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Dystonia and tremor secondary to a pediatric thalamic stroke
Parkinsonism & Related Disorders Parkinsonism and Related Disorders 4 (1998) 119–122
Dystonia and tremor secondary to a pediatric thalamic stroke Federico Micheli a,*, Graciela Cerso´simo a, Claudio Palacios b, Marı´a Clara Scorticati a, Silvia Tenembaum b, Juan Trı´poli b a
Hospital de Clı´nicas ‘‘Jose´ de San Martin’’, U.B.A. Department of Neurology, Olleros 2240-1426, Buenos Aires, Argentina b Hospital Nacional de Pediatrı´a ‘‘Juan P. Garrahan’’, Department of Neurology, Buenos Aires, Argentina Received 15 May 1998; received in revised form 13 August 1998; accepted 31 August 1998
Abstract A previously healthy 10-year-old girl developed a right hemiparesis with sensory loss secondary to a posterolateral thalamic infarct. Despite improvement in strength, three weeks later a 4 Hz kinetic tremor appeared in the right hand accompanied by dystonia in the right upper and lower limbs. Basal ganglia vascular lesions are rare in childhood and movement disorders secondary to such lesions even more so. A thorough work-up failed to disclose the etiology. Our patient illustrates that dystonia and tremor secondary to posterolateral thalamic infarctions are also apt to occur in children and, unlike the adult picture, abnormal movements may develop very soon after the insult. 䉷 1998 Elsevier Science Ltd. All rights reserved. Keywords: Thalamus; Stroke; Dystonia; Tremor
1. Introduction Basal ganglia infarctions are very unusual in childhood and have been poorly described in the literature [1, 2]. Abnormal involuntary movements secondary to such lesions are even more uncommon although recently greater interest has been focused on these complications [3], which include: tremor, myoclonus, dystonia, chorea and asterixis subsequent to either thalamic infarctions or hemorrhages [4–7]. We here describe a 10-year-old girl who presented with unilateral postural and kinetic tremor associated with dystonic posturing contralateral to a posterior thalamic infarct.
2. Case report This previously healthy 10-year-old girl suddenly developed a right facio-brachio-crural hemiparesis with ipsilateral sensory loss, heralded by a 12-hour contralateral headache. Relevant personal history was limited to severe headaches over the last year, recurring monthly. Family history was unremarkable. On neurological examination, the patient was fully * Corresponding author. Fax: 00-54-811-3076; E-mail: fmicheli@ sminter.com.ar.
oriented to time and space. Ocular fundi were normal and visual fields full. She had a right central facial palsy and dysarthria while the remainder of the cranial nerve testing was normal. A moderate right hemiparesis with hemihyopaesthesia was evident. Otherwise, the neurological examination was unremarkable. The hemiparesis and sensory disturbance markedly improved over the next three days, but distal right limb abnormal movements gradually developed featuring postural and kinetic tremor in the right upper limb and dystonic posturing in the right arm and, to a lesser extent, posturing in the right foot. Rapid alternating right hand movements were affected by dystonic spasms in the flexor and extensors of the wrist. Surface EMG recordings from antagonist muscles in the right upper limb showed 4Hz rhythmic discharges associated with sustained cocontractions of antagonist muscles consistent with dystonia. A CT scan performed four days later disclosed a hypodense lesion in the left posterior thalamus with slight posterior capsule involvement. MRI confirmed the location of the lesion which was visualized as hypointense in T1-weighted images, slightly enhancing with gadolinium and hyperintense in T2 weighted images, but lacking mass effect, consistent with an ischemic infarction (Figs 1 and 2). An extensive laboratory work-up, including antinuclear antibodies, coagulation studies, blood and CSF lactate, proteins C and S assays and antiphospholipid antibodies, was normal, as also were a cerebral angiogram and echocardiography findings.
1353-8020/98/$ - see front matter 䉷 1998 Elsevier Science Ltd. All rights reserved. PII: S1353-802 0(98)00029-7
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Fig. 1. T2-weighted MRI showing a hyperintense lesion in the left thalamic posterolateral region.
