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sábado, 12 de noviembre de 2011

Re: [amn-epilepsia-mexico:614] 500 cirugias encefálicas ilegales

Tu comentario es preciso y aclaratorio, lo difundo a toda la comunidad virtual y lo envio al blog del ameinnn, debería decir neurocirujanos,
Saludos muy cordiales Francisco

Gustavo

Enviado desde mi iPod

El 12/11/2011, a las 19:34, Francisco Jiménez Gil 

Estimado Gustavo, creo que esta nota es en detrimentos de los Neurólogos ya que los neurólogos no hacemos cirugía, es conveniente aclarar esto a la sociedad.
Saludos afectuosos
Francisco



De la agencia de noticias EFE, a la amable consideración de esta comunidad virtual, la presente noticia se difunde sin ánimo discriminatorio para la institución de de la que hemos sido parte, así como tampoco contra alguna persona en particular, se ofrece a esta comunidad virtual en vista de que esta en el dominio público de la web, el link: 500 cirugias ilegales

Gustavo



Neurólogos han practicado unas 500 cirugías encefálicas ilegales, según ONG

Por (foto) | EFE –  jue, 10 nov 2011
México, 10 nov (EFE).- Médicos del Instituto Nacional de Neurología y Neurocirugía de México han practicado unas 500 cirugías encefálicas experimentales a pacientes y todas de manera ilegal de los cuales fallecieron unos 370 entre 1994 y 2007, denunciaron hoy diversos organismos civiles.
Representantes de grupos como Médicos Democráticos, Red Solidaria Década contra la impunidad, Víctimas de Crimen de Lesa Humanidad, entre otros, explicaron en rueda de prensa que este proceso se ha practicado sin consentimiento de los pacientes.
Las organizaciones indicaron que esta denuncia ya fue presentada ante la Fiscalía mexicana y ante la Comisión Interamericana de Derechos Humanos (CIDH).
El representante del Médicos Democráticos, el médico Rodolfo Ordanza precisó que las cirugías consisten en colocar un dispositivo permanente intercraneal "no aprobado por autoridades internacionales de salud" a pacientes con hidrocefalia y que "han dejado graves secuelas hasta llevar a la muerte".
El especialista detalló que en este tipo de padecimientos a nivel mundial se utilizan unas válvulas y tubos costosos, pero "por ahorrarse casi el 90 % del material se sustituyen por unos centímetros de un material experimental denominado Tygon y que no tienen valor ni validez científica".
María de Lourdes Walkup, una de las víctimas de esta práctica en ese instituto debido a dicha intervención quedó paralítica a mitad de cuerpo, exigió a las autoridades castigo a los responsables y el reparo del daño.
Según los denunciantes, en éste hospital se han efectuado cientos de implantes de este dispositivo, incluyendo a recién nacidos, "sin llevar a cabo un control periódico de la investigación y no se proporciona información inmediata a los afectados de cada daño complicación".
La activista de Red Solidaria Década contra la Impunidad María López afirmó que este tipo de actos son considerados como un crimen de lesa humanidad y posiblemente una forma de tortura.
Agregó que estas intervenciones han afectado de manera sistemática a pacientes de grupos vulnerables, dañando la integridad física, moral, social, y económica por funcionarios públicos.
"Por este motivo, en los próximos meses tomará el caso la Comisión Interamericana de Derechos Humanos ".
Recordaron que de acuerdo a la Ley mexicana de Salud, los tratamientos o cirugías experimentales deben aplicarse bajo consentimiento de los pacientes, aunque aclararon que tampoco está definido el pago de los daños ocasionados por los mismos ni tampoco el tratamiento gratuito para revertir los efectos.
La Cámara de Diputados de México aprobó este jueves reformas a la Ley General de Salud para que las instituciones den atención médica a las personas que sufran algún daño por estudios de investigación científica, sin perjuicio de la indemnización que legalmente les corresponda.
Las reformas establecen una base para el desarrollo de la investigación en seres humanos, pero también la responsabilidad de la institución para proporcionar atención médica al sujeto que sufra algún daño. EFE
ea/jrm/cav


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miércoles, 9 de noviembre de 2011

Paralísis del tercer nervio craneal, etiología 32 art. de acceso libre, texto completo

Los neurólogos y neurocirujanos con alguna frecuencia enfrentamos el reto
diagnóstico-terapéutico de una parálisis aislada del tercer nervio craneal,
los extremos son sencillos: una parálisis secundaria a un TCE, con pérdida
de conciencia- período lúcido- somnolencia y afectación del tercero con
compromiso pupilar en esa secuencia en un paciente con fractura de la
escama del hueso temporal = hematoma epidural con herniación lateral.
 El otro extremo, es el paciente que siendo
diabético inicia con dolor supraorbitario ligero y es seguido de parálisis
incompleta del tercero con respeto pupilar. Estan por supuesto los aneurismas
rotos y no rotos de la comunicante posterior.
¿Pero que hay de aquellos casos no tan típicos?, aquí se impone seguir
una ruta crítica que implica hacer estudios de imagen de alta definición
CTA o ARM, estudios nde serología.
Va incuida aquí una pequeña revisión de 32 artículos de texto completo
libre, me sorprendió ver un caso secundario a amigdalítis aguda purulenta,
 el reporte de unos nigerianos que señalan a las causas  de ORL en un
20% (!!) y un hermoso artículo que viene en francés con unos gráficos
muy didácticos.
Acabo de ver por cierto, un caso de parálisis aislada con compromiso
pupilar de instalación aguda sin cefalea, en un paciente hipertenso, sin
otros datos. Le mande hacer una ARM incluyendo de vasos supraórticos

