Case Reports / Journal of Clinical Neuroscience 21 (2014) 1271–1273 [2] Uncini A. A common mechanism and a new categorization for anti-ganglioside antibody-mediated neuropathies. Exp Neurol 2012;235:513–6. [3] Uncini A, Susuki K, Yuki N. Nodo-paranodopathy: beyond the demyelinating and axonal classification in anti-ganglioside antibody-mediated neuropathies. Clin Neurophysiol 2013;124:1928–34. [4] Kuwabara S, Yuki N, Koga M, et al. IgG anti-GM1 antibody is associated with reversible conduction failure and axonal degeneration in Guillain-Barré syndrome. Ann Neurol 1998;44:202–8. [5] Capasso M, Notturno F, Manzoli C, et al. Involvement of sensory fibres in axonal subtypes of Guillain-Barre syndrome. J Neurol Neurosurg Psychiatry 2011;82:664–70. [6] Umapathi T, Tan EY, Kokubun N, et al. Non-demyelinating, reversible conduction failure in Fisher syndrome and related disorders. J Neurol Neurosurg Psychiatry 2012;83:941–8. [7] Capasso M, Notturno F, Manzoli C, et al. Reversible conduction failure in pharyngeal-cervical-brachial variant of Guillain-Barré syndrome. Muscle Nerve 2010;42:608–12.
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[8] Rajabally YA, Hassan-Smith G, Notturno F, et al. Motor and sensory conduction failure in overlap of Guillain-Barré and Miller Fisher syndrome: two simultaneous cases. J Neurol Sci 2011;303:35–8. [9] Chan YC, Ahmad A, Paliwal P, et al. Non-demyelinating, reversible conduction failure in a case of pharyngeal–cervical–brachial weakness overlapped by Fisher syndrome. J Neurol Sci 2012;321:103–6. [10] Nagashima T, Koga M, Odaka M, et al. Continuous spectrum of pharyngealcervical-brachial variant of Guillain-Barré syndrome. Arch Neurol 2007;64:1519–23. [11] Hiraga A, Kuwabara S, Ogawara K, et al. Patterns and serial changes in electrodiagnostic abnormalities of axonal Guillain-Barré syndrome. Neurology 2005;64:856–60. [12] Susuki K, Yuki N, Schafer DP, et al. Dysfunction of nodes of Ranvier: a mechanism for anti-ganglioside antibody-mediated neuropathies. Exp Neurol 2012;233:534–42. [13] Kiernan MC, Guglielmi JM, Kaji R, et al. Evidence for axonal membrane hyperpolarization in multifocal motor neuropathy with conduction block. Brain 2002;125:664–75.
http://dx.doi.org/10.1016/j.jocn.2013.10.022
Primary Hodgkin lymphoma of the central nervous system Nematullah Sharaf a, Bjorn Lobo b, Joung Lee b, Richard A. Prayson a,⇑ a b
Department of Anatomic Pathology, Cleveland Clinic Lerner College of Medicine, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA Department of Neurosurgery, Cleveland Clinic Lerner College of Medicine, Cleveland Clinic, Cleveland, OH, USA
a r t i c l e
i n f o
Article history: Received 28 August 2013 Accepted 30 October 2013
a b s t r a c t Primary involvement of the central nervous system by Hodgkin lymphoma is rare; most cases represent metastases. We report a primary Hodgkin lymphoma presenting in the cerebellum of a 77-year-old man and review the literature on primary Hodgkin lymphoma of the central nervous system. Ó 2014 Elsevier Ltd. All rights reserved.
