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4. Iida H, Yamamuro T. Kinetic analysis of the centre of gravity of the human body in normal and pathological gaits. J Biomech 1987;20:987‑95. 5. Gerschlager W, Münchau A, Katzenschlager R, Brown P, Rothwell JC, Quinn N, et al. Natural history and syndromic associations of orthostatic tremor: A review of 41 patients. Mov Disord 2004;19:788‑95. b
a
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c
d
Figure 1: Polymyographic recordings: Channels are right-sided biceps brachii, forearm flexor muscle, forearm extensor muscle, rectus femoris, anterior tibialis and gastrocnemius respectively. (a) A 10 Hz postural tremor of the upper extremity with no lower extremity tremor during sitting (sensitivity 200 µV/div, 0.1 ms/div). (b) A 16 Hz tremor over the rectus femoris, anterior tibialis, gastrocnemius muscles during standing (sensitivity 200 µV/div, 0.1 ms/div). A very high frequency tremor also appears on the upper extremity.(c) A 16 Hz tremor over lower extremity muscles similar to the Figure b, but this figure shows a longer period due to longer sweep time (sensitivity 200 µV/div, 0.5 ms/div). (d) Disappearance of high frequency tremor during swing phase of gait and its reappearance during stance phase with sweep time similar to the Figure c (sensitivity 200 µV/div, 0.5 ms/div)
the frontal plain. Unfortunately, this compensatory mechanism persists between 6 months to 3 years after surgery.[4] Because the trunk compensatory strategy causes a mechanical disadvantage with increased energy demand during walking, [2,3] the additional exertion can produce extra tremors. The 10 Hz postural tremor observed during sitting is most likely a concomitant essential tremor. The co‑existence of OT and essential tremor (ET) has been well documented.[5] Patients with OT should be informed of the possible worsening of their symptoms, especially after surgeries that may impact their balance.
Philip B. Adebayo1,2, Aysegul Gunduz1, Meral E. Kiziltan1, Guneş Kızıltan1 1
Department of Neurology, Cerrahpasa School of Medicine, Istanbul University, Istanbul, Turkey, 2Department of Medicine, Neurology Unit, Ladoke Akintola University of Technology, Ogbomoso, Nigeria E‑mail: [email protected]
References 1.
Wu YR, Ashby P, Lang AE. Orthostatic tremor arises from an oscillator in the posterior fossa. Mov Disord 2001;16:272‑9. 2. Nankaku M, Tsuboyama T, Kakinoki R, Kawanabe K, Kanzaki H, Mito Y, et al. Gait analysis of patients in early stages after total hip athroplasty: Effect of lateral trunk displacmemnt on walking efficiency. J Orthop Sci 2007;12:550‑4. 3. Nallegowda M, Singh U, Bhan S, Wadhwa S, Handa G, Dwivedi SN. Balance and gait in total hip replacement: A pilot study. Am J Phys Med Rehabil 2003;82:669‑77. Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
DOI: 10.4103/0028-3886.141280
Received: 18-07-2014 Review completed: 29-07-2014 Accepted: 24-08-2014
Diffusion MRI in transient global amnesia Sir, Transient global amnesia (TGA) is clinically defined as sudden onset anterograde amnesia with preserved alertness, attention, and personal identity, which occurs during a period of not more than 24 hours with no long‑term sequelae.[1] The precise etiology of TGA is unknown. Diffusion‑weighted imaging (DWI) magnetic resonance imaging (MRI) may help in the diagnosis of this condition. A 52‑year‑old male presented with acute confusion and memory disturbance. No history of any similar episodes or any medical illness in the past was noted; the family history was negative. Neurological examination showed awake, alert, and well‑oriented person with short‑term memory loss and long‑term memory was intact, was able to remember family members. He kept asking repetitive questions. He had no active hallucinations or delusions, and no speech disturbances or other deficits. The patient returned to baseline normal neurologic state over the course of a 24‑hour hospitalized observation period and has not had any further recurrences. Blood biochemistry and complete blood picture were normal. MRI brain showed no abnormality in conventional T1/T2‑weighted and FLAIR (Fluid attenuated inversion recovery) sequences [Figure 1a‑d]. However, DWI showed focal punctate area of restricted diffusion in left hippocampus [Figure 1e and g white arrow]. Corresponding ADC showed hypointense [Figure 1f and h white arrow] 457
