El cerebro dormido está bien despierto

La actividad mental durante la fase del descanso en la que se producen los sueños es muy similar a la de la vigilia.

Una de las cualidades más chocantes de los sueños es su imaginería vívida y asombrosamente detallada, su mundo visual intrincado y revestido de ese aire de realidad que deja perplejos cuando se recuerdan al despertar.

Un estudio neurofisiológico con 19 personas dormidas revela ahora la causa: la actividad cerebral durante el sueño REM —el sueño con sueños— es muy parecida a la de la vigilia, cuando estamos despiertos. Si las imágenes durante el sueño parecen reales es porque para el cerebro lo son. El resultado resta misterio al sueño, pero le añade lógica neuronal.

La investigación de Yuval Nir, Itzhak Fried y sus colegas del Laboratorio de Ciencias Cognitivas de París, la Universidad de Wisconsin en Madison y la Universidad de Tel Aviv se basa en un análisis extenso, durante la vigilia y el sueño, de la actividad eléctrica de un total de 2.057 neuronas individuales y unos electroencefalogramas particularmente precisos, con los electrodos situados dentro del cráneo. Han podido hacerlo porque los 19 voluntarios eran pacientes epilépticos sometidos a cirugía intracraneal. Los resultados aparecen en la revista Nature Communications.

El sueño sigue siendo tan misterioso hoy como en la antigüedad, y será difícil encontrar un tópico sobre el que se hayan escrito más tonterías sin el menor fundamento, pero uno de los descubrimientos seminales sobre esta materia ocurrió en los años cincuenta: el del sueño REM, la fase principal en la que ocurren los sueños. REM son las siglas de Rapid Eye Movements, o movimientos rápidos de los ojos. La pregunta obvia perdura desde su hallazgo: ¿son esos movimientos un signo de que el cerebro del durmiente está emulando el procesamiento de las señales visuales típicas de la vigilia?

El trabajo de Nir y sus colegas no llega a demostrar que ese sea el caso, pero sí convierte la idea en la hipótesis más probable sobre el sueño REM. Los científicos muestran que las neuronas individuales se comportan de un modo muy similar, en todos sus detalles (grado de actividad, frecuencia de las ondas de potencial, fases típicas de latencia y cese de actividad), a cuando están en vigilia.

Los científicos muestran que las neuronas individuales se comportan de un modo muy similar, en todos sus detalles, a cuando están en vigilia.

Esto es particularmente cierto en un área concreta del córtex cerebral —el lóbulo temporal medial— que, según se sabe por estudios anteriores, está directamente implicada en la formación de memorias visuales de alto nivel: el nivel en que, por ejemplo, los rasgos de una cara dejan de importar y la cara en su conjunto pasa a constituir un significado en sí misma, esté en la orientación que esté, y poniendo el gesto que se ponga.

“Dado que la actividad del lóbulo temporal medial está íntimamente relacionada con la consciencia visual”, dicen los científicos, “nuestros resultados pueden implicar que los movimientos rápidos de los ojos durante el sueño REM reflejan un cambio de la imaginería visual en los sueños, pero se necesitan investigaciones adicionales para establecer esta posibilidad de forma inequívoca”.

En los hombres, el sueño REM también se asocia a las frecuentes erecciones del pene que ocurren por la noche. Sobre este punto también se necesitan toda clase de estudios adicionales. Por cierto, no van necesariamente asociadas a sueños eróticos, como tal vez habría esperado Freud.

No solo las lecturas de las neuronas individuales revelan el gran parecido entre los sueños y la vigilia: también la detección por electroencefalograma (EEG) apunta en el mismo sentido. El EEG tiene el inconveniente de su escasa precisión cartográfica, pero la ventaja de que las grandes ondas y variaciones de potencial que detecta son fenómenos globales del córtex cerebral, y en muchos casos se asocian a procesos de alto nivel, como el procesamiento semántico del lenguaje.

La interpretación de los sueños está todavía lejos. Para descifrarlos, sin embargo, ayudará mucho saber lo mucho que se parecen a la vida misma.

