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1/22. hepatic encephalopathy--a physostigmine-reactive central anticholinergic syndrome?

    This report describes an association between hepatic encephalopathy and central anticholinergic syndrome (CAS). A 60-year-old anaemic woman was admitted unconscious and with a delayed reaction to pain but with no focal neurological deficits. She had signs of portal hypertension and a history of non-alcoholic liver cirrhosis grade child B. Suspecting upper gastro-intestinal bleeding, she was intubated for gastro-duodenoscopy and a fibrin-covered ulcer was revealed. Raised intra-abdominal pressure resulting from ascites caused cardiopulmonary failure, which required mechanical ventilation for 24 h, but extubation was possible after drainage of the ascites and blood volume replacement therapy. However, her neurological state remained unchanged despite normal blood ammonia concentration and no sedation. CAS was considered and physostigmine injected with immediate effect. The patient opened her eyes immediately and was fully orientated to personal and medical history. We suggest that hepatic encephalopathy may trigger CAS, although the significance of physostigmine in the treatment of hepatic encephalopathy remains to be addressed by controlled investigations.
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2/22. Acute dilated cardiomyopathy and central nervous system toxicity following propranolol intoxication.

    OBJECTIVE: We report a case of a 16-year-old boy who developed central nervous system (CNS) depression and acute dilated cardiomyopathy following ingestion of 3200 mg of propranolol in a suicide attempt. Early echocardiographic findings were the only sign of cardiac toxicity. DESIGN: A case report. SETTING: Pediatric intensive care unit of a teaching hospital. RESULTS: This child developed significant acute dilated cardiomyopathy and severe CNS depression 2 hours after ingesting 3200 mg of propranolol. The child was treated with gastric lavage, activated charcoal, and mechanical ventilation. Following the echocardiographic findings, treatment with isoprenaline hydrochloride and glucagon were given intravenously. Echocardiographic examination 12 hours following treatment showed normal left ventricular size and function. No change in pulse rate or blood pressure was reported on admission and during his hospitalization. DISCUSSION: In the early stages of propranolol and other lipophilic beta-blocker intoxication, severe CNS depression can develop in the absence of clinical signs of cardiac toxicity. Early echocardiographic evaluation is important and may prevent delay in diagnosis and treatment of cardiac toxicity.
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3/22. noise-induced neurologic disturbances in divers exposed to intense water-borne sound: two case reports.

    Divers may be exposed to intense noise underwater. Two cases of neurologic disturbances during experimental exposures to 15 min of continuous underwater sound are described. sound exposure in the first case consisted of a warble tone with center frequency of 240 Hz and a sound pressure level of 160 dB re 1 microPa. Symptoms during exposure consisted of somnolence, lightheadedness, and an inability to concentrate. No apparent effect on hearing was noted. In the second case, a center frequency of 1,000 Hz at 181 dB was used. Lightheadedness, inability to concentrate, agitation, and head vibrations were noted during the exposure. The diver also exhibited a temporary auditory threshold shift of 19.2 dB. In both cases, overt symptoms resolved within 30 min after exposure, but both divers reported recurrent symptoms days to weeks after the exposures. Medical histories and examinations, assessment of dive profiles, and breathing gas analysis failed to support a source other than the sound exposures to account for the symptoms observed. Potential mechanisms for the described symptoms are discussed.
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4/22. Thoracic spine arachnoid ossification with and without cord cavitation. Report of three cases.

    Thoracic spine arachnoid ossification is a relatively rare disease that affects mainly women and causes sensory, motor, and sphinctal symptoms associated with inferior limb pain. Based on three cases, the authors comment on pathogenic and surgery-related aspects of the disease. The patient in Case 1 was followed over the course of 23 years. Spinal cavitation is highlighted in Case 2, and yellow, gross, half-ring ossification is described in Case 3. calcium deposits usually occur in the middle and lower thoracic spine where the majority of trabeculated arachnoid cells are located. Operative treatment does not interrupt the ossification process, which continues over time, causing progressive deterioration in the patient. Spinal cavitation can occur due to spinal cord tethering, stretching, and central cord edema formation, accompanied by cerebrospinal fluid blockage and pulse pressure changes. The results of surgical intervention are poor, offering short-term recovery with later deterioration. Multiple pathogenic factors are involved in this clinical syndrome including metabolic changes.
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5/22. Subarachnoid cyst and ascent to high altitude--a problem?