[Downloaded free from http://www.neurologyindia.com on Thursday, September 25, 2014, IP: 202.177.173.189] || Click here to download free Android application this journal Letters to Editor
a
b
e
f
c
d
g
h
Figure 1: Axial Magnetic Resonance (MR) images performed on 1.5 T shows normal FLAIR (a and b) and T2 weighted images (c and d) which shows no abnormality. Diffusion weighted images (e and g) and ADC mapping (f and h) shows focal punctate area of restricted diffusion in the left hippocampus appearing bright on the DWI series (white arrow F) and appearing hypointense on the ADC mapping (white arrow H)
area in the region of hyperintensity in DWI. The MR angiography was normal. Electroencephalogram and color‑coded carotid Doppler were normal. Although not the first to report TGA, Fisher and Adams[2] were credited with naming the syndrome and monographing it in detail. The etiology and pathogenesis of TGA are uncertain, although several different causes suggested include: Ischemia, migraine, epileptic seizure, venous congestion, and psychological disturbances.[3] In addition, TGA is a well‑recognized complication of cerebral angiography with ionic or nonionic contrast agents.[4] Recent studies have indicated the presence of focal hyperintensities involving the hippocampus in TGA. The typical findings on MRI include hyperintensity signal at the hippocampal area on DWI with corresponding hypointensity on ADC, which support of ischemic etiology.[5,6] Transient ischemic changes and epileptic events are two major mechanisms proposed etiologies of TGA.[5] Hypothesis of transient cerebral ischemia, especially the hippocampus, is supported by the modern imaging studies.[6] Selective ischemic involvement of hippocampus is not clear. This may be related to the 458
vulnerability of CA‑1 (cornu ammonis) of hippocampus (Sommer sector) to ischemic insult. [6] Some triggers in patients with TGA include exertion, emotional stress, or sexual intercourse. These observations lead to the hypothesis of venous congestion mediated by intracranial venous reflux. The intracranial venous reflux may be caused by the valve incompetence of the internal jugular vein or the left brachiocephalic vein occlusion after a precipitating factor such as Valsalva maneuver.[7,8] The lesions detected by DWI are small and punctate (1-3 mm) and located within the lateral portion of the hippocampus. [9,10] The reported frequency of DWI range between 0% and 84%.[9,11] This discrepancy in the reported rates appears to be related to the timing of imaging from symptoms onset.[9] The combined use of a high b‑value (b = 2000) and thin section thickness (3 mm) is preferred for detection of lesions in TGA. If no lesion is detected on initial DWI, especially if performed within several hours of symptom onset, follow‑up DWI after several days is recommended.[12] To summarize, TGA is an important cause of acute transient anterograde amnesia. The characteristic Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
[Downloaded free from http://www.neurologyindia.com on Thursday, September 25, 2014, IP: 202.177.173.189] || Click here to download free Android application for this journal Letters to Editor
findings on DWI support the clinical diagnosis of TGA. It is important to diagnose this condition as it has benign outcome and treatment is generally not required, and the condition usually does not recur.
Harikiran Reddy, Keerthiraj Bele1, Z.K. Misri2, Santosh P.V. Rai Departments of Radiodiagnosis, 1Neuroradiology, and 2 Neurology, Kasturba Medical College, Manipal University, Mangalore, Karnataka, India E‑mail: [email protected]
References 1.
