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Abstract Background Muscle cramps (MCs) are prolonged, involuntary, painful muscle contractions characterized by an acute onset and short duration, caused by peripheral nerve hyperactivity. Objectives To provide a detailed description of the clinical features and diagnostic findings in dogs affected by MCs. Animals Fourteen dogs. Methods Multicenter retrospective case series. Cases were recruited by a call to veterinary neurologists working in referral practices. Medical records and videotapes were searched for dogs showing MCs. The follow-up was obtained by telephone communication with the owner and the referring veterinarian. Results Three patterns of presentation were identified depending on the number of affected limbs and presence/absence of migration of MCs to other limbs. In 9/14 (64%) of dogs, MCs were triggered by prompting the dogs to move. 8/14 (58%) dogs were overtly painful with 6/14 (42%) showing mild discomfort. The cause of MCs was hypocalcemia in 11/14 (79%) dogs: 9 dogs were affected by primary hypoparathyrodism, 1 dog by intestinal lymphoma and 1 dog by protein losing enteropathy. In 3/14 cases (21%) the cause was not identified, and all 3 dogs were German Shepherds. Conclusions and Clinical Importance Muscle cramps can manifest in 1 of 3 clinical patterns. Muscle cramps are elicited when dogs are encouraged to move and do not always appear as painful events, showing in some cases only discomfort. The main cause of MCs in this study was hypocalcemia consequent to primary hypoparathyroidism. In dogs having MCs of unknown etiology, idiopathic disease or paroxysmal dyskinesia could not be ruled out.

All details collected from owners and their dogs will be anonymised by the principal veterinary investigator (ML) and all identification data will remain strictly confidential.

Episodes consist of gait abnormalities ranging from ataxia to an inability to stand, contractions of the abdominal, neck and back muscles resulting in abnormal posturing, and contractions/cramping of the appendicular muscles (causing extensor rigidity or flexion of the limbs).

Two standard poodles were evaluated for painful, episodic muscle cramps affecting their thoracic and pelvic limbs. Both dogs had been diagnosed with hypoadrenocorticism and were being treated with fludrocortisone acetate and prednisone when evaluated for muscle cramps. However, the muscle cramping started approximately 1 month prior to the diagnosis of hypoadrenocorticism. Findings on general physical examination included lethargy and dehydration. Neurological examination was normal between episodes. Serum biochemical abnormalities included hyperalbuminemia, azotemia, hyponatremia, hypochloremia, and hyperkalemia. Altering treatment to desoxycorticosterone pivalate resolved the electrolyte abnormalities and the episodes of muscle cramping in both dogs. The authors conclude that hypoadrenocorticism can be associated with episodes of painful muscle cramping in standard poodles.

Myoclonus is a sudden brief, involuntary muscle jerk. Of all the movement disorders, myoclonus is the most difficult to encapsulate into any simple framework. On the one hand, a classification system is required that is clinically useful to aid in guiding diagnosis and treatment. On the other hand, there is need for a system that organizes current knowledge regarding biological mechanisms to guide scientific research. These 2 needs are distinct, making it challenging to develop a robust classification system suitable for all purposes. We attempt to classify myoclonus as “epileptic” and “nonepileptic” based on its association with epileptic seizures. Myotonia in people may be divided into 2 clinically and molecularly defined forms: (1) nondystrophic myotonias and (2) myotonic dystrophies. The former are a group of skeletal muscle channelopathies characterized by delayed skeletal muscle relaxation. Many distinct clinical phenotypes are recognized in people, the majority relating to mutations in skeletal muscle voltage-gated chloride (CLCN1) and sodium channel (SCN4A) genes. In dogs, myotonia is associated with mutations in CLCN1. The myotonic dystrophies are considered a multisystem clinical syndrome in people encompassing 2 clinically and molecularly defined forms designated myotonic dystrophy types 1 and 2. No mutation has been linked to veterinary muscular dystrophies. We detail veterinary examples of myotonia and attempt classification according to guidelines used in humans. This more precise categorization of myoclonus and myotonia aims to promote the search for molecular markers contributing to the phenotypic spectrum of disease. Our work aimed to assist recognition for these 2 enigmatic conditions.

