Temporal trauma

Dementias due to trauma usually do not progress in this manner. The injury damages the brain and causes dementia, but further deterioration does not occur. In contrast, a few dementias can be rapidly progressive. This includes most dementias due to infection (although syphilis and AlDS-related dementias are usually slowly progressive) as well as Pick s disease, a dementia associated with a relatively early age of onset, characterized by massive degeneration of frontal and temporal lobe tissue. 

The medial and caudal portions of the midbody of the CC contain interhemispheric projections from the auditory cortices, posterior cingulate, retrosplenial cortex, and insula, and somatosensory and visual cortices to a lesser extent. It also includes connections from the inferior parietal lobe to the contralateral superior temporal sulcus, cingulate, and parahippocampal gyrus (Pandya and Seltzer, 1986). Several of the regions with interhemispheric projections through the medial and caudal portions of the midbody of the CC are involved in the processing of emotional stimuli and various memory functions—core disturbances frequently observed in children with a history of early trauma. 

Historically, lesions (often due to accident or tumor), trauma history, and findings on neurological exam or neuropsychological testing have furnished evidence regarding localization. Two regions have most consistently been implicated the prefrontal cortex and temporal lobe. 

This syndrome has similarities to the paradoxical reaction seen with barbiturates or BZDs, as well as epileptoid syndromes, including temporal lobe seizures and intermittent explosive disorder. Brain injury from trauma or encephalitis may also predispose some to an abnormally excessive response to even small amounts of alcohol. 

Tenderness of the branches of the external carotid artery (occipital, facial, superficial temporal) points towards giant cell arteritis. Tenderness of the common carotid artery in the neck can occur in acute carotid occlusion but is more Ukely to be a sign of dissection, or arteritis. Absence of several neck and arm pulses in a young person occurs in Takayasu s arteritis (Ch. 6). Delayed or absent leg pulses suggest coarctation of the aorta or, much more commonly, peripheral vascular disease. Other causes of widespread disease of the aortic arch are atheroma, giant cell arteritis, syphihs, subintimal fibrosis, arterial dissection and trauma. 

Head Soft tissue injury Tender, thickened, or pulseless temporal artery Obliteration of flow through the trochlear artery with compression of the preauricular or supraorbital vessels Anhidrosis Tongue laceration Head trauma Temporal arteritis ICA occlusion or severe stenosis with retrograde ophthalmic flow CCA dissection with damage to sympathetic fibers or brainstem stroke with interruption of sympathetic tract Consider seizure as the cause of the neurologic deterioration... 

Violent offenders in prison have low cortical brain blood flow and hypometabolism in nondominant frontal and temporal lobes, when compared to control subjects. Others have abnormalities in prefrontal regions. Some criminals have metabolic diseases, infections, tumors, malnutrition, poisons, trauma, or take drugs. Many have psychiatric problems, are poor, come from broken homes, or have suffered social ostracism that leads to resentment and hostility. 

Hearing loss may result from physical trauma, such as a fracture of the temporal bone that lies just behind the ear or a puncture of the eardrum. These injuries typically heal on their own, and in most cases, the hearing loss is temporary. 

For the purpose of diagnosing cranial dysfunctions, the osteopathic physician must inquire about trauma and birth history. It is often surprising how widely varied symptoms are temporally associated with physical trauma and associated palpable tissue changes. 

Intracranial, e.g. space occupying lesion, trauma, infection, inflammation, temporal lobe epilepsy... 

Symptomology induced after bTBI is likely dependent on secondary effects of blast trauma. After exposme to blast overpressure, extensive tissue damage initiates nemo-inflammation and neuronal cell loss. To combat such effects, biochemical processes are activated to mitigate neuroinflammation, promote cell survival, and enhance proliferation. Because of their anatomic locations, the medial temporal lobe structures are extremely vulnerable to impacts of blast overpressure. Therefore, studies of histological and biochemical changes in these areas will help to reveal mechanisms underlying the prolonged... 

Perdiki M, Farooque M, Holtz A (1998) Expression of endothelial barrier antigen immunoreactivity in blood vessels following compression trauma to rat spinal cord. Temporal evolution and relation to the degree of the impact. Acta Neuropathol 96 8-12... 

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