Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 60 year-old man was admitted to our hospital because of gait disturbance and dizziness. At 57 years of age, he noticed his walking unstable. After then, he had dizziness due to orthostatic hypotension, urinary difficulty, loss of livid, and forgetfulness. Neurological examination revealed he had severe orthostatic hypotension, cerebellar ataxia, dysarthria, hyperreflexia of four limbs, myoclonus of right leg, and atonic bladder. His brain CT showed cerebellar atrophy. Thereafter he had recurrent syncopic attacks. His gait disturbance progressed steadily, so he became bedridden. In his terminal stage, his limbs showed rigidity. About 3 years later he died of pneumonia and sepsis. At autopsy brain weighted 1,230 g. Glossly the putamens was bilaterally shrunken, the color of the substantia nigra and locus ceruleus became pale. Base of the pons and the cerebellum were atrophic. Microscopical examination confirmed the degeneration of striato-nigral and olivo-ponto-cerebellar systems without Lewy body. In the spinal cord there was depletion of neuronal cells in the intermediolateral nuclei and Onufrowitz nuclei. In addition to the conventional neuropathological staining methods, we performed the immunohistochemical studies using monoclonal antibody against synthetic peptide of beta protein which detected senile plaque of every stages with formic acid pretreatment, and compared to the modified Bielschowsky method and Congo red method. Our case showed many very primitive and primitive senile plaque in neocortices and hippocampal region. A few neurofibrally tangle were seen in hippocampus. We supposed our case might combine multiple system atrophy and Alzheimer' pathology.
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PMID:[An autopsy case of multiple system atrophy with many senile plaques]. 262 28

Carotid body tumors (CBTs) are rare, usually benign, neoplasms of the extra-adrenal paraganglion system. They are almost always nonfunctional. The diagnosis is generally confirmed by an angiogram that shows a vascular tumor enlarging the space between the internal and external carotid arteries. A 55-year-old man with hypertension and episodes of flushing, palpitations, and dizziness was treated for a firm, nonmobile mass measuring 3 x 2 cm at the left carotid bifurcation. Plasma and urine catecholamines, and the vanilylmandelic acid/creatinine ratios were elevated. Carotid arteriograms showed a vascular mass displacing the vessels, but the space between the arteries was narrowed rather than enlarged, and an atherosclerotic plaque was present. At operation the CBT was removed by resection of the bifurcation and with a temporary shunt a saphenous vein graft was inserted between the common and internal carotid arteries. Pathologic examination revealed a typical paraganglionoma. Although most CBTs produce catecholamines, only 11 patients have been reported to have elevated plasma and urine levels, and most were symptomatic. Since these tumors slowly increase in size, early surgical removal is recommended, even in asymptomatic patients.
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PMID:Carotid body tumor: atypical angiogram of a functional tumor. 333 80

The management of patients with cerebral transient ischemic attacks and carotid artery stenosis remains controversial. Noninvasive techniques help to determine which patients require surgical intervention without exposing the majority of patients to the risk and discomfort of invasive procedures. Measurement of ophthalmic artery pressure by ophthalmodynamometry or oculoplethysmography gives a representation of perfusion pressure in the internal carotid artery circulation. Doppler ultrasound studies can define the extent of obstruction to flow at the carotid artery bifurcation and assess collateral flow from the external carotid artery. Real time B-mode ultrasonography can detect nonobstructive ulcerated plaque in the carotid artery bifurcation. Employing these examinations in a test battery can identify hemodynamically significant lesions, which are more likely to precipitate a stroke. The information obtained from these studies can be utilized in patients with episodes of cerebral transient ischemic attacks, asymptomatic carotid artery bruits and vertebrobasilar insufficiency. Noninvasive carotid artery testing is also useful in screening patients with nonspecific symptoms, such as dizziness or light-headedness, which may be related to decreased flow in the carotid circulation. Noninvasive carotid artery testing can provide valuable anatomic and physiologic information required in the appropriate management of patients with cerebrovascular disease. It is of particular value in managing patients with heart disease who are at high risk for complications from invasive procedures.
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PMID:Clinical applications of noninvasive carotid artery testing. 388 May 66

