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Cerebral blood flow and clinical outcome in patients with thalamic hemorrhages: a comparison with putaminal hemorrhages.

It has been reported that the reduction of cerebral blood flow (CBF) is more pronounced with thalamic hemorrhages than with putaminal hemorrhages, and the clinical outcome is worse with the former. However, the mechanism underlying these differences is not clear. We compared neurologic status, hematoma volumes, outcome scores. and early (< 1 month) and late (2-12 month) CBF values between 15 patients with thalamic hemorrhages and 28 patients with putaminal hemorrhages. We also correlated thalamic versus hemispheric CBF on each side and ipsilateral versus contralateral thalamic and hemispheric CBF. Finally, we evaluated the response to acetazolamide during the late stage. Thalamic hemorrhages were associated with a more pronounced reduction in CBF bilaterally, even though their hematoma volumes were much smaller. Contralateral to the hemorrhage, the discrepancy in CBF values between the two groups became greater in the late stage because CBF started to recover in putaminal hemorrhages but persistently deteriorated in thalamic hemorrhages. In the group with thalamic hemorrhages, the correlation between thalamic and hemispheric CBF ipsilateral to the hemorrhage and between thalamic CBF on both sides was disrupted in the early stage and restored in the late stage, whereas the correlation between the hemispheric CBF values was consistently preserved. Acetazolamide invariably augumented CBF during the late stage. The clinical outcome was worse in the thalamic group, but CBF values correlated negatively with outcome in both groups. We conclude that the reduction of CBF in the late stage may be secondary to metabolic depression due to transneural depression ('diaschisis'). The metabolic depression in thalamic hemorrhages is more extensive and persistent than in putaminal hemorrhages, which probably accounts for both the more pronounced CBF reduction and the worse outcome.

Acetazolamide↗

Hydrocephalus is a determinant of early mortality in putaminal hemorrhage.

BACKGROUND AND PURPOSE: Previous studies have shown that the volume of intracerebral hemorrhage and Glasgow Coma Score (GCS) on admission are powerful predictors of 30-day mortality. However, the significance of hydrocephalus associated with deep cerebral hemorrhage has not been studied extensively. The purpose of this study was to determine the prognostic indicators of 30-day mortality in patients with deep cerebral hemorrhage. METHODS: We studied 100 consecutive patients with deep cerebral hemorrhage between 1994 and 1998. Deep cerebral hemorrhage was divided into 2 groups: putaminal hemorrhage (lateral group) and thalamic and caudate hemorrhage (medial group). Univariate and multivariate logistic regression analyses were performed to determine independent prognostic indicators of 30-day mortality. RESULTS: Hydrocephalus was present in 40 of the 100 patients. The 30-day mortality was 29%, and hydrocephalus was present in 76% of those who died. Multivariate analyses showed 2 independent prognostic indicators of 30-day mortality for putaminal hemorrhage: GCS </=8 (P:=0.002, odds ratio [OR] 37.7, CI 3.6 to 396.9) and hydrocephalus (P:=0.005, OR 27.4, CI 2.7 to 282.6). However, only GCS </=8 (P:=0.0002, OR 16.5, CI 3.7 to 73.4) was predictive of 30-day mortality for thalamic and caudate hemorrhage. This model (GCS </=8 and hydrocephalus) has a sensitivity of 57% and a specificity of 91% for predicting 30-day mortality for putaminal hemorrhage. When both attributes were present in putaminal hemorrhage (GCS </=8 and hydrocephalus), 1 (11%) of 9 patients survived, and when both attributes were missing 28 (100%) of 28 patients survived. CONCLUSIONS: Obstructive hydrocephalus on admission in a comatose patient with a putaminal hemorrhage predicts 30-day mortality.

Adult↗

The effect of hematoma removal for reducing the development of brain edema in cases of putaminal hemorrhage.