Keywords: Brain tumor Central nervous system Cerebellum Epstein-Barr virus Primary Hodgkin lymphoma
1. Introduction Hodgkin lymphoma (HL) involvement in the central nervous system (CNS) is uncommon; only 0.02% of patients with HL have CNS involvement [1]. The majority of these cases represent metastatic involvement of the spine. HL confined to the CNS and presumed primary at that site is an even rarer occurrence with only exceptional cases reported in the literature [2]. We present a CNS HL arising in a 77-year-old man and presumed primary in the cerebellum. The literature on primary HL in the CNS is also reviewed. 2. Case report A 77-year-old man with a history of monoclonal paraproteinemia initially presented with increased right facial discomfort along with worsening imbalance and falls over the past 2 weeks. MRI study demonstrated a large enhancing juxtacortical mass in the inferior lateral left cerebellar hemisphere which measured 3.1 cm 2.1 cm 2.3 cm (Fig. 1) with significant fluid attenuated inversion recovery hyperintensity extending throughout the left cerebellum into the paramedian right cerebellar hemisphere and anteriorly in the left brachium pontis. The patient was started on steroids and underwent a left suboccipital craniectomy for resec⇑ Corresponding author. Tel.: +1 216 444 8805; fax: +1 216 445 3707. E-mail address: [email protected] (R.A. Prayson).
tion of the mass. A few weeks later, a positron emission topography–CT body scan with contrast revealed no systemic neoplasm. The patient received whole brain radiation (3600 cGy). There was no evidence of recurrent tumor at the most recent follow-up 7 months post-operatively. 3. Pathology Histologic sections from resected cerebellar tissue were marked by a diffuse inflammatory infiltrate with a vaguely nodular architecture and consisting of macrophages, plasma cells, eosinophils, neutrophils, lymphocytes and atypical lymphocytes. Focal areas containing large cells with multiple nuclear lobes and composed of pale chromatin, prominent eosinophilic nucleoli and moderate cytoplasm, consistent with Hodgkin Reed-Sternberg cells, were present (Fig. 2). The Reed-Sternberg cells demonstrated positive staining with antibodies to CD15 (1:40 dilution; Biogenex, Freemont, CA, USA), CD30 (1:10 dilution; DAKO, Carpinteria, CA, USA) (Fig. 3), PAX-5 (1:20 dilution; BD Transduction, San Jose, CA, USA), CD20 (1:25 dilution; DAKO), OCT-2 (1:200 dilution; Santa Cruz Biotechnology, Dallas, TX, USA) and fascin (1:50 dilution; DAKO). The atypical cells did not stain with antibodies to CD1a (prediluted; Serotec, Raleigh, NC, USA), CD138 (1:200 dilution; Biocare, Concord, CA, USA), myeloperoxidase (prediluted; Cell Marque, Rocklin, CA, USA), TdT (1:10 dilution; Supertech, Bethesda, MD, USA), muramidase (1:100 dilution; DAKO), cytokeratin CAM
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Case Reports / Journal of Clinical Neuroscience 21 (2014) 1271–1273
Fig. 1. Coronal (A) and axial (B) post-gadolinium contrasted T1-weighted MRI demonstrating a heterogeneously enhancing mass arising in the left cerebellar hemisphere and focally dural based. The tumor’s irregular margins and local parenchymal enhancement were consistent with brain invasion.
Fig. 2. Large atypical Reed-Sternberg cells were identified in a mixed inflammatory background (hematoxylin and eosin, original magnification 400).
Fig. 4. Reed-Sternberg cells stained positively for Epstein-Barr virus by chromogenic in situ hybridization (original magnification 400).
5.2 (1:10 dilution; Becton Dickinson, Franklin Lake, NJ, USA), cytokeratins AE1/3 (1:200 dilution; Millipore, Billerica, MD, USA), S-100 protein (1:800 dilution; DAKO), BOB-1 (1:100 dilution; Santa Cruz Biotechnology), CD45 (1:100 dilution; DAKO), ALK-1 (1:80 dilution; DAKO), CD5 (1:10 dilution; Biogenex), CD3 (prediluted; Ventana, Tuczon, AZ, USA), kappa (1:32000 dilution; DAKO), or lambda (1:64000 dilution; DAKO). Areas of geographic necrosis were present. The plasma cells which were present stained with both kappa and lambda antibodies. Chromogenic in situ hybridization for Epstein-Barr viral encoded RNA was positive in the large atypical cells (Fig. 4).
4. Discussion
Fig. 3. Reed-Sternberg cells demonstrated CD30 immunoreactivity (original magnification 400).
