Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients had clinical findings of encephalopathy that progressed in 4 to 5 months. One patient had headache, fatigue, lethargy, hemiparesis, and a seizure. The second patient had only forgetfulness, confusion, and lethargy without focal signs. Herpes simplex virus was grown from brain biopsy in the first patient and from CSF in the second patient. These cases suggest that herpes simplex virus caused the encephalitis and that it should be considered in the differential diagnosis of chronic encephalopathy.
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PMID:Chronic encephalitis possibly due to herpes simplex virus: two cases. 403 28

Three operated cases of congenital deficiency of factor XIII (fibrin-stabilizing factor) associated with intracranial hematomas were described and the diagnosis, replacement therapy of the factor were discussed. Congenital deficiency of factor XIII is quite rare coagulation disorder and only 100 patients were reported in the literatures in which we could find only one case who had craniotomy for associated intracranial hemorrhage. Case 1: A 41-year-old female with the history of unknown hemorrhagic diathesis complained of headache and right hemiparesis on August 2, 1980. CT scan showed left parietal intracerebral hematoma caused by unknown hemorrhagic diathesis and operated on under fresh blood transfusion. Postoperative state was uneventful but bleeding from the operated wound and rebleeding in the operated hematoma cavity were found on 5th postoperative day. The screening test for factor XIII was abnormal but replacement therapy with fresh plasma and factor XIII failed to control hemorrhagic diathesis. The patients died of GI bleeding and recurrent intracerebral hematoma on 21st postoperative day. Case 2: A 1.4-year-old boy with the history of umbilical bleeding on delivery and diagnosed as congenital deficiency of factor XIII in the other hospital fall down and struck his occiput on September 20, 1980. He vomited and became stuporous two days after injury, and was transferred to Ryukyu University Hospital. CT can revealed epidural hematoma at the left posterior fossa which extended to the supratentorium. The hematoma was successfully evacuated under infusion of fresh plasma and he showed uneventful recovery without rebleeding by postoperative appropriate replacement therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[3 operated cases of congenital deficiency of Factor XIII associated with intracranial hematomas]. 650 54

The case of a 26 year old woman who had been taking tranexamic acid to prevent uterine bleeding due to an IUD and who died from thrombosis of the left internal carotid artery is reported. The patient's father had died at age 54 of myocardial infarction. Otherwise the family history was entirely negative for thromboembolic disease. The patient was a mild smoker. She had been previously healthy and in particular, she was not affected with hypertension, diabetes, or dyslipidemia. She had carried to term 2 uncomplicated pregnancies. 40 days prior to hospital admission her gynecologist had inserted an IUD. The insertion of the IUD was followed by persistent uterine bleeding, and for this reason she began treatment with tranexamic acid (1.5 g/daily). Uterine bleeding persisted despite this treatment, and the IUD was removed. Because of persistence of a mild uterine bleeding, tranexamic acid was continued. 2 hours before admission the patient suddenly presented a left sided hemiparesis with disarthria and vomiting. On admission she was stuporous. The left side of her face drooped and the strength of the left arm and leg was markedly decreased. Both arm and leg reflexes were symmetrical. Her blood pressure was 110/70. An electroencephalogram on arrival confirmed a right sided cerebral lesion. Subsequently the patient's condition deteriorated rapidly. She developed a full left hemiplegia and became deeply comatose. A CAT scan performed 4 hours after admission showed no abnormalities. A CAT scan performed 3 days after admission showed a large cerebral infarction involving nearly the whole right cerebral hemisphere. The patient's condition remained essentially unchanged until she died 6 days after admission. Permission for autopsy was refused. Antifibrinolytic drugs competitively inhibit plasminogen activators and noncompetitively plasmin. Thromboembolic complications after the administration of antifibrinolytic drugs have long been recognized. The use of IUDs is often associated with troublesome uterine bleeding and particularly excessive menstrual bleeding. To avoid these complaints, antifibrinolytic drugs are increasingly used.
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PMID:Tranexamic acid, intrauterine contraceptive devices and fatal cerebral arterial thrombosis. Case report. 710 62

