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 6-year-old boy developed a flaccid hemiplegia and dysarthria following several transient episodes of nausea, vomiting, and ataxia. An anomly of the dens was discovered, permitting subluxation of C-1 on C-2. A segmental occlusion of the right vertebral artery and an aneurysm of the left vertebral artery were found at the C-2 level, as well as a thromboembolic occlusion of the rostral end of the basilar artery. It appeared that the repeated cervical subluxation produced occlusive, aneurysmal, and embolic vascular disease, and that clinical symptoms were the result of ischemia in the territory perfused by the vertebrobasilar arteries.
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PMID:Occlusive vertebrobasilar artery disease associated with cervical spine anomaly. 113 Mar 56

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

Transient global amnesia (TGA) is an unusual form of the amnestic syndrome, clinically characterized by profound disturbance of short-term memory with preservation of immediate recall and long-term memory. Spontaneous recovery is the rule and is usually complete within several hours. The etiology of TGA is not clear. It is considered to be caused by transient ischemia confined to the medial temporal lobe, an area supplied by branches of the vertebrobasilar system. Basilar artery migraine is a well-known syndrome, first described by Bickerstaff. Besides pulsating headache, the dominant symptoms are vertigo, ataxic gait, tinnitus, dysarthria, paraeshesia in the hands, homonymous hemianopsia and sometimes drop-attacks. These symptoms are associated with vertebrobasilar system dysfunction. In this paper, three migraine patients, suffering from one episode of TGA, were reported. All patients were women. Case 1 was a 48-year-old woman with a history of common migraine. Case 2 was a 48-year-old woman with a history of classic migraine. Case 3 was a 59-year-old woman with a common migraine. Family history of migraine exists in case 1 and case 3. Their migrainous attacks began in their twenties and thirties. They suddenly suffered migraine with the symptoms of vertebrobasilar dysfunction. These symptoms are ataxic gait (Case 1, 2, 3), dysarthria (Case 1, 2), vertigo (Case 1, 3) and homonymous hemianopsia (Case 1, 3). Simultaneously three patients had TGA. Duration of retrograde amnesia were about twenty-four hours (Case 1), about thirty minutes (Case 2) and about three hours (Case 3).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Basilar artery migraine associated with transient global amnesia]. 262 11

Two young patients are described who made good recoveries from a "locked-in" syndrome presumed to be due to ventral pontine ischemia. The first patient recovered completely from quadriplegia and mutism. In the second patient the only permanent sequellae were slight dysarthria and mild spasticity. Since patients may recover nearly completely from a "locked-in" syndrome, aggressive supportive therapy seems justified during the initial weeks or months.
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PMID:Reversible "locked-in" syndromes. 404 98

A 70-year-old man manifested during four years a progressive clinical picture consisting in palsy of gaze, axial rigidity, disorders of standing and gait, dysarthria, dysphagia. Neuroradiological investigations demonstrated proximal thrombosis of the left subclavian artery with subclavian steal. At necropsy, degenerative changes in several areas of the basal ganglia and brain stem, with presence of globose neurofibrillary tangles, were found, consistently with the pathologic pattern of the Progressive Supranuclear Palsy (PSP). The association of PSP and subclavian steal syndrome has not been previously reported, to our knowledge. We hypothesize that chronic ischemia, due to subclavian steal syndrome, in the vertebral basilar system and its watershed versus carotid system may have favoured the appearance, in these same areas, of the changes of the PSP.
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PMID:Progressive supranuclear palsy in the course of subclavian steal syndrome. 693 74

Sequential computed tomography (CT) scans were performed for up to 7 months on patients who presented with clinical evidence of lacunar infarction or ischemia. Sixty-nine percent of the patients showed lacunar infarction, and a negative scan did not suggest a better prognosis in stroke patients. Of patients with transient ischemic attacks (TIA) (lacunar), those with repeated bursts of hemiplegia (capsular warning syndrome) were more likely to be CT-positive (p less than 0.01). The clinical features of patients with lacunar infarction were examined and correlated with the features of infarction. Partial syndromes were found in 32% of the cases and included examples of monoparesis and dysarthria alone.
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PMID:A prospective study of lacunar infarction using computerized tomography. 719 33

Three patients with transient cerebellar dysfunction following head injury are described. Acute cerebellar signs, such as ataxia, nystagmus, and dysarthria, occurred just after trauma and resolved gradually, disappearing in every patient. Cerebrospinal fluid and computed tomography examinations were normal but magnetic resonance imaging and single photon emission computed tomography revealed cerebellar lesions. These findings distinguish cerebellar concussion from cerebellar contusion and suggest that the synergistic effect of trauma and ischemia may be the pathophysiological basis of this unusual syndrome.
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PMID:Cerebellar concussion--three case reports. 752 52

We report the successful management of cerebral vasculitis in a 46-year-old woman with longstanding rheumatoid arthritis with low-dose methotrexate. She suddenly developed dysarthria and left hemiparesis. Magnetic resonance imaging disclosed ischemia of the right pons, and angiography demonstrated cerebral vasculitis of vertebro-basilar arteries. The vasculitis was refractory with high-dose steroid therapy, which had only transient clinical benefit, and evolution to the pontine infarction followed. Her clinical status showed marked improvement in association with recovery of the vascular abnormalities after the initiation of the methotrexate therapy.
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PMID:Recovery from rheumatoid cerebral vasculitis by low-dose methotrexate. 782 78

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

We report the clinical findings and stroke mechanisms of 63 patients with cerebellar infarcts. We divided the intracranial vertebrobasilar circulation into the proximal territory (P), fed by the intracranial vertebral arteries and their branches; the middle territory (M), fed by the proximal and middle basilar artery and its branches; and the distal territory (D), fed by the rostral basilar artery and its branches. Cerebellar infarcts were classified by vascular territories P, M, D, P&D, and middle-plus (P&M, M&D, and P&M&D). Patients with P infarcts (11 patients) frequently had vertigo, gait instability, limb ataxia, and headache, whereas patients with D infarcts (15 patients) most often had limb ataxia, gait instability, and dysarthria. Patients with P&D infarcts (17 patients) had signs and symptoms of both groups combined. Infarcts in which the middle territory was involved, either alone (three patients) or combined with other territories (17 patients) were dominated by brainstem signs and symptoms. The predominant stroke mechanisms in the P, D, and P&D groups were embolic due to intra-arterial or cardiac embolism. When the M territory was involved, either alone or with P, D, or P&D territories, stroke mechanisms were more varied, and there was often large-artery occlusion with hemodynamic ischemia.
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PMID:Cerebellar infarcts in the New England Medical Center Posterior Circulation Stroke Registry. 805 34


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