Cases of primary CNS HL are exceptionally rare. In a report by the German Hodgkin Study Group, 13,568 patients with untreated HL and 1300 patients with relapsed disease were examined for the presence of CNS involvement [1]. The reported results suggest that HL of the CNS has a frequency of less than 0.02% [1]. A recent review of primary CNS HL reported only 16 patients [2]. The average age of presentation was 59 years (range 34–
Case Reports / Journal of Clinical Neuroscience 21 (2014) 1273–1276
84 years). There was a slight male predominance in the reported patients (n = 10). All cases in which the subtype was reported (n = 6) were nodular sclerosis type [2]. Our patient is unusual in that he represents the first case of mixed cellularity HL presumably presenting as a primary CNS tumor to our knowledge. In regard to location, six out of 16 tumors presented in the cerebellum and six cases arose in various lobes [2]. Our patient’s tumor presented in the left cerebellum. The current patient demonstrated Epstein-Barr virus (EBV) positivity via in situ hybridization. Seven other patients in the literature were assessed for EBV association; two patients showed immunoreactivity for EBV latency-associated protein and four out of five patients showed positivity by in situ hybridization for EBV [2]. The most common treatment approaches have included radiation therapy, either localized or whole brain, after resection (n = 12) [2]. Three patients underwent chemotherapy treatment in conjunction with radiation therapy. In 90% of patients, there was no evidence of disease at follow-up (range 1 month–10 years; median 12 months). Only one recurrence has been reported at 14 months after combined chemotherapy treatment [2]. Our pa-
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tient received whole brain radiation following resection with no evidence of recurrent tumor at his 7 month follow-up. Due to differing prognosis and treatment, it is important to distinguish HL from other CNS lymphomas such as diffuse large B cell lymphoma, which account for the majority of primary CNS lymphomas. It is also important to ensure that there is no evidence of lymphoma elsewhere in the body.
Conflicts of Interest/Disclosures The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication. References [1] Re D, Fuchs M, Schober T, et al. CNS involvement in Hodgkin’s lymphoma. J Clin Oncol 2007;25:3182. [2] Kresak J, Nguyen J, Kondi W, et al. Primary Hodgkin lymphoma of the central nervous system: two case reports and review of the literature. Neuropathology 2013;33:658–62. http://dx.doi.org/10.1111/neup.12035.
http://dx.doi.org/10.1016/j.jocn.2013.10.034
Clinical presentation and treatment considerations of a ruptured posterior spinal artery pseudoaneurysm Donnie L. Bell a,1, Christopher J. Stapleton b,⇑,1, Anna R. Terry b, James R. Stone c, Christopher S. Ogilvy d a
Division of Interventional Neuroradiology/Endovascular Neurosurgery, Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, ACC-745, Boston, MA 02114, USA Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA d Division of Neurosurgery, Department of Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA b c
a r t i c l e
i n f o
Article history: Received 30 December 2013 Accepted 13 January 2014
Keywords: Endovascular neurosurgery Posterior spinal artery Pseudoaneurysm Spinal subarachnoid hemorrhage Vascular neurosurgery
a b s t r a c t Spinal artery pseudoaneurysms are rare vascular lesions with poorly defined natural history, diagnostic paradigms, and treatment strategies. We present a 68-year-old woman with severe back pain and left lower extremity weakness with spinal subarachnoid hemorrhage due to a ruptured T5 region posterior spinal artery pseudoaneurysm, and review issues related to radiologic diagnosis and endovascular and open neurosurgical interventions. Ó 2014 Elsevier Ltd. All rights reserved.
1. Introduction Spinal artery pseudoaneurysms are rare vascular lesions of the craniospinal axis typically caused by inflammatory vasculopathies, spondyloarthropathies, and trauma. Natural history data, diagnostic paradigms, and treatment strategies are poorly defined for these lesions, as only 10 patients with ruptured posterior spinal artery (PSA) aneurysms have been published to our knowledge [1,2]. We present a 68-year-old woman with increasingly severe back pain with left lower extremity weakness and paresthesias who was found to have thoracolumbar spinal subarachnoid hemorrhage
⇑ Corresponding author. Tel.: +1 617 726 2000. 1
E-mail address: [email protected] (C.J. Stapleton). These authors have contributed equally to the manuscript.
