Gene/Protein Disease Symptom Drug Enzyme Compound
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Two cases of Aujeszky's disease in a cat and a dog belonging to the same owner are reported. The two animals each were five months of age. The symptoms shown by the cat were typical of Aujeszky's disease: intense itching, salivation and the head bent to one side. The main symptoms shown by the dog consisted in salivation, ptosis of one eye, a drooping ear, the head bent to one side and ataxia. As itching was not observed in the dog and the animal had spent the first months of its life in wooded surroundings, it could also have been affected with rabies, although it had been inoculated with LEP-Flury vaccine forty days prior to importation. It is of importance to the practitioner to know that itching may be absent in dogs with Aujeszky's disease and that rabies should also be suspected in these cases. Only a laboratory diagnosis will be conclusive. Studies were negative for rabies, the virus of Aujeszky's disease being found to be present in the two cases. The source of infection probably consisted in contaminated pork offal (larynges).
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PMID:[An atypical case of Aujeszky's disease in a dog (author's transl)]. 16 63

A method for testing a rat's physical-dependence liability to sedaditive-hypnotic agents and for evaluating that dependence was studied by using the method. Rats received phenobarbital- or barbital-admixed food on a graded-increase dosage schedule over 30-40 days. Manifestations of CNS-suppressing action of either drug (e.g., systemic muscle relaxation, motor incoordination, staggering gait, and ptosis) persisted day and night during the drug medication. Twenty-four to 48 h after withdrawal of either drug, abstinence symptoms (e.g., muscle fasciculation, nuchal twitching, vocalization, increased irritability, ataxia, hyperthermia, and clonic-tonic and grand mal-type convulsions) were evidenced in all animals (N = 6), some of which died after convulsions. These withdrawal signs in rats were classified and found to be closely correlated with the magnitude of weight loss during the withdrawal. The calssification provides a basis for quantitatively assessing physical-dependence liability. The data obtained in the present study suggest that rats, like dogs and monkeys, are suitable experimental animals for tests in early stages of dependence liability, and that the administration of drug-admixed food is a useful method of developing dependence on both barbiturate and morphine-type drugs.
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PMID:Experimental barbiturate dependence. I. Barbiturate dependence development in rats by drug-admixed food (DAF) method. 41 46

A new syndrome of autosomal recessive spastic ataxia has been isolated in the Charlevoix-Saguenay region of Quebec. This syndrome is remarkably homogeneous and includes: spasticity, dysarthria, distal muscle wasting, foot deformities, truncal ataxia, absence of sensory evoked potentials in the lower limbs, retinal striation reminiscent of early Leber's atrophy and the frequent presence (57%) of a prolapse of the mitral valve. Biochemically, many cases show impaired pyruvate oxidation, others have hyperbilirubinaemia and some have low serum beta-lipoproteins and HDL apoproteins. These features are similar to those found in typical Friedreich's ataxia.
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PMID:Autosomal recessive spastic ataxia of Charlevoix-Saguenay. 64 99

Ataxia and incoordination occurred in 7 lion cubs in a lion park. Postmortem examination of 3 cubs revealed thickened skull bones which compressed the brain and lead to prolapse of the posterior vermis of the cerebellum through the foramen magnum. In 2 of the lions compression of the anterior cervical spinal cord caused marked damage particularly in the dorsal funiculi. In both cubs the central canal of the spinal cord was abnormal being extended laterally. The pathological changes in the bones and the brain together with low liver vitamin A levels lead to a diagnosis of hypovitaminosis A.
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PMID:Neurologic lesions in young captive lions associated with vitamin A deficiency. 86 16

A pharmacological study was performed in the involved pupils to demonstrate the site of lesion in a patient with Fisher's syndrome who showed marked ptosis, complete external ophthalmoplegia, pupillary involvement with anisocoria, facial paresis, ataxia, areflexia, and albuminocytological dissociation in the cerebrospinal fluid. The instillation of 2.5% methacholine produced mild constriction of one pupil. This response was not detectable in the recovery stage. The instillation of 1.25% l-epinephrine produced marked bilateral dilation of the pupils, in both the early and recovery stages. Instillation of 5% tyramine produced pupillary dilation as in the normal pupil. The response to 5% cocaine, tested only in the recovery stage, was weak in one pupil. These results imply that the pupillary involvement was due to peripheral involvement of the sympathetic and parasympathetic nervous systems. The lesion in the sympathetic nervous system was preganglionic, but in the parasympathetic nervous system the precise localization could not be determined.
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PMID:Fisher's syndrome: a pharmacological study of the pupils. 90 Sep 8

