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)

In addition to a preceeding report the relation of motor development to ataxia and age at onset of symptoms and therapy as well as psychopathological symptoms in relation to intelligence and sex in 32 children with hypothyroidism are reported.
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PMID:[Psychological development of children with hypothyroidism. II. Motor development and psychopathology (author's transl)]. 63 94

This review focuses on the features of pseudotumor cerebri in the pediatric age group. There is no sex predilection in children, and obesity does not appear to be an important factor. Infants and young children may present with irritability, apathy, or somnolence, rather than headache. Dizziness and ataxia may also occur. Papilledema is infrequently noted in pediatric patients if the fontanelles are open or the sutures are split. Pre-adolescents appear more likely than adults or adolescents to have manifestations of their pseudotumor cerebri other than headache and papilledema, including lateral rectus pareses, vertical strabismus, facial paresis, back and neck pain. Among the etiologies that are particularly pertinent to children are tetracycline therapy, malnutrition or renutrition, and the correction of hypothyroidism. Children with pseudotumor cerebri are at risk for visual loss and their visual function must be closely monitored. Surgical intervention is imperative when vision is threatened.
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PMID:Pediatric pseudotumor cerebri (idiopathic intracranial hypertension). 147 50

Several cases of association between cerebellar ataxia and hypothyroidism have been reported, in which cerebellar symptoms regressed after euthyroid state was obtained, suggesting an etiologic relationship between hypothyroidism and ataxia. We present a further case of hypothyroidism and ataxia, with a peculiar positive family history for both thyroid and cerebellar disorders. Long-term replacement therapy with L-thyroxine determined the regression of hypothyroidism; however, no improvement in cerebellar symptoms was observed. The lack of response of the neurologic symptoms to L-thyroxine treatment suggests the absence of an etiological relationship between thyroid disease and cerebellar disease in this case.
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PMID:Familial occurrence of hypothyroidism and cerebellar ataxia. 191 58

A 42-year-old woman who presented phenytoin intoxication induced by acute hypothyroidism was reported. She had a 29-year history of hypothyroidism and a 18-year history of epilepsy. She was treated with phenytoin (PHT) 100 mg, mephobarbital (MPB) 200 mg, valproic acid (VPA) 400 mg and thyroid powder 100 mg daily for 2 years. She had no medical problem until she noticed gait disturbance and diplopia which appeared 1 month after sudden withdrawal of thyroid powder. On admission, she was somnolent and somewhat disoriented. She had nystagmus in horizontal direction of gaze. Her speech was slurred and she could not sit nor stand due to trunkal ataxia. There was prominent intentional tremor in finger-nose test and heel-shin test showed severe ataxia. Blood cell count and blood chemistry examinations were normal. Serum PHT, phenobarbital (PB) levels were elevated as to 26.4, 36.4 micrograms/ml, respectively. VPA level was low. The endocrinological examinations revealed primary hypothyroidism. EEG showed generalized slow background, but cranial MRI, EMG, SEP and ECG were normal. Thyroxine (T4) administration was started soon, and in the course of thyroid hormone replacement, her cerebellar symptoms gradually improved and serum PHT level decreased even to the subtherapeutical level with the same amount of antiepileptic drugs treatment. By the 40th day of admission, thyroid function became normal and cerebellar signs disappeared, however, she needed 200 mg PHT daily to obtain good control of epilepsy. Cerebellar symptoms of this patient were thought to be PHT intoxication rather than ataxia caused by hypothyroidism itself from the viewpoint of clinical manifestations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of phenytoin intoxication induced by hypothyroidism]. 193 66

Congenital hypothyroid dwarfism was diagnosed in a family of Giant Schnauzers. Three female and two male puppies from different litters were evaluated for dwarfism, lethargy, somnolence, gait abnormalities, and constipation. On physical examination, disproportionate dwarfism (n = 5), macroglossia (n = 3), hypothermia (n = 3), delayed dental eruption (n = 3), ataxia (n = 2), and abdominal distension (n = 1) were identified. Results of initial laboratory tests showed anemia (n = 4), hypercholesterolemia (n = 4), hypercalcemia (n = 2), and transudative abdominal effusion (n = 1). Radiographic skeletal surveys disclosed epiphyseal dysgenesis and delayed skeletal maturation (n = 5). A diagnosis of hypothyroidism was established on the basis of low basal serum thyroxine concentrations that failed to increase following the administration of TSH (n = 5) and markedly reduced to absent thyroid image when evaluated with gamma camera imaging of the thyroid gland (n = 4). In the two dogs that were most thoroughly evaluated, the results of thyroid histology, prolonged TSH testing, and repeat thyroid imaging, after three daily injections of TSH, were all consistent with secondary or tertiary, rather than primary, hypothyroidism. When TSH was administered over a period of 3 consecutive days (5 IU/day, subcutaneously), serum thyroid hormone response became normal and resulted in a normal thyroid image in the two dogs re-evaluated with gamma camera imaging. Daily treatment with oral levothyroxine (20 micrograms/kg) resulted in complete remission in puppies (n = 4) treated prior to 4 months of age. The other puppy failed to attain normal breed standards for height.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Congenital hypothyroid dwarfism in a family of giant schnauzers. 174 85

