Different Effects of Hematoma Expansion on Short-Term Functional Outcome in Basal Ganglia and Thalamic Hemorrhages.

PURPOSE: To investigate the impact of hematoma expansion (HE) on short-term functional outcome of patients with thalamic and basal ganglia intracerebral hemorrhage. METHODS: Data of 420 patients with deep intracerebral hemorrhage (ICH) that received a baseline CT scan within 6 hours from symptom onset and a follow-up CT scan within 72 hours were retrospectively analyzed. The poor functional outcome was defined as modified Rankin score (mRS) > 3 at 30 days. Receiver operating characteristic (ROC) curves for relative and absolute growth of HE were generated and compared. Multivariable logistic regression models were used to analyze the impact of HE on the functional outcome in basal ganglia and thalamic hemorrhages. The predictive values for different thresholds of HE were calculated, and correlation coefficient matrices were used to explore the correlation between the covariables. RESULTS: Basal ganglia ICH showed a higher possibility of absolute hematoma growth than thalamic ICH. The area under the curve (AUC) for absolute and relative growth of thalamic hemorrhage was lower than that of basal ganglia hemorrhage (AUC 0.71 and 0.67, respectively) in discriminating short-term poor outcome with an AUC of 0.59 and 0.60, respectively. Each threshold of HE independently predicted poor outcome in basal ganglia ICH (P < 0.001), with HE > 3 ml and > 6 ml showing higher positive predictive values and accuracy compared to HE > 33%. In contrast, thalamic ICH had a smaller baseline volume (BV, 9.55 ± 6.85 ml) and was more likely to initially involve the posterior limb of internal capsule (PLIC) (85/153, 57.82%), and the risk of HE was lower without PLIC involvement (4.76%, P = 0.009). Therefore, in multivariate analysis, the effect of thalamic HE on poor prognosis was largely replaced by BV and the involvement of PLIC, and the adjusted odds ratios (ORs) of HE was not significant (P > 0.05). CONCLUSION: Though HE is a high-risk factor for short-term poor functional outcome, it is not an independent risk factor in thalamic ICH, and absolute growth is more predictive of poor outcome than relative growth for basal ganglia ICH.

Biomechanical Analysis of the Head Movements of a Person Thrown by the Judo Technique 'Seoi-nage'.

The present study examined the kinematics and biomechanical parameters of the head of a person thrown forward by the judo technique 'Seoi-nage'. A judo expert threw an anthropomorphic test device (the POLAR dummy) five times. Kinematics data were obtained with a high-speed digital video camera. Linear and angular accelerations of the head were measured by accelerometers mounted at the center of gravity of the dummy's head. When Seoi-nage was performed, the dummy fell forward accompanied by contacting the anterior parietal regions of the head to the tatami, and the linear and angular accelerations of most axes reached peak values when the head contacted the tatami. Peak resultant linear and angular accelerations were 20.3 ± 9.8 G and 1890.1 ± 1151.9 rad/s2, respectively (means ± standard deviation). Peak values in linear and angular acceleration did not significantly differ between the three directional axes. Absolute angular accelerations in all axes observed in Seoi-nage were high and the resultant value was approximately equal to the already reported in Ouchi-gari, one of the predominant techniques causing judo-related acute subdural hematoma. However, the remarkable increase of linear acceleration in the longitudinal direction and/or angular acceleration in the sagittal plane, as previously reported in techniques being thrown backward (i.e., Ouchi-gari and Osoto-gari), was not detected. The likely mechanism of acute subdural hematoma caused by Seoi-nage is that a large angular acceleration causes large strains and deformations of the brain surface and subsequent rupture of cortical vessels.

Relationships between kinesiotherapy methods used in rehabilitation and the course of lost function recovery following surgical treatment of cranio-cerebral trauma.

