Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 49-year-old female with no history of hearing disturbance developed sudden onset of headache and was admitted with no neurological deficits other than mild nuchal rigidity. Computed tomography (CT) showed subarachnoid hemorrhage. Four-vessel cerebral angiography disclosed no aneurysm. A second angiogram obtained on the 14th day showed vasospasm of the bilateral posterior cerebral arteries and right anterior inferior cerebellar artery, but still failed to demonstrate an aneurysm. Following the second angiography, she developed mild disturbance of consciousness and cerebellar ataxia of the right limbs, and repeat CT showed an infarct in the right cerebellar hemisphere. When she regained consciousness a few days later, she was completely deaf on the right side. The third angiography revealed a right vertebral artery dissecting aneurysm. Following clipping of the proximal portion of the right vertebral artery, she did well and was discharged, although right cerebellar ataxia and deafness persisted. Neuro-otological evaluation, including pure-tone audiography, auditory brainstem responses, electrocochleography, and caloric testing, indicated that her deafness resulted from ischemia in the territory of the right internal auditory artery due to vasospasm.
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PMID:[Unilateral nerve deafness due to rupture of a right vertebral artery aneurysm. Case report]. 247 75

We reported a patient with bilateral cerebellar peduncle infarcts who had an abrupt onset of bilateral hearing loss. A hypertensive 56-year-old man suddenly experienced bilateral hearing loss without other accompanying neurological deficits. He was hospitalized and treated for "idiopathic deafness". In addition, dysarthria and ataxic gait appeared two days later and he was transferred to our hospital. On neurological examination, the patient presented with diplopia, neurosensory hearing loss (approximately 70 dB) ataxic dysarthria, bilateral cerebellar ataxia and bilateral Babinski's signs. Auditory brain stem evoked response demonstrated prolonged delay of interpeak latency between waves III-IV. CT and MRI revealed fresh ischemic lesions symmetrically located at the middle cerebellar peduncles and cerebellar medullary body. Cerebral angiography showed total occlusion of the left vertebral artery and a stenotic right vertebral artery at the ostium of the posterior inferior cerebellar artery. We postulated that hearing impairment in this patient resulted from transient ischemia of the bilateral auditory tract in the brain stem or the peripheral cochlear system, but the definitive cause of the transient hearing loss remains undetermined. Concomitant appearance of a symmetrical infarction at the cerebellar peduncles is rare. We suggest that a circulation defect involving a multivascular system, which resulted in "border zone infarction" occurred at these regions.
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PMID:[A case of bilateral cerebellar peduncle infarction with bilateral hearing impairment of a sudden onset]. 795 15

The authors report three cases with petrotentorial dural arteriovenous malformation who underwent surgical interruption of the draining vein or dural sinus. They discuss the rationale and feasibility of this surgical procedure. Case 1 (70-year-old man) presented with trigeminal neuralgia and cerebellar ataxia caused by subarachnoid and cerebellar hemorrhage. Case 2 (68-year-old man) with trigeminal neuralgia due to venous mass effect. Case 3 (48-year-old man) with dementia caused by venous ischemia in the bilateral thalami. Cases 1 and 2 underwent lateral suboccipital craniotomy followed by infratentorial supracerebellar approach, and the draining vein was interrupted by aneurysmal clip under the cerebellar tentorium. Case 3 underwent surgical occlusion of the straight sinus by occipital transfalcine transtentorial approach after transarterial embolization had failed. Intraoperative digital subtraction angiography revealed the disappearance of dural AVMs in all three cases. The clinical symptoms disappeared postoperatively, and follow-up 6-vessel-angiography 2, 20, 11 months later, respectively, revealed no recurrence of dural AVMs. It has recently been proposed that many cranial dural AVMs with leptomeningeal venous drainage require only interruption of the draining vein as it enters the subarachnoid space for successful, lasting elimination. The striking clinical and radiological improvement in these cases emphasizes the pivotal role of surgical occlusion of the draining vein for petrotentorial dural AVMs which are not amenable to cure by endovascular procedures.
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PMID:[Surgical interruption of draining vein or dural sinus: treatment for petrotentorial dural arteriovenous malformation]. 951 93

