880
Case Reports / Journal of Clinical Neuroscience 21 (2014) 880–882
3. Discussion Among the organic solvents of lacquer thinners, toluene is the main component responsible for neurotoxicity. Toluene intoxication following inhalation may lead to variable clinical presentations, from headache to death, depending on exposure duration and dose. In a large series of 41 paint thinner abusers, 3 years of exposure is the minimum duration to have MRI evidence of white matter changes, typically confluent lesions in the periventricular white matter and centrum semiovale [2]. However, unlike chronic inhalation exposure to organic solvents, a lacquer thinner explosion may expose patients to an extraordinarily high level of toluene [3]. We hypothesize that a high level of toluene exposure resulted in severe neurologic deterioration and white matter necrosis in our patient. Our patient’s MRI showed target-like lesions with rings of restricted water diffusion and contrast enhancement, findings indicating cytotoxic edema and disruption of the blood–brain barrier. The areas inside and outside the enhancing rings without restricted water diffusion represent necrosis and vasogenic edema, respectively. The heterogeneous signal intensities of the lesions on the T2-weighted images were probably contributed by hemorrhage, although this was not a prominent feature in the biopsy specimen. The target-like lesions on diffusion weighted imaging are unusual and are associated with limited differential diagnoses, including disseminated necrotizing leukoencephalitis (DNL), cerebral aspergillosis, and toxoplasma abscesses. DNL is a toxic leukoencephalopathy following intrathecal or intravenous administration of methotrexate. Pathologically, DNL lesions are characteristic of multifocal necrosis and occasional hemorrhage [4], which resemble features in our patient. Unlike pyogenic abscesses, cerebral
aspergillus and toxoplasma abscesses may show unrestricted water diffusion in the center of the enhancing rings, probably because the necrotic cores do not contain pus or proteinaceous fluid of high viscosity [5]. In our patient, the aspergillus infection of the burn wound and the MRI findings of the target-like cerebral lesions were suggestive of cerebral aspergillosis. In such circumstances, empirical antifungal therapy is mandatory until proven otherwise. In conclusion, our patient suffered acute inhalation of vaporized lacquer thinner, containing a high volume of toluene, and became deeply comatose with lesions in the bilateral cerebral white matter. Brain biopsy was necessary to exclude other treatable lesions and suggest that, although not previously described to our knowledge, the changes seen on imaging were a manifestation of acute toluene neurotoxicity. 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] Filley CM, Kleinschmidt-DeMasters BK. Toxic leukoencephalopathy. N Engl J Med 2001;345:425–32. [2] Aydin K, Sencer S, Demir T, et al. Cranial MR findings in chronic toluene abuse by inhalation. AJNR Am J Neuroradiol 2002;23:1173–9. [3] Yoshida M, Akane A, Okii Y, et al. Analysis of organic compounds in a case of suicide by ignition with lacquer thinner. Nihon Hoigaku Zasshi 1995;49:472–7. [4] Rubinstein LJ, Herman MM, Long TF, et al. Disseminated necrotizing leukoencephalopathy: a complication of treated central nervous system leukemia and lymphoma. Cancer 1975;35:291–305. [5] Chong-Han CH, Cortez SC, Tung GA. Diffusion-weighted MRI of cerebral toxoplasma abscess. AJR Am J Roentgenol 2003;181:1711–4.
http://dx.doi.org/10.1016/j.jocn.2013.07.036
Upper limb compartment syndrome: An unusual complication of stroke thrombolysis Wallace J. Brownlee a,⇑, Teddy Y. Wu a, Stephanie A. Van Dijck b, Barry J. Snow a a b
Department of Neurology, Auckland District Health Board, Auckland City Hospital, Park Road, Grafton, Auckland, New Zealand Department of Orthopaedics, Auckland District Health Board, Auckland, New Zealand
a r t i c l e
i n f o
Article history: Received 18 February 2013 Accepted 10 July 2013
Keywords: Compartment syndrome Stroke Thrombolysis
a b s t r a c t Bleeding is the most important complication of treatment with intravenous tissue plasminogen activator for acute ischemic stroke. Neurologists are familiar with intracranial hemorrhage, the most feared site for bleeding following thrombolysis, but extracranial bleeding can also occur resulting in substantial morbidity and mortality. We describe an 88-year-old woman with an acute stroke who developed bleeding into the left arm complicated by hemodynamic instability and compartment syndrome following intravenous thrombolysis. The patient was treated conservatively in view of the risks associated with fasciotomy and her other medical comorbidities. Ó 2013 Elsevier Ltd. All rights reserved.