The Role of Hemosiderin Excision in Seizure Outcome in Cerebral Cavernous Malformation Surgery: A Systematic Review and Meta-Analysis

The T2-weighted image show a cavernous malformation as heterogeneous and “popcorn-like” with a mixed signal intensity core and a hypointense hemosiderin rim.

T2WI and T2* gradient echo show multiple cavernomas. Notice the popcorn appearance with peripheral rim of hemosiderin on the T2WI. The lesions are almost completely black on the gradient echo due to blooming artefacts. T2* and susceptibility weighted imaging (SWI) markedly increase the sensitivity of MRI to detect small cavernomas. The five black dots in the left cerebral hemisphere on the T2* are also cavernomas and are not visible on the T2WI.

Importance

In ten studies comparing extended hemosiderin excision with only lesion resection were identified by searching the English-language literature. Meta-analyses, subgroup analyses and sensitivity analysis were conducted to determine the association between hemosiderin excision and seizure outcome after surgery.

Patients who underwent extended surrounding hemosiderin excision could exhibit significantly improved seizure outcomes compared to patients without hemosiderin excision. However, further well-designed prospective multiple-center RCT studies are still needed 1).

Previous works showed that extent of resection and its surrounding hemosiderin rim were found to consistently correlate with a more favorable post-operative seizure-free outcome 2) 3).

Patients with short duration of epilepsy associated with cavernous malformations could benefit greatly from complete resection of hemosiderin rim and cavernous malformations 4).

High field intraoperative MRI imaging (iopMRI) and neuronavigation might play a crucial role to achieve both goals 5).

26 patients (14 female, 12 male, mean age 39·1 years, range: 17-63 years) with CM related epilepsy were identified. Eighteen patients suffered from drug resistant epilepsy (69·2%). Mean duration of epilepsy was 11·9 years in subjects with drug resistant epilepsy (n = 18) and 0·3 years in subjects presenting with first-time seizures (n = 8).

24 lesionectomies and two lesionectomies combined with extended temporal resections were performed.

Seven lesions were located extratemporally.

Complete CM removal was documented by postsurgical MRI in all patients. As direct consequence of iopMRI, refined surgery was necessary in 11·5% of patients to achieve complete cavernoma removal and in another 11·5% for complete resection of additional adjacent epileptogenic cortex. Removal of the hemosiderin rim was confirmed by iopMRI in 92% of patients. Two patients suffered from mild (7·7%) and one from moderate (3·8%) visual field deficits. Complete seizure control (Engel class 1A) was achieved in 80·8% of patients with a mean follow-up period of 47·7 months 6).

1) Ruan D, Yu XB, Shrestha S, Wang L, Chen G. The Role of Hemosiderin Excision in Seizure Outcome in Cerebral Cavernous Malformation Surgery: A Systematic Review and Meta-Analysis. PLoS One. 2015 Aug 25;10(8):e0136619. doi: 10.1371/journal.pone.0136619. eCollection 2015. PubMed PMID: 26305879.
2) Stavrou I, Baumgartner C, Frischer JM, Trattnig S, Knosp E. Long-term seizure control after resection of supratentorial cavernomas: a retrospective single-center study in 53 patients. Neurosurgery. 2008 Nov;63(5):888-96; discussion 897. doi: 10.1227/01.NEU.0000327881.72964.6E. PubMed PMID: 19005379.
3) Kim W, Stramotas S, Choy W, Dye J, Nagasawa D, Yang I. Prognostic factors for post-operative seizure outcomes after cavernous malformation treatment. J Clin Neurosci. 2011 Jul;18(7):877-80. doi: 10.1016/j.jocn.2010.12.008. Epub 2011 May 10. Review. PubMed PMID: 21561775.
4) Jin Y, Zhao C, Zhang S, Zhang X, Qiu Y, Jiang J. Seizure outcome after surgical resection of supratentorial cavernous malformations plus hemosiderin rim in patients with short duration of epilepsy. Clin Neurol Neurosurg. 2014 Apr;119:59-63. doi: 10.1016/j.clineuro.2014.01.013. Epub 2014 Jan 25. PubMed PMID: 24635927.
5) Xie HW, Wang DM, Yuan QG, Sha C, Yang YM, Jiang HZ. [The utility of neuronavigation in the microsurgery for cerebral cavernous malformations]. Zhonghua Wai Ke Za Zhi. 2011 Aug 1;49(8):712-5. Chinese. PubMed PMID: 22168935.
6) Sommer B, Kasper BS, Coras R, Blumcke I, Hamer HM, Buchfelder M, Roessler K. Surgical management of epilepsy due to cerebral cavernomas using neuronavigation and intraoperative MR imaging. Neurol Res. 2013 Oct 23:0. [Epub ahead of print] PubMed PMID: 24070413.

