- Email: [email protected]
‘Posterior pusher syndrome’ or ‘psychomotor disadaptation syndrome’?
Clinical Neurology and Neurosurgery 113 (2011) 520–521
Contents lists available at ScienceDirect
Clinical Neurology and Neurosurgery journal homepage: www.elsevier.com/locate/clineuro
Letters to the Editor Helicobacter pylori may play an important role in both axonal type Guillain–Barré syndrome and acute inflammatory demyelinating polyradiculoneuropathy Dear Editor, In their paper, Ghabaee et al. [1] reported a relationship between Helicobacter pylori infection (Hp-I) and axonal damage rather than demyelination, which is to some extent against our study that proposed a possible association between Hp-I and acute inflammatory demyelinating polyradiculoneuropathy (AIDP) [2]. However, serum and cerebrospinal fluid anti-Hp IgG titers were significantly higher in their patients, consisting mainly of AIDP [10/15(67%)] patients and only 2 (13%) patients with acute motor axonal neuropathy (AMAN), than in controls. Moreover, the authors claimed that anti-Hp IgG may have an important role in Guillain–Barré syndrome; damage and leaky blood–nerve barrier (BNB) allows entry of these antibodies into endoneural space, and, through molecular mimicry, immune reactions occur between these antibodies and myelin or axon epitopes, thereby resulting not only in axonal damage, as the authors commented, but also in demyelination. BNB damage has been increasingly implicated in inflammatory demyelinating neuropathies (IDNs) [3], and a variety of proinflammatory cytokines are instrumental in the course of IDNs. They increase vascular permeability and BNB disruption (tumor necrosis factor (TNF)-alpha, vascular endothelial growth factor, vascular permeability factor); induce transmigration of leukocytes into the nerve, activation and proliferation of macrophages (interferon-gamma) and T-cells (interleukins1 and -2); and exert direct myelinotoxic activities (TNF-alpha and -beta) [4]. Besides, mast cells are located in close proximity to neurons in the peripheral and central nervous systems, signifying their role in normal and aberrant neurodegenerative conditions [5]. Hp-I, by releasing several of the aforementioned inflammatory mediators, could induce BNB/BBB breakdown, thereby possibly being involved in the pathogenesis of neuropathies including both AMAN and AIDP [6–9]. For instance, Hp could indirectly affect the peripheral and central nervous systems, through the release of numerous cytokines such as TNF-alpha acting at distance; TNF-alpha is involved in BBB/BNB disruption through matrix metalloproteinases upregulation [6,7]. Moreover, Hp-induced vacuolating cytotoxin A exhibits chemotactic activities to the bone marrow-derived mast cells (BMD-MCs) and induces BMD-MCs to produce proinflammatory cytokines involved in the BBB/BNB disruption [6,7]. Therefore, Hp-induced BBB/BNB breakdown might promote entry of immune cell infiltrations (autoreactive effector CD4+ and CD8+ T-cells) and Hp circulating antibodies into the peripheral and central neurons resulting in the development of neuronal pathologies [6,7,10–12] including AMAN and AIDP.
References [1] Ghabaee M, Ghanbarian D, Brujeni GN, Bokaei S, Siavoshi F, Gharibzadeh S. Could Helicobacter pylori play an important role in axonal type of Guillain–Barré syndrome pathogenesis? Clin Neurol Neurosurg 2010;112(April (3)):193–8. [2] Kountouras J, Deretzi G, Zavos C, Karatzoglou P, Touloumis L, Nicolaides T, et al. Association between Helicobacter pylori infection and acute inflammatory demyelinating polyradiculoneuropathy. Eur J Neurol 2005;12(February (2)):139–43. [3] Lilje O, Armati PJ. Restimulation of resting autoreactive T-cells by Schwann cells in vitro. Exp Mol Pathol 1999;67(December (3)):164–74. [4] Créange A, Barlovatz-Meimon G, Gherardi RK. Cytokines and peripheral nerve disorders. Eur Cytokine Netw 1997;8(June (2)):145–51. [5] Purcell WM, Atterwill CK. Mast cells in neuroimmune function: neurotoxicological and neuropharmacological perspectives. Neurochem Res 1995;20(May (5)):521–32. [6] Deretzi G, Kountouras J, Grigoriadis N, Zavos C, Chatzigeorgiou S, Koutlas E, et al. From the “little brain” gastrointestinal infection to the “big brain” neuroinflammation: a proposed fast axonal transport pathway involved in multiple sclerosis. Med Hypotheses 2009;73(November (5)):781–7. [7] Kountouras J. Helicobacter pylori: an intruder involved in conspiring glaucomatous neuropathy. Br J Ophthalmol 2009;93(November (11)):1413–5. [8] Harvey GK, Toyka KV, Hartung HP. Effects of mast cell degranulation on blood-nerve barrier permeability and nerve conduction in vivo. J Neurol Sci 1994;125(August (1)):102–9. [9] Kountouras J, Zavos C, Diamantidis MD, Deretzi G, Grigoriadis N, Tsapournas G, et al. A concept of Helicobacter pylori and stress-secreted mast cells’ potential involvement in brain metastases. J Neuroimmunol 2009;209(April (1–2)):121–2. [10] Kountouras J, Zavos C, Chatzopoulos D. Primary open-angle glaucoma: pathophysiology and treatment. Lancet 2004;364(October (9442)):1311–2. [11] Kountouras J, Tsolaki M, Gavalas E, Boziki M, Zavos C, Karatzoglou P, et al. Relationship between Helicobacter pylori infection and Alzheimer disease. Neurology 2006;66(March (6)):938–40. [12] Gavalas E, Kountouras J, Deretzi G, Boziki M, Grigoriadis N, Zavos C, et al. Helicobacter pylori and multiple sclerosis. J Neuroimmunol 2007;188(August (1–2)):187–9.
Jannis Kountouras ∗ Christos Zavos Georgia Deretzi Emmanuel Gavalas Stergios Polyzos Elizabeth Vardaka Constantinos Kountouras Evangelia Giartza-Taxidou Evangelos Koutlas Iakovos Tsiptsios Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece ∗ Corresponding
author at: Gastroenterologist, 8 Fanariou St, Byzantio, 551 33, Thessaloniki, Macedonia, Greece. Tel.: +30 2310 892238; fax: +30 2310 992794. E-mail addresses: [email protected], [email protected], [email protected] (J. Kountouras) 22 December 2009 Available online 12 February 2011 doi:10.1016/j.clineuro.2011.01.004
0303-8467/$ – see front matter © 2011 Elsevier B.V. All rights reserved.
Letters to the Editor / Clinical Neurology and Neurosurgery 113 (2011) 520–521
‘Posterior pusher syndrome’ or ‘psychomotor disadaptation syndrome’?夽 Keywords: Pusher behavior Posterior pusher syndrome Psychomotor disadaptation syndrome
Dear Editor, We read with great interest the case report recently published in the journal by Cardoen and Santens on the “posterior pusher syndrome” [1]. They reported two patients with a marked disturbance of body orientation in the sagittal plane with backward imbalance, posterior tilt and an active resistance to forward pulling or pushing. One 82-year old patient had history of a left frontal parafalcine meningioma and hydrocephalus with recurrent falling, decrease of cognitive abilities, frontal release sings, hypertonia of the four limbs, without asymmetrical findings on neurological examination; and one 65-year-old patient with a history of transient ischemic attacks (TIA), a large hypothalamic lymphoma and post-irradiation encephalopathy that was admitted with gait difficulties and tendency to fall backwards, apathy, frontal release sings and clear hypertonia in the four limbs [1]. By the description of Cardoen and Santens [1], it is not clear if the ‘posterior pusher syndrome’ is a new described neurological behavior or a severe reactive/protective postural reaction due to the already described ‘psychomotor disadaptation syndrome’ (PDS). The PDS, which was first described by Gaudet and colleagues in 1986, is a geriatric syndrome characterized by postural impairments, including ‘retropulsion’ or ‘backwards disequilibrium’ (BD), neurological signs as axial and limb rigidity and psychological disorders as fear of falling and phobia of the upright position [2–4]. Its severe presentation is also called ‘post fall syndrome’. According to Mourey et al. [3], the backward disequilibrium is a result of a backward projection of the center-of-mass to the posterior boundary of the base of support and is characterized as follows: “the backward position of the trunk while sitting, and a tendency to fall backward in the standing position. In severe cases, we sometimes observe a failure to reach an erect position because the center-of mass is projected outside the base of support. When the standing position is successful, forward trunk bending, knee flexion, and toe clenching can be observed as adaptive patterns that allow the patient to maintain the center-of-mass in the base of support. In the sitting position, the buttocks are commonly located on the anterior side of the seat while the trunk rests on the back of the armchair in patients without severe kyphosis. In severe cases, the transfer from sitting to standing is impossible without assistance because the subject cannot bend the trunk forward.”