Neurology Networks tries to offer broad exposure to various topics that may be presented on the veterinary neurology board exam.

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“Measurement of distal motor latency of the suprascapular nerve in dogs.”

Bolukbasi et al.

Vet REc 2007.


Suprascapular distal motor latency measurement was easy to make, and may supply additional data in the examination of neuromuscular diseases that affect the shoulder region. The results suggest that measurements longer than 3·20 ms in male dogs, and 2·78 ms in females, should be considered to indicate a suprascapular neuropathy.






“F-wave conduction velocity, persistence, and amplitude for the tibial nerve in clinically normal cats.”

Okunu et al.

AJVR 2008.


Objective―To establish a method of F-wave evaluation and to determine normative values of F-wave parameters, including F-wave conduction velocity, persistence, and amplitude for the tibial nerve in cats.

Animals―30 clinically normal cats.

Procedures―F-waves elicited in the interosseous muscles by stimulation of the tibial nerve were recorded, and linear regression analyses of the shortest latency versus the length of the tibial nerve and the limb length were performed. F-wave persistence was calculated by dividing the number of recorded F-waves by the number of stimuli.

Results―The correlation coefficient between F-wave latency and nerve length was 0.92, and that between F-wave latency and limb length was 0.58. Mean ± SD F-wave conduction velocity of the tibial nerve was calculated to be 97.1 ± 5.0 m/s. Linear regression analysis yielded the regression equation as follows: F-wave latency (milliseconds) = 2.60 + (0.02 X nerve length ). Mean F-wave persistence and amplitude were 98.7 ± 2.3% and 1.01 ± 0.62 mV, respectively.

Conclusions and Clinical Relevance―Results indicated that nerve length should be used for nerve conduction studies of F-waves in felids. The regression equation for F-wave latency, conduction velocity, persistence, and amplitude may contribute to the diagnosis of nervous system diseases or injury in cats, such as trauma to the spinal cord or diabetic neuropathy. F-wave persistence is the number of definable Fwaves divided by the number of stimuli and provides an indication of the state of excitability of the motor neurons examined. F-wave persistence varies depending on the muscle, nerve, and stimulation frequency and is nearly 100% for the tibial nerve in humans.13 F-wave persistence decreases in humans with injuries to the proximal portion of nerves or nerve roots, as does H-reflex persistence. F-wave amplitude reflects the proportion of a motor neuron pool activated by the stimulation, it is influenced by the excitability of the motor neuron in the spinal cord or by the conduction velocity of the impulse in the motor nerve.






“Tibial Nerve Somatosensory Evoked Potentials in Dogs with Degenerative Lumbosacral Stenosis.”

Meij et al.

Vet Surg 2006.


Animals—Dogs with DLS (n1/421) and 11 clinically normal dogs, age, and weight matched.

Methods—Under anesthesia, the tibial nerve was stimulated at the caudolateral aspect of the stifle, and lumbar SEP (LSEP) were recorded percutaneously from S1 to T13 at each interspinous space. Cortical SEP (CSEP) were recorded from the scalp.

Results—LSEP were identified as the N1–P1 (latency 3–6 ms) and N2–P2 (latency 7–13ms) wave complexes in the recordings of dogs with DLS and control dogs. Latency of N1–P1 increased and that of N2–P2 decreased as the active recording electrode was moved cranially from S1 to T13. Compared with controls, latencies were significantly delayed in DLS dogs: .8 ms for N1–P1 and 1.7ms for the N2–P2 complex. CSEP were not different between groups.

Conclusions—Surface needle recording of tibial nerve SEP can be used to monitor somatosensory nerve function of pelvic limbs in dogs. In dogs with DLS, the latency of LSEP, but not of CSEP, is prolonged compared with normal dogs.




“Somatosensory evoked potentials and sensory nerve conduction velocities in the thoracic limb of mallard ducks (Anas platyrhynchos).”

Brenner et al.

AJVR 2008.


Objective—To develop a clinically applicable technique for recording cord dorsum potentials (CDPs) following stimulation of the radial and ulnar nerves and establish reference values for radial and ulnar sensory nerve conduction velocities (SNCVs) in the wings of ducks.

Animals—8 clinically normal adult female mallard ducks (Anas platyrhynchos).