Saludos queridos amigos, esperando
sea de utilidad.
PD Estas revisiones también las encontraran en el blog de
los AMEINNNes


This message contains search results from the National Center for Biotechnology Information at the U.S. National Library of Medicine.
Sender's message: THIRD CRANEAL PALSY + ETIOLOGY
Sent on: Tue Nov 8 23:55:24 2011
32 selected items


pubmed Results
Items 1 -32 of 32

1. Arch Soc Esp Oftalmol. 2009 Aug;84(8):395-8.

[Third nerve palsy as the only manifestation of occult temporal arteritis].

[Article in Spanish]
Asensio-Sánchez VM, Morales-Gómez I, Rodríguez-Vaca I.

Source

Hospital General, Medina del Campo, Valladolid, España. victor_asensio@orangemail.es

Abstract

CASE REPORT: Two patients (80 and 67 year-old) presented with diplopia for a sudden right 3rd cranial nerve palsy without other ocular or systemic symptoms related to temporal arteritis. Erythrocyte sedimentation rate and C-reactive protein levels were normal. Subsequent biopsy of the superficial temporal artery confirmed the diagnosis of temporal arteritis. DISCUSSION: Patients with ocular nerve palsy could have occult temporal arteritis. Aged patients with an acute ocular ischemic lesion, without elevated erythrocyte sedimentation rate, C-reactive protein levels and systemic symptoms, should raise a high index of suspicion for temporal arteritis.
Free Article
PMID:
19728240
[PubMed - indexed for MEDLINE]
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2. Korean J Ophthalmol. 2008 Sep;22(3):201-4.

A case of oculomotor nerve palsy and choroidal tuberculous granuloma associated with tuberculous meningoencephalitis.

Moon S, Son J, Chang W.

Source

Department of Ophthalmology, Yeungnam University College of Medicine, Daegu, Korea.

Abstract

We report a rare case of oculomotor nerve palsy and choroidal tuberculous granuloma associated with tuberculous meningoencephalitis. A 15-year-old male visited our hospital for an acute drop of the left eyelid and diplopia. He has been on anti-tuberculous drugs (isoniazid, rifampin) for 1 year for his tuberculous encephalitis. A neurological examination revealed a conscious clear patient with isolated left oculomotor nerve palsy, which manifested as ptosis, and a fundus examination revealed choroidal tuberculoma. Other anti-tuberculous drugs (pyrazinamide, ethambutol) and a steroid (dexamethasone) were added. After 3 months on this medication, ptosis of the left upper eyelid improved and the choroidal tuberculoma decreasedin size, but a right homonymous visual field defect remained. When a patient with tuberculous meningitis presents with abrupt onset oculomotor nerve palsy, rapid re-diagnosis should be undertaken and proper treatment initiated, because the prognosis is critically dependent on the timing of adequate treatment.
PMCID: PMC2629901
Free PMC Article
PMID:
18784452
[PubMed - indexed for MEDLINE]
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3. Arch Iran Med. 2008 Jul;11(4):466-8.

Pituitary apoplexy presenting as acute painful isolated unilateral third cranial nerve palsy.

Bahmani Kashkouli M, Khalatbari MR, Yahyavi ST, Borghei-Razavi H, Soltan-Sanjari M.

Source

Department of Ophthalmology, Eye Research Center, Iran University of Medical Sciences, Tehran, Iran. bahmanik@yahoo.com

Abstract

A 40-year-old man presented with a sudden severe headache and complete right-sided ptosis. Neuro-ophthalmic examination revealed a right oculomotor nerve palsy. Computed tomography of the brain showed a round isodense intrasellar mass. Magnetic resonance imaging demonstrated a pituitary tumor with some areas of infarction and invasion into the right cavernous sinus, which was diagnosed as pituitary apoplexy. The patient received intravenous steroid for 10 days with no recovery of the oculomotor nerve palsy. He underwent trans-sphenoid tumor resection followed by complete recovery of the oculomotor nerve and no sign of tumor in postoperative MRI, two weeks after the surgery.
Free Article
PMID:
18588383
[PubMed - indexed for MEDLINE]
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4. AJNR Am J Neuroradiol. 2008 May;29(5):997-1002. Epub 2008 Feb 22.

Unruptured large and giant carotid artery aneurysms presenting with cranial nerve palsy: comparison of clinical recovery after selective aneurysm coiling and therapeutic carotid artery occlusion.

van Rooij WJ, Sluzewski M.

