Case Report
Parkinsonism after External Ventricular Drainage in a Patient with Intraventricular Hemorrhage Min Ho Chun, MD, PhD,* Chang Gu Kang, MD,* Eun Jung Kong, MD,† and Min Cheol Chang, MD*
We report a patient who presented with Parkinsonism after external ventricular drainage (EVD) for an intraventricular hemorrhage (IVH). We also demonstrate dopaminergic system dysfunction using 18F-florinated-N-3-fluoropropyl-2-b-carboxymethoxy-3-b-(4-lodophenyl) nortropane (18F-FP-CIT) positron emission tomography (PET) scanning. A 50-year-old woman presented with manifestations of Parkinsonism, including severe rigidity and 3-Hz resting tremor, immediately after EVD for IVH. 18F-FP-CIT PET images at 6 months after onset showed dysfunction of the bilateral caudate nuclei and putamen after EVD that seemed to have induced Parkinsonism, although no lesion was observed in those areas on either conventional computed tomography or magnetic resonance imaging. With a dose of 300/ 1200 mg/day carbidopa/levodopa, the rigidity of both upper and lower extremities was significantly reduced, and the tremor completely disappeared. The decreased rigidity also improved the activities of daily living performance. In summary, a patient developed Parkinsonism after EVD for IVH, and we demonstrated dopaminergic system dysfunction on 18F-FP-CIT PET images. Clinicians should pay particular attention to the occurrence of Parkinsonism when performing procedures that can reduce intraventricular pressure. Key Words: Parkinsonism—external ventricular drainage—intraventricular hemorrhage—18F-FP-CIT—positron emission tomography. Ó 2015 by National Stroke Association
Parkinsonism can be secondarily induced by various causes, such as stroke, encephalitis, drug poisoning, and hydrocephalus.1-4 Parkinsonism has also been reported in patients with obstructive hydrocephalus From the *Department of Physical Medicine and Rehabilitation, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea; and †Department of Nuclear Medicine, University of Yeungnam College of Medicine, Taegu, Republic of Korea. Received July 30, 2014; revision received September 5, 2014; accepted October 27, 2014. The authors declare no conflicts of interest. Address correspondence to Min Cheol Chang, MD, Department of Physical Medicine and Rehabilitation, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Pungnap-2 dong, Songpa-gu, Seoul 138-736, Republic of Korea. E-mail: [email protected]. 1052-3057/$ - see front matter Ó 2015 by National Stroke Association http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2014.10.013
after ventriculoperitoneal (VP) shunt placement.5,6 In such cases, it was proposed that shear forces arising from sudden changes in ventricular pressure after VP shunt placement caused mechanical disruption of the nigrostriatal pathways from the medial substantia nigra to the caudate nucleus and putamen or dysfunction of the basal ganglia and its frontal projection fibers. However, Parkinsonism after external ventricular drainage (EVD) has not yet been reported. In the present study, we report such a case involving a patient who presented with Parkinsonism after EVD for an intraventricular hemorrhage (IVH). We also demonstrate dopaminergic system dysfunction using 18 F-florinated-N-3-fluoropropyl-2-b-carboxymethoxy-3b-(4-lodophenyl) nortropane (18F-FP-CIT) positron emission tomography (PET) scanning.
Journal of Stroke and Cerebrovascular Diseases, Vol. 24, No. 3 (March), 2015: pp e75-e78
e75
e76
Case Presentation A 50-year-old, right-handed, woman with no history of neurologic or psychiatric illness underwent EVD via the anterior horns of both lateral ventricles for spontaneous IVH and intracerebral hemorrhage in the right corona radiata. She was treated at the neurosurgery department of a university hospital (Fig 1, A). At the onset of her hemorrhage, she experienced mental drowsiness. She also presented with complete weakness of the left extremities (Medical Research Council [MRC],7 0/5) and moderate weakness of the right extremities (MRC, 32/5; Table 1). After EVD (Fig 1, B), she regained alertness, but presented with cogwheel rigidity in both the upper and lower extremities. She also showed a 3-Hz resting tremor in both upper extremities. On computed tomography (CT) images obtained the day after the EVD, shrinkage of the ventricles (ie, slit-like ventricles) was observed. One month after onset, she was transferred to a local rehabilitative hospital where she underwent a comprehensive rehabilitative management program, including neuromuscular electrical stimulation therapy for her bilateral finger extensors, knee extensors, and ankle dorsiflexors (20 minutes 3 2 times/day, 6 days/week) and movement therapy (Monday through Friday, 2.5 hours/ day; Saturday, 1 hour/day). Five months after onset, CT showed a leukomalacic lesion in her right corona radiata
M.H. CHUN ET AL.