(SAH) due to a ruptured pseudoaneurysm of the PSA at the T5 level arising from a right T7 segmental artery. 2. Case report 2.1. History and examination A 68-year-old woman presented to her local emergency department with 10 days of severe, sharp low back pain that developed suddenly during physical exertion. Initial MRI of the thoracolumbar spine demonstrated a thoracic intradural lesion (Fig. 1A–C) and lumbar SAH (Fig. 1D–F). The patient was transferred to our institution, where her neurologic examination was notable for 4+/5 strength throughout the left lower extremity and diminished sensation to light touch along the left medial calf and foot. There was no clonus and her Babinski reflex was negative.
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[8] Rajabally YA, Hassan-Smith G, Notturno F, et al. Motor and sensory conduction failure in overlap of Guillain-Barré and Miller Fisher syndrome: two simultaneous cases. J Neurol Sci 2011;303:35–8. [9] Chan YC, Ahmad A, Paliwal P, et al. Non-demyelinating, reversible conduction failure in a case of pharyngeal–cervical–brachial weakness overlapped by Fisher syndrome. J Neurol Sci 2012;321:103–6. [10] Nagashima T, Koga M, Odaka M, et al. Continuous spectrum of pharyngealcervical-brachial variant of Guillain-Barré syndrome. Arch Neurol 2007;64:1519–23. [11] Hiraga A, Kuwabara S, Ogawara K, et al. Patterns and serial changes in electrodiagnostic abnormalities of axonal Guillain-Barré syndrome. Neurology 2005;64:856–60. [12] Susuki K, Yuki N, Schafer DP, et al. Dysfunction of nodes of Ranvier: a mechanism for anti-ganglioside antibody-mediated neuropathies. Exp Neurol 2012;233:534–42. [13] Kiernan MC, Guglielmi JM, Kaji R, et al. Evidence for axonal membrane hyperpolarization in multifocal motor neuropathy with conduction block. Brain 2002;125:664–75.
http://dx.doi.org/10.1016/j.jocn.2013.10.022
Primary Hodgkin lymphoma of the central nervous system Nematullah Sharaf a, Bjorn Lobo b, Joung Lee b, Richard A. Prayson a,⇑ a b
Department of Anatomic Pathology, Cleveland Clinic Lerner College of Medicine, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA Department of Neurosurgery, Cleveland Clinic Lerner College of Medicine, Cleveland Clinic, Cleveland, OH, USA
a r t i c l e
i n f o
Article history: Received 28 August 2013 Accepted 30 October 2013
a b s t r a c t Primary involvement of the central nervous system by Hodgkin lymphoma is rare; most cases represent metastases. We report a primary Hodgkin lymphoma presenting in the cerebellum of a 77-year-old man and review the literature on primary Hodgkin lymphoma of the central nervous system. Ó 2014 Elsevier Ltd. All rights reserved.
Keywords: Brain tumor Central nervous system Cerebellum Epstein-Barr virus Primary Hodgkin lymphoma
1. Introduction Hodgkin lymphoma (HL) involvement in the central nervous system (CNS) is uncommon; only 0.02% of patients with HL have CNS involvement [1]. The majority of these cases represent metastatic involvement of the spine. HL confined to the CNS and presumed primary at that site is an even rarer occurrence with only exceptional cases reported in the literature [2]. We present a CNS HL arising in a 77-year-old man and presumed primary in the cerebellum. The literature on primary HL in the CNS is also reviewed. 2. Case report A 77-year-old man with a history of monoclonal paraproteinemia initially presented with increased right facial discomfort along with worsening imbalance and falls over the past 2 weeks. MRI study demonstrated a large enhancing juxtacortical mass in the inferior lateral left cerebellar hemisphere which measured 3.1 cm 2.1 cm 2.3 cm (Fig. 1) with significant fluid attenuated inversion recovery hyperintensity extending throughout the left cerebellum into the paramedian right cerebellar hemisphere and anteriorly in the left brachium pontis. The patient was started on steroids and underwent a left suboccipital craniectomy for resec⇑ Corresponding author. Tel.: +1 216 444 8805; fax: +1 216 445 3707. E-mail address: [email protected] (R.A. Prayson).
