Traumatic Intracerebral Hemorrhage Research Articles

Palilalia after traumatic intracerebral hemorrhage (a case report)

This report refers to the 4-year long diachronic observation of a case of acquired palilalia caused by intracerebral hemorrhage due to head trauma. It was approximately 7 months after his trauma that the patient began exhibiting striking palilalia behavior along with echolalia and a global deterioration of mental activities. Palilalia was still present 2 years later in spite of some degree of general improvement. A peculiarity of this patient was that palilalia occurred in response to relatively complex questions whereas it was hardly present in response to simpler ones. Contrary to observations made in other cases of palilalia, instrumental sound analyses revealed that articulation speed, although somewhat fast, did not keep increasing as palilalic utterances went on, and that vocal intensity remained within normal ranges, i.e. did not decrease from the onset of a given palilalic utterance to its end. CT-scan and MRI imaging showed the brain lesion to be almost restricted to the cortex of the right frontal convexity and its underlying white matter. It is suggested that palilalia is, in certain cases caused by a disturbance of higher motor speech control mechanisms.

Delayed Traumatic Intracerebral Hemorrhage

Delayed traumatic intracerebral hemorrhage refers to the appearance of hemorrhage (usually within 48 hours of head trauma) in areas of the brain that were normal in appearance or nearly so on the CT scan taken shortly after injury. Neurologic deterioration is common but is not universally the rule. The frequency of delayed traumatic intracerebral hemorrhage is variable but is reported to occur in 1% to 8% of patients with severe head injury. The pathogenesis is multifactorial and may result from one or more of the following: coagulation abnormalities, necrosis of blood vessels in areas of brain injury, dysautoregulation, and release of tamponade effect with evacuation of extra-axial hematomas. Outcome is poor, and most series report a mortality of 50% or higher.

TWO CASES OF TRANSCUTANEOUS REMOVAL OF IVH CATHETER FARGMENTS IN THE RIGHT SIDE CIRCULATORY SYSTEM

In this paper two cases that IVH catheter fragments in the right side circulatory system were transcutaneously removed are reported. Case 1 is an 18-year-old man who was hospitalized for traumatic intracerebral hemorrhage. He pulled out a IVH catheter indwelling in the right subclavian vein by himself, when the catheter was broken and the fragment of it entered through the supra vena cava into right side circulatory system. Case 2 is a 47-year-old woman hospitalizing for cerebral infarction. She also pulled out the catheter by herself. In both cases, catheter fragments were transcutaneously removed by using a basket catheter via the right femoral vein.It is probable that IVH catheter frequently entered into right side circulatory system in daily medical care. In Japan, only 51 cases that IVH catheter fragments in the right side circulatory system were transcutaneously removed have been reported. The most common mechanism for loss of the catheter was iatrogenic (14 cases), followed by spontaneous break by patients (8 cases). In the all 51 cases the mean age was 47 years and the male-to-female ratio was 2:1, versus 58 years and 5:1 in spontaneous break cases. It can be said that spontaneous break commonly occurred in aged men. In Japan snare loop catheters via the right femoral vein are most commonly used for removals of fragments.

Follow-up of computerized tomography findings in traumatic intracerebral hematomas

CT controls and follow-ups were conducted in 27 patients who had suffered traumatic intracerebral hemorrhage. Only such patients were included who did not die before the 14th day after the trauma and in whom operation did not become necessary during this period. In these patients the volume of the hematoma and perifocal edema was determined via CT and clinical parameters were measured or recorded such as state of consciousness at the time of admission and the neurological outcome. It was found that the hematoma had attained its maximum size on about the fourth posttraumatic day. However, even the size of the freshly CT-detected hematoma shows good correlation to the outcome of the patients. Examination of the edema size points to the existence of two groups: one with only slight edema formation in the early posttraumatic stage, and another with an immediate considerable edematic border. From approximately the 8th posttraumatic day the hematoma/edema ratio is approximately the same in both groups, namely, 0.3. Anisocoria, or inequality of the pupils, occurred early in patients with an average hematoma volume of 37.7 cm. Of these, none left the hospital without neurologic signs, so that anisocoria must be considered as a prognostically unfavorable sign.

