Traumatic Spreading Depression Syndrome

Abstract

From 1476 hospital admissions with head injury, 37 patients were selected on the basis of distinctive clinical features which appeared to share a single and benign aetiology. In head injuries of this type, transient neurological disorders resulted from trivial or rather mild head injuries. These disorders, which included headache, nausea and vomiting, pallor, somnolence, irritability and restlessness, stupor, hemiparesis and aphasia, appeared after a lucid interval which was usually less than two hours; then the patient either recovered, or went on to develop convulsive attacks. Recovery without convulsions was usual in children and adolescents; convulsions occurred both in infants and younger children. The symptoms were not attributable to cerebral compression but were probably due to a self-limiting cortical phenomenon. It appears that convulsive attacks occurring within a few hours of this type of head injury may not be significant as precursors of post-traumatic epilepsy. It is suggested that there is a close relation between the convulsive attacks and the non-convulsive symptoms seen in this type of injury and that both are based on a common process which has the characteristics of the spreading depression of Leão. This type of head injury should be classified as a distinct clinical entity, in which no surgical treatment is required and the prognosis is good.

The young brain and concussion: Imaging as a biomarker for diagnosis and prognosis

“…Although the pathogenesis of post-traumatic headache is yet to be defined, current theories include; (i) a similar process to migraine (Packard and Ham, 1997) but provoked by damage to the trigemino-vascular system (viz., structures such as the circle of Willis, extracranial cephalic blood vessels, basilar artery, vessels of the dura and pia matter that receive innervation from the trigeminal ganglion) (Sakas and Whitwell, 1997); (ii) ‘fragility’ of the cranium in children whereby the skull is more malleable and dural damage thus more likely because the dura is tightly adherent to the cranium (Sakas and Whitwell, 1997); (iii) tearing of extracranial dural afferents (Levy et al, 2009; Zhang et al, 2010b); (iv) increased propensity to cortical spreading depression (Ayata, ; Leao, 1947; Oka et al, 1977; Sakas and Whitwell, 1997); and (iv) involvement of upper cervical trauma that affects the area of spinal nerves C1–C3 (Grgic, 2007). Of note whiplash associated disorder (WAD) patients report similar symptoms to those observed in mTBI including headache, cognitive disturbances such as impaired memory, poor concentration, mental fatigue, sleep impairment, sensory sensitivity, visual disturbances and vertigo, possibly linked to perfusion abnormalities (Linnman et al, 2009; Otte et al, 1998), but see also Evans (Evans, 2010).…”