On the other hand, there was little change in the pain score after single administration of amitriptyline or combinational administration of amitriptyline and clomipramine, or amitriptyline and ifenprodil, indicating that these agents have little effect on thalamic pain; therefore, the present study exhibited that only cilostazol has the analgesic effect. antidepressant, is usually used as a drug of first choice for CPSP 4, 5. Nevertheless, the recent evaluated therapies, including amitriptyline, have been largely unsuccessful in controlling CPSP 6, 7, indicating that few options are available for improving CPSP. Central post\stroke EG01377 TFA pain is considered to be persistent neuropathic pain of central origin that is generated after stroke. Some anticoagulants and antiplatelets, including triflusal, cilostazol, sarpogrelate, and miscellaneous drugs, may be effective for secondary stroke prevention 8. Cilostazol is also a drug of first choice for intermittent claudication in addition to secondary prevention of cerebral infarction 9, suggesting that the treatment of cilostazol may result in improvement in cerebral infarction. However, there have been no reports on the effects of cilostazol in patients with thalamic pain derived from cerebral infarction. Thus, cilostazol was administered to a patient with both thalamic pain and intermittent claudication, and its effect on thalamic pain was mainly evaluated. Case Description The patient was a 66\12 months\aged man with a history of hypertension, hypertensive retinopathy, severe pneumonia, and lacunar infarction. Three years previously, a left\side thalamic hemorrhage developed suddenly, and he experienced persistent pain and numbness of the right upper and lower limbs. Just before treatment, pain and numbness of the right side of face, upper and lower limbs, and intermittent claudication emerged. At the start of treatment, the visual analogue scale (VAS) without walking was 92, indicating severe pain, while he complained about pain in both legs after walking. Additionally, the dorsal arteries of both feet were impalpable, and he had depression, thalamic syndrome, hypertension, and probable arteriosclerosis obliterans. His score around the 21\item Hamilton Rating Scale for Depressive disorder (HAMD\21) was 20, indicating severe depressive disorder. Amitriptyline (25?mg/day), a tricyclic antidepressant, was administered throughout treatment and is currently still administered. Clomipramine (25?mg/day), another tricyclic antidepressant, was administered in addition to amitriptyline by intravenous drip for 8?days. Consequently, his HAMD\21 score was reduced to 4. No apparent changes in the VAS or intermittent claudication were observed. Thereafter, ifenprodil (30?mg/day), a cerebral circulation activator, was administered in addition to amitriptyline for 18?days. The VAS and intermittent claudication showed little change. Thus, ifenprodil was switched to cilostazol that has an antiplatelet effect on the cerebral circulation, and is thus widely used to treat intermittent claudication. Treatment with cilostazol (100?mg/day) for 1?week gradually improved the intermittent claudication and VAS score; indeed, the VAS score improved by 58 points, indicating mid\level pain. The administration of cilostazol (200?mg/day) for 2?weeks moreover improved the intermittent claudication, and he could walk and stretch voluntarily. Concurrently, his VAS score improved furthermore by 30 points, indicating slight pain (Fig.?1), and he was discharged from the hospital. He is currently continuing treatment as an outpatient and is receiving cilostazol and amitriptyline (Fig.?1). Open in a separate windows Physique 1 The clinical and therapeutic course of the patient. HAMD\21, 21\item Hamilton Rating Scale for Depressive disorder; VAS, visual analogue scale; DIV, intravenous drip infusion. The pain score (VAS) was decreased after the start of cilostazol treatment. T2\weighted magnetic resonance imaging (MRI) of the brain revealed a clear lesion derived from an obsolete hemorrhage, predominantly in the left thalamus (Fig.?2). Concurrently, 99mTc\ethylene cysteine diethylester (ECD) single\photon emission computed tomography (SPECT) exhibited deterioration in the blood flow of the brain, predominantly in the left thalamus (Fig.?3A), and the regional blood flow showed little change, or rather decrease, even after the start of cilostazol treatment (Fig.?3B). Open in a separate window Physique 2 T2\weighted MRI imaging of brain. Obsolete cerebral infarction was acknowledged in the left\dominated thalamus as illustrated by a circle. Open in a separate window Physique 3 99mTc\ECD SPECT with the easy Z\score imaging system findings from August 2015 (A) and January 2017 (B). A left\dominated reduction of cerebral blood flow was acknowledged in the thalamus EG01377 TFA before (A) and after treatment with cilostazol (B). Discussion Magnetic resonance imaging and SPECT imaging of the brain of a patient with thalamic pain exhibited