Localising Neurologic Lesions Using the NeuroMap: Spinal Cord
World Small Animal Veterinary Association World Congress Proceedings, 2013
Christine E. Thomson, BVSc (Hons), DACVIM (Neurology), DECVN, PhD
VetLearn, New Zealand Veterinary Association, Massey University, Palmerston North, New Zealand

The first step in neurology cases is to localise the lesion, but that can be challenging, particularly if it is not something you do frequently. The NeuroMap and associated table are simple aids that have been distilled from years of clinical practice and can assist you in localising lesions. As diseases are often location-specific, once you've localised the lesion, then you can list the possible causes and make a diagnostic plan.

The NeuroMap is derived from mapping the main neural functions on a diagram of the nervous system. If a lesion is in a particular area, you can read from the NeuroMap which neural functions could be disrupted and, conversely, which neural functions will be normal. Key point: Identifying both the neural functions that are disrupted and those functions that are still normal are essential in lesion localisation. Clinical signs of dysfunction indicate that a lesion is disrupting that neural system. However, if a neural system is functioning normally, that suggests the lesion is not in the region of the nervous system housing that neural system.

The Neurological Examination

The following neural functions are assessed in the neurological examination:

1.  Behaviour and arousal (awareness)

2.  Ascending sensory systems (tactile, proprioception, and nociception)

3.  Motor function

4.  Cranial nerve function

5.  Spinal reflexes

Spinal sensitivity/pain may help to further localise a spinal cord lesion. By noting from these test results which systems are functioning normally and which are abnormal, then by referring to the NeuroMap (and accompanying table), you can determine where the lesion is likely to be cited. Can a single lesion account for all the observed signs (normal and abnormal)? If not, then the animal may have a multifocal lesion, indicating specific aetiologies.

Functional Regions of the Spinal Cord

These are based around where the innervation to the limbs connects; they comprise specific spinal cord segments. In the dog, these are: cervical (C1–5: neck), cervical intumescence (C6–T2: thoracic limbs), thoracolumbar (T3–L3: trunk), lumbosacral intumescence (L4–S3: pelvic limbs and pelvic viscera), and caudal segments (Cd1–5: tail). As the clinical signs of spinal cord disease are characteristic for each of these regions, animals are considered to have a region-specific localisation: e.g., thoracolumbar disease.

Upper and Lower Motor Neurons

A UMN is confined to the central nervous system (CNS = brain and spinal cord), thus it might help to think of it as a 'central motor neuron.' An LMN has its cell body in the CNS, but the bulk of the cell (the axon) is in the periphery, thus it might help to think of it as a 'peripheral motor neuron.'


A reflex comprises three parts: sensory input from a peripheral receptor; a central connection in the brain or spinal cord for reflexes involving the cranial and spinal nerves, respectively; and output via a lower (peripheral) motor neuron that connects to the muscle via a neuromuscular junction. Damage to any one of those components will result in a reduction or loss of the reflex. Damage to LMNs results in reduced/lost reflexes, but when UMNs are damaged, reflexes will still be present; they may even be increased due to loss of inhibitory UMN influence.

UMN versus LMN Disease

When a lesion affects an intumescence (cervical or lumbosacral), it can damage cell bodies of the lower (peripheral) motor neuron cell bodies supplying the limbs, resulting in LMN signs such as reduced/lost Reflexes, Atrophy of specific muscles innervated by those LMNs, and reduced muscle Tone. Conversely, when the lesion is cranial to the intumescence, then the LMNs to that limb will be intact (good tone and intact reflex arcs); the animal is described as having UMN signs to the limbs as the upper (central) motor neuron has been compromised.

Table 1. Differentiating between UMN and LMN lesions


UMN disease

LMN disease


Normal to increased

Decreased to absent


Disuse: Mild, generalised

Neurogenic: severe, specific muscles


Normal to increased

Decreased to absent

Figure 1. The Neuro RAT (Reflexes, Atrophy, Tone)
Figure 1. The Neuro RAT (Reflexes, Atrophy, Tone)

The Neuro RAT is a useful mnemonic to help differentiate between the signs of UMN disease and LMN disease.

Sensory Function and Proprioception

Spinal cord lesions can also compromise sensory function caudal to the lesion. This can cause reduced/lost proprioception, and sensory input from the external (tactile, thermal and noxious stimuli) and the internal environment (e.g., viscera such as the distension of the urinary bladder or rectum). Proprioception is awareness of body position. Subconscious proprioception projects to a subconscious area of the brain - the cerebellum. SCP is used to keep the limbs located under the body's centre of gravity and is particularly important for setting posture both at rest and during locomotion. Thus, an animal with deficits in subconscious proprioception may stand base-wide or base-narrow, or cross its feet when ambulating, resulting in an ataxic (incoordinated) gait. Input from muscle and joint receptors is important in SCP. Conscious proprioception (CP) is projected to the sensory cortex of the contralateral forebrain and is used by the animal for voluntary or skilled motor function, e.g., the dog lifting paw to 'shake hands.' Tactile input is a key component of CP. An animal with deficits in CP may stand on top of its foot ('knuckling'). However, animals with spinal cord disease usually have both conscious and subconscious proprioceptive deficits, as both types of information travel up the spinal cord. Note: Normal proprioceptive reactions require both sensory and motor functions to be intact.