A case of arterio-venous malformation (AVM) at the right parietal area in association with agenesis of the left internal carotid artery (ICA) is described. A 27-year-old male complained of severe headache and vomiting on September 27th in 1980. He lost his consciousness and became stuporous within several minutes after the ictus. He was then transferred to Kurume University Hospital. On admission, he was semicomatose, anisocoria and left hemiparesis marked in the lower limbs, and bilateral Babinski reflex were noted. A emergency CT scan revealed a round high density area suggesting intracerebral hematoma at the right parieto-occipital area. Right retrograde brachial angiography was then performed which showed a small AVM at the right parietal lobe mainly fed by the right posterior parietal arterial branch, and drained into the superior sagittal sinus, via the subcortial veins. Left MCA bilateral PCA and SCA also were demonstrated on the angiogram. The angiogram suggested on abnormality of the Willis ring. Emergency operation fro the small AVM associated with intracerebral hematoma was then performed. The AVM was sufficiently removed and approximately 80 gr. of intracerebral clots were also evacuated completely. Histological examination indicated a typical small AVM. The postoperative course was uneventful. Left CAG performed by seldinger method from the femoral artery after the operation showed no demonstration of the left ICA. the left common carotid artery was terminated as the external carotid artery without carotid bifurcation at the neck. The left ophthalmic artery was fed by the meningeal artery of the internal maxillary artery. Left vertebrobasilar system was normal. From an angiogram, the agenesis of the left ICA was most suspected. An agenesis of ICA was uncommon among the literature in which there was no case with this anomaly associated with cerebral AVM. The embryological consideration about this case was mainly discussed.
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PMID:[A case of arterio-venous malformation associated with agenesis of unilateral internal carotid artery (author's transl)]. 734 82

An epidural hematoma associated with posttraumatic pseudoaneurysm of the middle meningeal artery is a very rare clinical entity. Only 31 such cases have been reported in the literature. A 54-year-old man was admitted with lethargy and right hemiparesis. A skull X-ray film revealed a linear fracture in the left parietal and temporal bone, extending to the base of the skull. A brain CT scan disclosed an acute epidural hematoma over the left cerebral hemisphere, contusional hematoma in the right frontal lobe and thalamus, and subarachnoid hemorrhage in the left Sylvian fissure. During an emergency craniotomy a large epidural hematoma was evacuated and external decompression was performed. Angiography, which was performed about one month after the head injury, revealed an aneurysm of the middle meningeal artery. The aneurysm was removed to avoid delayed rupture at the time of cranioplasty. Histological diagnosis was pseudoaneurysm. We discussed the pathogenesis of a pseudoaneurysm of the meningeal artery and the necessity to pay attention to the presence of a pseudoaneurysm when an active bleeding point is not observed during surgery of the epidural hematoma.
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PMID:[Posttraumatic pseudoaneurysm of the middle meningeal artery: a case report]. 747 11

Ornithine transcarbamylase deficiency is an X-linked recessive disorder of urea biosynthesis characterized by recurrent, often fatal, hyperammonemic encephalopathy in affected males; carrier females are usually asymptomatic. We report here the clinical and laboratory findings in five symptomatic heterozygous females with ornithine transcarbamylase deficiency. In each case, the onset of symptoms occurred in the 1st year of life, but diagnosis was delayed by up to 15 years. Symptoms included recurrent vomiting with lethargy (five patients), dietary protein intolerance (five), irritability (four), severe acute encephalopathy (three), ataxia (three), and acute hemiparesis (two). All eventually showed evidence of developmental delay or learning difficulties. Two of the three who experienced severe, acute, hyperammonemic encephalopathy suffered serious, permanent neurologic sequelae. Three of the patients showed decreased ornithine transcarbamylase activity in liver obtained by needle biopsy, and the other two had marked orotic aciduria associated with hyperammonemia. Neuroimaging studies demonstrated persistent abnormal lobar attenuation and abnormal signal on computed tomographic scan and magnetic resonance imaging. All patients showed marked symptomatic improvement on treatment with dietary protein restriction supplemented by pharmacologic measures to increase nonprotein nitrogen excretion. Ornithine transcarbamylase deficiency should be considered in the differential diagnosis of acute or chronic encephalopathy in females at any age.
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PMID:Ornithine transcarbamylase deficiency in females: an often overlooked cause of treatable encephalopathy. 749 56