clear stroke\derived lesions and decreased EG01377 TFA blood flow over an area of the left thalamus, respectively. In addition, stroke\derived lesions caused severe pain on the right\side extremities. The left and right reversed relationship between the thalamic lesion and the extremity pain is consistent with an ascending pathway of pain information, indicating that pain in the extremities was derived from thalamic lesions. This is.Judging from the effect of cilostazol on a patient with thalamic pain, it is possible that administration of cilostazol enhances axonal sprouting and, consequently, the function of inhibitory neurons in the thalamus is usually recovered and thalamic pain is alleviated, although the relationship between axonal sprouting and cAMP remains uncertain. drug of first choice for CPSP 4, 5. Nevertheless, the recent evaluated therapies, including amitriptyline, have been largely unsuccessful in controlling CPSP 6, 7, indicating that few options are available for improving CPSP. Central post\stroke pain is considered to be persistent neuropathic pain of central origin that is generated after stroke. Some anticoagulants and antiplatelets, including triflusal, cilostazol, sarpogrelate, and miscellaneous drugs, may be effective for secondary stroke prevention 8. Cilostazol is also a drug of first choice for intermittent claudication in addition to secondary prevention of cerebral infarction 9, suggesting that the treatment of cilostazol may result in improvement in cerebral infarction. However, there have been no reports on the effects of cilostazol in patients with thalamic pain derived from cerebral infarction. Thus, cilostazol was administered to a patient with both thalamic pain and intermittent claudication, and its effect on thalamic pain was mainly evaluated. Case Description The patient was a 66\12 months\old man with a history of hypertension, hypertensive retinopathy, severe pneumonia, and lacunar infarction. Three years previously, a left\side thalamic hemorrhage developed suddenly, and he experienced persistent pain and numbness of the right upper and lower limbs. Just before treatment, pain and numbness of the right side of face, upper and lower limbs, and intermittent claudication emerged. At the start of treatment, the visual analogue scale (VAS) without walking was 92, indicating severe pain, while he complained about pain in both legs after walking. Additionally, the dorsal arteries of both feet were impalpable, and he had depression, thalamic syndrome, hypertension, and probable arteriosclerosis obliterans. His score around the 21\item Hamilton Rating Scale for Depressive disorder (HAMD\21) was 20, indicating severe depressive disorder. Amitriptyline (25?mg/day), a tricyclic antidepressant, was administered throughout treatment and is currently still administered. Clomipramine (25?mg/day), another tricyclic antidepressant, was administered in addition to amitriptyline by intravenous drip for 8?days. Consequently, his HAMD\21 score was reduced to 4. No apparent changes in the VAS or intermittent claudication were observed. Thereafter, ifenprodil (30?mg/day), a cerebral circulation activator, was administered in addition to amitriptyline for 18?days. The VAS and intermittent claudication showed little change. Thus, ifenprodil PROCR was switched to cilostazol that has an antiplatelet effect on the cerebral circulation, and is thus widely used to treat intermittent claudication. Treatment with cilostazol (100?mg/day) for 1?week gradually improved the intermittent claudication and VAS score; indeed, the VAS score improved by 58 points, indicating mid\level pain. The administration of cilostazol (200?mg/day) for 2?weeks moreover improved the intermittent claudication, and he could walk and stretch voluntarily. Concurrently, his VAS score improved furthermore by 30 points, indicating slight pain (Fig.?1), and he was discharged from the hospital. He is currently continuing treatment as an outpatient and is receiving cilostazol and amitriptyline (Fig.?1). Open in a separate window Physique 1 The clinical and therapeutic course of the patient. HAMD\21, 21\item Hamilton Rating Scale for Depressive disorder; VAS, visual analogue scale; DIV, intravenous drip infusion. The pain score (VAS) was decreased after the start of cilostazol treatment. T2\weighted magnetic resonance imaging (MRI) of the brain revealed a clear lesion derived from an obsolete hemorrhage, predominantly in the left thalamus (Fig.?2). Concurrently, 99mTc\ethylene cysteine diethylester (ECD) single\photon emission computed tomography (SPECT) exhibited deterioration in the blood flow of the brain, mainly in the remaining thalamus (Fig.?3A), as well as the regional blood circulation showed little modification, or rather lower, even following the begin of cilostazol treatment (Fig.?3B). Open up in another window Shape 2 T2\weighted MRI imaging of mind. Outdated cerebral infarction was identified in the remaining\dominated thalamus as illustrated by.