Risk factors for development of status epilepticus in dogs with idiopathic epilepsy and effects of status epilepticus on outcome and survival time: 32 cases (1990-1996)

OBJECTIVE: To identify risk factors for episodes of status epilepticus (SE) in dogs with idiopathic epilepsy and determine how SE affects long-term outcome and survival time. DESIGN: Retrospective study. ANIMALS: 32 dogs with idiopathic epilepsy. PROCEDURE: Information on signalment, seizure onset, initiation of treatment, anticonvulsants administered, number of episodes of SE, overall seizure control, and long-term outcome was obtained from medical records and through telephone interviews. Differences between dogs that did and did not have episodes of SE were evaluated statistically. RESULTS: 19 (59%) dogs had 1 or more episodes of SE. Body weight was the only variable significantly different between dogs that did and did not have episodes of SE. Thirteen dogs (9 that did not have episodes of SE and 4 that did) were still alive at the time of the study and were > or = 10 years old. Six of the 19 (32%) dogs that had episodes of SE died of causes directly attributed to the seizure disorder. Mean life spans of dogs that did and did not have episodes of SE were 8.3 and 11.3 years, respectively. Survival time was significantly different between groups. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that a substantial percentage of dogs with idiopathic epilepsy will have episodes of SE. Dogs with greater body weights were more likely to have episodes of SE, and early appropriate seizure treatment did not appear to decrease the risk that dogs would have episodes. Most dogs with idiopathic epilepsy had an expected life span, but survival time was shorter for dogs that had episodes of SE.     

Laryngeal paralysis in immature and mature dogs as one sign of a more diffuse polyneuropathy

Six dogs with laryngeal paralysis had clinical, electrophysiologic, and pathologic evidence of a more generalized polyneuropathy. Three of the dogs were young Dalmatians, one was a young Bouvier des Flandres, and two were older, large-breed dogs. The results of this study suggest that laryngeal paralysis in dogs may frequently be one clinical sign of an underlying, more generalized polyneuropathy. Two forms of this generalized polyneuropathy may exist: an early form, as seen in young dogs with congenital or hereditary disease, and a delayed-onset form that is usually found in older dogs with so-called idiopathic laryngeal paralysis, some of which may have hypothyroidism.     

MAGNETIC RESONANCE IMAGING OF THE INTRATEMPORAL FACIAL NERVE IN IDIOPATHIC FACIAL PARALYSIS IN THE DOG

The most common cause of peripheral facial nerve paralysis in dogs, in the absence of otitis media, is thought to be idiopathic. Gadolinium-enhanced (Gd) magnetic resonance (MR) imaging has been used to study peripheral facial weakness in humans with a wide variety of disorders, including Bell's palsy, the clinical equivalent of idiopathic facial nerve paralysis in dogs. Gd-MR imaging may be useful to demonstrate abnormal enhancement of the intratemporal facial nerve. The aim of this study was to define the role of the Gd-MR imaging in dogs with idiopathic facial nerve paralysis, with regard to pattern of enhancement, and to search for prognostic information. Six dogs with peripheral facial nerve paralysis, followed between 2003 and 2005, were studied. Physical and neurologic examinations, as well as clinical tests, were performed, including routine hematology, serum biochemistry, thyroid screening, cerebrospinal fluid analysis, and MR imaging. The time interval between the onset of the clinical signs, the progress of the disease, and the final recovery was noted in each dog. The following four intratemporal segments of the facial nerve were analyzed: internal acoustic meatus, labyrinthine segment/geniculate ganglion, tympanic segment, and mastoid segment. Along its length, contrast enhancement was found in four dogs. In this group, contrast enhancement of the facial nerve was found in all segments of two dogs, in three segments of one dog, and in one segment of the other dog. In the four dogs with enhancement, one recovered completely in 8 weeks and three have not recovered completely. The two dogs without evidence of enhancement recovered completely in an average time of 4 weeks.     

