Raimund Firsching

Cerebellar haemorrhage: management and prognosis.

Of 26 patients with CT confirmed intracerebellar haematoma, 17 had ventricular drainage performed and 7 patients had the haematoma evacuated.Eleven patients died. Mortality was clearly related to state of consciousness. Seven out of 8 non-comatose patients survived but 10 out of 18 comatose patients died. As there was no incidence of deterioration immediately following placement of a ventricular drainage, the actual risk of upward transtentorial herniation seemed low. Absence of evoked potentials in 6 patients accurately predicted a fatal outcome but normal SEP and BAEP were of lesser value for predicting survival.

Brain death : practicability of evoked potentials

Multimodally evoked potentials were registered in 85 patients who fulfilled the criteria for brain death. While samatosensory and visual evoked potentials have been found to be of limited value for the diagnosis of brain death, the stepwise abolition of brain stem auditory evoked potentials (BAEP) confirmed brain death in 26 out of 85 patients, i. e. 31%.Registration of the abolition of BAEP is concluded to be a safe and acceptable confirmatory test. It is, however, more feasible for institutions, in which BAEP are analysed routinely. In spite of all efforts sequential BAEP could not be used for the diagnosis of brain death in the majority of cases either because of absence of reproducible responses at the initial registration or because the patient was already apnoic at the time of the initial BAEP. Assuming that bilateral preservation of wave I has the same significance as the stepwise abolition of BAEP, since it also proves the integrity of the peripheral receptor, BAEP are relevant for the declaration of brain death in approximately 30% of patients.

Contribution to the problem of giant cell astrocytomas.

Histological, immunocytochemical, and biological features of 38 giant cell gliomas were investigated. The invasion of these tumors and its giant cells by histiocytes, lymphocytes, plasma cells, and especially by eosinophilic granulocytes is viewed as an immune response, which may explain a favorable clinical course. Fifty-three percent of the patients were younger than 45 years at the time of surgery. The average postoperative survival of 27.4 months was clearly longer than in glioblastoma. These biological features suggest a differentiation from glioblastoma multiforme. The classification of this entity as “monstrocellular astrocytoma” is proposed.

Significance of eosinophilic granulocytes in chronic subdural hematomas

Despite a number of studies on infiltration of eosinophilic granulocytes into the outer membrane of chronic subdural hematomas, the significance of this phenomenon is not clear. We investigated histologically the membranes of 40 patients with chronic subdural encapsulated hematoma. Infiltrations with eosinophilic leucocytes were found in the granulation tissue of the inner layer of the outer membrane, either diffuse and sporadic (12 cases) or as massive agglomerations (28 cases). Fifty percent of the patients with marked infiltrations were between 61 and 80 years old. In 5 cases Charcot-Leyden crystals were identified. The numerous functions of the eosinophils play a more important role in repair than in maintenance of fluidity of hematomas.

Rehabilitation After Severe Head Injury

123 survivors of severely head injured patients presenting with coma grade III show a decreasing mean duration of coma with increasing age. The numbers and frequency of good recovery decrease, whereas poor recovery increases with age. Increase of the duration of coma grade III produces an increase of the mean latency and time of recovery and of the frequency of poor recovery, regardless of the age of the patients. Increasing age does not increase the mean latency and time of recovery systematically. The important conclusion of this analysis is, that the clinical feature of coma grade III, corresponding to GCS score of 4 and RLS of 6 and 7, indicates a different kind of brain damage at various age groups. It represents a lesser degree of brain damage for younger patients under 20, than for those over 20. In our opinion our observations do not demonstrate a better capacity of recovery of the young patients: but the young patients show a more severe clinical picture than the older patients do, if only the clinical syndrome of coma grade III with extensor rigidity, is considered as a yardstick for comparison.

Encapsulated subdural hematoma

In 45 out of 103 cases with chronic subdural hematoma a definite membrane was found. Membranectomy was performed in 37 cases, mostly as a secondary procedure after burr-hole evacuation and closed system drainage. The mortality rate was 6.6% and in the survivors a complete recovery was achieved in 90%. CT monitoring of the diameter of the hematoma and midline shift did not reveal any correlation of size of the hematoma with neurological findings. The indication for membranectomy can, therefore, not be based on radiological findings alone, but on the clinical course of events and with due regard to the CT findings.