Source

Department of Radiology, St. Elisabeth Ziekenhuis, Tilburg, the Netherlands. radiol@knmg.nl

Abstract

BACKGROUND AND PURPOSE:

Internal carotid artery (ICA) aneurysms may present with cranial nerve dysfunction. Therapeutic ICA occlusion, when tolerated, is an effective treatment resulting in improvement or cure of symptoms in most patients. When ICA occlusion is not tolerated, selective endovascular aneurysm occlusion can be considered. We compare recovery of cranial nerve dysfunction in patients treated with selective coil occlusion and with therapeutic ICA occlusion.

MATERIALS AND METHODS:

In 16 patients with 17 large or giant (11-45 mm) unruptured ICA aneurysms presenting with dysfunction of cranial nerves (CN) II, III, IV, or VI, selective coil occlusion was performed. From a cohort of 39 patients with ICA aneurysms treated with ICA occlusion and long-term follow-up, we selected 31 patients with aneurysms presenting with cranial nerve dysfunction. Clinical recovery at follow-up from oculomotor dysfunction and visual symptoms was compared for both treatment modalities.

RESULTS:

Of 17 aneurysms treated with selective coiling, symptoms of cranial nerve dysfunction resolved in 3, improved in 10, and remained unchanged in 4. In 9 of 17 patients, additional coiling during follow-up was required. Of 31 aneurysms treated with carotid artery occlusion, cranial nerve dysfunction resolved in 19, improved in 9, and remained unchanged in 3. These differences were not significant. There were no complications of treatment.

CONCLUSION:

Recovery of ICA aneurysm-induced cranial nerve dysfunction occurs in most patients, both after ICA occlusion and after selective coiling. In patients who cannot tolerate ICA occlusion, selective aneurysmal occlusion with coils is a valuable alternative.
Free Article
PMID:
18296545
[PubMed - indexed for MEDLINE]
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5. AJNR Am J Neuroradiol. 2008 May;29(5):988-90. Epub 2008 Feb 13.

Recovery of posterior communicating artery aneurysm-induced oculomotor palsy after coiling.

Hanse MC, Gerrits MC, van Rooij WJ, Houben MP, Nijssen PC, Sluzewski M.

Source

Department of Neurology, St Elisabeth Ziekenhuis, Tilburg, the Netherlands.

Abstract

BACKGROUND AND PURPOSE:

Recovery of oculomotor (cranial nerve [CN] III) palsy after surgery of posterior communicating artery (PcomA) aneurysms has been well documented, but recovery after coiling is poorly understood. In this study, we report the recovery after coiling of PcomA aneurysm-induced CN III palsy in 21 patients at follow-up of 1 to 7 years.

MATERIALS AND METHODS:

Of 135 patients with a PcomA aneurysm treated with coils between January 1997 and December 2003, there were 21 patients with initial CN III dysfunction who were selected and reevaluated. There were 2 men and 19 women with a mean age of 54.9 years. In 17 patients, CN III palsy was associated with subarachnoid hemorrhage (SAH). Timing of treatment after onset of symptoms was 1 to 3 days in 5 patients, 4 to 14 days in 13, and more than 14 days in 3. Mean size of the aneurysm was 9 mm. Initial CN III palsy was complete in 15 patients and partial in 6. Mean follow-up after coiling was 3.7 years (range, 1-7 years).

RESULTS:

Of 15 patients with initial complete CN III palsy, recovery was complete in 3 and partial in 10. In 2 patients, complete CN III palsy was unchanged. Of 6 patients with initial partial CN III palsy, recovery was complete in 5 and partial in 1. Initial partial CN III palsy was the only predictor of complete recovery at follow-up.

CONCLUSION:

PcomA aneurysm-induced CN III palsy improves or cures after coiling in most patients. Complete recovery is more likely with initial partial dysfunction of the nerve.
Free Article
PMID:
18272550
[PubMed - indexed for MEDLINE]
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6. J Fr Ophtalmol. 2007 Dec;30(10):e31.

[Third cranial nerve palsy related to an unruptured aneurysm of the posterior communicating artery].

[Article in French]
Beynat J, Bidot S, Ricolfi F, Creuzot-Garcher C, Bron A.

Source

Service d'Ophtalmologie, CHU, Dijon. jbeynat@free.fr

Abstract

The posterior communicating artery (PCA) aneurysm is a traditional cause of young subjects' painful ophthalmoplegia. We report the case of a patient presenting a complete, extrinsic and intrinsic, third cranial nerve palsy related to an unruptured aneurysm of the PCA. The diagnosis was made with the angio-CT, and the patient was treated with endovascular treatment for 6 days after the beginning of the cephalalgias. Recovery was complete at 8 weeks. We review the literature on the etiologies of this type of attack, the work-up, and the possible treatments.
Free Article
PMID:
18268434
[PubMed - indexed for MEDLINE]
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7. Indian J Ophthalmol. 2007 Jan-Feb;55(1):79; author reply 79.

Ocular motor nerve palsy.

Jethani J. Free Article
PMID:
17189900
[PubMed - indexed for MEDLINE]
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8. Indian J Ophthalmol. 2006 Sep;54(3):173-5.

Ocular motor nerve palsy: a clinical and etiological study.