Iatrogenic sciatic nerve injury in eighteen dogs and nine cats (1997-2006)

Objective— To report clinical features associated with iatrogenic peripheral nerve injury in dogs and cats admitted (1997–2006) to a referral teaching hospital.
Study Design— Retrospective study.
Animals— Dogs (n=18), 9 cats.
Methods— Patients had acute signs of monoparesis attributable to sciatic nerve dysfunction that developed after treatment. Neurologic examination and electrodiagnostic testing were performed. Surgical therapy was used for nerve entrapment and delayed reconstructive surgery used in other cases.
Results— Of 27 nerve injuries, 25 resulted from surgery (18 with treatment of pelvic injuries). Iliosacral luxation repair resulted in tibial (4 cats) and peroneal (3 dogs) nerve dysfunction. Other causes were intramedullary pinning of femoral fractures (3), other orthopedic surgery (cemented hip prosthesis [2] and tibial plateau-leveling osteotomy [1]), and perineal herniorrhaphy [1]. Nerve injury occurred after intramuscular injection (1 cat, 1 dog). Immediate surgical treatment was removal of intramedullary nails, extruded cement, or entrapping suture. Delayed nerve transplantation was performed in 2 dogs. Within 1 year, 13 patients recovered completely, clinical improvement occurred in 7, and there was no improvement in 7. Five of the 7 dogs that did not recover had acetabular or ilium fracture.
Conclusion— Iatrogenic sciatic nerve injury occurred most commonly during treatment of pelvic orthopedic diseases and had a poor prognosis. Clinical variation in sciatic nerve dysfunction in dogs and cats can be explained by species anatomic differences.
Clinical Relevance— Iatrogenic sciatic nerve injury leads to severely debilitating locomotor dysfunction with an uncertain prognosis for full-functional recovery.     

Idiopathic facial paralysis in the dog

Facial nerve paralysis of acute onset is reported in seven mature dogs, five of which were cocker spaniels. The clinical signs were characterised by ear drooping, lip commissural paralysis, sialosis, and collection of food on the paralysed side of the mouth. All dogs showed absent menace responses and trigeminofacial/acousticofacial reflexes. Horner's syndrome was not present in any dog. In four dogs, bilateral facial paralysis developed. The facial paralysis was unrelated to otitis media. Electrodiagnostic studies revealed denervation potentials and absent evoked muscle potentials. Facial nerve biopsies from two cases showed nerve fibre degeneration and apparent loss of larger diameter myelinated fibres. The condition has been termed idiopathic facial paralysis since the aetiopathogenesis is presently unknown.     

Inability to experimentally produce a polyneuropathy in dogs given chronic oral low level lead.

Electromyographic examinations were performed at various times over a 40 week period in four mature dogs receiving chronic oral low doses of lead acetate and a control dog receiving sodium acetate. Blood lead levels in the four dogs were elevated (mean values 1.15, 2.18, 1.13 and 1.72 mumol/liter). No clinical signs of lead intoxication were present. Two dogs had evidence of a nonregenerative anemia. Neither needle electromyographic nor nerve conduction velocity studies showed evidence of a polyneuropathy. Teased nerve fiber preparations of proximal and distal segments of the ulnar and tibial nerves and muscle biopsies of distal appendicular muscles were normal in all dogs. Light microscopic examination of the brain, kidneys and liver revealed no abnormalities in the two dogs necropsied. In conclusion, a polyneuropathy was not produced experimentally in dogs ingesting low doses of inorganic lead for up to 40 weeks.     