INTRODUCTION AND AIM: This paper aims to outline the relationships between kinesiotherapy methods used in rehabilitation and the recovery of the patient's ability to perform activities of daily living (ADLs), improvement of functional condition, regression of pareses and improvement of conscious state following surgical treatment of traumatic subdural haematomas. MATERIALS AND METHODS: The study was conducted on 84 patients treated surgically for traumatic subdural haematomas, divided into two groups. The key differentiating factor was the kinesiotherapy method used in rehabilitation. Patients were assessed using the International Scale of Muscle Weakness (ISMW), Barthel Index and modified Rankin Scale, while their conscious state was assessed using the Glasgow Coma Scale. RESULTS: A significant improvement of the assessed features was observed in all patients. However, patients treated with proprioceptive neuromuscular facilitation (PNF) and elements of the Bobath concept regained lost function significantly faster than patients treated with traditional kinesiotherapy. No significant differences were observed in the course of improvement of conscious state between the two groups. CONCLUSIONS: Treatment using functional elements may significantly accelerate the return of the ability to perform ADLs, improvement in functional condition and regression of pareses in comparison with traditional kinesiotherapy.

Assessment of prognostic factors in severe traumatic brain injury patients treated by mild therapeutic cerebral hypothermia therapy.

This study analyzed the predictable factors of outcome such as neuro-parameters and systemic complications to elucidate the indications for therapeutic hypothermia. In our institute, 35 patients with severe head injury (Glasgow Coma Scale 3-7) were treated with mild hypothermia therapy (33 degrees-35 degrees C). Twenty-two of these 35 patients underwent complete neuromonitoring and outcome assessments by Glasgow Outcome Scale (GOS) at three months after injury. GOS of hypothermia group was significantly better than another patient group which was treated without mild hypothermia therapy. The hypothermia group was divided into two groups: good outcome (GOOD) (good recovery or moderate disability; n = 9, 40.9%) and poor outcome (POOR) (severe disability, vegetative state, or death; n = 13, 59.1%). The mean age (mean 30.2 years, range 9-46) was significantly lower in GOOD than in POOR (mean 45.2 years, range 17-62). Patients aged over 50 years had poor outcome. CPP was significantly higher in GOOD during hypothermia. All patients with thrombocytopenia had poor outcome. Hypothermia therapy can improve outcome in patients with traumatic brain injury who are younger than 50 years old, without severe brain damage, and if improvement of cerebral perfusion is expected. Systemic complications must be prevented as far as possible by combination with other therapies.

Effects of hypothermia on intracranial pressure and brain edema formation: studies in a rat acute subdural hematoma model.

Acute subdural hematoma (SDH) is the most common mass lesion in severe head injury, and brain ischemia is the leading pathophysiological mechanism in the development of secondary brain damage following SDH. Hypothermia has been employed as an effective neuroprotective procedure in clinical and laboratory studies on cerebral ischemic and contusional injuries. In the present study, we used a rat acute SDH model to assess the effect of hypothermia on the intracranial pressure (ICP) and also on the brain edema formation at 4 h after hematoma induction. Mild (34 degrees C) and moderate (32 degrees C) hypothermia did not significantly affect the ICP or cerebral perfusion pressure, but they were associated with a significant lower cortical brain edema formation beneath the hematoma (81.09 +/- 0.49%, p<0.05; and 80.88 +/- 0.17%, p<0.01) when compared with the normothermic control group (81.65 +/- 0.52%). This reduction in brain edema formation was comparable to the results of MK-801 treatment (80.95 +/- 0.35%, p<0.01). The present findings indicate that hypothermia represents a potent neuroprotective strategy. The possible protective mechanisms of hypothermic protection afforded in this rat acute SDH model are discussed.

[Clinical study of cerebral blood flow in unilateral chronic subdural hematoma measured by 99mTc-HMPAO SPECT].

