Download Lesion localization

Companion Animal
Neurology & Neurosurgery
LESION LOCALIZATION
Simon R. Platt,
BVM&S, MRCVS, DACVIM
(Neurology), DECVN
College of Veterinary
Medicine, University of
Georgia
USA
[email protected]
The nervous system plays a role in nearly all body processes. Disease syndromes may
affect the central nervous system (CNS), which includes the brain and spinal cord, and
the peripheral nervous system, which includes cranial nerves, spinal cord nerve roots,
spinal nerves, peripheral nerve branches, and the neuromuscular junction.
Suspicion of neurological dysfunction arises from the history and physical examination.
The signalment, presenting chief complaint, time course of clinical signs, and history
may suggest the type of disease process or species-specific disorder. A complete
neurologic examination is necessary to localize the anatomic distribution, to determine
the severity of the disease process, and to assess the prognosis for patient recovery.
A neurological examination is easily integrated into a routine physical examination.
The objectives of the neurological examination are to confirm if there is a neurological
abnormality and to specifically localize the abnormality within the nervous system.
In conjunction with the history, signalment, presenting complaint and the physical
examination, the neurological lesion localization is a piece of a jigsaw essential to
creating a list of differential diagnoses for the disease. However, caution must be used
as some manipulations necessary for the neurological examination could exacerbate
problems such as spinal cord disease.
The overall aim when approaching neurological problems is essentially the same as
with any clinical problem. Initially it is necessary to identify the nature of the problem,
its extent and severity. Following this, it is necessary to determine the possible
differential diagnoses in order to formulate an effective diagnostic approach. In
this way an accurate diagnosis can be made and an appropriate treatment regime
formulated whilst additionally offering prognostic information to the owner of the
animal.
Primarily the aim is to address two main questions:
• Where is the lesion?
• What is the nature of the lesion?
Abstracts | European Veterinary Conference Voorjaarsdagen 2016
Anatomical localisation of the lesion is generally necessary with neurological cases
in order to make a definitive diagnosis. This relates to the fact that the clinical signs
observed in neurological cases reflect the location of the lesion and the function of the
section of the nervous system involved far more than the underlying aetiology of the
lesion. Hence the approach should generally be to determine the lesion site, primarily
employing the neurological examination in order to do this, and then to compile a
differential diagnosis list weighted according to the anatomical location.
Comprehensive knowledge of the anatomy and the physiology of the nervous system
is very useful in clinical neurology; however, the majority of neurologic problems
in clinical practice can be diagnosed and managed through knowledge of several
principles of nervous system organisation.
Functional Arrangement of the Nervous System
Simplistically, the nervous system can be broken down into motor and sensory systems.
The motor system consists of both upper and lower motor neurons, whilst the sensory
system consists primarily of proprioception and pain sensation neurons.
The Motor System
Lower Motor Neuron
The lower motor neuron (LMN) connects the central nervous system (CNS) to an effector
organ such as muscle and is the final common pathway responsible for movement.
Lower motor neurons are located in all spinal cord segments in the intermediate
and ventral horns of the gray matter, and in cranial nerve nuclei III-VII and IX-XII in
the brainstem. In other words, LMNs can be thought of as the main components of
peripheral spinal and cranial nerves. Frequently, the identification of LMN signs can
help to specifically localise a lesion within the nervous system because the loss of reflex
function highlights specific neuroanatomic dysfunction.
Upper Motor Neuron
Upper motor neuron (UMN) is a collective term for motor systems in the CNS that
control LMNs . The UMNs are responsible for (a) the initiation and maintenance of
movement as well as (b) the maintenance of tone in the weight bearing extensor
muscles of the limbs. The UMNs originate in the intracranial structures of the brain and
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brainstem. Signs of UMN dysfunction are listed in Table 1. However, because disease at
many different levels of the nervous system may produce signs of UMN dysfunction,
these signs are rarely helpful in localising a disease to particular place. Additional more
specific signs need to be considered in this situation in contrast to the situation with
LMN signs.