All cases of Chiari III

Chiari III malformation

Chiari III is one of the rarest of the Chiari malformations and is characterized by a high cervical or low occipital encephalocele and osseous defect with or without spinal cord involvement and may include many of the anatomical characteristics seen in the Chiari II malformation.

Type III is the most serious form of Chiari malformation (CM).

The cerebellum and brain stem protrude, or herniate, through the foramen magnum and into the spinal cord. Part of the brain’s fourth ventricle, a cavity that connects with the upper parts of the brain and circulates CSF, may also protrude through the hole and into the spinal cord.

In rare instances, the herniated cerebellar tissue can enter an occipital encephalocele, a pouch-like structure that protrudes out of the back of the head or the neck and contains brain matter. The covering of the brain or spinal cord can also protrude through an abnormal opening in the back or skull.

Type III causes severe neurological defects.

Out of 57 reported cases of Chiari III malformation, encephaloceles were in a high cervical/low occipital position in 23, 8 were in a high cervical position, 17 were in low occipital position, and the position in 9 cases was not reported. The pathogenesis of Chiari III malformation remains unclear. The majority of patients have concomitant hydrocephalus. Brain parts occurring in the sac from the most to least common include the following: cerebellum, occipital lobe, and parietal lobe. The severity of symptoms is correlated with the amount of brain structures within the encephalocele. Neurologic functional outcomes have been varied and depend on the neurological status of the patient before surgery 1).

1) Ivashchuk G, Loukas M, Blount JP, Tubbs RS, Oakes WJ. Chiari III malformation: a comprehensive review of this enigmatic anomaly. Childs Nerv Syst. 2015 Aug 9. [Epub ahead of print] PubMed PMID: 26255148.

Sign Up for the Stereotactic and Functional Neurosurgery Workshop Before Registration Closes on Aug. 17, 2015

Practitioners of stereotactic neurosurgery must use a variety of stereotactic devices to deliver a range of therapies safely and effectively, but have few venues to learn and practice these skills.

Led by course director Aviva Abosch, MD, PhD, FAANS, the Stereotactic and Functional Neurosurgery workshop helps practitioners use standard stereotactic devices to deliver therapies safely and effectively. Taking place Nov. 13-15, 2015, in Aurora, Colo., this workshop includes discussion with renowned faculty and hands-on training in a state-of-the-art lab.

Review the brochure online to view a detailed course description and a full list of course faculty. CME will be awarded for course participation.

Learn More and Register Today

Visit www.aans.org/sfncourse to learn more about this workshop, then register today to save your seat. Registration closes on Monday, Aug. 17, 2015, or when space runs out.

Stereotactic and Functional Neurosurgery workshop is presented by the American Association of Neurological Surgeons (AANS), the Neurosurgery Research and Education Foundation (NREF) and the American Society for Stereotactic and Functional Neurosurgery (ASSFN).

Lymphomatosis cerebri

Lymphomatosis cerebri

J.Sales-Llopis

Neurosurgery Department, University General Hospital of Alicante, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Alicante, Spain

A case study in 1999 coined the term ‘lymphomatosis cerebri’ (LC) to describe an exceedingly rare variant of Primary central nervous system lymphoma PCNSL characterised by diffuse parenchymal infiltration of lymphomatous cells 1).

Clinical Features

The patient with lymphomatosis cerebri may have variable clinical symptoms such as gait abnormality, focal weakness, cognitive decline, memory disturbance, personality changes, dementiaanorexia, orthostatic hypotension, paraparesis and weight loss 2) 3).

