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. 2023 Oct 17;9(6):2404–2409. doi: 10.1002/vms3.1308

Schiff–Sherrington phenomenon in a cat with complete spinal cord transection from traumatic dorsocranial luxation of the second lumbar vertebra

Christopher T Holland 1,✉
PMCID: PMC10650366  PMID: 37846941

Abstract

A young stray entire female domestic shorthair cat was presented with symmetrical forelimb extensor rigidity, neck hyperextension and hindlimb paraplegia, characteristic of Schiff–Sherrington phenomenon (SSP), within 30 min of a motor vehicle accident. Radiographic and post‐mortem studies disclosed complete transection of the spinal cord from traumatic dorsocranial luxation of the second lumbar vertebra, displacement of the sacrum from the ilium, seventh lumbar and first caudal vertebrae and multiple pelvic fractures. Other causes of forelimb extensor rigidity and neck hyperextension such as decerebrate and decerebellate rigidity were excluded by a lack of neurological signs consistent with these entities and unremarkable findings on post‐mortem examination of the cranial cavity and brain and histological examination of the cerebrum, brainstem and cerebellum. To the best of the author's knowledge, this is the first report of SSP in the cat outside the experimental arena of decerebrate or non‐decerebrate preparations following post‐brachial spinal cord transection/cold block.

Keywords: feline, Schiff–Sherrington phenomenon, spinal cord transection, spinal cord trauma, vertebral luxation

A young domestic shorthair cat presented with symmetrical forelimb extensor rigidity, neck hyperextension and hindlimb paraplegia, characteristic of Schiff–Sherrington phenomenon, within 30 min of a motor vehicle accident, due to complete transection of the spinal cord from traumatic dorsocranial luxation of the second lumbar vertebra. Other causes of forelimb extensor rigidity and neck hyperextension such as decerebrate and decerebellate rigidity were excluded by a lack of neurological and post‐mortem findings consistent with these entities. This is the first case report of Schiff–Sherrington phenomenon in the cat outside the experimental setting of decerebrate or non‐decerebrate preparations following post‐brachial spinal cord transection/cold block.

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1. INTRODUCTION

Schiff–Sherrington phenomenon (SSP), variously termed Schiff–Sherrington posture, syndrome or sign, is a well‐recognized entity in small animal neurology (Bagley, 2005; Braund, 1994; Chrisman, 1991; Chrisman et al., 2003; De Lahunta et al., 2020b; Dewey, 2016; Fitzmaurice, 2010; Freeman & Ives, 2020; Garosi, 2012; Griffiths, 1987; Jaggy & Platt, 2010; LeCouteur, 1986; LeCouteur & Child, 1989; Lorenz et al., 2011; Messonnier, 2000; Olby, 2013; Palmer, 1975; Sharp & Wheeler, 2005; Thomson & Hahn, 2012; Wheeler & Thomas, 1996). It is characterised by forelimb extensor rigidity (Bagley, 2005; Braund, 1994; Chrisman, 1991; Chrisman et al., 2003; De Lahunta et al., 2020b; Dewey, 2016; Fitzmaurice, 2010; Freeman & Ives, 2020; Garosi, 2012; Griffiths, 1987; Jaggy & Platt, 2010; LeCouteur, 1986; LeCouteur & Child, 1989; Lorenz et al., 2011; Messonnier, 2000; Olby, 2013; Palmer, 1975; Sharp & Wheeler, 2005; Thomson & Hahn, 2012; Wheeler & Thomas, 1996), neck hyperextension (Jaggy & Platt, 2010; LeCouteur & Child, 1989; Sharp & Wheeler, 2005) and hindlimb paraplegia that is often affected by transient spinal shock (Chrisman, 1991; De Lahunta et al., 2020b; Garosi, 2012; Lorenz et al., 2011; Thomson & Hahn, 2012). SSP arises as a consequence of a severe peracute transverse T3 to L3 myelopathy, usually attributable to spinal cord trauma, and less frequently, spinal cord infarction or peracute intervertebral disc extrusion (Chrisman, 1991; De Lahunta et al., 2020b; Freeman & Ives, 2020; Garosi, 2012; Lorenz et al., 2011; Thomson & Hahn, 2012).