This chapter reports the clinical and neuropathological findings of eight cases of "diffuse Lewy body disease" verified by autopsy. The age at onset was between 60 and 82 years; the age at death was between 75 and 92 years. The initial symptoms were amnesia in three cases, orthostatic dizziness in three, visual hallucination in two, but parkinsonism in none. The cardinal clinical symptoms included dementia in all cases, hallucinatory-delusional state in six, akinesia and rigidity in five, and orthostatic hypotension in five. Antemortem diagnoses were senile dementia in five, and hallucinatory-delusional state, Parkinson's disease and Shy-Drager syndrome in one each. Despite the clinical symptoms differences from each other, neuropathological findings were alike. Abundant Lewy bodies were present in the neurons of the cerebral cortex as well as in the brainstem nuclei and diencephalon. Concomitant senile changes including senile plaques and Alzheimer's neurofibrillary tangles (NFTs) were also present in varying degree. Immunocytochemical study with anti-ubiquitin for Lewy body, anti-tau protein for NFT, and beta-protein of amyloid for senile plaque suggested that dementia of DLBD might have resulted not from a single pathology but from the complex of Lewy bodies, NFTs and senile plaques.
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PMID:Clinical and neuropathological aspects of diffuse Lewy body disease in the elderly. 842 Jan 71

A 35-year-old woman presented with a 6-month history of intermittent headaches, vomiting and dizziness. CT showed a plaque-like mass with tiny calcifications along the surface of the left frontal lobe. The mass exhibited heterogeneous enhancement with a few low-density foci. Underlying sulcal obliteration and enhancement and white matter oedema were also noted. Histopathological examination of excised material was consistent with tuberculoma. Recognition of this unusual presentation of intracranial tuberculoma may facilitate appropriate diagnosis and management.
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PMID:Tuberculoma en plaque: CT. 883 90

Alefacept belongs to the new generation of drugs applied in the treatment of psoriasis. It is an immunomodulatory recombinant, fully human lymphocyte function associated antigen-3/immunoglobulin G1 fusion protein (LFA-3-Ig) CD2 antagonist that targets memory-effector T cells by binding CD2 on the T cell surface. It blocks the interactions of leukocyte functional antigen (LFA)-3 with CD2 interaction. This drug is used to treat moderate-to-severe chronic plaque psoriasis and there was conducted a pilot study of psoriatic arthritis. It was observed that Alefacept had reduced peripheral-blood memory effector T-lymphocyte (CD45RO+) counts, cells which are responsible for sustaining the disease. Pharyngitis, dizziness, increased cough, nausea, pruritus, myalgia, chills, injection site inflammation, and accidental injury were recorded. So far, in the conducted trials no generalised immunosuppression or increased risk of infection or malignancy were observed. The possibility of increased risk of infections and malignancies must be considered because of reduced lymphocyte counts.
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PMID:Possibilities of using alefacept in the treatment of psoriasis. 1532 11

Neurofibromatosis type 2 (NF2) is a tumour-prone disorder characterised by the development of multiple schwannomas and meningiomas. Prevalence (initially estimated at 1: 200,000) is around 1 in 60,000. Affected individuals inevitably develop schwannomas, typically affecting both vestibular nerves and leading to hearing loss and deafness. The majority of patients present with hearing loss, which is usually unilateral at onset and may be accompanied or preceded by tinnitus. Vestibular schwannomas may also cause dizziness or imbalance as a first symptom. Nausea, vomiting or true vertigo are rare symptoms, except in late-stage disease. The other main tumours are schwannomas of the other cranial, spinal and peripheral nerves; meningiomas both intracranial (including optic nerve meningiomas) and intraspinal, and some low-grade central nervous system malignancies (ependymomas). Ophthalmic features are also prominent and include reduced visual acuity and cataract. About 70% of NF2 patients have skin tumours (intracutaneous plaque-like lesions or more deep-seated subcutaneous nodular tumours). Neurofibromatosis type 2 is a dominantly inherited tumour predisposition syndrome caused by mutations in the NF2 gene on chromosome 22. More than 50% of patients represent new mutations and as many as one-third are mosaic for the underlying disease-causing mutation. Although truncating mutations (nonsense and frameshifts) are the most frequent germline event and cause the most severe disease, single and multiple exon deletions are common. A strategy for detection of the latter is vital for a sensitive analysis. Diagnosis is based on clinical and neuroimaging studies. Presymptomatic genetic testing is an integral part of the management of NF2 families. Prenatal diagnosis and pre-implantation genetic diagnosis is possible. The main differential diagnosis of NF2 is schwannomatosis. NF2 represents a difficult management problem with most patients facing substantial morbidity and reduced life expectancy. Surgery remains the focus of current management although watchful waiting with careful surveillance and occasionally radiation treatment have a role. Prognosis is adversely affected by early age at onset, a higher number of meningiomas and having a truncating mutation. In the future, the development of tailored drug therapies aimed at the genetic level are likely to provide huge improvements for this devastating condition.
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PMID:Neurofibromatosis type 2 (NF2): a clinical and molecular review. 1954 78

