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Organic personality disorder (OPD) or secondary personality change, is a condition described in the ICD-10 and ICD-11 respectively. It is characterized by a significant personality change featuring abnormal behavior due to an underlying traumatic brain injury or another pathophysiological medical condition affecting the brain.
A lesion affecting one side of the temporal lobe may cause damage to the inferior optic radiations (known as the temporal pathway or Meyer's loop) which can lead to superior quadrantanopia on the contralateral side of both eyes (colloquially referred to as "pie in the sky"); if the superior optic radiations (parietal pathway) are lesioned, the ...
This is a shortened version of the sixth chapter of the ICD-9: Diseases of the Nervous System and Sense Organs. It covers ICD codes 320 to 389. The full chapter can be found on pages 215 to 258 of Volume 1, which contains all (sub)categories of the ICD-9. Volume 2 is an alphabetical index of Volume 1.
The most frequent cause of the syndrome is brain damage to the frontal lobe. Brain damage leading to the dysexecutive pattern of symptoms can result from physical trauma such as a blow to the head or a stroke [6] or other internal trauma. It is important to note that frontal lobe damage is not the only cause of the syndrome.
Potential organic explanations that have been investigated but ruled out include ear problems, temporal lobe seizure, nerve dysfunction, or specific genetic changes. [2] Potential risk factors include psychological stress. [2] It is classified as a sleep disorder or headache disorder. [2] [5] People often go undiagnosed. [5]
The associated autobiographical memory impairment is, however, a more puzzling consequence of medial temporal lobe pathology on this theory. It could be that epileptiform activity originating in the medial temporal lobe has the potential to disrupt the distributed neocortical traces required to maintain detailed autobiographical memories.
In 1825, Bouchet and Cazauvieilh described palpable firmness and atrophy of the uncus and medial temporal lobe of brains from epileptic and non-epileptic individuals. [4]: 565 In 1880, Wilhelm Sommer investigated 90 brains and described the classical Ammon's horn sclerosis pattern, severe neuronal cell loss in hippocampal subfield cornum Ammonis 1 (CA1) and some neuronal cell loss in ...
] The disorder is primarily caused by thrombotic and embolic strokes, which cause a deficiency of oxygen in the brain. As a result, bilateral lesions may form in the junctions between the frontal lobe and temporal lobe , the parietal lobe and cortical lobe, or the subcortical region of the brain.