While SSP is frequently described in the dog (Bagley, 2005; Braund, 1994; Chrisman, 1991; Chrisman et al., 2003; De Lahunta et al., 2020b; Dewey, 2016; Fitzmaurice, 2010; Freeman & Ives, 2020; Garosi, 2012; Griffiths, 1987; Jaggy & Platt, 2010; LeCouteur, 1986; LeCouteur & Child, 1989; Lorenz et al., 2011; Messonnier, 2000; Olby, 2013; Palmer, 1975; Sharp & Wheeler, 2005; Thomson & Hahn, 2012; Wheeler & Thomas, 1996), its occurrence in the cat outside the experimental arena of decerebrate or non‐decerebrate preparations following post‐brachial spinal cord transection or cold block (Morrison & Bowker, 1971; Ruch, 1936; Ruch & Watts, 1934; Schadt & Barnes, 1980; Sprague, 1953; Wang, 1958) is poorly defined. Current textbooks of small animal neurology (Bagley, 2005; Braund, 1994; Chrisman, 1991; Chrisman et al., 2003; De Lahunta et al., 2020b; Dewey, 2016; Fitzmaurice, 2010; Freeman & Ives, 2020; Garosi, 2012; Griffiths, 1987; Jaggy & Platt, 2010; LeCouteur, 1986; Lorenz et al., 2011; Messonnier, 2000; Olby, 2013; Palmer, 1975; Sharp & Wheeler, 2005; Thomson & Hahn, 2012; Wheeler & Thomas, 1996), and their earlier editions, invariably refer to SSP in the dog or discuss its occurrence generically without specific reference to the cat. Likewise, no mention is given to SSP in many reviews on feline spinal cord disease (Goncalves et al., 2009; Marioni‐Henry, 2010; Marioni‐Henry et al., 2004), although it is discussed in one (LeCouteur, 2003) and described as ‘rarely seen in the cat’ in two others (Scott et al., 2021a, 2021b); however, corroborating data or citations to support these observations are lacking. From seven retrospective studies on spinal cord trauma in either the cat (Besalti et al., 2002; Grasmueck & Steffen, 2004) or cats and dogs (Bali et al., 2009; Bruce et al., 2008; Carberry et al., 1989; McKee, 1990; Selcer et al., 1991), totalling 199 feline cases, SSP was not described in any cat, and to the best of this author's knowledge no case reports or case series have been published in the peer‐reviewed veterinary literature.

The aim of the present report is to document the occurrence of SSP in a cat with complete traumatic transection of the spinal cord between the first and second lumbar vertebrae as a result of a motor vehicle accident.

2. CASE DESCRIPTION

A young (exact age unknown) stray entire female domestic shorthair cat weighing 4.2 kg was presented by a member of the public who had witnessed and then rescued the cat within 30 min of being run over by a motor vehicle. Clinical examination revealed tachycardia (200 beats/min), variable splintering of the nails of all paws and multiple small wounds around the perineum. Neurological examination disclosed symmetric hypotonic hindlimb paraplegia accompanied by hyperextension of the neck and a bilaterally symmetrical increase in forelimb extensor tone that was more pronounced in lateral recumbency (Figure 1). Patella reflexes were bilaterally increased, while the cranial tibial, gastrocnemius, flexor reflexes, as well as nociception were absent in the hindlimbs. The tail was flaccid, immobile and analgesic. Anal tone, perianal sensation and perianal reflexes were absent. The cutaneous trunci reflex was bilaterally absent caudal to the dorsal spinous process of the 12th thoracic vertebra. Despite these signs, conscious movement, proprioceptive positioning, hopping, visual and non‐visual wheelbarrowing, visual and non‐visual placing and sensation were symmetrically normal in the forelimbs, albeit under a prevailing level of increased extensor tone. In both forelimbs, flexor reflexes were judged as symmetrically normal; however, the biceps, triceps and extensor carpi radialis reflexes could not be elicited in the hyperextended state. Notably, consciousness was unimpaired and the resting pupillary diameters were equal and appropriate for the level of examination room lighting. Visual following, menace response, dazzle reflex, the oculocephalic reflex and direct and consensual pupillary light reflexes were normal in both eyes as well as the remaining cranial nerve examination.

FIGURE 1.

FIGURE 1

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Conscious cat in right lateral recumbency with symmetrical hindlimb paraplegia, hyperextension of the neck and bilaterally symmetrical increase in forelimb extensor tone characteristic of Schiff–Sherrington phenomenon.