and dilatation of the ventricular system. The patient underwent a VP shunt operation via the right posterior horn of the lateral ventricle for hydrocephalus (Fig 1, C). In spite of comprehensive rehabilitation after her EVD and VP shunt operations, her rigidity and tremor had not improved 6 months after onset, and she was transferred to the rehabilitation department of a university hospital for more active rehabilitation. At that time, she presented with severe rigidity in both the upper and lower extremities, which was worse on the right side. She was thus unable to perform any activities of daily living and could not ambulate at all, even with the support of another person. Her degree of motor weakness could not be assessed because of her severe rigidity. On conventional magnetic resonance imaging performed 6 months after symptom onset, leukomalacic lesions in the right corona radiata and right occipitotemporal lobe were visible, but lesions that could be related to her rigidity were not observed (Fig 1, D). To evaluate the integrity of the patient’s nigrostriatal dopaminergic system, 18F-FP-CIT PET scanning was performed 6 months after onset using a Biograph 40 TruePoint PET/CT camera (Siemens/CTI, Knoxville, TN).8 Image acquisition began 3 hours after intravenous injection of 18F-FP-CIT PET (173.9 MBq). Emission PET data were acquired for 10 minutes in 3-dimentional mode after brain CT, which was performed in spiral mode at 120 kVp
Figure 1. (A) Brain computed tomography (CT) images at onset showing an intraventricular hemorrhage and an intracranial cerebral hemorrhage in the right corona radiata of the study case. (B) Brain CT images acquired the day after external ventricular drainage showing that the catheters were inserted through the anterior horns of both lateral ventricles and revealing slit-like ventricles. (C) Brain CT images obtained 5 months after onset showing the ventriculoperitoneal shunt inserted via the right occipital lobe, an encephalomalacic lesion in the right corona radiata caused by intracerebral hemorrhage, and an encephalomalacic lesion in the right occipital lobe caused by the shunt. (D) T2-weighted magnetic resonance imaging images acquired 6 months after onset showing encephalomalacic lesions in the right corona radiata and the right occipital lobe (Color version of figure appears online.)
PARKINSONISM AFTER EVD
e77
Table 1. Changes in Medical Research Council scores of both extremities in the study case 6 months (after carbidopa/levodopa medication)
Onset Right Left Shoulder abductor Elbow flexor Finger flexor Finger extensor Hip flexor Knee extensor Ankle dorsiflexor
32 32 32 32 32 32 32
Right
Left
31 42 42 42 21 32 32
3 31 31 31 21 32 32
0 0 0 0 0 0 0
Medical Research Council scores are as follows: 0, no contraction; 1, palpable contraction but no visible movement; 2, movement without gravity; 3, movement against gravity; 4, movement against a resistance lower than the resistance overcome by the healthy side; and 5, movement against a resistance equal to the maximum resistance overcome by the healthy side.
and 380 mA (reference standard) using the CARE Dose4D program (Siemens Medical Solutions, Forchheim, Germany). 18F-FP-CIT PET images were reconstructed using CT data for attenuation correction with the True X algorithm and an all-pass filter using a 336 3 336 matrix. 18 F-FP-CIT PET imaging revealed reduced binding of dopamine transporter (DAT) with a heterogeneous distribution in the bilateral striatum. DAT binding was significantly decreased in the body and tail portions of the bilateral caudate nuclei, and multifocal 18F-FP-CIT defects were seen in the left posterior putamen and right middle putamen (Fig 2). A ventrodorsal gradient of striatal DAT loss, which indicates idiopathic Parkinson disease, was not seen (Fig 2). A movement disorder specialist diagnosed our patient with secondary Parkinsonism induced by an intraventricular pressure change after EVD. Carbidopa/levodopa was started with an initial dose of 75/300 mg/day on the seventh day of admission to our department, with a gradual increase. The daily dose of carbidopa/levodopa had increased to 300/1200 mg/day by the third week of admission. Three weeks after admission, the patient had significantly lessened rigidity, espe-
Figure 2. (A) Brain positron emission tomography. (B) positron emission tomography/ computed tomography, and (C) maximum intensity projection images of 18F-florinatedN-3-fluoropropyl-2-b-carboxymethoxy-3-b-(4lodophenyl) nortropane demonstrating dopamine transporter loss throughout the bilateral striatum with a heterogeneous pattern, especially in the body and tail portions of the bilateral caudate nuclei, left posterior, and right midputamen (Color version of figure appears online.)