Procedures—Radial and ulnar compound nerve action potentials (CNAPs) and CDPs were recorded following distal sensory nerve stimulation. The CDPs were recorded from the interarcuate space between the last cervical vertebra and the first thoracic vertebra. Surgical dissection and transection of the brachial plexus in 1 anesthetized duck were performed to identify nerve root location and confirm functional loss of nerve conduction assessed by loss of the CDP.

Results—Radial and ulnar CNAPs and CDPs were consistently recorded in all birds. Median radial SNCV was 38.3 m/s (range, 36.0 to 49.0 m/s), and ulnar SNCV was 35.3 m/s (range, 28.0 to 40.0 m/s). Surgical transection of the brachial plexus resulted in complete loss of the CDP.

Conclusions and Clinical Relevance—Measurement of radial and ulnar SNCV or CDP is feasible in isoflurane-anesthetized mallard ducks. The CDP accurately reflects sensory nerve conduction through the brachial plexus. Assessment of brachial plexus function in mallard ducks via evaluations of SNCVs and CDPs may have application for diagnosis of traumatic injuries to the brachial plexus, evaluation of neuropathies associated with exposure to toxic chemicals, and assessment of the efficacy of interventions such as brachial plexus nerve blockade.






“Middle-Latency Auditory-Evoked Potential in Acepromazine-Sedated Dogs.”

Murrell et al.

JVIM 2004.


The middle-latency auditory-evoked potential (MLAEP) has been investigated as means of monitoring anesthesia in dogs. The goals of this study were to develop a technique to record MLAEPs in awake dogs and to determine the effects of sedation. The MLAEP was recorded in 12 dogs with and without sedation with acepromazine. Three needle electrodes were inserted SC. Click stimuli were delivered biaurally. Signal acquisition, averaging, and analysis were performed by software developed in-house. Signals were recorded for 128 milliseconds, and the responses to 1,024 stimuli were averaged. The waveforms from 10 recordings were averaged, and the amplitudes and latencies of peaks that could be consistently identified were measured. Data measured were compared by means of a paired 2-sided Student’s t-test. Interpretable MLAEPs were recorded in 10 of the 12 dogs. Three peaks were consistently identified (Pa, Nb, and Pb). The latencies of these peaks were significantly (P 5 .032, .035, and .028, respectively) shorter in awake (mean 6 SD milliseconds) (Pa 5 18.85 6 1.36, Nb 5 30.50 6 3.55, and Pb 5 47.70 6 5.53) than in sedated (Pa 5 22.40 6 3.88, Nb 5 35.75 6 6.77, and Pb 5 55.30 6 10.55) dogs. The Pb amplitude was not significantly different (2.51 6 1.30 mV awake and 2.19 6 1.10 mV sedated). This study demonstrates that acepromazine sedation causes changes in MLAEP.




“Brainstem Auditory-Evoked Potential Assessment of Auditory Function and Congenital Deafness in Llamas (Lama glama) and Alpacas (L pacos).”

Gauly et al.

JVIM 2005.


Auditory function of llamas and alpacas was assessed objectively by means of brainstem auditory-evoked response audiometry (BAER) to establish the normal hearing range and to test the hypothesis of a correlation between blue eyes, white coat, and deafness. Sixty-three camelids were available for the study. Thirteen animals had blue irides; 1 animal had 1 blue and 1 pigmented iris. Wave latencies, amplitudes, and interpeak latencies were measured under general anesthetic. Click stimuli (dB ) were delivered by an insert earphone. Four to five positive peaks could be detected; waves I, II, and V were reproducible; wave II appeared infrequently; and wave IV generally merged with wave V to form a complex. Peak latencies decreased and peak amplitudes increased as stimulus intensity increased. A hearing threshold level of 10–20 dB (HL) was proposed as the normal range in llamas and alpacas. None of the animals with pigmentation of coat and iris showed any degree of hearing impairment. Seven of the 10 blue-eyed, pure-white animals were bilaterally deaf and one of them was unilaterally deaf. However, 2 blue-eyed, white animals exhibited normal hearing ability. Three blue-eyed animals with pigmented coat did not show any hearing impairment. All white animals with normal iris pigmentation had normal auditory function; so did the 1 animal with 1 normal and 1 blue iris. The high frequency (78%) of bilaterally deaf animals with pure white coat and blue iris pigmentation supports the hypothesis of a correlation between pigmentation anomalies and congenital deafness in llamas and alpacas.




