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)

Seven patients of temporal arteritis with eye involvement have been presented. These cases represent a spectrum of disease from intermittent diplopia with minimal 6th nerve weakness through mild retinal ischemia with recovery to permanent bilateral blindness. Temporal arteritis should be suspected when any form of ocular ischemia is suspected by history or found on examination of an elderly person. An early diagnosis may protect the vision in both eyes if vision is normal at the time of diagnosis. If vision in one eye is decreased because of ischemia, the vision in the other eye can usually be retained if proper therapy is instituted. Furthermore, adequate therapy may even result in improvement in vision in the involved eye. Patients with biopsy proven temporal arteritis should be continued on steroid therapy until the active disease is quiescent. Inactivity should be determined by carefully monitoring the ESR while steroids are being tapered. If the ESR rises, it is indicative of continued inflammation and if steroids are not continued, the eyes remain at risk as seen in Case 5. If the ESR remains elevated for a year or more despite continuation of high steroid levels, consideration should be given to repeating the temporal artery biopsy. Temporal arteritis should be considered in the differential diagnosis of any multisystem disease in older patients. Even central nervous system involvement may occur concomitantly, since the intracranial vessels are not immune from the disease process. Tuberculosis, systemic syphilis and more recently the collagen vascular diseases have been dubbed the "great imitators" and "the protean diseases." We suggest that the same terminology can be applied to temporal arteritis. Temporal arteritis can affect any organ. Moreover, there is a wide spectrum of variation in the degree of involvement of any particular tissue as illustrated by these 7 cases of ocular involvement.
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PMID:Temporal arteritis: a spectrum of ophthalmic complications. 118 Apr 60

We reported a patient with brainstem infarction who presented paralytic pontine exotropia (PPE) in acute phase and non-paralytic pontine exotropia (NPPE) during the recovery phase. On March 10, 1991, a 60-year-old man was brought to our hospital with chief complaints of double vision and right hemiparesis. The ocular position of the left eye on forward gaze was fixed at the midline, while the right eye was abducted, and skew deviation was observed. On leftward gaze, neither eye could pass the midline, and on rightward gaze the right eye was abducted and monocular nystagmus was noted in the abducted right eye, which indicated paralytic pontine exotropia. T2-weighted MRI showed high signal intensity lesions in the left paramedian portion of the mid-pontine tegmentum beneath the fourth ventricle, and in the midline of the pontine base extending to the left side. The next day, similar disturbance of ocular movement was seen on rightward gaze, but the limitation of leftward gaze had improved and NPPE was noted to have developed. On the third day, there was no abduction of the right eye on forward gaze, but left MLF syndrome was still present. Seven days later, the disturbances of ocular movement disappeared. The lesion was considered to be due to partial impairment of the left paramedian pontine reticular formation in addition to the MLF. PPE caused by ischemia due to the perforating arteries of the brainstem, different from that due to basilar artery occlusion may recover after progression through NPPE and MLF syndromes. Hence, one-and-a-half syndrome, PPE, NPPE, and MLF syndromes are considered to be analogous to one another.
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PMID:[A case of brainstem infarction presenting with paralytic pontine exotropia and non-paralytic pontine exotropia]. 181 90

We combined a recession or resection of recti muscles with a vertical or horizontal transposition to correct a complicated paralytic ocular deviation in eight patients. The transposed muscles were reattached to the globe parallel to the spiral of Tillaux and adjacent to the paralyzed muscle. Postoperatively, seven patients demonstrated fusion in the primary position or required a slight head turn to fuse. There were no surgical complications, and no patient developed symptomatic cyclotropia, diplopia, or anterior segment ischemia.
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PMID:A simple transposition procedure for complicated strabismus. 195 23

Symptoms compatible with vertebrobasilar ischemia have been reported in patients with unilateral or bilateral carotid occlusive disease. Intracranial steal phenomena have been proposed to explain the symptoms. In a review of 54 patients with angiographically documented severe bilateral carotid stenosis (less than or equal to 2 mm residual lumen) or occlusion, eight had symptoms suggesting vertebrobasilar insufficiency. Five patients were identified retrospectively, and the other three were evaluated prospectively. Symptoms included various combinations of hemodynamically mediated, transient bilateral motor, sensory, or visual impairment. Dysarthria, dysphagia, and diplopia were generally absent. Each patient also described additional symptoms compatible with transient hemispheric or retinal ischemia. The anatomic regions subserving the bilateral vertebrobasilar-like symptoms could be correlated with angiographically estimated arterial border zones in both hemispheres and may thus represent bilateral hemispheric border zone ischemia rather than brain stem ischemia. An intracranial steal need not be invoked.
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PMID:The syndrome of bilateral hemispheric border zone ischemia. 226 72