A single, conscious right lateral plain radiograph revealed marked dorsocranial displacement/luxation of the second lumbar vertebra relative to the first lumbar vertebra, displacement of the sacrum from the ilium, seventh lumbar and first caudal vertebrae and multiple pelvic fractures with a compound fracture of the left ischium (Figure 2). The skull, mandible, cervical and thoracic vertebral column, rib cage, sternum, forelimbs, hindlimbs, thorax and abdomen were unremarkable and no microchip was evident. On prognostic, compassionate and ethical grounds, the cat was humanely euthanized and the body kept in a frozen state (−18°C) to allow for possible owner reclamation.

FIGURE 2.

FIGURE 2

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Conscious right lateral plain radiograph of the cat showing marked dorsocranial displacement/luxation of the second lumbar vertebra relative to the first lumbar vertebra, displacement of the sacrum from the ilium, seventh lumbar and first caudal vertebrae and multiple pelvic fractures. Note the hyperextension of the neck and forelimbs.

After an appropriate period, when no person could be found or came forward to identify and claim ownership of the cat, the body was allowed to thaw at room temperature for 36 h and additional assessment was undertaken. Plain dorsoventral radiographs of the skull and entire vertebral column and pelvis showed left‐sided dorsocranial displacement of the luxated second lumbar vertebra with no other additional abnormalities identified. On post‐mortem examination, all internal organs were intact, the cat was in an early stage of pregnancy and no thoracic, pericardial, abdominal or retroperitoneal effusions were evident. The spinal cord was completely transected between the luxated first and second lumbar vertebrae (Figure 3). The brain, meninges and internal surfaces of the calvaria were all unremarkable. There was no evidence of calvarial fractures, brain contusion, tearing of neuronal tissues, falcine, transtentorial or foraminal herniation or epidural, subarachnoid or subdural space haemorrhage. The brain was placed in 10% neutral buffered formalin, kept for 5 days before repeat gross examination and scrutiny of multiple transverse sections disclosed no abnormal findings or intra‐parenchyma or ventricular system haemorrhage. Notably, the midbrain, rostral cerebellum, pons and medulla were unremarkable. Apart from significant freeze–thaw artefact, no lesions were identified on histopathological examination of the brain.

FIGURE 3.

FIGURE 3

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Post‐mortem dissection of the dorsal thoracolumbar vertebral column revealing complete spinal cord transection due to marked left dorsocranial displacement of the second lumbar vertebra (L2) relative to the first lumbar vertebra (L1).

3. DISCUSSION

This is the first report of SSP in a cat outside experimental settings which resulted from a complete traumatic spinal cord transection between the first and second lumbar vertebrae due to a motor vehicle accident.

In 1934, Ruch and Watts (Ruch, 1936; Ruch & Watts, 1934) detailed the increase in excitability of extensor and decrease in excitability of flexor muscles that occurred in the forelimbs of decerebrate cats following post‐brachial spinal cord transection and introduced the eponym SSP, in deference to earlier accounts of this phenomenon by Schiff in frogs in 1858 (Schiff, 1858) and subsequently, without knowledge of Schiff's work, by Sherrington in cats in 1898 (Sherrington, 1898).

The neural substrate subserving SSP originates from large neurons termed ‘border’ or ‘Cooper–Sherrington’ cells lying in a fringe of grey matter bordering the ventrolateral white columns (also termed the dorsolateral nucleus) (Cooper & Sherrington, 1940; Sprague, 1953). A majority of border cell axons cross at their point of origin to ascend deep in the contralateral lateral funiculus (Cooper & Sherrington, 1940; Sprague, 1953) (likely within the fasciculus proprius [De Lahunta, 1983]) to inhibit extensor and facilitate flexor motor neurons in the cervical intumescence (Ruch, 1936; Ruch & Watts, 1934; Sprague, 1953). When cervicothoracic motor neurons lack border cell input due to transverse thoracolumbar myelopathy, extensor muscle tone increases, while flexor muscle tone decreases (Ruch, 1936; Ruch & Watts, 1934; Sprague, 1953), secondary to hypo‐polarisation of extensor and hyper‐polarisation of flexor motor neurons (Schadt & Barnes, 1980), hence indicating the classic signs of SSP.

