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 10-year-old girl developed bilateral blindness and partial third nerve paresis immediately following a closed head injury. Bilateral optic atrophy developed subsequently. This is the first report of an association between second and third nerve injuries after minor head trauma in the absence of a preexisting lesion. The pathophysiology of indirect injury to the optic nerve under these circumstances is uncertain, but the lesions in this patient seemed to be due to ischemia.
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PMID:Total blindness after trivial frontal head trauma: bilateral indirect optic nerve injury. 57 Jun 62

Spinal cord blood flow (SCBF) was measured in 24 rhesus monkeys after injury to the cord produced by the inflatable circumferential extradural cuff technique. Measurement of regional blood flow in the white and gray matter of the cord in areas of 0.1 sq mm was achieved with the 14C-antipyrine autoradiographic technique and a scanning microscope photometer. After moderate cord injury (400 mm Hg pressure in the cuff maintained for 5 minutes), which produced paraplegia in 50% of animals and moderate to severe paresis in the other 50%, mean white matter SCBF was significantly decreased for up to 1 hour. White matter blood flow then rose to normal levels by 6 hours posttrauma and was significantly increased by 24 hours posttrauma. Gray matter SCBF was significantly decreased for the entire 24-hour period posttrauma. After severe cord injury (150 mm Hg pressure in the cuff maintained for 3 hours), which produced total paraplegia in almost all animals; SCBF in white and hours), which prodced total paraplegia in almost all animals, SCBF in white and gray matter was reduced to extremely low levels for 24 hours posttrauma. In addition, focal decreases in SCBF were seen in white and gray matter for considerable distances proximal and distal to the injury site. It is concluded that acute compression injury of the spinal cord is associated with long-lasting ischemia in the cord that increases in severity with the degree of injury.
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PMID:Effect of acute spinal cord compression injury on regional spinal cord blood flow in primates. 82 18

Vessels of the microcirculatory bed of the heart in myocardial infarction were studied on the basis of the material of 21 section observations using histological, histochemical methods and the technique of impregnation of films of the epicardium developed by V. V. Kupriyanov. In the ischemic stage in the zone of ischemia and in perifocal areas there were noted signs of increased vascular permeability and impairment of hemodynamics: plethora of the venous department of the microcirculatory system, stasis of the blood in capillaries, spasm and paresis of vessels of the microcirculation. In the necrotic stage in the zone of necrosis there were observed destruction of vessels of the microcirculatory bed; in the peri-infarction zone--drastic plethora of veins, venules and capillaries, higher vascular permeability, leucostasis, leucopedesis, perivascular cellular infiltrates, destruction of vessels of the microcirculatory bed, dilatation of lymphatic vessels; in the intact zone--venous plethora and elevated permeability. In cases of shocks and collapses in vessels of the microcirculatory bed of the heart beyond the zone of necrosis aggregations of erythrocytes were found. In the reparative stage newly formed vessels in the granulation tissue were observed; In the post-infarction scars sinusoid vascular cavities and arteries of the closing type were noted.
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PMID:[Vessels of the microcirculatory bed of the heart in myocardial infarction]. 122 73

Oculomotor nerve paresis, ocular hypotony, anterior segment ischemia, and the ocular ischemic syndrome are uncommon manifestations of giant cell arteritis. Four patients with these findings had giant cell arteritis documented by temporal artery biopsy. Cerebral angiography or ultrasonography, or both, performed in three patients, excluded hemodynamically significant stenosis of the internal carotid artery as the cause of ocular ischemia and cerebral aneurysms as the cause of oculomotor nerve paresis. Corticosteroid treatment, administered to three patients, resulted in resolution of the oculomotor deficits and the clinical signs of ocular ischemia, although the visual acuity in one patient improved from 20/400 to 20/60. Giant cell arteritis should be considered in the differential diagnosis of the ocular ischemic syndrome.
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PMID:Giant cell arteritis in the ocular ischemic syndrome. 159 63

Three cases of bilateral deafness with cytologically-demonstrated meningeal carcinomatosis are reported. The first patient, a 64-year old man, presented with bilateral deafness, gait disturbances, and bilateral facial paresis. The second patient, a 78-year-old man, had bilateral deafness, unsteady gait and fluctuations in consciousness. The last patient, a 69-year-old man, complained of bilateral deafness and severe headache, and presented with right facial paresis and left laterodeviation while walking. All three patients had abnormal cochleo-vestibular findings and brainstem auditory evoked responses (BAER) that suggested peripheral lesions with absent or very delayed I waves. The brain CT scans with an without contrast enhancement were entirely normal, and the diagnosis was established by lumbar puncture. From our own cases and a review of the literature, deafness in meningeal carcinomatosis may start unilaterally but becomes bilateral in less than a week. Vestibular disturbances may not be apparent, but they can be demonstrated in almost all cases. Facial paresis or plegia is also a very frequent finding. The destruction of the eighth and seventh cranial nerves is probably due to direct infiltration by neoplastic cells as well as to ischemia through compression of the nerve supplying vessels. The 3 cases presented here emphasize once again the important fact that meningeal carcinomatosis remains a cytological diagnosis, several lumbar punctures being sometimes necessary, and that cerebrospinal fluid studies cannot yet be supplanted by other diagnostic techniques like contrast-enhanced CT or MRI with gadolinium.
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PMID:[Bilateral deafness, an initial manifestation of meningeal carcinomatosis]. 160 23