Hodges JR, Warlow CP. Syndromes of transient amnesia: Towards a classification-A study of 153 cases. J Neurol Neurosurg Psychiatry 1990;53:834‑43. 2. Fisher CM, Adams RD. Transient global amnesia. Acta Neurol Scand 1964;40:1‑83. 3. Sander K, Sander D. New insights into transient global amnesia: Recent imaging and clinical findings. Lancet Neurol 2005;4:437‑44. 4. Schamschula RG, Soo MY. Transient global amnesia following cerebral angiography with non‑ionic contrast medium. Australas Radiol 1994;38:196‑8. 5. Ay H, Furie KL, Yamada K, Koroshetz WJ. Diffusion‑weighted MRI characterizes the ischemic lesion in transient global amnesia. Neurology 1998;51:901‑3. 6. Bartsch T, Alfke K, Deuschl G, Jansen O. Evolution of hippocampal CA‑1 diffusion lesions in transient global amnesia. Ann Neurol 2007;62:475‑80. 7. Sander D, Winbeck K, Etgen T, Knapp R, Klingehlofer J, Conrad B. Disturbance of venous flow patterns in patients with transient global amnesia. Lancet 2000;356:1982‑4. 8. Chung CP, Hsu HY, Chao AC, Chang FC, Sheng WY, Hu HH. Detection of intracranial venous reflux in patients of transient global amnesia. Neurology 2006;66:1873‑7. 9. Sedlaczek O, Hirsch JG, Grips E, Peters CN, Gass A, Worhle J, et al. Detection of delayed focal MR changes in the lateral hippocampus in transient global amnesia. Neurology 2004;62:2165‑70. 10. Bartsch T, Alfke K, Stingele R, Rohr A, Feritaq‑Wolf S, Jansen O, et al. Selective affection of hippocampal CA‑1 neurons in patients with transient global amnesia without long‑term sequelae. Brain 2006;129:2874‑84. 11. Winbeck K, Etgen T, von Einsiedel HG, Rottinger M, Sander D. DWI in transient global amnesia and TIA: Proposal for an ischaemic origin of TGA. J Neurol Neurosurg Psychiatry 2005;76:438‑41. 12. Weon YC, Kim JH, Lee JS, Kim SY. Optimal diffusion‑weighted imaging protocol for lesion detection in transient global amnesia. AJNR Am J Neuroradiol 2008;29:1324‑8.
Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.141283
Received: 06-08-2014 Review completed: 09-08-2014 Accepted: 24-08-2014
Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
Malignant infiltration of peripheral nerves: As initial presenting manifestation of lymphoreticular malignancies Sir, Neurologic complications in patients with cancer account for 20-25% of cases. Most often the peripheral nervous system (PNS) in patients with cancer is related to the adverse effects of chemotherapy. [1] Rarely PNS involvement may be due to infiltration, invasion and compression of nerves, particularly in leukemia (neuroleukemiosis) and lymphoma (neurolymphomatosis), and multiple myeloma (MM).[2] Diagnosis of such complications requires a high index of suspicion and is based on clinical, imaging as well as pathological studies obtained from nerves or the extraneural tissue and CSF.[3] This report presents three unusual patients in whom the initial manifestation was infiltrative peripheral neuropathy. The clinical characteristic and the associated malignancy are given in Table 1. Malignant cell infiltration of peripheral nerve associated with lymphoproliferative malignancies are exceedingly rare and may rarely be the first manifestation or the sole relapse site of the cancer. [2,3] There is limited information available on the mode of presentation, clinical course, diagnostic yield of various procedures, and response to therapy in patients with malignant cell infiltrative peripheral neuropathy. Lack of awareness of the condition may contribute to a diagnostic delay. [4] In published reports patients developed leukemic infiltration of peripheral nerves, while in remission. [2] Infiltrative peripheral neuropathy as the presenting feature of leukemia as seen in case 1 and 2 in this series is even rarer. Recognition of such presentation is important because exclusion of leukemia or hematologic malignancies is not usually part of the diagnostic algorithm of peripheral neuropathy. The most distinctive pattern of neuropathy in MM unrelated to therapy is a sensory‑motor and autonomic neuropathy due to light chain amyloidosis. Malignant cell infiltration of peripheral nerves can herald a relapse in a MM patients considered to be in full remission.[5] Early recognition and treatment of this rare neurologic manifestation cancer may improve outcome. Magnetic resonance neurography and positron emission tomography scan may provide a clue to the possibility of malignant cell infiltration of peripheral nerves. Cerebrospinal fluid shows