cially in the upper extremities, and she was able to move both upper extremities against gravity (MRC, 3-42/5; Table 1). As a result, she was able to grasp and release an object using either her right or left hand. She could also use a spoon with her right hand and independently feed herself. In addition, her rigidity in the lower extremities was improved, although the degree of the improvement was less than that of the upper extremities. She was able to move both her lower extremities against gravity, but not with a full range of motion (MRC, 21-32/5; Table 1) and ambulate with moderate assistance. The tremor, which had been gradually reducing from the start of the administration of carbidopa/levodopa, completely disappeared in the third week of admission.
Discussion Parkinsonism induced by a sudden decrease in pressure in the ventricles is rare but does occur.5,6 Our current patient presented with Parkinsonian symptoms, including rigidity and tremor, immediately after EVD for IVH. An EVD is a temporary system that drains cerebrospinal fluid (CSF) from the lateral ventricles in the center of the brain to an external reservoir. After EVD, significant shrinkage of the ventricles was observed on CT, which indicates overdrainage of CSF by the EVD. In addition, we confirmed dopaminergic dysfunction using the recently developed 18F-FP-CIT PET scan. 18F-FP-CIT PET is suitable for DAT imaging in clinical practice8 and has better spatial resolution and more sophisticated attenuation correction than singlephoton emission computed tomography (SPECT). In our 18 F-FP-CIT PET images, decreased DAT binding in the bilateral caudate nuclei and bilateral putamen was evident, and loss of striatal DAT was heterogeneously shown. The pattern of striatal DAT loss in 18F-FP-CIT PET reflects the pathologic basis of Parkinson disease.8 In a case of idiopathic Parkinson disease, a gradient in DAT loss from the ventral to the dorsal portion of the putamen is observed, whereas heterogeneous loss without a ventrodorsal gradient indicates secondarily induced Parkinsonism.9 Thus, we believe that our current patient’s Parkinsonian symptoms occurred secondarily and were attributable to a sudden decrease in ventricular pressure
M.H. CHUN ET AL.
e78
after overdrainage of the CSF after EVD, which is thought to induce mechanical damage to both the caudate nuclei and bilateral putamen. Moreover, we speculate that the hydrocephalus in our patient might have led to dysfunction in the caudate nuclei and putamen.3,4 However, given that the Parkinsonian symptoms manifested immediately after EVD in this case and that the placement of the VP shunt did not effectively relieve her symptoms, CSF overdrainage appears to bear the primary responsibility for her Parkinsonian symptoms. Thus far, 2 studies have reported on Parkinsonism or Parinaud sign after VP shunt placement. In 1998, Asamoto et al5 described a patient with acute Parkinsonism after a shunt revision. The sudden decrease in intraventricular pressure was thought to be partially involved in the Parkinsonian symptoms. The patient responded well to levodopa therapy, and the manifestations of Parkinsonism eventually completely disappeared. In 2006, Yomo et al6 reported a patient who presented with Parkinsonian symptoms, such as cogwheel rigidity that was worse on the left side, bradykinesia, and drooling, after a VP shunt placement for obstructive hydrocephalus. The authors suggested that overdrainage of the CSF was responsible for the Parkinsonian symptoms of their patient. The symptoms of their patient were refractory to treatment, including shunt revision and levodopa therapy. Unlike our present case, these previous studies did not demonstrate dysfunction of the dopaminergic system using tools such as PET/SPECT imaging. In conclusion, we here report a patient who had Parkinsonism after EVD for IVH. Using 18F-FP-CIT PET images, we confirmed the dysfunction of the bilateral caudate nuclei and putamen, which seems to have induced Parkinsonism after EVD in this case, although no lesion was observed in those areas on either conventional CT or magnetic resonance imaging. Therefore, clinicians should pay particular attention to the occurrence of Parkinsonism when performing procedures that can
reduce intraventricular pressure. To the best of our knowledge, this is the first case report detailing Parkinsonism after EVD. Moreover, we demonstrated dysfunction of the dopaminergic system using the recently developed 18F-FP-CIT PET scanning technique. However, our present report is based on a single case, and the etiology of this complication has not been definitively confirmed. Thus, complementary studies, including larger numbers of patients and investigating alterations of Parkinsonian symptoms after changes in intraventricular pressure, are warranted.