Butaclamol hydrochloride (AY-23,028) is a member of a new chemical class for which antipsychotic activity in humans has recently been demonstrated. The compound antagonized amphetamine-induced stereotyped behavior in rats, amphetamine toxicity in aggregated mice and apomorphine-induced emesis in dogs. It depressed both discriminated avoidance and continuous lever-pressing behavior in rats and inhibited ambulation and rearing in the open field. At higher doses, AY-23,028 induced catalepsy. Adrenergic blocking activity, measured by the antagonism of epinephrine-induced mortality, was weak. These pharmacological actions are characteristic of neuroleptic drugs. In the dose range where the aforementioned effects were observed AY-23,028 did not antagonize either the tetrabenazine-induced ptosis or the tremorine syndrome and did not cause either hypothermia or ataxia. The potency and onset of action of AY-23,028 were comparable to those of fluphenazine but AY-23,028 was of longer duration. The results are discussed in relation to current concepts of neuroleptic mechanisms.
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PMID:The behavioral pharmacology of butaclamol hydrochloride (AY-23,028), a new potent neuroleptic drug. 117 96

Three cases (case 1, female, aged 30; case 2, male, aged 32; case 3, male, aged 34) of benign brainstem encephalopathy with truncal ataxia were reported. Two patients had prodromal symptoms Neurological examination revealed truncal ataxia in all cases. As additional neurological signs, anisocoria, mydriasis, nystagmus, ptosis, transient opsoclonus, and facial palsy were seen. There was neither drowsiness nor myoclonus in the three cases. On laboratory examinations, cold agglutination test revealed significant elevation in two cases. The examination of cerebrospinal fluid showed a moderate rise of proteins in one case, but did not revealed pleocytosis in any of the cases. Magnetic resonance imaging of one patient revealed an area of high intensity in the left pontine tegmentum by T2-weighed imaging. The prognosis for all these cases was good, and the reappearance of neurological signs was not present until now. Our cases were different from brainstem encephalitis (Bickerstaff's encephalitis) because of an absence of disturbed consciousness and no pleocytosis in the cerebrospinal fluid. Our cases were also different from "myoclonus-opsoclonus syndrome" because of an absence of myoclonus. We discussed a possibility of a new clinical syndrome which we call "benign brainstem encephalopathy with truncal ataxia".
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PMID:[Benign brainstem encephalopathy with truncal ataxia--a clinical study of 3 cases]. 128 89

A 7-year-old boy presented with bilateral ptosis and atypical retinitis pigmentosa. Before age two, he had had an Fe-refractory anemia, with neutropenia and thrombopenia. Just prior to the ophthalmic examination, the patient developed lactate acidosis, muscular hypotonia, ataxia and increased protein in the spinal fluid. Pancytopenia, pancreas dysfunction and growth retardation are the main features of Pearson's syndrome, most children not surviving beyond age three. The cause of Pearson's syndrome in our patient turned out to be a 5 kb deletion in the mitochondrial DNA. Similar deletions have been described in the Kearns-Sayre syndrome. It seems that children who survive the initial phase of Pearson's syndrome, may develop Kearns-Sayre syndrome.
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PMID:Kearns-Sayre's syndrome developing in a boy who survived pearson's syndrome caused by mitochondrial DNA deletion. 130 30

Primary meningeal lymphoma was diagnosed in an 18-year-old Morgan gelding. The horse was examined because of a 3-day history of progressive ataxia and weakness. The gait abnormalities were worse on the left side, and the pelvic limbs were more affected than the thoracic limbs. Additional findings included signs of depression, miosis of the left pupil, ptosis of the left upper eyelid, and areas of muscle atrophy on the left side of the neck and over the dorsal aspect of the left scapula. Inflammatory changes were evident in the CSF. At necropsy, there was diffuse and irregular thickening of the dura mater along the entire spinal cord. Histologic examination revealed infiltration of the leptomeninges with neoplastic lymphocytes.
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PMID:Primary meningeal lymphoma in a horse. 142 63

A 15 year old patient developed ataxia 2 weeks after an upper respiratory infection. Absent reflexes, external ophthalmoplegia, bilateral ptosis, isochoric mydriasis and week photomotor reflexes (Bell's phenomenon) were noted. A slight increase in protein but not cell content of the CSF was observed. Miller-Fisher syndrome was diagnosed on clinical grounds and visual and auditory evoked potentials were explored and found to be normal. This is in complete agreement to the literature and indicates indemnity of the central nervous system in Miller-Fisher's syndrome. Peripheral nervous system abnormalities that have been identified by pathologic and radiologic studies may explain all of the alterations observed in this syndrome.
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PMID:[Auditory evoked potentials in Fisher's syndrome. A clinical case]. 184 57


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