459
Copyright of Neurology India is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
4. Iida H, Yamamuro T. Kinetic analysis of the centre of gravity of the human body in normal and pathological gaits. J Biomech 1987;20:987‑95. 5. Gerschlager W, Münchau A, Katzenschlager R, Brown P, Rothwell JC, Quinn N, et al. Natural history and syndromic associations of orthostatic tremor: A review of 41 patients. Mov Disord 2004;19:788‑95. b
a
Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: ***
c
d
Figure 1: Polymyographic recordings: Channels are right-sided biceps brachii, forearm flexor muscle, forearm extensor muscle, rectus femoris, anterior tibialis and gastrocnemius respectively. (a) A 10 Hz postural tremor of the upper extremity with no lower extremity tremor during sitting (sensitivity 200 µV/div, 0.1 ms/div). (b) A 16 Hz tremor over the rectus femoris, anterior tibialis, gastrocnemius muscles during standing (sensitivity 200 µV/div, 0.1 ms/div). A very high frequency tremor also appears on the upper extremity.(c) A 16 Hz tremor over lower extremity muscles similar to the Figure b, but this figure shows a longer period due to longer sweep time (sensitivity 200 µV/div, 0.5 ms/div). (d) Disappearance of high frequency tremor during swing phase of gait and its reappearance during stance phase with sweep time similar to the Figure c (sensitivity 200 µV/div, 0.5 ms/div)
the frontal plain. Unfortunately, this compensatory mechanism persists between 6 months to 3 years after surgery.[4] Because the trunk compensatory strategy causes a mechanical disadvantage with increased energy demand during walking, [2,3] the additional exertion can produce extra tremors. The 10 Hz postural tremor observed during sitting is most likely a concomitant essential tremor. The co‑existence of OT and essential tremor (ET) has been well documented.[5] Patients with OT should be informed of the possible worsening of their symptoms, especially after surgeries that may impact their balance.
Philip B. Adebayo1,2, Aysegul Gunduz1, Meral E. Kiziltan1, Guneş Kızıltan1 1
Department of Neurology, Cerrahpasa School of Medicine, Istanbul University, Istanbul, Turkey, 2Department of Medicine, Neurology Unit, Ladoke Akintola University of Technology, Ogbomoso, Nigeria E‑mail: [email protected]
References 1.
Wu YR, Ashby P, Lang AE. Orthostatic tremor arises from an oscillator in the posterior fossa. Mov Disord 2001;16:272‑9. 2. Nankaku M, Tsuboyama T, Kakinoki R, Kawanabe K, Kanzaki H, Mito Y, et al. Gait analysis of patients in early stages after total hip athroplasty: Effect of lateral trunk displacmemnt on walking efficiency. J Orthop Sci 2007;12:550‑4. 3. Nallegowda M, Singh U, Bhan S, Wadhwa S, Handa G, Dwivedi SN. Balance and gait in total hip replacement: A pilot study. Am J Phys Med Rehabil 2003;82:669‑77. Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
DOI: 10.4103/0028-3886.141280
Received: 18-07-2014 Review completed: 29-07-2014 Accepted: 24-08-2014
Diffusion MRI in transient global amnesia Sir, Transient global amnesia (TGA) is clinically defined as sudden onset anterograde amnesia with preserved alertness, attention, and personal identity, which occurs during a period of not more than 24 hours with no long‑term sequelae.[1] The precise etiology of TGA is unknown. Diffusion‑weighted imaging (DWI) magnetic resonance imaging (MRI) may help in the diagnosis of this condition. A 52‑year‑old male presented with acute confusion and memory disturbance. No history of any similar episodes or any medical illness in the past was noted; the family history was negative. Neurological examination showed awake, alert, and well‑oriented person with short‑term memory loss and long‑term memory was intact, was able to remember family members. He kept asking repetitive questions. He had no active hallucinations or delusions, and no speech disturbances or other deficits. The patient returned to baseline normal neurologic state over the course of a 24‑hour hospitalized observation period and has not had any further recurrences. Blood biochemistry and complete blood picture were normal. MRI brain showed no abnormality in conventional T1/T2‑weighted and FLAIR (Fluid attenuated inversion recovery) sequences [Figure 1a‑d]. However, DWI showed focal punctate area of restricted diffusion in left hippocampus [Figure 1e and g white arrow]. Corresponding ADC showed hypointense [Figure 1f and h white arrow] 457
