Head rebound test in the clinical neurological examination of veterinary patients: a case example and discussion of Stewart and Holmes’ rebound phenomenon

In human medical neurology, the clinical neurological examination is variably augmented by specific tests that may be either unsuitable for veterinary patients or not included in the clinical evaluation of veterinary neurological patients due to clinicians presumably being unfamiliar with these tests. An example of the latter can be found in testing for the Stewart and Holmes’ rebound phenomenon (“rebound test”). In this article, a veterinary case example is presented in which a modified version of this test was performed (“head rebound test”). The interpretation of the results of this test is discussed, and the literature on the Stewart and Holmes’ rebound phenomenon and testing thereof is reviewed

Case report: Traumatic hemorrhagic cervical myelopathy in a dog

A 1.5-year-old female entire French bulldog was referred for neurological evaluation, further diagnostic tests, and treatment 24 h after a road traffic accident. Initial emergency treatment, diagnostic tests, and stabilization had been performed by the referring veterinarian. Neurological examination revealed severe spastic non-ambulatory tetraparesis and was consistent with a C1-5 myelopathy. A magnetic resonance imaging (MRI) study revealed an irregular to elongated ovoid intramedullary lesion centered over the body of C2. The lesion showed marked signal heterogeneity with a central T2W and T2* hyperintense region, surrounded by a hypointense rim on both sequences. The lesion appeared heterogeneously T1W hypointense. The lesion was asymmetric (right-sided), affecting both white and gray matter. The C2-3 intervertebral disk appeared moderately degenerate with a Pfirrmann grade of 3. No evidence of vertebral fracture or luxation was found on radiographs or MRI of the vertebral column. Additional soft tissue abnormalities in the area of the right brachial plexus were suggestive of brachial plexus and muscle injury. A diagnosis of traumatic hemorrhagic myelopathy at the level of C2 and concurrent brachial plexus injury was formed. Conservative treatment was elected and consisted of physiotherapy, bladder care with an indwelling urinary catheter, repeated IV methadone based on pain scoring (0.2 mg/kg), oral meloxicam 0.1 mg/kg q24h, and oral gabapentin 10 mg/kg q8h. The dog was discharged after 4 days, with an indwelling urinary catheter and oral medication as described. The catheter was replaced two times by the referring veterinarian and finally removed after 10 days. Thereafter, voluntary urination was seen. During the 2 months after the road traffic accident, slow recovery of motor function was seen. The right thoracic limb recovery progressed more slowly than the left limb, also showing some lower motor neuron signs during follow-up. This was judged to be consistent with a right-sided brachial plexus injury. The dog was reported ambulatory with mild residual ataxia and residual monoparesis of the right thoracic limb at the last follow-up 3 months post-injury. This case report highlights the MRI-based diagnosis of traumatic hemorrhagic myelopathy in a dog. A fair short-term outcome was achieved with conservative treatment in this case

Longitudinal assessment of syringomyelia in Pomeranians

IntroductionChiari-like malformation (CM) and syringomyelia (SM) are disorders that, in dogs, affect mainly small and toy breeds, including the Pomeranian. These disorders are linked to a great number of (owner-reported) clinical signs (ORCS) suggestive of pain. Aging was associated with an increased risk of having SM in several studies. However, there are only a few longitudinal studies that assess the presence and severity of CM/SM over time in CKCS dogs and progression of SM was linked to progression of clinical signs. The aim of this study was to investigate ORCS, CM/SM classification, and quantitative syrinx parameters in relation to progression of time (age) within individual Pomeranians.Materials and methodsPomeranians with or without ORCS and with or without diagnoses of CM/SM were included that had undergone two (or more) MRI studies of the craniocervicothoracic region between January 2020 and June 2023. Classification of CM/SM and quantitative syrinx measurements were performed. Absolute values as well as ratios for syrinx height, width, and cross-sectional area were included for analysis.ResultsA total of 19 Pomeranians were included in the study, of which 11 were male (58%) and 8 were female (42%). The median age at the time of MRI1 was 26 months (range 7–44 months). The median scan interval was 26 months (range 11–49 months). Eleven dogs (58%) were presented with ORCS at the time of MRI1, whereas the other 8 dogs (42%) had no ORCS at that time. At the time of MRI2, there were 17/19 dogs (89%) with ORCS and 2/19 dogs without ORCS (11%). Dogs were significantly more likely to have ORCS at MRI2 than MRI1 (p = 0. 0411). There was no significant difference between CM/SM classification at the time of MRI1 and MRI2. Significant differences were found between MRI1 and MRI2 for syrinx height (based on transverse images) (absolute value and ratio P = 0.0059), syrinx width (absolute value P = 0.1055, ratio P = 0.0039), and syrinx cross sectional area (absolute value P = 0.0195, ratio P = 0.0217).DiscussionThere are differences in the presence or absence of ORCS as well as quantitative syrinx measurements in Pomeranians at different ages. This finding supports that longitudinal changes occur in the SM status of Pomeranians