[3]. Moreover, patients with PDS have an increase in muscle tone that counteracts movement execution. This hypertonia is called reactional or paratonia because it appears when a limb is mobilized passively by an investigator, and it decreases when confidence and relaxation are obtained [3]. Patients with PDS also have an alteration in postural reactions. When the examiner gives a slight push applied to the trunk, in severe cases, patients fall with no protective reactions of the arms [2,3]. Other features that suggest against the existence of a newly described ‘posterior pusher syndrome’ is that all the pusher
patients reported in the literature so far had an acute event and unilateral neurological deficits [5–7]. Besides the TIA that was not described as time-related to the ‘posterior pusher syndrome’, the patients reported by Cardoen and Santens had no acute encephalic lesion nor asymmetrical findings on neurological testing. Adversely, the PDS may be associated with several chronic diseases such as lymphomas of nervous system, multiple system atrophy, meningoencephalitis, normal pressure hydrocephalus, and depression [2–4]. In addition, the authors pointed out that the absence of patients’ attempts to correct their posterior tilt and to have protective actions when they fell backwards argue against the possibility of other underlying disorders different from pusher syndrome [1]. In contrast, we find this lack of reactive and protective reaction another feature that can argue in favor to the PDS as described above. Moreover, both patients presented frontal release sings that may be accompanied by paratonia. An interesting aspect recently published is that the backward disequilibrium is associated with a dysfunction of postural vertical perception [4] as occurs in pushing behavior [8,9]. Manckoundia et al. [4] found a close correlation between backward disequilibrium scale and the backward tilt of the subjective postural vertical, although the relatively low number of subjects. Future studies will be necessary to clarify the relationship between the pusher behavior with the backward disequilibrium. References [1] Cardoen S, Santens P. Posterior pusher syndrome: a report of two cases. Clin Neurol Neurosurg 2010;112(4):347–9. [2] Pfitzenmeyer P, Mourey F, Tavernier B, Camus A. Psychomotor desadaptation syndrome. Arch Gerontol Geriatr 1999;28(3):217–25. [3] Mourey F, Manckoundia P, Martin-Arveux I, Tavernier-Vidal B, Pfitzenmeyer P. Psychomotor disadaptation syndrome. A new clinical entity in geriatric patients. Geriatrics 2004;59(5):20–4. [4] Manckoundia P, Mourey F, Pfitzenmeyer P, Van Hoecke J, Perennou D. Is backward disequilibrium in the elderly caused by an abnormal perception of verticality? A pilot study. Clin Neurophysiol 2007;118(4):786–93. [5] Santos-Pontelli TE, Pontes-Neto OM, Colafemina JF, de Araujo DB, Santos AC, Leite JP. Contraversive pushing in non-stroke patients. J Neurol 2004;251(11):1324–8. [6] Paci M, Nannetti L. The pusher syndrome in a patient with cerebellar infarction. Physiother Res Int 2005;10(3):176–7. [7] Karnath HO. Pusher syndrome—a frequent but little-known disturbance of body orientation perception. J Neurol 2007;254(4):415–24. [8] Karnath HO, Ferber S, Dichgans J. The origin of contraversive pushing: evidence for a second graviceptive system in humans. Neurology 2000;55(9):1298–304. [9] Perennou DA, Mazibrada G, Chauvineau V, Greenwood R, Rothwell J, Gresty MA, et al. Lateropulsion, pushing and verticality perception in hemisphere stroke: a causal relationship? Brain 2008;131(Pt 9):2401–13.
T.E.G. Santos-Pontelli O.M. Pontes-Neto J.P. Leite ∗ Department of Neurology, University of São Paulo, School of Medicine at Ribeirão Preto, Brazil ∗ Corresponding
author at: Campus Universitário, Ribeirão Preto, CEP 14049-900, Brazil. Tel.: +55 16 3602 2556; fax: +55 16 3633 0760. E-mail address: [email protected] (J.P. Leite) 20 April 2010 Available online 12 February 2011
doi:10.1016/j.clineuro.2011.01.012 夽 J.P.Leite, O.M. Pontes-Neto and T.E.G. Santos-Pontelli are supported by Fundac¸ão de Apoio a Pesquisa do Estado de São Paulo (FAPESP) and Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq).
