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)

CD is an autoimmune-mediated disorder of the gastrointestinal tract. Initial symptom presentation is variable and can include neurologic manifestations that may comprise ataxia, neuropathy, dizziness, epilepsy, and cortical calcifications rather than gastrointestinal-hindering diagnosis and management. We present a case of a young man with progressive neurologic symptoms and brain MR imaging findings worrisome for ALS. During the diagnostic work-up, endomysium antibodies were discovered, and CD was confirmed by upper gastrointestinal endoscopy with duodenal biopsies. MR imaging findings suggestive of ALS improved after gluten-free diet institution.
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PMID:White matter lesions suggestive of amyotrophic lateral sclerosis attributed to celiac disease. 1991 Apr 50

The goals of epilepsy therapy are to achieve seizure freedom while minimizing adverse effects of treatment. However, producing seizure-freedom is often overemphasized, at the expense of inducing adverse effects of treatment. All antiepileptic drugs (AEDs) have the potential to cause dose-related, "neurotoxic" adverse effects (i.e., drowsiness, fatigue, dizziness, blurry vision, and incoordination). Such adverse effects are common, especially when initiating AED therapy and with polytherapy. Dose-related adverse effects may be obviated in most patients by dose reduction of monotherapy, reduction or elimination of polytherapy, or substituting for a better tolerated AED. Additionally, all older and several newer AEDs have idiosyncratic adverse effects which usually require withdrawal in an affected patient, including serious rash (i.e., Stevens-Johnson Syndrome, toxic epidermal necrolysis), hematologic dyscrasias, hepatotoxicity, teratogenesis in women of child bearing potential, bone density loss, neuropathy, and severe gingival hyperplasia. Unfortunately, occurrence of idiosyncratic AED adverse effects cannot be predicted or, in most cases, prevented in susceptible patients. This article reviews a practical approach for the definition and identification of adverse effects of epilepsy therapies, and reviews the literature demonstrating that adverse effects result in detrimental quality of life in epilepsy patients. Strategies for minimizing AED adverse effects by reduction or elimination of AED polytherapy, appropriately employing drug-sparing therapies, and optimally administering AEDs are outlined, including tenets of AED selection, titration, therapeutic AED laboratory monitoring, and avoidance of chronic idiosyncratic adverse effects.
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PMID:Minimizing AED adverse effects: improving quality of life in the interictal state in epilepsy care. 1994 68

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

Pregabalin (PGB), like its predecessor gabapentin, is a structural analogue (but not functional) of the gammaaminobutyric acid (GABA). PGB has analgesic, antoconvulsivant, and ansiolytic activities. Neuropathic pain (NP) initial recommended dose is 150 mg per day. Depending on the patient response or bodily resistance to the drug the initial dose can be increased up to 300 mg per day (divided in 2-3 daily doses) during a one-week period. PGB is quickly absorbed in the digestive system with high oral biodisponibility. The drug is eliminated almost exclusively by renal excretion (98%). PGB efficacy was evaluated by several studies by means of visual analog scales (VAS) in several NP conditions such as post-herpetic neuropathy (PHN) or painful diabetic neuropathy (PDN). When compared with placebo, PGB provided significant benefit with 150 mg doses in the treatment of PHN pain. In studies developed in patients with PDN, the significant difference between placebo and treatment group only was achieved in individuals with daily doses of 300 mg/day, and the response was clearly dose-dependent. Tolerability information obtained from a number of studies has shown that the drug has a very good safety and tolerability profile. Side effects were mild to moderate and dose-dependent. Based on controlled studies, the main adverse effects observed with PGB are dizziness (23.1%), drowsiness (14.6%), and peripheral aedema (10.4%). As these side effects are dosedependent, they can be easily managed by a simple dose reduction, with no need to discontinue the therapy. Thus, according to efficacy and tolerability data, PGB is an important therapeutic option in NP treatment.
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PMID:[Pregabalin--profile of efficacy and tolerability in neuropathic pain]. 2008 82