References 1. Kim MJ, Chung SJ, Sung YH, et al. Levodopa-responsive parkinsonism associated with hydrocephalus. Mov Disord 2006;21:1279-1281. 2. Pradhan S, Pandey N, Shashank S, et al. Parkinsonism due to predominant involvement of substantia nigra in Japanese encephalitis. Neurology 1999;53:1781-1786. 3. Prashantha DK, Netravathi M, Ravishankar S, et al. Reversible parkinsonism following ventriculoperitoneal shunt in a patient with obstructive hydrocephalus secondary to intraventricular neurocysticercosis. Clin Neurol Neurosurg 2008;110:718-721. 4. Racette BA, Esper GJ, Antenor J, et al. Pathophysiology of parkinsonism due to hydrocephalus. J Neurol Neurosurg Psychiatry 2004;75:1617-1619. 5. Asamoto S, Sugiyama H, Doi H, et al. Levodopa effective parkinsonism associated with aqueductal stenosis: a case report and review of the literature. No Shinkei Geka 1998;26:1089-1092. 6. Yomo S, Hngo K, Kuroyanagi T, et al. Parkinsonism and midbrain dysfunction after shunt placement for obstructive hydrocephalus. J Clin Neurosci 2006;13:373-378. 7. Medical Research Council. Aids to examination of the peripheral nervous system. London, England: Her Majesty’s Stationery Office 1976. 8. Lee SJ, Oh SJ, Chi DY, et al. One-step high-radiochemicalyield synthesis of [18F]FP-CIT using a protic solvent system. Nucl Med Biol 2007;34:345-351. 9. Townsend DW. Dual-modality imaging: combining anatomy and function. J Nucl Med 2008;49:938-955.
Parkinsonism after External Ventricular Drainage in a Patient with Intraventricular Hemorrhage Min Ho Chun, MD, PhD,* Chang Gu Kang, MD,* Eun Jung Kong, MD,† and Min Cheol Chang, MD*
We report a patient who presented with Parkinsonism after external ventricular drainage (EVD) for an intraventricular hemorrhage (IVH). We also demonstrate dopaminergic system dysfunction using 18F-florinated-N-3-fluoropropyl-2-b-carboxymethoxy-3-b-(4-lodophenyl) nortropane (18F-FP-CIT) positron emission tomography (PET) scanning. A 50-year-old woman presented with manifestations of Parkinsonism, including severe rigidity and 3-Hz resting tremor, immediately after EVD for IVH. 18F-FP-CIT PET images at 6 months after onset showed dysfunction of the bilateral caudate nuclei and putamen after EVD that seemed to have induced Parkinsonism, although no lesion was observed in those areas on either conventional computed tomography or magnetic resonance imaging. With a dose of 300/ 1200 mg/day carbidopa/levodopa, the rigidity of both upper and lower extremities was significantly reduced, and the tremor completely disappeared. The decreased rigidity also improved the activities of daily living performance. In summary, a patient developed Parkinsonism after EVD for IVH, and we demonstrated dopaminergic system dysfunction on 18F-FP-CIT PET images. Clinicians should pay particular attention to the occurrence of Parkinsonism when performing procedures that can reduce intraventricular pressure. Key Words: Parkinsonism—external ventricular drainage—intraventricular hemorrhage—18F-FP-CIT—positron emission tomography. Ó 2015 by National Stroke Association
Parkinsonism can be secondarily induced by various causes, such as stroke, encephalitis, drug poisoning, and hydrocephalus.1-4 Parkinsonism has also been reported in patients with obstructive hydrocephalus From the *Department of Physical Medicine and Rehabilitation, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea; and †Department of Nuclear Medicine, University of Yeungnam College of Medicine, Taegu, Republic of Korea. Received July 30, 2014; revision received September 5, 2014; accepted October 27, 2014. The authors declare no conflicts of interest. Address correspondence to Min Cheol Chang, MD, Department of Physical Medicine and Rehabilitation, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Pungnap-2 dong, Songpa-gu, Seoul 138-736, Republic of Korea. E-mail: [email protected]. 1052-3057/$ - see front matter Ó 2015 by National Stroke Association http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2014.10.013
after ventriculoperitoneal (VP) shunt placement.5,6 In such cases, it was proposed that shear forces arising from sudden changes in ventricular pressure after VP shunt placement caused mechanical disruption of the nigrostriatal pathways from the medial substantia nigra to the caudate nucleus and putamen or dysfunction of the basal ganglia and its frontal projection fibers. However, Parkinsonism after external ventricular drainage (EVD) has not yet been reported. In the present study, we report such a case involving a patient who presented with Parkinsonism after EVD for an intraventricular hemorrhage (IVH). We also demonstrate dopaminergic system dysfunction using 18 F-florinated-N-3-fluoropropyl-2-b-carboxymethoxy-3b-(4-lodophenyl) nortropane (18F-FP-CIT) positron emission tomography (PET) scanning.
