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The famous painter Francisco Goya y Lucientes (1746-1828) suffered during his life one or several diseases, the nature of which has not been determined with certainty. At age of 46, Goya suffered from severe illness that lasted a few months. It caused loss of vision and hearing, tinnitus, dizziness, a right-sides paralysis, weakness and general malaise. Although he recovered from a cerebral stroke which accompanied it, the deafness remained unaltered. The illness divides Goya's artistic life into two great different periods. After in the painter produces his greatest works. The visual experience after the illness was heightened by the exclusion of acoustics stimuli and the artist's talent rose to the highest level. His character became more withdrawn and introspective and his entire vitality was direscted to his painting. Goya's painting became progressively more gloom and satirical during his long convalescence. The artist suffered a stroke at age 73 that again rendered him paralysed on the right side. The precise cause of his illness has long been debated. Ome medical writers have favored the diagnosis of syphilis, some consider the possibility of an exogenous psychosis, and other suggests that the symptoms of the illness are more congruent with heavy metal poisoning, particulary lead. It is interesting to speculate how the Goya's deafness influenced the artist's mentality and the changes of his painting. Interesting is also the problem of the sensory compensation in fact of disturbance of physiological function of one of the senses.
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PMID:[Deafness and mentality in Francisco Goya's paintings]. 1968 94

The athletic performance supplement industry is a multibillion-dollar business and one popular category claims to increase nitric oxide (NO) production. We report three patients presenting to the emergency department with adverse effects. A 33-year-old man presented with palpitations, dizziness, vomiting, and syncope, after the use of NO(2) platinum. His examination and electrocardiogram (ECG) were normal. The dizziness persisted, requiring admission overnight. A 21-year-old man with palpitations and near syncope had used a "nitric oxide" supplement. He was tachycardic to 115 bpm with otherwise normal examination. Laboratory values including methemoglobin, and ECG were unremarkable. He was treated with 1 L of saline with no change in heart rate. He was admitted for observation. A 24-year-old man presented after taking NO-Xplode with palpitations and a headache. His examination, laboratory values, and ECG were normal. He was discharged. The purported active ingredient in these products is arginine alpha-ketoglutarate (AAKG), which is claimed to increase NO production by supplying the precursor L-arginine. The symptoms could be due to vasodilation from increased levels of NO, though other etiologies cannot be excluded. AAKG containing supplements may be associated with adverse effects requiring hospital admission.
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PMID:Adverse effects associated with arginine alpha-ketoglutarate containing supplements. 1975 57

The principal toxic ingredients of aconite roots include aconitine, mesaconitine and hypaconitine, which are known cardiotoxins and neurotoxins. A 58-year-old man took a decoction of 11 g each of processed 'chuanwu' (the main root of Aconitum carmichaeli) and processed 'caowu' (the root of A. kusnezoffii) as treatment for his neck pain. One hour later, he experienced numbness of tongue and the four limbs, generalized weakness, nausea, vomiting, diarrhoea and dizziness. Three hours after ingestion, he was admitted to hospital. His blood pressure was 106/53 mmHg and heart rate 65 beats/min. Six hours after ingestion, he became hypotensive (systolic blood pressure <100 mmHg) with bradycardia (heart rate <60 beats/min). As treatments for the hypotension, he was given intravenous infusions of 0.9% saline (125 mL/hour) for 15 hours (7-21 hours after ingestion) and dopamine (3 microg/kg/min) for 36 hours (10-45 hours after ingestion). He was given atropine 0.6 mg intravenously 7 and 24 hours after ingestion. He was hypotensive for 31 hours (6-36 hours after ingestion), with a systolic blood pressure of 84-106 mmHg (mean 93.5) and a diastolic blood pressure of 40-59 mmHg (mean 51.8). He had bradycardia for 36 hours (6-41 hours after ingestion), with a heart rate of 45-68 beats/min (mean 56.5). On discharge (48 hours after ingestion), his blood pressure was 117/82 mmHg and heart rate 70 beats/min. In patients with aconite poisoning, prolonged hypotension and sinus bradycardia may occur and supportive therapy with close monitoring of blood pressure and cardiac rhythm are essential.
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PMID:Aconite poisoning presenting as hypotension and bradycardia. 1988 Jun 59

