Three Domestic Long-haired cats from a litter of five afflicted with alpha-mannosidosis (alpha-mannosidosis) were studied clinically and pathologically. Many of these findings contrasted with those made previously in kittens with deficiency of alpha-mannosidase. In these cats, the clinical signs were generally milder, more slowly progressive, and did not include the prominent skeletal deformities, ocular abnormalities, or hepatomegaly that were reported in prior studies of Persian and Domestic Short-haired kittens. While the Domestic Long-haired cats were spared the central nervous system (CNS) myelin deficiency, which was severe in the Persian but mild in the Domestic Short-haired cats, the extensive loss of Purkinje cells in their cerebellar cortices was without precedent. Additionally, ultrastructural study of the neuronal cytosomes showed a diversity not recorded in the earlier cases. The observed phenotypic heterogeneity was sufficient enough to consider separating feline alpha-mannosidosis into severe, acute and milder, chronic forms in a manner analogous to the Type I and Type II distinctions made in infants and juveniles.

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Multisystemic chromatolytic neuronal degeneration in Cairn terriers. A case with generalized cataplectic episodes.

Multisystemic chromatolytic neuronal degeneration, a newly recognized disease of Cairn Terriers, is described in a second affected North American puppy. In this puppy, the early onset of hind limb weakness at 11 weeks and rapid development of signs of diffuse CNS involvement were distinctive. Signs of cerebellar dysfunction were prominent, but bouts of cataplectic collapse in this puppy constituted the most distinguishing clinical feature. Although electroencephalograph (EEG) recordings lacked a true rapid eye movement (REM) pattern during cataplectic episodes, cervical electromyograph (EMG) potentials ceased or diminished, and imipramine injection was associated with arousal. Postmortem studies revealed that chromatolytic degeneration was very widespread, affecting many neuronal populations in the brain and spinal cord as well as neurons in sensory ganglia. Although the pattern of chromatolysis varied among affected perikarya, chromatolysis was consistently related to dispersion and loss of ribosomes. In this puppy, as opposed to six studied previously, thoracolumbar myelomalacia also occurred symmetrically in the dorsal horns and adjoining funicular white matter. The metabolic derangement underlying this chromatolytic neuronal degeneration and myelomalacia remains unknown.

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PubMedDate not supplied

The diagnostic utility of cerebrospinal fluid creatine kinase activity in the horse.

We evaluated creatine kinase (CK) activity in the cerebrospinal fluid (CSF) of 128 horses with various neurological disorders. No association was found between CSF CK activity and CSF red blood cell count, CSF nucleated cell count, CSF total protein concentration, or serum CK activity. The sensitivity and specificity of CSF CK activity as a diagnostic test for protozoal myelitis in horses (61% and 56%, respectively) was higher than for cervical stenotic myelopathy, degenerative myelopathy, or motor neuron disease, but was considered to be inadequate to be of use diagnostically. Contamination of CSF with whole blood, hemolyzed red blood cells, or serum did not substantially contribute to increases in CSF CK activity. Addition of epidural fat or dura to CSF significantly increased CSF CK activity in all cases. We suggest that the use of CSF CK activity as a diagnostic indicator of neurological disease in the horse in unreliable, and that CSF CK activity may be falsely increased by contamination of CSF with epidural fat or dura during CSF collection.

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Results of diagnostic investigations and long-term outcome of 33 dogs with brain infarction (2000-2004).

Medical records of 33 dogs presented for acute onset, nonprogressive, intracranial dysfunction that had a magnetic resonance imaging diagnosis of brain infarction were reviewed. Postmortem confirmation of brain infarction was available in 10 dogs. All dogs were evaluated by CBC, serum biochemistry, thyroid and adrenal testing, urinalysis, thoracic and abdominal imaging, and cerebrospinal fluid analysis. Results of coagulation profile and arterial blood pressure were available in 32/33 and 28/33 dogs, respectively. On the basis of the imaging findings, infarcts were classified depending on their type (territorial or lacunar) and location within the brain (telencephalic, 10/33; thalamic/midbrain, 8/33; cerebellar, 15/33). No marked associations among location or type of infarct and patient age and sex, occurrence of systemic hypertension, and the presence or absence of a concurrent medical condition were identified. Small breed dogs (< or =15 kg) were significantly more likely to have territorial cerebellar infarcts, whereas large breed dogs (>15 kg) were significantly more likely to have lacunar thalamic or midbrain infarcts. A concurrent medical condition was detected in 18/33 dogs with brain infarcts, with chronic kidney disease (8/33) and hyperadrenocorticism (6/ 33) being most commonly encountered. Of 33 dogs, 10 were euthanized because of the severity and lack of improvement of their neurologic status or the severity of their concurrent medical condition. No association was identified between type or location of infarct and patient outcome. Dogs with concurrent medical conditions had significantly shorter survival times than those with no identifiable medical condition and were significantly more likely to suffer from recurrent neurologic signs because of subsequent infarcts.

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PubMedDate not supplied

Clinical and topographic magnetic resonance characteristics of suspected brain infarction in 40 dogs.

Medical records of 40 dogs presented for evaluation of acute-onset, nonprogressive, intracranial dysfunction by means of magnetic resonance imaging (MRI) diagnosis of brain infarction were reviewed. Location of the brain infarcts was: 11 of 38, telencephalic; 8 of 38, thalamic/midbrain; 18 of 38, cerebellar; and 3 of 38, multifocal. Telencephalic infarcts developed within the territory of the middle cerebral (4/11), rostral cerebral (2/11), and striate (5/11) arteries. Thalamic/midbrain infarcts developed within the territory of perforating arteries of the caudal portion of the thalamus and rostral portion of the brainstem (8/8). All cerebellar infarcts (18/38) were within the territory of the rostral cerebellar artery or one of its branches. All infarcts appeared nonhemorrhagic, with marked contrast enhancement observed in only 3 of 38 dogs, all of which were imaged more than 7 days after the onset of signs of neurologic dysfunction. Diffusion-weighted imaging (DWI) sequences were available from 6 dogs, all imaged within 5 days of the onset of signs of neurologic dysfunction. Suspected infarcts were hyperintense on DWI sequences and were hypointense on the apparent diffusion coefficient map. Telencephalic infarcts caused abnormal mental status, contralateral postural reaction deficit, contralateral nasal hypalgesia, contralateral menace deficit, and ipsilateral circling. Thalamic/midbrain infarcts caused contralateral or ipsilateral postural reaction deficit, contralateral menace deficit, ipsilateral head tilt or turn, nystagmus, ventrolateral strabismus, and anisocoria. Cerebellar infarcts caused ipsilateral asymmetric cerebellar quality ataxia, head tilt, intermittent opisthotonus, nystagmus, and ipsilateral menace deficit with apparent normal vision.

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