Three patients with spinal dural arteriovenous fistula presented with acute and/or progressive myelopathy. The thoracic cord was focally enlarged and poorly defined on MR images in two of the patients. One individual showed focal cord atrophy, and one demonstrated abnormal intrathecal vessels. In all patients MR studies revealed cord enhancement after IV administration of gadopentetate dimeglumine. The MR findings are believed to represent disruption of the blood-cord barrier associated with cord ischemia and/or infarction, which, in turn, is caused by venous stasis resulting from the fistula. The diagnosis in each case was confirmed by the combined results of myelography, spinal arteriography, and surgery. Surgical excision or embolization of the fistula produced a poor return of lost function but an arrest in the progression of paresis. One of the patients had constant severe back and leg pain postoperatively, and a follow-up MR study 5 months after surgery showed focal atrophy and persistent enhancement of the thoracic cord. The patient with preoperative focal cord atrophy had an MR examination 1 year prior to surgery, which revealed enhancement of the cord similar to that seen on the immediate preoperative MR study. This patient also had severe pain in the back and lower extremities preoperatively, which accompanied her progressive paraparesis. It is believed that long-standing enhancement of the spinal cord in patients with dural arteriovenous fistula probably results from chronic progressive venous ischemia, which may be irreversible and cause pain of a central type.
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PMID:Venous infarction of the spinal cord resulting from dural arteriovenous fistula: MR imaging findings. 188 56

Medical personnel should be able to recognize vascular injuries. Knowing the key signs of ischemia, namely pallor, pulselessness, pain, paresis, and paresthesia and the soft signs of vascular injury will help to prevent limb loss.
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PMID:Recognition of vascular injury in the trauma patient. 211 86

A 58-year-old woman developed bilateral internuclear ophthalmoplegia, probable right oculosympathetic paresis (Horner's syndrome), and right facial dysesthesias with acute cervical hyperextension upon sustaining a rear-end automobile collision. There was no head trauma. A nuclear magnetic resonance scan revealed a discrete area of increased signal in the tegmentum of the pons to the left. Extensive recovery was noted 1 year later. The acute cervical hyperextension suggested acute shearing and stretching of axons from brain stem deceleration rather than transient vertebral artery ischemia. Internuclear ophthalmoplegia representing intracranial pathology without direct head trauma has not previously been described with acute cervical hyperextension injury.
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PMID:Bilateral internuclear ophthalmoplegia due to acute cervical hyperextension without head trauma. 252 55

Three men developed acute esotropia, stupor, and impaired upward gaze. Vestibulo-ocular stimulation showed that the adducted eye remained immobile while the fellow eye responded normally. The alteration of consciousness, the long-tract neurologic signs, and the esotropia quickly resolved. Upgaze paresis and brief bursts of convergence-retraction nystagmus were the major residual signs. Imaging techniques demonstrated lesions of the contralateral posterior thalamus in each patient. Several mechanisms are proposed to explain the acute esotropia. Impairment of monocular projections in the contralateral posterior thalamus could disinhibit neurons in the oculomotor complex, or ischemia of inputs to neurons involved with vergence control in the midbrain could result in tonic activation of the medial rectus. The clinical and radiographic findings are consistent with infarction in the territory of penetrating branches of the basilar-communicating (mesencephalic) artery. Embolism to the top of the basilar artery is presumed to be the precipitating event.
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PMID:Acute thalamic esotropia. 1117 22

The term "top of the basilar" has been used in reference to a group of signs and symptoms of midbrain, diencephalic, and posteroinferior hemispheric dysfunction. It has been attributed to ischemia in the territory of second- and third-order vessels that arise from the uppermost portion of the basilar artery. We report our experience with four patients who had alteration of consciousness, confusion, and vertical gaze paresis accompanied by other physical abnormalities. Extensive evaluation did not help in documenting the lesions or in understanding their pathogenesis. The top of the basilar syndrome is a not uncommon form of stroke and carries a variable prognosis. Treatment by anticoagulation may prevent further infarction in selected patients who are seen early.
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PMID:Altered sensorium, confusion, and vertical gaze paresis: the top of the basilar syndrome. 339 40


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