INTRODUCTION: Surgical intervention in putaminal hemorrhage has been a controversial issue. The aim of this research is to evaluate the benefits of surgery for reducing the development of brain edema. MATERIALS AND METHODS: Sixteen cases of putaminal hemorrhage were examined. Eight patients were treated conservatively (C group), and the other 8 patients were treated surgically (S group). Head CT scans were performed on the day of onset (day 0) in C group or performed just after surgery (day 0) in S group, and performed again once per period on days 1-7, 8-14, and 15-21. The volume of the mass including hematoma and edema (H + E) was measured using CT scans and the (H + E)/H0 ratios were calculated (H0; hematoma volume on day 0). The (H + E)/H0 ratios for each period were compared statistically between the 2 groups using a t-test. RESULTS: The mean values of(H + E)/H0 ratios at each period were 2.19, 2.63, 2.53 in C group, and 1.29, 1.29, 0.66 in S group. The values in S group were significantly lower as compared with C group in every period (p < 0.01, < 0.05, < 0.01). CONCLUSIONS: Hematoma volume reduction by surgery reduced the development of brain edema.

Adult↗

Failure of surgery to improve outcome in hypertensive putaminal hemorrhage. A prospective randomized trial.

Hypertensive putaminal hemorrhage remains a major cause of hemorrhagic stroke carrying extremely high morbidity. Considerable controversy remains regarding the optimal form of therapy. Between 1983 and 1989 we conducted a prospective randomized trial with three treatment strategies: best medical management, best medical management plus intracranial pressure monitoring, and surgical evacuation. Only patients with significant deficit harboring a putaminal hematoma at least 3.0 cm in diameter were entered. The study was interrupted after 21 patients had been studied (9, best medical management; 4, intracranial pressure monitoring; and 8, surgical evacuation). No differences were found among groups for age, admission blood pressure, and time interval between onset of symptoms and arrival at hospital. None of the subjects were capable of returning to prestroke activity. Fifteen (71%) died or remained vegetative at 6 months, and only 4 (19%) were capable of independent life at home. Of the 9 patients in the best medical management arm, 7 were dead or vegetative. In the surgical group, 4 patients died and only 2 were capable of independent life. These results suggest that current medical and neurosurgical therapies remain ineffective in preventing the devastating neurologic consequences of hypertensive putaminal hemorrhage.

Adult↗

[Three cases of cryptic arteriovenous malformation in basal ganglia manifested by putaminal hemorrhage].

Three cases of histologically proven cryptic arteriovenous (AV) malformation of the basal ganglia are reported. Seventeen cases of patients showing putaminal hemorrhage in the CT scan underwent craniotomy for evacuation of a hematoma between January 1986 and December 1988. The preoperative diagnosis was hypertensive putaminal hemorrhage. In all three cases a network of abnormal vessels around the internal capsule was detected at surgery. Case 1: A 62-year-old male was admitted to our hospital with consciousness disturbance (JCS 20), total aphasia and right hemiparesis. The CT scan showed left putaminal hemorrhage. The volume of the hematoma was 45 ml by CT criteria. Left carotid angiography did not demonstrate any abnormal findings. Case 2: 69-year-old male was admitted with consciousness disturbance (JCS 10) and right hemiparesis. Left putaminal hemorrhage (volume 25 ml) was recognized on the CT scan. Two hours after admission, the consciousness level suddenly deteriorated (JCS 100). At that moment, the volume of the putaminal hematoma had increased to 100 ml. AV malformation was not detected by left carotid angiography. Case 3: A 50-year-old male was admitted with consciousness disturbance (JCS 20), total aphasia and right hemiparesis. The CT scan showed left putaminal hemorrhage of 73 ml. Pathohistological examination proved AV malformation in each case. The three cases described here suggest the following; 1) The incidence of the basal ganglia cryptic AV malformation has been considered low, but meticulous examination shows that among the cases diagnosed as hypertensive hemorrhage, AV malformation is not infrequently the hidden cause.(ABSTRACT TRUNCATED AT 250 WORDS)

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Bilateral putaminal hemorrhage with cerebral edema in hyperglycemic hyperosmolar syndrome.

Bilateral putaminal hemorrhages rarely occur simultaneously in hypertensive patients. The association of intracerebral hemorrhage with cerebral edema (CE) has been rarely reported in diabetic patients. We present a patient with bilateral putaminal hemorrhage (BPH) and CE during the course of hyperglycemic hyperosmolar syndrome (HHS). A 40-year-old man with a history of diabetes mellitus and chronic alcoholism was admitted with acute impaired mentality. His blood pressure was within the normal range on admission. Laboratory results revealed hyperglycemia and severe metabolic acidosis without ketonuria. After aggressive treatment, plasma sugar fell to 217 mg/dl, but brain CT showed BPH and diffuse CE. Our case demonstrated that HHS should be considered as a cause of BPH with CE. Initial brain imaging study may be recommended for patients with diabetic coma.

