Small-cell carcinoma of the lung resembling a brachial plexus tumour

A small-cell carcinoma of the lung was identified in a six-year-old female German shepherd dog with a history of chronic lameness of the left forelimb, Horner's syndrome and sensory deficits on the caudal portion of the left forelimb below the elbow. A mass, the exact location of which was difficult to ascertain, was identified during radiographic examination of the thorax. It was easily identified, using magnetic resonance imaging, as an apical tumour of the left lung with dorsal extension and involvement of paraspinal structures, such as spinal nerve roots C8 to T1 and the sympathetic trunk. Postmortem examination confirmed a mass in the left apical lobe of the lung, compatible with a diagnosis of small-cell carcinoma by histopathology and immunohistochemistry. This clinical presentation is similar to Pancoast syndrome described in humans.     

Hydrocephalus with visual deficits in a cat

A 22-month-old male Japanese mongrel cat with a history of dysuria and recurrent generalised tonic-clonic seizure was examined by neuro-opthalmological testing and computed tomography (CT). Vision testing revealed narrowing of the visual field in the right eye, and complete visual deficits in the left eye. Pupillary reactions, and motor and sensory function in the eyelids and the eyes were normal. The cat was diagnosed as hydrocephalus by CT examination, because dilation of the right lateral ventricle, and compression of the right temporal and occipital cortices was shown. The etiology of the hydrocephalus was unclear. Although a unilateral lesion of the upper visual pathway was suspected, a complete homonymous hemianopsia was not shown.     

Neuroradiographic diagnosis and surgical repair of tethered cord syndrome in an English bulldog with spina bifida and myeloschisis

A 3-month-old English Bulldog had excretory incontinence and sensory deficits in the distribution of pudendal nerves. Noncontrast radiography, myelography, and computed tomography revealed spina bifida beginning at L7, an expanded subarachnoid space caudal to L7, and a taut, thick filum terminale. Microsurgical exploration of the lumbosacral spine confirmed the presence of a tethered cord, and the filum terminale was transected. The spinal cord immediately migrated cranially about 1 cm. Although some sensory improvement was evident during a 2-week postoperative period, the dog was euthanatized. Postmortem examination confirmed spina bifida and atrophy of sacral nerve roots and perineal muscles, thoracic hemivertebrae, and hydrocephalus.     

Sensory neuropathy in two Border collie puppies

A peripheral sensory neuropathy was diagnosed in two Border collie puppies. Neurological, electrophysiological and histopathological examinations suggested a purely sensory neuropathy with mainly distal involvement. Urinary incontinence was observed in one of the puppies and histological examination of the vagus nerve revealed degenerative changes. An inherited disorder was suspected.     

Trigeminal neuropathy in dogs: a retrospective study of 29 cases (1991-2000)

The medical records of 29 dogs unable to close their mouths due to flaccid paralysis or paresis of the muscles innervated by the mandibular branch of the trigeminal nerve, were reviewed. Idiopathic trigeminal neuropathy was diagnosed in 26 dogs based on complete resolution of clinical signs and lack of any long-term neurological disease. Of these dogs, golden retrievers were overrepresented. No age, sex, or seasonal predispositions were identified. Trigeminal sensory innervation deficits were observed in 35% (9/26), facial nerve deficits were observed in 8% (2/26), and Horner's syndrome was observed in 8% (2/26) of dogs. Electromyographic examination of the muscles of mastication revealed abnormalities in seven of nine dogs. Results of cerebrospinal fluid analysis were abnormal in seven of eight dogs. Corticosteroid therapy did not affect the clinical course of the disease. Mean time to recovery was 22 days. Lymphosarcoma, Neospora caninum infection, and severe polyneuritis of unknown origin were diagnosed in three of 29 dogs at necropsy.     

Diagnosis of sciatic nerve tumour in two dogs by electromyography and magnetic resonance imaging

Sciatic nerve tumour was diagnosed in a Staffordshire Bull Terrier cross-bred and a Bichon Frise, both presenting with chronic left hind limb lameness. Neurological examination in each case was consistent with left sciatic nerve deficits and this was confirmed by EMG studies. Rectal examination of both dogs revealed a palpable intrapelvic mass that was not apparent on survey radiographs. A sciatic nerve tumour was identified using MRI in each case. Histological examination of tissue taken from the Staffordshire Bull Terrier cross-bred was consistent with a malignant peripheral nerve sheath tumour.     

