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)

Three case histories of patients with large tumors in the posterior fossa who were operated on in a sitting position subsequently developed 1 or more symptoms referable to the temporoparietooccipital regions of the brain 24 to 48 hours postoperatively. Initially, it was believed that such symptoms were due to a stimulation of the association pathways causing firing of remote association areas (See Ch. 4). Subsequent studies of the rotation of blood vessels of the brain in the developing embryo and a review of the anatomical location of the arteries supplying the temporoparietooccipital region led to the conclusion that some compromise of the posterior cerebral artery was responsible for the symptoms. The symptomatology in these brain tumor patients was not unlike that seen in the cosmonauts and astronauts in space flight, designated as "motion sickness" in the space literature. A suggestion was made as to clarification of the definitions. This author advocated that the term "motion sickness" be confined to those symptoms of dizziness, nausea, and vomiting, due to involvement of the peripheral end organ, the inner ear. "Space sickness" might include these symptoms but also might have the addition of disorientation or the inversion of image in space and formed or unformed hallucinations. These relate to the temporoparietooccipital area, the midtemporal, and the occipital regions. In such instances, there must be central involvement or a stimulation of this interpretive cortex of the brain. The remote symptoms from the supratentorial cotex were believed to be due to hypoxia related to the posterior cerebral artery compromise, resulting in delayed "luxury perfusion" and the development of local lactic acidosis. Transaxial transmission of force with an uncal tentorial herniation causing compression of the posterior cerebral artery was suggested as a mechanism responsible for the vascular compression.
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PMID:Remote cerebral hemisphere symptoms from surgically treated patients with posterior fossa brain tumors; vascular factors: a basis for a theory concerning space sickness. 56 32

Three patients who had large, benign cerebellar tumors were operated upon in the sitting position and developed symptoms referable to the temporoparieto-occipital region of the brain 24-48 h postoperatively. They consisted of dizziness, nausea, vomiting, formed and unformed hallucinations, and inversion of image or disorientation in space, some of which were experienced by some of the astronauts and cosmonauts during space flight. Such findings are not due to stimulation of the cerebellum, the site of the lesion, but must come from the cerebral hemisphere. The symptoms were believed to be caused by "the luxury perfusion" of Lassen with the development of local lactic acidosis secondary to vascular insufficiency to the brain in the distribution of the posterior cerebral artery thus stimulating the temporoparieto-occipital region. This theory is suggested to some degree by the work of Endo et al. using CT scans, which showed the shifting of increased blood flow from the frontal region to the temporoparieto-occipital region following removal of a benign posterior fossa tumor. The mechanism for the compression of the posterior cerebral artery may be due to uncal herniation at the tentorium. The authors believe that it might be well to consider further testing in a vertical or oblique plane rather than only in a centrifugal horizontal one. This method would tend to cause uncal herniation more readily. Monitoring of such effects could be done with the colored CT scan.
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PMID:Motion sickness: part III--a clinical study based on surgery of posterior fossa tumors. 736 52

Accumulation of D-lactate after gastrointestinal surgery, particularly jejuno-ileal bypass, is an uncommon and often misdiagnosed clinical disturbance. The syndrome may be complicated by dizziness, ataxia, confusion, headache, memory loss, and aggressive behavior. Serum chemistries are often deceptive because the anion gap is frequently normal in spite of severe metabolic acidosis. Moreover, the urine anion gap may be positive, incorrectly suggesting a defect in renal net acid excretion. Indeed, the combination of a normal anion gap metabolic acidosis and positive urine anion gap may erroneously suggest a diagnosis of renal tubular acidosis. Importantly, all reported cases of D-lactic acidosis secondary to bypass surgery have been encountered within 5 to 10 years following the surgery. Here we present an unusual case of D-lactic acidosis (complicated by encephalopathy) presenting 23 years after a jejuno-ileal bypass procedure. The patient was initially diagnosed with a drug intoxication secondary to benzodiazepines. Ultimately, the diagnosis of D-lactate encephalopathy was established after challenging the patient with a carbohydrate load. Thus, administration of 40 kcal/kg over 16 hours reproduced the clinical syndrome and was accompanied by a marked increment in serum and urine D-lactate concentration. The patient had sustained resolution of her symptoms after treatment with oral vancomycin.
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PMID:D-lactic acidosis 23 years after jejuno-ileal bypass. 1092 30

