Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 66-year-old female suffering from HTLV-1 associated myelopathy (HAM) for more than 30 years was hospitalized because of memorial impairment, deafness, dysarthria, dysphagia, and complete paraplegia. She first noticed stiffness and weakness of the right leg at 35 years of age. Gait disturbance was slowly progressed and complete paraplegia developed 18 years later. Neurological examinations on admission revealed that she was bedridden with decubitus, mental deterioration (pre-dementia of subcortical type), bilateral optic nerve atrophy, severe sensory-neural deafness, dysarthria, complete paraplegia, and marked neurogenic bladder. Laboratory data showed mild normocytic anemia and moderate diabetes mellitus. Anti-HTLV-1 antibody titers in serum and CSF were 78,192X and 1,024X, respectively (PA method). Serum levels of soluble IL-2 receptor was markedly elevated (2,200 U/ml). Peripheral blood lymphocytes showed spontaneous proliferation when cultured for 5 days (3H-thymidine uptake; 45,285 cpm/5 X 10(4) cells). MRI examinations of the spinal cord disclosed a predominant atrophy of lower thoracic cord without any compressive lesions. Brain MRI showed diffuse high intensity lesions of the periventricular area on T2 weighted images. Such abnormalities were predominantly found in fronto-parietal region and were quite similar to those of leuko-ariosis. Single photon emission CT using 123I-iodoamphetamine showed hypoperfusion of cerebral white matter on delayed image. It has been reported that intellectual impairment and brain atrophy are not usually seen in HAM patients. The present case, however, shows that such abnormalities of the central nervous system could occur in HAM patients with a long duration of illness.
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PMID:[A case of HTLV-1 associated myelopathy progressed in course over 30 years]. 189 70

The authors report a clinical review of 16 childhood cases with early-onset cerebellar ataxia with retained tendon reflexes. The preservation of tendon reflexes distinguishes this disorder from Friedreich's ataxia. The mean age of onset of symptoms was 7.1 years. The main presenting symptom was abnormal gait (100%). Ataxia of gait and limbs and normal or increased tendon reflexes were found in all cases. This disorder is associated with dysarthria, pyramidal signs in the limbs, and in some instances, sensory loss. Other important differences from Friedreich's ataxia are absence of optic atrophy, diabetes mellitus, cardiomyopathy and severe skeletal deformity. Sensory nerve conduction was found to be normal, excluding one case. This finding constitutes another aspect of the syndrome different from Freidreich's ataxia. CT scans were normal in 2 of the 4 cases. The remaining two cases showed cerebellar atrophy. Inheritance is probably autosomal recessive in the majority of cases.
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PMID:Early-onset cerebellar ataxia with retained tendon reflexes. 261 87

The clinical features of six women with spinal cord meningioma are presented. These cases comprise the neurosurgical experience of one of the authors (B.B.) over approximately a 3-year period. Median age was 76 years with a range of 65-89 years. Previous reports of this disorder have not emphasized the occurrence of this tumour in the later decades. A notable feature was delay in diagnosis. Only one patient had a correct diagnosis of spinal cord compression prior to admission. Incorrect diagnoses included diabetes mellitus, osteoarthritis, degenerative spinal disease, gait disturbance secondary to fall and a thalamic cerebrovascular accident. Gait disorders at presentation included paraparesis, wide-based gait and unclassified disability. All patients had pyramidal tract signs and five had a truncal sensory level. Plain radiographs of the spine were unhelpful and can dissuade the physician from the diagnosis. All tumours were in the thoracic region. Surgery resulted in cure in all patients and diverted one patient from planned institutional care. Spinal cord meningioma should be considered in elderly patients presenting with gait disorder.
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PMID:Spinal cord meningiomas in the elderly. 342 85

Stiff-man syndrome is a well-described, but rare and often overlooked, neuromuscular syndrome of rigidity, spasm, and gait abnormality that is associated with several endocrinologic and autoimmune disorders. A patient exhibiting many typical features of stiff-man syndrome had intermittent symptoms for 22 years before the correct diagnosis was made. Similar to many described patients, she was diabetic, hyperthyroid, and had elevated islet cell, antithyroid, and glutamic acid decarboxylase antibody levels. The high frequency of diabetes mellitus among patients with stiff-man syndrome is emphasized, as is increasing evidence to suggest that elaboration of anti-glutamic acid decarboxylase and anti-islet cell antibodies may play a role in the pathophysiologic state of the disorder.
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PMID:Stiff-man syndrome. Report of a case. 820 96