The tumors infiltrating to the diencephalon have been reported to cause the diencephalic syndrome 4).

Diagnosis

MRI

MRI study of LC typically reveals diffuse leukoencephalopathy.

Typical MR findings of the lymphomatosis cerebri are extensive, diffuse T2 and FLAIR-weighted hyperintense lesions without contrast enhancement in both cerebral hemispheres and brainstem 5).


Diagnosis of LC requires additional examinations generally not performed in the other white matter disorders. In suspected cases, biopsy should be performed to avoid deferring adequate cytostatic treatment

Diffuse infiltrations of both cerebral hemispheres by lymphoma cells without discernible lesions 6) 7).

Differential diagnosis

It is not well recognized and may be misdiagnosed with infiltrating tumors, degenerative disorders, ischemic diseases, and infectious diseases developed in the brain 8).

Awareness of the possibility of this rare disease and early biopsy are required for differential diagnosis and preventing poor clinical outcomes.

Subtle or patchy enhancements may be seen in some cases in MRI. These radiological findings may be similar with those of the gliomatosis cerebri which has to be differentiated in this case. In the gliomatosis cerebri, T1-weighted hypo-intense lesions on MRIs, low-density lesions on CT, and focal enhancements are typical radiological findings 9).

Anaplastic large-cell lymphoma 10).

Treatment

Where LC was diagnosed premortem, many cases responded to steroids alone, at least initially.

To achieve complete remission, steroid use has been followed by radiotherapy, cisplatin or methotrexate 11).

Optimal treatment for lymphomatosis cerebri remains unclear. However, better outcomes may be expected than previously reported ones because lymphomatosis cerebri is identical to PCNSL pathologically 12).

Case series

2005

3 immunocompetent individuals who developed rapidly progressive dementia. Magnetic resonance imaging features mimicked other disorders of white matter and prompted preoperative diagnoses of Binswanger’s disease (subcortical ischemic vascular dementia), unknown leukoencephalopathy, viral infection, or infiltrating glioma. Neuropathologic examination at biopsy and autopsy demonstrated nonnecrotic, diffusely infiltrating, large-cell B-cell lymphoma of white matter, with relative sparing of gray matter, and without significant leptomeningeal involvement or bulky periventricular disease at autopsy. Microglial and astrocytic reactions, but only subtle myelin pallor, were evident as individual tumor cells permeated the entire brain and spinal cord, albeit with considerable variation in cell density. Individual tumor cells could be identified from the optic nerve to spinal cord, documenting the “whole-brain” nature of the disease. CD20 immunostaining was necessary to fully appreciate the extent of individual lymphoma cell percolation through the white matter. The neurobehavioral deficits manifested by these patients demonstrate that lymphomatosis cerebri is an additional neoplastic cause of white matter dementia and can be added to the growing list of disorders responsible for this syndrome 13).

1999

2 cases from the UCLA Medical Center who developed a rapidly progressive dementia due to extensive gray and white matter cerebral lesions involving much of the brain. In the patient who came to autopsy, widely infiltrating, focally necrotic B-cell plasmacytoid lymphoma was noted throughout the cerebral neuraxis. MRI findings in case 2 were consistent with diffuse lymphomatous brain infiltration without mass lesions, which was biopsy proven. We conclude that PCNSL may occur in a diffusely infiltrating form which may occur without MRI evidence of mass lesions or blood-brain barrier compromise. We refer to this entity as ‘lymphomatosis cerebri’ and add it to the differential diagnosis of a rapidly progressive dementia 14).

Case reports

It has been reported less than 20 cases till 2012 15).