Mwanza JC, Ngweme GB, Kayembe DL.

Source

Kinshasa University Hospital, Kinshasa, Democratic Republic of Congo. jcmwanza@hotmail.com

Abstract

PURPOSE:

To clinically describe cases of ocular motor nerve palsy and to determine the possible causes.

MATERIALS AND METHODS:

Thirty-one consecutive patients with ocular motor nerve palsies were investigated. All underwent complete ophthalmological, as well as neurological, otorhinolaryngological and general examination. Computerised tomography (CT)-scan of the brain and complementary laboratory tests were obtained from each participant.

RESULTS:

Paralysis of the sixth (38.4%) and the third (35.3%) cranial nerve were the most common. The Lees screen test was found to be very sensitive, confirming the diagnosis of ocular motor nerve palsy, even in cases with minimal manifestations. Complete ptosis and full mydriasis were mostly seen in isolated cases of the third cranial nerve palsy. The majority of eyes (63.2%) with third cranial nerve palsy had pupil sparing. Overall, an etiological diagnosis was made in 93.5% of cases. The common causes were vascular conditions (25.8%), otorhinolaryngologic diseases (19.7%) and trauma (12.9%). CT scan failed to reveal any abnormality in 54.8% of cases.

CONCLUSION:

Patients with ocular motor nerve palsy should be carefully examined in close collaboration with other specialists, especially where sophisticated, complementary investigations are impossible.
Free Article
PMID:
16921214
[PubMed - indexed for MEDLINE]
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9. Intern Med. 2005 Jun;44(6):638-40.

Isolated oculomotor nerve palsy in Churg-Strauss syndrome.

Tsuda H, Ishikawa H, Majima T, Sawada U, Mizutani T.

Source

Division of Neurology, Nihon University, School of Medicine, Oyaguchikamicho, Tokyo.

Abstract

A 30-year-old man with bronchial asthma complained of horizontal diplopia. Partial oculomotor nerve palsy with restrictions of elevation and adduction, and mydriasis was observed in the left eye. Cranial magnetic resonance imaging demonstrated an infarct lesion in the territory of the left superior median mesencephalic branch of the posterior cerebral artery. Based on bronchial asthma, hypereosinophilia, mononeuropathy multiplex, pulmonary eosinophilia and positive perinuclear antineutrophil cytoplasmic antibody in the serum, the patient was diagnosed as having Churg-Strauss syndrome. This is the first case of oculomotor nerve palsy due to midbrain infarction associated with Churg-Strauss syndrome.
Free Article
PMID:
16020896
[PubMed - indexed for MEDLINE]
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10. Br J Sports Med. 2005 Aug;39(8):e34.

Isolated oculomotor nerve palsy from minor head trauma.

Chen CC, Pai YM, Wang RF, Wang TL, Chong CF.

Source

Shin Kong Wu Ho-Su Memorial Hospital, Taipei 111, Taiwan.

Abstract

Isolated third cranial nerve palsies in head trauma patients can be the result of direct or indirect damage to the oculomotor nerve. They are usually associated with severe head trauma. We reported a case of isolated oculomotor nerve palsy associated with minor head injury. No initial loss of consciousness was recalled. Computed tomography (CT), magnetic resonance imaging (MRI), and magnetic resonance angiography (MRA) of the brain were normal. Previous reports in the literature were reviewed and the possible mechanism of injury was discussed. Head injuries are commonly seen in sports settings. Our case illustrated that even minor head trauma can cause isolated oculomotor nerve palsy in the absence of abnormal brain imaging findings.
PMCID: PMC1725282
Free PMC Article
PMID:
16046322
[PubMed - indexed for MEDLINE]
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11. Acta Neurol Taiwan. 2005 Mar;14(1):21-3.

Tuberculous meningitis with initial manifestation of isolated oculomotor nerve palsy.

Huang P, Tai CT.

Source

Department of Neurology, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.

Abstract

Tuberculous meningitis (TB meningitis) is a subacute meningitis known for its various form of initial manifestations, which often make early diagnosis difficult. The present case report demonstrates a patient with TB meningitis, who had initial manifestation of isolated right oculomotor nerve palsy. High vigilance is needed in diagnosing TB meningitis. A 75 year-old female was hospitalized due to acute onset of right side ptosis. Thorough neurological examination at admission revealed isolated right oculomotor nerve palsy. Brain magnetic resonance imaging and cerebral angiography showed no specific finding. Lumbar puncture was performed two days later due to low grade fever. Cerebrospinal fluid (CSF) study and the polymerase chain reaction on CSF confirmed the diagnosis of TB meningitis. Because TB meningitis is a chronic disease, cranial nerve palsies are common manifestations. This report suggests that TB meningitis should be a disease of differential diagnosis for isolated oculomotor nerve palsy.
Free Article
PMID:
15835285
[PubMed - indexed for MEDLINE]
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12. Med Sci (Paris). 2004 Mar;20(3):357-62.

[The control of gaze (3). Neurological defects].

[Article in French]
Pierrot-Deseilligny C.