Adult↗

[Evaluation of the hypertensive intracerebral hematoma based on the study on long-term outcome--Part I. Mode of hematoma extension and its clinical significance in putaminal hemorrhage].

A retrospective analysis of our series of 355 cases of putaminal hemorrhage revealed some interesting aspects of its pathogenesis. All the cases were studied in detail with special attention to clinical presentation, diagnostic findings and the long-term clinical outcome. Role of surgery in management of putaminal hemorrhage is still controversial. Inability to form proper useful classification has been one of the reasons responsible for this controversy. A new classification is formulated which divides putaminal hemorrhage into four types. Mild type has hematoma localized to external capsule while moderate type shows hematoma extension to corona radiata from external capsule. In severe type, hematoma extends to internal capsule also while in very severe type it further extends to midbrain. These four types could be very well correlated to long-term clinical outcome. Accessory hematoma is discussed in detail. It is found to be more common in severe and very severe types. Its presence in mild or moderate types results in worse clinical outcome. Hypertension (BP greater than 200 mm of Hg) may play an important role in further extension of hematoma.

Cerebral Hemorrhage↗

[Hypertensive putaminal hemorrhage with extensive subarachnoid hemorrhage presenting extravasation of contrast material during angiography: case report].

The authors describe a case of hypertensive putaminal hemorrhage with extensive subarachnoid hemorrhage. On admission, the patient aged 71 presented right-sided motor weakness. CT scan on admission revealed left putaminal hemorrhage with extension into the ipsilateral thalamus and lateral ventricle as well as into the subarachnoid space of the suprasellar, ambient, interhemispheric and contralateral sylvian cisterns. To exclude vascular lesions, left carotid angiography was performed just after admission. The lateral view was unremarkable, but the anterior-posterior view demonstrated extravasation of contrast material from the left lateral lenticulostriate artery. The angiographic sylvian point was shifted to the lateral side. No abnormal vessels were revealed. CT scan after angiography showed exacerbation of both intracerebral and subarachnoid hemorrhages, but the consciousness level was unchanged. CT-guided stereotactic aspiration of the hematoma was performed 4 days after the onset, but failed to remove much hemtoma. The patient died of aspiration pneumonia 9 days after onset. The authors emphasize that extensive subarachnoid hemorrhage in cases with hypertensive putaminal hemorrhage may be an important finding which indicates high risk of rebleeding.

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Putaminal hemorrhage: clinical-computed tomographic correlations.

Ninety-two percent of 100 patients with putaminal hemorrhage were hypertensive. Of the eight normotensive patients, seven were substance abusers or had bilateral putaminal hemorrhages. The one other normotensive patient was less than 40 years old. The 100 hemorrhages had the following locations: 1. medial putaminal (17 cases; six were normotensive and less than 40 years old and five were substance abusers); 2. lateral putaminal extending through the external capsule (eleven cases); 3. putaminal-capsular and subcortical white matter (32 cases); 4. putaminal cerebral hemispheric (19 cases); 5. putaminal-thalamic (19 cases); 6. bilateral (two cases). A disproportionate number of black patients suffered hematoma extension to the cerebral hemispheres or thalamus (46%) compared to Caucasians (23%). Overall mortality was 20% (17 blacks and three Caucasians) and occurred in patients with hematoma extension to the thalamus or cerebral hemispheres. Contrast-enhanced CT was performed in all 100 patients and provided no additional diagnostic yield. This indicates limited use for enhanced CT in hypertensive patients with putaminal hemorrhage who have a characteristic appearance of the acute hemorrhage on the nonenhanced CT.

Adult↗

Putaminal hemorrhage disrupts thalamocortical projection to secondary somatosensory cortex: case report.

Putaminal hemorrhage presenting pure sensory stroke is rare. We describe a case of left putaminal hemorrhage presenting contralateral hemisensory disturbance without hemiparesis. A 52-year-old man developed analgesia and thermoanesthesia in the right half of his body, but deep sensation was relatively well preserved. Neuroradiological and somatosensory evoked potential findings suggested that thalamocortical sensory pathways to the secondary somatosensory cortex (S2) were involved, whereas those to the primary somatosensory cortex (S1) were spared. In experimental animals, spinothalamic projections from the thalamic nucleus input directly to S2. In humans, thalamocortical pathways are still a subject of debate, but results of recent functional imaging studies suggest that the pathway of pain inputs directly to S2 and that of tactile sensation to S2 via S1. Our findings support these reports.

