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 78-year-old hypertensive woman suddenly developed blurred vision, followed shortly by dizziness, difficulty walking with a tendency to veer to the left, and vertical diplopia. Examination 3 weeks later revealed a unique neuro-ophthalmologic motility pattern, which may be described as periodic alternating skew deviation. This previously unreported motility disturbance was associated with downbeat nystagmus in our patient, and a focal lesion at the level of the interstitial nucleus of Cajal was demonstrated on computed tomography. The spectrum of physiologically related motility patterns--including periodic alternating nystagmus, cyclic oculomotor paralysis, see-saw nystagmus, periodic alternating gaze deviation, "ping-pong" gaze, and intermittent aperiodic alternating skew deviation--has been considered and is helpful in topical neuro-ophthalmologic diagnosis.
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PMID:Periodic alternating skew deviation. 621 44

A 50-year-old woman with antiphospholipid antibody syndrome (APAS) awoke in a morning to notice dizziness, so she came to our hospital. Several hours later she developed left oculomotor paralysis. Further two hours later she developed right oculomotor paralysis and could not stand. Brain MRI showed high signal intensity lesion of paramedian thalamic and midbrain on the T2-weighted image. Cerebral angiography did not reveal any occlusion. Transesophageal echocardiography disclosed mitral valvular vegetation. We thought this valvular abnormality was non-bacterial thrombotic vegetation associated with APAS and this suggests that cerebral infarction was due to emboli from this vegetation.
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PMID:[Brain infarct due to non-bacterial thrombotic valvular vegetation associated with primary antiphospholipid antibodies--a case report]. 1020 77

The Kearns-Sayre (K-S) syndrome which includes the triad of progressive external ophthalmoplegia, pigment retinopathy, and disorder of cardiac conduction was first described in 1958. The mitochondria disorder is believed to be the cause of this syndrome. Involvement of the cardiac conduction system is the most importent prognostic factor in K-S syndrome. A 34-year-old male K-S syndrome patient, manifesting as ptosis and weakness of limbs since the age of 15 years, suffered from dizziness and weakness. Twelve-lead eletrocardiography (ECG) showed a 2:1 atrioventricular (AV) block with slow ventricular rate. Intermittent complete AV block, complete left bundle branch block and torsades de pointes were noted in Holter ECG. The electrophysiology study demonstrated prolonged HV interval (85 ms) on conduction beat and infra-His block on non-conduction beat. A VVIR mode of permanent pacemaker was implanted and the patient's condition was stable during this period of follow-up.
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PMID:Atrioventricular block in Kearns-Sayre syndrome: a case report. 1155 73

Although ophthalmoplegia following snake bites is not indicative of a serious neurotoxic complication, symptoms of diplopia, dizziness and ocular discomfort can be emotionally devastating for patients. The authors experienced two cases of ophthalmoplegia following snake bites in Korea. The patients complained of diplopia that had developed several hours after the snake bites. The diplopia did not improve with antivenom treatment, but resolved completely after several injections of neostigmine.
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PMID:Anticholinesterase therapy for patients with ophthalmoplegia following snake bites: report of two cases. 1530 63

The brainstem is an uncommon site of a brain abscess. Such lesions, which were invariably fatal, changed with the arrival of computed tomography and magnetic resonance imaging (MRI). These not only helped in the diagnosis but also in treatment management. A 51-year old patient was diagnosed of widespread pontomesencephalic abscess. He was admitted with a clinical picture of dizziness, headache and involvement of multiple cranial nerves with near complete ophthalmoplegia and cerebellar syndrome in the side of the lesion and contralateral hemiplegia. Microbiologic investigations were negative and the medical management decided was broad spectrum antibiotic and periodic MRI controls. The length of the lesion decreased (from 4 cm in diameter to 0.5 cm) with progressive improvement of the neurological deficits. Treatment of large brainstem abscesses includes primary antibiotic therapy combined with stereotaxic drainage, but in individual cases empirical medical therapy can be effective. Sequential MRI examinations are very important for monitoring treatment efficacy.
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PMID:[Widespread brainstem abscess resolved with medical therapy]. 1732 39

Between 1994 and 2006, a total of 280 cases of varying degrees of tetrodotoxin poisoning following ingestion of the toxic eggs of the horseshoe crab, Carcinoscorpius rotundicauda, were admitted to the medical service of Chon Buri Hospital. The severity of the poisoning was classified into four stages based on clinical signs and symptoms of human tetrodotoxication. Of 245 available medical records; 100 were in stage 1, 74 were in stage 2, 3 were in stage 3 and 68 were in stage 4. The frequencies of symptoms and signs included the following : circumoral and lingual numbness (98%), hands and feet numbness (94.7%), weakness (59.6%), dizziness and vertigo (54.3%), nausea and vomiting (52.6%), transient hypertension (39.6%), respiratory paralysis (27.7%), fixed dilated pupils (14.7%), ophthalmoplegia (12.2%), blood pressure lower than 90/60 mmHg (5.7%), and polyuria (0.4%). All patients received symptomatic and supportive treatment. Endotracheal intubation and mechanical ventilation were considered when paralysis was progressing rapidly. The results of treatment are as follows: 239 patients (97.5%) showed complete recovery, 5 patients (2%) died, and 1 patient (0.4%) suffered anoxic brain damage. Horseshoe crab poisoning occurs both sporadically and epidemically in Chon Buri. Seasonal variation in the number of cases of poisoning was observed with a peak from December through March.
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PMID:Tetrodotoxin poisoning following ingestion of the toxic eggs of the horseshoe crab Carcinoscorpius rotundicauda, a case series from 1994 through 2006. 1856 17

