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)

The clinical significance of temporal minor slow and sharp activity (TMSSA) is discussed on the basis of earlier literature and personal observations (209 patients, 227 EEG records). This pattern consists of mixed 2-7/sec and 8-14/sec activity with intermingled minor sharp transients (occasionally even frank spikes) over the anterior temporal-midtemporal region and, in the vast majority (84% in our material) predominantly on the left side. This pattern is most prominent in early drowsiness, and may change to rhythmical spiky discharges in light NREM sleep ("wicket spikes"). The origin of TMSSA is unclear. There is reason to believe that hippocampic ischemia might be the underlying substratum but the evidence remains tenuous. Vertebrobasilar artery insufficiency states may result in TMSSA since the hippocampus largely depends on this vascular system (via posterior cerebral artery). The occurrence of TMSSA usually represents a mild abnormality of potentially considerable clinical significance.
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PMID:Temporal minor slow and sharp EEG activity and cerebrovascular disorder. 311 43

A patient suffering from acute left subclavian artery thrombosis presented with an unusual syndrome of prominent somnolence, right cerebellar signs, and left upper extremity ischemia. Clinical, angiologic, and electrophysiologic studies confirmed a brain stem and reticular formation dysfunction due to vertebrobasilar ischemia. Urgent thromboembolectomy led to neurologic improvement and satisfactory revascularization of the involved upper limb.
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PMID:Prominent somnolence and cerebellar syndrome in subclavian artery thrombosis--a case report. 342 77

The clinical signs and morphological brain lesions associated with histotoxic hypoxia induced by subcutaneous injection of 3-nitropropionic acid (NPA) in rats are described, and compared to hypoxic brain damage from other causes including ischemia and hypoglycemia. The brains were perfusion-fixed with paraformaldehyde/glutaraldehyde fixative, and examined by light and electron microscopy. Intoxicated rats developed severe neurological disease characterized by somnolence, uncoordinated gait with stereotypical paddling movements, and ventral or lateral recumbency. Recumbent rats had a selective, bilaterally symmetrical pattern of severe morphological injury in the caudate-putamen, hippocampus, and thalamus. Recumbency was a consistent indicator of the development of morphological brain lesions. In contrast to reports describing rat models of ischemia and hypoglycemia, morphological injury was not seen in the cerebral and cerebellar cortices of NPA-intoxicated rats. Ultrastructurally, neuronal alterations ranged from chromatin clumping with increased cytoplasmic lucency to severe cellular shrinkage or swelling with marked mitochondrial swelling (high amplitude swelling). White matter alterations included axonal swelling and adaxonal splitting of myelin lamellae. Vascular changes included perivascular deposits of proteinaceous material presumably from leakage of serum proteins, variable electron lucency of endothelial cell cytoplasm, an apparent increase in pinocytotic vesicles, rare platelet thrombosis of capillaries, and rare intravascular blebs of luminal plasma membrane. As a model of brain damage following energy deficiency, NPA intoxication has the advantages of producing morphological brain injury in a highly predictable anatomical pattern, and at a time paralleling the onset of clinical recumbency.
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PMID:Nature and distribution of brain lesions in rats intoxicated with 3-nitropropionic acid: a type of hypoxic (energy deficient) brain damage. 356 9

Absence spells in adults have been recognized in association with disorders of excessive somnolence, transient ischemia of the temporal lobes, and seizure disorders. A 66-year-old man who presented with a history of absence spells for more than 20 years is described. After diagnosis of a hyperventilation syndrome without an associated seizure disorder, educational and behavioral therapy without the use of medication has produced a long, continuing remission of these spells. The hyperventilation syndrome continues to present in many ways, often without recognition by physicians for prolonged periods. The case presented exemplifies this problem and may be the first report of absence spells caused by hyperventilation.
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PMID:Absence spells. Hyperventilation syndrome as a previously unrecognized cause. 642 1

Bilateral ophthalmoplegia may be an unusual sign of vertebrobasilar ischemia. We report the cases of two patients (75 and 73 years old), who suddenly developed drowsiness, bilateral ophthalmoplegia with bilateral ptosis and mild right hemiparesis. In both patients, MRI revealed bilateral thalamic and midbrain infarcts, ECG showed the presence of atrial fibrillation and Doppler study of the extracranial and intracranial vertebral arteries found no significant alterations. Ischemia involving the midbrain and thalamic paramedian regions may cause bilateral ophthalmoplegia and consciousness disturbances. In these two cases, the most plausible etiologic mechanism was cardiac embolism, and the prognosis for bilateral ocular palsy was poor.
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PMID:Bilateral ophthalmoplegia: an unusual sign of the top of the basilar artery syndrome. 891 63

Although hypercalcemia may cause drowsiness, lethargy, weakness, confusion and coma it rarely causes seizures or cerebral infarction. The patient presented had a clinical evolution from hallucinosis to a generalized tonic-clonic seizure, and subsequent cortical blindness with occipital cerebral ischemia as evidenced by SPECT and MRI scans. EEG revealed occipital PLEDs. With reversal of hypercalcemia, there was a return of vision, resolution of EEG epileptiform activity, although with some residual occipital infarction. This case, in concert with a literature review of hypercalcemia, reveals examples of occipital and watershed ischemia, blindness, seizures and hypertension, a pattern markedly similar to that of eclampsia. Furthermore, medications such as magnesium sulfate, believed to reverse cerebrovasospasm responsible for the eclamptic neurologic findings, may counter the effects of hypercalcemia at a cellular level, lending support to a calcium-mediated injury in eclampsia.
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PMID:Reversible hypercalcemic cerebral vasoconstriction with seizures and blindness: a paradigm for eclampsia? 966 11