Evoked Potentials, Somatosensory↗

[A case of aneurysm of the peripheral middle cerebral artery presenting putaminal hemorrhage--pitfall in diagnosis].

A case mimicking hypertensive putaminal hemorrhage which was first treated by CT-guided stereotactic aspiration and eventually diagnosed as a sequence of the ruptured aneurysm of the left peripheral middle cerebral artery on postoperative angiography is presented. This 41 old, right-handed, hypertensive female suffered sudden onset of headache and right hemiparesis. Next day hematoma was evacuated by the CT-guided stereotactic aspiration because of progressive deterioration of the consciousness and patient recovered well. Fourteen days after the evacuation when she presented mild right hand weakness and motor aphasia, angiography revealed a saccular aneurysm with broad neck derived from left posterior parietal artery. A neck clipping necessitated an additional anastomosis between superficial temporal artery and distal middle cerebral artery because of parent artery stenosis. Postoperatively she is doing well with slight motor aphasia. Among the typical hypertensive putaminal hemorrhage diagnosed on CT scan, it is stressed that there may be a possibility of ruptured aneurysm situated on the peripheral middle cerebral artery.

Adult↗

Superacute phase blood pressure elevation may relate to massive hematoma in hypertensive putaminal hemorrhage.

A restrospective clinical investigation has been performed to elucidate the relationship between hematoma size in putaminal hemorrhage and blood pressure (BP) changes during the immediate post-hemorrhagic phase in the emergency room (ER). Thirty-seven adult patients brought to the emergency department by ambulance within 6 hours after onset of symptoms with a confirmed diagnosis of acute putaminal hemorrhage on CT have been involved. Two BP measurements during the superacute phase in the ER have been studied: immediately after arrival at the ER (BP-I), and immediately prior to CT examination (BP-II). Patients have been divided into 6 categories: 1) those whose BP decreased with treatment (D+), 2) those whose BP decreased without treatment (D-), 3) those whose BP increased in spite of treatment (I+), 4) those whose BP increased without treatment (I-), 5) those whose BP remained unchanged in spite of treatment (U+), and 6) those whose BP remained unchanged without treatment (U-). Hematoma size has been compared among 5 categories (D+, D-, I-, U+, U-) using factorial ANOVA (analysis of variance). The hematoma sizes have been found to be (D+) 54 +/- 44 ml, (D-) 22 +/- 25 ml, (I-) 102 +/- 58 ml, (U+) 11 +/- 5 ml, (U-) 21 +/- 9 ml (mean +/- S.D.), respectively. (I-) has been significantly larger than any of the other categories (p < 0.001 - 0.05). Additional ANOVA has shown that BP-II in category (I-) was significantly higher than that of the other categories. Patients with putaminal hemorrhage whose BP was elevating during the superacute phase in the ER were shown to have massive hematomas.

Acute Disease↗

[Cortical deafness following bilateral hypertensive putaminal hemorrhage].

A case of cortical deafness is reported, which was caused by two episodes of bilateral hypertensive putaminal hemorrhage. Such a case has not appeared in literature up to this time. The patient was a right-handed, 69-year-old man, admitted to us after the stroke with right hemiparesis and disturbance of consciousness. CT scans showed right putaminal hemorrhage. After recovery of consciousness, the patient complained of hearing difficulty of the right ear. The right hemiparesis improved and he was followed ambulatorily after two months hospitalization. He returned to his work and was able to drive a car. His hearing difficulty of the right ear progressed and became stone deaf six months after onset of the initial stroke. Two years after the first stroke, he was attacked by the second stroke with left hemiparesis. CT scans showed left putaminal hemorrhage larger than the previous one in the right. When the patient recovered consciousness, he complained of total deafness. Audiometry test showed that hearing was lost completely to both high and low notes, and there was absence of bone conduction bilaterally. Auditory brain stem response test revealed normal pattern from wave I through wave V bilaterally. Middle latency response showed normal component Po on the right ear and it was absent on the left. The component Pa was not identified on both ears. He showed skill and reliance on lip reading two years after the onset of the complete deafness. Now he can speak fluently and communicate with lip reading and written language, although no improvement of the complete deafness being noticed.(ABSTRACT TRUNCATED AT 250 WORDS)

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[Outcome evaluation in putaminal hemorrhage by multiple regression analysis].