We report a case of subacute encephalopathy with seizures in chronic alcoholism (age 34 years). This syndrome clearly differs from the known neurological complications of chronic alcoholism. One of the authors has observed (and reported) such cases in the Baltimore area. Subacute encephalopathy is characterized by lethargy, confusion and neurological deficits such as hemiparesis, homonymous hemianopsia and aphasia. Epileptic seizures (generalized tonic-clonic, focal) are obligatory. The EEG shows very prominent slowing and periodic lateralized paroxysmal discharges (PLEDs). The condition is complicated by a variety of internal-medical complications. Structural neuroradiological tests are either normal or irrelevant. The cause and pathogenesis remain obscure. The subacute course ends with gradual resolution.
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PMID:[Subacute encephalopathy with seizures in chronic alcoholism]. 768 29

From the literature and our own experience, 11 cases of hemorrhage or infarction of a pituitary adenoma associated with cardiac surgery have been identified over a 13-year period. Males outnumbered females by 10 to 1. Symptoms observed were headache, lethargy, confusion, obtundation, unilateral ptosis, meiosis, and opthalmoplegia involving cranial nerves III, IV, and VI, visual field deficits, and hemiparesis. Diagnosis in most recent cases has been confirmed with computerized tomography or magnetic resonance imaging. All patients received adrenocortical steroid therapy initially. Eight patients underwent transsphenoidal hypophysectomy and all survived. One patient underwent decompression craniotomy and died. Intracranial surgery was deferred in 1 patient who survived and in another who died of a massive stroke. Residual neurological deficits were noted to be either absent, minimal, or resolving in 7 of the 9 patients who survived their initial hospitalization. While numerous mechanisms have been proposed to explain the hemorrhage and necrosis of a pituitary adenoma during heart surgery, no direct cause has been clearly identified. Surgical treatment is commonly necessary since untreated pituitary apoplexy is often fatal. Transsphenoidal hypophysectomy with decompression is the preferred method of treatment with a low perioperative mortality and fairly good long-term prognosis.
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PMID:Pituitary adenomas complicating cardiac surgery: summary and review of 11 cases. 777 76

Traumatic aneurysms (TAs) are an unusual etiology for late neurological deterioration after traumatic brain injury (TBI) and represent less than 1% of all cerebral aneurysms. TAs most often are diagnosed acutely but may be delayed in presentation. To increase awareness of this serious but treatable condition when diagnosed early, we report a delayed TA after a motor vehicle accident. The patient experienced a seizure on day 46 postinjury while in rehabilitation and demonstrated persistent lethargy and hemiparesis. Neuroimaging revealed a large, ruptured left pericallosal artery TA, which was surgically clipped. The patient completed his rehabilitation course and was eventually discharged home with family. Among TBIs, TAs are associated with penetrating injuries and skull base or anterior cranial fossa fractures. Associated mortality is high, especially if rupture has occurred. Although TAs are rare, the clinician should be vigilant in the at-risk patient.
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PMID:Delayed traumatic cerebral aneurysm after brain injury. 934 11

A normally healthy 6-year-old woke in an agitated state, limp, and moving only her left extremities. Upon arrival at the emergency department, a blood glucose measurement was 34 mg/dL. The child was lethargic, not responding to questions appropriately, and not moving her right extremities. The right arm was flexed, and the right leg was flexed and abducted. Pupils were equal and reactive, and eyes were deviated to the left. Six loose tablets of the grandmother's glyburide were found at home in the child's outdoor playhouse. Administration of glucose produced no change in the child's clinical condition. Intravenous glucose was begun at 4 mg glucose/kg/min, and the blood glucose level did not fall below 74 mg/dL after that. Over the next 48 h, the hemiparesis and mental status changes resolved without sequelae. The events of the case suggest a hypoglycemia-induced seizure with subsequent Todd's paralysis. Early direct medical evaluation in suspected glyburide ingestions in children is suggested.
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PMID:Hemiparesis and altered mental status in a child after glyburide ingestion. 961 Sep 73


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