33 research outputs found
Nimodipineμ΄ μ₯μ λκ²½μμ λ―ΈμΉλ μν₯
μνκ³Ό/λ°μ¬[μλ¬Έ]
[νκΈ]
λνλ₯μ κ°μλ‘ λ°μλλ ννμ± λμ§νμ λΉκ°μμ μΈ λμμμ νν μμΈμΌλ‘ μλ €μ Έ
μμΌλ©° ννμ± μμμΌλ‘ λΆν° λλ₯Ό 보νΈνλ κ²μ μ€μν μμκ³Όμ λ‘ μκ°λλ€. ννμ±
λμμμ κ΅μνν νμ μ€λ μ§μ°μ± μ κ΄λ₯μ λΉκ°μμ μΈν¬μμμ μ΄λνλ μΈν¬λ§λ³μ±
μ μν΄μ μΌκΈ°λλ€κ³ νλ©° μΉΌμμ΄μ¨μ λκ°μ§ λννμ λ³νμ리 κΈ°μ μ μ€μν μν μ
νλ€κ³ μλ €μ Έ μλ€. μΉΌμν΅λ‘ μ°¨λ¨μ λ ννμ± λμ§νμ κ°λ₯ν μΉλ£μ λ‘μ μκ°λμ΄ μ§
λ€. μΉΌμν΅λ‘ μ°¨λ¨μ μ€μ νλμΈ nimodipineμ dihydropyridine μ λ체λ‘μ κ°λ ₯ν νκ΄
νμ₯ μμ©μ΄ μμΌλ©° λνκ΄μ μ νμ μΌλ‘ μμ©νλ κ²μΌλ‘ μλ €μ Έ μλ€. μ μλ μ₯μ κ΅
μλνν λͺ¨λΈμ λμμΌλ‘ nimodipineμ ν¬μ¬νμ¬ nimodipineμ λννμ λν ν¨κ³Όλ₯Ό 보
κ³ μ νμλ€. μ€λλλλ§₯ νμ 1μκ°, 2μκ° κ·Έλ¦¬κ³ 6μκ° νμ nimodipine νΉμ μ리μ
μΌμλ₯Ό ν¬μ¬νμκ³ νμ 24μκ° λ€μ μνν μ κ²½νμ κ²μ¬μ λ³λ¦¬νμ μ견μ ν΅νμ¬ ni
modipine ν¬μ¬κ΅°κ³Ό μ€λλλλ§₯ νμλ§ μνν λμ‘°κ΅° λ° μ리μμΌμ ν¬μ¬κ΅°μ μλ‘ λΉκ΅
νμ¬ λ€μκ³Ό κ°μ κ²°κ³Όλ₯Ό μ»μ μ μμλ€.
1. Nimodipine ν¬μ¬κ΅°μ μ리μμΌμ ν¬μ¬κ΅° λ° λμ‘°κ΅°λ³΄λ€ λκ²½μμ λ©΄μ μ΄ μ½ 5βΌ11%
κ°μ λμλ€.
2. νμ 1μκ° νμ nimodipine ν¬μ¬κ΅°μ νμ 2μκ° λ° 6μκ° νμ nimodipine ν¬μ¬κ΅°
λ³΄λ€ λκ²½μμ λ²μκ° μμμΌλ ν΅κ³νμ μμλ μμλ€.
3. λμ‘°κ΅°κ³Ό μ리μμΌμ ν¬μ¬κ΅° κ°μλ λκ²½μ λΉμ¨μ λλ Έν μ°¨μ΄κ°, μμλ€.
4. Nimodipine ν¬μ¬κ΅°μ μ리μμΌμ ν¬μ¬κ΅° λ° λμ‘°κ΅°λ³΄λ€ μ κ²½νμ μκ²¬μ΄ μνΈνμλ€
.
μ΄μμ κ²°κ³Όλ‘ λ³΄μ λννμ nimodipineμ μ κ²½νμ μ견μ νΈμ μν€κ³ λκ²½μμ λ²μ
λ₯Ό κ°μμν¬ μ μλ€κ³ μκ°λλ€. Nimodipineμ μμ©κΈ°μ μ νμ€ν μλ €wu μμ§ μμΌλ n
imodipineμ λνλ₯λ₯Ό μ¦κ°μν€κ±°λ νμ μ κ²½μΈν¬μ μ§μ μμ©νμ¬ ννμ μν λμμ
μΌλ‘ λΆν° λλ₯Ό 보νΈνλ€κ³ μκ°λλ€.
The Effects of Nimodipine on Focal Cerebral Ischemia in Rats
Se Hyuck Park
Department of Medical Science The Graduate School, Yonsei University
(Directed by Professor Kyu Chang Lee, M.D.)