Delayed traumatic intracerebral hemorrhage in children

This report describes delayed traumatic intracerebral hemorrhage in five pediatric patients. The phenomenon has been considered extremely rare in children. Cranial computed tomography preceding and following the ictal hemorrhages provides the best documentation of this phenomenon and suggests some insights into the pathogenic mechanism.

Head and neck injuries.

A survey of cranial, intracranial and neck injuries caused by blunt trauma to the head is presented. The different types of fractures to the skull (impression fractures, linear fractures and ring fractures) are discussed as well as the injury mechanisms. Brain injuries are discussed under the heading of focal brain injury (i.e. brain laceration, cortical contusion, hemorrhages of the meninges and traumatic intracerebral hemorrhages). The different types of neck injuries, including atlanto-occipital dislocation, are listed and the stability of the different fractures are discussed. Facial injury is not included.

Reversible Causes of Mental Impairment

To the Editor.— The article entitled Senility Reconsidered: Treatment Possibilities for Mental in the Elderly by the Task Force sponsored by the National Institute on Aging (1980;244:259) is informative and helpful. There are, however, inaccuracies that have crept into it, especially in the table entitled Reversible Causes of Mental Impairment on p 261. The first one is Cushing's syndrome, which is denoted as a cause of dementia. In fact, Cushing's syndrome produces acute psychosis and confusional states more frequently when drug induced. Cushing's disease, itself, produces an organic brain syndrome or depression-like syndrome with about 10% making suicidal attempts. 1 Second, traumatic intracerebral hemorrhage is known to cause an acute organic brain syndrome (OBS), and during the recovery phase, varying degrees of neurological and intellectual impairment. 2(p1065-1078) Therefore, it should be denoted as a cause of both dementia and delirium. Epidural hematoma can cause both acute OBS and dementia.

Delayed traumatic intracerebral haemorrhage.

Twenty-one out of 7,866 head injuries were complicated by the development of delayed intracerebral haematomata. The age distribution of patients with this condition closely resembled that of patients with subdural haematomata and differed sharply from patients with extradural haemorrhage. This finding, combined with the fact that the two conditions often coexisted, suggests the possibility of similar aetiological factors operating in their production. The injury producing the lesion was often minor and the larger haematomata appeared to be associated with longer `asymptomatic' intervals. The neurological deterioration was in most instances clearly the result of an increase in intracranial pressure. When possible, angiography followed by definitive craniotomy was the most satisfactory method of management and multiple burr holes even when combined with needling of the hemisphere yielded unsatisfactory results. The distribution of lesions tended to confirm their traumatic origin. On no occasion was there a vascular abnormality to account for the haemorrhage and, despite the fact that the ages of most patients were in the seventh and eighth decades, the incidence of degenerative vascular disease was small. Contusional injury causes a local failure of the mechanisms that regulate cerebral blood flow. Hypoxia, hypercapnia, and venous congestion produce cerebral hyperaemia which encourages gradual haematoma formation particularly at the sites of injury. This explains not only the situation of the lesions but also the latency between the trauma and their development.

DELAYED TRAUMATIC INTRACEREBRAL HEMORRHAGE

SUMMARYA case of delayed traumatic intracerebral hemorrhage (Bollinger's “Spät‐apoplexie”) is discussed. A 2 1/2‐years old boy falls from some steps on to a road, strikes his head, develops a hematoma in the upper part, and has signs of concussion and fracture of the skull. Signs of right‐sided hemiparesis thereafter. Sudden death 23 months later after he had felt out of sorts for 3 weeks. A post‐mortem examination showed cyst formation in the brain stem (medulla oblongata) bounded by glia scar tissue containing some old blood pigment. A massive recent hemorrhage into and about the cyst. This case seems to meet all the requirements demanded for the diagnosis of “Spät‐apoplexie”.The literature of the subject is dealt with in full, particularly with reference to the genesis of these hemorrhages and the requirements to be fulfilled if this diagnosis is to be accepted as definite.

Delayed traumatic intracerebral haemorrhage (Traumatische Spätapoplexie).

