Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over-the-counter availability of drugs in developing countries poses the risk of their abuse and overdosing in animals by the owners. This report describes ivermectin toxicosis and its treatment with neostigmine methylsulfate in 2 kittens and an adult cat that had been massively overdosed by their owners. Of two 4-w-old 300 g kittens, one was injected with 1.5 ml ivermectin (15 mg; corresponding to 250 times the recommended dose) by the owner and became comatose, started salivation and died after 2 1/2 h. The other kitten was treated with about 0.75 ml ivermectin (7.5 mg; corresponding to 125 times the recommended dose) by the same owner and developed ataxia and salivation after 2 h, went into coma the next morning and was presented for treatment with mydriasis, coma, slight fever (102.4 F), tachypnea (48/min) and severe tachycardia. This kitten was treated twice at a half hourly interval with neostigmine methylsulfate (25 microg) and 5% dextrose (20 ml) iv showed a transient improvement but died 12 h later. A 2-y-old, 4.5 kg male cat was treated s.c. with 1.5 ml ivermectin (15 mg; corresponding to 16.6 times the recommended dose) by its owner and developed slight salivation, lacrimation. mydriasis, protrusion of third eye-lid, tachypnea (42 breaths/min), tachycardia (128 beats/min) and ataxia. The patient was treated with neostigmine methylsulfate (150 microg) and 5% dextrose (100 ml) i.v., and 200 ml of Heartmann's solution i.v. Treatment was repeated after 6 h Follow up treatment over next 2 d was with daily i.v. administration of neostigmine and dextrose. The patient completely recovered 5 d after initiation of treatment.
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PMID:Use of neostigmine in massive ivermectin toxicity in cats. 1474 14

The medical records of 19 horses with acute hemoperitoneum were reviewed. The causes for the hemoperitoneum were idiopathic (8 horses), splenic hematoma with capsular tear (7), bleeding from the reproductive tract (3), multicentric hemangiosarcoma (1), and systemic amyloidosis (1). The affected horses were between 4 and 32 years of age (median 11.5 years). The most consistent findings on initial examination were depression, tachycardia, tachypnea, pale mucous membranes, prolonged capillary refill time, colic, and abdominal discomfort. Less common clinical signs included abdominal distention, profuse sweating, ataxia, and broad ligament mass palpated on rectal examination. Clinicopathologic abnormalities commonly detected were anemia, neutrophilia, lymphopenia, thrombocytopenia, hypoproteinemia, hypocalcemia, azotemia, increased creatinine kinase, and sorbitol dehydrogenase activity. Hemoperitoneum was diagnosed on the basis of abdominocentesis, transabdominal ultrasonography, and postmortem examination. Sixteen horses were treated, and 3 horses were euthanized at owners' request because of severe clinical signs. The treatment consisted of the administration of intravenous fluids, plasma or blood transfusion, nonsteroidal drugs, antimicrobial drugs, and antifibrinolytic and procoagulant agents. Rapid clinical deterioration was observed in 2 horses, necessitating euthanasia. The remaining 14 horses survived the abdominal bleeding (survival rate 74%) and were discharged 3-15 days (median 7.0 days) after presentation. Postmortem examination of the 6 nonsurvivors showed massive abdominal hemorrhage from splenic hematoma with capsular tear (2 horses), multicentric hemangiosarcoma with liver rupture (1), systemic amyloidosis with splenic hematoma and capsular tear (1), and bilateral ruptured ovarian hematomas (1). In one horse, no origin of the bleeding could be determined during postmortem examination.
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PMID:Acute hemoperitoneum in horses: a review of 19 cases (1992-2003). 1595 49

A 5-year-old, 29-kg, female Labrador retriever developed tachypnea, tachycardia, and ataxia following ingestion of approximately 48 mg/kg of phenylpropanolamine. Initial diagnostic tests showed multiform ventricular tachycardia, left ventricular dilatation with a focal dyskinetic region in the dorsal interventricular septum, and elevations in creatinine kinase and cardiac troponin I. All abnormalities resolved within 6 months. The transient electrocardiographic, echocardiographic, and biochemical abnormalities were consistent with myocardial necrosis from infarction or direct catecholamine-induced myocardial toxicity.
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PMID:Cardiac toxicity from phenylpropanolamine overdose in a dog. 1626 67

A tiletamine hydrochloride-zolazepam hydrochloride combination was used successfully to immobilize 27 free-ranging maned wolves (Chrysocyon brachyurus) at a mean dose of 2.77+/-0.56 (mean+/-SD) mg/kg. The induction time ranged from 3-15 min. Animals remained immobilized for periods of 48.56 +/-12.65 min. Compulsive licking, excessive salivation, muscle twitching, muscle tremors, tachypnea, and bradycardia were observed associated with the induction of the anesthesia in 13 of 27 maned wolves. Muscle twitching, pedal withdrawal reflex, muscle tremors, and ataxia were observed during recovery in three (11%) maned wolves. There were no significant differences in heart rates (P = 0.44), respiratory rates (P = 0.82), and rectal temperatures (P = 0.54) recorded at 5, 15, and 25 min after induction at these dosages. The tiletamine hydrochloride-zolazepam hydrochloride combination was shown to be an effective and safe immobilizing agent for free-ranging maned wolves.
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PMID:Immobilization of free-ranging maned wolf (Chrysocyon brachyurus) with tiletamine and zolazepam in central Brazil. 1731 18