“Brain auditory-evoked response in dogs.”

Wilson et al.

AJVR 2005.


**Wave characteristics

First wave begins at 1.0-1.5 msec, each successive wave at 0.5-1 msec

Amplitudes <1 uv to 6 uV

Wave IV often absent in dogs

Wave V is the positive peak immediately before the deeply negative peak

Waves I, II, V are largest, III, IV, VII, small

Wave VI usually present, wave VII usually absent

Waves III and IV may merge to form the III-IV complex

Waves IV and V may merge to form wave dominated by V

Waves I, II, III generated by CN VIII, cochlear nucleus, and superior olivary complex

Waves IV, V, VI, VII generated by one or more of: nucleus of lateral lemniscus, caudal colliculus, MGN

With the exception of waves I and II, other waves contributed by more than one structure

Cochlea does not contribute to wave I, cochelar microphonics occur before wave I and are separate from the BAER (in people)

Wave I – far-field representation of afferent CAP of CN VIII fibers as they pass through the internal auditory canal – negative trough after wave reflects activity as it exits at cerebellopontine angle

Wave II – likely proximal portion of CN VIII as it enters brainstem

Wave III – thought to be second order neurons in or near the cochlear nucleus; negative trough after III arises from trapezoid body

Waves IV and V – difficult to differentiate because of close association to each other and multiple decussations

IV – superior olivary complex in pons with likely contributions from cochlear nucleus and nucleus lateral lemniscus

V – termination of lateral lemniscus fibers in the contralateral caudal colliculus

VI, VII – potentially thalamus, potentially caudal colliculus


Nonpathologic Subject features

**Effect of age

BAER can be recorded after approximately 2 weeks of age, waves I and II appear first; adult levels by 6-8 weeks

Caudal to rostral development of brain with increased neuronal myelination contributes

Amplitudes increase, latencies decrease, and response to lower decibels improves

**Hypothermia leads to increased latency

**Ototoxic drug effects – antimicrobials, loop diuretics, lidocaine, high dose phenytoin, alcohol

            Complete loss observed after IV admin of neomycin

            No changes with chlorihexidine or entamicing instilled in the ears x 21 days

            Reversible changes after kanamycin administered IV

            IV admin of thiamylal and inhaled 3% methoxyflurane has been shown to prolong latencies


Stimulus factors


  1. msec stimulus

Wave I thought to reflext high frequency (more basal) activity while wave V reflects midfrequency (mor apical) activity

Tone bursts – short duration tones that attempt to balance the rapid onset of the click with the frequency specificity of the tone


decibels sound pressure level (dBSPL) – absolute physical measure of sound intensity (referenced to 20 micropascals)

decibels peak equivalent sound pressure level (dBpeSPL)– measure of intensity of a complex sound (simple sound laid over complex so has same maximum amplitude)

decibels hearing level (dBHL)– threshold of hearing of young healthy adult human (0 is quietest) for pure tone; dBnHL refers to not pure tone

decibels sensation level (dBSL)– number of decibels above an individuals threshold

Amplitudes increase and latencies decrease with higher stimulus intensity, but interwave latencies remain stable

As stimulus decreases to less than 50 dBSL in dogs, waves IV, VI, and VII begin to disappear, followed by I, II, and III until only V remains

            Wave V considered the BAER threshold (<25 dBnHL in dogs with normal hearing)

High intensity activates the basilar membrane at the base of the cochlea; moves progressively towards apical end with lower stimulus intensities

At high stimulus intensities, can be transmitted via skull from test ear directly to cochlea of non-test ear (cross-over effect)


Stimulus rates up to 20 clicks/sec have little effect on BAER; above this, latencies increase and amplitudes decrease


Rarefacting pulls toward transducer  – initially depolarizes cochelar hair cells yielding BAER responses with shorter latency and greater amplitude

Condensing pushes tympanic membrane away from transducer – initially hyperpolarizes

Alternating – cancels out the stimulus related electromagnetic and cochlear microphonic artifacts associated with each polarity

