Louisa Garrett Anderson (1873-1943), surgeon and suffragette.

Louisa Garrett Anderson, daughter of Britain's first woman doctor, has been largely forgotten today despite the fact that her contribution to the women's movement was as great as that of her mother. Recognized by her contemporaries as an important figure in the suffrage campaign, Anderson chose to lend her support through high-profile action, being one of the few women doctors in her generation who risked their professional as well as their personal reputation in the fight for women's rights by becoming a suffragette - in her case, even going so far as to spend a month in prison for breaking a window on a demonstration. On the outbreak of war, with only the clinical experience she had gained as outpatient surgeon in a women's hospital, Anderson established a series of women-run military hospitals where she was a Chief Surgeon. The most successful was the Endell Street Military Hospital in London, funded by the Royal Army Medical Corps and the only army hospital ever to be run and staffed entirely by women. Believing that a doctor had an obligation to take a lead in public affairs, Anderson continued campaigning for women's issues in the unlikely setting of Endell Street, ensuring that their activities remained in the public eye through constant press coverage. Anderson's achievement was that her work played no small part in expunging the stigma of the militant years in the eyes of the public and - more importantly - was largely instrumental in putting women doctors on equal terms with their male colleagues.

The Women's Hospital Corps: forgotten surgeons of the First World War.

Under the leadership of the former militant suffragists Flora Murray and Louisa Garrett Anderson, a group of women doctors calling themselves the Women's Hospital Corps (WHC) successfully ran two military hospitals in France from September 1914 to January 1915. In 1915 the War Office invited them to run a military hospital in London where large numbers of new beds were being created. It gave them former workhouse premises in Covent Garden, which they transformed into a 573-bed hospital, staffed and administered entirely by women. The Endell Street Military Hospital, the first hospital in the UK established for men by medical women, was open from May 1915 to December 1919; in that time, its doctors saw 26,000 patients and performed over 7000 major operations. A key feminist organization of the First War, the WHC has largely been forgotten, partly because of its relatively small size and partly because of its anomalous status as a female-run hospital under the direct patronage of the War Office.

Stretch-associated injury in cervical spondylotic myelopathy: new concept and review.

The simple pathoanatomic concept that a narrowed spinal canal causes compression of the enclosed cord, leading to local tissue ischemia, injury, and neurological impairment, fails to explain the entire spectrum of clinical findings observed in cervical spondylotic myelopathy. A growing body of evidence indicates that spondylotic narrowing of the spinal canal and abnormal or excessive motion of the cervical spine results in increased strain and shear forces that cause localized axonal injury within the spinal cord. During normal motion, significant axial strains occur in the cervical spinal cord. At the cervicothoracic junction, where flexion is greatest, the spinal cord stretches 24% of its length. This causes local spinal cord strain. In the presence of pathological displacement, strain can exceed the material properties of the spinal cord and cause transient or permanent neurological injury. Stretch-associated injury is now widely accepted as the principal etiological factor of myelopathy in experimental models of neural injury, tethered cord syndrome, and diffuse axonal injury. Axonal injury reproducibly occurs at sites of maximal tensile loading in a well-defined sequence of intracellular events: myelin stretch injury, altered axolemmal permeability, calcium entry, cytoskeletal collapse, compaction of neurofilaments and microtubules, disruption of anterograde axonal transport, accumulation of organelles, axon retraction bulb formation, and secondary axotomy. Stretch and shear forces generated within the spinal cord seem to be important factors in the pathogenesis of cervical spondylotic myelopathy.

Ependymoma with neuropil-like islands: a case report with diagnostic and histogenetic implications.

We describe a case of ependymoma with neuronal differentiation in form of neuropil-like islands. A 6-year-old boy presented at clinical examination for a short history of headaches and vomiting. Brain computed tomography showed a large, partially cystic, parieto-occipital lesion. The tumor was composed by glial fibrillary acidic protein-positive round cells with a perivascular arrangement and scattered neuropil-like islands, showing intense positivity for synaptophysin. Despite radiotherapy, the tumor recurred, showing frank features of anaplasia, but lacking the neuropil-like islands. The histological features of the tumor are discussed in the light of the concept that neuronal differentiation can occur occasionally in gliomas of different lineage without affecting the expected biological behavior.