[Downloaded free from http://www.neurologyindia.com on Thursday, September 25, 2014, IP: 202.177.173.189] || Click here to download free Android application this journal Letters to Editor
a
b
e
f
c
d
g
h
Figure 1: Axial Magnetic Resonance (MR) images performed on 1.5 T shows normal FLAIR (a and b) and T2 weighted images (c and d) which shows no abnormality. Diffusion weighted images (e and g) and ADC mapping (f and h) shows focal punctate area of restricted diffusion in the left hippocampus appearing bright on the DWI series (white arrow F) and appearing hypointense on the ADC mapping (white arrow H)
area in the region of hyperintensity in DWI. The MR angiography was normal. Electroencephalogram and color‑coded carotid Doppler were normal. Although not the first to report TGA, Fisher and Adams[2] were credited with naming the syndrome and monographing it in detail. The etiology and pathogenesis of TGA are uncertain, although several different causes suggested include: Ischemia, migraine, epileptic seizure, venous congestion, and psychological disturbances.[3] In addition, TGA is a well‑recognized complication of cerebral angiography with ionic or nonionic contrast agents.[4] Recent studies have indicated the presence of focal hyperintensities involving the hippocampus in TGA. The typical findings on MRI include hyperintensity signal at the hippocampal area on DWI with corresponding hypointensity on ADC, which support of ischemic etiology.[5,6] Transient ischemic changes and epileptic events are two major mechanisms proposed etiologies of TGA.[5] Hypothesis of transient cerebral ischemia, especially the hippocampus, is supported by the modern imaging studies.[6] Selective ischemic involvement of hippocampus is not clear. This may be related to the 458
vulnerability of CA‑1 (cornu ammonis) of hippocampus (Sommer sector) to ischemic insult. [6] Some triggers in patients with TGA include exertion, emotional stress, or sexual intercourse. These observations lead to the hypothesis of venous congestion mediated by intracranial venous reflux. The intracranial venous reflux may be caused by the valve incompetence of the internal jugular vein or the left brachiocephalic vein occlusion after a precipitating factor such as Valsalva maneuver.[7,8] The lesions detected by DWI are small and punctate (1-3 mm) and located within the lateral portion of the hippocampus. [9,10] The reported frequency of DWI range between 0% and 84%.[9,11] This discrepancy in the reported rates appears to be related to the timing of imaging from symptoms onset.[9] The combined use of a high b‑value (b = 2000) and thin section thickness (3 mm) is preferred for detection of lesions in TGA. If no lesion is detected on initial DWI, especially if performed within several hours of symptom onset, follow‑up DWI after several days is recommended.[12] To summarize, TGA is an important cause of acute transient anterograde amnesia. The characteristic Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
[Downloaded free from http://www.neurologyindia.com on Thursday, September 25, 2014, IP: 202.177.173.189] || Click here to download free Android application for this journal Letters to Editor
findings on DWI support the clinical diagnosis of TGA. It is important to diagnose this condition as it has benign outcome and treatment is generally not required, and the condition usually does not recur.
Harikiran Reddy, Keerthiraj Bele1, Z.K. Misri2, Santosh P.V. Rai Departments of Radiodiagnosis, 1Neuroradiology, and 2 Neurology, Kasturba Medical College, Manipal University, Mangalore, Karnataka, India E‑mail: [email protected]
References 1.