3. Discussion Our patient suddenly developed a right hemiparesis with sensory loss, which resolved over a few days when severe, low frequency postural and action tremor in the right upper limb associated with mild dystonic posturing in both the right hand and foot became evident. Brain imaging revealed a posterolateral thalamic infarction, probably resulting from occlusion of the thalamogeniculate branches of the posterior cerebral artery [8]. Three clinical syndromes associated with posterolateral thalamic lesions have been recognized: pure sensory stroke, sensory motor stroke and the so-called thalamic syndrome of Dejerine and Roussy [9], on occasion featuring chorea or choreoathetosis secondary to the interruption of the extrapyramidal and cerebellar tracts synapsing in the lateral thalamus [8]. Several weeks after the injury, a slow frequency tremor at a rate of 3 to 5 Hz may appear [10]. Our patient presented two noteworthy features. On the one hand, the presence of a vascular lesion involving the posterior thalamus in a child and on the other the develop-
Fig. 2. The same lesion in T1-weighted images.
ment of unilateral postural and kinetic tremor as well as dystonia as its clinical expression. Despite a thorough work-up including fibrinogen, plasminogen, proteins C and S assays as well as urinary homocysteine, a collagenogram, an echocardiogram and a brain angiogram, no etiology was ascertained. However, the most frequent causes of cerebrovascular accidents in childhood such as congenital heart disease, falciform anemia, vasculitis and hypercoagulation states were ruled out [11– 15]. It could be speculated that our patient’s headaches were migraines that led to the thalamic infarction, but this seems unlikely since only migraine preceded by aura is currently recognized to cause stroke [16]. Mitochondrial DNA defects may present with stroke in young patients with estimates of frequency ranging from 0.5 to 8% [17]. A history of migraine is also common in such cases. Unfortunately blood molecular genetic analysis was not available for our patient. However, blood and CSF lactate was normal and there was no history of maternal neurological diseases. According to the literature, in 30% of cases, most likely including our patient, the cause of cerebrovascular accidents
F. Micheli et al. / Parkinsonism and Related Disorders 4 (1998) 119–122
in childhood remains unknown. Fortunately, the risk of recurrence in such cases is lower than in those with a discernible etiology [14]. Recently Miwa et al. [18] reported two patients with thalamic stroke who developed contralateral postural and resting tremor of the upper limb and they reviewed the literature. Both patients had lesions confined to the posterolateral thalamic region closely resembling our patient’s infarction. In adults, tremor has been reported as a late complication of stroke [18–26] appearing from 3 months to 3 years after the vascular insult, while age at onset ranges from 23 to 77 years. In such cases tremor has been ascribed to the development of postsynaptic supersensitivity or secondary reorganization of the involved pathways rather than to the lesion itself [27]. Only a single case of tremor due to infarction in the ventrolateral thalamus has been reported [28]. Instead, our case differed in two aspects from those previously described in that the patient was a child and that involuntary movements developed within a few days of the stroke, when the hemiparesis had already resolved. It has been speculated that tremor can be triggered either by interruption of ascending inputs to the posterolateral, rather than to the ventrolateral thalamic region, originating in the brainstem or cerebellum, or by destruction of the posterolateral thalamic neurons [18]. In addition, thalamic lesions have also been held responsible for symptomatic dystonia [29–31]. As in our patient, dystonia has been described in cases of posterolateral thalamic lesions [18, 19, 32] in which tremor is usually the predominant feature [33]. In such cases, dystonia is commonly restricted to the hand, and action and pastural myoclonic jerks are also frequently associated and may even be the most prominent feature [6]. In most cases, dystonia secondary to stroke develops promptly after the cerebrovascular episode [6]. In our patient, surface EMG was performed in order to rule out myoclonus and to confirm a 4-Hz tremor, as positive or negative myoclonus can mimic tremor [34]. As the sensory disturbances were very mild, the dystonia cannot be ascribed to deafferentation (pseudoathetosis). The clinical features in our patient closely resemble those reported in patients with either posterolateral [21, 28] or posterior [21, 28, 35] thalamic infarctions. Our case further supports the relevance of thalamic lesions in the generation of both tremor and dystonia and illustrates that movement disorders like these resulting from thalamic stroke are not unknown in children.