521
Contents lists available at ScienceDirect
Clinical Neurology and Neurosurgery journal homepage: www.elsevier.com/locate/clineuro
Letters to the Editor Helicobacter pylori may play an important role in both axonal type Guillain–Barré syndrome and acute inflammatory demyelinating polyradiculoneuropathy Dear Editor, In their paper, Ghabaee et al. [1] reported a relationship between Helicobacter pylori infection (Hp-I) and axonal damage rather than demyelination, which is to some extent against our study that proposed a possible association between Hp-I and acute inflammatory demyelinating polyradiculoneuropathy (AIDP) [2]. However, serum and cerebrospinal fluid anti-Hp IgG titers were significantly higher in their patients, consisting mainly of AIDP [10/15(67%)] patients and only 2 (13%) patients with acute motor axonal neuropathy (AMAN), than in controls. Moreover, the authors claimed that anti-Hp IgG may have an important role in Guillain–Barré syndrome; damage and leaky blood–nerve barrier (BNB) allows entry of these antibodies into endoneural space, and, through molecular mimicry, immune reactions occur between these antibodies and myelin or axon epitopes, thereby resulting not only in axonal damage, as the authors commented, but also in demyelination. BNB damage has been increasingly implicated in inflammatory demyelinating neuropathies (IDNs) [3], and a variety of proinflammatory cytokines are instrumental in the course of IDNs. They increase vascular permeability and BNB disruption (tumor necrosis factor (TNF)-alpha, vascular endothelial growth factor, vascular permeability factor); induce transmigration of leukocytes into the nerve, activation and proliferation of macrophages (interferon-gamma) and T-cells (interleukins1 and -2); and exert direct myelinotoxic activities (TNF-alpha and -beta) [4]. Besides, mast cells are located in close proximity to neurons in the peripheral and central nervous systems, signifying their role in normal and aberrant neurodegenerative conditions [5]. Hp-I, by releasing several of the aforementioned inflammatory mediators, could induce BNB/BBB breakdown, thereby possibly being involved in the pathogenesis of neuropathies including both AMAN and AIDP [6–9]. For instance, Hp could indirectly affect the peripheral and central nervous systems, through the release of numerous cytokines such as TNF-alpha acting at distance; TNF-alpha is involved in BBB/BNB disruption through matrix metalloproteinases upregulation [6,7]. Moreover, Hp-induced vacuolating cytotoxin A exhibits chemotactic activities to the bone marrow-derived mast cells (BMD-MCs) and induces BMD-MCs to produce proinflammatory cytokines involved in the BBB/BNB disruption [6,7]. Therefore, Hp-induced BBB/BNB breakdown might promote entry of immune cell infiltrations (autoreactive effector CD4+ and CD8+ T-cells) and Hp circulating antibodies into the peripheral and central neurons resulting in the development of neuronal pathologies [6,7,10–12] including AMAN and AIDP.
References [1] Ghabaee M, Ghanbarian D, Brujeni GN, Bokaei S, Siavoshi F, Gharibzadeh S. Could Helicobacter pylori play an important role in axonal type of Guillain–Barré syndrome pathogenesis? Clin Neurol Neurosurg 2010;112(April (3)):193–8. [2] Kountouras J, Deretzi G, Zavos C, Karatzoglou P, Touloumis L, Nicolaides T, et al. Association between Helicobacter pylori infection and acute inflammatory demyelinating polyradiculoneuropathy. Eur J Neurol 2005;12(February (2)):139–43. [3] Lilje O, Armati PJ. Restimulation of resting autoreactive T-cells by Schwann cells in vitro. Exp Mol Pathol 1999;67(December (3)):164–74. [4] Créange A, Barlovatz-Meimon G, Gherardi RK. Cytokines and peripheral nerve disorders. Eur Cytokine Netw 1997;8(June (2)):145–51. [5] Purcell WM, Atterwill CK. Mast cells in neuroimmune function: neurotoxicological and neuropharmacological perspectives. Neurochem Res 1995;20(May (5)):521–32. [6] Deretzi G, Kountouras J, Grigoriadis N, Zavos C, Chatzigeorgiou S, Koutlas E, et al. From the “little brain” gastrointestinal infection to the “big brain” neuroinflammation: a proposed fast axonal transport pathway involved in multiple sclerosis. Med Hypotheses 2009;73(November (5)):781–7. [7] Kountouras J. Helicobacter pylori: an intruder involved in conspiring