Conflicting opinions as to which is best



Insert earphone – reduces electrical artifact and prevents auditory canals from closing, may delay 0.8-1.0 msec

Bone conductor – useful when significant conductive hearing loss is suspected; has large amount of electrical artifact which limits recordings to stimulus intensities below 40 dBnHL

**Binaural stimulation causes amplitudes to increase


Recording factors

**Analysis time – 10 msecs (must finished by 8 msec, 9 msec with insert earphones)

**Electrode placement

            Noninverting (active) – vertex

            Inverting (reference) – rostral to tragus of test ear

            Ground – rostral to tragus of non-test ear

Moving even a short distance from midline has big effect on wave I


100,000-150,000 gain setting because wave forms are so small


High pass filters pass frequencies higher than their cut-off; Low pass filters pass frequencies lower than their cut-off

BAER contains frequencies ranging from 30-1960 Hz

**Averaging – do approximately 1000 sweeps

**Recommended protocols

Suprathreshold >70 dBnHL

**Wave form analysis

            Waveform morphology

                        Is there waveform?

                        All clinically important waves present?

                        Sharply defined or morphologically degraded?

            Waveform repeatability

                        Do waves overlay well?

                        Frequencies similar?

            Absolute wave latencies

            Interwave latencies

            Interaural comparisons – similar between ears?

            Wave amplitudes

**Site-of-lesion diagnostic tool

            Conductive lesions in outer/middle ear – affect wave I, delay onset and reduce amplitude; interwave latencies remain the same (same effect as reduction in stimulus level)

            Sensory lesion in inner ear – similar to conductive with delayed latency and reduced amplitude with normal interwave latencies; at high stimulus intensities may look normal; complete loss of inner function à flatline BAER

            Neural lesions of CN VIII – BAER waves absent, delayed, or deduced in amplitude

            Lesion between CN VIII and caudal brainstem, wave I may be normal but II and after may be absent, delayed, or decreased in amplitude; often creates a delayed interwave latency between the early but not the late waves

            Lesion in rostral brain stem – early waves normal but later waves absent, delayed, or reduced in amplitude

            Key finding that differentiates neural lesion in CN VIII or brainstem from outer, middle, or inner ear is prolonged interwave latency




“Frequency-specific Electric Response Audiometry (ERA) and its clinical application in the diagnosis of hearing defects in the dog.”

Schacks et al.

Vet Quarterly 2006.


Useful for detecting partial high and low frequency hearing loss; 1-4 kHz




“The Use of Cont ralateral Masking Noise in the Detect ion of Unilateral Deafnes s in Dalmatian Puppies.”

Goncalves et al.

JVIM 2008.


Methods: The BAER was elicited with 80 and 100 dB normalized hearing level (dBnHL) stimulus intensity in the deaf ear. The 100 dBnHL stimulus was repeated while simultaneously applying 80 dBnHL white masking noise to the nontest ear.

Results: Ten dogs were excluded because of BAER trace baseline fluctuation. In the remaining 46 dogs, 8 dogs had no waveforms,nbut 38 dogs had an identifiable wave-V in the deaf ear BAER at 80 dBnHL intensity stimulus. At 100 dBnHL intensity stimulus, all but 1 dog had a discernible wave-V in the deaf ear BAER. The deaf ear BAER waveforms were abolished by white masking noise at 80 dBnHL in the nontest ear in all dogs.

Conclusions and Clinical Importance: Abolition of BAER wave-V in the deaf ear by white masking noise in the nontest ear suggests that this wave is caused by the crossover effect. b distribution indicates 95% confidence that white masking noise, at 20 dB below click stimulus intensity, would abolish this crossover effect in over 90% of the dogs. This supports using masking noise in the nontest ear during canine BAER.






“Diagnosis of Rapid Eye Movement Sleep Disorder With Electroencephalography and Treatment With Tricyclic Antidepressants in a Dog.”

Bush et al.

JAAHA 2004.