Between 10%-28% of patients who receive the immunosuppressant cyclosporine (CsA) experience some form of neurotoxic adverse event. Both sensorial motoric functions may be adversely affected, and thus patients present with a wide range of neurological and psychiatrical disorders. Mild symptoms are common and include tremor, neuralgia, and peripheral neuropathy. Severe symptoms affect up to 5 % of patients and include psychoses, hallucinations, blindness, seizures, cerebellar ataxia, motoric weakness, or leukoencephalopathy. Tacrolimus is associated with similar neurotoxic adverse events. Neurotoxicity may result in serious complications for some patients, particularly recipients of orthotopic liver transplants. Factors that may promote the development of serious complications include advanced liver failure, hypertension, hypocholesterolemia, elevated CsA or tacrolimus blood levels, hypomagnesemia, and methylprednisolone. Occipital white matter appears to be uniquely susceptible to the neurotoxic effects of CsA; injury to both the major and minor vasculature may cause hypoperfusion or ischemia and local secondary toxicity in the white matter. Calcineurin inhibition by CsA and tacrolimus alters sympathetic outflow, which may play a role in the mediation of neurotoxic and hypertensive adverse events. The symptoms of CsA- and tacrolimus-associated neurotoxicity may be reversed in most patients by substantially reducing the dosage of immunosuppressant or discontinuing these drugs. However, some patients have experienced permanent or even fatal neurological damage even after dose reduction or discontinuation. CsA-sparing and tacroli-mus-sparing drug regimens that use the immunosuppressant mycophenolate mofetil, which has no neurotoxic effects, may reduce the incidence and severity of neurotoxic adverse events while maintaining an adequate level of immunoisuppression.
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PMID:Neurotoxicity of calcineurin inhibitors: impact and clinical management. 1105 66

A 71-year-old-woman was admitted to the S. Eugenio Hospital for a history of progressively impaired standing and gait. Anamnesis revealed systemic hypertension, gastric polyposis and juvenile pulmonary tuberculosis. Neurological examination showed a severe truncal and gait ataxia, without any sensory-motor impairment. Motor and somato-sensory evoked potentials were normal. Brain Magnetic Resonance Imaging (MRI) showed minimal signs of chronic ischemia only at a supratentorial level. Cerebral Single Photon Emission Computed Tomography, spinal MRI, total body computed tomography, Esophagogastroduodenoscopy, and finally total body Positron Emission Tomography resulted negative for neoplasms. Oncological serum markers were negative. Serum antibody against Purkinje's cells (Anti-Yo) was detected and titer was 1:80, while normally it should be undetectable. Other autoantibodies (Anti-Hu, Anti-Ri) were undetectable. Two sessions of plasma exchange (PE) were thus performed, leading to a rapid, marked and durable improvement of standing and gait and to a reduction of the autoantibody, which became undetectable. No serious adverse effect was noted. Although no definite therapy for autoimmune cerebellar ataxia has been established, PE should be considered as one of the main therapeutic choices.
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PMID:A case report of plasma exchange therapy in non-paraneoplastic cerebellar ataxia associated with anti-Yo antibody. 1566 51

Paraneoplastic neurological syndromes (PNS) can be defined as remote effects of cancer that are not caused by the tumor and its metastasis, or by infection, ischemia or metabolic disruptions. PNS are rare, affecting less than 1/10,000 patients with cancer. Only the Lambert-Eaton myasthenic syndrome is relatively frequent, occurring in about 1% of patients with small cell lung cancer. PNS can affect any part of the central and peripheral nervous system, the neuromuscular junction, and muscle. They can be isolated or occur in association. In most patients, the neurological disorder develops before the cancer becomes clinically overt and the patient is referred to the neurologist who has the charge of identifying a neurological disorder as paraneoplastic. PNS are usually severely disabling. The most common PNS are Lambert-Eaton myasthenic syndrome (LEMS), subacute cerebellar ataxia, limbic encephalitis (LE), opsoclonus-myoclonus (OM), retinopathies (cancer-associated retinopathy (CAR) and melanoma-associated retinopathy (MAR), Stiff-Person syndrome (SPS), chronic gastrointestinal pseudoobstruction (CGP), sensory neuronopathy (SSN), encephalomyelitis (EM) and dermatomyositis. PNS are caused by autoimmune processes triggered by the cancer and directed against antigens common to both the cancer and the nervous system, designated as onconeural antigens. Due to their high specificity (> 90%), the best way to diagnose a neurological disorder as paraneoplastic is to identify one of the well-characterized anti-onconeural protein antibodies in the patient's serum. In addition, as these antibodies are associated with a restricted range of cancers, they can guide the search for the underlying tumor at a stage when it is frequently not clinically overt. This is a critical point as, to date, the best way to stabilize PNS is to treat the cancer as soon as possible. Unfortunately, about one-third of patients do not have detectable antibodies and 5% to 10% have an atypical antibody that is not well-characterized. As PNS are believed to be immune-mediated, suppression of the immune response represents another treatment approach.
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PMID:Paraneoplastic neurological syndromes. 1748 Feb 25