1. Introduction Bleeding is the most important complication of treatment with intravenous tissue plasminogen activator (tPA) for acute ischemic stroke. Neurologists are familiar with intracranial hemorrhage, the most feared site for bleeding following tPA, but extracranial ⇑ Corresponding author. Tel.: +64 2154 5705; fax: +64 9375 4309. E-mail address: [email protected] (W.J. Brownlee).
bleeding can also occur resulting in substantial morbidity and mortality. We describe a patient who developed upper limb compartment syndrome following stroke thrombolysis and review other reported patients. 2. Case report An 88-year-old woman presented following the sudden onset of left-sided weakness and slurred speech. Her daughter reported
Case Reports / Journal of Clinical Neuroscience 21 (2014) 880–882
881
Fig. 1. (a) Photograph of the left upper arm showing significant soft tissue swelling following administration of tissue plasminogen activator (tPA). (b) Photograph 14 days following tPA administration showing significant improvement in soft tissue swelling. (This figure is available in colour at http://www.sciencedirect.com/.)
supporting her by the left arm as she slumped to one side. There was minor bruising on the dorsal aspect of her left hand without any other signs of trauma. Her National Institutes of Health Stroke Scale score was 8. A non-contrast brain CT scan showed no acute changes and routine blood tests including a coagulation profile were normal. She was treated with alteplase 0.9 mg/kg at 2 hours 40 minutes after symptom onset through an intravenous catheter placed in the right arm. During the infusion her blood pressure was monitored using non-invasive blood pressure (NIBP) monitoring from the left upper arm. An hour later the patient became hypotensive and was noted to have significant swelling of the left upper arm (Fig. 1a). There was no evidence of neurovascular compromise with good peripheral pulses and no change in the neurological deficit. Her hemoglobin had fallen from 110 g/L to 79 g/L. A CT scan of the left upper limb showed marked swelling in the anterior and posterior compartments of the arm with no underlying fracture seen (Fig. 2). A CT angiogram showed several areas of contrast extravasation in muscle consistent with sites of acute bleeding (Fig. 2). Delayed venous phase scanning showed no contrast filling the arm veins, in keeping with compression related to a compartment syndrome (CS). Compartment pressure in the left arm was elevated; 75 mmHg in the anterior compartment and 42 mmHg in the posterior compartment (normal range 10–12 mmHg) with a diastolic blood pressure of 74 mmHg. Orthopedic and vascular surgical opinions were obtained. Fasciotomy was considered but a decision was made to manage the patient conservatively in view of the risks associated
Fig. 2. (a) Axial CT scan of the left upper arm with marked soft tissue swelling (long arrows) and small areas of hemorrhage (arrow heads). (b) Sagittal CT scan of the left arm showing intact humeral cortex, soft tissue swelling (long arrows) and small areas of hemorrhage (arrow heads).
with surgical intervention. The patient’s condition remained stable and the arm swelling reduced significantly over the next 2 weeks (Fig. 1b). 3. Discussion Acute CS is caused by bleeding or swelling within a closed fascial space resulting in increased interstitial pressures and ultimately complications related to muscle and nerve ischemia [1]. The causes of acute CS include fractures, vascular and soft tissue injuries [1]. The diagnosis of CS is primarily a clinical one, but requires a high index of suspicion. A common finding is pain that is out of proportion to an injury. Intracompartmental pressure monitoring can be done if there is uncertainty about the diagnosis using an 18 G needle attached to manometry to estimate compartment pressures [1]. The normal pressure within muscle
882
Case Reports / Journal of Clinical Neuroscience 21 (2014) 882–884
compartments is 10–12 mmHg. As the pressure rises there is progressive impairment of the microcirculation leading to tissue hypoperfusion [1] The absolute pressure may be less important than the perfusion pressure. A difference between the diastolic blood pressure and the compartment pressure of less than 30 mmHg is associated with a higher risk of ischemic complications. A single other case report describes a patient with CS following stroke thrombolysis [2]. Yip et al. reported a patient who collapsed with a left hemiparesis and injured the left arm. Pain and swelling was noted in the left elbow but a radiograph showed no evidence of a fracture. The patient was treated with tPA but subsequently developed CS in the left forearm. An occult fracture was later identified