glaucomatous neuropathy. Br J Ophthalmol 2009;93(November (11)):1413–5. [8] Harvey GK, Toyka KV, Hartung HP. Effects of mast cell degranulation on blood-nerve barrier permeability and nerve conduction in vivo. J Neurol Sci 1994;125(August (1)):102–9. [9] Kountouras J, Zavos C, Diamantidis MD, Deretzi G, Grigoriadis N, Tsapournas G, et al. A concept of Helicobacter pylori and stress-secreted mast cells’ potential involvement in brain metastases. J Neuroimmunol 2009;209(April (1–2)):121–2. [10] Kountouras J, Zavos C, Chatzopoulos D. Primary open-angle glaucoma: pathophysiology and treatment. Lancet 2004;364(October (9442)):1311–2. [11] Kountouras J, Tsolaki M, Gavalas E, Boziki M, Zavos C, Karatzoglou P, et al. Relationship between Helicobacter pylori infection and Alzheimer disease. Neurology 2006;66(March (6)):938–40. [12] Gavalas E, Kountouras J, Deretzi G, Boziki M, Grigoriadis N, Zavos C, et al. Helicobacter pylori and multiple sclerosis. J Neuroimmunol 2007;188(August (1–2)):187–9.
Jannis Kountouras ∗ Christos Zavos Georgia Deretzi Emmanuel Gavalas Stergios Polyzos Elizabeth Vardaka Constantinos Kountouras Evangelia Giartza-Taxidou Evangelos Koutlas Iakovos Tsiptsios Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece ∗ Corresponding
author at: Gastroenterologist, 8 Fanariou St, Byzantio, 551 33, Thessaloniki, Macedonia, Greece. Tel.: +30 2310 892238; fax: +30 2310 992794. E-mail addresses: [email protected], [email protected], [email protected] (J. Kountouras) 22 December 2009 Available online 12 February 2011 doi:10.1016/j.clineuro.2011.01.004
0303-8467/$ – see front matter © 2011 Elsevier B.V. All rights reserved.
Letters to the Editor / Clinical Neurology and Neurosurgery 113 (2011) 520–521
‘Posterior pusher syndrome’ or ‘psychomotor disadaptation syndrome’?夽 Keywords: Pusher behavior Posterior pusher syndrome Psychomotor disadaptation syndrome
Dear Editor, We read with great interest the case report recently published in the journal by Cardoen and Santens on the “posterior pusher syndrome” [1]. They reported two patients with a marked disturbance of body orientation in the sagittal plane with backward imbalance, posterior tilt and an active resistance to forward pulling or pushing. One 82-year old patient had history of a left frontal parafalcine meningioma and hydrocephalus with recurrent falling, decrease of cognitive abilities, frontal release sings, hypertonia of the four limbs, without asymmetrical findings on neurological examination; and one 65-year-old patient with a history of transient ischemic attacks (TIA), a large hypothalamic lymphoma and post-irradiation encephalopathy that was admitted with gait difficulties and tendency to fall backwards, apathy, frontal release sings and clear hypertonia in the four limbs [1]. By the description of Cardoen and Santens [1], it is not clear if the ‘posterior pusher syndrome’ is a new described neurological behavior or a severe reactive/protective postural reaction due to the already described ‘psychomotor disadaptation syndrome’ (PDS). The PDS, which was first described by Gaudet and colleagues in 1986, is a geriatric syndrome characterized by postural impairments, including ‘retropulsion’ or ‘backwards disequilibrium’ (BD), neurological signs as axial and limb rigidity and psychological disorders as fear of falling and phobia of the upright position [2–4]. Its severe presentation is also called ‘post fall syndrome’. According to Mourey et al. [3], the backward disequilibrium is a result of a backward projection of the center-of-mass to the posterior boundary of the base of support and is characterized as follows: “the backward position of the trunk while sitting, and a tendency to fall backward in the standing position. In severe cases, we sometimes observe a failure to reach an erect position because the center-of mass is projected outside the base of support. When the standing position is successful, forward trunk bending, knee flexion, and toe clenching can be observed as adaptive patterns that allow the patient to maintain the center-of-mass in the base of support. In the sitting position, the buttocks are commonly located on the anterior side of the seat while the trunk rests on the back of the armchair in patients without severe kyphosis. In severe cases, the transfer from sitting to standing is impossible without assistance because the subject cannot bend the trunk forward.”