This paper presents a case of cardiac tamponade with idiopathic hemorrhagic pericarditis as the initial symptom of human immunodeficiency virus (HIV) infection. A 29-year-old male came to the emergency room with a sudden onset of dizziness. Upon arrival, he was hypotensive although not tachycardic, and his jugular venous pressure was not elevated. His chest X-rays revealed a mild cardiomegaly. Transthoracic echocardiography revealed a large amount of pericardial effusion with a diastolic collapse of the right ventricle, a dilated inferior vena cava with little change in respiration, and exaggerated respiratory variation of mitral inflow velocities, representing echocardiographic evidence of cardiac tamponade. After pericardiocentesis, his blood pressure improved to 110/70 mmHg without inotropics support. Serial 12-lead electrocardiograms during hospitalization revealed upwardly concave diffuse ST-segment elevation followed by a T-wave inversion suggestive of acute pericarditis. Pericardial fluid cytology and cultures for bacteria, mycobacteria, adenovirus, and fungus were all negative. HIV enzyme-linked immunosorbent assay (ELISA) was positive and confirmed by Western blot. The CD4 cell count was 168/mm(3). Finally, the diagnosis of cardiac tamponade due to HIV-associated hemorrhagic pericarditis was made. It was concluded that HIV infection should be considered in the diagnosis of unexplained pericardial effusion or cardiac tamponade in Korea.
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PMID:Acute idiopathic hemorrhagic pericarditis with cardiac tamponade as the initial presentation of acquired immune deficiency syndrome. 2019 Oct 22

A 56 year old male with a past medical history of hypertension and dyslipidemia presented with recurrent dizziness. Routine EKG was performed, which suggested frequent junctional extra systoles with compensatory pauses. During telemetry periods of 2:1 block with effective ventricular rate of 34 bpm was observed. His bundle study suggested frequent His extra systoles causing functional AV block. Treatment with anti-arrhythmic medication, paradoxically improved AV block and symptoms in our patient.
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PMID:Unusual pauses in sinus rhythm and intermittent 2 to 1 AV block in a patient with concealed his extra systoles--a rare cause of bradycardia. 2023 12

A 30-year-old man was referred in our department for treatment of a midbasilar trunk aneurysm. His presenting symptoms included headache and dizziness. A CT scan at another hospital showed no significant findings whereas a digital subtraction angiogram disclosed a dissecting aneurysm in the midbasilar trunk, and there was severe stenosis in the basilar artery. After discussion, we planned to use stent-assisted-coil embolization technique. During the procedure, a LEO stent (Balt, Montmorency, France) was implanted into the basilar artery across the aneurysm neck, but fearing acute basilar artery occlusion because of stent collapse or thrombus we did not fill coils into the aneurysm. After the procedure, the completion angiography demonstrated considerably decreased flow into the aneurysm, with stasis persisting into the venous phase of angiography. The patient awoke from general anaesthesia after the procedure and had no additional neurological symptoms, he was discharged three days later and used clopidogrel and aspirin for antiplatelet therapy. Six months later when he was admitted for a recheck, a DSA showed the basilar artery was occluded completely and the aneurysm had disappeared even though the patient remained neurologically normal.
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PMID:Delayed thrombosis of the basilar artery after stenting for a basilar trunk dissection aneurysm. A case report and review of the literature. 2037 83