in the proximal radius. A collapse is relatively common following a stroke and patients need to be carefully assessed for fractures and soft tissue injuries, which can be difficult to detect in the context of dysphasia or sensory impairment. In our patient there was no history of trauma, however, during the infusion of tPA the patient was monitored with a NIBP cuff on the left arm which is a potential source of iatrogenic soft tissue injury. CS has been reported previously in this setting in a patient treated with streptokinase for myocardial infarction [3]. Vascular injuries are another potential source cause of CS following thrombolysis. Repeated attempts at arterial line placement in a patient treated with thrombolysis for a myocardial infarction resulted in bilateral forearm and hand CS [4]. The treatment of acute CS is emergent fasciotomy in order to decompress the affected compartment, particularly if there is evidence of arterial compromise [1]. Management decisions are more complicated when soft tissue hemorrhage and CS develops in patients who have been treated with thrombolysis because of the
potential for further bleeding complications plus the risks associated with anesthesia from the initial vascular event. In our case the patient was elderly, had multiple medical comorbidities and had adequate arterial supply to the affected limb. The surgical team who assessed the patient suggested close observation in the first instance and fasciotomy was recommended if neurovascular compromise developed. In summary, we report an 88-year-old woman with an acute stroke who developed atraumatic upper limb CS as a complication of thrombolysis. Soft tissue bleeding is an extremely unusual site of extracranial hemorrhage in patients treated with tPA. Neurologists need to be aware of this complication particularly among patients who have sustained trauma or collapsed at the time of the stroke. Care should be taken with NIBP monitoring and vascular access avoided if possible in the immediate period post-thrombolysis.
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] Gourgiotis S, Villias C, Germanos S, et al. Acute limb compartment syndrome: a review. J Surg Educ 2007;64:178–86. [2] Yip T, Demaerschalk B. Forearm compartment syndrome following intravenous thrombolytic therapy for acute ischemic stroke. Neurocrit Care 2005;2:47–8. [3] Rudoff J, Ebner S, Canepa C. Limb-compartmental syndrome with thrombolysis. Am Heart J 1994;128:1267–8. [4] Thomas W, Harris C, D’Amore T, et al. Bilateral forearm and hand compartment syndrome following thrombolysis for acute myocardial infarction: a case report. J Emerg Med 1994;12:467–72.
http://dx.doi.org/10.1016/j.jocn.2013.07.018
Thalamic stimulation alleviates levodopa-resistant rigidity in a patient with non-Parkinson’s disease parkinsonian syndrome Kazumichi Yamada a,b,⇑, Tadashi Hamasaki a, Jun-ichi Kuratsu a a b
Department of Neurosurgery, Graduate School of Life Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto 860-8556, Japan Department of Functional Neurosurgery, Kumamoto University Hospital, Kumamoto, Japan
a r t i c l e
i n f o
Article history: Received 8 April 2013 Accepted 13 July 2013
Keywords: Deep brain stimulation Parkinsonism Rigidity Thalamus Tremor
a b s t r a c t Deep brain stimulation (DBS) to the thalamic ventrointermediate nucleus (Vim) is a useful treatment in patients with tremor-dominant Parkinson’s disease (PD). Efficacy to alleviate rigidity remains controversial. We report a 65-year-old right-handed man with persistent severe rigidity and bradykinesia on the right side despite daily administration of levodopa/carbidopa (600/60 mg). His right-hand tremor was continuous at rest and present at action. His antiparkinsonian medications appeared ineffective and he reported difficulties with writing and eating. Repeated 123I-meta-iodobenzylguanidine myocardial scintigraphy studies demonstrated a non-PD pattern. He underwent the stereotactic implantation of a DBS electrode into the left Vim. Using contacts 1 and 2 we started continuous unipolar stimulation with a pulse generator implanted in a subclavian pocket. This improved the tremor and the rigidity and bradykinesia of his right hand. Postoperative image analysis revealed the likelihood of simultaneous stimulation of the Vim and the nucleus ventralis oralis posterior. Our findings suggest thalamic stimulation as a therapeutic option for drug-resistant rigidity (and tremor) in patients with parkinsonian syndromes ineligible for DBS targeted at the globus pallidus internus or subthalamic nucleus. Ó 2013 Elsevier Ltd. All rights reserved.
⇑ Corresponding author. Tel.: +81 96 373 5219; fax: +81 96 371 8064. E-mail address: [email protected] (K. Yamada).