Remarkable anecdotes illustrating the nature and effect of seizure-precipitating factors in Border Collies with idiopathic epilepsy

Epilepsy is one of the most common chronic neurological syndromes in dogs and has serious implications for the quality of life of both the dogs and owners. Seizure-precipitating factors (SPFs) (also termed "triggers" or "provocative factors") have been studied and reported in both humans and dogs with idiopathic epilepsy. In dogs stress, hormones, sleep deprivation, and the weather have been reported as SPFs. The Border Collie (BC) is a breed of dog that is predisposed to idiopathic epilepsy, and the outcome is often poor. BC is described as a very sensitive dog with a strong focus on their owners, and this may have an influence on their and their owners' stress level. In this article, we described six unrelated BCs with idiopathic epilepsy in which several remarkable SPFs were identified, and avoiding them improved the outcome of these dogs. The possible SPFs were different for each dog. The SPFs were, among others, the other dog in the family, the lack of intellectual challenge, the presence of an autistic child, a busy street, the relation with the owner, and throwing a ball at the beach. These cases illustrate that recognizing the SPF(s) and taking measures with regard to management can lead to a reduction in epileptic seizure frequency or even achieving seizure freedom

Canine paroxysmal dyskinesia—a review

Paroxysmal dyskinesias (PDs) are a group of involuntary, hyperkinetic movement disorders that recur episodically and may last seconds to hours. An important feature of PD is that there is no loss of consciousness during the episode. Using a clinical classification, three main types of PDs have been distinguished in canine PD: (1) paroxysmal kinesigenic dyskinesia (PKD) that commences after (sudden) movements, (2) paroxysmal non-kinesigenic dyskinesia (PNKD) not associated with exercise and can occur at rest, and (3) paroxysmal exertion-induced dyskinesia (PED) associated with fatigue. Canine PDs are diagnosed based on the clinical presentation, history, and phenomenology. For the latter, a video recording of the paroxysmal event is extremely useful. An etiological classification of canine PDs includes genetic (proven and suspected), reactive (drug-induced, toxic, metabolic, and dietary), structural (neoplasia, inflammatory, and other structural causes), and unknown causes. In this review, an overview of all reported canine PDs is provided with emphasis on phenotype, genotype, and, where possible, pathophysiology and treatment for each reported canine PD

Microanatomical findings with relevance to trigeminal ganglion enhancement on post-contrast T1-weighted magnetic resonance images in dogs

Trigeminal ganglion contrast enhancement (TGCE) is reported to be a normal and a common finding on magnetic resonance imaging studies of dogs, cats and humans. The intent of the present study was to describe the anatomical characteristics of the trigeminal ganglion, its surrounding structures, and histological features that are relevant to explain or hypothesize on the reason for TGCE on T1-weighted post-contrast MRI studies of the brain in dogs. Eight dog cadavers were dissected to study the anatomy of the trigeminal ganglion. The presence and anatomy of vessels was studied by dissection and by histological techniques. Two trigeminal ganglia were isolated and stained with hematoxylin-eosin (HE). Two other trigeminal ganglia included in the trigeminal canal and trigeminal cavity were decalcified with formic acid/formalin for 12 weeks and stained with HE to study the related vessels. Additionally, a corrosion cast was obtained from a separate canine specimen. Leptomeninges and a subarachnoid space were identified at the level of the trigeminal nerve roots and the trigeminal ganglion. No subarachnoid space was identified and leptomeninges were no longer present at the level of the three trigeminal nerve branches. Small arterial vessels ran to and supplied the trigeminal ganglion, passing through the dura mater. No venous plexus was visualized at the level of the trigeminal ganglion in the dissections. A complex arterial vascular network was identified within the leptomeningeal covering of the trigeminal ganglion and was best appreciated in the corrosion cast. Histological examination revealed small-to moderate-sized blood vessels located in the epineurium around the ganglion; from there a multitude of arterioles penetrated into the perineurium. Small endoneurial branches and capillaries penetrated the ganglion and the trigeminal nerve branches. Limitations to this study include the limited number of canine specimens included and the lack of electron microscopy to further support current hypotheses included in our discussion. In conclusion, this study provides further support to the theory that TGCE in dogs may be due an incomplete blood-nerve barrier or blood-ganglion barrier at the interface between the central nervous system and the peripheral nervous system