Australian and New Zealand Journal of SurgeryVolume 23, Issue 4 p. 300-307 DELAYED TRAUMATIC INTRACEREBRAL HAEMORRHAGE (TRAUMATISCHE SPÄTAPOPLEXIE) Kenneth G. Jamieson, Kenneth G. Jamieson Alfred Hospital, MelbourneSearch for more papers by this author Kenneth G. Jamieson, Kenneth G. Jamieson Alfred Hospital, MelbourneSearch for more papers by this author First published: May 1954 https://doi.org/10.1111/j.1445-2197.1954.tb05059.xCitations: 6AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume23, Issue4May 1954Pages 300-307 RelatedInformation

The neurosurgical treatment of spontaneous intracerebral hemorrhage simulating the common stroke.

Article1 October 1952THE NEUROSURGICAL TREATMENT OF SPONTANEOUS INTRACEREBRAL HEMORRHAGE SIMULATING THE COMMON STROKEMICHAEL SCOTT, M.D.MICHAEL SCOTT, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-37-4-751 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe appalling mortality from massive hemorrhage into the cerebrum is common knowledge. The Metropolitan Life Insurance Company in 1946 listed this condition as fourth in the cause of death.1This fact has encouraged neurosurgeons to attempt removal of the clot and control of hemorrhage in selected cases. The results in small series as reported by various neurosurgeons have been encouraging.2-17 This has stimulated the author to operate on a group of carefully selected cases, and then gradually to extend the procedure in some instances to those with grave prognosis with the hope that life might be saved.The first step...Bibliography1. Bulletin, Metropolitan Life Insurance Company, April 29, 1948. Google Scholar2. Cushing H: Blood pressure reaction of acute cerebral compression, Am. J. M. Sc. 125: 1017, 1903. CrossrefGoogle Scholar3. RussellSargent HEP: Apoplectiform cerebral hemorrhage: operation: evacuation of blood: slow improvement, Proc. Roy. Soc. Med. (Sect. Neurol.) 2: 44, 1909. Google Scholar4. Bagley C: Spontaneous cerebral hematomas: discussion of four types with surgical consideration, Arch. Neurol. and Psychiat. 27: 1133 (May) 1932. CrossrefGoogle Scholar5. Penfield W: The operative treatment of spontaneous intracerebral hemorrhage, Canad. M. A. J. 28: 369, 1933. MedlineGoogle Scholar6. CraigAdson WMAW: Spontaneous intracerebral hemorrhage: etiology and surgical treatment, Arch. Neurol. and Psychiat. 35: 701 (April) 1936. CrossrefGoogle Scholar7. FurlowCarrWattenberg LTADC: Spontaneous cerebral hemorrhage: the surgical treatment of selected cases, Surgery 9: 758, 1941. Google Scholar8. Pilcher C: Subcortical hematoma, Arch. Neurol. and Psychiat. 46: 416 (Sept.) 1941. CrossrefGoogle Scholar9. Hamby WR: Gross intracerebral hematomas, New York State J. Med. 45: 866, 1945. Google Scholar10. RowbothamOgilvie GEAG: Chronic intracerebral haematomata: their pathology, diagnosis and treatment, British M. J. 1: 146, 1945. CrossrefMedlineGoogle Scholar11. Scott M: Surgical treatment of spontaneous non-traumatic hematomas, J. A. M. A. 130: 845, 1946. CrossrefMedlineGoogle Scholar12. GrossWechsler SWIS: Arteriography in cerebral vascular accidents, J. A. M. A. 39: 502, 1949. Google Scholar13. Sirois J: Surgical treatment of cerebral hemorrhage, Laval méd. 15: 457-466 (April) 1950. MedlineGoogle Scholar14. GrantAustin FCGM: The surgical treatment of spontaneous and traumatic intracerebral hemorrhage, Am. J. M. Sc. 219: 237, 1950. CrossrefMedlineGoogle Scholar15. Ferey D: The surgical therapy of spontaneous cerebral hemorrhage, Concours Med. 72: 1235-1236 (April) 1950. MedlineGoogle Scholar16. LusignanCross FWGO: Intracranial angiography in treatment of cerebrovascular accidents, California Med. 73: 240, 1950. MedlineGoogle Scholar17. GurdjianWebster ESJE: Cerebrovascular accidents, Arch. Surg. 62: 724, 1951. CrossrefGoogle Scholar18. Zimmerman HJ: Cerebral apoplexy, New York State J. Med. 49: 2153, 1949. MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Philadelphia, Pennsylvania*Presented at the Thirty-third Annual Session of the American College of Physicians, Cleveland, Ohio, April 25, 1952. (Presented in part before the Section on Neurology, American Medical Association Convention, June, 1951.)From the Department of Neurosurgery, Temple University Hospital and Medical School, and the Jewish Hospital, Philadelphia, Pennsylvania. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byBibliographyDiagnosis and Treatment of Facial Pain 1 October 1952Volume 37, Issue 4Page: 751-754KeywordsHemorrhageHemorrhagic strokeMortalityNeurologyNeurosurgeryStroke ePublished: 1 December 2008 Issue Published: 1 October 1952 PDF downloadLoading ...