Failure to identify an association between serologic or molecular evidence of Bartonella infection and idiopathic rhinitis in dogs

OBJECTIVE: To determine whether infection with or exposure to Bartonella spp was associated with idiopathic rhinitis in dogs. DESIGN: Case-control study. ANIMALS: 44 dogs with idiopathic nasal discharge and 63 age- and weight-matched control dogs without nasal discharge and no clinical signs of bartonellosis. Procedures-Serum was tested for antibodies against Bartonella henselae and Bartonella vinsonii subsp berkhoffii with indirect fluorescent antibody assays. Blood was tested for Bartonella DNA with a PCR assay. RESULTS: Results of the antibody and PCR assays were negative for all 44 dogs with idiopathic nasal discharge. One control dog had antibodies against B henselae; a second control dog had positive PCR assay results. We did not detect a significant association between assay results and group designation. CONCLUSIONS AND CLINICAL RELEVANCE: The present study failed to confirm an association between idiopathic rhinitis and exposure to or infection with Bartonella spp in dogs. Findings do not rule out the possibility that Bartonella infection may cause nasal discharge in some dogs, but the failure to find any evidence of exposure to or infection with Bartonella spp in dogs with idiopathic nasal discharge suggested that Bartonella infection was not a common cause of the disease.     

Distal peripheral polyneuropathy in a great dane

A spayed female five year old Great Dane dog was diagnosed as having a chronic, progressive, symmetrical distal polyneuropathy and concurrent hypothyroidism. Axonal degeneration and segmental demyelination were evident in teased nerve fiber preparations. Clinical signs included hindlimb weakness and muscle atrophy of the head and distal limbs. Diagnosis was based on clinical, electrophysiological, and nerve and muscle biopsy findings. Thyroxine supplementation for one month was of no benefit. The etiology of the polyneuropathy was not established but several causes were considered. The extent of demyelination in our case was of greater magnitude than described in a previous report of a similar idiopathic distal symmetrical polyneuropathy in a Great Dane.     

Pneumonia after intracranial surgery in dogs

OBJECTIVE: To determine factors associated with the occurrence of pneumonia after intracranial surgery in dogs. STUDY DESIGN: Retrospective cohort study. Animals-Forty-nine client-owned dogs. METHODS: The medical records of 49 dogs with space-occupying intracranial disease that underwent craniotomy were reviewed. Development of pneumonia after surgery was considered highly likely in 12 dogs (affected dogs) based on clinical signs, including acute dyspnea or coughing in association with typical radiographic findings or abnormal transtracheal wash results. Pneumonia was confirmed in 6 dogs based on necropsy findings. Affected dogs were compared with 37 dogs that did not develop pneumonia (unaffected dogs) subsequent to intracranial surgery. Based on the medical records of affected dogs, determinations were made regarding time between development of pneumonia and surgery, surgical procedure, intracranial lesion type, and intracranial lesion location. Risk factors examined for both affected and unaffected dogs included level of consciousness, body position during the postoperative recovery period, duration of anesthesia, occurrence of vomiting or regurgitation, presence of seizures, cranial nerve deficiencies, and the presence of megaesophagus before and after surgery. We also compared the feeding protocol after surgery for each group. RESULTS: Pneumonia typically occurred within the first week after surgery (median, 6.5 days); however, this was variable (range, 1-96 days). Of the factors that were present within 24 hours before the clinical signs of pneumonia, vomiting or regurgitation and megaesophagus were found to be significant risk factors. Dogs that vomited or regurgitated were 2.71 times more likely to develop pneumonia than dogs that did not. Vomiting or regurgitation occurred in 63% of the dogs that developed pneumonia in this cohort. Dogs with megaesophagus were 9.25 times more likely to develop pneumonia than dogs without megaesophagus. Seven dogs with pneumonia died. Five of these 7 dogs appeared to have died as a direct sequel to pneumonia. CONCLUSION: Dogs undergoing craniectomies for space-occupying intracranial disease may be at higher risk for development of pneumonia due to several factors, including vomiting, regurgitation, and megaesophagus.     