Jamestown Canyon virus (JCV) is a mosquito-borne zoonotic pathogen belonging to the California serogroup of bunyaviruses. Although JCV is widely distributed throughout temperate North America, reports of human JCV infection in the United States are rare. This is the first report of human JCV infection detected in Montana, one of only 15 cases reported in the United States since 2004, when JCV became reportable. On May 26, 2009, a man aged 51 years with no travel history outside of Montana went to a local emergency department immediately following onset of fever, severe frontal headache, dizziness, left-sided numbness, and tingling. His blood pressure was elevated. Stroke was ruled out, oxygen was administered, medication was prescribed for hypertension, and the patient was sent home. One week later, the patient visited his primary-care physician complaining of continued neurologic symptoms consistent with acute febrile encephalitis and recent mosquito bites. Although West Nile virus (WNV) disease was diagnosed based on detection of WNV-immunoglobulin M (IgM) and G (IgG) antibodies, subsequent testing indicated that the WNV antibodies were from a past infection and that his illness was caused by JCV. The final diagnosis of JCV infection was based on positive JCV-specific IgM enzyme-linked immunosorbent assay (ELISA) results and a fourfold rise in paired sample JCV plaque reduction neutralization test (PRNT) titers. This finding represents a previously unrecognized risk for JCV infection in Montana; clinicians should consider JCV infection when assessing patients for suspected arboviral infections.
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PMID:Human Jamestown canyon virus infection --- Montana, 2009. 2161 30

Alzheimer disease is the most common form of dementia, affecting nearly one-half [corrected] of Americans older than 85 years. It is characterized by progressive memory loss and cognitive decline. Amyloid plaque accumulation, neurofibrillary tau tangles, and depletion of acetylcholine are among the pathologic manifestations of Alzheimer disease. Although there are no proven modalities for preventing Alzheimer disease, hypertension treatment, omega-3 fatty acid supplementation, physical activity, and cognitive engagement demonstrate modest potential. Acetylcholinesterase inhibitors are first-line medications for the treatment of Alzheimer disease, and are associated with mild improvements in cognitive function, behavior, and activities of daily living; however, the clinical relevance of these effects is unclear. The most common adverse effects of acetylcholinesterase inhibitors are nausea, vomiting, diarrhea, dizziness, confusion, and cardiac arrhythmias. Short-term use of the N-methyl-D-aspartate receptor antagonist memantine can modestly improve measures of cognition, behavior, and activities of daily living in patients with moderate to severe Alzheimer disease. Memantine can also be used in combination with acetylcholinesterase inhibitors. Memantine is generally well tolerated, but whether its benefits produce clinically meaningful improvement is controversial. Although N-methyl-D-aspartate receptor antagonists and acetylcholinesterase inhibitors can slow the progression of Alzheimer disease, no pharmacologic agents can reverse the progression. Atypical antipsychotics can improve some behavioral symptoms, but have been associated with increased mortality rates in older patients with dementia. There is conflicting evidence about the benefit of selegiline, testosterone, and ginkgo for the treatment of Alzheimer disease. There is no evidence supporting the beneficial effects of vitamin E, estrogen, or nonsteroidal anti-inflammatory drug therapy.
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PMID:Treatment of Alzheimer disease. 2167 41

Multiple sclerosis (MS) causes dizziness and vertigo. Reports suggest responsible lesions are often in the intra-pontine 8th nerve fascicle. We sought to determine frequency and clinical features of demyelinating acute vestibular syndrome (AVS). This is a prospective observational study (1999-2011). Consecutive AVS patients (vertigo, nystagmus, nausea/vomiting, head-motion intolerance, unsteady gait) with a risk for central localization underwent structured bedside examination and neuroimaging. When applicable, we identified MS based on clinical, imaging, and laboratory features. Of 170 AVS presentations, 4% (n = 7) were due to demyelinating disease. Five had an acute MS plaque likely responsible for the clinical syndrome. Lesion location varied-1 medulla; 1 inferior cerebellar peduncle; 1 middle cerebellar peduncle; 1 posterior pontine tegmentum; 1 in the intrapontine 8th nerve fascicle; 1 superior cerebellar peduncle; 1 midbrain. Only two had a lesion in or near the intra-pontine 8th nerve fascicle. Three were first presentations (i.e., clinically isolated demyelinating syndrome), while the others were known MS. All had central oculomotor signs. In two patients, the only central sign was a normal horizontal head impulse test (h-HIT) of vestibular function. All patients improved with steroid therapy. Demyelinating disease was an uncommon cause of AVS in our series. Symptomatic lesions were not restricted to the 8th nerve fascicle. Five patients had relatively obvious oculomotor signs, making differentiation from vestibular neuritis straightforward. Two patients had unidirectional, horizontal nystagmus that followed Alexander's law and was suppressed with fixation (true pseudoneuritis). The presence of a normal h-HIT in these suggested central localization.
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PMID:Multiple sclerosis as a cause of the acute vestibular syndrome. 2339 81


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