Journal of Stroke and Cerebrovascular Diseases, Vol. 24, No. 3 (March), 2015: pp e75-e78
e75
e76
Case Presentation A 50-year-old, right-handed, woman with no history of neurologic or psychiatric illness underwent EVD via the anterior horns of both lateral ventricles for spontaneous IVH and intracerebral hemorrhage in the right corona radiata. She was treated at the neurosurgery department of a university hospital (Fig 1, A). At the onset of her hemorrhage, she experienced mental drowsiness. She also presented with complete weakness of the left extremities (Medical Research Council [MRC],7 0/5) and moderate weakness of the right extremities (MRC, 32/5; Table 1). After EVD (Fig 1, B), she regained alertness, but presented with cogwheel rigidity in both the upper and lower extremities. She also showed a 3-Hz resting tremor in both upper extremities. On computed tomography (CT) images obtained the day after the EVD, shrinkage of the ventricles (ie, slit-like ventricles) was observed. One month after onset, she was transferred to a local rehabilitative hospital where she underwent a comprehensive rehabilitative management program, including neuromuscular electrical stimulation therapy for her bilateral finger extensors, knee extensors, and ankle dorsiflexors (20 minutes 3 2 times/day, 6 days/week) and movement therapy (Monday through Friday, 2.5 hours/ day; Saturday, 1 hour/day). Five months after onset, CT showed a leukomalacic lesion in her right corona radiata
M.H. CHUN ET AL.
and dilatation of the ventricular system. The patient underwent a VP shunt operation via the right posterior horn of the lateral ventricle for hydrocephalus (Fig 1, C). In spite of comprehensive rehabilitation after her EVD and VP shunt operations, her rigidity and tremor had not improved 6 months after onset, and she was transferred to the rehabilitation department of a university hospital for more active rehabilitation. At that time, she presented with severe rigidity in both the upper and lower extremities, which was worse on the right side. She was thus unable to perform any activities of daily living and could not ambulate at all, even with the support of another person. Her degree of motor weakness could not be assessed because of her severe rigidity. On conventional magnetic resonance imaging performed 6 months after symptom onset, leukomalacic lesions in the right corona radiata and right occipitotemporal lobe were visible, but lesions that could be related to her rigidity were not observed (Fig 1, D). To evaluate the integrity of the patient’s nigrostriatal dopaminergic system, 18F-FP-CIT PET scanning was performed 6 months after onset using a Biograph 40 TruePoint PET/CT camera (Siemens/CTI, Knoxville, TN).8 Image acquisition began 3 hours after intravenous injection of 18F-FP-CIT PET (173.9 MBq). Emission PET data were acquired for 10 minutes in 3-dimentional mode after brain CT, which was performed in spiral mode at 120 kVp
Figure 1. (A) Brain computed tomography (CT) images at onset showing an intraventricular hemorrhage and an intracranial cerebral hemorrhage in the right corona radiata of the study case. (B) Brain CT images acquired the day after external ventricular drainage showing that the catheters were inserted through the anterior horns of both lateral ventricles and revealing slit-like ventricles. (C) Brain CT images obtained 5 months after onset showing the ventriculoperitoneal shunt inserted via the right occipital lobe, an encephalomalacic lesion in the right corona radiata caused by intracerebral hemorrhage, and an encephalomalacic lesion in the right occipital lobe caused by the shunt. (D) T2-weighted magnetic resonance imaging images acquired 6 months after onset showing encephalomalacic lesions in the right corona radiata and the right occipital lobe (Color version of figure appears online.)