The Sensory System
Pain sensation
Sensory neurons are located in the ganglia of dorsal roots along the spinal cord, and in
the ganglia of some cranial nerves. One spinal nerve innervates an area of skin called
a dermatome, which are arranged in a roughly segmental fashion. Alterations in the
sensation of a dermatome can be used to localise a lesion to a spinal nerve or a dorsal
root. The area of skin innervated by the sensory neurons of an appendicular nerve also
allow specific localisation of lesions. Superficial pain pathways are located primarily
in the dorsolateral portion of the spinal cord and project to the contralateral cerebral
cortex for conscious recognition of pain. The deep pain pathway, responsible for the
perception of severe pain from bones and joints, is a bilateral multisynaptic system,
which also projects to the cerebral cortex.
Lesions of the sensory neurons produce characteristic signs, which include (a)
anaesthesia – complete loss of pain sensation, (b) hypaesthesia – partial loss of pain
sensation, (c) hyperaesthesia – increased pain sensation, and (d) loss of reflexes.
Increased or decreased pain sensation can be assessed by pinching the skin, which can
help map out sensory nerve damage accurately. Lesions of the deep pain pathways
within the spinal cord cause loss of deep pain sensation; this is poor prognostic
indicator as it indicates severe, potential total damage to the spinal cord pathways with
limited potential for complete resolution.
Proprioception
Proprioceptive pathways are located in the dorsal and dorsolateral portions of the
spinal cord. They project to the cerebral cortex and the cerebellum. Signs of damage
to these pathways cause proprioceptive deficits and ataxia. They may often be
accompanied by weakness (motor dysfunction) due to concurrent damage to the
neighbouring motor pathways.
Abstracts | European Veterinary Conference Voorjaarsdagen 2016
Localisation of Disease within the Central Nervous System
Spinal Cord
The examination of the motor system should enable localisation of spinal disease to
one of five segments of the spinal cord. It is essential to note that the divisions of the
spinal cord listed below refer to spinal cord segments, which do not correspond exactly
with vertebrae of the same number. Motor dysfunction can also occur with brainstem
disease but there will be an association with cranial nerve dysfunction in this situation;
this is considered separately below.
The most common signs of spinal cord dysfunction are ataxia or incoordination,
weakness caudal to the lesion and spinal pain. Ataxia can also be a feature of vestibular
and cerebellar diseases (see below). The presence of focal spinal pain is localising
and suggests a compressive lesion such as disc extrusion or neoplasia (extradural or
intradural-extramedullary lesions). Non-painful spinal diseases are usually lesions that
affect the spinal cord parenchyma only (intramedullary lesions), such as degenerative
and vascular disorders. The degree of weakness of the patient often parallels the
severity of the lesion. Proprioceptive deficits are an early indicator of compressive spinal
cord lesions. In severe cases, superficial and deep pain perception are absent caudal to
the lesion. In all cases of focal spinal cord disease, whatever the location, there are no
mentation changes or signs of cranial nerve dysfunction.
Spinal Segments Cervical 1-Cervical 5
Lesions affecting the spinal cord segments C1-C5 can cause weakness or paralysis in
all four limbs (tetraparesis / tetraplegia) or in the limbs on just one side (hemiparesis).
Lesions in the centre of the spinal cord in this region can cause weakness in the thoracic
limbs with minimal deficits in the pelvic limbs (central cord syndrome). Segmental
spinal reflexes are not affected by lesions in this region of the spinal cord and therefore
remain intact. Severe lesions can cause respiratory weakness or apnoea.
Spinal Segments Cervical 6 – Thoracic 2
Lesions affecting spinal cord segments C6-T2 can result in the same pattern of motor
dysfunction in the thoracic and pelvic limbs as that seen with C1-C5 lesions, with the
addition of weak or absent spinal reflexes in the thoracic limbs. Segmental spinal
reflexes are intact in the pelvic limbs. With mild extradural lesions, the pelvic limbs can
be more severely affected than the thoracic limbs.
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Spinal Segments Thoracic 3 – Lumbar 3
Lesions affecting the T3 through L3 spinal segments may cause varying degrees of
ataxia and weakness in the pelvic limbs with normal motor function in the thoracic
limbs. The segmental spinal reflexes in all limbs remain intact with lesions in this region.
Acute lesions in this region may cause a Schiff-Sherrington posture but this does not
have prognostic significance. The cutaneous trunci reflex (panniculus) may be absent
two vertebral levels caudal to the site of the lesion.
Spinal Segments Lumbar 4 – Sacral 2
Lesions affecting the L4 through the second sacral spinal segments cause weakness in
the pelvic limbs with limited ataxia and reduced spinal reflexes (patella reflex /femoral
nerve L4-L5; flexor withdrawal reflex / sciatic nerve L6-S2).
