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Year Old Woman (year + old_woman)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

NS14P PRIMARY FALCINE CHONDROSARCOMA

ANZ JOURNAL OF SURGERY, Issue 2007
Y. Kathiravel
Primary intracranial chondrosarcomas account for under 0.16% of intracranial neoplasms and have been predominantly located in the skull base (1). Seventy five percent of intracranial chondrosarcomas originate from the skull base but they can arise from the meninges along the falx, tentorium and convexity (2). An intracranial classic chondrosarcoma arising from the falx is extremely rare and to date there is only a limited number of cases described in the literature (3). Falcine or parasagittal chondrosarcomas reported in the literature tend to be of a mesenchymal type. We present a case of a classic falcine chondrosarcoma in a 32 year old woman. Due to its rarity, there is little data on the management of these tumours. We review the diagnostic and management options pertaining to this tumour. [source]

Androgenic adult granulosa cell tumour with prolongation of the activated partial thromboplastin time in a 29 year old woman

BJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 4 2003
Tsuyoshi Honda
No abstract is available for this article. [source]

Motor aprosodia due to isolated brainstem stroke in a young woman

ACTA NEUROLOGICA SCANDINAVICA, Issue 3 2005
M. Hoffmann
A 21 year old woman presented with coma and quadriparesis secondary to bilateral pontine infarction. Three weeks later motor aprosodia was the most notable neurological finding apart from mild asymmetric limb weakness. No other supratentorial lesion was noted on initial and subsequent multimodality magnetic resonance imaging and magnetic resonance perfusion imaging revealed right frontotemporal hypoperfusion. This is the first report of aprosodia with an isolated brainstem lesion. [source]

AML with bilateral retinal detachment

ACTA OPHTHALMOLOGICA, Issue 2007
E SARKADY
Purpose: To present a case of thrombotic ocular and CNS involvement complicating acute myeloid leukaemia (AML). Methods: A 42 year old woman developed blurred vision shortly after diagnosis and treatment of M6 AML. Investigations showed anterior orbital infiltration, retinal detachment and panuveitis. Iris biopsy and vitreous aspirate were negative. She developed right temporal lobe infarction and died following further CNS infarction two months after initial diagnosis. Results: Post mortem examination showed cerebral oedema, multiple cerebral infarctions and hepatosplenomegaly; both eyes contained vitreous exudates, retinal detachment and uveal thickening. Microscopy showed exudative and haemorrhagic retinal detachment, without inflammatory or neoplastic infiltrate, and bilateral uveal leukaemic infiltration with infarction. Neoplastic cells infiltrated the leptomeninges and brain parenchyma with focal vascular occlusion. Lung vessels were occluded by neoplastic cells. The spleen and bone marrow were heavily infiltrated. Partial immunophenotyping suggested a diagnosis of acute promyelocytic leukaemia (APL). Conclusions: Acute leukaemia involves the eye occurs in 39-53% cases. Visual loss is uncommon. Retinal involvement most frequently occurs in the form of superficial haemorrhages, detachment is uncommon. Acute lymphoblastic leukaemia (ALL) treated with L-asparaginase, acute promyelocytic leukaemia (APL) and non-M3 AML may present with a prothrombotic state which may be catastrophic, as occurred in this fatal case. [source]

Ataxia with vitamin E deficiency in southeast Norway, case report

ACTA NEUROLOGICA SCANDINAVICA, Issue 2009
J. Koht
Background,, Ataxia with vitamin E deficiency (AVED) is a rare cause of hereditary ataxia in north European countries with unknown prevalence. Few cases are reported from these countries. Methods ,Through a systematic population based study of hereditary ataxia in southeast Norway subjects were classified and investigated. Aims , To report a subject with ataxia due to vitamin E deficiency in Norway. Results , One patient with AVED was identified. The subject was a 45 years old woman with progressive ataxia from preschool age. When she was 12 years old Friedreich's ataxia was diagnosed after neurological examination. At the age of 45 re-evaluation and re-examination was performed and genetic analysis of the Frataxin gene was negative. At that time she had truncal and extremities ataxia, titubation of the head, pes cavus, inverted plantar response, loss of proprioceptive and vibration sense and a severe sensory neuropathy. Vitamin E in serum was undetectable and genetic analysis detected a compound heterozygous mutation, p.A120T and p.R134X, in the ,-tocopherol transport protein gene on chromosome 8q13. Discussion , Vitamin E should always be assessed in progressive ataxia of genetic or unexplained causes and especially with a Friedreich's ataxia-like phenotype since treatment is available. Conclusion,, AVED is rare in Norway, but exists, and we here report the first genetically confirmed subject with ataxia due to vitamin E deficiency in Norway. [source]