Source

Inserm U.289 et Service de Neurologie 1, Hôpital de la Salpêtrière, 47, boulevard de l'Hôpital, 75651 Paris Cedex 13, France. cp.deseilligny@psl.ap-hop-paris.fr

Abstract

Eye movements serve vision, which has two different aims: changing images using saccades, i.e. rapid eye movements, and stabilizing new images on the retina using slow eye movements. Eye movements are performed by ocular motor nuclei in the brainstem, on which supranuclear pathways--originating in the cerebral cortex, cerebellum and vestibular structures--converge. It is useful for the neurologist to know the clinical abnormalities of eye movements visible at the bedside since such signs are helpful for localization. Eye movement paralysis may be nuclear or infranuclear (nerves), involving all types of eye movements, i.e. saccades as well as the vestibulo-ocular reflex (VOR), or supranuclear, in which case the VOR is usually preserved. Lateral eye movements are organized in the pons, with paralysis of adduction (and preservation of convergence) when the lesion affects the medial longitudinal fasciculus (internuclear ophthalmoplegia), paralysis of conjugate lateral eye movements when the lesion affects the abducens nucleus (VI) and the "one-and-a-half" syndrome when both these structures are involved. Vertical eye movements are organized in the midbrain, with ipsilateral oculomotor (III) paralysis and contralateral paralysis of the superior rectus muscle when the third nerve nucleus is unilaterally damaged, supranuclear upward gaze paralysis when the posterior commissure is unilaterally damaged and supranuclear downward gaze paralysis (often coupled with upward gaze paralysis) when the mesencephalic reticular formations are bilaterally damaged. Numerous types of abnormal eye movements exist, of which nystagmus is the most frequent and usually due to damage to peripheral or central vestibular pathways. Cerebral hemispheric or cerebellar damage results in subtle eye movement abnormalities at the bedside, in general only detected using eye movement recordings, because of the multiplicity of eye movement pathways at these levels and their reciprocal compensation in the case of a lesion. Lastly, eye movements can also help the neuroscientist to understand the organization of the brain. They are a good model of motricity allowing us, using eye movement recordings, to study the afferent pathways of the cortical areas that trigger them, and thus to analyze relatively complex neuropsychological processes such as visuo-spatial integration, spatial memory, motivation and the preparation of motor programs.
Free Article
PMID:
15067583
[PubMed - indexed for MEDLINE]
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13. J Clin Endocrinol Metab. 2004 Feb;89(2):574-80.

Tumors metastatic to the pituitary gland: case report and literature review.

Komninos J, Vlassopoulou V, Protopapa D, Korfias S, Kontogeorgos G, Sakas DE, Thalassinos NC.

Source

Department of Endocrinology, Diabetes and Metabolism, Evangelismos General Hospital, 10676 Athens, Greece. jokomni@otenet.gr

Abstract

Tumors metastatic to the pituitary gland are an unusual complication of systemic cancer typically seen in elderly patients with diffuse malignant disease. Breast and lung are the commonest sites of the primary tumor, whereas diabetes insipidus is the most frequent symptom at presentation. Their rarity and usually indolent course, as well as the lack of specific clinical and radiological features, impede their differentiation from other more common sellar area lesions, particularly when history of malignancy is absent. Management of these patients may also be very difficult because the prognosis depends on the course of the primary neoplasm. A 68-yr-old man, with no history of malignancy, presented with recent onset of hypopituitarism, mild diabetes insipidus, headaches, left oculomotor nerve palsy, and progressive bilateral deterioration of visual acuity and visual fields. Magnetic resonance imaging revealed a large sellar mass compressing the optic chiasm and invading the left cavernous sinus, whereas a prolactin elevation at 438.6 ng/ml (19.73 nmol/liter) was noted. Decompression of the sellar region was attempted, and pathology disclosed a metastatic hepatocellular carcinoma. On postoperative investigation, primary liver tumor was identified and confirmed by biopsy. The patient improved transiently but died 3 months after diagnosis because of deterioration of the liver disease. The relevant literature is reviewed in light of this unusual case, illustrating the problems in the diagnosis and management of patients with metastasis to the pituitary.
Free Article
PMID:
14764764
[PubMed - indexed for MEDLINE]
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14. Neurol Med Chir (Tokyo). 2003 Oct;43(10):484-7.

Unilateral oculomotor nerve paresis associated with anterior communicating artery aneurysm rupture--two case reports.

Aiba T, Fukuda M.

Source

Department of Neurosurgery, Shibata Hospital, Shibata, Niigata, Japan. aiba@sbt.lamen.or.jp

Abstract

Two cases of complete unilateral oculomotor nerve palsy occurred after subarachnoid hemorrhage (SAH) due to a ruptured anterior communicating artery aneurysm. A 61-year-old female suffered left oculomotor nerve paresis after mild SAH. This paresis was probably related to pre-existing oculomotor nerve stretching caused by abnormal positioning of the posterior cerebral and superior cerebellar arteries in the premesencephalic cistern. A 70-year-old female suffered right oculomotor nerve paresis after severe SAH. Elevated intracranial pressure might have caused this paresis, but the reason for the unilateral occurrence was undetermined. Both patients were treated by clipping of the aneurysm, and the signs of oculomotor nerve paresis gradually resolved. A pattern of pupil-sparing paresis was observed during the early recovery stage in both patients.
Free Article
PMID:
14620199
[PubMed - indexed for MEDLINE]
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15. Neurocirugia (Astur). 2003 Oct;14(5):423-5; discussion 425.