[3]. Moreover, patients with PDS have an increase in muscle tone that counteracts movement execution. This hypertonia is called reactional or paratonia because it appears when a limb is mobilized passively by an investigator, and it decreases when confidence and relaxation are obtained [3]. Patients with PDS also have an alteration in postural reactions. When the examiner gives a slight push applied to the trunk, in severe cases, patients fall with no protective reactions of the arms [2,3]. Other features that suggest against the existence of a newly described ‘posterior pusher syndrome’ is that all the pusher
patients reported in the literature so far had an acute event and unilateral neurological deficits [5–7]. Besides the TIA that was not described as time-related to the ‘posterior pusher syndrome’, the patients reported by Cardoen and Santens had no acute encephalic lesion nor asymmetrical findings on neurological testing. Adversely, the PDS may be associated with several chronic diseases such as lymphomas of nervous system, multiple system atrophy, meningoencephalitis, normal pressure hydrocephalus, and depression [2–4]. In addition, the authors pointed out that the absence of patients’ attempts to correct their posterior tilt and to have protective actions when they fell backwards argue against the possibility of other underlying disorders different from pusher syndrome [1]. In contrast, we find this lack of reactive and protective reaction another feature that can argue in favor to the PDS as described above. Moreover, both patients presented frontal release sings that may be accompanied by paratonia. An interesting aspect recently published is that the backward disequilibrium is associated with a dysfunction of postural vertical perception [4] as occurs in pushing behavior [8,9]. Manckoundia et al. [4] found a close correlation between backward disequilibrium scale and the backward tilt of the subjective postural vertical, although the relatively low number of subjects. Future studies will be necessary to clarify the relationship between the pusher behavior with the backward disequilibrium. References [1] Cardoen S, Santens P. Posterior pusher syndrome: a report of two cases. Clin Neurol Neurosurg 2010;112(4):347–9. [2] Pfitzenmeyer P, Mourey F, Tavernier B, Camus A. Psychomotor desadaptation syndrome. Arch Gerontol Geriatr 1999;28(3):217–25. [3] Mourey F, Manckoundia P, Martin-Arveux I, Tavernier-Vidal B, Pfitzenmeyer P. Psychomotor disadaptation syndrome. A new clinical entity in geriatric patients. Geriatrics 2004;59(5):20–4. [4] Manckoundia P, Mourey F, Pfitzenmeyer P, Van Hoecke J, Perennou D. Is backward disequilibrium in the elderly caused by an abnormal perception of verticality? A pilot study. Clin Neurophysiol 2007;118(4):786–93. [5] Santos-Pontelli TE, Pontes-Neto OM, Colafemina JF, de Araujo DB, Santos AC, Leite JP. Contraversive pushing in non-stroke patients. J Neurol 2004;251(11):1324–8. [6] Paci M, Nannetti L. The pusher syndrome in a patient with cerebellar infarction. Physiother Res Int 2005;10(3):176–7. [7] Karnath HO. Pusher syndrome—a frequent but little-known disturbance of body orientation perception. J Neurol 2007;254(4):415–24. [8] Karnath HO, Ferber S, Dichgans J. The origin of contraversive pushing: evidence for a second graviceptive system in humans. Neurology 2000;55(9):1298–304. [9] Perennou DA, Mazibrada G, Chauvineau V, Greenwood R, Rothwell J, Gresty MA, et al. Lateropulsion, pushing and verticality perception in hemisphere stroke: a causal relationship? Brain 2008;131(Pt 9):2401–13.
T.E.G. Santos-Pontelli O.M. Pontes-Neto J.P. Leite ∗ Department of Neurology, University of São Paulo, School of Medicine at Ribeirão Preto, Brazil ∗ Corresponding
author at: Campus Universitário, Ribeirão Preto, CEP 14049-900, Brazil. Tel.: +55 16 3602 2556; fax: +55 16 3633 0760. E-mail address: [email protected] (J.P. Leite) 20 April 2010 Available online 12 February 2011
doi:10.1016/j.clineuro.2011.01.012 夽 J.P.Leite, O.M. Pontes-Neto and T.E.G. Santos-Pontelli are supported by Fundac¸ão de Apoio a Pesquisa do Estado de São Paulo (FAPESP) and Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq).
521