A 9-month-old, female Labrador retriever mix was presented for two types of seizure-like episodes, one of which occurred only during sleep. The two types of episodes were morphologically distinct. An electroencephalogram (EEG) demonstrated that the sleep-associated episodes occurred during rapid eye movement (REM) sleep, supporting a diagnosis of a REM behavior disorder. Based on their morphology and response to antiseizure medications, the waking episodes were diagnosed as seizures. The animal was also diagnosed with an obsessive-compulsive and generalized anxiety disorder. The REM behavior disorder and anxiety-related behaviors improved with tricyclic antidepressant therapy. Rhythmic jaw movements, padding, standing up disoriented before going back down. Responded to Phenobarb and returned when off




“Electroencephalography Findings in Heal thy and Finnish Spitz Dogs with Epilepsy: Visual and Background Quantitative Analysis.”

Jeserevics et al.

JVIM 2007.


Animals: Sixteen healthy and 15 Finnish Spitz dogs with epilepsy.

Methods: A prospective clinical EEG study performed under medetomidine sedation. Blinded visual and quantitative EEG analyses were performed and results were compared between study groups.

Results: Benign epileptiform transients of sleep and sleep spindles were a frequent finding in a majority of animals from both groups. The EEG analysis detected epileptiform activity in 3 Finnish Spitz dogs with epilepsy and in 1 healthy Finnish Spitz dog. Epileptiform activity was characterized by spikes, polyspikes, and spike slow wave complexes in posterior-occipital derivation in dogs with epilepsy and with midline spikes in control dog. The healthy dogs showed significantly less theta and beta activity than did the dogs with epilepsy (P , .01), but the only significant difference between healthy dogs and dogs with untreated epilepsy was in the alpha band (P , .001). Phenobarbital treatment increased alpha, beta (P , .001), and theta (P ,.01), and decreased delta (P , .001) frequency bands compared with dogs with untreated epilepsy.

Conclusions and Clinical Importance: Benign epileptiform transients of sleep could be easily misinterpreted as epileptiform activity. Epileptiform activity in Finnish Spitz dogs with epilepsy seems to originate from a posterior-occipital location. The EEG of dogs with epilepsy exhibited a significant difference in background frequency bands compared with the control dogs. Phenobarbital treatment markedly influenced all background activity bands. Quantitative EEG analysis, in addition to visual analysis, seems to be a useful tool in the examination of patients with epilepsy.






“Evoked potentials induced by transcranial stimulation in dogs.”

Kraus et al.

AJVR 1990.


Evoked potentials were induced by transcranial stimulation and recovered from the spinal cord, and the radial and sciatic nerves in six dogs. Stimulation was accomplished with an anode placed on the skin over the area of the motor cortex. Evoked potentials were recovered from the thoracic and lumbar spinal cord by electrodes placed transcutaneously in the ligamentum flavum. Evoked potentials were recovered from the radial and sciatic nerves by surgical exposure and electrodes placed in the perineurium. Signals from 100 repetitive stimuli were averaged and analyzed. Waveforms were analyzed for amplitude and latency. Conduction velocities were estimated from wave latencies and distance traveled. The technique allowed recovery of evoked potentials that had similar characteristics among all dogs. Conduction velocities of potentials recovered from the radial and sciatic nerves suggested stimulation of motor pathways; however, the exact origin and pathway of these waves is unknown.




“Magnetic Motor Evoked Potentials in Ponies.”

Mayhew et al.

JVIM 1996.


Increasing stimulator output resulted in shorter latency and higher amplitude of the evoked responses. A consistent, well-defined early waveform and 2 less well defined, slower evoked potentials were identified (Fig 3). Latencies of early (approximately 20 milliseconds for ECRM and 30 milliseconds for CTM) potentials were measured from tracings that were consistent and of robust amplitude requiring settings of 80% to 100% stimulator output. Recorded waveforms were of better quality and of greater amplitude from ECRM than from CTM. Motor pathway conduction velocities to the forelimb and hindlimb were determined to be 53.8 5 9.6 m/s-’ and 63.4 5 8.3 mls-’, respectively.




“Correlation between severity of clinical signs and motor evoked potentials after transcranial magnetic stimulation in large-breed dogs with cervical spinal cord disease.”

Poma et al.

JAVMA 2002.


Objective—To evaluate use of transcranial magnetic motor evoked potentials for assessment of the functional integrity of the cervical spinal cord in largebreed dogs with cervical spinal cord disease.

Design—Randomized, controlled, masked study.

Animals—10 healthy large-breed control dogs and 25 large-breed dogs with cervical spinal cord diseases.