Evaluation of Fenestration for Treatment of Degenerative Disc Disease in the Caudal Cervical Region of Large Dogs

Seventeen large dogs (15 Doberman pinschers, one Labrador retriever, and one German short-haired pointer) with pain and gait abnormalities resulting from caudal cervical intervertebral disc degeneration were treated by disc fenestration. Four dogs recovered completely, two dogs appeared to have recovered but nerve root compression and pain returned 3 years later, five did not recover completely or did not improve, and six became progressively worse. In the dogs that recovered, preoperative myelograms showed that traction on or flexing the neck relieved the spinal cord compression. Such manipulation did not relieve slight persistent compression in the dogs that did not improve nor did it relieve severe compression by disc herniation or spinal canal stenosis in the dogs that became progressively worse. The return of nerve root compression after 3 years in two dogs was attributed to incomplete removal of dorsal anulus fibrosus. It was concluded that disc fenestration alone provided inadequate treatment of caudal cervical degenerative disc disease in large dogs.     

Characterization of renal defects in dogs with a syndrome similar to the Fanconi syndrome in man.

Ten adult dogs with multiple spontaneous defects of renal tubular reabsorption were studied. Clinical signs included polydipsia, polyuria, and glycosuria for 2 to 12 months. Eight of the dogs were Basenjis. Urinalyses revealed hyposthenuria, glycosuria, and amino aciduria in most dogs. Renal function was normal in 5 dogs and slightly reduced in the remainder. Moderate metabolic acidosis had developed in 3 dogs. Renal clearance studies revealed reduced tubular reabsorption of glucose, phosphate, sodium, potassium, and uric acid. Abnormal glucose tubular maximal curves were found. Results of oral glucose tolerance tests were normal. Two patterns of abnormal amino aciduria were evident: generalized amino aciduria and a pattern similar to that of cystinuria in dogs. Radiography of long bones and bone densitometry did not reveal any skeletal abnormalities. Five of the dogs died within 90 days of diagnosis; death was due to acute renal failure associated with profound dehydration, acidosis, and papillary necrosis. The other dogs remained stable without treatment after 18 months. Histopathology of kidneys did not reveal uniform abnormalities; some dogs had variable and nonspecific changes and others were normal. Electron microscopy did not reveal ultrastructural abnormalities in renal tubular cells. It was concluded that the syndrome in these dogs represents a new entity of renal disease in dogs, similar to idiopathic Fanconi syndrome in man.     

Postoperative results of unilateral arytenoid lateralization for treatment of idiopathic laryngeal paralysis in dogs: 39 cases (1996-2002)

OBJECTIVE: To evaluate postoperative results for dogs with idiopathic laryngeal paralysis that underwent unilateral arytenoid lateralization (UAL). DESIGN: Retrospective case series. ANIMALS: 39 dogs with idiopathic laryngeal paralysis. PROCEDURE: Medical records were reviewed, and information on surgical technique, hospitalization time, postoperative treatment, and complications was obtained. Owners were contacted by telephone for additional information if necessary. RESULTS: In all dogs, UAL had been performed by a single surgeon who used a standard surgical technique. Long-term follow-up information was available for all 39 dogs; mean follow-up time was 29.6 months (range, 3 to 61 months). Seven (18%) dogs developed postoperative pneumonia, and 6 of the 7 recovered with treatment. Twenty-two of the 39 (56%) dogs had minor complications, including unresolved coughing or gagging, continued exercise intolerance, vomiting, and seroma formation. Owners of 35 of the 39 (90%) dogs reported an improvement in postoperative quality-of-life score. Median survival time was 12 months; only 1 dog was euthanized because of respiratory tract disease following surgery. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that UAL will improve quality of life in most dogs with idiopathic laryngeal paralysis. However, the complication rate is high, with postoperative pneumonia being the most important major complication. Minor complications were common but did not adversely affect owner-assigned quality-of-life scores in most dogs.     