We present a case of a 4-year-old previously healthy child who had a possible first-time seizure at home, and upon a second Emergency Department evaluation was found to have gross cerebellar ataxia suggestive of acute stroke. Initial computed tomography scan and metabolic work-up were unrevealing. Subsequent neuroimaging demonstrated stroke in the left medulla and cerebellum secondary to left vertebral artery dissection. Cervical artery dissection may cause up to 20% of strokes in childhood and adolescence. Unlike typical adult presentations, antecedent or concurrent head and neck pain occurs less often in pediatric dissections. Symptoms of posterior circulation ischemia resulting from vertebral artery dissection may include vertigo, vomiting, ataxia, dysarthria, and seizure. Willingness to utilize newer, non-invasive imaging modalities may lead to earlier recognition of cervical artery dissection when patients have prodromal symptoms or episodes of transient ischemia. Vertebral artery dissection should be included in the differential diagnosis when evaluating children with first time seizure, headache, or neck pain.
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PMID:A preschool-age child with first-time seizure and ataxia. 1797 66

Neuropsychiatric manifestations are commonly observed in systemic lupus erythematosus (SLE) patients; however, cerebellar involvement has rarely been reported. In the presence of acute cerebellar ataxia, etiologies related (focal edema and ischemia) and not related (infections, malignancy and paraneoplastic syndromes) to lupus have to be considered and they imply different treatment strategies. We report the clinical and radiological features of 3 SLE patients who presented with acute cerebellar ataxia. A review of the literature was performed by documenting cases of cerebellar ataxia in SLE and the importance of neuroimaging in the evaluation of these patients.
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PMID:Cerebellar ataxia in systemic lupus erythematosus. 1902 81

We report a 28-year-old male who presented with severe vertigo, vomiting, diplopia, clumsiness of right extremities. Physical examination revealed low reading of blood pressure in the left upper limb and evidence of mild left upper limb ischemia. On neurological examination he had right cerebellar ataxia. Computed tomography and magnetic resonance imaging, revealed an acute right cerebellar infarction in the anterior inferior cerebellar artery territory. Doppler ultrasono-graphy revealed an aneurysm of the left subclavian artery. The patient was tested positive for serology of syphilis.
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PMID:Left subclavian artery aneurysm secondary to syphilitic arteritis presenting with a right ischemic cerebellar infarction. 2013 37

Vascular disrupting agents (VDAs) are an exciting new group of targeted therapies under active clinical research in many solid tumors, in particular, lung cancer. Small-molecule VDAs are the focus of current clinical research, and consist of the flavonoids and the tubulin-binding agents. Toxicities of single-agent VDAs are characterized by acute, transient, and generally noncumulative side effects including headaches, nausea and vomiting, tumor pain, hypertension, and tachycardia. Flavonoid agents can also cause infusion site pain, visual disturbances, electrocardiac abnormalities, and symptoms consistent with an acute release of serotonin. Tubulin-binding agents can result in cardiac ischemia, abdominal pain, neuromotor abnormalities and cerebellar ataxia, and acute hemodynamic changes. Clinical trials investigating VDAs in combination with traditional chemotherapy have also shown the potential for significant pharmacologic and adverse toxicity interactions. Further research will need to focus on pharmacokinetic and pharmacodynamic parameters to optimize dosing schedules, determine effective combinations with chemotherapy, and minimize toxicities associated with VDAs.
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PMID:Classification and toxicities of vascular disrupting agents. 2127 75


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