Acquired idiopathic laryngeal paralysis as a prominent feature of generalised neuromuscular disease in 39 dogs

A retrospective evaluation of 17 dogs treated surgically for idiopathic acquired laryngeal paralysis demonstrated a marked variability in outcome, with many dogs continuing to exhibit weakness and exercise tolerance. In a subsequent prospective study, 22 consecutive affected dogs were tested for neurological deficits by neurological examination, electrodiagnostic evaluation, and blood analysis to measure thyroxine and thyroid-stimulating hormone and to detect any evidence of myasthenia gravis. Clinical neurological deficits and/or electrodiagnostic abnormalities were found in each case. There was limited evidence that specific neurological deficits were associated with a poor prognosis for full recovery of exercise tolerance. None of the dogs was positive for anti-acetylcholine receptor antibodies, and only three showed evidence of thyroid dysfunction.     

Acute non-ambulatory tetraparesis in a 6-month-old Standardbred weanling caused by a cervical vertebral epidural haematoma

A 6-month-old Standardbred weanling presented with acute non-ambulatory tetraparesis. Cranial nerve examination was normal and neuroanatomic localisation suggested there was a focal C1-C5 spinal cord lesion. Post-mortem examination identified a cervical vertebral epidural haematoma at the level of C2-C3 causing spinal cord compression and neurological deficits. Histological examination determined the haematoma was several weeks old making the lesion chronic. Since the clinical progression was acute, this suggests an acute on chronic pathophysiology. Even with no history of trauma, an epidural haematoma should be on the differential list in young horses with acute tetraparesis.     

Neurologic deficits associated with severe hyponatremia in 2 foals

Objective: To describe the neurologic deficits associated with profound hyponatremia in 2 critically ill foals. Series summary: A 4‐month‐old Thoroughbred colt and an 11‐day‐old Paint filly presented for acute diarrhea and depression. Severe neurologic deficits including blindness and head pressing were noted upon initial examination along with marked hyponatremia observed on biochemistry profile. Aggressive intravenous sodium replacement increased the serum sodium concentration to subnormal values with concurrent resolution of neurologic deficits. Intensive monitoring and fluid therapy were continued; the Thoroughbred colt was euthanized due to lack of response to the primary disease while the Paint filly was discharged clinically healthy without further complications. New or unique information provided: Mild hyponatremia (122–132 mEq/L) is a common clinicopathologic finding in equine medicine associated with a variety of diseases. The vast majority of horses with mild hyponatremia do not demonstrate direct clinical manifestations as a result of low serum sodium concentration. However, when severe acute hyponatremia occurs (<122 mEq/L), such as with acute enterocolitis, subtle to profound neurologic deficits may be observed and immediate and rapid treatment as well as serial evaluations of serum sodium concentration are warranted. Significant, and potentially permanent, neurologic deficits can occur if water balance and tonicity are not properly addressed. The cases presented here describe additional cases of a previously published disease in foals, acute hyponatremia and associated neurologic deficits, and describe the microscopic examination of the central nervous system in one foal that did not survive.     

Urethral haemangiosarcoma in a boxer

A seven-year-old, entire female boxer presented with a history of restless behaviour and inappetence. Physical examination revealed that the dog was listless and had a hunched gait. Neurological examination was normal. Abdominal ultrasonography revealed a 4 cm x 4 cm mass in the cranial pelvic canal. Neurological abnormalities were detected three days after presentation, and progressed from proprioceptive deficits to loss of deep pain sensation in the pelvic limbs over a two-day period. The dog was euthanased and postmortem examination revealed that the pelvic mass was a urethral haemangiosarcoma with metastasis to the second lumbar vertebra. This case is unusual as urethral tumours are usually transitional cell carcinomas and frequently present with signs of dysuria.     

Solitary plasmacytoma of bone in two successfully treated cats

This is the first report of feline solitary plasmacytoma of bone. We describe the clinical, clinico-pathological, radiographic and pathological findings of two successfully treated cats with long-term follow-up. The first case presented with spinal pain and neurological deficits. Radiographs demonstrated sclerosis of lumbar vertebra L6 and a myelogram confirmed interference to flow of contrast in the L4-7 region. A biopsy of L6 revealed neoplastic plasma cell infiltration. There was no evidence of paraproteinaemia on serum protein electrophoresis. The cat underwent hypofractionated megavoltage radiotherapy. Clinical signs resolved completely and 4 years after diagnosis the cat remains well and has no electrophoretically detectable paraproteinaemia. The second case presented with neurological deficits of the tail and spinal radiographs revealed extensive osteolysis of the sacrum. A biopsy of sacral bone demonstrated neoplastic plasma cell infiltration. The animal was normoglobulinaemic. The cat improved clinically with induction chemotherapy (melphalan and methylprednisolone). The same chemotherapeutics were continued at maintenance doses for 4.3 years, at which time there was recurrence of neurological deficits and a palpable sacral mass. Cytological examination of a fine needle aspirate confirmed recurrence of plasma cell neoplasia. A low concentration monoclonal paraproteinaemia was detected. Vincristine was administered resulting in resolution of neurological deficits and a palpably smaller sacral mass. Eighteen months into vincristine therapy, there was recurrence of clinical signs and the cat was euthanased, more than 6 years after the initial diagnosis.     