The Asiatic or Himalayan black bear (Selenarctos thibetanus) is an endangered species. In South Asian countries, captive tamed Himalayan bears are commonly used by roving bear-charmers to entertain the people in rural and urban areas. In captivity, this species confronts several psychophysical traumas and communicable diseases, which are prevalent in other domestic species. The present report describes four cases of Trypanosoma evansi infection in live Himalayan charming bears, which originated from the Faisalabad and Jhang districts of Pakistan. The condition was characterized by pyrexia, accelerated pulse, tachypnea, depression, anemic mucous membranes, and ataxia (n = 3). Microscopic examination of peripheral blood films revealed moderate (n = 2) or high (n = 2) numbers of T. evansi. All four bears were treated twice at 3-day intervals with suramin sodium by using almost twice the dosage recommended for common domestic animals (10 mg/kg). The treated bears were found aparasitemic on repeat blood testing on days 5, 7, and 10 post-treatment. No adverse effects were noted and all four cases recovered in 3-7 days after completion of the second round of treatment. One bear died 8 days after the second treatment (day 11). This is the first report of T. evansi in bears.
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PMID:Trypanosoma evansi infections in Himalayan black bears (Selenarctos thibetanus). 1746 82

Biotinidase deficiency is a treatable cause of severe neurological disorders and skin problems. Spinal cord impairment is a rare complication of this disease and is commonly unrecognized. The authors encountered 3 Chinese patients with progressive spinal cord demyelination associated with biotinidase deficiency. Case 1 exhibited fatigue, proximal muscular weakness, and hypotonic paraplegia from the age of 7 years 4 months. Demyelination of cervical and thoracic cord was evident on magnetic resonance imaging (MRI). Case 2 developed visual impairment, blepharoconjunctivitis, and optic nerve atrophy from 5 years of age, which combined with progressive hypertonic paralysis, ataxia, and alopecia from the age of 7 years. His spinal MRI T2-weighted sequence revealed an extensive hyperintense lesion involving the cervical spinal cord C(2) to C(4). Bilateral optic nerves were significantly thick. In case 3, intercurrent wheezing, tachypnea, dyspnea, and lethargy occurred from the age of 1 year. Medulla and upper cervical spine edema and demyelination were found on MRI. Markedly elevated urine organic acids and decreased blood biotinidase activities were observed in the 3 patients. Biotin supplementation led to a dramatic improvement of clinical symptoms in 3 patients. The findings indicate that biotinidase deficiency should be considered in the differential diagnosis of unexplained spinal cord demyelination because prompt diagnosis and treatment with biotin may enable an excellent recovery.
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PMID:Spinal cord demyelination associated with biotinidase deficiency in 3 Chinese patients. 1762 76

Joubert syndrome is a rare genetic disorder characterised by dysplasia of the cerebellar vermis and a malformed brainstem causing ataxia, tachypnoea, nystagmus, hypotonia and mental retardation. An early case of a two-month-old infant presenting with the symptoms mentioned above with the diagnosis of Joubert syndrome is presented here. MRI revealed characteristic "molar tooth" appearance of superior cerebellar peduncles. This case is unusual as it was diagnosed in early infancy.
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PMID:Joubert syndrome: a major brain malformation. 1817 93

A 25-year-old man was referred to our hospital because of repetitive cessation of breathing during sleep. He had a history of longstanding ataxia, motor delay, and mental retardation and had been diagnosed with cerebral palsy. Neurological examination revealed ataxia, general hypotonia and wide-based, shuffling gait. Magnetic resonance imaging showed vermian aplasia and dilated fourth ventricle, consistent with Joubert syndrome. Polysomnography revealed repetitive tachypnea followed by central apnea. Tachypneic episodes were elicited by brief arousals. Nasal continuous positive airway pressure eliminated neither tachypnea nor apnea. This case indicates that a patient with Joubert syndrome may survive into adulthood and present as a case of sleep-disordered breathing.
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PMID:[Joubert syndrome diagnosed based on sleep-disordered breathing in a 25-year-old man--case report]. 1830 70

Abnormalities of deep cerebellar nuclei in Joubert syndrome have been previously reported only in rare autopsy cases. Epilepsy in association with Joubert syndrome is also rarely reported. In two new cases of patients with Joubert syndrome, bilateral hypoplasia of deep cerebellar nuclei was detected in vivo by magnetic resonance imaging. One of the patients had drug-resistant epilepsy. Both patients received clinical examination, electroencephalography, neuropsychologic testing, and high-resolution magnetic resonance imaging (1.5 T). Patient 1, a 7-year-old boy, had muscular hypotonia, periodic tachypnea, mild ataxia, global developmental delay, exotropia, and polydactyly. Patient 2, a 23-year-old woman, had muscular hypotonia, epilepsy with pharmacoresistant generalized tonic-clonic seizures, learning disability, esotropia, and mild gait ataxia. Abnormalities of deep cerebellar nuclei might contribute to the pathophysiology of epilepsy in patients with Joubert syndrome.
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PMID:Hypoplasia of deep cerebellar nuclei in joubert syndrome. 1943 86

Joubert syndrome is an autosomal recessive disorder that is characterized by a variable combination of central nervous system, respiratory and eye anomalies. It is a syndrome with a variable phenotype: partial or complete absence of the cerebellar vermis is seen in all patients, while other cardinal findings include episodic tachypnea and apnea in the neonatal period, jerky eye movements, hypotonia, severe mental handicap, developmental delay, ataxia and impaired equilibrium. Even within sibships the phenotype may vary, making it difficult to establish the exact clinical diagnostic boundaries of Joubert syndrome. A case of Joubert syndrome in a newborn is reported and the importance of recognizing the syndrome in the neonatal period so that specific and effective supportive measures can be started as soon as possible is stressed.
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PMID:Joubert syndrome: Report of a neonatal case. 2001 35


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