References [1] Brower MC, Rollins N, Roach ES. Basal ganglia and thalamic infarction in children. Arch Neurol. 1996;53:1252-1256. [2] Broderick J, Falbot T, Prenger E et al. Stroke in children within a major metropolitan area: the surprising importance of intracerebral hemorrhage. J Child Neurol 1993;8:250-255.
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[3] Lee MS, Marsden CD. Movement Disorders following lesions of the thalamus or subthalamic region. Mov Disord 1994;9:493-507. [4] Ghika J, Bogousslavsky J, Henderson J, Maeder P, Regli F. The jerky dystonic unsteady hand: a delayed motor syndrome in posterior thalamic infarctions. J Neurol 1994;241:537-542. [5] Rio J, Montalban J, Pujadas F, Alvarez Sabini, Roviar A, Codina A. Asterixis associated with anatomic cerebral lesions: a study of 45 cases. Acta Neurol Scand 1995;91:377-381. [6] Leherecy S, Vidailhet M, Dormont D et al. Striatopallidal and thalamic dystonia. Arch Neurol 1996;53:241-250. [7] Massey EW, Goodman JC, Stewart C et al. Unilateral asterixis: motor integrative dysfunction in focal vascular disease. Neurlogy 1979;29:1188-1190. [8] Barth A, Bogousslavsky J, Caplan LR. Thalamic infarcts and hemorrhages. In: Bogousslavsky J, Caplan LR, editors. Stroke syndromes. New York: Cambridge University Press, 1995:276-83. [9] Dejerine J, Roussy G. Le syndrome thalamique. Rev Neurol (Paris) 1906;14:521-32. [10] Brazis PW, Masdeu JC, Biller J. Localization in clinical neurology. 3rd ed. Boston: Little Brown, 1996. [11] Riele AR, Roach ES. Choreoathetosis in an infant with tuberculous meningitis. Arch Neurol 1982;24:173-178. [12] Roach ES, Riela AR. Pediatric cerebrovascular disorders. 2nd ed. New York, NY: Future, 1995. [13] Inagaki M, Koeda T, Takeshite K. Prognosis and MRI after ischemic stroke of the basal ganglia. Pediatr Neurol 1992;8:104-108. [14] Zimmerman RA, Bilaniuk LT, Packer RJ et al. Computed tomographic arteriographic correlates, in acute basal ganglionic infarction in childhood. Neuroradiology 1983;24:241-248. [15] Wood DH. Cerebrovascular complications of sickle cell anaemia. Stroke 1978;9:73–75. [16] Welch KM, Levine SR. Migraine related stroke in the context of the IMS classification. Arch Neurol 1990;47:458-462. [17] Chinnery PF, Turnbull DM. Diagnosis and management of mitochondrial DNA defects. J Neurol Neurosurg Psychiatry 1997;63: 559-563. [18] Miwa M, Matori K, Kondo T, Imai M, Mizuno Y. Thalamic tremor: case reports and implications of the tremor generating mechanism. Neurology 1996;46:75-79. [19] Ferbert A, Gerwig M. Tremor due to stroke. Mov Disord 1993;8:179182. [20] Mossuto-Agatiello L, Puccetti G, Castellano AE. Rubral tremor after thalamic haemorrhage. J Neurol 1993;241:27-30. [21] Kim JS. Delayed onset hand tremor caused by cerebral infarction. Stroke 1992;23:292-294. [22] Solomon DH, Barohn RJ, Bazan C, Grissom J. The thalamic ataxia syndrome. Neurology 1994;44:810-814. [23] Lee MS, Lee SA, Heo JH, et al. A patient with a resting tremor and a lacunar infarction at the border between the thalamus and the internal capsule. Mov Disor 1993;8:244-246. [24] Mano Y, Nakamuro T, Takayanagi T et al. Ceruletide therapy in action tremor following thalamic hemorrhage. J Neurol 1993;240:144-148. [25] Berkovic SF, Bladin PF. Rubral tremor: clinical features and treatment of three cases. Clin Exp Neurol 1984;20:119-128. [26] Schlitt M, Brown JW, Zeiger HE. Appendicular tremor as a late complication of intracerebral hemorrhage. Surg Neurol 1986;25:181-184. [27] Louis ED, Lynch T, Ford B, Greene P, Bressman S, Fahn S. Delayed onset cerebellar syndrome. Arch Neurol 1996;53:450-454. [28] Qureshi Fi, Morales A, Elbe RJ. Tremor due to infarction in the ventrolateral thalamus. Mov Disord 1996;11:440-459. [29] Marsden CD, Obeso JA, Zarrans JJ, Lang AE. The anatomical basis of symptomatic dystonia. Brain 1985;108:463-483. [30] Bhatia KP, Marsden CD. Behavioral and motor consequences of focal lesions of the basal ganglia in man. Brain 1994;117:859-879. [31] Narbona J, Obeso JA, Tuon T, Martinez Lage JM, Marsden CD.
