tics/hemorrhage

The etiology of tic disorder includes idiopathic, postencephalitic, head injury, carbon monoxide poisoning, stroke, and developmental syndromes. We report a case of new-onset complex motor and vocal tics that began after hemorrhage of an arteriovenous malformation located in the left frontal lobe.

BACKGROUND While efforts have been made to document short-term outcomes following poor grade aneurysmal subarachnoid hemorrhage (aSAH), no data exist concerning the degree of delayed improvement in neurological function. Here we assess cognitive function, level of independence, and quality of life

BACKGROUND Cognitive impairment is widely considered the main cause of disability and handicap after subarachnoid hemorrhage (SAH). The impact of depression on recovery after SAH remains poorly defined. We sought to determine the frequency of post-SAH depression, identify risk factors for its

Background: Severe traumatic haemorrhage is the leading cause of death in young adults. Trauma Induced Coagulopathy is a complex and multifactorial phenomenon associated with severe traumatic haemorrhage. Fibrinogen is one of the first

Hemorrhage remains one of the leading causes of trauma-related deaths. Uncontrolled diffuse microvascular bleeding in the course of initial care is common, potentially resulting in exsanguination. Early and aggressive hemostatic intervention increases survival and reduces the incidence of massive

Even nowadays and at specialized centers, one of the leading causes of death is exsanguination. Trauma-induced coagulopathy (TIC) occuring with massive blood loss primarily results from loss of coagualtion factors and platelets and is aggravated by hemodilution. In addition, hyperfibrinolysis,

OBJECTIVE Subarachnoid haemorrhage (SAH) accounts for 5-10% of all strokes, strikes at a mean age of 50 years and results in a pattern of deficits similar to that of traumatic brain injury. This study is an extension of a previous study which described outcome at discharge from inpatient

BACKGROUND Severe traumatic injury and haemorrhagic shock are frequently associated with disruptions of coagulation function (such as trauma-induced coagulopathy TIC) and activation of inflammatory cascades. These pathologies may be exacerbated by current standard of care resuscitation protocols.

Uncontrolled hemorrhage and subsequent trauma-induced coagulopathy (TIC) are still the principle causes for preventable death after trauma and early detection and aggressive management have been associated with reduced mortality. Despite increasing knowledge about trauma resuscitation, best practice

Death from uncontrolled haemorrhage is one of the leading causes of trauma-related mortality and is potentially preventable. Advances in understanding the mechanisms of trauma-induced coagulopathy (TIC) have focused attention on the role of blood products and procoagulants in mitigating the sequelae

Trauma-induced coagulopathy (TIC) is present soon after injury and is associated with increased transfusion requirements and worse outcomes. The pathophysiological mechanisms, which result in the widespread derangements of hemostasis following major trauma hemorrhage, are as yet not fully defined.