tion of the mass. A few weeks later, a positron emission topography–CT body scan with contrast revealed no systemic neoplasm. The patient received whole brain radiation (3600 cGy). There was no evidence of recurrent tumor at the most recent follow-up 7 months post-operatively. 3. Pathology Histologic sections from resected cerebellar tissue were marked by a diffuse inflammatory infiltrate with a vaguely nodular architecture and consisting of macrophages, plasma cells, eosinophils, neutrophils, lymphocytes and atypical lymphocytes. Focal areas containing large cells with multiple nuclear lobes and composed of pale chromatin, prominent eosinophilic nucleoli and moderate cytoplasm, consistent with Hodgkin Reed-Sternberg cells, were present (Fig. 2). The Reed-Sternberg cells demonstrated positive staining with antibodies to CD15 (1:40 dilution; Biogenex, Freemont, CA, USA), CD30 (1:10 dilution; DAKO, Carpinteria, CA, USA) (Fig. 3), PAX-5 (1:20 dilution; BD Transduction, San Jose, CA, USA), CD20 (1:25 dilution; DAKO), OCT-2 (1:200 dilution; Santa Cruz Biotechnology, Dallas, TX, USA) and fascin (1:50 dilution; DAKO). The atypical cells did not stain with antibodies to CD1a (prediluted; Serotec, Raleigh, NC, USA), CD138 (1:200 dilution; Biocare, Concord, CA, USA), myeloperoxidase (prediluted; Cell Marque, Rocklin, CA, USA), TdT (1:10 dilution; Supertech, Bethesda, MD, USA), muramidase (1:100 dilution; DAKO), cytokeratin CAM
1272
Case Reports / Journal of Clinical Neuroscience 21 (2014) 1271–1273
Fig. 1. Coronal (A) and axial (B) post-gadolinium contrasted T1-weighted MRI demonstrating a heterogeneously enhancing mass arising in the left cerebellar hemisphere and focally dural based. The tumor’s irregular margins and local parenchymal enhancement were consistent with brain invasion.
Fig. 2. Large atypical Reed-Sternberg cells were identified in a mixed inflammatory background (hematoxylin and eosin, original magnification 400).
Fig. 4. Reed-Sternberg cells stained positively for Epstein-Barr virus by chromogenic in situ hybridization (original magnification 400).
5.2 (1:10 dilution; Becton Dickinson, Franklin Lake, NJ, USA), cytokeratins AE1/3 (1:200 dilution; Millipore, Billerica, MD, USA), S-100 protein (1:800 dilution; DAKO), BOB-1 (1:100 dilution; Santa Cruz Biotechnology), CD45 (1:100 dilution; DAKO), ALK-1 (1:80 dilution; DAKO), CD5 (1:10 dilution; Biogenex), CD3 (prediluted; Ventana, Tuczon, AZ, USA), kappa (1:32000 dilution; DAKO), or lambda (1:64000 dilution; DAKO). Areas of geographic necrosis were present. The plasma cells which were present stained with both kappa and lambda antibodies. Chromogenic in situ hybridization for Epstein-Barr viral encoded RNA was positive in the large atypical cells (Fig. 4).
4. Discussion
Fig. 3. Reed-Sternberg cells demonstrated CD30 immunoreactivity (original magnification 400).