2015

A 71-year-old immunocompetent man developed cognitive decline and gait abnormalityBrain magnetic resonance imaging (MRI) revealed bilateral diffuse leukoencephalopathy without a mass lesion. An analysis of the cerebrospinal fluid (CSF) showed elevated levels of interleukin 10(IL-10). The condition of the patient progressively deteriorated, and intravenous high-dose steroids proved ineffective. Detection of non-destructive, diffusely infiltrating, large B cell lymphoma in biopsy and autopsy specimens led to a diagnosis of lymphomatosis cerebri (LC). On serial MRI, the basal ganglia and white matter lesions increased in parallel with the levels of IL-10. These findings suggest that the IL-10 level in the CSF may represent a potentially useful biomarker for the early diagnosis and monitoring of the disease progression in LC 16).

2013

A case with lymphomatosis cerebri who presented with rapid neurological deterioration 17).

2012

A 55-year-old man presenting with subacute progressive dementia and ataxic gait. Brain MRI showed diffuse hyperintense lesions in the cerebral white matter of both hemispheres, left amygdala, brainstem and cerebellar peduncles on FLAIR image. No contrast-enhanced lesion was observed. Cerebrospinal fluid analysis showed elevated levels of soluble interleukin-2 receptor and β2-microglobulin. Based on MRI findings and 123I-IMP SPECT, stereotactic biopsy targeting white matter of the left medial temporal lobe was performed (day 0). On the day after the brain biopsy, corticosteroid therapy was initiated and improved the patient’s cognitive function and gait disturbance. Pathological diagnosis of large B-cell lymphoma was obtained on day 9. High-dose intravenous methotrexate chemotherapy was started on day 14 and led to complete remission by day 52. This case highlighted the importance of brain biopsy for diagnosis of LC. This report raises a possibility that timely and proper treatment leads to a favorable outcome of LC that has been regarded as an intractable disease with poor prognosis 18).


A 56-year-old immunocompetent woman who complained of rapid deterioration of her higher brain function over a 4-month period. Magnetic resonance imaging showed extensive white-matter lesions. During brain biopsy, a diffusely infiltrating lymphoma with distinctive immunohistochemical features was detected. Awareness of this unique presentation and early tissue diagnosis provide the best hope for instituting appropriate treatments 19).

2009

A patient with subacute dementia and diffuse bilateral white matter changes in the cerebral hemispheres and additional involvement of the brainstem, basal ganglia and thalamus on MRI. Initially, she was considered to suffer from an autoimmune encephalitis, transiently responded to immunosuppression but then developed multiple solid appearing cerebral lymphomas 20).

2008

A 53-year-old, immunocompetent man who had an insidiously progressive dementia and right weakness. On serial MRI in 4 months duration, diffuse white matter lesions without contrast enhancement gradually progressed, which was clinically consistent with his worsening condition. Biopsy specimen demonstrated nondestructive, diffusely infiltrating, large B-cell lymphoma, diagnosing LC. After the biopsy, corticosteroids were initiated, which dramatically alleviated his symptoms. Afterwards, he was treated by whole brain irradiation (total 36Gy) and discharged without noticeable deficits 21).


A 56-year-old female who had clinical signs and symptoms of sub-acute dementia. Computerised axial tomography and MRI of the head revealed extensive, diffuse and bilateral involvement of the white matter, basal nuclei, mesencephalon and pons, with no mass effect or contrast enhancement. A stereotactic biopsy of the white matter (which was not conclusive) showed a perivascular mixed mononuclear-cell inflammatory infiltrate of B and T cells. No cytologic atypia was observed. Treatment was established with corticoids, which produced a clinical and radiological improvement in the first two months. During the next month the patient underwent rapid clinical deterioration with sleepiness and a worsening of the ability to walk. In an MRI scan the lesion had a more heterogeneous appearance with mass effect on adjacent structures and patchy contrast enhancement. A wedge biopsy of brain tissue led to a diagnosis of high-grade B-cell lymphoma.

The imaging and histological appearance of LC may not be the one typically found in primary lymphomas of the central nervous system, and its clinical presentation may be similar to that of other diffuse processes involving compromise of the white matter (cerebral gliomatosis, inflammatory diseases of the white matter, such as Behçet’s disease, Sjögren’s disease or systemic lupus erythematosus) 22).