TRAUMATIC HEMORRHAGE OF THE INTERNAL CAPSULE

The existence of traumatic intracerebral hemorrhage is generally conceded, yet the finding of a blood clot in the region of the internal capsule at autopsy is ordinarily accepted as positive evidence that the lesion represents a spontaneous hemorrhage. If signs of trauma are present, the temptation is to consider such trauma as secondary to the unconsciousness and fall resulting from the apoplexy. Courville and Blomquist, 1 in a discussion of traumatic intracranial hemorrhage, presented 38 instances occurring among 439 cases of fatal craniocerebral injuries. Only 7 cases of traumatic hemorrhage into the ganglionic region (external capsule and lenticular nucleus) were included. They stated: . . . . No example of gross hemorrhage into the posterior limb of the internal capsule, such as appears spontaneously in cases of hypertension or arteriosclerosis, has been observed by us. It may, therefore, be safely assumed that gross hemorrhage in this region is not the result of trauma, for,

DELAYED TRAUMATIC INTRACEREBRAL HEMORRHAGE

The syndrome of delayed traumatic intracerebral hemorrhage, ortraumatische Spatapoplexie, was first described in 1891 by Bollinger,1who stated that even a mild injury to the head might be followed by the development of foci of softening in the cerebrum or medulla, alterations in the blood vessel walls and intracranial hemorrhage. The syndrome has not aroused a great deal of interest during the fifty years that have elapsed, but there have been occasional reports of the onset of hemiplegia or other evidences of cerebral damage days, or even weeks, after what appeared to have been a slight injury to the head. In spite of some controversy, both with respect to the exact mechanism of the hemorrhage and its relationship to preexisting vascular disease, delayed traumatic apoplexy has come to be regarded as a disease entity. The symptoms may resemble those of ordinary cerebral hemorrhage, embolism or thrombosis or those

Delayed Traumatic Intracerebral Hemorrhage.

CURRENT LITERATURE: III. SYMBOLIC NEUROLOGY PSYCHOLOGY, PSYCHOANALYSIS, NEUROSES, PSYCHONEUROSES, PSYCHOSES: PDF Only

TRAUMATIC INTRACEREBRAL HEMORRHAGE

To those familiar with the effects of trauma on the brain and its envelopes, the importance of the mechanism by which the injury is produced in interpreting the pathologic picture is quite evident. Each type of injury is now known to produce its own characteristic train of lesions. The appalling increase in craniocerebral injuries consequent to traffic accidents has brought into prominence a number of effects which appear to be the direct consequence of striking of a stationary or relatively stationary object by the head in motion. These effects have been long described as coup-contrecoup effects. One of the lesions belonging to this group which to date has not been given any selective attention is gross hemorrhage into the cerebral substance—traumatic intracerebral hemorrhage. In 1891, Bollinger described 4 cases in which death occurred rather suddenly from twelve to fifty days after an injury to the head and proved at autopsy

Delayed Traumatic Intracerebral Haemorrhage

Delayed Traumatic Intracerebral Haemorrhage