Lumbar spinal 'juxtaarticular' cyst in a Gordon setter

An 11-year-old Gordon setter bitch was presented with a history of progressive weakness in the right hind limb associated with pain in the lumbar spine. Neurological deficits consisted of ataxia, monoparesis, muscle atrophy and spontaneous over-knuckling of the affected limb. A large 'juxtaarticular' cyst located in a right dorsolateral position of the intervertebral foramen at L3-L4 was diagnosed by magnetic resonance imaging. The cyst was removed through a modified laminectomy. The dog recovered quickly and returned to the owners 4 days after surgery with slight neurological symptoms. During the follow-up examination 2 and 6 months later, the Setter showed normal gait and neurological examination.     

Gait deficits in liver disease: Hepatic encephalopathy and hepatic myelopathy

In this issue, the unusual clinical presentation of a horse diagnosed is described with severe liver cirrhosis and hepatic encephalopathy. The horse initially presented for thoracic and pelvic limb ataxia and weakness, and signs of forebrain disease were not apparent until later in the disease process. The typical pathology of central nervous system disease associated with liver disease is related to encephalopathy and forebrain disease; however, the spinal cord is occasionally also involved. Hepatic myelopathy is a rare syndrome usually associated with surgical or acquired portosystemic shunts, liver cirrhosis and/or portal hypertension in man. Where a gliopathy is the most prominent pathological feature seen in hepatic encephalopathy, in hepatic myelopathy the most remarkable feature is demyelination of the corticospinal tracts of the distal cervical and thoracic spinal cord with occasional axon loss. The clinical signs of hepatic myelopathy are spastic paresis/paralysis with normal sensory findings and preserved sphincter function. The prognosis for hepatic myelopathy is generally poor. In summary, in severe liver disease, motor deficits can occur secondary to the encephalopathy, but motor deficits can also occur as a result of spinal cord pathology such as seen in hepatic myelopathy. In examination of horses with myelopathies, liver disease as a cause of myelopathy should be included in our list of differentials.     

Imaging diagnosis and clinical presentation of a Chiari malformation in a Thoroughbred foal

A newborn Thoroughbred foal was presented to the clinic with ambiguous neurological deficits, spinal anomalies and a soft tissue swelling dorsal to the lumbar vertebral column. The foal was alert but unable to rise and stand. With radiography, ultrasonography, computed tomography (CT) and magnetic resonance imaging (MRI) a lumbar dysraphic anomaly, cerebellar herniation and coincidental skeletal abnormalities were documented. Finally, a meningomyelocele was defined and, in context with the cerebellar herniation through the foramen magnum, the foal was diagnosed to have a Chiari malformation. The MRI examination corresponded best with the post mortem findings. Although 3‐dimensional imaging methods have been considered superior regarding full and detailed assessment of the congenital malformation, radiography and ultrasonography also provide essential information to diagnose dysraphic lesions at reduced costs and efforts. A Chiari malformation should be considered as a differential diagnosis in foals with neurological deficits.     

Adult-onset cerebellar cortical abiotrophy and retinal degeneration in a domestic shorthair cat.

A 4-year-old, neutered male domestic shorthair cat presented for evaluation of ataxia and visual deficits. Neurological examination revealed severe cerebellar ataxia with symmetrical hypermetria and spasticity, a coarse whole-body tremor, positional vertical nystagmus, and frequent loss of balance. A menace response was absent bilaterally, and the pupils were widely dilated in room light. A funduscopic examination revealed markedly attenuated to absent retinal vessels and pronounced tapetal hyperreflectivity, findings consistent with end-stage retinal degeneration. Blood work evaluation included retroviral testing, a complete blood count, serum biochemistry analysis, taurine levels, and toxoplasma immunoglobulin G and immunoglobulin M titers. All were within reference ranges. The patient was euthanized, and a necropsy was performed. Microscopically, lesions of the nervous system were confined to the cerebellum and were consistent with cerebellar cortical abiotrophy. Selective photoreceptor degeneration was seen on histopathological examination of the retina with a reduction in the number of rods and cones. The combination of clinical findings and histopathological lesions seen here has not been previously reported in the cat.     