Case Reports / Journal of Clinical Neuroscience 21 (2014) 880–882
3. Discussion Among the organic solvents of lacquer thinners, toluene is the main component responsible for neurotoxicity. Toluene intoxication following inhalation may lead to variable clinical presentations, from headache to death, depending on exposure duration and dose. In a large series of 41 paint thinner abusers, 3 years of exposure is the minimum duration to have MRI evidence of white matter changes, typically confluent lesions in the periventricular white matter and centrum semiovale [2]. However, unlike chronic inhalation exposure to organic solvents, a lacquer thinner explosion may expose patients to an extraordinarily high level of toluene [3]. We hypothesize that a high level of toluene exposure resulted in severe neurologic deterioration and white matter necrosis in our patient. Our patient’s MRI showed target-like lesions with rings of restricted water diffusion and contrast enhancement, findings indicating cytotoxic edema and disruption of the blood–brain barrier. The areas inside and outside the enhancing rings without restricted water diffusion represent necrosis and vasogenic edema, respectively. The heterogeneous signal intensities of the lesions on the T2-weighted images were probably contributed by hemorrhage, although this was not a prominent feature in the biopsy specimen. The target-like lesions on diffusion weighted imaging are unusual and are associated with limited differential diagnoses, including disseminated necrotizing leukoencephalitis (DNL), cerebral aspergillosis, and toxoplasma abscesses. DNL is a toxic leukoencephalopathy following intrathecal or intravenous administration of methotrexate. Pathologically, DNL lesions are characteristic of multifocal necrosis and occasional hemorrhage [4], which resemble features in our patient. Unlike pyogenic abscesses, cerebral
aspergillus and toxoplasma abscesses may show unrestricted water diffusion in the center of the enhancing rings, probably because the necrotic cores do not contain pus or proteinaceous fluid of high viscosity [5]. In our patient, the aspergillus infection of the burn wound and the MRI findings of the target-like cerebral lesions were suggestive of cerebral aspergillosis. In such circumstances, empirical antifungal therapy is mandatory until proven otherwise. In conclusion, our patient suffered acute inhalation of vaporized lacquer thinner, containing a high volume of toluene, and became deeply comatose with lesions in the bilateral cerebral white matter. Brain biopsy was necessary to exclude other treatable lesions and suggest that, although not previously described to our knowledge, the changes seen on imaging were a manifestation of acute toluene neurotoxicity. 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] Filley CM, Kleinschmidt-DeMasters BK. Toxic leukoencephalopathy. N Engl J Med 2001;345:425–32. [2] Aydin K, Sencer S, Demir T, et al. Cranial MR findings in chronic toluene abuse by inhalation. AJNR Am J Neuroradiol 2002;23:1173–9. [3] Yoshida M, Akane A, Okii Y, et al. Analysis of organic compounds in a case of suicide by ignition with lacquer thinner. Nihon Hoigaku Zasshi 1995;49:472–7. [4] Rubinstein LJ, Herman MM, Long TF, et al. Disseminated necrotizing leukoencephalopathy: a complication of treated central nervous system leukemia and lymphoma. Cancer 1975;35:291–305. [5] Chong-Han CH, Cortez SC, Tung GA. Diffusion-weighted MRI of cerebral toxoplasma abscess. AJR Am J Roentgenol 2003;181:1711–4.
http://dx.doi.org/10.1016/j.jocn.2013.07.036
Upper limb compartment syndrome: An unusual complication of stroke thrombolysis Wallace J. Brownlee a,⇑, Teddy Y. Wu a, Stephanie A. Van Dijck b, Barry J. Snow a a b
Department of Neurology, Auckland District Health Board, Auckland City Hospital, Park Road, Grafton, Auckland, New Zealand Department of Orthopaedics, Auckland District Health Board, Auckland, New Zealand
a r t i c l e
i n f o
Article history: Received 18 February 2013 Accepted 10 July 2013
Keywords: Compartment syndrome Stroke Thrombolysis
a b s t r a c t Bleeding is the most important complication of treatment with intravenous tissue plasminogen activator for acute ischemic stroke. Neurologists are familiar with intracranial hemorrhage, the most feared site for bleeding following thrombolysis, but extracranial bleeding can also occur resulting in substantial morbidity and mortality. We describe an 88-year-old woman with an acute stroke who developed bleeding into the left arm complicated by hemodynamic instability and compartment syndrome following intravenous thrombolysis. The patient was treated conservatively in view of the risks associated with fasciotomy and her other medical comorbidities. Ó 2013 Elsevier Ltd. All rights reserved.