2007

A 64-year-old woman presenting with rapidly progressive dementia, brain magnetic resonance imaging revealed a diffuse leukoencephalopathy without gadolinium enhancement, and the 14.3.3 protein was found to be positive in the cerebrospinal fluid. An electroencephalogram showed diffused slow waves and epileptic seizures without periodic paroxysmal activity. The patient died 3 months after onset of symptoms, and an autopsy restricted to the brain was performed. Gross examination was not informative, and only microscopic examination permitted identification of scattered lymphomatous cells on all sections from the brain hemispheres, brain stems and cerebellum. Immunopositivity of these tumor cells for CD20 attested their B phenotype 23)


A case of an elderly patient referred to a tertiary-care center for further evaluation of a rapidly progressive dementia, whose definitive diagnosis was delayed by nonspecific MRI findings, presence of 14-3-3 protein in the CSF, and nonspecific cutaneous lesions. At brain biopsy, he was thought to have a diffusely infiltrating lymphoma, with distinctive immunohistochemical features.

This case is notable in that it presents a patient with progressive dementia whose diagnosis of primary central nervous system lymphoma (PCNSL) was delayed because of the lymphoma’s atypical diffusely infiltrating nature. Awareness of this unique presentation may hasten the time between clinical presentation, diagnosis, and subsequent treatment 24).

References

1) , 14) Bakshi R, Mazziotta JC, Mischel PS, et al. Lymphomatosis cerebri presenting as a rapidly progressive dementia: clinical, neuroimaging and pathologic findings. Dement Geriatr Cogn Disord 1999;10:152–7.
2) , 5) Keswani A, Bigio E, Grimm S. Lymphomatosis cerebri presenting with orthostatic hypotension, anorexia, and paraparesis. J Neurooncol. 2012;109:581–586.
3) , 15) , 19) Kitai R, Hashimoto N, Yamate K, Ikawa M, Yoneda M, Nakajima T, et al. Lymphomatosis cerebri : clinical characteristics, neuroimaging, and pathological findings. Brain Tumor Pathol. 2012;29:47–53.
4) Ashworth B. Cerebral histiocytic lymphoma presenting with loss of weight. Neurology. 1982;32:894–896.
6) Lewerenz J, Ding X, Matschke J, Schnabel C, Emami P, von Borczyskowski D, et al. Dementia and leukoencephalopathy due to lymphomatosis cerebri. J Neurol Neurosurg Psychiatry. 2007;78:777–778.
7) , 8) Rollins KE, Kleinschmidt-DeMasters BK, Corboy JR, Damek DM, Filley CM. Lymphomatosis cerebri as a cause of white matter dementia. Hum Pathol. 2005;36:282–290.
9) Chen S, Tanaka S, Giannini C, Morris J, Yan ES, Buckner J, et al. Gliomatosis cerebri : clinical characteristics, management, and outcomes. J Neurooncol. 2013;112:267–275.
10) Sugino T, Mikami T, Akiyama Y, Wanibuchi M, Hasegawa T, Mikuni N. Primary central nervous system anaplastic large-cell lymphoma mimicking lymphomatosis cerebri. Brain Tumor Pathol. 2013 Jan;30(1):61-5. doi: 10.1007/s10014-012-0094-0. Epub 2012 Mar 18. PubMed PMID: 22426596.
11) Leschziner G, Rudge P, Lucas S, et al. Lymphomatosis cerebri presenting as a rapidly progressive dementia with a high methylmalonic acid. J Neurol 2011;258: 1489–93.
12) , 17) Choi CY, Lee CH, Joo M. Lymphomatosis cerebri. J Korean Neurosurg Soc. 2013 Nov;54(5):420-2. doi: 10.3340/jkns.2013.54.5.420. Epub 2013 Nov 30. PubMed PMID: 24379950; PubMed Central PMCID: PMC3873356.
13) Rollins KE, Kleinschmidt-DeMasters BK, Corboy JR, Damek DM, Filley CM. Lymphomatosis cerebri as a cause of white matter dementia. Hum Pathol. 2005 Mar;36(3):282-90. PubMed PMID: 15791573.
16) Hashiguchi S, Momoo T, Murohashi Y, Endo M, Shimamura M, Kawasaki T, Kanada S, Nozawa A, Tada M, Koyano S, Tanaka F. Interleukin 10 Level in the Cerebrospinal Fluid as a Possible Biomarker for Lymphomatosis Cerebri. Intern Med. 2015;54(12):1547-52. doi: 10.2169/internalmedicine.54.3283. Epub 2015 Jun 15. PubMed PMID: 26073248.
18) Watanabe M, Satoi H, Takahashi Y, Nishida N, Toda H, Matsumoto S. [Remission of lymphomatosis cerebri induced by corticosteroid and high-doses intravenous methotrexate]. Rinsho Shinkeigaku. 2012;52(7):486-90. Japanese. PubMed PMID: 22849990.
20) Lewerenz J, Ding XQ, Matschke J, Schnabel C, Emami P, von Borczyskowski D, Buchert R, Krieger T, de Wit M, Münchau A. Dementia and leukoencephalopathy due to lymphomatosis cerebri. BMJ Case Rep. 2009;2009. pii: bcr08.2008.0752. doi: 10.1136/bcr.08.2008.0752. Epub 2009 Feb 2. PubMed PMID: 21686648; PubMed Central PMCID: PMC3028137.
21) Kanai R, Shibuya M, Hata T, Hori M, Hirabayashi K, Terada T, Fujii K. A case of ‘lymphomatosis cerebri’ diagnosed in an early phase and treated by whole brain radiation: case report and literature review. J Neurooncol. 2008 Jan;86(1):83-8. Epub 2007 Jul 5. Review. PubMed PMID: 17611716.
22) de Toledo M, López-Valdés E, Ferreiro M, Cervera JL, Ramos A, Cabello A, Hernández-Laín A, Montes-Montes S, Lagares A, Alvarez-Linera Prado J. [Lymphomatosis cerebri as the cause of leukoencephalopathy]. Rev Neurol. 2008 Jun 1-15;46(11):667-70. Spanish. PubMed PMID: 18509825.
23) Vital A, Sibon I. A 64-year-old woman with progressive dementia and leukoencephalopathy. Brain Pathol. 2007 Jan;17(1):117-8, 121. PubMed PMID: 17493046.
24) Weaver JD, Vinters HV, Koretz B, Xiong Z, Mischel P, Kado D. Lymphomatosis cerebri presenting as rapidly progressive dementia. Neurologist. 2007 May;13(3):150-3. PubMed PMID: 17495760.