Surgical management of acute ear canal separation in a cat

A 5-year-old cat presented with haemorrhagic left aural discharge, 2 days following a road traffic accident. Otoscopic examination identified disruption of the external ear canal at the auricular/annular cartilage junction. This was managed by total ear canal ablation and lateral bulla osteotomy. Left sided facial nerve deficits were present following surgery. Eighteen months postoperatively there were no auricular problems, however facial nerve deficits persisted. There are no previous reports describing management of acute separation at the auricular/annular cartilage junction of the external ear in the cat or dog. This case report describes the presentation, diagnosis and surgical management of an acute ear canal separation at the auricular/annular junction of the external ear canal in a cat.     

Cerebellar granuloprival degeneration in an Italian hound

A severe atrophy of the cerebellum was observed in a 7-month-old male Italian hound with a history of progressive ataxia and head tremor from the age of 3 months. On clinical examination, signs included severe hypermetric gait, head tremors and proprioception deficits in all limbs. At necropsy, a pronounced symmetrical reduction in size of the cerebellum was the only gross lesion observed. Histological examination of the cerebellum revealed marked thinning of the granular and molecular layers with almost complete loss of granule cells. Purkinje cells had normal morphology and distribution. These findings differ from those of previous reports of cerebellar cortical abiotrophy in dogs, which were mainly characterized by prominent Purkinje cell degeneration and loss.     

Sensory and motor neuropathy in a Border Collie

A 5-month-old female Border Collie was evaluated because of progressive hind limb ataxia. The predominant clinical findings suggested a sensory neuropathy. Sensory nerve conduction velocity was absent in the tibial, common peroneal, and radial nerves and was decreased in the ulnar nerve; motor nerve conduction velocity was decreased in the tibial, common peroneal, and ulnar nerves. Histologic examination of nerve biopsy specimens revealed considerable nerve fiber depletion; some tissue sections had myelin ovoids, foamy macrophages, and axonal degeneration in remaining fibers. Marked depletion of most myelinated fibers within the peroneal nerve (a mixed sensory and motor nerve) supported the electrodiagnostic findings indicative of sensorimotor neuropathy. Progressive deterioration in motor function occurred over the following 19 months until the dog was euthanatized. A hereditary link was not established, but a littermate was similarly affected. The hereditary characteristic of this disease requires further investigation.     

Electrophysiological evaluation of traumatic forelimb paralysis of the dog

The results of clinical neurological, electromyographic and electroneurographic examinations in 26 dogs with traumatic forelimb paralysis are presented. The results of neurological examination varied considerably among the cases. Electromyographic evidence of denervation in the epaxial muscles was observed in 22 dogs. A post ganglionic dorsal root lesion was diagnosed in 14 cases by the presence of an evoked sensory nerve action potential in association with loss of conscious pain perception in the appropriate area. Motor nerve studies in the ulnar nerve were not helpful in discriminating root lesions from spinal nerve involvement. It was concluded that electromyographic examination of the ipsilateral epaxial muscles under general anaesthesia is essential for the detection of root involvement. Sensory conduction studies in the radial nerve are indicated if conscious pain perception is absent in the fifth digit. Motor and sensory conduction studies of the ulnar nerve system seldom provide additional diagnostic information seldom provide additional diagnostic information. The absence of electrophysiological signs of root involvement does not exclude a post ganglionic dorsal root lesion.     

Management of fluorouracil toxicity in a Labrador retriever-poodle crossbred dog

A juvenile, neutered male, Labrador retriever-poodle crossbred dog was brought to a veterinary hospital for overnight care after ingesting fluorouracil 5.0% (5-FU) topical solution. The exposure occurred the night before and involved an unknown amount of fluorouracil. The dog survived the acute toxicity but developed status epilepticus requiring control with general anesthesia and spent multiple days hospitalized in a comatose state, eventually waking with sensory deficits in both vision and smell which resolved over time. Blood samples taken at a recheck visit 1 week after ingestion, showed the dog had developed severe thrombocytopenia and moderate leukopenia. Ten days after initial intoxication, the dog developed progressive alopecia which eventually affected the entire body.