When mentioned in the veterinary neurological literature, the distribution of border cells is variably given as occurring between L1 and L7 spinal cord segments (Bagley, 2005; De Lahunta, 1983; De Lahunta et al., 2020b; Dewey, 2016; Jaggy & Platt, 2010; Lorenz et al., 2011; Olby, 2013; Sharp & Wheeler, 2005) with maximal numbers between L1 and L4 (Bagley, 2005), L2 and L4 (De Lahunta, 1983; Dewey, 2016) or L1 and L5 (De Lahunta et al., 2020b). However, these distribution data correspond to studies in the rhesus macaque monkey (Macaca mulatta) (Cooper & Sherrington, 1940; Sprague, 1953). Distribution data for feline border cells are limited to just one cat in one study, occurring between L3 and L6 with maximal numbers between L3 and L4 (Cooper & Sherrington, 1940), with the cat reportedly having fewer cells than the monkey (Cooper & Sherrington, 1940; Sprague, 1953).

The salient finding in the present case was the forelimb extensor rigidity and neck hyperextension characteristic of SSP (Bagley, 2005; Braund, 1994; Chrisman, 1991; Chrisman et al., 2003; De Lahunta et al., 2020b; Dewey, 2016; Fitzmaurice, 2010, Jaggy & Platt, 2010; Freeman & Ives, 2020; Garosi, 2012; Griffiths, 1987; LeCouteur, 1986; LeCouteur & Child, 1989; Lorenz et al., 2011; Messonnier, 2000; Olby, 2013; Palmer, 1975; Sharp & Wheeler, 2005; Thomson & Hahn, 2012; Wheeler & Thomas, 1996) in a cat with complete traumatic transection of the spinal cord between first and second lumbar vertebrae. As an increase in forelimb extensor tone can occur with cervical spinal cord lesions, and forelimb extensor rigidity and neck hyperextension are classical signs of decerebrate and decerebellate rigidity (De Lahunta et al., 2020b; De Lahunta et al., 2020a; Freeman & Ives, 2020; Jaggy & Platt, 2010; LeCouteur, 1986; LeCouteur & Child, 1989), all of which could arise from trauma, it was imperative to rule out these considerations if a clear cut diagnosis of SSP was to be made. The presence of voluntary movement, postural reactions, proprioceptive positioning and superficial pain sensation in the forelimbs largely ruled out the possibility of a cervical spinal cord lesion (Braund, 1994; De Lahunta et al., 2020b; Dewey, 2016; Freeman & Ives, 2020; LeCouteur & Child, 1989), particularly given the absence of radiographic evidence of spinal cord trauma. Additionally, neck hyperextension is generally not a recognised feature of cervical spinal cord lesions (Braund, 1994; De Lahunta et al., 2020b; Dewey, 2016; LeCouteur & Child, 1989). Likewise, decerebrate rigidity, which arises from a lesion in the midbrain, was excluded due to an absence of neurological signs characteristic for this entity such as increased extensor tone in all limbs, paresis or postural reaction deficits in the forelimbs, altered level of consciousness, ventrolateral strabismus or abnormalities in pupil size or pupillary light reflexes (Braund, 1994; De Lahunta et al., 2020a; Dewey, 2016; Freeman & Ives, 2020). This was further supported by a lack of external visible signs, radiological or gross post‐mortem evidence of craniocerebral trauma and an absence of lesions, other than freeze–thaw artefact, on histopathological examination of the cerebrum, brainstem and cerebellum. These later observations, combined with a lack of active hip flexion or extensor rigidity of the hindlimbs, both signs of decerebellate rigidity of varying severity (Dewey, 2016; Freeman & Ives, 2020; Holliday, 1980), also discounted this possibility.

The occurrence of neck hyperextension in the present case is in accord with similar observations in dogs with SSP (Jaggy & Platt, 2010; LeCouteur & Child, 1989; Sharp & Wheeler, 2005) and parallels findings from two experimental studies in non‐decerebrate cats following post‐brachial spinal cord transection (Morrison & Bowker, 1971; Wang, 1958). The first described forelimb extension with the head being raised, but without opisthotonus, immediately following crushing injury at T10 while under bulbocapnine induced cataplexy, with the postoperative posture of the head and forelimbs lasting the duration of the experiment (Wang, 1958). The second documented forelimb extensor rigidity and an opisthotonic posture with the head dorsiflexed within 1 h following crushing injury at T8 performed under halothane anaesthesia that lasted approximately 8 h while in a drowsy state post‐recovery (Morrison & Bowker, 1971). From these observations, it is tempting to speculate that border cell inhibitory input may also influence the activity of cervico‐spinal extensor muscles in dogs and cats.