Somatic and germline mosaicism in sporadic early-onset Alzheimer's disease.

Alzheimer's disease (AD) is the commonest neurodegenerative disease worldwide. Rare familial cases may be caused by mutations in one of three genes-amyloid precursor protein, presenilin-1 and presenilin-2; however, the molecular basis of >99% of AD cases is unknown. Somatic mutation has been considered to be a mechanism that may account for a proportion of sporadic cases of AD, but to date there has been no evidence for this. We now report a sporadic early-onset patient with AD, and show that this individual is a somatic mosaic for a mutation in the presenilin-1 gene, suggesting a novel molecular mechanism for AD. Quantification of the mosaicism demonstrated the degree of mosaicism at 8% in peripheral lymphocytes and 14% in cerebral cortex in the index patient; a clear gene dosage effect on age of presentation and clinical phenotypic presentation is demonstrated. This finding has important implications for the aetiology of sporadic AD, and for other apparently sporadic neurodegenerative diseases such as Parkinson's disease, motor neuron disease and Creutzfeldt-Jakob disease.

Sarcoid polyneuropathy responsive to intravenous immunoglobulin.

We describe a 38-year-old woman with a predominantly sensory axonal polyneuropathy in whom a nerve biopsy demonstrated sarcoid granulomas. The neuropathy did not respond to oral steroid therapy but there was a rapid and repeated response to intravenous immunoglobulin, which gradually diminished over subsequent treatments, but remained beneficial. The systemic sarcoidosis remained active.

Localization of the neuronal class III beta-tubulin in oligodendrogliomas: comparison with Ki-67 proliferative index and 1p/19q status.

The class III beta-tubulin isotype (betaIII) is widely regarded as a neuronal marker in development and neoplasia. Whereas the expression of betaIII in neuronal/neuroblastic tumors is differentiation-dependent, the aberrant expression of this cytoskeletal protein in astrocytomas is associated with an ascending gradient of malignancy. To test the generality of this observation we have compared the immunoreactivity (IR) profiles of the betaIII isotype with the Ki-67 nuclear antigen proliferative index in 41 archival, surgically excised oligodendrogliomas (32 classical [WHO grade II] and 9 anaplastic [WHO grade III]). Seventeen of 41 tumors were examined by quantitative microsatellite analysis for loss of 1p and/or 19q. Minimal deletion regions were defined on 1p (D1S468, D1S214) and 19q (D19S408, D19S867). Three of 10 classical oligodendrogliomas had combined 1p/19q loss, while 2 exhibited loss of either 1p or 19q. Three of 7 anaplastic tumors had combined 1p/19q loss. BetaIII IR was present in all tumors, but was significantly greater in the anaplastic (median labeling index [MLI] 61%, interquartile range [IQR] 55%-64%) as compared with the classical variants (MLI, 19%, IQR, 11-36%) (p < 0.0001). A highly significant relationship was found to exist between betaIII and Ki-67 LIs (betaIII, p < 0.0001 and Ki-67, p < 0.0001. r = 0.809). BetaIII localization delineated hitherto understated unipolar or bipolar tumor phenotypes with growth cones and leading cell processes resembling migrating oligodendrocyte progenitor cells. Codistribution of betaIII and GFAP IR was present in "gliofibrillary" tumor areas. Synaptophysin IR was detected in rare tumor cells (mean LI, 0.7%), and only in 4/41 samples (10%), denoting a lack of relationship between betaIII and synaptophysin expression. No significant differences in betaIII LIs were observed in tumors with 1p and/or 19q loss as compared to those with 1p/19q intact status. Increased betaIII IR in oligodendrogliomas is associated with an ascending degree of malignancy and thus is a potentially useful tumor marker. However, the significance of high betaIII LIs in low-grade oligodendrogliomas with respect to prognostic and predictive value requires further evaluation. Class III beta-tubulin expression in oligodendrogliomas should not be construed as a priori evidence of divergent neuronal differentiation.