Meningitis and meningococcal sepsis are emergency conditions associated with high mortality. The outcome is worsened by the onset of disseminated intravascular coagulation. This may present, particularly in children, with the clinical picture of purpura fulminans, characterized by extensive necrotic-hemorrhagic skin lesions, ischemia of the extremities and multiorgan failure. It has been observed that depletion of coagulation inhibitors, particularly protein C, plays a key role in the development of this severe complication. We describe the case of a woman who presented in the Emergency Room with signs of meningitis, drowsiness, hypotension and petechie. Bacterioscopic examination of the cerebrospinal fluid evidenced characteristic gram-negative diplococci. Laboratory data disclosed initial disseminated intravascular coagulation with low levels of proteins C and S. Following intravenous infusion of antibiotics, fluids and fresh frozen plasma, the patient's condition rapidly improved. However, multiple skin lesions appeared on her fingers, toes and heels. It is likely that the infusion of coagulation inhibitors contained in fresh frozen plasma, prevented evolution to full-blown purpura fulminans. The first choice treatment for purpura fulminans in meningococcal sepsis is infusion of protein C concentrate, which is not, however, currently available on the market.
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PMID:[Meningococcal meningitis in the adult complicated by cutaneous necrosis: description of a clinical case]. 1120 31

The authors report an unusual case of low intracranial pressure (ICP) syndrome that was successfully treated by the placement of an anti-siphon device (ASD). This 36-year-old male had suffered suprasellar germinoma with hydrocephalus and had had a V-P shunt following radiotherapy. Sixteen years later he developed gait disturbance and somnolence and MRI demonstrated a small lateral ventricle as well as a diffuse dural enhancement. A lumbar tap revealed a low ICP of 12 mmH2O. Because of this, an ASD was placed in the patient. Postoperatively, his symptoms of gait and consciousness disturbance improved. Typical clinical findings of low ICP syndrome such as headache were not observed in this case. To our knowledge, no symptom of gait disturbance with low ICP has been reported previously. We present an interesting case of low ICP syndrome with gait disturbance and discuss the mechanism of the symptoms. Symptoms of this patient were due at first to brain ischemia. After convulsion and consciousness disturbance due to low intracranial pressure, the symptoms increased in strength until gait disturbance occurred. The possibility is suggested that gait disturbance in this patient was due both to brain ischemia and low intracranial pressure.
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PMID:[Successful treatment of a patient with low pressure syndrome associated with gait disturbance]. 1159 68

Diffuse neurological manifestations of preeclampsia are due to endothelial involvement that lead to ischemia, hemorrhage, or edema. We analyzed clinical and radiological features and the course of brainstem ischemic strokes in a preeclampsia patient. We report a case of severe preeclampsia in a 30-year-old woman who was admitted 10 hr after a vaginal delivery at home. The pregnancy was at 39 wk, with no prenatal care. At her admission, she was conscious, and she had tetraparesia, swinging deep tendon reflex testing, drowsiness, and dysarthria; the BP was at 160/100 mmHg and 4 + proteinuria; magnetic resonance imaging revealed brainstem ischemic stroke. The evolution was favorable with symptomatic treatment. The patient was discharged on the 16th day; 2 months later she had a normal recovery. Brainstem strokes are rare. They are frequently due to hemorrhage; sometimes, they can also be ischemic. Their course is favorable.
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PMID:Brainstem ischemia and preeclampsia. 1561 26

This review summarizes the well-known clinical features of the obstructive sleep apnea-hypopnea syndrome (OSAHS) and emphasizes new research on this syndrome. Though described in the seventies, the prevalence OSAHS is known mainly in the US. A dramatic increasing in prevalence has been related to the increase prevalence of obesity, raising a substantial public health problem. Discussion continues on the proper definition of the syndrome and degrees of severity. Multiple factors are involved in the pathogenesis of sleep apnea: anatomic abnormalities, mechanical factors, nervous alterations, muscular imbalance between pharyngeal constrictor and dilator muscles or part of a metabolic syndrome? Indeed, obstructive sleep apnea with and without obesity is increasingly implicated in the initiation and progression of metabolic disorders and of cardiovascular diseases (hypertension, cardiac ischemia and probably congestive heart failure, cardiac arrhythmias and strokes). An extended literature reports the neural, humoral, thrombotic, metabolic and inflammatory mechanisms linking OSAHS to endocrinology and cardiovascular diseases. Daytime sleepiness, cognitive, memory and performance deficits with their risks are also stressed. These consequences require treating this syndrome as soon as possible. Multiple interventions (medical, mechanical-nasal positive airway pressure or oral appliances, and sometimes surgical management) can be used but nasal continuous positive airway pressure is the "gold standard" treatment in severe OSAHS. More often multiple interventions are appropriate in a given patient. Finally, there is growing evidence that genetic factors influence the expression of OSAHS. Numerous genetic studies have investigated the etiology of OSAHS with the goal of improving our understanding of its pathogenesis.
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PMID:[Obstructif sleep apnea-hypopnea syndrome: evolution of an old concept]. 1718 49


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