In concert with classical signs of SSP in the forelimbs, there was a complex admixture of upper and lower motor neuron signs in the hindlimbs. The absent flexor reflex could have arisen from transient spinal shock that often accompanies SSP (Chambers et al., 1966; De Lahunta et al., 2020b; Smith & Jeffery, 2005) and/or traumatic dysfunction to L7 to S1(2) spinal cord segments and/or nerve roots in the distribution of the sciatic nerve (De Lahunta et al., 2020b; Dewey, 2016; LeCouteur & Child, 1989). The bilateral patella hyper‐reflexia could have occurred as an upper motor neuron sign from transection of the spinal cord between L1 and L2 vertebra (De Lahunta et al., 2020b; Dewey, 2016; LeCouteur & Child, 1989) and/or from patella pseudo‐hyperreflexia as a result of sciatic nerve dysfunction (Dewey, 2016). This finding suggests that any potential influence of spinal shock on the patella reflex (Chambers et al., 1966; Smith & Jeffery, 2005) would have subsided by the time of examination, which occurred between 30 and 60 min after the trauma. Given radiographic evidence of displacement of the sacrum from the ilium, seventh lumbar and first caudal vertebrae, it is likely the flaccid, immobile and analgesic tail and absence of anal tone, perianal sensation and perianal reflexes were due to traumatic dysfunction of S1 to Cd5 spinal cord segments and/or associated nerve roots (De Lahunta et al., 2020b; Dewey, 2016; LeCouteur & Child, 1989).

It is of particular comparative interest that naturally occurring SSP is extremely rare in the cat, in contrast to the dog, where it is well recognized following a peracute transverse thoracolumbar myelopathy (Bagley, 2005; Braund, 1994; Chrisman, 1991; Chrisman et al., 2003; De Lahunta et al., 2020b; Dewey, 2016; Fitzmaurice, 2010; Freeman & Ives, 2020; Garosi, 2012; Griffiths, 1987; Jaggy & Platt, 2010; LeCouteur, 1986; LeCouteur & Child, 1989; Lorenz et al., 2011; Messonnier, 2000; Olby, 2013; Palmer, 1975; Sharp & Wheeler, 2005; Thomson & Hahn, 2012; Wheeler & Thomas, 1996). It has been speculated that this may involve faster adaptation times or differences in upper motor neuron input to feline cervicothoracic motor neurons or interneurons (Bali et al., 2009). Alternatively, species differences in neural networks of border cells and their input to extensor and flexor motor neurons of the cervical intumescence may underscore this disparity. However, unlike the cat, no neurophysiological or neurohistological studies on the neural substrate subserving SSP have been published in the dog, and until this work is undertaken, the reason for the discordance must remain enigmatic.

4. CONCLUSION

This is the first report of SSP in a cat outside experimental settings, which resulted from a complete traumatic spinal cord transection between the first and second lumbar vertebrae due to a motor vehicle accident.

AUTHOR CONTRIBUTIONS

Christopher T. Holland: Conceptualisation; data curation; investigation; methodology; resources; validation; visualization; writing—original draft preparation; writing—review and editing.

CONFLICT OF INTEREST STATEMENT

The author declares no conflicts of interest.

FUNDING INFORMATION

None.

ETHICS STATEMENT

None.

PEER REVIEW

The peer review history for this article is available at https://publons.com/publon/10.1002/vms3.1308.

ACKNOWLEDGEMENTS

The author would like to thank Dr. Karen Catchpole, Niki Myan, Lucy Cook, and Dianne Jenkins for technical assistance and Dr. David Taylor for histopathological examination of the brain.

Holland, C. T. (2023). Schiff–Sherrington phenomenon in a cat with complete spinal cord transection from traumatic dorsocranial luxation of the second lumbar vertebra. Veterinary Medicine and Science, 9, 2404–2409. 10.1002/vms3.1308

DATA AVAILABILITY STATEMENT

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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