Procedure—Affected dogs were allocated to 3 groups on the basis of neurologic status: signs of neck pain alone, ambulatory with ataxia in all limbs, or nonambulatory. Transcranial magnetic stimulation was performed on each dog with the same standard technique. Motor evoked potentials (MEP) were recorded from electrodes inserted in the tibialis cranialis muscle. Following the procedure, each dog was anesthetized and cervical radiography, CSF analysis, and cervical myelography were performed. The MEP latencies and amplitudes were correlated with neurologic status of the dogs after correction for neuronal path length.

Results—Mean MEP latencies and amplitudes were significantly different between control dogs and dogs in each of the 3 neurologic categories, but were not significantly different among dogs in the 3 neurologic categories. A linear association was evident between MEP latencies and amplitudes and severity of neurologic deficits; the more severe the neurologic deficits, the more prolonged the latencies and the more decreased the amplitudes.

Conclusions and Clinical Relevance—Transcranial magnetic MEP are useful to assess severity of cervical spinal cord disease in large-breed dogs. Impairment of the functional integrity of the cervical spinal cord was found even in dogs with neck pain alone.




“Transcranial magnetic stimulation: review of the technique, basic principles and applications.”

Nollet et al.

Vet Jour 2003.


Magnetic stimulation is a technique for stimulating peripheral nerves and cerebral cortex in order to help quantify the integrity of the motor nervous system, especially to measure conduction times. Its purpose is to create a pulsed electric current, induced by the timevarying magnetic field that will momentarily depolarise the nervous system. It is important to acknowledge that the actual pathways being investigated are not known; however, they incorporate the fastest conducting fibres which presumably include the pyramidal tracts (in humans). A magnetic field is generated by passing an electric current through a coil of wire, called the magnetic coil (Fig. 1), which is placed above the scalp. Faraday!s law (Faraday, 1839) says that whenever a magnetic field changes there is an induced electric field which impedes the changing magnetic field. The magnetic pulse produced from an electric current pulse will thus induce in turn a current in an electrically conductive region, such as the human or animal body. This induced electric current flows perpendicularly to the magnetic field and circulates up to a few centimetres away from the coil!s external edge, and with a direction opposite to the current flowing in the coil and an intensity proportional to the magnetic field. Such a rapidly changing magnetic field induces electric eddy currents in any conductive structures nearby. Because the skull presents a low impedance to magnetic fields of this frequency, eddy currents are produced in the brain, and these currents can stimulate neural tissue. Currents induced on the scalp by magnetic stimulation are much weaker than those produced by transcranial electrical stimulation, because they crossed the extracerebral layers (scalp, skull and meninges) with minimal or no activation of the pain receptors and resulted in a well tolerated procedure. The magnetic motor evoked potential (MMEP) testing can be regarded as a counterpart of the longer-established procedure of somatosensory evoked potential (SSEP) monitoring, where small ‘‘cortical’’ potentials are recorded over the scalp in response to peripheral nerve stimulation. When magnetic stimulation is performed on the motor cortex, electromyographic responses (MMEPs, magnetic motor evoked potentials) can be recorded in contralateral, particularly distal, appendicular muscles. However, large pulses of magnetic field need to be generated in order to induce electric fields in the body of sufficient amplitude and duration to cause stimulation of the neural tissue in its vicinity. Magnetic stimulation has three main advantages over conventional electrical stimulation. First, the primary benefit of magnetic stimulation is its ability to penetrate all body structures without attenuation. Because this increased field penetration compared to surface electrical stimulation, it allows to stimulate regions below layers of bone, for instance the brain. The cells are still activated by electric currents, but the magnetic field penetrates the tissue more efficiently and induces current within the brain itself. The mechanism of stimulation at the neural level is thought to be the same for both magnetic and electrical stimulation, namely current passes across a nerve membrane and into the axon, resulting in depolarisation and the initiation of an action potential that then propagates by the normal method of nerve conduction. Although the magnetic field and hence the induced electric field theoretically should be unaffected by the bone of the spine, there is however a stimulation of the nerve roots at their spinal exit but not the spinal cord when the magnetic coil is placed over the spine. Machida et al. (1992) showed that magnetic stimulation could excite the thoracolumbar spinal cord after laminectomy and pediculotomy in dogs. It is suggested that the bony structure surrounding the spinal cord interferes with the spread of magnetically induced eddy currents to the spinal cord. Therefore, the bony vertebrae act as an insulator between the spinal cord and the external tissue and the current probably tends to flow around the spinal cord rather than through it. Hence stronger magnetic fields are needed for spinal stimulation and novel coil geometries may be able to improve the coupling between the induced currents and the anatomy of the spine. Magnetic stimulation differs from electrical stimulation in that it uses a pulse of magnetic field to cause an electric field (a voltage difference between two points) in the tissue and results in stimulation. Hence the magnetic field functions as the vehicle that causes ion flow (or electric current) in the body and does not itself stimulate the nerve. The magnetic field generated by the current flow in the coil is proportional to the rate of change of the magnetic field with respect to time. At the frequencies used in magnetic stimulation, the magnetic field is not affected by the electrical properties of the body and passes through both bone and soft tissue (and even clothing and air) without being affected by them and without causing large electrical fields at the surface. The electric field resulting from magnetic stimulation is much more homogeneous and is parallel to the surface of the coil at all points and hence will tend to stimulate structures with a different orientation Magnetic stimulation does not require either physical or electrical contact with the body.