Young French neurosurgeons: Working conditions and outlook

Young French neurosurgeons: Working conditions and outlook

Due to the increase in the number of French neurosurgeon residents the neurosurgical workforce is changing. The main objective of this survey was to assess working conditions and perspectives for young French neurosurgeons.

METHOD:

An on-line survey was sent to young French neurosurgeons based on a mailing-list (219 mail addresses of Residents and Fellows obtained during previous meetings). The form contained questions about career, amount of work, salary, quality of life, teaching and university work.

RESULTS:

We received 78 replies from January to March 2014. A total of 56% from fellows saying they had undergone difficulties in obtaining a fellowship, although 78% were satisfied. Fellows considered a private career more often than residents. Overall, young neurosurgeons were worried about future employment. Some 33% admitted contemplating a different career from one they originally wanted. The average weekly working time of 76.8hours was deemed to be excessive. Security rests after overnight shifts were lacking or incomplete in 91% of cases. The work atmosphere was good overall (3.7/5), and so was the quality of life (3.2/5). Theoretical teaching was unsatisfactory (2.43/5) as well as the time allowed for academic work (approximately 1.58 half-days per month). However, practical teaching was considered rewarding (3.63/5).

CONCLUSION:

This study provides some guidance for upcoming reforms, and should be considered again at a later date to evaluate progress.

Pommier B, Manet R, Gay E, Vassal F, Nuti C, Hladky JP. [Young French neurosurgeons: Working conditions and outlook]. Neurochirurgie. 2015 Aug 4. pii: S0028-3770(15)00096-X. doi: 10.1016/j.neuchi.2015.04.003. [Epub ahead of print]
French. PubMed PMID: 26254124.

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