PARKINSONISM AFTER EVD
e77
Table 1. Changes in Medical Research Council scores of both extremities in the study case 6 months (after carbidopa/levodopa medication)
Onset Right Left Shoulder abductor Elbow flexor Finger flexor Finger extensor Hip flexor Knee extensor Ankle dorsiflexor
32 32 32 32 32 32 32
Right
Left
31 42 42 42 21 32 32
3 31 31 31 21 32 32
0 0 0 0 0 0 0
Medical Research Council scores are as follows: 0, no contraction; 1, palpable contraction but no visible movement; 2, movement without gravity; 3, movement against gravity; 4, movement against a resistance lower than the resistance overcome by the healthy side; and 5, movement against a resistance equal to the maximum resistance overcome by the healthy side.
and 380 mA (reference standard) using the CARE Dose4D program (Siemens Medical Solutions, Forchheim, Germany). 18F-FP-CIT PET images were reconstructed using CT data for attenuation correction with the True X algorithm and an all-pass filter using a 336 3 336 matrix. 18 F-FP-CIT PET imaging revealed reduced binding of dopamine transporter (DAT) with a heterogeneous distribution in the bilateral striatum. DAT binding was significantly decreased in the body and tail portions of the bilateral caudate nuclei, and multifocal 18F-FP-CIT defects were seen in the left posterior putamen and right middle putamen (Fig 2). A ventrodorsal gradient of striatal DAT loss, which indicates idiopathic Parkinson disease, was not seen (Fig 2). A movement disorder specialist diagnosed our patient with secondary Parkinsonism induced by an intraventricular pressure change after EVD. Carbidopa/levodopa was started with an initial dose of 75/300 mg/day on the seventh day of admission to our department, with a gradual increase. The daily dose of carbidopa/levodopa had increased to 300/1200 mg/day by the third week of admission. Three weeks after admission, the patient had significantly lessened rigidity, espe-
Figure 2. (A) Brain positron emission tomography. (B) positron emission tomography/ computed tomography, and (C) maximum intensity projection images of 18F-florinatedN-3-fluoropropyl-2-b-carboxymethoxy-3-b-(4lodophenyl) nortropane demonstrating dopamine transporter loss throughout the bilateral striatum with a heterogeneous pattern, especially in the body and tail portions of the bilateral caudate nuclei, left posterior, and right midputamen (Color version of figure appears online.)
cially in the upper extremities, and she was able to move both upper extremities against gravity (MRC, 3-42/5; Table 1). As a result, she was able to grasp and release an object using either her right or left hand. She could also use a spoon with her right hand and independently feed herself. In addition, her rigidity in the lower extremities was improved, although the degree of the improvement was less than that of the upper extremities. She was able to move both her lower extremities against gravity, but not with a full range of motion (MRC, 21-32/5; Table 1) and ambulate with moderate assistance. The tremor, which had been gradually reducing from the start of the administration of carbidopa/levodopa, completely disappeared in the third week of admission.
Discussion Parkinsonism induced by a sudden decrease in pressure in the ventricles is rare but does occur.5,6 Our current patient presented with Parkinsonian symptoms, including rigidity and tremor, immediately after EVD for IVH. An EVD is a temporary system that drains cerebrospinal fluid (CSF) from the lateral ventricles in the center of the brain to an external reservoir. After EVD, significant shrinkage of the ventricles was observed on CT, which indicates overdrainage of CSF by the EVD. In addition, we confirmed dopaminergic dysfunction using the recently developed 18F-FP-CIT PET scan. 18F-FP-CIT PET is suitable for DAT imaging in clinical practice8 and has better spatial resolution and more sophisticated attenuation correction than singlephoton emission computed tomography (SPECT). In our 18 F-FP-CIT PET images, decreased DAT binding in the bilateral caudate nuclei and bilateral putamen was evident, and loss of striatal DAT was heterogeneously shown. The pattern of striatal DAT loss in 18F-FP-CIT PET reflects the pathologic basis of Parkinson disease.8 In a case of idiopathic Parkinson disease, a gradient in DAT loss from the ventral to the dorsal portion of the putamen is observed, whereas heterogeneous loss without a ventrodorsal gradient indicates secondarily induced Parkinsonism.9 Thus, we believe that our current patient’s Parkinsonian symptoms occurred secondarily and were attributable to a sudden decrease in ventricular pressure
M.H. CHUN ET AL.
