Concussion Syndrome Research Articles

Head Injury and Post Concussive Syndrome

Head Injury and Post Concussive Syndrome

Minor Traumatic Brain Injury: A Review of Physiogenesis and Psychogenesis.

Mild Traumatic Brain Injury (TBI) has a well defined neuropathology. The natural history of recovery is well understood. The appropriate somatic and psychological treatments are known. Nevertheless, a subset of patients do not recover and may even worsen with time-the persistent post concussive syndrome (PPCS). They are frequently involved in litigation. The risk factors for PPCS are known, and management strategies are available. There is a great risk of inappropriately attributing PPCS to direct neurological injury that cannot be supported by any objective measure. The symptoms and the cognitive deficits in these patients, even when defined by ostensibly objective testing, have no specificity. Accurately distinguishing among the many possible diagnoses in these patients is critical to avoid iatrogenic disability and incorrect treatment.

Not so minorhead injuries?

Sue Jackson offers an analysis of the incidence and severity of Post Concussion Syndrome in mild head injured patients

Biochemical and biophysical changes in guinea pigs after acute head injury.

Animal experiments were set up mainly to derive additional diagnostic data from the study of biochemical changes after acute head injury. In standardized experiments guinea pigs were subjected in groups of 20 to three identical head injuries, each of either 1.0 J or 1.5 J intensity. The trauma was likely to result in a concussion or contusion syndrome similar to that found in man; 40 animals served as controls. During the 60 min after injury observation and measurement of body functions did not reveal signs of a shock-like condition or hypoxaemia in the traumatized animals compared with control animals. Superficial anaesthesia probably did not influence the findings. Temperature and respiration were altered significantly in all the animals receiving head injuries. Blood gas analysis showed a decrease of standard bicarbonate only after the 1.5 J injury but even though hypoxaemia was not present 2,3-diphosphoglycerate values and P50 increased, compared with the control animals. The fall of plasma lipid concentrations reported probably had to be seen as a sympathomimetic effect of the minor (1.0 J) trauma. Of special significance was the increased activity of malate dehydrogenase and aldolase, found only in the blood of severely traumatized animals, as this could serve as an early diagnostic aid for evaluating head injuries.

Etiology and treatment of post concussion syndrome.

Etiology and treatment of post concussion syndrome.

SPINAL CORD INJURIES IN WARFARE; SYMPTOMATOLOGY AND DIAGNOSIS

Introductory Remarks 471 Injuries (Direct and Indirect) 473 1. Pathology 2. General Symptomatology Muscle Tone and Reflex Action Inferior Cervical Syndrome Contractures Cerebrospinal Hypertension Syndrome State of Sensibility State of Bladder 3. Complete Cord Section Symptomatology Suture of the Divided Cord Electrical Reactions Cauda Equina Injuries 482 Syndrome of Cauda Equina Concussion 483 1. Direct Concussion Mechanism and Pathology Cervical Concussion Syndrome from Vertebral Dislocation Cervical Concussion Syndromes from Injury to Surrounding Soft Parts Spinal Hemiplegia with Injury to XI, Cranial Nerve 2. Indirect Concussion Effects of High Explosives Mechanism State of Cerebrospinal Fluid Asthenic Syndrome Sphincter Disturbances Complications and Other Conditions 492 Trophic Lesions Camptocormia Operative Indications and Prognosis 493 Introduction The exceptional opportunities which the war has offered for observation of injuries to the nervous system has resulted in a voluminous literature on the subject. It appears that brain and peripheral nerve injuries have been relatively more numerous