caudal thigh muscles may also occur. The gastrocnemius is primarily an extensor of the hock and is innervated by the tibial branch of the sciatic nerve (with origin in the L7-S1 segments of the spinal cord in the dog). The gastrocnemius reflex is interpreted in the same manner as the cranial tibial reflex but is even less reliable. Sciatic Reflex Sciatic reflex is also tested with the animal in lateral recumbency. This is performed by placing your index finger in the sciatic notch (the indentation between the ischiatic tuberosity and treater trochanter). Once this region is palpated, strike your finger with the plexor. The limb should be relaxed when this is performed. The sciatic nerve is innervation to the hamstrings (with origin in the L6-S1 segments of the spinal cord in the dog). Striking the region of the sciatic notch causes the stifle to flex. The sciatic reflex is interpreted in the same manner as the cranial tibial and gastrocnemius reflex. Crossed Extensor The crossed extensor reflex may be observed when the flexor reflex is elicited. The response is an extension of the limb opposite the stimulated limb. The crossed extensor reflex is a part of the normal supporting mechanism of the animal. The weight of an animal in a standing position is evenly distributed among the limbs. If one limb is flexed, increased support is required of the opposite limb. The flexor reflex sensory fibers send collaterals to interneurons on the opposite side of the spinal cord, which excite extensor motor neurons. The crossed extensor reflex generally is considered an abnormal reflex except in the standing position. In the normal recumbent animal, the extension response is inhibited through descending pathways. Crossed extensor reflexes result from lesions in ipsilateral descending Extensor Toe (Babinski) Reflex The animal is positioned in lateral recumbency (the same position as that for the myotatic reflex). The pelvic limb is held proximal to the hock, with the hock and the digits slightly flexed. The handle of the plexor or a forceps is used to stroke the limb on the caudolateral surface from the hock to the digits. The normal animal exhibits no response or a slight flexion of the digits. The abnormal response is an extension and a fanning of the digits. The extensor toe reflex has been compared with the Babinski reflex in human beings. The two reflexes are not strictly analogous because the Babinski reflex includes elevation and fanning of the large toe, which is not present in domestic animals; it is reported to be a sign of pyramidal tract damage in human beings. The extensor toe reflex has Perineal (Bulbocavernosus, Anal) Reflex The perineal reflex is elicited by light stimulation of the perineum with forceps. Noxious stimuli that are painful usually are not necessary. The reaction is a contraction of the anal sphincter muscle and a flexion of the tail. One can obtain a similar reaction by squeezing the penis or the vulva (bulbocavernosus reflex). If the anal sphincter appears weak or if the response is questionable, the examiner can insert a gloved digit into the anus because minimal responses often can be felt in this manner. Sensory innervation occurs through the pudendal nerves and spinal cord segments S1-2 (sometimes S3) in the dog and the cat. Motor innervation of the anal sphincter also occurs through the pudendal nerves. Tail flexion is mediated through the caudal nerves. The organization of the reflex is similar to that of the flexor reflex. Cutaneous Trunci (formerly panniculus) reflex With the patient standing or in straight sternal recumbency, lightly pinch the skin just lateral to the vertebral column. Start at the region of the wings of the ilium (L6) and proceed cranially, one vertebral level at a time. The opposite side is tested similarly. The normal response is a bilateral contraction of the cutaneous trunci muscle, resulting in a twitch of the skin over the thorax and abdomen. This reflex is present in the thoracolumbar region and is absent in the neck and sacral regions. An obvious cutoff point suggests a spinal cord lesion 1–4 cord segments cranial to the level of cutoff (the rule of thumb is approximately two vertebral bodies cranial to the cutoff point). Cutaneous Trunci Reflex Continued A lesion affecting the brachial plexus may cause a loss of the ipsilateral cutaneous trunci reflex with a normal response on the other side, regardless of the level at which the skin is stimulated. Thoracotomies typically transect the lateral thoracic nerve, also causing ipsilateral loss of the cutaneous trunci reflex. The cutaneous trunci reflex assesses the sensory integrity of all dermatomes over the thoracolumbar vertebral column (with their corresponding spinal cord segments and nerves). The efferent component is mediated by the lateral thoracic nerve and C8–T1 spinal cord segments. Palpation Light palpation helps detect swelling or atrophy. Light palpation is also useful to evaluate the vertebral column for areas of luxation or crepitus. Deep palpation and manipulation detect painful regions. If crying, whimpering, or muscle tensing occurs on palpation, more vigorous maneuvers, such