The aim of this study was to determine the factors that influence the prognosis of hypertensive putaminal hemorrhage. We investigated the outcome of the activity of daily living (ADL 1: full recovery at social life, 2: self cared, 3: required partial care at home, 4: remained bedridden, 5: vegetative state, 6: dead) one year after the onset of putaminal hemorrhage in comparison with initial data obtained on the day when it occurred. The following parameters were assessed: sex, age, side of hematoma, classification of computed tomography (CT) findings, neurological grade, degree of muscle power, hematoma volume, treatment, past history of cerebrovascular disease, and laboratory data. In 67 patients with putaminal hemorrhage, the relationships among these parameters were examined using Spearman's rank correlation analysis. Additionally, in 55 patients (24 male and 31 female) with complete data from the day of onset, multiple regression analysis was performed. The data of muscle power were handled by the quantification method. The result of Spearman's rank correlation coefficient indicated that the outcome had a positive correlation with age (correlation coefficient = 0.375), CT classification (0.595), neurological grade (0.714), hematoma volume (0.689), a past history of cerebrovascular disease (0.475), the white blood cell count (0.541), and the lactate dehydrogenase level (0.347). The outcome had a negative correlation with muscle power (-0.579) and the cholinesterase (-0.340).(ABSTRACT TRUNCATED AT 250 WORDS)

Activities of Daily Living↗

[A study of aphasia caused by putaminal hemorrhage].

Aphasia was evaluated in 21 right-handed patients (39-74 years old) with putaminal hemorrhage, and compared with that caused by thalamic hemorrhage. The patients were divided into three groups by the volume of the hematoma: small hematoma (I, n = 6), middle hematoma (II, n = 8) and large hematoma (III, n = 7) groups in computed tomographic findings. Aphasia examination was performed 8-37 days (mean 21 days) after the onset. In group I, aphasia was not seen or just transient, if any. In group II, aphasia was mainly a mixed type, and the prognosis was excellent in many patients. In group III there were expressive type at anterior lesion, receptive type at posterior lesion and global aphasia at anterior-posterior lesion, and the prognosis was not good. It is suggested that the putamen itself does not participate in language behavior, and that aphasia caused by putaminal hemorrhage is due to destruction of the surrounding tissue of the putamen. The type of aphasia and prognosis are varied by the site of a lesion and a hematoma volume. It is also suggested that the thalamus is related to language behavior in a circle of thalamus-cortical language area-thalamus. Aphasia caused by putaminal or thalamic hemorrhage was observed to be different from classical cortical aphasia. But there was no significant difference between aphasia caused by putaminal lesions and that by thalamic lesions.

Adult↗

Computed tomographic findings of good prognosis for hemiplegia in hypertensive putaminal hemorrhage.

Computed tomography (CT) findings were analyzed in 17 patients with hypertensive putaminal hemorrhage accompanied by hemiplegia which had subsided almost completely by conservative therapy within one month after the onset. In such patients a high density area was not seen at the level of the lateral ventricles on CT scan. To study the reason for this, the relationship between the extent of a hematoma and the level at which the pyramidal tract was destroyed was investigated. From consideration of the process of destruction of the pyramidal tract by a hematoma, it seemed that CT findings at the level of the bodies of the lateral ventricles, rather than at the level of the posterior limb of the internal capsule, were of value in evaluating the prognosis of hemiplegia in putaminal hemorrhage.

Adult↗

Semiquantitative regional cerebral blood flow evaluation using 123I-IMP SPECT in a case showing transient ischemic attack caused by putaminal hemorrhage.

A 69-year-old woman presented a transient cerebral ischemic attack, showing left arm weakness and slurred speech which recovered within 4 h of onset, while computed tomography indicated a putaminal hemorrhage. The regional cerebral blood flow distribution, measured semiquantitatively by use of 123I amphetamine emission tomography, was disturbed, which persisted more than one month up to a maximum of 4.5 months from the onset of symptoms. This case illustrates a variety of putaminal hemorrhage of good functional and vital prognosis, and provides an example in which the regional cerebral blood flow disturbances might persist for more than one month up to 4.5 months after the occurrence of a transient ischemic attack caused by a putaminal hemorrhage.

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