OPA1 mutations are known to cause autosomal dominant optic atrophy (ADOA), and some types of OPA1 mutations also cause auditory neuropathy. In the present study, we evaluated the vestibular dysfunction that accompanied auditory neuropathy in a patient with an OPA1 mutation. A caloric test failed to elicit nystagmus or dizziness in either ear. Vestibular evoked myogenic potentials (VEMPs) in the right ear were characterized by a normal biphasic waveform. In contrast, no VEMPs were evoked in the left ear. Model building suggested that the OPA1 mutation, p.R445H, indirectly distorts the catalytic structure of the GTPase reaction center and decreases GTPase activity. The patient complained of instability while walking or moving but thought these symptoms were caused by visual dysfunction. This is the first report of a detailed evaluation of vestibular dysfunction in a patient with an OPA1 mutation. This case suggests that vestibular dysfunction may be involved in motor instability in patients with an OPA1 mutation, even when patients do not complain of vestibular symptoms. Based on this case, we suggest that vestibular evaluation should be performed in auditory neuropathy patients carrying an OPA1 mutation, even if the patients are free of symptoms of vestibular dysfunction.
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PMID:Vestibular dysfunction in a Japanese patient with a mutation in the gene OPA1. 2038 91

Vertigo can be defined as an illusion or hallucination of movement. The control of balance is complicated. Vertigo can be caused by many different pathologies, some of which are potentially life threatening. An important differentiation is whether the symptoms of vertigo originate from a central or peripheral origin. Clues to a central origin are other brainstem symptoms or signs of acute onset such as headache, deafness and other neurological findings. These patients warrant urgent referral and investigation. Red flags in patients with vertigo include: headache; neurological symptoms; and neurological signs. It is useful to categorise vertigo into acute and chronic. The former usually has a single mechanism whereas chronic dizziness is often multifactorial. History is usually the most important part of the assessment. Key questions should be asked and it is vital to establish if the patient is suffering from vertigo or some other complaint such as anxiety or syncope. A neurological and otological examination should be performed, appropriate to the history. Assessment of gait and posture is crucial. If the patient has positional vertigo then a Hallpike test should be performed. Visual acuity should be checked as vision is a vital part of the balance system. The cranial nerves should be tested in particular eye movements for any ophthalmoplegia pointing to focal cranial nerve pathology and for nystagmus. The rest of the neurological examination should exclude evidence of central disease, in particular cerebellar disease, and neuropathy. If syncope is suspected it is wise to perform an extensive systemic examination in particular lying and standing BP, and cardiovascular and respiratory system assessments.
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PMID:Systematic approach needed to establish cause of vertigo. 2151 May 8

Bortezomib is a new chemotherapeutic agent approved for the treatment of relapsed/refractory and newly diagnosed multiple myeloma. One of the major side effects of bortezomib is a peripheral length-dependent sensory axonal neuropathy and, less frequently, a small fiber neuropathy. Autonomic symptoms like postural dizziness, syncope, diarrhoea, ileus, impotence and urinary disturbances have been reported, nevertheless, autonomic neuropathy has never been characterized. We describe by means of immunofluorescence, the involvement of autonomic skin nerve fibers in three patients with small fiber neuropathy induced by bortezomib treatment.
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PMID:Somatic and autonomic small fiber neuropathy induced by bortezomib therapy: an immunofluorescence study. 2129 Jan 60