Case report: Radiofrequency-induced thermal burn injury in a dog after magnetic resonance imaging

A 10-year-old male Shar-Pei was referred for lethargy and proprioceptive deficits of the left thoracic limb. An magnetic resonance imaging (MRI) examination of the cervical spinal column and the brain was performed. The MRI examination of the brain was normal. A left-sided C3-C4 intervertebral disc extrusion with spinal cord compression was diagnosed. Medical treatment was elected. Within a week after the MRI examination, the dog presented with deep partial-thickness skin burn wounds in both axillae. Since the specific absorption rate had not exceeded the safety limits during any of the scans and no other procedures or circumstances were identified that could possibly have resulted in burn injuries, the thermal burn injuries were diagnosed as radiofrequency (RF) burns. The wounds healed by secondary intent over the next month. RF burns are the most reported complication in humans undergoing MRI but have not been reported in veterinary patients. Clinicians and technicians should consider the potential risk for RF burns in veterinary patients and take precautions regarding positioning of the patient and take notice of any signs of burn injury when performing follow-up examinations

Invasive nasal histiocytic sarcoma as a cause of temporal lobe epilepsy in a cat

Case summary A 10-year-old neutered female domestic shorthair cat was presented with an acute onset of neurological signs suggestive of a right-sided forebrain lesion, temporal lobe epilepsy and generalised seizure activity. MRI of the head revealed an expansile soft tissue mass in the caudal nasal passages (both sides but predominantly right-sided) involving the ethmoid bone and extending through the cribriform plate into the cranial vault affecting predominantly the right frontal lobe and temporal lobe. Histopathological examination of the tumour revealed a histiocytic sarcoma. Relevance and novel information This is the first report of a cat with clinical signs of temporal lobe epilepsy due to an invasive, histiocytic sarcoma. Histiocytic sarcoma, although rare, should be included in the list of differential diagnoses for soft tissue masses extending through the cribriform plate. Other differential diagnoses are primary nasal neoplasia (eg, adenocarcinoma, squamous cell carcinoma, chondrosarcoma and other types of sarcomas), lymphoma and olfactory neuroblastoma. Temporal lobe epilepsy in cats can be the consequence of primary pathology of temporal lobe structures, or it can be a consequence of pathology with an effect on these structures (eg, mass effect or disruption of interconnecting neuronal pathways)

Dystonia in veterinary neurology

Dystonia is a clinical sign and main feature of many movement disorders in humans as well as veterinary species. It is characterized by sustained or intermittent involuntary muscle contractions causing abnormal (often repetitive) movements, postures, or both. This review discusses the terminology and definition of dystonia, its phenomenology, and its pathophysiology, and provides considerations regarding the diagnosis and treatment of dystonia in dogs and cats. In addition, currently recognized or reported disorders in dogs and cats in which dystonia is a particular or main feature are discussed and comparisons are made between disorders featuring dystonia in humans and animals. We suggest that when describing the phenomenology of dogs and cats with dystonia, if possible the following should be included: activity being performed at onset (e.g., resting or running or exercise-induced), body distribution, duration, responsiveness (subjective), severity, temporal pattern (i.e., paroxysmal or persistent, severity at onset and at later stages), presence or absence of autonomic signs (e.g., salivation), presence or absence of preceding signs (e.g., restlessness), presence or absence of signs after dystonia subsides (e.g., sleepiness), coexistence of other movement disorders, any other neurological manifestations, and possible links to administered medications, intoxications or other associated factors. We also suggest that dystonia be classified based on its etiology as either structural genetic, suspected genetic, reactive, or unknown