Dementias which are either reversible or avoidable are discussed in the light of the literature. The frequency is between 6 and 32%. The most important etiological groups are immunological vasculopathies, hyperlipidemia, some types of encephalitis and, mainly, progressive dementia of the insane, benign tumors and in particular meningioma, low pressure hydrocephalus, intoxications due to drugs, industrial products and alcohol, metabolic disturbances, encephalopathy in dialysed patients, ileo-jejunal-bypass encephalopathy and encephalopathy due to neoplasms. Dementias are also seen in endocrinological disturbances and particularly in hypothyroidism. Vitamin B12 and folate deficiency, as well as epilepsy, may be causes of dementia. Depression may mimic a state of dementia. Some features of reversible dementias are listed, including in particular the somewhat more rapid onset, the younger age of patients, and accompanying neurological symptoms such as headache, gait disturbances, ataxia, polyneuropathy, myoclonus or epileptic fits.
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PMID:[Reversible and preventable dementias]. 361 87

A 6-year-old, obese, spayed female Doberman pinscher dog was presented for clinical examination with a 1-day history of repeated seizures and a long-term history of periodic bouts of ataxia, circling, and head tilt. The seizures were controlled with phenobarbital, but the dog died 2 days after presentation. Necropsy revealed severe, diffuse, follicular atrophy of the thyroid gland (primary hypothyroidism), severe generalized atherosclerosis, severe pseudolaminar cortical necrosis and acute vasculitis in the cerebrum, and congestive heart failure. The neurologic signs were explained by the pseudolaminar necrosis and associated cerebrovascular atherosclerosis. The cerebrocortical necrosis was believed to be caused by tissue hypoxia secondary to progressive vascular occlusion. Cerebrovascular atherosclerosis, secondary to primary hypothyroidism, was considered the most important cause of the hypoxia.
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PMID:Neurologic manifestations of cerebrovascular atherosclerosis associated with primary hypothyroidism in a dog. 397 13

A case of hypothyroidism with ataxia is described. At necropsy there were degenerative changes in the cerebellum, particularly in the anterosuperior portion of the vermis, together with atrophy of ventral portion of the pons, transverse pontine fibres, and middle and superior peduncles. The relationship between ataxia and pathological findings in myxoedema is discussed.
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PMID:Pathological findings in a case of hypothyroidism with ataxia. 515 93

Trichothiodystrophy is characterized by sparse, short, sulfur-deficient hair. Numerous symptom complexes have been described in which the hair abnormality represents a constant feature. We report a boy with trichothiodystrophy, ichthyotic skin changes, onychodystrophy, chronic neutropenia, osteosclerosis, hypothyroidism, nystagmus, growth and mental retardation, and microcephaly, who developed a progressive encephalopathy with ataxia and optic atrophy at 2.5 years of age. In addition to a deficient cystine level identified on a hair sample, a disturbance in the composition of other amino acids was present. Although features were reminiscent of osteosclerosis, ichthyosis, brittle hair due to trichothiodystrophy, impaired intelligence, decreased fertility, and short stature (SIBIDS) and could represent a variant of this disorder, findings in our patient may reflect a new trichothiodystrophy symptom complex that carries a poor prognosis for survival beyond childhood.
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PMID:Trichothiodystrophy and associated anomalies: a variant of SIBIDS or new symptom complex? 834

A 65 year old woman, referred for differential diagnosis of dementia, presented with cognitive and mnestic deficits. Typical signs and symptoms of hypothyroidism led to the diagnosis of severe autoimmune thyroiditis. After six months of treatment with thyroid hormone, dementia, myopathy and ataxia had disappeared. The neurologic and neuropsychologic manifestations of hypothyroidism are discussed. In dementia the diagnosis of secondary and reversible forms is of great importance with regard to prognosis and treatment. Hypothyroidism is known to be a common and treatable cause of pseudodementia. Early diagnosis and adequate treatment are important to prevent further permanent deterioration of cerebral function.
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PMID:[Reversible dementia]. 965 92


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