Prospective survey of tick paralysis in dogs

OBJECTIVE: To obtain information on tick paralysis in dogs, including the nature of disease, host signalment, tick-host relationship, treatment, disease progression and recovery, and preventive measures. DESIGN: A prospective survey of 577 dogs affected by tick paralysis was conducted during 1998. Forty-two veterinary clinics along the eastern coast of Australia were instructed to complete survey forms for the first 15 dogs that presented with tick paralysis during September to November. RESULTS: Five percent of dogs died from tick paralysis. Younger dogs were more likely to survive. Long coat length was associated with a greater tick burden but not greater tick size, whereas coat thickness had no bearing on either. Dogs with mild disease recovered more quickly from tick paralysis. Respiratory and gait scores reflected disease severity and were good prognostic indicators. The size of the tick did not reflect the severity of the clinical condition it induced in the host. No method of tick removal or in situ treatment improved recovery time or reduced mortality. However, the time spent in hospital was significantly less for dogs from which the live tick was manually removed. Inspiratory stridor, evident in some dogs with tick paralysis, was not related to tick attachment on the neck. The use of acepromazine maleate or dexamethasone did not reduce recovery time or mortality. Increasing the dose of tick antitoxin serum (TAS) above 0.1 mL/kg had no effect on mortality or recovery time. Dogs with severe disease that received an additional dose of TAS were significantly less likely to survive. Subcutaneous use of TAS at the site of tick attachment was of no benefit in reducing mortality or time to initial clinical improvement. A registered preventative product had not been used on the majority of dogs. Clipping the coat to search for ticks did not reduce mortality. CONCLUSIONS: Therapy needs to address cardiopulmonary dysfunction that may be due directly to the effect of tick toxin and not just respiratory compromise caused by progressive respiratory muscle failure.     

Effects of atracurium on intraocular pressure, eye position, and blood pressure in eucapnic and hypocapnic isoflurane-anesthetized dogs

OBJECTIVE: To determine effects of atracurium on intraocular pressure (IOP), eye position, and arterial blood pressure in eucapnic and hypocapnic dogs anesthetized with isoflurane. ANIMALS: 16 dogs. PROCEDURE: Ventilation during anesthesia was controlled to maintain Paco2 at 38 to 44 mm Hg in group- I dogs (n = 8) and 26 to 32 mm Hg in group-II dogs (8). Baseline measurements for IOP, systolic, diastolic, and mean arterial blood pressure, central venous pressure (CVP), and heart rate (HR) were recorded. Responses to peroneal nerve stimulation were monitored by use of a force-displacement transducer. Atracurium (0.2 mg/kg) was administered i.v. and measurements were repeated at 1, 2, 3, and 5 minutes and at 5-minute intervals thereafter for 60 minutes. RESULTS: Atracurium did not affect IOP, HR, or CVP Group II had higher CVP than group I, but IOP was not different. There was no immediate effect of atracurium on arterial blood pressure. Arterial blood pressure increased gradually over time in both groups. Thirty seconds after administration of atracurium, the eye rotated from a ventromedial position to a central position and remained centrally positioned until 100% recovery of a train-of-four twitch response. The time to 100% recovery was 53.1 +/- 5.3 minutes for group I and 46.3 +/- 9.2 minutes for group II. CONCLUSIONS AND CLINICAL RELEVANCE: Atracurium did not affect IOP or arterial blood pressure in isoflurane-anesthetized dogs. Hyperventilation did not affect IOP or the duration of effect of atracurium.     

Nutritional Management of Idiopathic Chronic Colitis in the Dog

Idiopathic chronic colitis was diagnosed in 13 dogs. Owners sought veterinary care because of semiformed to liquid feces, fresh blood and/or mucus in the feces, tenesmus, increased frequency of defecation, vomiting, weight loss, and flatulence in their dogs. A lymphocytic, plasmacytic infiltration in the colonic lamina propria was found on colonic biopsy specimens. Signs resolved in all 13 dogs after they were fed a low residue, easily assimilated, relatively hypoallergenic diet. In 11 dogs, two commercial diets not previously fed to these dogs were successfully substituted for the initial test diet, without causing recurrence of signs. Only two of these 11 dogs subsequently tolerated a switch to diets that had been fed at the time of onset of signs of colitis. All 13 dogs have been successfully managed from 2 months to 28 months following the initiation of dietary therapy. The results of these dietary challenges strongly suggest a dietary role in the pathogenesis of this disorder, and also illustrate the importance of dietary therapy in the management of idiopathic chronic colitis.     

