Cases reported "Paresis"

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1/12. Pituitary abscess presenting with cranial nerve paresis. Case report and review of literature.

    Non-adenomatosus lesions of the pituitary represent a small part of the intrasellar processes and they have heterogeneous presentation. Making a precise diagnosis is of great importance, as it may lead to more efficient management. A 65-year-old man was admitted to the hospital because of headache and right cranial nerve III palsy. Basic laboratory work-up was normal whereas endocrinological assessment revealed hypopituitarism without diabetes insipidus. Plain radiography showed an enlarged sella and frontal and paranasal sinusitis. Computed tomography (CT) and magnetic resonance imaging (MRI) of the sella revealed an intrasellar lesion with extension to the sphenoid and cavernous sinuses as well as the suprasellar region, exerting pressure on the optic chiasm. On T1-weighted images the mass had a low-intensity signal with a smooth enhancing rim with bright signal. Given the presence of multiple sinusitis and imaging characteristics a pre-operative diagnosis of pituitary abscess was made. The patient was operated via transphenoidal route and purulent material was drained out. Cultures of the material were positive for staphylococcus aureus. Antibiotics as well as cortisol replacement therapy were given. Three months later hypopituitarism persisted but there was significant improvement in the neurological findings. We report a case of an unusual presentation of a pituitary abscess. High index of suspicion, the presence of associated conditions such as pituitary tumors, meningitis or sinusitis, as well as diabetes insipidus and specific imaging features are the main diagnostic clues. Pre-operative diagnosis, which will lead to prompt antibiotic therapy and transphenoidal drainage, can decrease high mortality and morbidity associated with this disease.
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2/12. Sonographic detection of diffuse peripheral nerve enlargement in hereditary neuropathy with liability to pressure palsies.

    Hereditary neuropathy with liability to pressure palsies (HNPP) is a disorder characterized by a tendency to develop focal neuropathies after trivial traumas. On teased nerve fiber studies, sausage-shaped myelin sheath swellings (tomacula) are found. We report the sonographic findings in a patient with genetically proven HNPP. We were able to demonstrate enlargement of several peripheral nerves, even nerves that were clinically unaffected. Enlargement was found not only at typical nerve entrapment sites but also outside these sites. This diffuse nerve enlargement may play an important role in the pathogenesis of entrapment neuropathies in HNPP patients.
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3/12. Interhemispheric intracranial pressure gradients in massive cerebral infarction.

    We report continuous bilateral intracranial pressure (ICP) monitoring immediately after transtentorial herniation in a patient with massive cerebral infarction to: 1) determine presence and time course of compartmental ICP differences, and 2) to study effects of therapy on both hemispheres. A 55-year-old man admitted with watershed infarctions in the left anterior-middle-posterior cerebral arteries distribution. Initial investigations demonstrated highly narrowed left extracranial internal carotid artery. Eight days later he developed unexplained lethargy and anisocoria. Head computerized tomography (CT) showed massive left hemispheric infarction, edema, and midline shift. Bilateral subarachnoid bolts demonstrated equally elevated ICP in both hemispheres. hyperventilation and osmotic therapy produced near-identical ICP reduction bilaterally with resolution of anisocoria. Later, plateau waves and autonomic instability developed. Shortly before loss of brainstem function, interhemispheric ICP gradients (left greater than right) of 30-40 mm Hg developed. intracranial pressure did not equalize prior to brain death determination. Bilateral ICP monitoring did not reveal an interhemispheric ICP gradient soon after transtentorial herniation in massive MCA infarction. The presence of interhemispheric ICP gradients in massive stroke remains unproven and further clinical study is necessary.
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4/12. Late onset seizures, hemiparesis and blindness in hemolytic uremic syndrome.

    Neurologic complications of hemolytic uremic syndrome, including seizures, usually occur early during the acute phase of the illness. We report a3-year-old girl with classic diarrhea-associated hemolytic uremic syndrome who developed late onset seizures, hemiparesis and transient blindness on the 17th hospital day, at which time her recovery was characterized by improvement in her blood pressure, serum electrolytes, renal function, hematocrit and platelet count. A CT and MR revealed brainstem and posterior parietal and occipital infarct/edema. The association of these radiologic findings within the posterior distribution along with visual loss and seizures are unique to posterior reversible encephalopathy syndrome. Within 7 days, she regained motor function and vision and had no further seizure activity. At 6 months follow-up, physical examination revealed normal motor function and vision and a repeat MR showed near resolution of the previous findings with minimal occipital lobe gliosis. This case report describes the uncommon finding of late onset seizures occurring during the recovery phase of hemolytic uremic syndrome with MR findings consistent with posterior reversible encephalopathy syndrome.
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5/12. Pure distant, leptomeningeal metastasis of esthesioneuro-epithelioma.