e78
after overdrainage of the CSF after EVD, which is thought to induce mechanical damage to both the caudate nuclei and bilateral putamen. Moreover, we speculate that the hydrocephalus in our patient might have led to dysfunction in the caudate nuclei and putamen.3,4 However, given that the Parkinsonian symptoms manifested immediately after EVD in this case and that the placement of the VP shunt did not effectively relieve her symptoms, CSF overdrainage appears to bear the primary responsibility for her Parkinsonian symptoms. Thus far, 2 studies have reported on Parkinsonism or Parinaud sign after VP shunt placement. In 1998, Asamoto et al5 described a patient with acute Parkinsonism after a shunt revision. The sudden decrease in intraventricular pressure was thought to be partially involved in the Parkinsonian symptoms. The patient responded well to levodopa therapy, and the manifestations of Parkinsonism eventually completely disappeared. In 2006, Yomo et al6 reported a patient who presented with Parkinsonian symptoms, such as cogwheel rigidity that was worse on the left side, bradykinesia, and drooling, after a VP shunt placement for obstructive hydrocephalus. The authors suggested that overdrainage of the CSF was responsible for the Parkinsonian symptoms of their patient. The symptoms of their patient were refractory to treatment, including shunt revision and levodopa therapy. Unlike our present case, these previous studies did not demonstrate dysfunction of the dopaminergic system using tools such as PET/SPECT imaging. In conclusion, we here report a patient who had Parkinsonism after EVD for IVH. Using 18F-FP-CIT PET images, we confirmed the dysfunction of the bilateral caudate nuclei and putamen, which seems to have induced Parkinsonism after EVD in this case, although no lesion was observed in those areas on either conventional CT or magnetic resonance imaging. Therefore, clinicians should pay particular attention to the occurrence of Parkinsonism when performing procedures that can
reduce intraventricular pressure. To the best of our knowledge, this is the first case report detailing Parkinsonism after EVD. Moreover, we demonstrated dysfunction of the dopaminergic system using the recently developed 18F-FP-CIT PET scanning technique. However, our present report is based on a single case, and the etiology of this complication has not been definitively confirmed. Thus, complementary studies, including larger numbers of patients and investigating alterations of Parkinsonian symptoms after changes in intraventricular pressure, are warranted.
References 1. Kim MJ, Chung SJ, Sung YH, et al. Levodopa-responsive parkinsonism associated with hydrocephalus. Mov Disord 2006;21:1279-1281. 2. Pradhan S, Pandey N, Shashank S, et al. Parkinsonism due to predominant involvement of substantia nigra in Japanese encephalitis. Neurology 1999;53:1781-1786. 3. Prashantha DK, Netravathi M, Ravishankar S, et al. Reversible parkinsonism following ventriculoperitoneal shunt in a patient with obstructive hydrocephalus secondary to intraventricular neurocysticercosis. Clin Neurol Neurosurg 2008;110:718-721. 4. Racette BA, Esper GJ, Antenor J, et al. Pathophysiology of parkinsonism due to hydrocephalus. J Neurol Neurosurg Psychiatry 2004;75:1617-1619. 5. Asamoto S, Sugiyama H, Doi H, et al. Levodopa effective parkinsonism associated with aqueductal stenosis: a case report and review of the literature. No Shinkei Geka 1998;26:1089-1092. 6. Yomo S, Hngo K, Kuroyanagi T, et al. Parkinsonism and midbrain dysfunction after shunt placement for obstructive hydrocephalus. J Clin Neurosci 2006;13:373-378. 7. Medical Research Council. Aids to examination of the peripheral nervous system. London, England: Her Majesty’s Stationery Office 1976. 8. Lee SJ, Oh SJ, Chi DY, et al. One-step high-radiochemicalyield synthesis of [18F]FP-CIT using a protic solvent system. Nucl Med Biol 2007;34:345-351. 9. Townsend DW. Dual-modality imaging: combining anatomy and function. J Nucl Med 2008;49:938-955.