    A 31-year-old man suffered diplopia and ataxia on two occasions when he ascended from sea level to 4,000 m. Evaluation revealed a moderate-sized subarachnoid cyst in the left frontal region, which did not communicate with the cerebral ventricles. The cyst might have acted as a space-occupying lesion, and caused symptoms on ascent due to hypoxic brain swelling, brain compression against the cyst, and elevated intracranial pressure. Subarachnoid cysts are common, and they should be considered in the differential diagnosis of neurological problems at high altitude.
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6/22. Respiratory failure in the neurological patient: the diagnosis of neurogenic pulmonary edema.

    Neurogenic pulmonary edema (NPE) is a potential complication of a central nervous system (CNS) insult such as intracranial hemorrhage, uncontrolled generalized seizures, head trauma, tumors, and neurosurgical procedures. The proposed etiology is massive sympathetic discharge following a CNS event. The pathogenesis is not completely understood. However, there are two theories on how NPE occurs: the blast theory and the permeability defect theory. There is evidence for both theories, and NPE is probably the result of a combination of the two. The treatment is mainly supportive with the use of mechanical ventilation and alpha-adrenergic blocking agents while managing increased intracranial pressure. A thorough understanding of the pathophysiological mechanisms behind the development of NPE aids in the management of these patients to prevent further complications.
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7/22. Langerhans' cell histiocytosis and the nervous system.

    We report two cases of Langerhans' cell histiocytosis with unusual central nervous system (CNS) involvement. The first patient had behavioural disturbances, memory loss and diabetes insipidus. His response to a range of treatments was poor. The second patient presented with seizures and headaches suggestive of raised intracranial pressure. etoposide (VP16) chemotherapy led to a dramatic clinical and radiological improvement. The various CNS manifestations of Langerhans' cell histiocytosis and their management are discussed.
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8/22. Neurogenic pulmonary edema: case reports and review.

    Neurogenic pulmonary edema (NPE) is a relatively common though often subclinical complication of a variety of central nervous system insults (trauma, hemorrhage, seizures, etc.) in children and adults. The syndrome probably results from massive centrally mediated sympathetic discharge and generalized vasoconstriction, and often presents in the emergency department (ED). The symptoms are likely to be mistaken for aspiration pneumonia. Treatment consists of ventilatory support, including positive end-expiratory pressure, and aggressive measures to reduce intracranial pressure. We present four cases of NPE and review its recognition and emergent management.
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9/22. Spontaneous intracranial hypotension with pachymeningeal enhancement on MRI.

    Spontaneous intracranial hypotension (SIH) is a rarely reported syndrome of spontaneously occurring postural cephalalgia associated with low CSF pressure. We report a case of SIH in which MRI of the brain revealed diffuse symmetric pachymeningeal enhancement that resolved without specific therapy.
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10/22. neurocysticercosis and nursing implications.

    neurocysticercosis causes significant neurologic morbidity and mortality in many countries and is increasing in frequency in the united states. The disease should be considered in any patient who has lived in or traveled to an area where it is endemic and who presents clinically with signs of increased intracranial pressure, stroke, seizures, or other neurologic deficits. neurocysticercosis can be a life-threatening disease depending on the size, location, and active or inactive status of the cysts. neurocysticercosis is treatable both medically and surgically according to symptoms. The sooner the correct diagnosis is made, the greater the chances for recovery and prevention of further neurologic deterioration. The nurse who is knowledgeable about the cause and treatment for neurocysticercosis can assist in controlling the incidence of this disease, decreasing complications, and averting needless mortality.
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