Cerebral reperfusion in brain death of a newborn. Case report

A case of “sudden infant death” after 15 minutes of successful resusciation of cardiovascular function is presented. While apnoic cranial nerve areflexia and electrocerebral silence persisted, angiography and transcranial Doppler sonography demonstrated nearly normal cerebral perfusion, which even increased day by day inspite of the persistence of other signs of brain death. The phenomenon “cerebral reperfusion” is concluded to be compatible with the diagnosis of brain death.

Celebral Contusions, Lacerations and Hematomas

Biomechanics of Brain Injuries.- Basic Injury Mechanics.- Force, Strain, Duration of Load.- Injurious Parameters.- Specific Brain Injury Mechanisms.- Anatomical Features.- Characteristics of Loading.- Cranial Effects of Loading.- Skull Deformation - Angular Acceleration Theory.- Pressure Gradient - Translational Acceleration Theory.- Cavitation.- Cranio-spinal Junction Movements.- Primary Injuries.- Fractures.- Focal Injuries.- Diffuse Injuries.- Aspects of Injury Reduction.- References.- Cerebral Hemispheric Contusions and Lacerations.- Contusions.- Immediate Cerebral Effects.- Types of Brain Contusions.- Macroscopic Pathology.- Microscopic Pathology.- Vascular Alterations.- Neuronal Lesions.- Glial Lesions.- Fiber Lesions.- Late Cerebral Effects.- General Remarks.- Posttraumatic Encephalopathies.- Macroscopic Pathology.- Microscopic Pathology.- Punch-drunk Encephalopathy.- Macroscopic Pathology.- Microscopic Pathology.- Lacerations.- Immediate Cerebral Effects.- Types of Brain Lacerations.- Macroscopic Pathology.- Microscopic Pathology.- Lacerations as Component of Cranio-cerebral Wounds.- Progressive Continuous Form of Brain Lacerations.- Late Lesionai Effects of Brain Lacerations.- Meningo-cerebral Scars.- Macroscopic Pathology.- Microscopic Pathology.- Summary.- References.- Diffuse Brain Injury and Brainstem Dysfunction.- Experimental Confirmation of Diffuse Brain Injury.- Types of Diffuse Brain Injury.- Diffuse Brain Swelling.- Diffuse Degeneration.- Gliding Contusion.- Clinical Aspects of Diffuse Brain Injury.- Diagnostic Criteria.- Cerebral Concussion.- Cerebral Shearing Injury.- Diffuse Axonal Shearing Injury.- Primary Brainstem Injury.- References.- Cerebral Contusions and Lacerations. A Clinical Study.- Symptomatology.- Disturbances of Consciousness.- Signs of Localization.- Diffuse Neurological Signs.- Clinical Synthesis.- Anatomo-clinical Forms.- Cerebral Contusion.- Cerebral Laceration.- Hematoma Contusions.- Evolutive Forms.- Extremely Serious Forms.- Serious Forms.- Less Serious Forms.- Benign Forms.- References.- Traumatic Brain Swelling and Brain Edema.- Diagnosis and Pathogenesis.- 1. Traumatic Brain Swelling.- 1.1. Diagnosis.- 1.2. Pathogenesis.- 2. Traumatic Brain Edema.- 2.1. Diagnosis.- 2.2. Pathogenesis.- 2.2.1. Vasogenic Brain Edema.- 2.2.2. Cytotoxic Brain Edema.- 3. Mediators.- Frequency and Temporal Development.- 1. Frequency.- 2. Temporal Development.- Intracranial Pressure.- Management.- 1. Brain Swelling.- 1.1. Basic Principles.- 1.2. Hyperventilation.- 1.3. Buffering of Brain Tissue Acidosis.- 2. Brain Edema.- 2.1. Removal of Mass Lesion.- 2.2. Repair of the Defective BBB.- 2.3. Improvement of Microcirculation.- 2.4. Control of Mediators.- 2.5. Support of Edema Clearance Rate.- 3. Intracranial Hypertension.- 3.1. Hyperosmotic Solutions.- 3.2. Loop Diuretics.- 3.3. Barbiturates.- Outcome.- 1. Early Outcome.- 2. Follow-up.- References.- Posttraumatic Intracerebral Hematomas.- Definition.- Incidence.- Etiology and Pathogenetic Mechanism.