1. Introduction Bleeding is the most important complication of treatment with intravenous tissue plasminogen activator (tPA) for acute ischemic stroke. Neurologists are familiar with intracranial hemorrhage, the most feared site for bleeding following tPA, but extracranial ⇑ Corresponding author. Tel.: +64 2154 5705; fax: +64 9375 4309. E-mail address: [email protected] (W.J. Brownlee).
bleeding can also occur resulting in substantial morbidity and mortality. We describe a patient who developed upper limb compartment syndrome following stroke thrombolysis and review other reported patients. 2. Case report An 88-year-old woman presented following the sudden onset of left-sided weakness and slurred speech. Her daughter reported
Case Reports / Journal of Clinical Neuroscience 21 (2014) 880–882
881
Fig. 1. (a) Photograph of the left upper arm showing significant soft tissue swelling following administration of tissue plasminogen activator (tPA). (b) Photograph 14 days following tPA administration showing significant improvement in soft tissue swelling. (This figure is available in colour at http://www.sciencedirect.com/.)
supporting her by the left arm as she slumped to one side. There was minor bruising on the dorsal aspect of her left hand without any other signs of trauma. Her National Institutes of Health Stroke Scale score was 8. A non-contrast brain CT scan showed no acute changes and routine blood tests including a coagulation profile were normal. She was treated with alteplase 0.9 mg/kg at 2 hours 40 minutes after symptom onset through an intravenous catheter placed in the right arm. During the infusion her blood pressure was monitored using non-invasive blood pressure (NIBP) monitoring from the left upper arm. An hour later the patient became hypotensive and was noted to have significant swelling of the left upper arm (Fig. 1a). There was no evidence of neurovascular compromise with good peripheral pulses and no change in the neurological deficit. Her hemoglobin had fallen from 110 g/L to 79 g/L. A CT scan of the left upper limb showed marked swelling in the anterior and posterior compartments of the arm with no underlying fracture seen (Fig. 2). A CT angiogram showed several areas of contrast extravasation in muscle consistent with sites of acute bleeding (Fig. 2). Delayed venous phase scanning showed no contrast filling the arm veins, in keeping with compression related to a compartment syndrome (CS). Compartment pressure in the left arm was elevated; 75 mmHg in the anterior compartment and 42 mmHg in the posterior compartment (normal range 10–12 mmHg) with a diastolic blood pressure of 74 mmHg. Orthopedic and vascular surgical opinions were obtained. Fasciotomy was considered but a decision was made to manage the patient conservatively in view of the risks associated
Fig. 2. (a) Axial CT scan of the left upper arm with marked soft tissue swelling (long arrows) and small areas of hemorrhage (arrow heads). (b) Sagittal CT scan of the left arm showing intact humeral cortex, soft tissue swelling (long arrows) and small areas of hemorrhage (arrow heads).
with surgical intervention. The patient’s condition remained stable and the arm swelling reduced significantly over the next 2 weeks (Fig. 1b). 3. Discussion Acute CS is caused by bleeding or swelling within a closed fascial space resulting in increased interstitial pressures and ultimately complications related to muscle and nerve ischemia [1]. The causes of acute CS include fractures, vascular and soft tissue injuries [1]. The diagnosis of CS is primarily a clinical one, but requires a high index of suspicion. A common finding is pain that is out of proportion to an injury. Intracompartmental pressure monitoring can be done if there is uncertainty about the diagnosis using an 18 G needle attached to manometry to estimate compartment pressures [1]. The normal pressure within muscle
882
Case Reports / Journal of Clinical Neuroscience 21 (2014) 882–884
compartments is 10–12 mmHg. As the pressure rises there is progressive impairment of the microcirculation leading to tissue hypoperfusion [1] The absolute pressure may be less important than the perfusion pressure. A difference between the diastolic blood pressure and the compartment pressure of less than 30 mmHg is associated with a higher risk of ischemic complications. A single other case report describes a patient with CS following stroke thrombolysis [2]. Yip et al. reported a patient who collapsed with a left hemiparesis and injured the left arm. Pain and swelling was noted in the left elbow but a radiograph showed no evidence of a fracture. The patient was treated with tPA but subsequently developed CS in the left forearm. An occult fracture was later identified