Spinal Segments Sacral 1 – Sacral 3
Lesions affecting the sacral spinal segments can cause mild pelvic limb weakness with
reduced or absent flexor withdrawal reflexes but may predominantly cause urinary
and faecal incontinence with reduced or absent perineal or anal reflex, in addition to
reduced motor function in the tail.
Brain Stem
The brain stem includes the midbrain, pons and medulla oblongata with cranial nerves
III through XII. Severe brain stem lesions can cause severe depression, stupor or coma,
but the animal’s personality and behaviour is appropriate unless there is concurrent
cerebral disease. Tetraparesis or tetraplegia with decerebrate rigidity, conscious
proprioception deficits and intact spinal reflexes are often seen with brain stem disease.
Ipsilateral cranial nerve deficits are possible in isolation or in conjunction with central
motor and sensory dysfunction, depending on whether the cranial nerve is affected
after it has exited the brainstem or before respectively. In addition to the above signs,
there is the potential for cardiac and respiratory abnormalities, including apnoea and
cardiac arrest.
Vestibular System
The function of the vestibular system is to send messages to the brain about the
gravitational forces acting on the head and any movement that the head experiences.
The brain can then determine the position of the head in space and can coordinate
subsequent movements of the eyes and limbs.
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(i) PERIPHERAL COMPONENT
The peripheral component of the vestibular system is located in the inner ear and is
made up of a membranous labyrinth and the vestibular portion of cranial nerve VIII. This
system is intricately associated with the auditory system and is enclosed in the petrous
temporal bone close to cranial nerve VII and the sympathetic supply to the eye and face.
(ii) CENTRAL COMPONENT
The central component of the vestibular system consists of vestibular nuclei in the
caudal brainstem (medulla oblongata) and the flocculonodular lobe of the cerebellum.
These nuclei are connected to the nuclei of cranial nerves III, IV, and VI to control the
movement of the eyes so that the eyes move in a coordinated fashion with the head.
The vestibular nuclei are also connected via the vestibulospinal tract to the extensor
muscles of the neck and the limbs; they are responsible for extensor tone in the
ipsilateral limbs and cause contralateral extensor inhibition.
Clinical Signs of Vestibular Disease
Damage to either the peripheral or the central components of the vestibular system will
cause vestibular dysfunction. It is most common to see unilateral lesions and therefore
asymmetric signs but bilateral lesions are possible. The signs exhibited by the patient
depend upon the portion of the vestibular system affected. Indeed, it is important to
use these differences in lesion localization, as peripheral and central vestibular diseases
have several different differentials to be considered as well as different prognoses.
Head Tilt – this is the most common sign of unilateral vestibular disease and occurs
because of the loss of muscle tone on one side of the neck. The head tilt is towards the
side of the lesion in peripheral disease whereas it can be to any side if there is a central
lesion. Often, there is no head tilt if there is bilateral disease and instead there are wide
excursions of the head and neck from side to side.
Ataxia & Dysequilibrium – the loss of general balance that is experienced by the
animal with vestibular disease is manifested by a base-wide stance and swaying of
the head and trunk. This can progress to rolling, leaning or falling to one side with
unilateral lesions. Peripheral vestibular disease occurs without any deficits in conscious
proprioception or strength, whereas a central lesion may cause these abnormalities.
Nystagmus – this is rhythmic movement of the eyes with a fast and a slow phase. The
direction of the nystagmus is often described as the direction of the fast phase but
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can be horizontal, rotational or vertical in its direction. In normal animals, a physiologic
nystagmus should be induced by rotation of the head, with the direction being in the
plane of the head movement and the fast phase being towards the side of rotation
(this may also be termed the occulocephalic reflex). This may be altered or absent in
animals with vestibular disease. Nystagmus can be spontaneous which means that
it occurs when the head is stationary in a normal position. With unilateral peripheral
lesions, the fast phase is away from the side of the disease and the direction can be
horizontal or rotational. With central lesions, the fast phase is usually away from the
side of the disease but the direction can be vertical as well as horizontal or rotatory. If
the nystagmus is detected only when the head is placed in an unusual position, this is
called positional nystagmus and can occur with both peripheral and central lesions but
may be more common with the latter. Animals with bilateral disease usually do not have
spontaneous or positional nystagmus.