Hodges JR, Warlow CP. Syndromes of transient amnesia: Towards a classification-A study of 153 cases. J Neurol Neurosurg Psychiatry 1990;53:834‑43. 2. Fisher CM, Adams RD. Transient global amnesia. Acta Neurol Scand 1964;40:1‑83. 3. Sander K, Sander D. New insights into transient global amnesia: Recent imaging and clinical findings. Lancet Neurol 2005;4:437‑44. 4. Schamschula RG, Soo MY. Transient global amnesia following cerebral angiography with non‑ionic contrast medium. Australas Radiol 1994;38:196‑8. 5. Ay H, Furie KL, Yamada K, Koroshetz WJ. Diffusion‑weighted MRI characterizes the ischemic lesion in transient global amnesia. Neurology 1998;51:901‑3. 6. Bartsch T, Alfke K, Deuschl G, Jansen O. Evolution of hippocampal CA‑1 diffusion lesions in transient global amnesia. Ann Neurol 2007;62:475‑80. 7. Sander D, Winbeck K, Etgen T, Knapp R, Klingehlofer J, Conrad B. Disturbance of venous flow patterns in patients with transient global amnesia. Lancet 2000;356:1982‑4. 8. Chung CP, Hsu HY, Chao AC, Chang FC, Sheng WY, Hu HH. Detection of intracranial venous reflux in patients of transient global amnesia. Neurology 2006;66:1873‑7. 9. Sedlaczek O, Hirsch JG, Grips E, Peters CN, Gass A, Worhle J, et al. Detection of delayed focal MR changes in the lateral hippocampus in transient global amnesia. Neurology 2004;62:2165‑70. 10. Bartsch T, Alfke K, Stingele R, Rohr A, Feritaq‑Wolf S, Jansen O, et al. Selective affection of hippocampal CA‑1 neurons in patients with transient global amnesia without long‑term sequelae. Brain 2006;129:2874‑84. 11. Winbeck K, Etgen T, von Einsiedel HG, Rottinger M, Sander D. DWI in transient global amnesia and TIA: Proposal for an ischaemic origin of TGA. J Neurol Neurosurg Psychiatry 2005;76:438‑41. 12. Weon YC, Kim JH, Lee JS, Kim SY. Optimal diffusion‑weighted imaging protocol for lesion detection in transient global amnesia. AJNR Am J Neuroradiol 2008;29:1324‑8.
Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.141283
Received: 06-08-2014 Review completed: 09-08-2014 Accepted: 24-08-2014
Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
Malignant infiltration of peripheral nerves: As initial presenting manifestation of lymphoreticular malignancies Sir, Neurologic complications in patients with cancer account for 20-25% of cases. Most often the peripheral nervous system (PNS) in patients with cancer is related to the adverse effects of chemotherapy. [1] Rarely PNS involvement may be due to infiltration, invasion and compression of nerves, particularly in leukemia (neuroleukemiosis) and lymphoma (neurolymphomatosis), and multiple myeloma (MM).[2] Diagnosis of such complications requires a high index of suspicion and is based on clinical, imaging as well as pathological studies obtained from nerves or the extraneural tissue and CSF.[3] This report presents three unusual patients in whom the initial manifestation was infiltrative peripheral neuropathy. The clinical characteristic and the associated malignancy are given in Table 1. Malignant cell infiltration of peripheral nerve associated with lymphoproliferative malignancies are exceedingly rare and may rarely be the first manifestation or the sole relapse site of the cancer. [2,3] There is limited information available on the mode of presentation, clinical course, diagnostic yield of various procedures, and response to therapy in patients with malignant cell infiltrative peripheral neuropathy. Lack of awareness of the condition may contribute to a diagnostic delay. [4] In published reports patients developed leukemic infiltration of peripheral nerves, while in remission. [2] Infiltrative peripheral neuropathy as the presenting feature of leukemia as seen in case 1 and 2 in this series is even rarer. Recognition of such presentation is important because exclusion of leukemia or hematologic malignancies is not usually part of the diagnostic algorithm of peripheral neuropathy. The most distinctive pattern of neuropathy in MM unrelated to therapy is a sensory‑motor and autonomic neuropathy due to light chain amyloidosis. Malignant cell infiltration of peripheral nerves can herald a relapse in a MM patients considered to be in full remission.[5] Early recognition and treatment of this rare neurologic manifestation cancer may improve outcome. Magnetic resonance neurography and positron emission tomography scan may provide a clue to the possibility of malignant cell infiltration of peripheral nerves. Cerebrospinal fluid shows
459
Copyright of Neurology India is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