- Biomechanics.- Location.- Clinical Manifestations.- Localizing Signs.- Differential Diagnosis.- Intracerebral Hematomas Concerning Their Appearance in Time.- Intracerebral Bleeding in Children.- Paraclinical Investigations.- Radiography of the Skull.- Pneumoencephalography, Ventriculography.- Cerebral Angiography.- Isotope Scintigraphy.- Echoencephalography.- CT and MRI.- Clinicopathological Correlation.- Predicting Outcome with CT and MRI.- Treatment.- How to Do It.- References.- Posttraumatic Cerebellar Contusions and Hematomas.- Cerebellar Contusions.- Incidence, Distribution of Age and Sex.- Clinical Signs and Symptoms.- Diagnosis.- Differential Diagnosis.- Posterior Fossa Hematomas.- Epidural Hematomas.- Age and Sex Distribution Location.- Etiology.- Pathological Effect.- Acute Epidural Hematoma.- Subacute and Chronic Hematomas.- Accompanying Lesions.- Clivus Extradural Hematoma.- Diagnosis.- Treatment.- Mortality.- Subdural Hematomas.- Incidence.- Pathology.- Diagnosis.- Treatment.- Mortality.- Intracerebellar Hematomas.- Incidence.- Signs, Symptoms, Diagnosis.- Surgical Treatment.- Results.- Conservative Treatment.- Subtentorial Subdural Hygroma.- Incidence.- Signs, Symptoms, Diagnosis.- Treatment.- Results.- Depressed Fractures.- How to Do It.- References.- Early Dynamic Evolution of Cerebral Contusions and Lacerations. Clinical and Radiological Findings.- Definition.- Radiological Findings.- Correlation of Clinical Manifestation and CT-findings.- Type of Lesions.- Time of Investigation.- Size of Contusions.- Location of Contusions.- Multiple Contusions, Accompanying Lesions.- State of Consciousness.- Enlargement of Contusions on Repeat Scan.- Dynamics of Cerebral Contusions.- Early CT scans.- Temporal Course.- Intracerebral Hematoma.- Frequency.- Secondary Delayed Intracerebral Hematoma.- Treatment.- Prognosis.- Mortality.- Manifestations.- Probability.- Overall Mortality.- Summary.- References.- Evoked Potentials in Head Injury.- Anatomical and Neurophysiological Considerations.- Somatosensory Evoked Potentials.- Visual Evoked Response.- Auditory Evoked Responses.- Prognostic Value of Evoked Potentials in Severe Head Injury.- Patients and Methods.- Results.- Discussion.- Conclusion.- Auditory Evoked Responses in Non-severe Head Injury.- Brain Death.- Patients and Methods.- Supratentorial Lesions.- Infratentorial Lesions.- Discussion.- Reliability of Evoked Potentials.- Conclusion.- How to Do It.- References.

Differentiation of oxytalan fibres from elastic fibres with reagents for detection of magnesium

Elastic fibres in various human and animal tissues revealed positive results with reagents for the detection of magnesium. By contrast, no Mg could be detected in oxytalan fibres or in zonular fibres of the ciliary body, which are composed of microfibrils not containing elastin. Mg is therefore concluded to be associated with the elastin core of elastic fibres. Its antagonism to calcium is speculated to play a protective role in maintaining the extensibility of elastin.

Acute hydrocephalus in infectious spinal disorder

Two patients with infectious spinal disorders and increased intracranial pressure are described. One patient with spinal empyema lapsed into coma but improved after external ventricular drainage to relieve increased intracranial pressure. The second patient, who had a severe wound infection after repeated operative stabilization of a cervical spine fracture, developed increased intracranial pressure and subsequent hydrocephalus 6 months after the trauma. The pathogenesis of hydrocephalus in infectious spinal disorder is discussed.