Strabismus – Vestibular disease may cause one eye to be deviated ventrally or
ventrolaterally when the neck is extended – positional strabismus. The ventrally deviated
eye is usually on the side of the lesion. Occasionally, a constant ventral strabismus is
present with vestibular disease.
Cranial Nerve Abnormalities – Peripheral vestibular lesions may be accompanied
by ipsilateral facial nerve paresis and, or Horner’s syndrome due to the anatomical
proximity of these two nerve supplies. It is possible that multiple cranial nerve defects
be present with central vestibular disease.
Cerebellum
Cerebellar disease is one of the most readily recognizable syndromes in veterinary
practice. The cerebellum coordinates movements. It controls the rate and range of
movements but not the initiation of the movement itself. Cerebellar disease results in
an inability to regulate the rate, range, and force of a movement (i.e., dysmetria). Clinical
signs include an exaggerated limb response when a movement is initiated, such as
“goose-stepping” (hypermetria) when walking. Limb movements are typically spastic
and clumsy. Initiation of movement is delayed and often accompanied by tremors (i.e.,
intention tremors). Tremors are especially noticeable involving the head. Intention
tremors disappear at rest. Fine, pendular, or oscillatory eye movements also may be
Abstracts | European Veterinary Conference Voorjaarsdagen 2016
present. A bilateral menace deficit may be noted, although vision is not affected. If the
lesion involves only one side of the cerebellum, the menace deficit will be ipsilateral.
Infrequently observed signs associated with specific areas of the cerebellum include
opisthotonus (e.g., when a lesion involves the rostral lobe of the cerebellum), and
vestibular signs (e.g., when a lesion occurs in the flocculonodular lobe or fastigial
nuclear area of the cerebellum).
Thalamus and Hypothalamus (Diencephalon)
The hypothalamus is intimately involved in autonomic visceral body functions,
including appetite, sexual activity, sleep-wake cycle, body temperature, blood pressure
regulation, heart rate, and emotions. It also regulates much of the body’s endocrine
activity. Animals with the hypothalamic syndrome may show signs of altered mental
status (e.g., disorientation, lethargy, or coma); and / or behaviour changes (e.g.,
aggression, hyperexcitability, pacing, wandering, hiding, tight circling, head pressing,
and trembling). Gait is usually normal. Abnormal temperature regulation may be
manifested as hyperthermia, hypothermia, or poikilothermia. Abnormalities in appetite
are seen as polyphagia and obesity, or anorexia and cachexia. Vision is frequently
impaired if the lesion extends to involve the optic chiasm, in which case pupils may
be dilated and weakly or non-responsive to light stimulation. Endocrine disturbances
most often include diabetes insipidus or hyperadrenocorticism (clinical signs include
polydypsia, polyuria, polyphagia, alopecia, pendulous abdomen, and muscular
weakness).
Pure thalamic lesions are infrequently reported in dogs and cats; however, signs
might include postural reaction deficits (contralateral), mild ataxia, visual deficits
(contralateral), hypalgesia (contralateral and especially involving the head), an
“adversive” syndrome (propulsive circling and head/eye deviation toward the side of
the lesion) with rostral thalamic lesions, and possible disturbances in consciousness
(depression, semi-coma) or seizures.
Cerebrum
Diseases of the cerebrum usually cause alterations in behaviour and / or mental status,
seizures, blindness with normal pupillary reactivity, and contralateral proprioception
deficits. Many animals will present with just one of these signs representing a lesion in a
focal area of the brain.
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Behavioural changes include those seen with lesions of the thalamus and
hypothalamus in addition to circling (usually to the side of the lesion), compulsive
pacing, head pressing, standing in corners, and getting trapped under furniture.
Circling however, can also be seen with lesions of the brain stem, so is not a definitively
localising sign. With cerebral disease, the animal’s gait is reasonably normal in most
cases although with severe lesions, there may be a moderate ataxia. Depression,
stupor or coma represent decreasing levels of consciousness seen with disease of the
cerebrum. These signs can also be seen with brain stem disease, so the clinician should
attempt to discern whether there is an inappropriate mentation (dementia) in addition
to the altered consciousness, which would confirm the cerebral origin of the disease.
Abstracts | European Veterinary Conference Voorjaarsdagen 2016
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