A patient of MELAS is reported. A 28-year-old woman was admitted to Shimada Municipal Hospital because of nausea, vomiting, and right homonymous hemianopsia. She had past history of dizziness and convulsion. A brain magnetic resonance imaging showed an ischemic lesion in the left occipital lobe, which disappeared in the follow-up study. Laboratory examination indicated elevated lactate and pyruvate levels in both blood and cerebrospinal fluid. The muscle biopsy demonstrated ragged-red fibers and strongly SDH-reactive blood vessels. PCR-RFLP analysis of DNA extracted from her muscle and blood as well as her mother's blood revealed a T to C mutation at nucleophile position of 3271 in mitochondrial DNA. She was diagnosed as having MELAS and discharged. One year after the first admission, she re-visited our hospital because of three days' duration of fatigability and generalized muscle pain after alcohol intake. She had severe lactic acidosis, rhabdomyolysis and acute renal failure. Despite a continuous hemodialysis and other intensive efforts, the patient died 20 hours later. Alcohol intake has been reported to induce rhabdomyolysis in myopathy with mitochondrial DNA deletions. The course of this patient suggests that alcohol intake can be an aggravating factor also in MELAS.
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PMID:[A patient of MELAS with 3271 mutation with fatal outcome after alcohol intake]. 1108 93

The short bowel syndrome appears for the reduction of intestinal absorptive surface due to functional or anatomical loss of part of the small bowel. We present the case of a 35-year-old woman with severe short bowel syndrome secondary to acute intestinal ischemia in adults, who presented at 5 years of evolution episodes of dizziness with gait instability and loss of strength in hands. The diagnosis was D-lactic acidosis. D-lactic acidosis is a rare complication, but important for their symptoms, of this syndrome. It is due to a change in intestinal flora secondary to an overgrowth of lactic acid bacteria that produce D-lactate. D-lactic acidosis should be looked for in cases of metabolic acidosis in which the identity of acidosis is not apparent, neurological manifestations without focality and the patient has short bowel syndrome or patients who have had jejunoileal bypass surgery. Appropriate treatment usually results in resolution of neurologic symptoms and prevents or reduces further recurrences.
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PMID:[D-Lactic acidosis secondary to short bowel syndrome]. 2133 48

Hydrogen sulfide is a toxic gas produced as a by-product of organic waste and many industrial processes. Hydrogen sulfide exposure symptoms may vary from mild (dizziness, headaches, nausea) to severe lactic acidosis via its inhibition of oxidative phosphorylation, leading to cardiac arrhythmias and death. Treatment is generally supportive. We report the case of a patient presenting with cardiac arrest secondary to hydrogen sulfide exposure treated with both hyperbaric oxygen therapy and therapeutic hypothermia to achieve full neurologic recovery.
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PMID:Utilization of hyperbaric oxygen therapy and induced hypothermia after hydrogen sulfide exposure. 2200 89

A 68-year-old man presented at the emergency room with sudden blindness. The day before, he had eaten sashimi and eel and drank alcohol for dinner. He experienced nausea, vomiting, and dizziness afterward. His medical history included hypertension and diabetes, and the latter was treated with metformin. Initial laboratory tests revealed severe metabolic acidosis (lactic acidosis). Massive hydration and intravenous sodium bicarbonate replacement therapies were initiated, but severe metabolic acidosis (lactic acidosis) did not resolve, in turn, leading to hemodialysis, which decreased metabolic acidosis. The patient's blindness improved, and his vision gradually recovered. As it is not easy to distinguish between blindness related to metformin-associated lactic acidosis (MALA) and blindness related to other causes, rapid correction of metabolic acidosis through hemodialysis might be helpful in differentiating this from of blindness from blindness related to other causes.
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PMID:Transient Blindness in a Patient with Severe Metformin-Associated Lactic Acidosis (MALA). 3133 10

BACKGROUND A 70-year-old African American man presented with fatigue, dizziness, generalized weakness, and considerable weight loss of over 20 pounds in 3 weeks. History-taking revealed he was positive for HIV, hepatitis C, and severe chronic condyloma acuminatum, which had been progressing for 16 years. Treatment and surgical intervention had been continuously postponed due to the patient's long-standing history of heroin abuse. CASE REPORT Physical exam and diagnostics showed evidence of sepsis. He was hypotensive, with lactic acidosis and significant leucocytosis, and had acute-on-chronic kidney disease. Urinalysis was positive for nitrites and leukocyte esterase; therefore, broad-spectrum antibiotics were initiated. Additional sources of sepsis were considered due to persistent leucocytosis despite appropriate antibiotic coverage. An MRI of the pelvis was done to evaluate for necrosis of fistulization from potential internal warts as a source of sepsis. The lesions extended from the inguinal areas bilaterally, covering the medial thighs, lower scrotal wall, and wall junction. It had infiltrated the perineum and the entire rectal area, including the gluteal cleft and anus. The patient was consulted by colorectal surgery, urology, and infectious disease services. CONCLUSIONS Surgical biopsies found that he had both low- and high-grade squamous intraepithelial neoplasia. There was no evidence of invasive carcinoma, which was a concern given his weight loss. Surgery devised a plan that included a diverting colostomy (allowing the infected anal area to heal), followed by resection of his giant condyloma, and re-anastomosing of the bowels to return him to a normal baseline anatomy. A favorable prognosis was expected.
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PMID:The Conundrum of an Accumulating Acuminatum. 3208 23