Cases reported "Coma"

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1/36. pituitary apoplexy after cardiac surgery presenting as deep coma with dilated pupils.

    Acute clinical deterioration due to infarction or haemorrhage of an existing, often previously unrecognized, pituitary tumour is a rare but well-described complication. It can occur spontaneously or may be caused e.g. by mechanical ventilation, infection or surgical procedures. We report on a case of pituitary apoplexy occurring in a 64-year-old patient 3 weeks after cardiac surgery. The patient presented with deep coma and dilated pupils. magnetic resonance imaging revealed a haemorrhagic pituitary tumour. After prompt endocrinologic replacement therapy with levothyroxine and hydrocortisone the patient regained consciousness. Neurological examination revealed right oculomotor nerve palsy and bilateral cranial nerve VI palsy. Subsequent trans-sphenoidal removal of a nonfunctional macroadenoma with large necrotic areas was performed. The patient recovered completely. To our knowledge, pituitary tumours presenting with a combination of deep coma and dilated pupils must be considered exceedingly rare. Possible pathophysiologic mechanisms are discussed. As our case illustrates, even in severe cases complete recovery is possible if the diagnosis is suspected, and diagnostic and therapeutic measures are initiated in time.
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2/36. Right median nerve electrical stimulation to hasten awakening from coma.

    Electrical stimulation of the right median nerve may hasten the awakening of closed head injured, comatose patients. A series of 25 comatose patients have been treated. These patients made better recoveries than similar individuals reported in the literature. In a double-blind pilot project patients in the treated group scored better on interval glasgow coma scale scores, spent fewer days in the intensive care unit, and showed better Glasgow Outcome Scores at 1 month post-injury. Peripheral electrical stimulation of the right median nerve, through activation of the ascending reticular activating system, may be sufficient to arouse the moderate to severely comatose patient.
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keywords = median nerve, median, nerve
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3/36. Early rebleeding from intracranial dural arteriovenous fistulas: report of 20 cases and review of the literature.

    OBJECT: In this study the authors sought to estimate the frequency, seriousness, and delay of rebleeding in a homogeneous series of 20 patients whom they treated between May 1987 and May 1997 for arteriovenous fistulas (AVFs) that were revealed by intracranial hemorrhage (ICH). The natural history of intracranial dural AVFs remains obscure. In many studies attempts have been made to evaluate the risk of spontaneous hemorrhage, especially as a function of the pattern of venous drainage: a higher occurrence of bleeding was reported in AVFs with retrograde cortical venous drainage, with an overall estimated rate of 1.8% per year in the largest series in the literature. However, very few studies have been designed to establish the risk of rebleeding, an omission that the authors seek to remedy. methods: Presenting symptoms in the 20 patients (17 men and three women, mean age 54 years) were acute headache in 12 patients (60%), acute neurological deficit in eight (40%), loss of consciousness in five (25%), and generalized seizures in one (5%). Results of the clinical examination were normal in five patients and demonstrated a neurological deficit in 12 and coma in three. Computerized tomography scanning revealed intracranial bleeding in all cases (15 intraparenchymal hematomas, three subarachnoid hemorrhages, and two subdural hematomas). A diagnosis of AVF was made with the aid of angiographic studies in 19 patients, whereas it was a perioperative discovery in the remaining patient. There were 12 Type III and eight Type IV AVFs according to the revised classification of Djindjian and Merland, which meant that all AVFs in this study had retrograde cortical venous drainage. The mean duration between the first hemorrhage and treatment was 20 days. Seven patients (35%) presented with acute worsening during this delay due to radiologically proven early rebleeding. Treatment consisted of surgery alone in 10 patients, combined embolization and surgery in eight, embolization only in one, and stereotactic radiosurgery in one. Three patients died, one worsened, and in 16 (80%) neurological status improved, with 15 of 16 AVFs totally occluded on repeated angiographic studies (median follow up 10 months). CONCLUSIONS: The authors found that AVFs with retrograde cortical venous drainage present a high risk of early rebleeding (35% within 2 weeks after the first hemorrhage), with graver consequences than the first hemorrhage. They therefore advocate complete and early treatment in all cases of AVF with cortical venous drainage revealed by an ICH.
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4/36. Predicting outcome from coma: man-in-the-barrel syndrome as potential pitfall.

    The glasgow coma scale motor score is often used in predicting outcome after hypoxic-ischemic coma. Judicious care should be exerted when using this variable in predicting outcome in patients with coma following hypotension since borderzone infarction can obscure the clinical picture. We describe a patient who underwent skull base surgery for a schwannoma of the left facial nerve. The operation, which lasted for 10 h, was conducted under controlled hypotension. After the intervention the patient remained comatose with absent arm movements upon painful stimuli. An absent motor score usually carries a poor prognosis. However, magnetic resonance inversion recovery imaging of the brain showed bilateral hyperintense lesions in the arm-hand area indicative of borderzone ischemic damage. The patient received optimal supportive care and after 17 days he regained consciousness with 'man-in-the-barrel syndrome', which also further improved over time.
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5/36. guillain-barre syndrome occurring in two women after ketoacidosic comatose state disclosing an insulin-dependent diabetes mellitus.