Spontaneous retroperitoneal hemorrhage is one of the most serious and often lethal complications of anticoagulation therapy. The clinical symptoms vary from femoral neuropathy to abdominal compartment syndrome or fatal hypovolemic shock. Of these symptoms, abdominal compartment syndrome is the most serious of all, because it leads to anuria, worsening of renal failure, a decrease in cardiac output, respiratory failure, and intestinal ischemia. We report a case of a spontaneous retroperitoneal hemorrhage in a 48-year-old female who had been receiving warfarin and aspirin for her artificial aortic valve. She presented with a sudden onset of lower abdominal pain, dizziness and a palpable abdominal mass after prolonged straining to defecate. Computed tomography demonstrated a huge retroperitoneal hematoma and active bleeding from the right internal iliac artery. After achieving successful bleeding control with transcatheter arterial embolization, surgical decompression of the hematoma was performed for management of the femoral neuropathy and the abdominal compartment syndrome. She recovered without any complications. We suggest that initial hemostasis by transcatheter arterial embolization followed by surgical decompression of hematoma is a safe, effective treatment method for a spontaneous retroperitoneal hemorrhage complicated with intractable pain, femoral neuropathy, or abdominal compartment syndrome.
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PMID:Abdominal compartment syndrome due to spontaneous retroperitoneal hemorrhage in a patient undergoing anticoagulation. 2131 59

Insulinoma, usually benign (90%), is clinically characterized by symptoms as tremulousness, tachycardia, weakness, sweating, fatigue, hunger, headache, dizziness, disorientation and unconsciousness. However rarely it has an unusual presentation. We present a case of insulinoma misdiagnosed as neurologic disease. A 48-year-old man was admitted to our Emergency Division because of car accident caused by loss of consciousness. A diagnosis of complex partial seizure was made one year before. The patient appeared pale, tachycardic, BP 130/85 mmHg. Laboratory tests showed a severe hypoglycemia (30 mg/dl). He was treated with hypertonic glucose solution and the resolution of symptoms was obtained. Dosages of insulin and C-peptide, CT-scan and RMN confirmed a diagnosis of insulinoma. Seizure disappeared after surgical excision. The diagnosis of insulinoma is sometimes delayed up to more than 20 years. Neurologic or psychiatric presentation like disorientation, personality changes, amnesia, irritability, seizures, bizarre behavior, visual difficulties, neuropathy in patients affected by insulinoma could be cause of misdiagnosis. Diagnosis of insulinoma should always be considered whenever these symptoms occur, especially if unresponsive to specific therapy. Insulinoma is curable in most cases and an early diagnosis can avoid adverse consequences including neurologic damage.
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PMID:[Complex partial seizure in patient with insulinoma: importance of early diagnosis]. 2135 8

Although vestibular schewannomas (VSs) are relatively rare as compared to other intracranial tumors, growing attention is required to achieve better outcomes with less morbidities among patients. In this retrospective study, we compared functional outcomes of retrosigmoid approach microsurgery (RSAMS) and gamma knife stereotactic radiosurgery (GKSRS) in VSs patients with serviceable hearing. Forty-six patients in inclusion criteria, who underwent RSAMS (n = 15) or GKSRS (n = 31) between January 2004 and June 2009 were reviewed. We evaluated symptoms at initial presentation, pre- and posttreatment pure-tone audiometry, speech discrimination score, tumor size, pre- and posttreatment assessments of facial nerve function, and pre- and posttreatment tinnitus, dizziness and facial paresthesia in vestibular schwannoma patients, who were treated with RSAMS or GKSRS. Hearing disturbance was the most common presenting symptom in both the groups. The hearing preservation rates in the RSAMS and GKSRS patients were 7% (1/15) and 45% (14/31), respectively. Two RSAMS patients and one GKSRS patient developed new facial neuropathy, defined as a temporary or permanent decline in House-Brackmann facial nerve grade. Tumor recurrence was observed in one RSAMS patient, whereas tumor size increase was observed in one GKSRS patient (3%). Tinnitus score was decreased after the treatment in both the groups. The results imply that GKSRS for vestibular schwannoma can possibly preserve hearing preservation with proper indication and treatment planning.
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PMID:Functional outcomes in retrosigmoid approach microsurgery and gamma knife stereotactic radiosurgery in vestibular schwannoma. 2147 79


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