Measuring parameters –

MMEP latency is affected by the size of the fibre, the abundance of myelin, and the number of synapses the impulse must cross. The configuration of the MMEPs evoked in the muscles of the hand is in most instances bi- or triphasic (Maertens de Noordhout, 1998). A polyphasic configuration (more than five phases) has to be considered as abnormal in those muscles, whereas a polyphasic configuration is more frequently seen with MMEPs evoked in more proximal muscles and muscles of the leg, even in normal subjects.




“Role of transcranial magnetic stimulation in differentiating motor nervous tract disorders from other causes of recumbency in four horses and one donkey.”

Nollet et al.

Vet Rec 2005.


Transcranial magnetic stimulation and measurement of the magnetic motor-evoked potentials (MMEPs) in the thoracic and pelvic limbs of four recumbent horses and one recumbent donkey were used to assess the integrity of the descending motor pathways, in order to confirm or exclude a descending motor tract lesion as the cause of the recumbency. In two of the animals abnormal MMEPs were recorded; in one of the horses a lesion along the cervical spinal cord due to a fracture of the fifth cervical vertebra was diagnosed and confirmed by radiography and postmortem examination; in another horse, damage to the peripheral nerves of the left forelimb was diagnosed and confirmed postmortem when a large abscess was found to have been compressing the peripheral nerves at the level of the last cervical vertebra. In the three other animals, normal MMEPs were recorded, and laminitis, rhabdomyolysis and physitis were diagnosed as the causes of the recumbency.






“Magnetic stimulation of the radial nerve in dogs and cats with brachial plexus trauma: A report of 53 cases.”

Van Soens et al.


Magnetic stimulation of the radial nerve and consequent recording of the magnetic motor evoked potential (MMEP) was examined in 36 dogs and 17 cats with unilateral brachial plexus trauma. In 22 dogs and 12 cats, magnetic stimulation of the radial nerve resulted in biphasic to polyphasic potentials. However, in 14 dogs and 5 cats, no MMEP could be evoked in the affected thoracic limb. Statistically significant differences in onset latencies and peak-to-peak amplitudes were found between the normal and the affected thoracic limb in all animals. In all animals, the inability to evoke a MMEP after magnetic stimulation in the affected limb resulted in an unsuccessful outcome. Between affected limbs, a significant difference in peak-to-peak amplitude in dogs with an unsuccessful versus a successful outcome was found; i.e. peak-to-peak amplitude in dogs with an unsuccessful outcome was significantly lower than peak-to-peak amplitude in dogs with a successful outcome. Interestingly, even in the animals that were presented earlier than 5 days after the traumatic injury, statistically significant differences were found between the affected and the normal limb. These findings may indicate the value of magnetic stimulation as an early electrodiagnostic tool in comparison to electromyography.




“Magnetic stimulation of peripheral nerves in dogs: A pilot study.”

Van Soens et al.

Vet Jour 2008.