Cerebral blood flow (CBF) measured by 99mTc-HMPAO SPECT before operation was studied in 60 patients with unilateral chronic subdural hematoma. The regional CBF was measured in 26 regions of the fronto-occipital 10 cortices, putamen, thalamus and cerebellar hemisphere on both sides. Sixty cases with unilateral chronic subdural hematoma were classified into four groups on the basis of clinical symptoms: 17 cases with headache (headache group), 34 cases with hemiparesis (hemiparesis group) and 9 cases with consciousness disturbance or dementia (consciousness disturbance group), and into three groups on the basis of the degree of midline brain shift on MRI: 7 cases of mild shift group, 24 cases of moderate shift group and 29 cases of severe shift group. The average CBF in 60 patients in each region indicated that the regional CBF was reduced in frontal, occipital cortices and cerebellum on the non-hematoma side, and in putamen and thalamus on the hematoma side. In the headache group, the regional CBF reduction on the non-hematoma side was found in only frontal and occipital cortices compared with the corresponding regions on the hematoma side. In the hemiparesis group, the regional CBF was reduced in frontal and occipital cortices on the non-hematoma side and in putamen and thalamus on the hematoma side. The part of CBF reduction in both hemispheres was also noted in the hemiparesis group. In the consciousness disturbance group, the CBF reduction was markedly noted in whole brain. The CBF reductions in frontal and occipital cortices on the non-hematoma side and in putamen, thalamus and cerebellum on the hematoma side was not mutually related with the degree of midline brain shift. We concluded that the disturbance of CBF in chronic subdural hematoma was started from frontal and occipital cortices on the non-hematoma side observed in the headache group, and which was extended to putamen and thalamus on the hematoma side and a part of both hemispheres observed in the hemiparesis group. And such disturbance was finally observed as the CBF reductions in whole brain in the consciousness disturbance group.

Blood degradation products play a role in cerebral ischemia caused by acute subdural hematoma.

The pathogenesis of ischemic brain lesions with traumatic hematoma is multifactorial. It has been suggested that the presence of subdural hematoma in patients with severe head injury is associated with elevated intracranial pressure and higher mortality. In this study we created acute subdural mass in the rats by injecting 250 microliters of autologous blood and silicone oil into the subdural space. The goal of this study was to determine the effect of subdural hematoma versus silicone oil on the adjacent brain parenchyma. Twenty-four hours after the injection, of the hematoma in the subdural space in rats produced an extensive zone of underlying ischemic damage but silicone oil did not. This study has shown that pressure alone caused by silicone oil is insufficient to cause significant neuronal damage or loss.

Hematoma subdural crónico en paciente joven / Chronic subdural hematoma in young patient

Entre julio de 1984 y junio de 1989 en el I.N.C. e I.C. Dr. A. Asenjo, se operaron de hematoma subdural crónico, H.S.D.Cr, 140 pacientes, 14 de los cuales eran menores de 30 años, 10 por ciento, representando un promedio de 2,8 pacientes por año. 10 pacientes fueron varones, 71,4 por ciento, y 4 mujeres, 28,6 por ciento. En 12 encontramos antecedente de trauma craneal, 85,7 por ciento, pero en solo 8 ésta databa de por lo menos 3 semanas antes del ingreso. En 2 habían antecedentes mórbidos: un hidrocefálico y un niño con un anemia y desnutrición severas. El tiempo entre el inicio de la clínica y el diagnóstico fluctuó entre los 2 meses y 1 día, haciéndose en 4 el diagnóstico de tumor cerebral. En el 71,4 por ciento hubo cefalia con atributos de hipertensión intracraneal, 10pacs.; 42,9 por ciento, 6pac signos focales deficitarios; 21,4 por ciento, 3pac compromiso de conciencia y 7,1 por ciento, 1pac fue asintomático. El tratamiento fue en todos quirúrgico. En 2 hubo complicaciones respiratorias, 14,2 por ciento. Al alta: 13 se encontraban normales, 92,3 por ciento, y 1 falleció, 7,1 por ciento