    We report two women who presented with a guillain-barre syndrome just after a ketoacidosic comatose state disclosing an insulin-dependent diabetes mellitus. One had characteristic clinical signs and the other had major motor involvement. At neurophysiologic investigations, one had typical demyelinating neuropathy whereas the second had mainly axonal degeneration. At ultrastructural examination of a peripheral nerve biopsy, features of macrophage-associated demyelination were present in both nerve specimens, thus confirming the diagnosis of acute inflammatory demyelinating polyneuropathy, i.e., guillain-barre syndrome. Prominent axonal involvement was also present in the motor nerves of the second patient. insulin therapy had to be permanently continued and these two cases are quite different from the transient diabetes sometimes observed in certain cases of guillain-barre syndrome. Both the latter and insulin-dependent diabetes mellitus probably have auto-immune mechanisms. It is likely that in our two patients both auto-immune diseases were triggered by a common event. Such cases of guillain-barre syndrome have to be distinguished from other acute diabetic neuropathies.
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6/36. ethylene glycol ingestion resulting in brainstem and midbrain dysfunction.

    INTRODUCTION: ethylene glycol toxicity has produced central nervous system abnormalities including coma, cerebral edema, and cranial nerve dysfunction. CASE REPORT: A 26-year-old male developed widespread brainstem and midbrain dysfunction with corresponding cranial computed tomography findings after ingesting ethylene glycol. The computed tomography scan which was obtained 3 days after ethylene glycol ingestion showed low density areas in the basal ganglia, thalami, midbrain, and upper pons. The neurologic findings in our patient reflected dysfunction of all the areas of hypodensity on the cranial computed tomography scan. A magnetic resonance imaging of the brain obtained 24 days after ingestion revealed bilateral putamen necrosis. The patient's neurologic sequelae resolved over the following 4 months.
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7/36. Auditory brainstem response and temporal bone pathology findings in a brain-dead infant.

    The criteria for assessing adult brain death have been already established, but those for infant brain death have not been yet established in japan. We report auditory brainstem response (ABR) and postmortem pathology of the temporal bone and brain of a brain-dead 9-month-old female. During the comatose state, her ABR showed only waves I and II bilaterally. autopsy revealed the presence of a left cerebellar astrocytoma, herniation and anoxic encephalopathy. The pathological examination of the temporal bone revealed the destruction of the inner ear particularly on the left side. In the auditory pathway of brain-dead patients, degeneration occurs first in the cerebrum, followed by the cochlear nerve. Thus, ABR is one of the useful means to assess brain death even in infants.
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8/36. miller fisher syndrome with transient coma: comparison with Bickerstaff brainstem encephalitis.

    We herein report a 4-year-old boy with miller fisher syndrome (MFS) who presented with transient coma in addition to the typical triad of internal and external ophthalmoplegia, cerebellar ataxia and areflexia after an influenza type B infection. The electroencephalogram findings revealed intermittently generalized slow wave bursts. The cerebrospinal fluid revealed high protein and a lack of any cellular response. The serum anti-GQ1b IgG antibody was elevated in the acute phase and disappeared in the convalescent phase. The transient coma with the triad of MFS in this patient indicated an extended brainstem lesion including a reticular formation, which is also the responsible lesion of Bickerstaff brainstem encephalitis (BBE), but the magnetic resonance imaging repeatedly showed no abnormal finding. Our patient suggested the involvement of central nervous system in addition to the peripheral nerve injury in MFS. He also suggested that MFS and BBE may belong to the same group of disorders as syndrome of ophthalmoplegia, ataxia and areflexia (SOAA).
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9/36. Paroxysmal apnea and vasomotor instability following medullary infarction.

    BACKGROUND: Central hypoventilation and paroxysmal hypertension are uncommon complications of medullary infarction. To our knowledge, the combination of these autonomic complications of medullary stroke has not previously been reported. OBJECTIVE: To describe a patient who experienced life-threatening paroxysmal attacks of central apnea and vasomotor instability 3 months after medullary infarction, a combination of symptoms that is unusual. PATIENT, methods, AND RESULTS: Following a right lateral medullary infarction, an otherwise stable 70-year-old woman developed recurrent episodes of apnea (PCO2), > 100 mm Hg), blood pressure instability (systolic blood pressure, > 200 to < 100 mm Hg), and mental status changes (from agitation to coma) within hours of removal from mechanical ventilation. These attacks occurred repeatedly after removal from mechanical ventilation and were prevented by diaphragm pacing with a phrenic nerve pacemaker and nocturnal mechanical ventilation via a tracheostomy. CONCLUSIONS: A syndrome of life-threatening central hypoventilation and vasomotor instability can occur after medullary infarction. Placement of a phrenic nerve pacemaker can prevent these complications, without the functional limitations imposed by continuous mechanical ventilation.
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10/36. A life-threatening complication of the Nuss procedure for pectus excavatum.

    We describe a delayed, life-threatening complication in a boy operated on using the Nuss-procedure 2 months earlier. On admittance he was in shock with cardiac tamponade. An immediate needle aspiration of blood from the pericardium was done before a median sternotomy. The Nuss-bar was removed, and we identified a 1.5-cm laceration in the adventitial layer of the ascending aorta as the source of bleeding. The tear was closed, and the patient had an uneventful recovery. Careful positioning of the bar is necessary to avoid complications. Measures must be taken postoperatively to confirm that the steel bar does not rotate.
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