The results demonstrate that magnetic stimulation is a feasible method for stimulating the radial and sciatic nerves in dogs. No significant differences were observed in onset-latencies and peak-to-peak amplitudes during magnetic and electrical stimulation, indicating conformity between the techniques. Orthodromic or antidromic magnetic nerve stimulation resulted in no significant differences. For magnetic stimulation of the radial nerve, the magnetic coil was placed in the axillary region, medial to the radial nerve, and the cranial part of the circle on the coil was held tangentially to the radial nerve (Fig. 1). For magnetic stimulation of the sciatic nerve, the magnetic coil was placed lateral to the hind limb and the caudal part of the circle on the coil was held tangentially to the sciatic nerve between the greater trochanter and the ischial tuberosity.  The disadvantages of the technique are (1) problems in obtaining a consistent supramaximal response as compared to the response obtained after electrical stimulation and (2) defining the exact site of localization.






“Quantitative assessment of nociceptive processes in conscious dogs by use of the nociceptive withdrawal reflex.”

Bergadano et al.

AJVR 2006.


Conclusions and Clinical Relevance—In dogs, the NWR can be evoked from limbs and correlates with behavioral reactions. Results suggest that NWR evaluation may enable quantification of nociceptive system

excitability and efficacy of analgesics in individual dogs.




“Assessment of impulse duration thresholds for electrical stimulation of muscles (chronaxy) in dogs.”

Swaya et al.

AJVR 2008.


Objective—To determine the electrical impulse duration thresholds (chronaxy) for maximal motor contraction of various muscles without stimulation of pain fibers in dogs.

Animals—10 healthy adult Beagles.

Procedures—The dogs were used to assess the minimal intensity (rheobase) required to elicit motor contraction of 11 muscles (5 in the forelimb , 5 in the hind limb , and the erector spinae). The rheobase was used to determine the chronaxy for each of the 11 muscles in the 10 dogs; chronaxy values were compared with those reported for the corresponding muscles in humans.

Results—Compared with values in humans, chronaxy values for stimulation of Aα motor fibers in the biceps femoris and semitendinosus muscles and muscles of the more distal portions of limbs were lower in dogs. For the other muscles evaluated, chronaxy values did not differ between dogs and humans.

Conclusions and Clinical Relevance—Application of the dog-specific chronaxy values when performing electrical stimulation for strengthening muscles or providing pain relief is likely to minimize the pain perceived during treatment in dogs.

The electric current delivered to the motor nerve to generate these muscle contractions has to be greater than a threshold value to depolarize Aα (motor) nerve fibers and create muscle contractions.4–7 Theoretically, the rheobase is the intensity threshold that leads to Aα fiber depolarization when the pulse duration is infinitely long; practically, the rheobase is determined by use of pulse duration > 100 milliseconds. The chronaxy of a muscle is the pulse duration needed to obtain Aα fiber depolarization with an intensity value twice that of the rheobase. For each muscle, intensity (l), pulse duration (t), rheobase (Rh), and chronaxy (Ch) are linked as follows: I = Rh (Ch/t + 1). The chronaxy of each muscle is considered to be the optimal pulse duration required to depolarize Aα fibers and create muscle contraction without stimulating Aδ and C nociceptive fibers.

Muscle chronaxy ranged from 100 to 300 microseconds (mean values, 155 to 270 microseconds).

The differences between chronaxy values in humans and dogs are likely linked to the differing proportions of slow- (type I) and fast-twitch (type II) fibers in hind limb muscles and in the more distal portion of the forelimb.

The hind limbs of quadrupeds in general and of dogs in particular have a high proportion of fast-twitch fibers, compared with the legs of humans.18–23 Fast-twitch fibers are activated by motor nerves that have action potentials with higher conduction velocity and higher motor neuron discharge frequency than the action potentials of motor nerves that activate slow-twitch fibers.24 These fast-twitch fibers have shorter chronaxy values than slow-twitch fibers.25

Muscle chronaxy is primarily influenced by abnormalities of peripheral nerves and neuromuscular junctions.41 During temporary denervation, muscle chronaxy increases within a few days of denervation

and returns to predenervation values over a period of weeks to months.42–44 Change in chronaxy, combined with assessment of nerve accommodation index, is 100% sensitive for detection of denervations that are complete or have a sudden onset.