Structural Causes of Stupor and Coma

2019 ◽  
pp. 93-124
Author(s):  
Jerome B. Posner ◽  
Clifford B. Saper ◽  
Nicholas D. Schiff ◽  
Jan Claassen
Keyword(s):  
Structural Lesion ◽  
Structural Injury ◽  
The Brain

Chapters 3 is the first of two chapters to discuss pathophysiology and specific causes of structural injury to the brain that result in defects of consciousness. It divides structural lesions causing coma into compressive and destructive lesions. It further indicates that lesions could be supratentorial, compressing, or destroying the diencephalon and upper midbrain, or infratentorial, directly affecting the pons and cerebellum. A physician attempting to determine the cause of coma resulting from a structural lesion must establish, first, the site of the lesion, determining whether the lesion is supratentorial or infratentorial, and, second, whether the lesion is causing its symptoms by compression or destruction or both.

Metabolic and Diffuse Encephalopathies: Disruption of the Internal Milieu

2019 ◽  
pp. 183-290
Author(s):  
Jerome B. Posner ◽  
Clifford B. Saper ◽  
Nicholas D. Schiff ◽  
Jan Claassen
Keyword(s):  
Metabolic Disease ◽  
Neurological Examination ◽  
Focal Lesions ◽  
Diagnostic Features ◽  
Brain Functions ◽  
Internal Milieu ◽  
Neurological Findings ◽  
Structural Lesion ◽  
The Brain ◽  
Metabolic Encephalopathies

Chapter 5 examines the broad range of metabolic causes of unconsciousness and the specific treatments they require. The main feature distinguishing diffuse or metabolic impairment of consciousness is that it is normally not associated with focal neurological findings that would suggest a structural lesion of the brain. However, there are some features of the neurological examination of patients with metabolic encephalopathies that can help to pinpoint the cause of the disturbance. In addition, there are some findings on examination that may appear to be due to focal lesions, but which can be due to diffuse or metabolic disease. The chapter first examines the diagnostic features of metabolic encephalopathies. It then looks at the internal metabolic milieu in which the brain functions normally. It also considers specific types of metabolic and diffuse disturbances of that internal milieu that can cause encephalopathy. Finally, it considers various endogenous and exogenous toxins that produce toxic encephalopathies.

scholarly journals Traumatic cerebral contusion: pathobiology and critical aspects

2013 ◽  
Vol 20 (2) ◽  
pp. 125-137
Author(s):  
Hernando Alvis-Miranda ◽  
Gabriel Alcala-Cerra ◽  
Luis Rafael Moscote-Salazar
Keyword(s):  
Traumatic Brain Injury ◽  
Developed Countries ◽  
Primary Lesion ◽  
Cerebral Contusion ◽  
Brain Contusion ◽  
Significant Percentage ◽  
Structural Lesion ◽  
Parenchymal Injury ◽  
The Brain ◽  
Critical Aspects

AbstractTraumatic brain injury is a major cause of mortality in developed countries. Cerebral parenchymal injury is evidenced by a significant percentage of patients. The most important structural lesion of the brain is the cerebral contusion, which is a complex and dynamic area, a result of the primary lesion and which is associated with ischemic and inflammatory phenomena that need to be known by the neurosurgeon. We present a review of the most important aspects of brain contusion.

Specific Causes of Structural Coma

2019 ◽  
pp. 125-182
Author(s):  
Jerome B. Posner ◽  
Clifford B. Saper ◽  
Nicholas D. Schiff ◽  
Jan Claassen
Keyword(s):  
Brain Injuries ◽  
Sinus Thrombosis ◽  
Traumatic Brain Injuries ◽  
Venous Sinus ◽  
Venous Sinus Thrombosis ◽  
Inflammatory Disorders ◽  
Basilar Occlusion ◽  
Structural Injury ◽  
The Brain

This chapter is the second of two chapters to discuss the pathophysiology and specific causes of structural injury to the brain that result in defects of consciousness. This chapter examines, in turn, the specific causes of supratentorial and infratentorial compressive and destructive lesions that cause coma. It also gives brief descriptions of the approach to treatment. Among the insults and injuries described are various hematomas, abscesses, empyema, tumors, infections, and, as well as infarctions, distal basilar occlusion, venous sinus thrombosis, vasculitis. Concussion and other traumatic brain injuries are described and discussed, as are vascular destructive and inflammatory disorders like basilar migraine, leukoencephalopathy syndrome, and myelinolysis.

Hereditary haemochromatosis

2010 ◽  
pp. 1673-1688
Author(s):  
William J. H. Griffiths ◽  
T. M. Cox
Keyword(s):  
Iron Homeostasis ◽  
Endocrine System ◽  
Genetic Syndromes ◽  
Iron Storage ◽  
Life Saving ◽  
Tissue Iron ◽  
Endocrine Organs ◽  
Structural Injury ◽  
The Brain ◽  
Prompt Diagnosis

Haemochromatosis is a hereditary disorder generally caused by inappropriate absorption of iron by the small intestine which leads to iron deposition in the viscera, endocrine organs, and other sites, causing structural injury and impaired function. The most common form is classical adult haemochromatosis, but juvenile and neonatal forms are recognized, and several other genetic syndromes associated with iron storage have been identified; these may rarely involve specific tissues selectively, such as the lens of the eye or basal ganglia of the brain, or a characteristic range of tissues including the liver, heart, and endocrine system. Early-onset (juvenile) haemochromatosis has a predilection for the heart, pituitary gonadotrophs and the pancreatic islet—thus myocardial disease (which may be fatal if untreated), hypogonadism and diabetes mellitus are prominent features. Prompt diagnosis and depletion of tissue iron by chelating agents—and venesection where possible—may be life-saving. Unravelling the molecular genetics of haemochromatosis is underpinning promising new therapies for disorders of iron homeostasis....

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