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F. Micheli et al. / Parkinsonism and Related Disorders 4 (1998) 119–122
Hemidystonia secondary to localized basal ganglia tumor. J Neurol Neurosurg Psychiatry 1984;47:704-709. [32] Berkovic SF, Bladin PF. Rubral tremor: clinical features and treatment of three cases. Clin Exp Neurol 1984;20:119-128. [33] Micheli F, Gran˜ana N, Scorticati MC, Giannaula R, Reboredo G. Unilateral postural and action tremor resulting from thalamic toxoplasmosis in a patient with acquired immunodeficiency syndrome. Mov Disord 1997;12:1096-1098.
[34] Hallet M. Electrophysiologic evaluation of tremor and central disorders of movements. In de Aminoff MJ, editor. Electrodiagnosis in Clinical Neurology. 2nd ed. New York: Churchill Livingstone, 1986:385-401. [35] Pettigrew LC, Jankovic J. Hemidystonia: a report of 22 patients and a review of the literature. J Neurol Neurosurg Psychiatry 1985;48:650657.
Dystonia and tremor secondary to a pediatric thalamic stroke Federico Micheli a,*, Graciela Cerso´simo a, Claudio Palacios b, Marı´a Clara Scorticati a, Silvia Tenembaum b, Juan Trı´poli b a
Hospital de Clı´nicas ‘‘Jose´ de San Martin’’, U.B.A. Department of Neurology, Olleros 2240-1426, Buenos Aires, Argentina b Hospital Nacional de Pediatrı´a ‘‘Juan P. Garrahan’’, Department of Neurology, Buenos Aires, Argentina Received 15 May 1998; received in revised form 13 August 1998; accepted 31 August 1998
Abstract A previously healthy 10-year-old girl developed a right hemiparesis with sensory loss secondary to a posterolateral thalamic infarct. Despite improvement in strength, three weeks later a 4 Hz kinetic tremor appeared in the right hand accompanied by dystonia in the right upper and lower limbs. Basal ganglia vascular lesions are rare in childhood and movement disorders secondary to such lesions even more so. A thorough work-up failed to disclose the etiology. Our patient illustrates that dystonia and tremor secondary to posterolateral thalamic infarctions are also apt to occur in children and, unlike the adult picture, abnormal movements may develop very soon after the insult. 䉷 1998 Elsevier Science Ltd. All rights reserved. Keywords: Thalamus; Stroke; Dystonia; Tremor
1. Introduction Basal ganglia infarctions are very unusual in childhood and have been poorly described in the literature [1, 2]. Abnormal involuntary movements secondary to such lesions are even more uncommon although recently greater interest has been focused on these complications [3], which include: tremor, myoclonus, dystonia, chorea and asterixis subsequent to either thalamic infarctions or hemorrhages [4–7]. We here describe a 10-year-old girl who presented with unilateral postural and kinetic tremor associated with dystonic posturing contralateral to a posterior thalamic infarct.