Friedreich's ataxia (FRDA) is the most frequent cause of recessive ataxias. Neurological examination shows oculo-motor ataxia, dysarthria, limbs ataxia, tendon areflexia, pyramidal signs and sensory deficits. Extra-neurological involvement consists in osteoarticular deformities, cardiomyopathy and diabetes mellitus. Neurological deficits and osteoarticular deformities both contribute to the gait disorder, which is the main disabling deficit. In 98% of the cases, a trinucleotide repeat is found in chromosome 9. Gene implicated in FRDA codes for a protein called frataxin. Experimental studies have revealed iron accumulation in mitochondria of neurons and cardiomyocytes, suggesting that frataxin plays a determinant role in intramitochondrial iron homeostasis. These discoveries are now considered as a clue for new strategies of treatment in this hereditary disease.
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PMID:[Friedreich's ataxia: recent developments and prospects for treatment]. 1033

Vascular parkinsonism (VP) is characterized by predominantly lower body involvement with gait impairment and postural instability, often without tremor, and by relative levodopa unresponsiveness. Neuroimaging studies demonstrate multiple infarcts or ischemic changes in periventricular white matter. Anticardiolipin antibodies (ACLA) are associated with hypercoagulable states and increased stroke risk. Review of our Movement Disorders Clinic records identified 44 individuals with a diagnosis of VP. ACLA have been obtained in 22 of these patients (mean age, 78.3 years; mean Mini-Mental Status Exam score, 25.8). Gait disturbance was the initial clinical feature in 82% of the patients, and levodopa responsiveness was present in 18% of those treated. In 9 of the 22 (40.9%), ACLA immunoglobulin G was positive. No significant differences in clinical features or risk factors (hypertension, diabetes, coronary artery disease, and clinical stroke) were evident between ACLA+ and ACLA- groups. Since the presence of ACLA in individuals with stroke is usually treated by full-scale anticoagulation with warfarin, our findings raise the question whether such treatment should also be used in persons with VP who are ACLA positive.
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PMID:Anticardiolipin antibody in vascular parkinsonism. 1236 May 48

The vertebral artery lesion has a variety of clinical characteristics. We sought to clarify the clinical patterns and the location of the intracranial vertebral artery (ICVA) diseases according to analyses of images obtained using magnetic resonance angiography (MRA). We studied vascular lesions, risk factors, symptoms, signs, and outcomes in 35 patients with ICVA disease (3 had bilateral occlusion; 9, unilateral occlusion; 6, bilateral stenosis; and 17, unilateral stenosis). The most common site of unilateral and bilateral lesions was the distal ICVA after the origin of posterior inferior cerebellar artery (PICA). We found accompanying basilar artery disease in 28.6% of patients with unilateral and bilateral ICVA disease. The majority of the ICVA lesions were associated with internal carotid arteries disease (48.8%). The common vascular risk factors were hypertension (71%), diabetes mellitus (34%), hyperlipidemia (31%), smoking (29%), and coronary artery disease (23%). Eighteen patients (51.4%) had transient ischemic attacks (TIAs) only, 10 patients (28.6%) had TIAs before stroke, and 5 patients (14.3%) had strokes without TIAs. Most patients (80%) with TIAs, with or without stroke, had multiple episodes. Vertigo or dizziness, ataxia, limbs weakness and abnormal gait were the common symptoms and signs. At 6 months follow-up, 66.7% patients had no symptoms or only slight symptoms that caused no disability. Our data showed (1) the usual location of ICVA disease (occlusion or severe stenosis) was distal to PICA, especially near the vertebrobasilar junction; (2) the risk factors were hypertension, diabetes mellitus, hyperlipidemia, smoking, and coronary artery disease; (3) patients with ICVA disease had a high frequency of accompanying internal carotid, middle cerebral, or basilar artery disease; (4) vertigo or dizziness, and ataxia were the common symptoms and signs; (5) TIA was the most common clinical pattern; (6) the outcome was favorable, except in cases with bilateral ICVA occlusion.
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PMID:Clinical findings of intracranial vertebral artery disease using magnetic resonance angiography. 1550 38