Lupus anticoagulants and anticardiolipin antibodies are antiphospholipid antibodies (APLAb) with related antigenic specificities and are newly recognized markers for an increased risk of thrombosis. We studied 48 patients who presented with cerebral or visual dysfunction associated with APLAb to help clarify the diagnostic, clinical, laboratory, radiologic, and pathologic features in these patients. Most patients presented with transient cerebral ischemia or cerebral infarction. Recurrent and stereotypic events were frequent. Visual disturbances resulted from amaurosis fugax, retinal arterial or venous occlusion, occipital ischemia, diplopia, and migraine-like disturbances. Three patients presented with severe atypical classic migraine. Recurrent infarcts of brain and eye were significantly associated with the presence of cigarette smoking, hyperlipidemia, and a positive antinuclear antibody. During 44.4 patient-years of prospective follow-up, the combined stroke and systemic thrombotic event rate was 0.27 events per patient-year and was 0.54 events per patient-year if TIA and death were included. Forty (83%) of the patients did not have systemic lupus erythematosus (SLE). Thrombocytopenia was present in 15 (31%) and a false-positive VDRL in 11 (23%) of the patients. Cerebral angiography was normal or revealed large-vessel occlusion or stenosis without changes suggestive of vasculitis. Patients with only transient dysfunction generally had normal radiologic studies, including angiography. Organs and arterial vessels studied pathologically revealed thrombotic occlusive disease without vasculitis. APLAb are strongly associated with an immune-mediated thrombotic tendency, generally in the absence of SLE. Other stroke risk factors may add to the risk of recurrent ischemic events in patients with APLAb.
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PMID:Cerebrovascular and neurologic disease associated with antiphospholipid antibodies: 48 cases. 238 25

This study was designed to investigate the hemodynamic characteristics of cavernous angiomas of the brain. Five adult patients with a cavernous angioma underwent local cortical blood flow studies and vascular pressure measurements during surgery for the excision of the cavernous angioma. Clinical presentation included headache in four patients, seizures in four patients, and recurring diplopia in one patient. Magnetic resonance imaging demonstrated the cavernous angiomas in all patients and revealed an associated small hematoma in two. Four patients with a cerebral cavernous angioma were operated on in the supine position and the remaining patient, whose lesion involved the brain stem, was operated on in the sitting position. Mean local cortical blood flow (+/- standard error of the mean) in the cerebral cortex adjacent to the lesion was 60.5 +/- 8.3 ml/100 gm/min at a mean PaCO2 of 35.0 +/- 0.6 torr. Mean CO2 reactivity was 1.1 +/- 0.2 ml/100 gm/min/torr. The local cortical blood flow results were similar to established normal control findings. Mean pressure within the lesion in the patients undergoing surgery while supine was 38.2 +/- 0.5 mm Hg; a slight decline in cavernous angioma pressure occurred with a drop in mean systemic arterial blood pressure and PaCO2. Mean pressure in the cavernous angioma in the patient operated on in the sitting position was 7 mm Hg. Jugular compression resulted in a 9-mm Hg rise in cavernous angioma pressure in one supine patient but no change in the patient in the sitting position. Direct microscopic observation revealed slow circulation within the lesions. The hemodynamic features demonstrated in this study indicate that cavernous angiomas are relatively passive vascular anomalies that are unlikely to produce ischemia in adjacent brain. Frank hemorrhage would be expected to be self-limiting because of relatively low driving pressures.
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PMID:Vascular pressures and cortical blood flow in cavernous angioma of the brain. 239 87