2. Case report This previously healthy 10-year-old girl suddenly developed a right facio-brachio-crural hemiparesis with ipsilateral sensory loss, heralded by a 12-hour contralateral headache. Relevant personal history was limited to severe headaches over the last year, recurring monthly. Family history was unremarkable. On neurological examination, the patient was fully * Corresponding author. Fax: 00-54-811-3076; E-mail: fmicheli@ sminter.com.ar.
oriented to time and space. Ocular fundi were normal and visual fields full. She had a right central facial palsy and dysarthria while the remainder of the cranial nerve testing was normal. A moderate right hemiparesis with hemihyopaesthesia was evident. Otherwise, the neurological examination was unremarkable. The hemiparesis and sensory disturbance markedly improved over the next three days, but distal right limb abnormal movements gradually developed featuring postural and kinetic tremor in the right upper limb and dystonic posturing in the right arm and, to a lesser extent, posturing in the right foot. Rapid alternating right hand movements were affected by dystonic spasms in the flexor and extensors of the wrist. Surface EMG recordings from antagonist muscles in the right upper limb showed 4Hz rhythmic discharges associated with sustained cocontractions of antagonist muscles consistent with dystonia. A CT scan performed four days later disclosed a hypodense lesion in the left posterior thalamus with slight posterior capsule involvement. MRI confirmed the location of the lesion which was visualized as hypointense in T1-weighted images, slightly enhancing with gadolinium and hyperintense in T2 weighted images, but lacking mass effect, consistent with an ischemic infarction (Figs 1 and 2). An extensive laboratory work-up, including antinuclear antibodies, coagulation studies, blood and CSF lactate, proteins C and S assays and antiphospholipid antibodies, was normal, as also were a cerebral angiogram and echocardiography findings.
1353-8020/98/$ - see front matter 䉷 1998 Elsevier Science Ltd. All rights reserved. PII: S1353-802 0(98)00029-7
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Fig. 1. T2-weighted MRI showing a hyperintense lesion in the left thalamic posterolateral region.
3. Discussion Our patient suddenly developed a right hemiparesis with sensory loss, which resolved over a few days when severe, low frequency postural and action tremor in the right upper limb associated with mild dystonic posturing in both the right hand and foot became evident. Brain imaging revealed a posterolateral thalamic infarction, probably resulting from occlusion of the thalamogeniculate branches of the posterior cerebral artery [8]. Three clinical syndromes associated with posterolateral thalamic lesions have been recognized: pure sensory stroke, sensory motor stroke and the so-called thalamic syndrome of Dejerine and Roussy [9], on occasion featuring chorea or choreoathetosis secondary to the interruption of the extrapyramidal and cerebellar tracts synapsing in the lateral thalamus [8]. Several weeks after the injury, a slow frequency tremor at a rate of 3 to 5 Hz may appear [10]. Our patient presented two noteworthy features. On the one hand, the presence of a vascular lesion involving the posterior thalamus in a child and on the other the develop-
Fig. 2. The same lesion in T1-weighted images.