[Isolated oculomotor palsy. An unusual presentation of chronic subural hematoma].

[Article in Spanish]
Ortega-Martínez M, Fernández-Portales I, Cabezudo JM, Rodríguez-Sánchez JA, Gómez-Perals LF, Giménez-Pando J.

Source

Servicio de Neurocirugía. Hospital Regional Universitario Infanta Cristina. Badajoz, Spain.

Abstract

Isolated oculomotor palsy is an unusual symptom in chronic subdural hematomas and it is very rare as initial manifestation. We report a patient with a chronic subdural hematoma that presented with a complete third nerve palsy and normal consciousness. Complete recovery was achieved after surgical evacuation. Rebleeding within the hematoma cavity, most possibly favored by antiaggregating agents, was considered responsible for this rare presentation. In these cases expeditious surgical evacuation is indicated.
Free Article
PMID:
14603390
[PubMed - indexed for MEDLINE]
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16. Arq Neuropsiquiatr. 2003 Sep;61(3A):668-70. Epub 2003 Sep 16.

Isolated oculomotor nerve palsy in spontaneous internal carotid artery dissection: case report.

Campos CR, Massaro AR, Scaff M.

Source

Department of Neurology, Hospital das Clínicas, University of São Paulo, São Paulo, SP, Brazil. cynthia-98@rocketmail.com

Abstract

Partial oculosympathetic palsy followed by ischemic manifestations in brain or retina are the main symptoms of extracranial internal carotid artery (ICA) dissection. Unusually, cranial nerves may be affected. Isolated oculomotor nerve palsy is found only rarely. CASE: We present a 50-year-old nondiabetic man who experienced acute onset of right occipital headache which spread to the right retro-orbital region. Five days later he noticed diplopia and right blurred vision sensation. Neurologic examination disclosed only impaired adduction and upward gaze of right eye, slight ipsilateral pupillary dilatation, without ptosis. Brain MRI was normal. Angiography showed right internal carotid artery dissection with forward occlusion to the base of the skull. Intravenous heparin followed by warfarin was prescribed. The headache and the oculomotor nerve deficit gradually resolved in the next three weeks. DISCUSSION: Isolated oculomotor nerve palsy is underrecognized as a clinical presentation of extracranial ICA dissection. If the angiographic evaluation is incomplete without careful study of extracranial arteries, misdiagnosis may lead to failure to initiate early treatment to prevent thromboembolic complications. For this reason we draw attention to the need for careful evaluation of cervical arteries in patients with oculomotor nerve palsy. Mechanical compression or stretching of the third nerve are possible mechanisms, but the direct impairment of the blood supply to the third nerve seems to be the most plausible explanation.
Free Article
PMID:
14513178
[PubMed - indexed for MEDLINE]
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17. J Fr Ophtalmol. 2002 May;25(5):480-7.

[Diagnostic approach for acquired and isolated third cranial nerve palsy: 18 case reports].

[Article in French]
Fogliarini C, Denis D.

Source

Service d'ophtalmologie Hôpital Nord, 15 chemin des Bourrelly, 13015 Marseille, France.

Abstract

PURPOSE:

The aim of this work was to establish a clinical diagnostic flow chart for third nerve palsy.

MATERIAL AND METHODS:

[corrected] We report a series of 18 patients with third nerve palsy seen at the department of ophthalmology in the Marseille North Hospital between 1997 and 1999. All patients had a complete clinical examination and were classified into four clinic types. An etiological diagnosis was given in all cases after a systematic approach, including first intention MRI.

RESULT:

Three patients presented abnormal pupil reflex secondary to an aneurysm diagnosed by carotid angiography; the MRI was pathological in two cases. The 15 other patients had pupil sparing. Among them, eight patients had a total external involvement secondary to diabetes mellitus; the MRI suggested an ischelic origin in four cases (50%) showing nuclear infarctus. In seven cases the external involvement was incomplete secondary to multiple etiologies: demyelinating illness, traumatic lesions, orbital tumor, metastasis or myasthenia gravis. The MRI contributed to diagnosing four cases.

CONCLUSION:

The MRI must be systematically used in all the patients with isolated third nerve palsy, except for patients with pupil sparing associated with total external involvement. Ischemic etiology was the rule: simple clinical surveillance is proposed, total spontaneous regression being the norm.
Free Article
PMID:
12048511
[PubMed - indexed for MEDLINE]
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18. Rev Neurol. 2002 Feb 1-15;34(3):296.

[Oculomotor nerve paralysis and purulent acute tonsillitis. A case report].

[Article in Spanish]
Arteaga-Rodríguez C, De Cassias AL, Hernández-Fustes O. Free Article
PMID:
12022085
[PubMed - indexed for MEDLINE]
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19. Emerg Med J. 2001 Jul;18(4):310-1.