A 42-year-old black African patient was admitted in the emergency department with severe headache, dizziness, and visual problems. He had been treated for hypertension diagnosed eight months ago after a similar episode. He was taking atenolol 100 mg /day, amlodipine 10 mg/day, and a combination of lisinopril 20 mg/hydrochlorothiazide 12.5 mg daily but experienced several hypertension peaks and hypotension. He adhered to treatment and was neither using traditional herbal medication nor illicit drugs. He did not smoke, but used to drink 1-2 glasses of wine after dinner. At admission, his blood pressure was 235/145 mm of Hg. His body mass index was 25.5 kg/m(2) and the waist/hip ratio was 0.9. Physical examination was unremarkable. Fundoscopic examination revealed hypertensive retinopathy. Biochemical and imaging explorations were compatible with diagnosis of pseudopheochromocytoma. Evolution was favourable after treatment with alpha-1 and beta-blokers.
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PMID:Pseudopheochromocytoma: An uncommon cause of malignant hypertension. 2043 34

Crouzon syndrome is one of the most common craniofacial syndromes and is inherited as autosomal dominant with variable expression. We report an 11 and a half-year-old boy with Crouzon syndrome with severe growth retardation. He had hydrocephalus since infancy and recently suffered from frequent dizziness. His bone age was only 5 years according to the Greulich and Pyle atlas. Magnetic resonance imaging showed shallow orbits, obstructive hydrocephalus, and cerebellar tonsil herniation. Growth hormone provocative tests revealed a reduced peak growth hormone response in both insulin and clonidine tests. Severe iron deficiency anemia was noted at the same time. Molecular analysis identified a common mutation point of Cys278Phe for Crouzon syndrome in exon IIIa of the fibroblast growth factor receptor 2 (FGFR2) gene. Since growth retardation is not a common feature of Crouzon syndrome, we reviewed the literature for the incidence of hydrocephalus in Crouzon syndrome and the association with growth hormone deficiency.
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PMID:Growth hormone deficiency in a case of crouzon syndrome with hydrocephalus. 2058 60

We present two cases of rare human poisoning in one family following ingestion of cooked leaves from the tobacco tree plant, Nicotiana glauca. The toxic principle of N. glauca, anabasine (C10H14N2), is a small pyridine alkaloid, similar in both structure and effects to nicotine, but appears to be more potent in humans. A 73-year-old female tourist from France, without remarkable medical history, collapsed at home following a few hours long prodrome of dizziness, nausea, vomiting, and malaise. The symptoms developed shortly after eating N. glauca cooked leaves that were collected around her daughter's house in Jerusalem and mistaken for wild spinach. She was found unconscious, with dilated pupils and extreme bradycardia. Following resuscitation and respiratory support, circulation was restored. However, she did not regain consciousness and died 20 days after admission because of multi-organ failure. Anabasine was identified by gas chromatography/mass spectrometry method in N. glauca leaves and in the patient's urine. Simultaneously, her 18-year-old grandson developed weakness and myalgia after ingesting a smaller amount of the same meal. He presented to the same emergency room in a stable condition. His exam was remarkable only for sinus bradycardia. He was discharged without any specific treatment. He recovered in 24 h without any residual sequelae. These cases raise an awareness of the potential toxicity caused by ingestion of tobacco tree leaves and highlight the dangers of ingesting botanicals by lay public. Moreover, they add to the clinical spectrum of N. glauca intoxication.
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PMID:Nicotiana glauca (tree tobacco) intoxication--two cases in one family. 2065 61

This paper discusses a case study of a 19-year-old male student who engaged in daily long distance running and presented with complaints of fatigue and dizziness. Laboratory test revealed a hemoglobin of 7.7 g/dl and a bone marrow negative for iron. After a complete evaluation no source of blood loss was identified. His iron deficient state may be caused by his exposure to long distance running for some years. Recent work from Sweden reports iron deficiency in eight runners, demonstrated by bone marrow examination. Further work in West Germany shows low ferritin values in runners. Source of iron loss may be from hemoglobinuria and/or excessive sweating. Hemoglobin and ferritin values should be monitored in runners every six to 12 months.
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PMID:Iron deficiency anemia in a distance runner. 2128 10


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