ment of unilateral postural and kinetic tremor as well as dystonia as its clinical expression. Despite a thorough work-up including fibrinogen, plasminogen, proteins C and S assays as well as urinary homocysteine, a collagenogram, an echocardiogram and a brain angiogram, no etiology was ascertained. However, the most frequent causes of cerebrovascular accidents in childhood such as congenital heart disease, falciform anemia, vasculitis and hypercoagulation states were ruled out [11– 15]. It could be speculated that our patient’s headaches were migraines that led to the thalamic infarction, but this seems unlikely since only migraine preceded by aura is currently recognized to cause stroke [16]. Mitochondrial DNA defects may present with stroke in young patients with estimates of frequency ranging from 0.5 to 8% [17]. A history of migraine is also common in such cases. Unfortunately blood molecular genetic analysis was not available for our patient. However, blood and CSF lactate was normal and there was no history of maternal neurological diseases. According to the literature, in 30% of cases, most likely including our patient, the cause of cerebrovascular accidents
F. Micheli et al. / Parkinsonism and Related Disorders 4 (1998) 119–122
in childhood remains unknown. Fortunately, the risk of recurrence in such cases is lower than in those with a discernible etiology [14]. Recently Miwa et al. [18] reported two patients with thalamic stroke who developed contralateral postural and resting tremor of the upper limb and they reviewed the literature. Both patients had lesions confined to the posterolateral thalamic region closely resembling our patient’s infarction. In adults, tremor has been reported as a late complication of stroke [18–26] appearing from 3 months to 3 years after the vascular insult, while age at onset ranges from 23 to 77 years. In such cases tremor has been ascribed to the development of postsynaptic supersensitivity or secondary reorganization of the involved pathways rather than to the lesion itself [27]. Only a single case of tremor due to infarction in the ventrolateral thalamus has been reported [28]. Instead, our case differed in two aspects from those previously described in that the patient was a child and that involuntary movements developed within a few days of the stroke, when the hemiparesis had already resolved. It has been speculated that tremor can be triggered either by interruption of ascending inputs to the posterolateral, rather than to the ventrolateral thalamic region, originating in the brainstem or cerebellum, or by destruction of the posterolateral thalamic neurons [18]. In addition, thalamic lesions have also been held responsible for symptomatic dystonia [29–31]. As in our patient, dystonia has been described in cases of posterolateral thalamic lesions [18, 19, 32] in which tremor is usually the predominant feature [33]. In such cases, dystonia is commonly restricted to the hand, and action and pastural myoclonic jerks are also frequently associated and may even be the most prominent feature [6]. In most cases, dystonia secondary to stroke develops promptly after the cerebrovascular episode [6]. In our patient, surface EMG was performed in order to rule out myoclonus and to confirm a 4-Hz tremor, as positive or negative myoclonus can mimic tremor [34]. As the sensory disturbances were very mild, the dystonia cannot be ascribed to deafferentation (pseudoathetosis). The clinical features in our patient closely resemble those reported in patients with either posterolateral [21, 28] or posterior [21, 28, 35] thalamic infarctions. Our case further supports the relevance of thalamic lesions in the generation of both tremor and dystonia and illustrates that movement disorders like these resulting from thalamic stroke are not unknown in children.
References [1] Brower MC, Rollins N, Roach ES. Basal ganglia and thalamic infarction in children. Arch Neurol. 1996;53:1252-1256. [2] Broderick J, Falbot T, Prenger E et al. Stroke in children within a major metropolitan area: the surprising importance of intracerebral hemorrhage. J Child Neurol 1993;8:250-255.
121