in the proximal radius. A collapse is relatively common following a stroke and patients need to be carefully assessed for fractures and soft tissue injuries, which can be difficult to detect in the context of dysphasia or sensory impairment. In our patient there was no history of trauma, however, during the infusion of tPA the patient was monitored with a NIBP cuff on the left arm which is a potential source of iatrogenic soft tissue injury. CS has been reported previously in this setting in a patient treated with streptokinase for myocardial infarction [3]. Vascular injuries are another potential source cause of CS following thrombolysis. Repeated attempts at arterial line placement in a patient treated with thrombolysis for a myocardial infarction resulted in bilateral forearm and hand CS [4]. The treatment of acute CS is emergent fasciotomy in order to decompress the affected compartment, particularly if there is evidence of arterial compromise [1]. Management decisions are more complicated when soft tissue hemorrhage and CS develops in patients who have been treated with thrombolysis because of the
potential for further bleeding complications plus the risks associated with anesthesia from the initial vascular event. In our case the patient was elderly, had multiple medical comorbidities and had adequate arterial supply to the affected limb. The surgical team who assessed the patient suggested close observation in the first instance and fasciotomy was recommended if neurovascular compromise developed. In summary, we report an 88-year-old woman with an acute stroke who developed atraumatic upper limb CS as a complication of thrombolysis. Soft tissue bleeding is an extremely unusual site of extracranial hemorrhage in patients treated with tPA. Neurologists need to be aware of this complication particularly among patients who have sustained trauma or collapsed at the time of the stroke. Care should be taken with NIBP monitoring and vascular access avoided if possible in the immediate period post-thrombolysis.
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] Gourgiotis S, Villias C, Germanos S, et al. Acute limb compartment syndrome: a review. J Surg Educ 2007;64:178–86. [2] Yip T, Demaerschalk B. Forearm compartment syndrome following intravenous thrombolytic therapy for acute ischemic stroke. Neurocrit Care 2005;2:47–8. [3] Rudoff J, Ebner S, Canepa C. Limb-compartmental syndrome with thrombolysis. Am Heart J 1994;128:1267–8. [4] Thomas W, Harris C, D’Amore T, et al. Bilateral forearm and hand compartment syndrome following thrombolysis for acute myocardial infarction: a case report. J Emerg Med 1994;12:467–72.
http://dx.doi.org/10.1016/j.jocn.2013.07.018
Thalamic stimulation alleviates levodopa-resistant rigidity in a patient with non-Parkinson’s disease parkinsonian syndrome Kazumichi Yamada a,b,⇑, Tadashi Hamasaki a, Jun-ichi Kuratsu a a b
Department of Neurosurgery, Graduate School of Life Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto 860-8556, Japan Department of Functional Neurosurgery, Kumamoto University Hospital, Kumamoto, Japan
a r t i c l e
i n f o
Article history: Received 8 April 2013 Accepted 13 July 2013
Keywords: Deep brain stimulation Parkinsonism Rigidity Thalamus Tremor
a b s t r a c t Deep brain stimulation (DBS) to the thalamic ventrointermediate nucleus (Vim) is a useful treatment in patients with tremor-dominant Parkinson’s disease (PD). Efficacy to alleviate rigidity remains controversial. We report a 65-year-old right-handed man with persistent severe rigidity and bradykinesia on the right side despite daily administration of levodopa/carbidopa (600/60 mg). His right-hand tremor was continuous at rest and present at action. His antiparkinsonian medications appeared ineffective and he reported difficulties with writing and eating. Repeated 123I-meta-iodobenzylguanidine myocardial scintigraphy studies demonstrated a non-PD pattern. He underwent the stereotactic implantation of a DBS electrode into the left Vim. Using contacts 1 and 2 we started continuous unipolar stimulation with a pulse generator implanted in a subclavian pocket. This improved the tremor and the rigidity and bradykinesia of his right hand. Postoperative image analysis revealed the likelihood of simultaneous stimulation of the Vim and the nucleus ventralis oralis posterior. Our findings suggest thalamic stimulation as a therapeutic option for drug-resistant rigidity (and tremor) in patients with parkinsonian syndromes ineligible for DBS targeted at the globus pallidus internus or subthalamic nucleus. Ó 2013 Elsevier Ltd. All rights reserved.
⇑ Corresponding author. Tel.: +81 96 373 5219; fax: +81 96 371 8064. E-mail address: [email protected] (K. Yamada).
