SUMMARY

Other demographic studies of epilepsy have revealed mean annual incidence rates ranging from 17/100,000 (Sato, 1964) to 70/100,000 (Pond et al., 1960) and prevalence rates from 2.8/S, OOO to as high as 15/1,000. Comprehensive review of their methods indicates that, although rates may indeed differ among different populations, a major problem is the wide variation in the completeness of case ascertainment and the definitions of epilepsy used.

The epidemiology of epilepsy in Rochester, Minnesota, 1935 through 1967.

V ASCULAR malformations of the central nervous system have been known for at least three hundred years (Olivecrona and Ladenheim '57), hu t are still surrounded by considerable confusion and associated with a complex classification. Detailed morphologic studies of large numbers of cases are rare. Reviews of the many classifications can be found in the works of Evans and Courville '39, Noran '45, Olivecrona and Ladenheim '57, and Rayno r and Kingman '65. While the relationship of vascular malformations to vascular neoplasms is still less than completely clear (Raynor and Kingman '65), it seems relatively certain tha t arteriovenous malformations are true developmental malformations and not neoplasms (Wolf and Brock '35, Noran '45, Manuelidis '50, Olivecrona and Ladenheim '57, Zttlch '57, Russell and Rubinstein '59, Bailey '61, Kaplan et al. '61, McCormick and Nofzinger '66). Ztilch '57 states tha t the distinction between vascular malformations and vascular neoplasms is difficult, and distinguishes between the two groups on the basis of the autonomous growth seen in the la t ter group. However , as Russell and Rubinstein '59 and others have noted, "in common with the t rue neoplasms, it is clear tha t some [malformations] at least are not static bu t grow and inflict progressive destruct ion on the adjacent bra in ." Noran '45 considered tha t the presence of brain parenchyma between the vessels of the angioma was of "pa ramoun t impor tance" in concluding tha t it is a malformat ion ra ther than a vascular neoplasm. Clearly, however, this does not hold for all malformations, most notably the cavernous angiomas. In spite of these difficulties, one considers the malformations to be distinct from the t rue

The Pathology of Vascular (“Arteriovenous”) Malformations

Of 153 patients presenting with acute transient amnesia, 114 fulfilled the proposed strict diagnostic criteria for transient global amnesia (TGA). The prognosis of this group was excellent with the exception of a small subgroup (7%), largely identifiable because of atypically brief or recurrent attacks, who developed epilepsy of temporal lobe type on follow up. Computerised tomography (CT) scans performed on 95 patients were normal, evidence for covert alcoholism was lacking and there was a familial incidence of approximately 2%. By contrast, the group of 39 patients who did not meet the criteria for TGA had a significantly worse prognosis with a high incidence of major vascular events. The groups could not be distinguished on the basis of behavioural characteristics during the attack. The following classification was proposed: 1) pure TGA--attacks fulfilling the strict criteria, and of more than one hour in duration which do not require detailed investigation, 2) probable epileptic amnesia--attacks of less than an hour or rapidly recurrent, 3) probable transient ischaemic amnesia, a minority of cases with additional focal neurological deficits during the attack.

https://jnnp.bmj.com/content/jnnp/53/10/834.full.pdf

Syndromes of transient amnesia: towards a classification. A study of 153 cases.

https://nmr.mgh.harvard.edu/~bradd/dickerson_neuropsychopharmacologyreviews_2009.pdf

The Episodic Memory System: Neurocircuitry and Disorders

Horizontal versus vertical associative memory concepts are denned. Vertical associative memory involves chunking: the specification of new (previously free) nodes to represent combinations of old (bound) nodes. Chunking is the basis of semantic memory, configuring in conditioning, and cognitive (as opposed to stimulus-response) learning. The cortex has the capacity for chunking, but the hippocampal (limbic) arousal system plays a critical role in this chunking process by differentiall y priming (partially activating) free, as opposed to bound, neurons. Binding a neuron produces negatively accelerated repression of its connections to the hippocampal arousal system, consolidating the memory by protecting the newly bound neuron from diffuse hippocampal input and thus retarding forgetting. Disruption of the hippocampal arousal system produces the amnesic syndrome of an inability to do new chunking (cognitive learning)—anterograde amnesia—and an inability to retrieve recently specified chunks—retrograde amnesia.

Chunking and Consolidation: A Theoretical Synthesis of Semantic Networks, Configuring in Conditioning, S-R versus Cognitive Learning, Normal Forgetting, the Amnesic Syndrome, and the Hippocampal Arousal System.

C M Fisher

Papers

Transient global amnesia.