REGIONAL BRAIN PERFUSION IN EPILEPTIC DOGS EVALUATED BY TECHNETIUM-99m-ETHYL CYSTEINATE DIMER SPECT

We evaluated the feasibility of interictal single photon emission computed tomography (SPECT) to detect alterations in regional cerebral blood flow and neuronal activity in dogs with idiopathic epilepsy. Twelve dogs with idiopathic epilepsy underwent interictal technetium-99m-ethyl cysteinate dimer SPECT of the brain. Different cortical regions of interest (ROIs), 1 ROI at the cerebellum and 1 ROI at the subcortical area were evaluated by semiquantitative analysis and compared with a control group (18 dogs). Significant hypoperfusion ( P =0.02) was present in the subcortical area of epileptic dogs. This hypoperfusion was not associated with seizure frequency, age at onset of seizures, duration of epilepsy, or time since the last seizure. Interictal SPECT did not reveal cortical or cerebellar perfusion alterations. The subcortical area may play an important role in the pathophysiology of canine idiopathic epilepsy.     

Cardiac troponins I and T in dogs with pericardial effusion

Cardiac troponin I (cTnI) and cardiac troponin T (cTnT) are sensitive and specific markers for myocardial ischemia and necrosis. Dogs with pericardial effusion frequently have myocardial ischemia and necrosis, and these changes are more severe in dogs with hemangiosarcoma (HSA). We investigated the utility of using serum cTnI and cTnT concentrations to identify the idiopathic pericardial effusion from that associated with HSA. Blood samples for measurement of cTnI and cTnT concentrations were collected before pericardiocentesis in 37 dogs with pericardial effusion. Eighteen dogs had a mass consistent with HSA, 6 dogs had idiopathic pericardial effusion, 1 dog had mesothelioma, and 1 dog had a heart base tumor. No final diagnosis was achieved for 11 dogs. Dogs with pericardial effusion had significantly higher serum concentrations of cTnI (P < .001) but not cTnT (P = .16) than did normal dogs. Dogs with HSA had significantly higher concentrations of cTnI (2.77 ng/dL; range: 0.09-47.18 ng/dL) than did dogs with idiopathic pericardial effusion (0.05 ng/dL; range: 0.03-0.09 ng/dL) (P < .001). There was no difference in the concentration of cTnT between dogs with HSA and those with idiopathic pericardial effusion (P = .08). Measurement of cTnI may be useful in helping to distinguish between idiopathic pericardial effusion and pericardial effusion caused by HSA.     

Results of thoracic duct ligation in dogs with chylothorax

Thoracic duct lymphangiography and ligation were done on 15 dogs with idiopathic chylothorax. Lymphangiography revealed thoracic lymphangiectasia in all dogs; none had a thoracic duct rupture. Lymphangiography immediately after ligation demonstrated missed branches of the thoracic duct in 4 of the 15 dogs. Eleven of the 15 dogs are alive and doing well. Eight of the 11 had no radiographic or clinical signs of pleural effusion (mean follow-up, 31.5 months; range, 4 to 75 months). The other 3 living dogs had persistent effusion; 2 were successfully managed with a pleuroperitoneal shunt (follow-up, 15 months) or pleurodesis (follow-up, 5 months), respectively, and 1 was not treated because the effusion was mild and the dog did not have clinical signs of disease (follow-up, 14 months). Four of the 15 dogs died or were euthanatized because of persistent effusion (mean follow-up, 11.5 months; range, 3 to 24 months). Considering the lack of treatment alternatives for dogs with idiopathic chylothorax, these results support thoracic duct ligation as a treatment method for dogs.     