    BACKGROUND: Esthesioneuro-epithelioma is a very rare variant of olfactory neuroblastoma that originates in the region of the cribriform plate. Its intracranial manifestation is due to infiltration of the anterior skull base and frontal lobes. methods: The authors describe a 52-year-old man with a history of a subtotally resected right maxillary sinus ethesioneuro-epithelioma 2 years earlier who presented with a left hemiparesis and signs of increased intracranial pressure. CT examination revealed a tumour of the right temporoparietal region. The tumour and its dural attachment were totally removed. The patient made a full recovery postoperatively. FINDINGS: The features of esthesioneuro-epithelioma were found on histopathological examination. INTERPRETATION: The intracranial tumour resected was a distant, leptomeningeal metastasis of esthesioneuro-epithelioma. To our knowledge such a documented case has not been published before.
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6/12. Hereditary neuropathy with liability to pressure palsies in childhood: report of a case and a brief review.

    We present a 10-year-old female diagnosed having hereditary neuropathy with liability to pressure palsies (HNPP). She had suffered from acute, recurrent monoplegic episodes affecting both the sciatic nerves and the left brachial plexus since the age of 7 years. The paresis seemed to be triggered by hiking and athletic training. Electrophysiological studies showed a conduction block in the proximal portions of affected nerves. The FISH method disclosed a deletion of the peripheral myelin protein 22 gene. This school child having HNPP is considered to be susceptible to the influence of abundant physical training, rather than minor trauma or compression at sites of entrapment of peripheral nerves.
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7/12. Trigonal cavernous angiomas: report of three cases and review of literature.

    BACKGROUND: Intraventricular cavernous angiomas are very rare. Only few cases of trigonal angiomas have been reported. CASE DESCRIPTION: We report three cases of trigonal cavernous angiomas who presented with raised intracranial pressure or seizures and who underwent total excision with a good recovery. We also review the literature and discuss surgical approaches. CONCLUSION: On magnetic resonance imaging, intraventricular cavernous angiomas lack the hemosiderin ring characteristically seen around parenchymal cavernous angiomas. This explains why trigonal cavernous angiomas can mimic malignant neoplasm on imaging, and they should be considered in the differential diagnosis of intraventricular masses. Total excision should be the goal of surgery.
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8/12. A febrile child with seizure and hemiparesis.

    Febrile seizures are the most common neurological disorders in children and are among the more common symptoms that lead to an emergency department visit. Although most febrile seizures are simple and benign, these seizures can infrequently create a diagnostic dilemma. The diagnosis of cerebral venous thrombosis is challenging to emergency physicians because it can mimic the presentation of many other disorders, including ischemic and hemorrhagic stroke, tumor, and abscess. In addition, the broad variety of signs and symptoms makes the clinical diagnosis difficult. The patients may be presented with signs of increased intracranial pressure or focal neurological deficits. It is an uncommon but potentially dangerous cause of hemiparesis after seizure. Early recognition of this condition and appropriate management may reduce the mortality rate. We present a young child with dural sinus thrombosis who presented with seizures associated with fever and subsequent hemiparesis, and explained a possible mechanism of focal neurological deficit.
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9/12. Bilateral trochlear nerve paresis in hydrocephalus.

    Three patients with nonneoplastic hydrocephalus had bilateral paresis of the trochlear nerves. Associated signs, including paresis of upgaze, light-near dissociation of the pupils, and convergence-retraction nystagmus, suggested rostral involvement of the mesencephalon. trochlear nerve paresis and accompanying signs improved after revision of ventricular shunts in two patients. Bilateral trochlear nerve paresis may be a localizing sign of involvement of the superior medullary velum (the anatomic site of trochlear nerve decussation) by a dilated sylvian aqueduct and/or downward pressure from an enlarged III ventricle.
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10/12. Neurologic symptoms after epidural anaesthesia. Report of three cases.

    We describe 3 patients, who exhibited neurological symptoms after single dose epidural anaesthesia. In patient 1 an unrecognized spinal arteriovenous fistula (AVF) caused paraparesis following epidural block. The dilated veins draining an AVF are space-occupying structures and the injection of the anaesthetic solution may have precipitated latent ischaemic hypoxia of the spinal cord due to raised venous pressure. In patient 2, epidural block was followed by postoperative permanent saddle pain and hypoaesthesia. The injection of the anaesthetic in a narrow spinal canal with multiple discal protrusions and restriction of interlaminar foramina may have acutely produced mechanical compression of the spinal cord or roots. Patient 3 exhibited post-epidural block spinal arachnoiditis. Although the few reported cases of this syndrome exhibit severe neurological damage, our patient presented with scarse symptoms. Our cases point out the importance of accurate neurological history and examination of candidates for epidural anaesthesia and of accurate anaesthetic history for neurological patients.
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