Myasthenia gravis (MG) is a chronic neuromuscular disease which leads to varying degrees of weakness in the skeletal muscles. Some of the symptoms of the disorder include weakness of the eye muscles, difficulty in swallowing and slurred speech. When only the muscles of the eyes are affected, the illness is termed ocular myasthenia, which is often characterized by abrupt onset of diplopia and ptosis of the eyelid. In most patients with ocular-onset MG, there is a progression to involvement of other muscle groups within the first two years (generalized myasthenia). In the case reported here, a 39-year-old male of Ecuadorian descent complained of difficulty seeing, double vision, dizziness, unsteady gait, difficulty maintaining balance and fatigue for the previous two days. Neurological examination was remarkable for total external ophthalmoplegia. There was no external bulbar muscle paralysis, motor weakness, muscle wasting, sensory deficits or sphincter dysfunction. His laboratory workup was significant for elevated acetylcholine receptor antibody. He was diagnosed with ocular MG after differential diagnoses were ruled out based on the onset and presentation of symptoms, the patient's age and a normal magnetic resonance imaging exam. No signs of generalized myasthenia were detected. His symptoms improved dramatically after treatment with Acetyl cholinesterase (AchE) inhibitors and steroids, regaining much of his ocular mobility and ability to walk without gait imbalance. At follow-up visits, the patient remained healthy with no evidence development of other myasthenic signs. This case is atypical since ocular MG does not normally occur in the absence of other myasthenic forms.
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PMID:An atypical course of myasthenia gravis. 1860 52

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

Unpleasant visual symptoms including oscillopsia and dizziness may occur when there is unexpected motion of the visual world across the subject's retina ("retinal slip") as in an acute spontaneous nystagmus or on head movement with an acute ophthalmoplegia. In contrast, subjects with chronic ocular dysmotility, e.g., congenital nystagmus or chronic progressive external ophthalmoplegia, are typically symptom free. The adaptive processes that render chronic patients asymptomatic are obscure but may include a suppression of oscillopsia perception as well as an increased tolerance to perceived oscillopsia. Such chronic asymptomatic patients display an attenuation of vestibular-mediated angular velocity perception, implying a possible contributory role in the adaptive process. In order to assess causality between symptoms, signs (i.e., eye movements), and vestibular-perceptual function, we prospectively assessed symptom ratings and ocular-motor and perceptual vestibular function, in a patient with acute but transient ophthalmoplegia due to Miller Fisher Syndrome (as a model of visuo-vestibular adaptation). The data show that perceptual measures of vestibular function display a significant attenuation as compared to ocular-motor measures during the acute, symptomatic period. Perhaps significantly, both symptomatic recovery and normalization of vestibular-perceptual function were delayed and then occurred in a parallel fashion. This is the first report showing that symptomatic recovery of visuo-vestibular symptoms is better paralleled by vestibular-perceptual testing than vestibular-ocular reflex (VOR) measures. The findings may have implications for the understanding of patients with chronic vestibular symptoms where VOR testing is often unhelpful.
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PMID:Symptomatic Recovery in Miller Fisher Syndrome Parallels Vestibular-Perceptual and not Vestibular-Ocular Reflex Function. 2135 Jul 34

A 42-year-old young lady presented with acute onset of dizziness, drooping of left eye with binocular diplopia and inability to walk unassisted. She had past history of uncontrolled diabetes mellitus and hypertension. On examination, she had left fascicular type of third nerve palsy, vertical one and half syndrome (VOHS), left internuclear ophthalmoplegia and skew deviation with ipsilesional hypertropia. She also had thalamic astasia and right unilateral asterixis. Her MRI revealed T2 and Flair hyper intense signal changes with restricted diffusion in the left thalamus, subthalamus and left midbrain. MR Angiography was normal. Thalamic-subthalamic paramedian territory infarct is relatively uncommon. It can present with oculomotor abnormalities including vertical one and half syndrome, skew deviation, thalamic astasia and asterixis. This case is reported for the rarity of the presenting clinical findings in unilateral thalamo-mesencephalic infarcts.
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PMID:Unilateral asterixis, thalamic astasia and vertical one and half syndrome in a unilateral posterior thalamo-subthalamic paramedian infarct: An interesting case report. 2391 12


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