A Maltese dog was presented with a stiff gait, secondary to muscle hypertonicity, affecting the axial and proximal appendicular muscles, which had progressively worsened over the last 4 years, associated with episodes of muscle spasms. Neuroanatomical localization was upper motor neuron (UMN) or generalized neuromuscular system. Cerebrospinal fluid (CSF) analysis was normal. Magnetic resonance imaging (MRI) of the brain and cervical spinal cord was performed and showed hypoplasia of the dorsal part of the left hippocampus, unchanged compared to the MRI performed 4 years earlier, and mild C6–C7 disk extrusion, with no evidence of compression of the spinal cord. Conscious electromyography showed continuous motor unit action potentials (MUAPs) in agonist and antagonist muscles. Indirect immunofluorescence (IFT) detected the presence of antibodies against glutamic acid decarboxylase (GAD). These findings were consistent with a human condition called “Stiff Person Syndrome” (SPS). A condition similar to SPS has only been described once before in a Beagle dog (“Stiff Dog Syndrome”). A therapeutic protocol based on human guidelines for SPS was initiated with a partial improvement. “Stiff Dog Syndrome” (SDS) is a possible cause of muscle hypertonicity and spasms in dogs.

Bovine tetanus is a serious infectious disease of the central nervous system caused by the exotoxin produced by Clostridium tetani and is characterized by persistent tension and spasm of the rhabdomyocytes. Currently, many studies have focused on diagnosing tetanus; however, only a few studies on treatment methods have been conducted. Therefore, cattle with tetanus have been treated using symptomatic therapy. In this case, severe muscle spasticity and spasms were observed in a 9-month-old Hanwoo (Korean indigenous cattle) bull, and aspartate aminotransferase and creatine kinase levels were increased in serum biochemical tests. Clinically, bovine tetanus was strongly suspected, and metronidazole was administered orally for 5 days. To treat the intensifying bloat, a temporary rumenostomy was performed on the third day of onset, and the toxin gene (tetanospasmin) of C. tetani was amplified by polymerase chain reaction analysis from the collected ruminal fluid. Magnesium and sedatives (acepromazine) were administered for 7 days to treat muscle spasticity and spasms. Muscle spasticity and spasm markedly improved, and the bull stood up from the lateral recumbent position. On the 17 th day after onset, all tetanus-related symptoms resolved and a normal diet was started. Our findings demonstrated that treatment with metronidazole, magnesium, and acepromazine was effective in the bull with tetanus.

We conducted a retrospective study of the case files of 64 multiple sclerosis (MS) patients presenting severe spasticity, who had received intrathecal (IT) baclofen test injections between 1992 and 2004 in a rehabilitation unit. In almost all cases of our series, IT baclofen was proposed to patients who were no longer able to walk. IT baclofen is a safe and effective treatment to reduce spasticity in MS patients. Despite an advanced stage of the disease at the time of pump placement, the complication rate was low and the efficacy of this treatment was maintained over time.

Introduction Dibucaine is a potent, long-lasting local anesthetic (LA). Topical dibucaine ointments are marketed directly to consumers in the USA without prescription. Dibucaine ointment is intended to treat discomfort associated with sunburn, eczema, minor rashes, minor scratches, insect bites, and poison ivy and is used alone or in combination with other active ingredients to treat pain associated with hemorrhoids or other anorectal disorders. Oral dibucaine toxicosis has been reported in children and includes gastrointestinal upset and neurologic and cardiovascular dysfunction. Case Report An 18-month-old, female, Parson Russell terrier ingested approximately 23 g of 1% dibucaine ointment (approximately 38 mg/kg dibucaine) recommended to the owner for the treatment of hemorrhoids. Onset and resolution of clinical signs were relatively rapid, 5 min and 60 min, respectively. Clinical signs included vomiting, ptyalism, whole-body muscle fasciculations, disorientation, and severe ataxia. Discussion Oral dibucaine toxicosis in dogs is similar to oral dibucaine toxicosis in children. Dibucaine ointment poses a real and potentially serious toxicological risk to pets and thus should be stored in a safe location.