Brain ischemia due to a critical reduction in cerebral blood flow is a well
recognized and common cause of irreversible brain damage. Therefore protecting the
human brain from ischemic damage is an important clinical problem. Two major
factors influence the sequelae of cerebral ischemic injury : the delayed
hypoperfusion that occurs after focal ischemia and membrane failure that leads to
irreversible cell injury. Calcium ions play a major role in both pathophysiological
mechanisms. And so calcium channel blockers are a logical choice for investigation
as possible therapeutic agents for the treatment of cerebral ischemia. Nimodipine,
a dihyropyridine derivative, is one of the most potent calcium channel blocking
agents with a selective action on the intracranial vessels. The present study was
designed to test the effects of nimodipine on focal cerebral ischemia in rats. At
1, 2 or 6 hours after occlusion of the middle cerebral artery (MCA), rats were
treated with either nimodipine or saline. Neurological and pathological evaluation
was performed at 24 hours after occulusion. Neurological outcome was better in
nimodipine-treated rats and the size of the infarcted area was statistically
smaller in rats treated with nimodipine 1, 2 or 6 hours after occlusion (p<0.001,
p<0.001,p < 0.001 respectively) when compared with control rats (MCA occlusion
only) or saline-treated rats. The results show that nimodipine improves
neurological outcome and decreases the size of the infarcted area after ischemic
insult. The mechanism of action of nimodipine is not fully understood but
nimodipine could influene cerebral postischemic changes by improving blood flow
and/or by a direct action on neurons.restrictio
Clinical Observation of the Chronic Subdural Hematomas
μνκ³Ό/μμ¬[μλ¬Έ]
[νκΈ]
1976λ
1μλΆν° 1983λ
9μκΉμ§ μ°μΈμλ μ κ²½μΈκ³Όν κ΅μ€μμ μΉνν λ§μ±κ²½λλ§νν
μ’
103μμ λν μμμ κ³ μ°°, νΉν κ° μμ λ°©λ²μ λν κ²°κ³Όλ₯Ό μλ‘ λΉκ΅νμ¬ λ€μκ³Ό κ°
μ κ²°κ³Όλ₯Ό μ»μλ€.
1. μ°λ ΉλΆν¬λ 41μΈλΆν° 60μΈκΉμ§κ° 49λͺ
(47.5%)μΌλ‘ κ°μ₯ λ§μκ³ 40λ μ΄μμμλ 74
λͺ
(71.8%)μ΄μλ€. λ¨λ
λΉλ λ¨μκ° 87λͺ
(84.5%), μ¬μκ° 16λͺ
(15.5%) μ΄μλ€.
2. μ λ°μΈμμμλ λλΆμΈμλ ₯μ΄ μλ κ²½μ°λ 72λͺ
(79.6%)μ΄μκ³ μμ½μ€λ
μλ 13λͺ
(12
.6%)μ΄μμΌλ©° μ§μ£Όλ§λμ’
1μ, μ§μ£Όλ§λμ’
λ° λμμ’
μΌλ‘ λμ’
볡κ°κ°λκ΄μ ν μν 1μ
λ° λ§μ±κ³¨μμ±λ°±νλ³ 1μκ° μμλ€.
3. μμμ¦μΈ λ° μ κ²½νμ μ견μ 보면 λν΅μ΄ 82μ (77.6%)λ‘μ κ°μ₯ λ§μμΌλ©° λ§λΉμ¦
μμ΄ 46μ (44.7%), μμμ₯μ λ° μμ μ견μ μ λλΆμ’
κ°μ μ λλΆ λ³νκ° κ°κ° 45μ(43.
7%) λ° 44μ(42.7%)μλ€. κ·Έ μΈ κ΅¬ν , λ곡λΆλμ¦, κ²½λ ¨, μΈμ΄μ₯μ λ° μκ°μ¦μμ΄ μμλ€
.
4. λμ μ°νλ¨μΈ΅μ΄¬μμ΄ μ§λ¨ λ° μμ λ°©λ²μ κ²°μ κ³Ό μννμ μ μ€μν μν μ νλ©° ν
μ’
μ λ°λλ₯Ό λ³Ό λ μ λ°λνμ’
μ΄ 32μ(43.3%), λλ°λνμ’
28μ(37.8%), κ³ λ°λνμ’
10μ
(13.5%)μκ³ κ·ΈμΈ νΌν©λ°λλ 4μ (5.4%)μ νμ’
μμ λ³Ό μ μμλ€. μμ ν 3μ£Όλ΄μ μν
ν λμ μ°νλ¨μΈ΅μ΄¬μμμμ λν½μ°½μ¨μ λμ΄κ° λ€μλ‘ κ°μνμ¬ 40λ μ΄μμμλ 80% μ΄
νλ‘ κ°μνλ€.
5. νμ’
μ λ°μλΆμλ μ’μΈ‘μ΄ 47μ (45.6%), μ°μΈ‘μ΄ 43μ(41.8%)λ‘μ ν° μ°¨μ΄λ μμκ³
μμΈ‘μ±μ 13μ (12.6%)κ° μμλ€. λ¨μνμλ°°μΆμ μ νμ’
μ λ°°μΆλμ μμ λΉμΌλ κ°μ₯
λ§μ 49%μ λ¬νκ³ μμ λ€μλ 33%λ‘μ μμ ν μ 2μΌκΉμ§ μ 체μ 95%κ° λ°°μΆλμλ€.