Cases of primary CNS HL are exceptionally rare. In a report by the German Hodgkin Study Group, 13,568 patients with untreated HL and 1300 patients with relapsed disease were examined for the presence of CNS involvement [1]. The reported results suggest that HL of the CNS has a frequency of less than 0.02% [1]. A recent review of primary CNS HL reported only 16 patients [2]. The average age of presentation was 59 years (range 34–
Case Reports / Journal of Clinical Neuroscience 21 (2014) 1273–1276
84 years). There was a slight male predominance in the reported patients (n = 10). All cases in which the subtype was reported (n = 6) were nodular sclerosis type [2]. Our patient is unusual in that he represents the first case of mixed cellularity HL presumably presenting as a primary CNS tumor to our knowledge. In regard to location, six out of 16 tumors presented in the cerebellum and six cases arose in various lobes [2]. Our patient’s tumor presented in the left cerebellum. The current patient demonstrated Epstein-Barr virus (EBV) positivity via in situ hybridization. Seven other patients in the literature were assessed for EBV association; two patients showed immunoreactivity for EBV latency-associated protein and four out of five patients showed positivity by in situ hybridization for EBV [2]. The most common treatment approaches have included radiation therapy, either localized or whole brain, after resection (n = 12) [2]. Three patients underwent chemotherapy treatment in conjunction with radiation therapy. In 90% of patients, there was no evidence of disease at follow-up (range 1 month–10 years; median 12 months). Only one recurrence has been reported at 14 months after combined chemotherapy treatment [2]. Our pa-
1273
tient received whole brain radiation following resection with no evidence of recurrent tumor at his 7 month follow-up. Due to differing prognosis and treatment, it is important to distinguish HL from other CNS lymphomas such as diffuse large B cell lymphoma, which account for the majority of primary CNS lymphomas. It is also important to ensure that there is no evidence of lymphoma elsewhere in the body.
Conflicts of Interest/Disclosures The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication. References [1] Re D, Fuchs M, Schober T, et al. CNS involvement in Hodgkin’s lymphoma. J Clin Oncol 2007;25:3182. [2] Kresak J, Nguyen J, Kondi W, et al. Primary Hodgkin lymphoma of the central nervous system: two case reports and review of the literature. Neuropathology 2013;33:658–62. http://dx.doi.org/10.1111/neup.12035.
http://dx.doi.org/10.1016/j.jocn.2013.10.034
Clinical presentation and treatment considerations of a ruptured posterior spinal artery pseudoaneurysm Donnie L. Bell a,1, Christopher J. Stapleton b,⇑,1, Anna R. Terry b, James R. Stone c, Christopher S. Ogilvy d a
Division of Interventional Neuroradiology/Endovascular Neurosurgery, Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, ACC-745, Boston, MA 02114, USA Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA d Division of Neurosurgery, Department of Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA b c
a r t i c l e
i n f o
Article history: Received 30 December 2013 Accepted 13 January 2014
Keywords: Endovascular neurosurgery Posterior spinal artery Pseudoaneurysm Spinal subarachnoid hemorrhage Vascular neurosurgery
a b s t r a c t Spinal artery pseudoaneurysms are rare vascular lesions with poorly defined natural history, diagnostic paradigms, and treatment strategies. We present a 68-year-old woman with severe back pain and left lower extremity weakness with spinal subarachnoid hemorrhage due to a ruptured T5 region posterior spinal artery pseudoaneurysm, and review issues related to radiologic diagnosis and endovascular and open neurosurgical interventions. Ó 2014 Elsevier Ltd. All rights reserved.
1. Introduction Spinal artery pseudoaneurysms are rare vascular lesions of the craniospinal axis typically caused by inflammatory vasculopathies, spondyloarthropathies, and trauma. Natural history data, diagnostic paradigms, and treatment strategies are poorly defined for these lesions, as only 10 patients with ruptured posterior spinal artery (PSA) aneurysms have been published to our knowledge [1,2]. We present a 68-year-old woman with increasingly severe back pain with left lower extremity weakness and paresthesias who was found to have thoracolumbar spinal subarachnoid hemorrhage
⇑ Corresponding author. Tel.: +1 617 726 2000. 1
E-mail address: [email protected] (C.J. Stapleton). These authors have contributed equally to the manuscript.
(SAH) due to a ruptured pseudoaneurysm of the PSA at the T5 level arising from a right T7 segmental artery. 2. Case report 2.1. History and examination A 68-year-old woman presented to her local emergency department with 10 days of severe, sharp low back pain that developed suddenly during physical exertion. Initial MRI of the thoracolumbar spine demonstrated a thoracic intradural lesion (Fig. 1A–C) and lumbar SAH (Fig. 1D–F). The patient was transferred to our institution, where her neurologic examination was notable for 4+/5 strength throughout the left lower extremity and diminished sensation to light touch along the left medial calf and foot. There was no clonus and her Babinski reflex was negative.