Noxious (tissue-damaging) stimuli travel via spinal nerves into the spinal cord. There they can stimulate local reflex function (e.g., withdrawal reflex). The nociceptive information is also projected to the forebrain for conscious perception. There are many nociceptive pathways travelling to the brain, bilaterally; thus only severe spinal cord lesions, compromising the width of the cord, will result in loss of nociception. If such a lesion is cranial to an intumescence, then the withdrawal reflex to that limb will still be intact, but there will be no conscious perception of the stimulus. But if the lesion is in the intumescence, both the withdrawal reflex and conscious perception will be lost.

Innervation of the Urinary Bladder and Anal Sphincter

The innervation of the urinary bladder, rectum, anal sphincter and perineum is associated mainly with the sacral spinal cord (S1–3). It receives sensory input from pelvic viscera and perineum and gives rise to parasympathetic LMNs supplying the bladder wall (for detrusor muscle tone and its contraction in urination) and somatic LMNs supplying the striated urinary and anal sphincters (urine and faecal retention). Sympathetic fibres originate from the cranial lumbar spinal cord; they stimulate contraction of smooth muscle at the neck of the bladder and relaxation of bladder wall muscle for urine storage. Sensory input synapses in the sacral spinal cord triggering reflex activity (e.g., perineal reflex) and also projects cranially to the brain, conveying information about the distension of the bladder and rectum for conscious perception. When LMNs originating in the sacral cord are damaged, there is reduced or lost muscle tone (bladder wall and sphincters) and reflexes. Such an animal will have a bladder that is large, flaccid, and easy to express; it may dribble urine. Loss of LMN supplying the anal sphincter may lead to a dilated sphincter and faecal incontinence; the perineal reflex will also be compromised. Conversely, with UMN lesions cranial to the sacral spinal cord, LMN innervation will be intact, and the bladder wall and striated urinary and anal sphincters will still have tone - thus, the bladder will be full, turgid, and difficult to express; the perineal reflex will also be intact.

Using the NeuroMap

If you cover a region of the NeuroMap with your finger or a coin (representing a lesion in it) you will be able to see which neurological functions will be compromised and which will still function normally. Conversely, if you have an animal with particular signs, you can use the NeuroMap to help localise the lesion. For example, consider an animal that is tetraparetic, with proprioceptive deficits in all four limbs and intact reflexes in all limbs. Identify on the NeuroMap where the wiring is for one of those functions. Where would a lesion have to be to compromise the proprioceptive tracts for all four limbs? C1–5 or C6–T2. Would that cause the tetraparesis? Yes. But as the thoracic reflexes are intact, then the lesion can't be at C6–T2. That makes it likely that it is a C1–5 lesion. That all fits. The pelvic limb reflexes are intact, implying that their LMN are intact - yes, that is possible with a lesion in the C1–5 region. Thus, both the signs of dysfunction and signs of normal function have helped you localise the lesion.

Figure 2. The NeuroMap for the spinal cord and spinal nerves
Figure 2. The NeuroMap for the spinal cord and spinal nerves


Table 2. Summary of effects of lesions in different areas of the spinal cord

Location of lesion

Loss of sensory input

Presence of UMN signs

Presence of LMN signs to limbs
Loss of other reflexes

Loss of urinary and faecal continence

Cervical C1–5

TL, trunk, PL, tail

TL and PL both affected

No LMN signs in TL and PL.
Cutaneous trunci and perineal reflexes intact

UMN bladdera
Faecal incontinencec

intumescence C6–T2

TL, trunk, PL, tail

PL only

TL, loss of cutaneous trunci reflex if lesion in C8–T2.
Perineal reflex intact

UMN bladder
Faecal incontinencec


Trunk (caudal to lesion), PL, tail

PL only
(TL normal)

No LMN signs in TL or PL
Cutaneous trunci reflex lost caudal to lesion, perineal reflex intact

UMN bladder
Faecal incontinence


PL, tail

No UMN signs to limbs

LMN signs in PL
Cutaneous trunci reflex intact, perineal reflex intact

UMN bladder
Faecal incontinence


Tail, PL probably normald

No UMN signs to limbs

LMN signs to pelvic viscera.
Loss of perineal reflex

LMN bladderb
LMN anal sphincter (dilated anus), faecal incontinence

Caudal nerves


No UMN signs

LMN signs to tail

Normal continence

TL = thoracic limb, PL = pelvic limb
a = UMN bladder - turgid, full, difficult to express
b = LMN bladder - flaccid, distended, easy to express, dribbling urine
c = Animal will deposit faeces with good emptying of colon, but may not be aware that it is defaecating.
Note: Whether or not all signs are present depends on lesion severity.


1.  Thomson C, Hahn C. Veterinary Neuroanatomy: A Clinical Approach. Elsevier Health Sciences; 2012. ISBN 9780702034824.


Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Christine E. Thomson, BVSc (Hons), DACVIM (Neurol), DECVN, PhD
VetLearn, New Zealand Veterinary Association
Massey University
Palmerston North, New Zealand

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