Normal pressure hydrocephalus (NPH) is one of the few reversible causes of dementia in older adults and accounts for approximately 6% of all dementias. The cardinal sign of NPH is a hypokinetic gait disorder in which the older adult's feet look as though they are glued to the floor. The gait also has been described as magnetic. People with NPH also may have mild dementia and bladder and bowel incontinence. A 78-year-old man exhibited symptoms of NPH for at least 4 years before being diagnosed. A neurological assessment of the patient revealed gait, posture, and balance abnormalities; mild dementia; and urinary urgency, frequency, nocturia, and incontinence at least once a day. His risk factors for NPH included diabetes and hypertension. A computed tomography (CT) scan revealed dilated lateral ventricles in the brain. A lumbar puncture was used to remove 50 ml of cerebrospinal fluid, which resulted in a transient improvement in his gait for approximately 18 hours. A ventriculoperitoneal shunt was then inserted in the patient, and during a 1-year period his symptoms gradually improved. He recovered without any complications and was eventually able to resume his usual activities. When the gait associated with NPH is observed in an older adult, he or she should be referred to a neurologist or multidisciplinary team for a comprehensive evaluation. If an individual receives treatment for NPH, he or she may have an improved quality of life and the opportunity to reduce functional limitations and disability. Families may also experience positive outcomes, such as having a loved one who is cognitively improved and requires less care.
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PMID:Gait disorder is the cardinal sign of normal pressure hydrocephalus: a case study. 1759 8

Vascular dementia (VaD) is heterogeneous in its clinical, imaging, and etiological characteristics. Although VaD is common in India, its pattern is not completely known. In a hospital-based cohort, we aimed to characterize VaD by its subtypes and study patterns of risk factors and clinical, and neuropsychological profiles. Vascular mechanisms, known to have racial and genetic variations were identified. NINDS-AIREN criteria were used to diagnose VaD. Patients were subtyped into subcortical, cortical, cortical-subcortical, and strategic infarct dementia. Vascular mechanisms were detected by vascular imaging, cardiac evaluation, and laboratory tests. In the 42 consecutive patients with VaD, subcortical dementia was the most common type (52.4%), followed by cortical-subcortical (26.2%), strategic infarcts in (14.3%), and cortical dementia (7.1%). Stroke (81%), hypertension (71.4%), and diabetes (35.7%) were important risk factors. Small artery disease was the underlying vascular mechanism in 42.9%; intracranial large artery disease, in 16.7%; extracranial disease, in 2.3%; cardioembolism, in 2.3%; multiple mechanisms, in 19%; and unknown, in 16.7%. Subtypes were similar in risk factor profile and neuropsychological features but differed in clinical characteristics and vascular mechanisms. Gait disorder (59.1% vs. 0%) and urinary symptoms (77.3% vs. 16.7%) were more common in subcortical dementia than in strategic infarct dementia (P < .05). Small artery disease was most common in subcortical dementia (72.7%). Intracranial large artery disease was associated with all subtypes. The pattern of VaD demonstrated in our study is a reflection of mechanisms of cerebrovascular disease in India. Outcome depends on underlying mechanisms and thus is likely to differ from that in other ethnic populations.
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PMID:Pattern of vascular dementia in India: study of clinical features, imaging, and vascular mechanisms from a hospital dementia registry. 1790 48

In this review we present a pragmatic approach to the patient with chronic vestibular symptoms. Even in the chronic patient a retrospective diagnosis should be attempted, in order to establish how the patient reached the current situation. Simple questions are likely to establish if the chronic dizzy symptoms started as benign paroxysmal positional vertigo (BPPV), vestibular neuritis, vestibular migraine, Meniere's disease or as a brainstem stroke. Then it is important to establish if the original symptoms are still present, in which case they need to be treated (e.g. repositioning maenouvres for BPPV, migraine prophylaxis) or if you are only dealing with chronic dizzy symptoms. In addition the doctor or physiotherapist needs to establish if the process of central vestibular compensation has been impeded due to additional clinical problems, e.g. visual problems (squints, cataract operation), proprioceptive deficit (neuropathy due to diabetes or alcohol), additional neurological or orthopaedic problems, lack of mobility or confidence, such as fear of falling or psychological disorders. A general neurological examination should also be conducted, amongst other reasons to make sure your patient's ;chronic dizziness' is not due to a neurological gait disorder. Treatment of the syndrome of chronic dizziness is multidisciplinary but rehabilitation and simple counselling should be available to all patients. In contrast, vestibular suppressants or tranquilisers should be reduced or, if possible, stopped.
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PMID:Management of the patient with chronic dizziness. 2008 85


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