6. μΉλ£λ°©λ²μΌλ‘ 102μμμλ μμ μ λ°©λ²μΌλ‘ μΉλ£νκ³ λλ¨Έμ§ 1μμμλ steroidμ L
asixλ₯Ό μ¬μ©νμ¬ λΉμμ μ μΌλ‘ μΉλ£νλ€. μμ λ°©λ²μΌλ‘λ 32μμμλ λ¨μνμλ°°μΆμ μ,
31μμμλ λκ°μ²κ³΅μ λ° κ°λ°©λ°°μΆμ μ, 1μ°¨ μμ ν λ€μ νμ’
μ΄ νμ±λ 2μλ₯Ό ν¬ν¨ν 31
μμμλ μ±νμ κ°λμ λ° νμ’
λ§ μ κ±°μ μ μννκ³ λλ¨Έμ§ 10μμμλ λκ°κ³¨ μ κ±°μ
ν νμ’
λ§μ μ κ±°νλ€. μμ λ²μ μλ‘ λΉκ΅ν κ²°κ³Ό λ¨μνμλ°°μΆμ μ΄ μΌμ°¨μ μΈ μΉλ£λ²μΌ
λ‘ μκ°λλ€. κ·Έλ¬λ μΌμ°¨ μμ ν νμ’
μ΄ λ€μ κ³ μΈ κ²½μ°, κ³ νμ± νμ’
μΈ κ²½μ° λ° λν½μ°½
μ΄ μ μλμ΄ κ²½λ§νκ°μ΄ μ€λ«λμ λ§νμ§ μλ κ²½μ°μλ κ°λμ ν νμ’
λ§ μ κ±°μ μ μ
νν΄μΌ νλ€.
CLINICAL OBSERVATION OF THE CHRONIC SUBDURAL HEMATOMAS
Se Hyuck Park
Department of Medical Science The Graduate School Yonsei University
(Directed by Prof. Kyu Chang Lee, M.D.)
One hundred three chronic subdural hematomas were treated from January, 1976 to
September, 1983, of which 102 cases were operated and 1 case was treated with
medication. The clinical analysis and surgical results were summerized as follows.
1. The chronic subdural hematomas were the most common in the 5th and 6th decade
(47.5%) and prominent over 5th decade(71.8%). The proportion of males(84.5%) was
much greater than females (15.5%)
2. 79.6% of crises had previous head injuries and 12.6% were chronic alcholics.
One case was associated with the arachnoid cyst in the middle cranial fossa and
another one case in the postoperative state of cystoperitoneal shunt due to
hydrocephalus and arachnoid cyst in the supratentorial and infratentorial area. One
case was under management of chronic myelocytic leukemia .
3. The common symptoms were headache(79.6%), motor weakness(44.7%), alternation
of consciousness(43.7%), change of fundus such as papilledema (42.7%) and vomiting
(35.0%). In addition there were pupillary inequality, seizure, speech disturbance
and visual symptoms.
4. Brain CT scan was the most effective and noninvasive diagnostic tool for
detecting chronic subdural hematoma and important in planning operative
intervention and evaluation of prognosis. Chronic subdural hematomas presented in 4
different forms in CT scans: hypodense subdural hematoma(43.3%), isodense subdural
hematoma(37.8%), hyperdense subdural hematoma(13.5%)and mixed density subdural
hematoma(5.4%). CT scanning was the most accurate method of determining the age of
a chronic subdural hematoma. The cerebral expansion rate (reduction in diameter of
the subdural space) decreased with aging and it was less than 80% in average over
5th decade within postoperative 3 weeks.
5. The right sided chronic subdural hematomas were 45.6%and the left were 41.8%
with bilaterality in 12.6%. Average amount of chronic subdural hematomas drained
daily in 32 patients treated with simple burr-hole and closed-system drainage were
as follows: 49% on the duty of operation, 33% on POD 1 and 13% on POD 2, and almost
all of the hematoma was drained out within two days doter surgery.
6. In 103 patients, operation were performed in 102 patients, and the other one
patient was treated conservatively. thirtytwo patients were underwent simple
burr-hole and closed-system drainage and in 1 patient craniotomy and and
membranectomy was necessary. The blood bags were used in 31 patients and Hemovac in
1 patient. Four patients were operated under local anesthesia. thirtyone patients
were treated with burr holes and open drainage and one patient required craniotomy
and membranectomy. In 31 patients underwent craniotomy and membranectomy.
Craniectomy and membranectomy were performed in 10 patients. One patient died of
hypertensive intracerebral hematoma 1 developed during operation under local
anesthesia and another 1 patient was unchanged following simple burr-hole and
closed-system drainage. Three patients were unchanged or deteriorted after burr
holes and open drainage and 8 patients following craniotomy and membranectomy. The
results of simple burr-hole and closed-system drainage were better than other
methods. Simple burr-hole and closed-system drainage is today's most rational
approach to the chronic subdural hematoma in children beyond the infant period and
in adults. Craniotomy, membranectomy and craniectomy should be reserved for
instances :the subdural recollection, failure of the brain to expands solid
hematoma and extensive swelling of white matter subjacent to the hematoma.restrictio