Clinical Forms of Acquired Myasthenia Gravis in Dogs: 25 Cases (1988–1995)

The purpose of this project was to investigate the clinical forms of acquired myasthenia gravis in dogs. The medical records from 25 dogs with seropositive acquired myasthenia gravis were reviewed, and the following data were recorded for each patient: signalment, history, clinical findings; results of IV edrophonium chloride administration, repetitive nerve stimulation, and presence or absence of muscle membrane staining by immunocytochemical methods; serum acetyl-choline receptor antibody concentration; treatment; and outcome. Several clinical forms of acquired myasthenia gravis were identified. Nine of the 25 patients (36%) had no historical or clinical evidence of appendicular muscle weakness, and were designated as focal myasthenics. These dogs exhibited focal weakness in one or more of the following muscle groups: facial {3 of 9), pharyngeal (3 of 9), and laryn-geal (3 of 9). The remaining 16 dogs (64%) exhibited appendicular muscle weakness. Four of these 16 dogs had acute onset and rapid development of clinical signs, and were designated as acute fulminating myasthenics. The remaining 12 dogs were classified as generalized myasthenics. All 4 dogs with acute fulminating myasthenia gravis had megaesophagus, 2 had facial muscle weakness, and 1 had pharyngeal muscle weakness. Ten of the 12 dogs with generalized myasthenia gravis had megaesophagus, 4 had facial muscle weakness, 4 had pharyngeal muscle weakness, and 3 had laryngeal muscle weakness. Historical or clinical evidence of exercise-associated appendicular weakness was found in only 6 of the 12 (50%) dogs with generalized myasthenia gravis, and in none of the dogs with acute fulminating myasthenia gravis. Seven of the 12 dogs with generalized myasthenia gravis had weakness primarily (n = 1) or exclusively (n = 6) of the pelvic limbs. Two of the 4 dogs with acute fulminating myasthenia gravis had primarily pelvic limb weakness. Twelve of the 25 dogs (48%) died or were euthanized shortly after admission to the hospital due to aspiration pneumonia. The dogs with acute fulminating myasthenia gravis had a markedly higher 1-year mortality rate in comparison with the other 2 groups. The use of immunosuppressive therapy had a significant positive effect on patient survival, regardless of the type of myasthenia gravis. This investigation demonstrates that acquired myasthenia gravis in dogs is a disorder with a wide spectrum of clinical forms, similar to the analagous disorder in people.     

Tongue atrophy as a neurological finding in hereditary polyneuropathy in Alaskan malamutes

BackgroundTongue atrophy with wrinkling as a clinical sign of inherited polyneuropathies has not been reported in dogs.ObjectivesClinically describe tongue atrophy as well as morphology of the tongue and hypoglossal nerve in Alaskan malamute polyneuropathy (AMPN).AnimalsSix client‐owned Alaskan malamute dogs diagnosed with AMPN, all homozygous for the causative mutation in the N‐myc downstream‐regulated gene 1 (NDRG1) and 1 neurologically normal control Alaskan malamute.MethodsProspective case study. Clinical and neurological examinations were performed on affected dogs. Necropsy samples from the tongue muscle and hypoglossal nerve were examined by light and electron microscopy.ResultsAll affected dogs had abnormal wrinkles and grooves on the dorsal surface of the tongue, a clinical sign not described previously in dogs with AMPN. Electromyography of the tongue performed in 2 dogs showed spontaneous activity. Five affected dogs underwent necropsy studies. Histopathology of the tongue showed groups of angular atrophic myofibers and changes in the hypoglossal nerve included thinly myelinated fibers, small onion bulbs, folded myelin, and axonal degeneration.Conclusion and Clinical ImportanceHistopathologic changes in the tongue and hypoglossal nerve were consistent with previously reported changes in skeletal muscle and other nerves from dogs with AMPN. Therefore, we conclude that macroscopic tongue atrophy is part of the disease phenotype of AMPN and should be considered a potential clinical sign in dogs with polyneuropathies.