[3] Lee MS, Marsden CD. Movement Disorders following lesions of the thalamus or subthalamic region. Mov Disord 1994;9:493-507. [4] Ghika J, Bogousslavsky J, Henderson J, Maeder P, Regli F. The jerky dystonic unsteady hand: a delayed motor syndrome in posterior thalamic infarctions. J Neurol 1994;241:537-542. [5] Rio J, Montalban J, Pujadas F, Alvarez Sabini, Roviar A, Codina A. Asterixis associated with anatomic cerebral lesions: a study of 45 cases. Acta Neurol Scand 1995;91:377-381. [6] Leherecy S, Vidailhet M, Dormont D et al. Striatopallidal and thalamic dystonia. Arch Neurol 1996;53:241-250. [7] Massey EW, Goodman JC, Stewart C et al. Unilateral asterixis: motor integrative dysfunction in focal vascular disease. Neurlogy 1979;29:1188-1190. [8] Barth A, Bogousslavsky J, Caplan LR. Thalamic infarcts and hemorrhages. In: Bogousslavsky J, Caplan LR, editors. Stroke syndromes. New York: Cambridge University Press, 1995:276-83. [9] Dejerine J, Roussy G. Le syndrome thalamique. Rev Neurol (Paris) 1906;14:521-32. [10] Brazis PW, Masdeu JC, Biller J. Localization in clinical neurology. 3rd ed. Boston: Little Brown, 1996. [11] Riele AR, Roach ES. Choreoathetosis in an infant with tuberculous meningitis. Arch Neurol 1982;24:173-178. [12] Roach ES, Riela AR. Pediatric cerebrovascular disorders. 2nd ed. New York, NY: Future, 1995. [13] Inagaki M, Koeda T, Takeshite K. Prognosis and MRI after ischemic stroke of the basal ganglia. Pediatr Neurol 1992;8:104-108. [14] Zimmerman RA, Bilaniuk LT, Packer RJ et al. Computed tomographic arteriographic correlates, in acute basal ganglionic infarction in childhood. Neuroradiology 1983;24:241-248. [15] Wood DH. Cerebrovascular complications of sickle cell anaemia. Stroke 1978;9:73–75. [16] Welch KM, Levine SR. Migraine related stroke in the context of the IMS classification. Arch Neurol 1990;47:458-462. [17] Chinnery PF, Turnbull DM. Diagnosis and management of mitochondrial DNA defects. J Neurol Neurosurg Psychiatry 1997;63: 559-563. [18] Miwa M, Matori K, Kondo T, Imai M, Mizuno Y. Thalamic tremor: case reports and implications of the tremor generating mechanism. Neurology 1996;46:75-79. [19] Ferbert A, Gerwig M. Tremor due to stroke. Mov Disord 1993;8:179182. [20] Mossuto-Agatiello L, Puccetti G, Castellano AE. Rubral tremor after thalamic haemorrhage. J Neurol 1993;241:27-30. [21] Kim JS. Delayed onset hand tremor caused by cerebral infarction. Stroke 1992;23:292-294. [22] Solomon DH, Barohn RJ, Bazan C, Grissom J. The thalamic ataxia syndrome. Neurology 1994;44:810-814. [23] Lee MS, Lee SA, Heo JH, et al. A patient with a resting tremor and a lacunar infarction at the border between the thalamus and the internal capsule. Mov Disor 1993;8:244-246. [24] Mano Y, Nakamuro T, Takayanagi T et al. Ceruletide therapy in action tremor following thalamic hemorrhage. J Neurol 1993;240:144-148. [25] Berkovic SF, Bladin PF. Rubral tremor: clinical features and treatment of three cases. Clin Exp Neurol 1984;20:119-128. [26] Schlitt M, Brown JW, Zeiger HE. Appendicular tremor as a late complication of intracerebral hemorrhage. Surg Neurol 1986;25:181-184. [27] Louis ED, Lynch T, Ford B, Greene P, Bressman S, Fahn S. Delayed onset cerebellar syndrome. Arch Neurol 1996;53:450-454. [28] Qureshi Fi, Morales A, Elbe RJ. Tremor due to infarction in the ventrolateral thalamus. Mov Disord 1996;11:440-459. [29] Marsden CD, Obeso JA, Zarrans JJ, Lang AE. The anatomical basis of symptomatic dystonia. Brain 1985;108:463-483. [30] Bhatia KP, Marsden CD. Behavioral and motor consequences of focal lesions of the basal ganglia in man. Brain 1994;117:859-879. [31] Narbona J, Obeso JA, Tuon T, Martinez Lage JM, Marsden CD.
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F. Micheli et al. / Parkinsonism and Related Disorders 4 (1998) 119–122
Hemidystonia secondary to localized basal ganglia tumor. J Neurol Neurosurg Psychiatry 1984;47:704-709. [32] Berkovic SF, Bladin PF. Rubral tremor: clinical features and treatment of three cases. Clin Exp Neurol 1984;20:119-128. [33] Micheli F, Gran˜ana N, Scorticati MC, Giannaula R, Reboredo G. Unilateral postural and action tremor resulting from thalamic toxoplasmosis in a patient with acquired immunodeficiency syndrome. Mov Disord 1997;12:1096-1098.
[34] Hallet M. Electrophysiologic evaluation of tremor and central disorders of movements. In de Aminoff MJ, editor. Electrodiagnosis in Clinical Neurology. 2nd ed. New York: Churchill Livingstone, 1986:385-401. [35] Pettigrew LC, Jankovic J. Hemidystonia: a report of 22 patients and a review of the literature. J Neurol Neurosurg Psychiatry 1985;48:650657.