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)

Between 1986 and 1988 a door-to-door survey was conducted on a stable rural population of 60,820 in central Ethiopia. Trained lay health workers made a complete census and identified cases with symptoms and signs of neurological disorders, using specially designed questionnaires which, in a previous pilot study, were found to have a sensitivity of 91% and specificity of 85%. Neurological disorders in the rural population were epilepsy, postpoliomyelitis paralysis, mental retardation, peripheral neuropathy (mainly due to leprosy), and deaf-mutism with prevalence rates (cases/100,000 population) of 520, 240, 170, 150 and 130, respectively. The prevalence rates of the other less common neurological disorders were 62 for hemiparesis (15 of which were for cerebrovascular accidents), 20 for cerebral palsy, 16 for optic atrophy, 12 for perceptive deafness, 10 for tropical spastic paraparesis, 7 for Parkinson's disease and 5 for motor neuron disease, ataxia and chorea/athetosis. Among related non-neurological conditions, blindness, locomotor disability and deafness were predominant. The significance and role of such a neuroepidemiological study in laying the strategies for the prevention of neurological disorders and rehabilitation of patients are discussed in the context of a developing country.
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PMID:Community-based study of neurological disorders in rural central Ethiopia. 208 51

A Hansen type I cervical intervertebral disc prolapse was diagnosed in a 16-year-old American Saddler showing clinical signs of paresis and ataxia. An ante-mortem diagnosis was made by means of plain radiographs and a myelogram. The horse was euthanased and the diagnosis confirmed on a post-mortem examination.
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PMID:[Cervical intervertebral disk prolapse in a horse]. 336 56

The sensory loss which occurs in leprosy is essentially cutaneous, resulting from centripetally ascending infection, the host cellular response and fibrosis, from dermal to certain mixed nerves. The hallmark is pain/temperature and touch/pressure loss. Muscle denervation is a byproduct of mixed nerve involvement. Leprous sensory and motor neuropathy presents a stereotyped picture, with preservation of position sense, noninvolvement of the large girdle muscles, and retained deep tendon reflexes. We report clinical and investigative details of 7 patients (3 males, 4 females) with mild-to-moderate polyneuritic leprosy who manifested severe proprioceptive loss in the upper per limbs; the lower limbs were similarly affected in 4 of them. Tendon reflexes were absent in the ataxic limbs. No other cause was found for the ataxia. Electrophysiological studies confirmed damage to large cutaneous and muscle afferents, and a normal EMG pattern in hip and shoulder muscles. Of great interest was the histology of a lumbar sensory ganglion biopsied in a severely disabled patient. There was extensive neuron loss and degeneration and reactive proliferation of capsular cells ("nodules of Nageotte"), an inflammatory focus of lymphocytes, and no bacilli. This suggests to us that the proprioceptive loss in these patients could well be the result of an unusual "leprous ganglionitis." Further clarification of the mechanism of ganglion degeneration and the frequency of inflammation could come from immunohistology of tissues from African green monkeys with experimental polyneuritic leprosy.
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PMID:Severe pan-sensory neuropathy in leprosy. 818 85

A 35-year-old man with borderline tuberculoid leprosy developed Type I lepra reaction 12 days after anti-leprosy treatment. There was acute worsening of neuropathic symptoms and skin lesions. He developed severe sensory ataxia and pseudoathetosis resulting in marked disability. His symptoms significantly improved on corticosteroid therapy.
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PMID:Pseudoathetosis in a patient with leprosy. 1272 78

Western medicine was introduced to Taiwan in 1865 when Dr. James L. Maxwell, a missionary doctor of the English Presbyterian Church, established a hospital in nowadays Tainan. The period of the missionary medicine lasted for over 30 years until Japanese took over. During this period, however, official records of diseases in Taiwan that were based on Western medicine were scanty or not available. Fortunately, port surgeons stationing respectively in Tamsui and Kelung in the north and in Takow and Taiwan-fu in the south reported semi-annually diseases seen in the ports, foreign communities and missionary hospitals that they volunteered to work. The diseases reported by port surgeons were either cases or summary of cases with classification and statistics. Their medical reports covered from 1871 to 1900. The data show that neurological diseases and/or disorders in the late 19th century Taiwan were uncommon, comprising only 2-3% of total diseases. The data further show that common neurological diseases were leprosy, opium smoking, syphilitic dementia (GPI), paralysis, hysteria, neuralgia, epilepsy, mania, sciatica, meningitis and ataxia. Stroke was uncommon while Parkinson's disease and Alzheimer's disease were not mentioned, indicating that neurological diseases related to old age and neurodegeneration were not yet a threat to health. Similarly, headache, insomnia, anxiety and depression, hallmark of functional disorders of the modern society, were also not mentioned, suggesting that these disorders were indeed rare or did not cause sufficient concern for patients to seek help from doctors of Western medicine.
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PMID:[Neurological diseases in late 19th century Taiwan--medical reports of the Chinese Imperial Maritime Customs]. 1642 51

Peripheral neuropathy refers to disorders of the peripheral nervous system. They have numerous causes and diverse presentations; hence, a systematic and logical approach is needed for cost-effective diagnosis, especially of treatable neuropathies. A detailed history of symptoms, family and occupational history should be obtained. General and systemic examinations provide valuable clues. Neurological examinations investigating sensory, motor and autonomic signs help to define the topography and nature of neuropathy. Large fiber neuropathy manifests with the loss of joint position and vibration sense and sensory ataxia, whereas small fiber neuropathy manifests with the impairment of pain, temperature and autonomic functions. Electrodiagnostic (EDx) tests include sensory, motor nerve conduction, F response, H reflex and needle electromyography (EMG). EDx helps in documenting the extent of sensory motor deficits, categorizing demyelinating (prolonged terminal latency, slowing of nerve conduction velocity, dispersion and conduction block) and axonal (marginal slowing of nerve conduction and small compound muscle or sensory action potential and dennervation on EMG). Uniform demyelinating features are suggestive of hereditary demyelination, whereas difference between nerves and segments of the same nerve favor acquired demyelination. Finally, neuropathy is classified into mononeuropathy commonly due to entrapment or trauma; mononeuropathy multiplex commonly due to leprosy and vasculitis; and polyneuropathy due to systemic, metabolic or toxic etiology. Laboratory investigations are carried out as indicated and specialized tests such as biochemical, immunological, genetic studies, cerebrospinal fluid (CSF) examination and nerve biopsy are carried out in selected patients. Approximately 20% patients with neuropathy remain undiagnosed but the prognosis is not bad in them.
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PMID:Diagnostic approach to peripheral neuropathy. 1989 45