We reported a 51-year-old male with ischemic disturbance of right inner ear resembling Meniere's disease. The patient had a sudden-onset episode of vertigo, right severe hearing disturbance, nausea, vomiting and gait disturbance. Two days after, he had hypersomnia, vertical gaze palsy, double vision, left Horner's sign, and sensory disturbance of pain and temperature of right half body involving face. Brain MRI disclosed high intensity area in T2-weighted image and proton density in bilateral paramedian thalamo-mesencephalic region and right cerebellum (area of the anterior inferior cerebellar artery). Cerebral angiography showed 90% or more stenosis of the right vertebral artery, 50% stenosis of the left vertebral artery before the posterior inferior cerebellar artery (PICA), and 60% stenosis of distal portion of the basilar artery. Furthermore, stem portion of the posterior cerebral artery, and the right anterior cerebellar artery and the left vertebral artery after the PICA were absent or occluded. Right deafness was evaluated to be Jerger type II, namely disturbance of inner ear. Caloric tests showed no response, and right auditory brainstem response showed no waves. Main cause of this vertigo and right deafness was considered to be disturbance of inner ear due to ischemia of right labyrinthine artery, though this patient was not a typical case of the anterior cerebellar artery syndrome. Ischemic disturbances of inner ear have been reported only in patients with the anterior cerebellar artery syndrome, therefore this patient who had only acute ischemic disturbance of inner ear and did not have disturbance of caudo-lateral portion of the pons was considered to be very rare.
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PMID:[A case of ischemic disturbance of inner ear]. 259 43

Ten adult patients developed sixth-nerve palsy after trauma or a cerebral tumor. No clinical evidence of recovery of function was noted by at least 8 months after onset. All patients underwent total transposition of the superior and inferior rectus muscle insertions to the area of the lateral rectus insertion, accompanied by botulinum toxin (Oculinum) injection of the ipsilateral medial rectus. These patients developed a mean diplopia-free field of 51 degrees, with a diplopia-free field in the abducted field of 20 degrees. This procedure involved surgery on only two rectus muscles, but the results compared favorably with surgical strategies involving three rectus muscles. Thus, the risk of developing anterior segment ischemia was greatly reduced.
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PMID:Vertical rectus muscle transposition and botulinum toxin (Oculinum) to medial rectus for abducens palsy. 192 13

Giant-cell arteritis is a polysymptomatic disease of the elderly. Systemic symptomatology includes headaches, arthralgias, myalgias, tender temporal arteries, jaw claudication, low-grade fever, anemia, anorexia, malaise, and weight loss. Visual loss from anterior ischemic optic neuropathy and diplopia resulting from ischemia of the ocular muscles represents the major ocular manifestations of giant cell arteritis. When the diagnosis is suspected, blood for a sedimentation rate should be drawn, and, if it confirms the clinical impression, high dose prednisone should be started immediately and a temporal artery biopsy performed at a later date. Only by asking the proper questions and suspecting the diagnosis will this preventable form of blindness receive the prompt attention it deserves.
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PMID:Giant-cell arteritis. Signs and symptoms. 715 21

Cortical blindness is defined as a loss of vision due to bilateral retrogeniculate lesions (geniculocalcarine blindness). Gerstmann's syndrome is a combination of disorientation for left and right, finger agnosia, and profound agraphia, alexia, and acalculia. It is due to a lesion in the left angular gyrus, situated at the confluence of the temporal, parietal, and occipital lobes. We report on a patient who suffered from severe underdiagnosed eclampsia and who developed bilateral extensive medial temporal, parietal, and calcarine ischemic infarctions during an eclamptic fit. In addition, ischemia destroyed the left angular gyrus. The combination of these lesions led to Gerstmann's syndrome with additional cortical agnosia and cortical diplopia. For the first few months following the ischemic insult, the patient had been cortically blind. Thereafter, the patient slowly regained a visual acuity of 0.1 in both eyes. She then experienced monocular and binocular diplopia. Her ocular motility was normal; there was no phoria or tropia. Monocular and binocular diplopia slowly became less severe over the following year. Now, 2 years after the incident, the patient has a visual acuity of 0.2 in both eyes and no double vision. However, the handicapping symptoms of Gerstmann's syndrome, which make leading a normal life impossible, have persisted--the patient still cannot cope alone, mainly due to the severe disorientation for left and right. The picture of cortical agnosia, cortical diplopia, and Gerstmann's syndrome is a very rare combination. Visual recovery and rehabilitation in cortical blindness are severely affected and made difficult by the symptoms of Gerstmann's syndrome. In our case the reason for such a dramatic clinical picture was eclampsia, whose prodomes had not been diagnosed in time.
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PMID:Eclamptogenic Gerstmann's syndrome in combination with cortical agnosia and cortical diplopia. 749 36


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