Mild head injury with isolated third nerve palsy.

Muthu P, Pritty P.

Source

Accident and Emergency Department, Queen's Medical Centre, Nottingham NG7 2UH, UK. palmut@aol.com

Abstract

Traumatic isolated cranial nerve palsies are uncommon and when they do occur, they are usually associated with severe head trauma. Cranial nerve palsy associated with mild head injury is rare. A case is reported of complete left third nerve palsy associated with mild head injury. The rate of recovery for complete third nerve palsy is slow and prolonged. The ptosis recovered in 10 months; the divergent squint required botulinum toxin to the lateral rectus muscle followed by surgery.
PMCID: PMC1725604
Free PMC Article
PMID:
11435377
[PubMed - indexed for MEDLINE]
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20. Postgrad Med J. 2002 Feb;78(916):105, 111.

An elderly lady with collapse.

Huwez FU, Umasankar U, Aggarwal D.

Source

Stroke Unit (Lister Ward), Orsett Hospital, Orsett, Grays, Essex RM16 3EU, UK.
PMCID: PMC1742274
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PMID:
11807201
[PubMed - indexed for MEDLINE]
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21. Br J Radiol. 2000 May;73(869):569-70.

A case of isolated third nerve palsy with pupil involvement.

Lenthall RK, Jaspan T.

Source

Department of Neuroradiology, Queen's Medical Centre, University Hospital, Nottingham, UK.
Free Article
PMID:
10884760
[PubMed - indexed for MEDLINE]
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22. Neurol Med Chir (Tokyo). 1999 May;39(5):367-71.

Bilateral chronic subdural hematomas resulting in unilateral oculomotor nerve paresis and brain stem symptoms after operation--case report.

Okuchi K, Fujioka M, Maeda Y, Kagoshima T, Sakaki T.

Source

Department of Neurosurgery, Nara Emergency and Critical Care Center.

Abstract

An 85-year-old male presented with bilateral chronic subdural hematomas (CSDHs) resulting in unilateral oculomotor nerve paresis and brainstem symptoms immediately after removal of both hematomas in a single operation. Initial computed tomography on admission demonstrated marked thick bilateral hematomas buckling the brain parenchyma with a minimal midline shift. Almost simultaneous removal of the hematomas was performed with the left side was decompressed first with a time difference of at most 2 minutes. However, the patient developed right oculomotor nerve paresis, left hemiparesis, and consciousness disturbance after the operation. The relatively marked increase in pressure on the right side may have caused transient unilateral brain stem compression and herniation of unilateral medial temporal lobe during the short time between the right and left procedures. Another factor was the vulnerability of the oculomotor nerve resulting from posterior replacement of the brain stem and stretching of the oculomotor nerves as seen on sagittal magnetic resonance (MR) images. Axial MR images obtained at the same time demonstrated medial deflection of the distal oculomotor nerve after crossing the posterior cerebral artery, which indicates previous transient compression of the nerve and the brain stem. Gradual and symmetrical decompression without time lag is recommended for the treatment of huge bilateral CSDHs.
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PMID:
10481440
[PubMed - indexed for MEDLINE]
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23. AJNR Am J Neuroradiol. 1999 Mar;20(3):411-3.

Resolution of third nerve paresis after endovascular management of aneurysms of the posterior communicating artery.

Birchall D, Khangure MS, McAuliffe W.

Source

Interventional Neuroradiology Unit, Royal Perth Hospital, Western Australia.

Abstract

The effect of endovascular treatment on the recovery of neural function in patients with third nerve palsy caused by an aneurysm of the posterior communicating artery is poorly documented. We report three cases in which third nerve paresis resolved completely within 2 to 3 weeks of endovascular occlusion of a posterior communicating artery aneurysm.
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PMID:
10219405
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24. Intern Med. 1997 Apr;36(4):301-3.

Oculomotor nerve palsy caused by lung cancer metastasis.

Ishikawa H, Satoh H, Fujiwara M, Kamma H, Yamashita YT, Naito T, Ohtsuka M, Hasegawa S.

Source

Department of Respiratory Medicine, University of Tsukuba.

Abstract

A 39-year-old man with a known diagnosis of lung adenocarcinoma developed intermittent double vision with right pupil dilatation. His symptoms eventually progressed to complete oculomotor nerve palsy on the right. Postmortem examinations revealed a metastasis of the adenocarcinoma involving the root of right oculomotor nerve.
Free Article
PMID:
9187571
[PubMed - indexed for MEDLINE]
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25. AJNR Am J Neuroradiol. 1995 Sep;16(8):1665-72.

MR of oculomotor nerve palsy.

Blake PY, Mark AS, Kattah J, Kolsky M.

Source

Department of Neurology, Georgetown University Medical Center, Washington, DC 20007, USA.

Abstract

PURPOSE:

To assess the utility of MR in third cranial nerve palsy.

METHODS:

We reviewed precontrast and postcontrast MR of 50 patients with third cranial nerve palsy.