as manipulation, are unnecessary and may be dangerous in patients with unstable fractures or luxations. Also, palpation is usually more specific because the manipulation of one region often produces movement in other areas. Palpation - Head Check the calvarium for masses, defects, or persistent fontanelles. After palpating the muscles of mastication, gently open the mouth to detect pain or reduced range of motion of the temporomandibular joints. Retropulse the globe by gently pressing on the closed eyelids to detect pain or a retrobulbar mass. Sometimes lightly squeezing the head by grasping above the zygomatic arch elicits a painful response in dogs and cats with structural brain disease. Palpation – Vertebral Column Lightly palpate the vertebral column to detect any curvature, displacement, atrophy, masses, or swelling. Deeply palpate the paraspinal muscle for pain. Palpate, extend, and flex the tail. Downward pressure on the sacrum often elicits pain in animals with lumbosacral lesions. When palpating the thoracolumbar vertebral column, lightly place one hand on the abdomen to detect tensing of the abdominal muscles as the affected area is palpated. Avoid applying pressure in the abdomen as it can elicit abdominal pain, which can be confused with spinal pain. The spinous processes, articular processes, and transverse processes or ribs are palpated separately. If palpation is not painful, the vertebral column can be gently manipulated by applying ventral and lateral pressure to extend Palpation – Vertebral Column Obvious cervical pain can be readily appreciated on posture examination and it is unnecessary to further palpate or manipulate the area. In less obvious cases, cervical pain is often manifested by tensing of the cervical muscles and twitching of the ears during palpation or manipulation. If palpation does not induce pain, gently extend and flex the head with one hand while placing the other hand on the cervical muscles to detect muscle tensing. This has to be done carefully and avoiding forcing it excessively as severe neurologic deterioration can ensue if the patient has potentially unstable vertebral conditions (such as atlantoaxial subluxation). A safer method is to use a food treat and make the dog follow it in all directions. This would more closely assess the natural cervical range of motion and the patient will stop if the movement becomes painful. The main advantage of this technique is that it does not carry the risk of neurologic worsening. Palpation - Limbs Limbs are initially palpated with the patient standing. Contralateral limbs are compared for symmetry. The limbs are more closely examined with the animal in lateral recumbency, when the spinal reflexes are tested. Palpate specific structures, not general regions. Carefully move overlying muscles to palpate bones without compressing adjacent structures. Palpate muscles without compressing or moving adjacent bones and joints. Pain Perception (Nociception) In addition to evaluating the patient for areas of hypersensitivity (hyperpathia), it is important, especially in nonambulatory patients, to determine whether noxious stimuli applied to the limbs are traversing the damaged segment of spinal cord to reach the brain for conscious perception. Nociception has been classically divided into superficial and deep. This division has been questioned because the pathways responsible for these two degrees of noxious stimuli are poorly divided. Superficial pain, also called fast pain, is sharp, well-localized pain most commonly originating in the skin. Deep pain, also called slow pain, is felt as burning, aching, poorly localized pain originating from the skin or deeper structures. Nociception The pathways that carry “deep” nociception are more resistant to damage than other pathways, including those responsible for proprioception, motor function, and superficial pain. Therefore, testing deep pain perception is necessary only if superficial pain or motor is absent. When there is no response to pinching with the fingers, use a hemostat to compress the digits or tail. The degree of compression is gradually increased until a response is elicited. Always test both the medial and lateral digits of the pelvic limbs. If no response is seen, evaluate the tail. Withdrawal of the limb indicates only an intact reflex arc (peripheral nerve and spinal segments). A behavioral response such as turning the head or vocalization indicates conscious perception. Localization As discussed in the Neurolocalization Part 1, all findings are put together to come up with a neurolocalization. Start with either an central or peripheral localization. If central is suspected, then decide if it is brain or spinal cord. If peripheral is expected, decide if it is either sensory or motor unit. If brain is suspected, then localize as: forebrain, brainstem, vestibular or cerebellum. If spinal cord is suspected, then localize as: C1-C5, C6-T2, T3-L3 or L4-S3. Differentials The localization is then combined with the history and signalment to develop a differential diagnosis list. The differential diagnosis directly relates to treatment recommendations, and prognosis.