RESULTS:

MR demonstrated an appropriate lesion in 32 cases. Of these patients, 6 had brain stem lesions and 15 had involvement of the nerve in the cavernous sinus; lesions of the cisternal segment of the nerve were present in 11 patients, with enhancement of this segment observed in 9 patients. An inflammatory or infiltrative source of the palsy was indicated in 19 of these 32 cases. Of 7 patients with pupillary involvement suggestive clinically of a compressive lesion, 4 demonstrated thickening and enhancement consistent with an infiltrative lesion of the nerve. Eighteen patients with pupil-sparing third cranial nerve palsies and a history of diabetes or vascular disease had normal MR findings, with no enhancement of the third cranial nerve observed.

CONCLUSIONS:

Patients who do not have a history of diabetes or hypertension and in whom a complete or incomplete third cranial nerve palsy develops with or without pupil sparing should undergo MR imaging initially (unless there are clear symptoms or signs of subarachnoid hemorrhage) to exclude the presence of an infiltrative lesion or intraparenchymal process. Patients who have a history of vascular disease and a clinical presentation that is suggestive of an ischemic event may be observed initially, but should undergo imaging if improvement does not occur within 3 months.
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PMID:
7502972
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26. Indian J Ophthalmol. 1984 Sep-Oct;32(5):447-53.

Aetiological patterns of ocular motor nerve palsies.

Menon V, Singh J, Prakash P. Free Article
PMID:
6545339
[PubMed - indexed for MEDLINE]
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27. Br J Ophthalmol. 1984 Aug;68(8):538-43.

Traumatic third nerve palsy.

Elston JS.

Abstract

Twenty patients with a traumatic third nerve palsy had sustained a closed head injury with prolonged loss of consciousness in a high-speed deceleration accident. Sixteen were male, and the average age was 25 years. Seven had skull or facial fractures, 15 damage to the anterior visual pathways, and 16 other permanent neurological damage. Nineteen developed the misdirection/regeneration syndrome. Thirteen had strabismus surgery, and an area of binocular single vision was enlarged or achieved in three.
PMCID: PMC1040409
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PMID:
6743622
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28. Br J Ophthalmol. 1984 Feb;68(2):128-34.

Ophthalmoplegia in carotid cavernous sinus fistula.

Leonard TJ, Moseley IF, Sanders MD.

Abstract

The aetiology of ophthalmoplegia in 15 patients with carotid-cavernous sinus fistula is discussed, and the clinical findings are correlated with angiographic and orbital CT appearances. After closure of the fistula the majority of patients with generalised ophthalmoplegia recovered full ocular movements rapidly, while patients with an isolated abduction weakness required much longer to return to normal. Orbital CT studies showed enlarged extraocular muscles in the patients with generalised ophthalmoplegia but muscles of normal size in those with abduction failure alone. After closure of the fistula repeat CT studies of patients with enlarged extraocular muscles showed a diminution in muscle size. We suggest that generalised ophthalmoplegia in carotid cavernous sinus fistula is due to hypoxic, congested extraocular muscles. Isolated abduction weakness is due to a sixth nerve palsy, which probably occurs either in the cavernous sinus or more posteriorly near the inferior petrosal sinus. A combination of these 2 mechanisms may be found in some patients.
PMCID: PMC1040270
Free PMC Article
PMID:
6691956
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29. Indian J Ophthalmol. 1980 Apr;28(1):13-6.

Ophthalmoplegia. (A study of ninety cases).

Rama V, Vimala J, Chandrasekhar M, Anjaneyulu C, Dinakar I. Free Article
PMID:
7203590
[PubMed - indexed for MEDLINE]
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30. Indian J Ophthalmol. 1972 Dec;20(4):159-63.

Aetiological study of the third, fourth and sixth cranial nerve paralysis.

Reddy PS, Reddy RC, Satapathy M. Free Article
PMID:
4671307
[PubMed - indexed for MEDLINE]
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31. Indian J Ophthalmol. 1971 Mar;19(1):40-1.

Abnormal regeneration of oculomotor nerve (case report).

Narang SK, Patel JK. Free Article
PMID:
15744965
[PubMed - indexed for MEDLINE]
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32. Can Med Assoc J. 1963 Oct 26;89:871-3.

THE OCULAR SEQUELAE OF THIRD CRANIAL NERVE PALSY.

JOHNSTON AC, PRATT-JOHNSON JA.

Abstract

The ocular sequelae in nineteen patients who had suffered from a complete paralysis of the third cranial nerve were analyzed. In eleven of these patients, the paralysis was associated with an aneurysm of the internal carotid artery system. None of the cases in this group showed complete recovery of the third nerve function; however, six recovered sufficiently to permit binocular single vision in most fields of gaze. Two cases of aberrant regeneration of the third nerve were diagnosed.Trauma accounted for four cases of third nerve paralysis. One of these recovered completely and one showed features of aberrant regeneration. Of the cases of oculomotor paralysis associated with herpes zoster ophthalmicus, encephalitis, or an obscure etiology (two cases), all recovered completely.
PMCID: PMC1921927
Free PMC Article
PMID:
14069610
[PubMed - indexed for MEDLINE]
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